Mo Reda Mrcs

ANATOMY
SPINE & BACK MRCS Part B Notes by Mo
ANATOMY SPINE MO’s MRCS B NOTES (Previously called Reda’s Notes) 1

Typical cervical vertebrae
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY SPINE

Examiner will show you x-ray with fracture odontoid (note that the below XR is normal)
Other than the fracture, what are the abnormal signs in this radiograph?
1. Abnormal alignment (the distance between the dens and the lateral masses of c1 on both sides is not equal)
2. Prevertebral soft tissue swelling due to fracture edema
Ligaments attached to the odontoid process?

• Transverse Atlantal ligament
• Apical odontoid ligament
• Alar ligament
Type of Atlanto axial joint?

Synovial pivot

Ligaments between C1 and C2?
• Ant. atlanto axial ligament
• Post. atlanto axial ligament
• Transverse ligament
What is the first spinous process to be felt?

Spinous process of C7 (has a long spine = vertebra prominence)
Demonstrate it on the subject?
Why we cannot feel the upper spinous processes?

As they are short, bifid and attached to the nuchal ligament
Atypical cervical vertebrae and the atypical features?

• C1 (atlas): no body, no spine
• C2 (axis): body projects upwards to form the odontoid process,
thick spine
• C7 (vertebra prominence): very long spine, smaller foramen
transversum
How many vertebrae make the spinal column: How many spinal nerves?
• 7 cervical, 8 cervical
• 12 thoracic, 12 thoracic
• 5 lumbar, 5 lumbar
• 5 fused sacral, 5 sacral
• 3 fused coccygeal, 1 coccygeal

Lumbar and sacral vertebral column showing termination of spinal cord and continuation and termination of
dural/arachnoid sac. T2-weighted MR image in sagittal plane

Characteristics of lumbar vertebrae
Lumbar vertebrae have very large vertebral bodies, which are kidney-shaped. They lack the characteristic features
of other vertebrae, with no transverse foramina, costal facets, or bifid spinous processes.
However, like the cervical vertebrae, they have a triangular-shaped vertebral foramen. Their spinous processes are
shorter than those of thoracic vertebrae and do not extend inferiorly below the level of the vertebral body.

Structures passing through the intervertebral foramen?
• The root of each spinal nerve,
• Dorsal root ganglion,
• The spinal artery of the segmental artery
• Communicating veins between the internal
and external plexuses,
• Recurrent meningeal (sinuvertebral) nerves
• Transforaminal ligaments.
Level of the lumbar puncture?

L4/L5. (at the supracrestal line)
Layers to pass through?

• Skin, subcutaneus fat, fascia
• Supraspinous ligament
• Interspinous ligament
• Ligamentum flavum
• Epidural space
• Dura matter
• Arachnoid matter
• CSF

IV disc anatomy?
Internal nucleus pulposus surrounded by
fibrocartilagenous annulus fibrosus
Type of IV joint?
Secondary cartilaginous joint
Movement on lumbar vertebrae?

Flexion, extension, lateral flexion, axial rotation
Level of the spinal cord in newborn and adult?

L3 (at birth), L1/2(adult)
Contents of the spinal canal below L2?

Cauda equina
Location of the paravertebral venous plexus?

• Anterior external vertebral venous plexus, the small system around the vertebral bodies;
• Posterior external vertebral venous plexus, the extensive system around the vertebral processes;
• Anterior internal vertebral venous plexus, the system running the length of the vertebral canal anterior to the
dura
• Posterior internal vertebral venous plexus, the system running the length of the vertebral canal posterior to the
dura

Contents of epidural space?
• Lymphatics
• Spinal nerve roots
• Loose connective tissue
• Fatty tissue
• Small arteries
• Network of internal vertebral venous plexuses
How does spinal metastasis happen?

• Spread from primary tumors is mainly by the arterial route
• Retrograde spread through the Batson plexus.
• Direct invasion through the intervertebral foramina.
Batson venous plexus

Is a network of veins with no valves that connect deep pelvic
veins draining the bladder, prostate, and rectum to the
internal vertebral venous plexus.

Tumors metastasizing to the spine?
• Breast • Kidney
• Lung • Lymphoma
• Thyroid • Melanoma
• GI tract • Unknown
• Prostate • Others including multiple myeloma - 13%
Structures found at C6?

• Termination of the pharynx and beginning of the esophagus
• Termination of the larynx and beginning of the trachea
• Entry of the vertebral artery to the foramen transversum
• Intermediate tendon of omohyoid cross the carotid sheath
• Middle thyroid vein emerging from the thyroid gland
• Inferior thyroid artery entering the thyroid gland

Demonstrate the boundaries of the posterior triangle on a subject?
Demonstrate the hyoid bone (C3) and the cricoid cartilage (C6) on a subject?

ANATOMY
UPPER LIMB MRCS Part B Notes by Mo
Brachial Plexus........................................................................................................................................................................... 2
Shoulder .................................................................................................................................................................................... 7
Arm and Forearm .................................................................................................................................................................... 18
Hand......................................................................................................................................................................................... 33
Anatomical Snuff Box .............................................................................................................................................................. 40
ANATOMY UPPER LIMB MO’s MRCS B NOTES (Previously called Reda’s Notes) 1
Brachial Plexus
Origin Anterior rami of C5 to T1
Sections of • Roots, trunks, divisions, cords, branches
the plexus • Mnemonic: Real Teenagers Drink Cold Beer
Roots • Located in the posterior triangle
• Pass between scalenus anterior and medius
Trunks • Located posterior to middle third of clavicle
• Upper and middle trunks related superiorly to the subclavian artery
• Lower trunk passes over 1st rib posterior to the subclavian artery
Divisions Apex of axilla
Cords Related to axillary artery
Terminal Cords Divisions Roots

nerves (anterior rami)
Medial pectoral nerve

Medial cutaneus nerve of arm
Medial cutaneus nerve of forearm
Lateral pectoral nerve
Long thoracic nerve
Intercostobrachial nerve
(lateral cutaneous branch of T2)
Superior subscapular nerve
Thoracodorsal nerve
Inferior subscapular nerve
Medial cutaneous nerve of the arm

Median nerve
Medial cutaneous nerve of the forearm
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY UPPER LIMB
Demonstrate where brachial plexus run on a subject?
Where are parts of brachial plexus found?

• Roots: exits from IV foramina between scalenus anterior and medius
• Trunks: base of the posterior triangle of the neck behind the 3rd part of the subclavian artery
• Divisions: behind middle ⅓ of the clavicle
• Cords: related to the 2nd part of axillary artery
Erb's paralysis?
• Damage to the upper nerve roots (C5, C6)
• Motor affection: (waiter’s tip deformity)
o Paralysis of arm abductors (supraspinatus + deltoid) → arm adduction
o Paralysis of arm external rotators (infraspinatus +teres minor) → arm internal rotation
o Paralysis of forearm flexors and supinators (biceps, brachialis, brachioradialis) → forearm extension
and pronation
• Sensory affection: loss of sensation of radial side of arm and forearm
Klumpke’s paralysis?
• Injury to lower trunk (C8, T1)
• Motor affection: (claw hand deformity)
o Paralysis of all intrinsic muscles of the hand
o Paralysis of wrist flexors (except flexor carpi radialis)
o Hyperextension of MCP joints with flexion of IP joints
• Sensory affection: loss of sensation over ulnar border of forearm and hand
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Shoulder
Scapula. A. Posterior view of right scapula. B. Anterior view of costal surface. C. Lateral view.
Pectoralis major, Trapezius, Serratus anterior and Deltoid?
Muscle Origin Insertion Action Innervation
Clavicular head
• From the medial half of • Adduction and medial rotation of
the anterior surface of the arm (the whole muscle) Medial (C8-
the clavicle Humerus • Clavicular head: flexion of the T1) and
Pectoralis Sternocostal head (lateral ITG) arm Lateral (C5-
major • Anterior surface of the (lateral lip of • Sternocostal head: extends the C7) pectoral
sternum bicipital groove) flexed arm nerves
• Upper 6 costal • Acts as accessory respiratory
cartilages muscle by elevating the ribs
• EOA
• SP C7-T12 Clavicle, Scapula
Accessory
Trapezius • Occipital protuberance (acromion, Rotating scapula
nerve (CN XI)
• Ligamentum nuchae spine)
Serratus Scapula (ventral Long thoracic
Ribs 1-9 Preventing winging
anterior medial) nerve
Anterior fibres: flexion and medial
rotation.
Humerus
Posterior fibres: extension and lateral
Deltoid Lateral clavicle, scapula (deltoid Axillary nerve
rotation.
tuberosity)
Middle fibres: the major abductor of
the arm (after 15°).
Rotator cuff muscles?

Ventral scapula Humerus Internally rotating arm Upper and lower
Subscapularis
(subscapular fossa) (LT) Providing anterior stability subscapular nerves
Abducting
Superior scapula
Supraspinatus Providing stability
(supraspinatus fossa) Humerus
Externally rotating arm Suprascapular nerve
(greater
Dorsal scapula
Infraspinatus tuberosity) Providing stability
(infraspinatus fossa)
Externally rotating arm
Teres minor Scapula (dorsolateral) Axillary nerve
Trapezius Levator scapulae
Rhomboid minor
Latissimus
dorsi
Supraspinatus Suprascapular notch (foramen)
Cut edge
of deltoid
Surgical neck
of humerus
Medial lip of
intertubercular
sulcus
Quadrangular
space
Triangular interval
Teres major Deltoid tuberosity
of humerus
Long head
of triceps
brachii
Cut edge of lateral head

of triceps brachii
Borders Structures
Triangular Space
• Sup. Teres minor
• Inf. Teres major • Circumflex
• Lat. Triceps (Long scapular artery
head)
Quadrangular space
• Sup. Teres minor
Borders Structures
• Inf. Teres major • Axillary nerve
Triangular interval
• Med. Triceps (long • Posterior
• Sup. Teres major • Radial nerve head) circumflex a.
• Med. Triceps (long head) • Deep artery of arm • Lat. Humerus • Humeral a.
• Lat. Triceps (lateral head) (medial border)
Axillary artery?
Divided by pectoralis minor into 3 parts
Mnemonic for branches “Screw The Lawyer, Save A Patient”
Part Branch Course

I Sup. Thoracic a. Medial to serratus anterior and pectoral muscles
II Thoracoacromial a. Four branches: deltoid, acromial, pectoralis, clavicular
Lateral thoracic a. Descends to serratus anterior
III Subscapular a. (largest br.) Two branches: thoracodorsal and circumflex scapular (triangular space)
Anterior humeral circumflex a. Blood supply to humeral head: arcuate artery lateral to bicipital groove
Posterior humeral circumflex a. Branch in the quadrangular space accompanying the axillary nerve
Subclavius Pectoralis minor
Superior thoracic artery
Subscapularis
Subscapular artery
Anterior circumflex humeral artery
Posterior circumflex humeral artery

(quadrangular space)
Latissimus dorsi
Circumflex scapular branch
(triangular space)
Teres major
Thoracodorsal artery
Profunda brachii artery

(triangular interval)
Surface marking of the coracoid
This can be felt 2 cm inferior to the junction between
the middle and lateral thirds of the clavicle.
Structures attached to the coracoid process?

• Ligaments
o Coracoclavicular (trapezoid, conoid)
o Coracoacromial
o Coracohumeral
• Muscles
o Pectoralis minor (insertion)
o Coracobrachialis (origin)
o Short head of biceps (origin)
Muscles inserted in bicipital groove?

‘PLT sandwich’ or ‘Lady between 2 majors’
• Teres major (medial lip)
• Latissimus dorsi (floor)
• Pectoralis major (lateral lip)
Tendon of long head of biceps lies in the groove
Shoulder joint abduction?

• Supraspinatus (0-15ᵒ)
• Deltoid (middle fibres) (15-90ᵒ)
• Trapezius and serratus anterior (over 90ᵒ):
which will require upward rotation of the
scapula with lateral rotation of the humerus
Factors decreasing the stability of the shoulder

joint?
The shoulder is stabilized by both static and dynamic restraints.
• Shallow glenoid cavity
• Static restraints
• Lax capsule with few ligaments Structures that provide unidirectional limitations to
• Inferior aspect is not supported due to translation
the presence of quadrangular space o Glenoid labrum
o Articular version
The main stabilizer of the shoulder joint? o Articular conformity
Rotator cuff muscles o Negative intraarticular pressure
o Capsule (posterior capsule and rotator interval)
Quadrangular space? o Glenohumeral ligaments
See before
• Dynamic restraints
These include joint concavity compression produced by
synchronized contraction of the rotator cuff, acting to
stabilize the humeral head within the glenoid; increased
capsular tension produced by direct attachments of the
rotator cuff to the capsule; the scapular stabilizers that act
to maintain a stable glenoid platform (“ball on a seal’s
nose”); and proprioception.
N.B Synovial Joints

These are freely moving joints in which the articulating bony
surfaces are covered in smooth (hyaline) articular cartilage and
separated by a film of viscous synovial fluid that serves as a
lubricant (Fig. 5.31). Joint stability is provided by a fibrous
capsule (which usually has intrinsic ligamentous thickenings),
and often by internal or external accessory ligaments. Synovial
fluid, which also aids metabolite transport to cells in the
articular cartilages, is synthesized by the synovial membrane
that lines the joint capsule.
Axillary nerve
Motor supply?
• Deltoid
• Teres minor
Sensory supply?
• Skin to the lower half of deltoid (badge area)
Injury?
• Inability to abduct the shoulder over 15ᵒ
• Loss of sensation over the badge area
Upper limb reflexes?
• Biceps reflex (C5/6) – located in the antecubital fossa, tap your finger overlying the biceps tendon
• Triceps reflex (C7) – place forearm rested at 90º flexion
• Supinator reflex (C6) – located 4 inches proximal to base of the thumb
Upper limb dermatomes?

Myotomes
Elbow flexors/Biceps C5
Wrist extensors C6
Elbow extensors/Triceps C7
Long finger flexors C8
Small finger abductors T1
1, 2 Buckle my shoe (Ankle).

3, 4 Kick the door (Knee).
5, 6 Pick up sticks (Biceps & Brachioradialis).
7, 8 Shut the gate (Triceps).
C5, 6, 7 Raise your arms up to heaven (Serratus
anterior) Nerve root for Long Thoracic Nerve.
Findings in nerve root compression

Root Sensory Deficit Muscle Weakness Reflex Changes
• Lateral neck
C4 • Scapula • None
• Shoulder
• Deltoid
C5 • Upper lateral arm and elbow • Biceps
• Biceps (variable)
• Lateral forearm • Biceps
C6 • Brachioradialis
• Thumb and index finger • Wrist extensors
• Triceps
C7 • Middle finger • Wrist flexors • Triceps
• Long finger extensors
• Little and ring finger
C8 • Ulnar border of palm • Finger flexors • None
• Medial forearm
• Dorsal interossei
T1 • Medial arm • None
• Abductor digiti minimi
Arm and Forearm
Articulate bones of the shoulder
Articulate humerus, radius and ulna?
• Capitulum of the humerus + radial head
• Trochlea of the humerus + trochlear notch of the ulna
• Olecranon of the ulna+ olecranon fossa of the humerus
Muscles flexing the elbow joint?

• Biceps
• Brachialis
• Brachioradialis
• Pronator teres
• Flexor carpi radialis
Structures passing in spiral groove?

• Radial nerve
• Profunda brachii vessels
Clinical picture of radial nerve injury at the spiral groove?

• Paralysis of wrist extensors → wrist drop
• Paralysis of finger extensors → finger drop
• Loss of sensation in the 1st web space
Identify x-ray?
Supracondylar fracture of the humerus
Associated injuries?
• Brachial artery injury (absent distal
pulse)
• Anterior interosseus nerve injury (unable
to flex the interphalangeal joint of his
thumb and the distal interphalangeal
joint of his index finger)
• Ulnar nerve injury (claw hand)
• Radial nerve injury (wrist drop and finger
drop)
Biceps and Triceps?
Coracobrachialis Coracoid Mid-humerus (medial) Flexion, adduction Musculocutaneous
Biceps brachii Coracoid (short head) Radial tuberosity Supination, flexion Musculocutaneous
Supraglenoid
(long head) Relations to bicipital
tendon:
Medially: Median n. and
brachial a.
Lateral: Radial nerve
Brachialis Anterior humerus Ulnar tuberosity (anterior) Flexing forearm Musculocutaneous,
Radial
Triceps brachii Infraglenoid (long head) Olecranon Extending forearm Radial
Posterior humerus (Elbow extension).
(lateral head) The long head can Blood supply by
Posterior humerus adduct the humerus Profunda brachii
(medial head)* and extend it from a artery
flexed position
* The radial nerve and profunda brachii vessels lie between the lateral and medial heads
Transverse humeral ligament
Short head of biceps

brachii muscle
Coracobrachialis muscle
Radial tuberosity
Superficial Flexors of the Forearm
Pronator teres Medial epicondyle and coronoid Mid-lateral radius Pronating, Median nerve
flexing forearm
Flexor carpi radialis Medial epicondyle 2nd & 3rd MC bases Flexing wrist Median nerve
Palmaris longus Medial epicondyle Palmar aponeurosis Flexing wrist Median nerve
Flexor carpi ulnaris Medial epicondyle and posterior ulna Pisiform Flexing wrist Ulnar nerve
Flexor digitorum Medial epicondyle, proximal anterior Base of middle Flexing PIP Median nerve
superficialis ulna and anterior radius phalanges joint
Humeral head of
pronator teres
Humeral head of
flexor carpi ulnaris
Ulnar head of
pronator teres Ulnar head of
Ulnar artery flexor carpi ulnaris
Median nerve
Separates the ulnar a.

from the median n. Flexor carpi ulnaris
Pisohamate ligament
Pisiform
Pisometacarpal ligament
Hook of hamate
Deep Flexors of the Forearm
Flexor digitorum Anterior and Base of distal Flexing DIP joint Median–anterior interosseous/ulnar
profundus medial ulna phalanges nerves
Flexor pollicis Anterior and Base of distal Flexing IP joint, Median–anterior interosseous nerve
longus lateral radius phalanges thumb
Pronator quadratus Distal ulna Volar radius Pronating hand Median–anterior interosseous nerve
Humero-ulnar head of
flexor digitorum
superficialis
Interosseous
membrane
Flexor
Flexor digitorum digitorum
superficialis profundus
Flexor digitorum
superficialis
tendon (cut)
Superficial Extensors of the Forearm
Brachioradialis Lateral supracondylar Lateral distal radius Flexing forearm Radial nerve
humerus
Extensor carpi Lateral supracondylar Second metacarpal Extending wrist Radial nerve
radialis longus humerus base
Extensor carpi Lateral epicondyle of humerus Third metacarpal Extending wrist Radial nerve
radialis brevis base
Anconeus Lateral epicondyle of humerus Proximal dorsal ulna Extending forearm Radial nerve
Extensor Lateral epicondyle of humerus Extensor aponeurosis Extending digits Radial–posterior
digitorum interosseous nerve
Extensor digiti Common extensor tendon Small finger extensor Extending small Radial–posterior
minimi expansion over P1 finger interosseous nerve
Extensor carpi Lateral epicondyle of humerus Fifth metacarpal base Extending/adducting Radial–posterior
ulnaris hand interosseous nerve
Extensor carpi
radialis longus
Extensor carpi
radialis brevis
Extensor carpi
ulnaris
Anterior View Posterior View
Deep Extensors of the Forearm
Supinator Lateral epicondyle of Dorsolateral radius Supinating forearm Radial–posterior
humerus, ulna interosseous nerve
Abductor Dorsal ulna/radius First metacarpal base Abducting/extending Radial–posterior
pollicis longus thumb interosseous nerve
Extensor Dorsal radius Thumb proximal phalanx Extending thumb Radial–posterior
pollicis brevis base MCP joint interosseous nerve
Extensor Dorsolateral ulna Thumb dorsal phalanx Extending thumb IP Radial–posterior
pollicis longus base joint interosseous nerve
Extensor indicis Dorsolateral ulna Index finger extensor Extending index Radial–posterior
proprius apparatus (ulnarly) finger interosseous nerve
Supinator
(deep head)
Supinator
(superficial head)
Abductor pollicis longus
Extensor indicis
Extensor carpi
radialis longus
Extensor carpi
radialis brevis
Abductor
pollicis longus
Extensor digiti minimi Extensor
pollicis brevis
Posterior View
Cubital fossa?
Boundaries:
• Superolateral: Brachioradialis muscle
• Medially: Pronator teres
• Floor: Brachialis
Contents: (from medial to lateral)
• Median nerve
• Brachial artery
• Biceps tendon
Triceps brachii
Artery
Medial intermuscular septum (brachial)
Nerve
Cubital fossa
(Median)
Line between
lateral and medial
epicondyles
Bicipital
Forearm flexors aponeurosis
Radial artery
Brachioradialis
Ulnar artery
Median nerve Ulnar nerve

Forearm extensors Radial nerve
Ulnar nerve
Musculocutaneous nerve
Medial cutaneous
nerve of the forearm
Pronator teres
(humeral head)
Brachioradialis Lateral cutaneous

(pulled back) nerve of the forearm Median cubital vein
(separated from the
Pronator teres brachial artery by the
Deep branch of (ulnar head) bicipital aponeurosis)
radial nerve
Ulnar artery
Median nerve
Supinator
Radial artery
Superficial branch of radial nerve Cephalic vein Basilic vein
Median nerve sensory distribution in the hand?
• Lateral ⅔ of the palm of the hand
• Lateral (radial) 3½ digits on the palmar side
• Dorsum of the tips of index, middle and thumb
Median nerve motor distribution in hand?

LOAF muscles
• Lateral 2 lumbricals
• Opponens pollicis
• Abductor pollicis brevis
• Flexor pollicis brevis
Clinical picture of median nerve injury at elbow?

Ape-like hand
• Hyperextended thumb (paralysis of FPB)
• Adducted thumb (paralysis of abductor pollicis brevis)
• Flat thenar eminence
• Loss of sensations from:
o Lateral ⅔ of the palm of the hand
o Lateral 3½ digits (palmar and distal dorsal aspect)
Clinical picture of ulnar nerve injury at wrist?

Complete claw hand
• Clawing of the 4th and 5th digits (paralysis of the medial lumbricals and interossei)
• Loss of sensation of the medial ⅓ of the palmar and dorsal aspects of hand and fingers
Cause of ulnar paradox?

In proximal ulnar nerve injuries, there will be paralysis of the medial ½ of the FDP which will decrease flexion of the IP
joints
Hand
Identify Median nerve?

Identify Ulnar nerve?
Identify ulnar artery, radial artery, superficial palmar arch?
Superficial palmar arch?

Formed mainly by the arch of
the superficial division of the
ulnar artery and is completed
by the superficial palmar
branch of the radial artery
Identify carpal bones? Scared Lovers Try Positions That They Can't Handle
Navicular (Scaphoid) bone blood supply?
It receives its blood supply primarily from
lateral and distal branches of the radial
artery, via palmar and dorsal branches.
These provide an "abundant" supply to
middle and distal bone, but neglects the
proximal portion, which relies on retrograde
flow
How to test ulnar artery (Allen' s test)?

• Elevate the hand and ask the patient to make a fist for 30 sec.
• Apply pressure on both ulnar and radial aa. To occlude both
• While still elevated, open the hand, it should be blanched
• Release pressure over the ulnar artery, colour should return in 7 seconds
Demonstration of Allen’s test: Demonstration of Allen’s test:

Maintaining occlusion as Release the radial artery and
Demonstration of Allen’s test: patient repeatedly clenches the watch for reperfusion Demonstration of Allen’s test:
Occluding the radial and ulnar fist Repeat the first two steps then
arteries release the ulnar artery and
watch for reperfusion
Identify styloid process of the radius?
Identify Lister’s tubercle?
Clinical application?
Tubercle on dorsal radius. “Lighthouse of the wrist.” EPL tendon runs around it.
(It serves as a pulley for the tendon of the EPL (Extensor pollicis longus), which wraps around the medial side and
takes a 45 degree turn)
Attachment of flexor retinaculum?
• Proximal
o Pisiform
o Tubercle of scaphoid
• Distal
o Hook of hamate
o Trapezium
Structures passing through carpal tunnel?

• 4 tendons of flexor digitorum superficialis
• 4 tendons of flexor digitorum profundus
• 1 tendon of flexor pollicis longus
• 1 tendon of flexor carpi radialis
• Median nerve.
Palmaris longus tendon
Flexor retinaculum
Median nerve
Flexor carpi radialis tendon
Flexor digitorum
superficialis tendons Flexor pollicis longus tendon
Extensor pollicis brevis tendon
Extensor carpi ulnaris Cephalic vein
Radial artery
Extensor pollicis longus tendon

Extensor digiti minimi tendon Extensor carpi radialis longus tendon
Extensor digitorum tendons Extensor carpi radialis brevis tendon

Extensor indicis tendon
Movements of the thumb?

Movement Muscles Innervation
Flexor pollicis longus Median (anterior interosseous n.)
Flexion at MCP/IPJ
Flexor pollicis brevis Median (recurrent branch)
Extensor pollicis longus
Extension at MCP/IPJ Radial (PIN)
Extensor pollicis brevis
Flexion (flexion/transpalmar Flexor pollicis brevis Median (recurrent branch)
adduction) Adductor pollicis Ulnar (deep branch)
Abductor pollicis longus
Extension (radial abduction) Radial (PIN)
Extensor pollicis brevis
Abductor pollicis longus Radial (PIN)
Abduction (palmar)
Abductor pollicis brevis Median (recurrent branch)
Adduction (ulnar adduction) Adductor pollicis Ulnar (deep branch)
Opponens pollicis
Opposition Flexor pollicis brevis Median recurrent branch
Abductor pollicis brevis
How to test FDP?
By fixing the PIP
How to test FDS?

Adjacent digits must be held in extension, in order to
eliminate FDP motion in adjacent fingers, which
otherwise might give the impression of FDS motion in
the examined finger
Assessing the flexor digitorum superficialis. Assessing the flexor digitorum profundus.
Where do the tendons of FDS and FDP insert?

FDS: Split tendon on both sides of the middle phalanx
FDP: Passes through the split tendon of FDS to be inserted into the terminal phalanx
Tendon attached to pisiform?

Flexor carpi ulnaris
What makes extensor tendons attached to the phalanges?

Extensor expansion
What is the function of intertendinous connections?

• Create space between extensor tendons
• Redistribute force between tendons
• Coordinate extension of fingers
• Stabilize MCP joint
Identify Extensor Digitorum?

Insertion? Extensor expansion of middle and distal phalanges of the 2nd, 3rd, 4th, and 5th fingers
Identify?
Identify the two tendons inserting

into the index finger?
• Extensor indicis (medial)
• Extensor digitorum (lateral)
First dorsal interosseous?

Origin: From the first metacarpal
Mnemonic “PAD & DAB”
Insertion: Into the lateral side of extensor expansion of the index finger
• Palmar interossei ADduct
Action: Abduction of index finger
• Dorsal interossei ABduct
N. Supply: Deep branch of the ulnar nerve
When you are doing power grip of the hand, what is the role of radial nerve?
Radial nerve supplies wrist extensors which give mechanical advantage to power grip by synergistic activity which cause
more efficient flexion of the digits
Why hand grip is powerful in extension than flexion?

Because the flexor muscles in extension position is in a state of tension than in flexion position, so contraction in this
position is more powerful
Anatomical Snuff Box
Boundaries?
Posterior border Extensor pollicis longus tendon
(medially)
Anterior border Extensor pollicis brevis tendon
(laterally) Abductor pollicis longus tendon
Proximal border Styloid process of the radius
Distal border Apex of snuffbox triangle
Floor Trapezium and scaphoid
Content Radial artery
What does tenderness of the scaphoid mean?

Possible fracture of the scaphoid bone.
Blood supply of scaphoid? See before
1st dorsal
interosseous muscle
Anatomical
snuffbox
Extensor pollicis brevis tendon
Extensor pollicis
longus tendon
Abductor pollicis longus tendon
Cephalic vein
Insertion of EPL?
Dorsum of the base of the terminal phalanx of the thumb
Insertion of EPB?
Dorsum of the base of the proximal phalanx of the thumb
Surface markings / Show me anatomical snuff box on your hand?
Anatomical snuffbox
Extensor pollicis longus tendon
ANATOMY
LOWER LIMB MRCS Part B Notes by Mo
Pelvis .......................................................................................................................................................................................... 2
Thigh/Hip ................................................................................................................................................................................... 8
Popliteal Fossa ......................................................................................................................................................................... 14
Femoral Triangle ..................................................................................................................................................................... 17
Adductor Canal ........................................................................................................................................................................ 18
Leg ............................................................................................................................................................................................ 20
Muscles of The Leg .............................................................................................................................................................. 22
Foot and Ankle ........................................................................................................................................................................ 25
Arches of the foot ............................................................................................................................................................... 25
Bones of the foot ................................................................................................................................................................. 25
Ligaments of the foot and ankle ......................................................................................................................................... 28
ANATOMY LOWER LIMB MO’s MRCS B NOTES (Previously called Reda’s Notes) 1
Pelvis
Where else does the gluteus maximus muscle insert?

Onto the gluteal tuberosity of the femur
What is the nerve supply and nerve roots of gluteus maximus?

Gluteus maximus is supplied by the inferior gluteal nerve (L5, S1, S2)
What are the actions of gluteus maximus?

Gluteus maximus performs external rotation and extension of the hip
What nerve supplies tensor fasciae lata?

The superior gluteal nerve supplies tensor fascia lata.
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY LOWER LIMB
Where does the gluteus medius muscle insert?
Onto the lateral surface of the greater trochanter. Gluteus minimus also inserts onto the greater trochanter deep to
gluteus medius.
What is the action of gluteus medius? Causes of Trendelenburg gait

During standing, it is a hip abductor. During gait, gluteus • Weak abductor muscles
medius, together with gluteus minimus, support the body • Avulsion of the abductor muscle tendon
whilst one leg is in the air, preventing the pelvis from • L5 radiculopathy
dropping to the opposite side • Superior gluteal nerve injury
• Myopathy
What clinical sign is evident with weakness of gluteus medius • Neurological conditions such as stroke
and minimus / How to test? and multiple sclerosis
A Trendelenburg gait or a positive Trendelenburg test • Trauma / fractures of the pelvis and hip
• DDH, congenital coxa vara or coxa valga
Damage to what nerve can produce this distinctive gait? • Painful hip
Damage to the superior gluteal nerve • Unequal leg length
• Wide walking base
Quadratus femoris origin, insertion, nerve supply and action?
Muscle Origin Insertion Nerve Segment
External Rotators
Gluteus maximus Ilium, posterior gluteal line Iliotibial band Inferior gluteal L5-S2 (P)
Gluteal sling (femur)
Piriformis Anterior sacrum/sciatic notch Proximal greater Piriformis S2 (P)
trochanter
Obturator externus Ischiopubic rami/obturator Trochanteric fossa Obturator L2-L4 (A)
Obturator internus Ischiopubic rami/obturator Medial greater Obturator internus L5-S2 (A)
membrane trochanter
Superior gemellus Outer ischial spine Medial greater Obturator internus L5-S2 (A)
trochanter
Inferior gemellus Ischial tuberosity Medial greater Quadratus femoris L5-S1 (A)
trochanter
Quadratus femoris* Lateral border of the upper Quadrate line of femur Quadratus femoris L5-S1 (A)
part of the Ischial tuberosity
Abductors
Gluteus medius Ilium between posterior and Greater trochanter Superior gluteal L4-S1 (P)
anterior gluteal lines
Gluteus minimus Ilium between anterior and Anterior border of Superior gluteal L4-S1 (P)
inferior gluteal lines greater trochanter
Tensor fasciae latae Anterior iliac crest Iliotibial band Superior gluteal L4-S1 (P)
(tensor fasciae
femoris)
A, anterior; P, posterior.
*Don’t confuse quadratus with quadriceps femoris
Gluteus minimus
Mnemonic for muscle attachment

Gemellus inferior
on greater trochanter: P-GOGO:
• Piriformis Quadratus femoris
• Gluteus medius and minimus
• Obturator internus Greater sciatic foramen
• Gemelli below piriformis
• Obturator externus
Where does the iliotibial tract attach?
The Iliotibial tract is attached to the anterolateral iliac tubercle of the iliac crest proximally and the lateral condyle of the
tibia distally.
What muscles insert onto it?

• Gluteus maximus
• Tensor fasciae lata
What is its clinical significance?

The iliotibial tract stabilizes the knee in extension and in partial flexion. It is important in walking and running
Tubercle of crest of ilium
Gluteus minimus
Attachment of deep
fibers to gluteal
tuberosity
Deep fascia of leg
What are the surface markings of the sciatic nerve?
The sciatic nerve (L4,5, S1,2,3) exits the pelvis via the greater sciatic foramen from below the piriformis muscle. The
surface marking of the sciatic nerve is a curved line drawn from 2 points: halfway between the posterior superior iliac
spine to the ischial tuberosity to halfway between the ischial tuberosity and the greater trochanter.
Highest point
on iliac crest
Greater
trochanter
Ischial
tuberosity
Gluteal
fold
Which vessels exit the greater sciatic foramen from above?

The superior gluteal vessels and nerve exit above piriformis.
What variations do you know with regard to the sciatic nerve exiting the pelvis?
In the majority of cases the sciatic nerve exits beneath the piriformis. Alternatively, either the whole nerve may pass
through piriformis, or it may divide high with one division passing through or around the piriformis
Identify arteries
A. Common femoral
artery
B. Lateral circumflex
femoral artery
C. Superficial femoral
artery
D. Profunda femoris
artery
Thigh/Hip
What muscles attach to the lesser trochanter of the femur?

• Psoas major
• Iliacus
Where does the psoas major originate?

The deep part of psoas major originates from the transverse processes of L1-L4. The superficial part originates from the
lateral surfaces of T12-L4 and the intervening vertebral discs.
What is the action of psoas major?

Psoas major flexes and externally rotates the hip
Describe the blood supply to the head of
the femur?
The majority of the blood supply to the
head of the femur is from retinacular
arteries, which arise as ascending cervical
branches from the extracapsular arterial
anastomosis. This is formed posteriorly by
the medial femoral circumflex artery and
anteriorly from branches of the lateral
femoral circumflex artery with minor
contributions from the superior and
inferior gluteal arteries.
There is also supply from the artery of the
ligamentum teres, also known as the artery
of the round ligament of
the femoral head (a branch of the
obturator artery).
Where do these arteries originate?

The medial and lateral circumflex
femoral arteries originate from
the profunda femoris
The artery of the ligamentum
teres originates from the
obturator artery
Identify origin and insertion of quadriceps muscle on the skeleton?
Muscle Origin Insertion Innervation
Quadriceps muscles
Vastus lateralis Iliotibial line / greater trochanter / lateral linea Lateral patella Femoral
aspera
Vastus medialis Iliotibial line / medial linea aspera / Medial patella Femoral
supracondylar line
Vastus intermedius Proximal anterior femoral shaft Patella Femoral
Rectus femoris Straight head: Anterior inferior iliac spine, Patella and tibial tubercle Femoral
Reflected head: acetabular rim
Vastus lateralis
Vastus intermedius
Posterior compartment of thigh
Vastus intermedius
Rectus femoris
Vastus medialis
Adductor canal
Suprapatellar bursa
Quadriceps femoris
tendon
Tibial tuberosity
Attachment Sartorius
of pes Gracilis
anserinus Semitendinosus
Hamstrings?
Muscle Origin Insertion Innervation
Muscles of the Posterior Thigh
Biceps femoris (long head) Medial ischial tuberosity Fibular head/lateral tibia Tibial
Biceps (short head) Lateral linea aspera/lateral Lateral tibial condyle Peroneal
intermuscular septum
Semitendinosus Distal medial ischial tuberosity Anterior tibial crest Tibial
Semimembranosus Proximal lateral ischial tuberosity Oblique popliteal ligament Tibial
Posterior capsule
Posterior/medial tibia
Popliteus
Medial meniscus
Actions of the hamstring muscles

All three muscles:
Flexion of the leg at the knee joint.
Extension of thigh at the hip.
Biceps
Lateral rotation of the hip and knee
Ischial tuberosity
Semitendinosus and Semimembranosus
Medially rotates the thigh at the hip joint
and the leg at the knee joint.
Structures at risk in supracondylar fracture of the

femur
Short head of biceps

femoris
Part of semimembranosus
that inserts into capsule
around knee joint
On anterior aspect of tibia

attaches to pes anserinus
Popliteal Fossa
Boundaries of the popliteal fossa
Laterally Biceps femoris above, lateral head of gastrocnemius and plantaris below
Medially Semimembranosus and semitendinosus above, medial head of gastrocnemius below
Floor Popliteal surface of the femur, posterior ligament of knee joint and popliteus muscle
Roof Superficial and deep fascia
Contents
Supracondylar fracture of femur
• Common peroneal nerve
Occurs in older patients, usually due to
• Tibial nerve
low energy trauma such as a fall
• Popliteal vein
(osteoporotic bone). Can occur in young
• Popliteal artery
patients due to a high energy trauma.
• Lymph nodes Popliteal artery is at risk, check distal
• Small saphenous vein pulses, ABPI (consider CTA or arteriogram)
• Posterior cutaneous nerve of the thigh
• Genicular branch of the obturator nerve
The tibial nerve lies superior to the vessels in the inferior aspect of the popliteal fossa. In the upper part of the fossa the
tibial nerve lies lateral to the vessels, it then passes superficial to them to lie medially. The popliteal artery is the deepest
structure in the popliteal fossa.
Biceps femoris muscle Posterior cutaneous

Semimembranosus muscle
(short head) nerve of thigh
Femoral vein
Adductor
hiatus
Popliteal Tibial nerve

fossa Popliteal vein
Plantaris Popliteal
muscle artery
Common
fibular nerve
Popliteus muscle Small saphenous vein Posterior cutaneous Small

nerve of thigh saphenous
vein
Differential diagnosis of lump from popliteal fossa?

• Backer's cyst
• Popliteal artery aneurysm
• Lipoma
• Schwannoma
• Popliteal vein varicosities
MRA of popliteal artery and its branches
Femoral Triangle
Boundaries
Superiorly Inguinal ligament
Laterally Sartorius
Medially Adductor longus
Floor Iliopsoas, pectineus and adductor longus
Roof • Fascia lata and Superficial fascia
• Superficial inguinal lymph nodes (palpable below the inguinal ligament)
• Long saphenous vein
Contents
• Femoral vein (medial to lateral)
• Femoral artery-pulse palpated at the mid
inguinal point
• Femoral nerve
• Deep and superficial inguinal lymph nodes
• Lateral cutaneous nerve
• Great saphenous vein
• Femoral branch of the genitofemoral nerve
Anterior superior
iliac spine
Inguinal ligament
Lymphatics passing Sartorius muscle

through femoral canal
Pubic tubercle
Medial margin of Adductor hiatus

sartorius muscle
Pubic symphysis
Medial margin of
adductor longus
muscle
• The iliacus lies posterior to the femoral nerve in the femoral triangle.
• The femoral sheath lies anterior to both the iliacus and pectineus.
Adductor Canal
What is Hunter's canal?
Hunter's canal, also known as the subsartorial or adductor canal, runs from the apex of the femoral triangle to the
popliteal fossa.
What are the boundaries of Hunter's canal?

Borders
Laterally Vastus medialis muscle
Posteriorly Adductor longus, adductor magnus
Roof Sartorius
What are the contents of Hunter's canal?

Contents
Saphenous nerve
Superficial femoral artery
Superficial femoral vein
(posterior to the artery in the upper part then posterolateral)
Nerve to vastus medialis
What is the surface marking of the adductor hiatus?

The adductor hiatus lies ⅔ along the line between the ASIS and the adductor tubercle of the femur.
What are the surface markings of the femoral artery?

The femoral artery can be palpated at the mid-inguinal point, which lies halfway between the pubic symphysis and the
ASIS
The inguinal region and femoral triangle

1) anterior superior iliac spine;
2) lateral femoral cutaneous nerve and its zone of
emergence into femoral triangle (white): range 0.3–7.3
cm (mean 2.1–3.5 cm) from anterior superior iliac spine;
3) inguinal ligament;
4) femoral artery and zone of emergence into femoral
triangle (white): mid-inguinal point ± 1 cm either side,
femoral nerve (yellow cross) and vein (blue cross) sit
lateral and medial, respectively, to the femoral artery;
5) femoral head: located 2–4 cm above the midpoint of
the greater trochanter to pubic tubercle line;
6) pubic tubercle;
7) greater trochanter to pubic tubercle line;
8) profunda femoris artery: almost always arises 6.5 ± 1.5
cm distal to the mid-inguinal point, or superior to or at
the level of the inguinal/groin crease;
9) zone of saphenofemoral junction location: almost
always sits within a 3 cm × 3 cm zone situated 1–4 cm
lateral and 0–3 cm inferior to the pubic tubercle;
10) sartorius;
11) inguinal/groin crease;
12) adductor longus.
Vascular lacuna?
It’s the compartment beneath the inguinal ligament which allows for passage of the femoral vessels, lymph vessels and
lymph nodes.
The muscular lacuna is the lateral compartment of the thigh inferior to the inguinal ligament, it is separated by the
iliopectineal arch from the vascular lacuna
Lacuna vasorum (vascular lacuna) is medially, while lacuna musculorum (muscular lacuna) is laterally.
Contents of lacuna vasorum? (order from

medial part)
• Deep inguinal lymph nodes
• Femoral vein,
• Femoral artery
• Femoral branch of the
genitofemoral nerve
Contents of lacuna musculorum?

• Femoral nerve
• Iliopsoas
• Lateral femoral cutaneous nerve
Leg
What nerve supplies the muscles in the posterior compartment of the leg?
The tibial nerve supplies the posterior compartments of the leg (deep and superficial)
• Superficial (GPS): Gastrocnemius, soleus and plantaris
• Deep (Pfft): Popliteus, flexor hallucis longus, flexor digitorum longus, tibialis posterior
How many compartments are there in the leg and what structures are in each compartment?
Separated by the interosseous membrane (anterior and posterior compartments), anterior fascial septum (separate
anterior and lateral compartments) and posterior fascial septum (separate lateral and posterior compartments)
Compartment Nerve Muscles Blood supply
Anterior Deep peroneal nerve • Tibialis anterior Anterior tibial artery
compartment • Extensor digitorum longus
• Extensor hallucis longus
• Peroneus tertius
Superficial Posterior Tibial “GPS” Posterior tibial
compartment • Gastrocnemius
• Soleus
• Plantaris
Deep Posterior “Pfft…”
compartment • Popliteus
• Flexor hallucis longus
• Flexor digitalis longus
• Tibialis posterior
Lateral compartment Superficial peroneal • Peroneus longus Peroneal artery
• Peroneus brevis
What nerve supplies the anterior compartment of the leg?

The deep peroneal nerve (anterior tibial nerve)
Demonstrate on the subject the actions of tibialis anterior, tibialis posterior, peroneus longus, brevis, gastrocnemius,
soleus?
Tibialis anterior: Dorsiflexion and inversion
Tibialis posterior: Plantarflexion and inversion
Peroneus longus: Eversion and abduction
Peroneus brevis: Eversion
GPS: Plantar flexion
How would you recognize compartment syndrome in the lower leg?

Compartment syndrome is an emergency that presents with pain out of proportion to the injury sustained, in someone
with a swollen leg, particularly acute on passive stretching of the ankle. There may be paresthesia, pulselessness and
paralysis, all late signs and suggestive of impending limb necrosis.
Orientate and articulate the tibia and fibula?
Muscles of The Leg
Anterior Compartment
Tibialis anterior Lateral tibia Medial cuneiform, Dorsiflexing, inverting Deep peroneal (L4)
first metatarsal foot nerve
Extensor hallucis Mid-fibula Great toe, distal Dorsiflexing, extending Deep peroneal (L5)
longus phalanx toe nerve
Extensor Tibial condyle/fibula Toe, middle and Dorsiflexing, extending Deep peroneal (L5)
digitorum longus distal phalanges toe nerve
Peroneus tertius Fibula and extensor Fifth metatarsal Everting, dorsiflexing, Deep peroneal (S1)
digitorum longus tendon abducting foot nerve
Lateral Compartment
Peroneus longus Proximal fibula Medial cuneiform, Everting, plantar Superficial peroneal
1st metatarsal flexing, abducting foot (S1) nerve
Peroneus brevis Distal fibula Tuberosity of 5th Everting foot Superficial peroneal
metatarsal (S1) nerve
Subcutaneous
surface of tibia
Anterior
surface of
fibula
Tibialis Common fibular
Origin of
anterior nerve
tibialis
anterior
Lateral surface
of fibula
Origin of
extensor
digitorum
longus
Origin of
extensor
hallucis
longus
Fibularis
tertius Groove on
inferior Fibularis
aspect of brevis
cuboid tendon
Medial
cuneiform
Fibularis
longus
Metatarsal I
Attachment to inferior tendon
surface of medial
cuneiform and metatarsal I
Superficial Posterior Compartment (“GPS”)
Gastrocnemius Posterior medial and Calcaneus Plantar flexing foot Tibial (S1) nerve
lateral femoral condyles
Plantaris Lateral femoral condyle Calcaneus Plantar flexing foot Tibial (S1) nerve
Soleus Fibula/tibia Calcaneus Plantar flexing foot Tibial (S1) nerve
Medial head of
gastrocnemius Plantaris
Lateral head of gastrocnemius
Popliteal vessels and tibial nerve
Gastrocnemius
Calcaneal tendon
Calcaneus
Deep Posterior Compartment (“Pfft…”)
Popliteus Lateral femoral condyle, Proximal tibia Flexing, internally Tibial (L5, S1) nerve
fibular head rotating knee
Flexor hallucis Fibula Great toe, distal Plantar flexing great toe Tibial (S1) nerve
longus phalanx
Flexor digitorum Tibia Second to fifth toes, Plantar flexing toes, foot Tibial (S1, S2) nerve
longus distal phalanges
Tibialis posterior Tibia, fibula, Navicular, medial Inverting/plantar flexing Tibial (L4, L5) nerve
interosseous membrane cuneiform foot
ANTERIOR VIEW
Tibialis
posterior
Extensor
digitorum
longus
Synovial
sheaths
Flexor hallucis
longus Extensor
Origin of flexor digitorum
hallucis longus brevis
Extensor
hallucis
brevis
Groove on Extensor
medial Groove on posterior hallucis
malleolus surface of talus longus
Groove on inferior
Tuberosity of surface of sustentaculum
navicular tali of calcaneus bone Extensor
hood
Medial
cuneiform
POSTERIOR VIEW
Foot and Ankle
Arches of the foot
What are the components of the Medial/Lateral longitudinal and Transvers arches?
Arch Medial longitudinal arch Lateral longitudinal arch Transverse arch
Construction • Calcaneus, Talus, Navicular • Calcaneus
• 3 cuneiform • Cuboid • Cuboid, 3 cuneiform
• 3 medial metatarsals • 2 lateral metatarsal • Bases of metatarsals
Function High arch concerned with the Low arch concerned mainly Elastic propulsion of foot and
elastic propulsion of the foot with body weight transmission body weight transmission
during walking
Factors Ligaments Ligaments Ligaments
maintaining • Interosseus ligaments • Interosseus ligaments • Interosseus ligaments
• Plantar aponeurosis • Plantar aponeurosis
• Long planter ligament • Short planter ligament
• Deltoid and spring ligaments
Muscles Muscles Muscles
• Tibialis anterior & posterior • 3 Peronei muscles • Peroneus longus
• Short muscles of the big toe • Short muscles of little toe • Transverse head of
• FHL adductor hallucis
Bones of the foot
Identify bones of the foot?
Ligaments of the foot and ankle
Identify ligaments on the medial and lateral aspects of the ankle?

Ligament Origin Insertion
Capsule Tibia Talus
Anterior tibiotalar Anteromedial surface of talus
Anterior colliculus of medial
Deltoid
(4 parts)
Tibionavicular Navicular tuberosity

malleolus
Tibiocalcaneal Sustentaculum tali
Posterior tibiotalar (deep) Post. colliculus of medial malleolus Medial talus & medial tubercle
Anterior talofibular Lateral malleolus Transversely to talus anteriorly
(3 parts)
LCL
Posterior talofibular Lateral malleolus Transversely to talus posteriorly

Calcaneofibular Lateral malleolus Obliquely to calcaneus posteriorly
Attachments of deltoid ligament? Lateral collateral ligament (LCL)

Superior: • Anterior talofibular
• Medial malleolus • Posterior talofibular
Inferior: • Calcaneofibular
• Tuberosity of the navicular Syndesmotic complex
• Spring ligament • Anterior tibiofibular
• Neck of talus • Posterior tibiofibular
• Sustentaculum tali • Inferior transverse tibiofibular
• Body of talus (deep fibers of posterior tibiofibular)
Midtarsal joint (of “Chopart”)?
The transverse tarsal joint or midtarsal joint or Chopart’s joint is formed by the
• Articulation of the calcaneus with the cuboid (calcaneocuboid joint) (saddle)
• Articulation of the talus with the navicular (talocalcaneonavicular joint) (ball & socket)
What movements occur at the subtalar (talocalcaneal) joint?

Inversion and eversion of the foot occur at the subtalar joint.
Which muscles perform these actions?

Inversion: Tibialis anterior and posterior (with some help from the extensor and flexor hallucis longus muscles)
Eversion: Peroneus longus and brevis
What is the type of the subtalar (talocalcaneal) joint?

Synovial plane joint
What is the type of the ankle (talocrural) joint?

Synovial hinge joint
What are the bones forming ankle joint?

Trochlear surface of talus, lower end of tibia and fibula
Movements at the ankle joint?

Plantar flexion:
• Gastrocnemius
• Soleus
• Plantaris
• Flexor digitorum longus
Dorsiflexion:
• Tibialis anterior
• Extensor digitorum longus
Ankle joint is most stable in dorsiflexion why?

Dorsiflexion is more stable than plantarflexion. The talus is stabilized due to the wider anterior side of the trochlea being
immobilized by the tibial articulation. In plantarflexion, the narrower posterior side is articulating more and so more
movement is possible since it does not completely fill the space allowed the anterior side.
What is the type of inferior tibiofibular joint?

Syndesmosis
Associated injury in syndesmotic fracture?
Fractures lateral malleolus
Point to the Achilles tendon
What muscles make this up?

Three muscles insert into the Achilles or calcaneal tendon:
• Soleus
• Gastrocnemius
• Plantaris
Structures passing behind the medial malleolus?

Structures posterior to the medial malleolus: Deep to flexor retinaculum (Posteromedially)
Tom Does Very Nice Hats
• Tibialis posterior tendon
• Flexor Digitorum longus
• posterior tibial Vessels
• posterior tibial Nerve
• Hallucis longus
Structures deep to extensor retinaculum

(Anterior):
Tom Has Very Nice Dogs & Pigs
• Extensor Hallucis longus
• Anterior tibial Vessels
• Anterior tibial Nerve
• Extensor Digitorum longus
Arteries of the foot?
Dorsalis pedis artery
• It is the continuation of the anterior tibial
artery and begins as the anterior tibial
artery crosses the ankle joint.
• It passes anteriorly over the dorsal aspect
of the talus, navicular, and intermediated
cuneiform bones, and then passes
inferiorly, as the deep planter artery,
between the two heads of the first dorsal
interosseous muscle to join the deep
planter arch in the sole of the foot.
Medial and lateral plantar arteries
• Arteries which supply the sole of the foot
• Branches of posterior tibial artery
• Run in the sole between the 1st and 2nd
layer of muscles
• Lateral plantar artery forms plantar arch
along with dorsalis pedis artery
Where to palpate dorsalis pedis and posterior tibial

arteries?
• Lateral to the EHL tendon
• Halfway between the posterior border of
the medial malleolus and achilles tendon
Demonstrate the foot pulses on this actor?

The dorsalis pedis pulse is found between the first
two metatarsal bones
The posterior tibial pulse is found 2-3cm below and
behind the medial malleolus
Identify tendons on the dorsum of the foot?
Surface markings of EHL?
What movements does extensor hallucis longus perform?
It extends the big toe, dorsiflexes the foot and assists with inversion of the foot.
What vessels would you find deep to extensor hallucis longus?

The anterior tibial artery and vein
And what nerve that lies deep to it?

The deep peroneal nerve
Where would you test sensation of…

S1?
S1 is tested on the lateral aspect of the foot
L4?
L4 is tested over the medial malleolus
Deep peroneal nerve?
The deep peroneal nerve is tested at the first web interspace
Superficial peroneal nerve?
The superficial peroneal nerve is tested over the dorsum of the foot, other than the first web interspace
Sural Nerve?
The sural nerve is tested over the lateral malleolus
On an actor demonstrate how you would test the knee and ankle reflexes?
Knee reflex:
The foot should be unsupported, relaxed and off the ground. The thigh should be fully exposed.
Test by tapping the patellar tendon with a tendon hammer. You are looking for reflex contraction of the quadriceps
muscles.
Ankle reflex:
The foot should be pointing laterally, be flexed, and relaxed. the leg should be fully exposed.
Test by tapping the Achilles tendon with a tendon hammer. You are looking for reflex contraction of the calf muscles.
What nerve roots do these reflexes originate from?

Ankle: S1
Knee: L3/4
What movement is ankle dorsiflexion?

Dorsiflexion is the upwards movement of the foot in relation to the leg
At which joint does dorsiflexion occur?

At the ankle joint between the tibia/fibula and the talus
What muscles are involved in dorsiflexion?

Muscles of the anterior compartment of leg are involved:
• Extensor digitorum longus
How would you demonstrate ankle plantarflexion?
Plantarflexion is the downwards movement of the
foot in relation to the leg.
What muscles are involved?

Both the superficial and deep posterior
compartments of the leg are involved
Superficial posterior compartment:
• Gastrocnemius
• Soleus
• Plantaris (only weak participation)
Deep posterior compartment:
• Flexor digitorum longus
• Popliteus
What action occurs when tibialis anterior and tibialis

posterior contract together?
Ankle inversion
At which joint does this occur?

Inversion and eversion both occur at the
subtalar joint
What muscles are responsible for ankle eversion?

Peroneus brevis and peroneus longus
Which nerve innervates them?

The superficial peroneal nerve
What motor and sensory function is lost with

damage to the superficial peroneal nerve?
Inability to evert the foot and loss of sensation over
the dorsum of the foot, apart from the first web
space, which is innervated by the deep peroneal
nerve
Identify lower limb dermatomes?
Myotomes
Hip flexors (psoas) L1 and L2
Knee extensors (quadriceps) L3
Ankle dorsiflexors (tibialis anterior) L4 and L5
Toe extensors (hallucis longus) L5
Ankle plantar flexors (gastrocnemius) S1
Findings in nerve root compression

Root Sensory Deficit Muscle Weakness Reflex Changes
L2 • Anteromedial thigh • Iliopsoas • None
L3 • Anterior thigh • Quadriceps • None
L4 • Anteromedial leg • Tibialis anterior • Patella tendon
• Lateral leg • Extensor hallucis longus • Medial hamstring
L5
• Dorsum foot/big toe • Gluteus medius
• Posterior calf • Gastrosoleus complex • Achilles tendon
S1
• Plantar foot • Gluteus maximus
S2, 3, 4 • Perianal • Bowel/Bladder • Cremasteric
ANATOMY
HEAD & NECK MRCS Part B Notes by Mo
Neck ........................................................................................................................................................................................... 2
Anterior Triangle of the Neck ................................................................................................................................................... 4
Posterior Triangle of the Neck .................................................................................................................................................. 5
External Carotid Artery ............................................................................................................................................................. 6
Thyroid Gland ............................................................................................................................................................................ 8
Parathyroid ................................................................................................................................................................................ 9
Larynx....................................................................................................................................................................................... 10
Inferior Laryngeal Nerve (Recurrent Laryngeal Nerve) (RLN) ............................................................................................... 11
Skull .......................................................................................................................................................................................... 12
Foramina.................................................................................................................................................................................. 16
Cavernous Sinus ...................................................................................................................................................................... 21
Dural / Cranial Venous Sinuses ............................................................................................................................................... 22
Facial Nerve (VII) ..................................................................................................................................................................... 25
Parotid Gland........................................................................................................................................................................... 26
Tongue ..................................................................................................................................................................................... 30
Ear Anatomy ............................................................................................................................................................................ 31
Brain ......................................................................................................................................................................................... 32
CSF ........................................................................................................................................................................................ 34
Circle of Willis ...................................................................................................................................................................... 36
Carotid arteriogram ............................................................................................................................................................ 38
ANATOMY HEAD & NECK MO’s MRCS B NOTES (Previously called Reda’s Notes) 1
Neck
Identify strap muscles?

Infrahyoid muscle
Deep:
• Sternothyroid
• Thyrohyoid
Superficial:
• Sternohyoid
• Omohyoid
Nerve supply?
All parts by ansa cervicalis C1 to C3 except for thyrohyoid which is innervated by C1
Action?
Depress the hyoid bone and larynx during swallowing and speaking
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY HEAD & NECK
Identify spinal accessory nerve? Identify great auricular nerve?
Supplies? Supply? (C2, C3)
• Trapezius (shrug the shoulder) • Skin over the angle of the mandible
• Sternomastoid (turns the head to the • Skin over the parotid gland
contralateral side) • Skin of the lower ½ of the auricle
Surface anatomy?
It crosses the posterior triangle of neck between the
point of the junction between upper ⅓ and lower ⅔ of
the sternomastoid to the junction between upper ⅔
and the lower ⅓ of the trapezius
Anterior Triangle of the Neck
Boundaries Anterior Midline of the neck
Posterior Anterior border of sternocleidomastoid
Superior Lower border of the mandible
Sub triangles (divided by Digastric above and Omohyoid)

• Submandibular Triangle (Digastric)
• Muscular triangle: Neck strap muscles
• Carotid triangle: Carotid sheath
Contents of the anterior triangle

Digastric triangle Submandibular gland
(submandibular) Submandibular nodes
Facial vessels
Hypoglossal nerve (XII)
Muscular Strap muscles
triangle External jugular vein
Carotid triangle Carotid sheath (Common carotid, Vagus and IJV)
Ansa cervicalis
Nerve supply to digastric muscle

• Anterior: Mylohyoid nerve
• Posterior: Facial nerve Stylohyoid muscle
Submandibular triangle Posterior belly of digastric
Anterior belly of
digastric muscle
Hyoid bone
Muscular triangle
Superior belly of omohyoid
Posterior Triangle of the Neck
Apex Sternocleidomastoid and the Trapezius muscles at the Occipital bone
Boundaries
Anterior Posterior border of the Sternocleidomastoid
Posterior Anterior border of the Trapezius
Base Middle third of the clavicle
Nerves •
Accessory nerve
•
Phrenic nerve
•
Three trunks of the brachial plexus
•
Branches of the cervical plexus: Supraclavicular nerve, transverse cervical
Contents
nerve, great auricular nerve, lesser occipital nerve

Vessels • External jugular vein
• Subclavian artery (3rd part)
Muscles • Inferior belly of omohyoid
• Scalene
Lymph nodes • Supraclavicular
• Occipital
The IJV does not lie in the posterior triangle. However, the terminal branches of the external jugular vein do.
Retromandibular vein
Lesser occipital nerve

Great auricular nerve
Supraclavicular nerves
External Carotid Artery
Identify external carotid artery?
Course?
Origin: as one of the 2 terminal branches of CCA at the upper border of the thyroid cartilage (C4)
Termination: behind the neck of the mandible inside the parotid gland by dividing into superficial temporal and maxillary
branches
Nerve passing anterior to it?

Hypoglossal nerve 'Some Angry Lady Figured Out PMS' (in order)
Superior thyroid (superior laryngeal artery branch)
Branches?
Ascending pharyngeal
It has six main branches, three in front, two behind and one deep.
Lingual
Three in front Superior thyroid
Facial (tonsillar and labial artery)
Lingual
Occipital
Facial
Two behind Occipital Posterior auricular
Posterior auricular Maxillary (inferior alveolar artery, middle meningeal a.)
Deep Ascending pharyngeal Superficial temporal
Occipital artery
Internal carotid artery

Ascending pharyngeal artery
External carotid artery
Superior thyroid artery
Carotid body?
On the posterior aspect of the bifurcation of CCA contains chemoreceptors sensitive to changes in pH.
Carotid sinus?
The carotid sinus is a dilated area at the base of the internal carotid artery just superior to the bifurcation of the internal
carotid and external carotid at the level of the superior border of thyroid cartilage. It contains baroreceptors for
maintaining blood pressure.
Thyroid Gland
Identify left and right lobes and isthmus?
Arterial supply and venous drainage?

Arterial • Superior thyroid artery (1st branch of external carotid)
• Inferior thyroid* artery (from thyrocervical trunk from subclavian a. 1st part)
• Thyroidea ima (in 10% of population -from brachiocephalic artery or aorta)
Venous • Superior and middle thyroid veins - into the IJV
• Inferior thyroid vein - into the brachiocephalic veins
* Also supplies parathyroid glands
Lymphatic drainage?
Pre-laryngeal, pre-tracheal, para-tracheal, upper and lower deep cervical, brachiocephalic lymph nodes.
Pretracheal fascia Trachea
Pyramidal
lobe
Thyroid
gland
Common carotid artery

Right recurrent
laryngeal nerve
Left lobe
thyroid
Right internal jugular vein Left internal jugular vein

Embryology of thyroid?
The thyroid gland develops from the foramen caecum (⅔ along the length of tongue from the tip) to pass forward and
loop around beneath the hyoid bone.
A thyroglossal cyst is a fibrous cyst
Incomplete descent → lingual or pyramidal thyroid
that forms from a persistent
Incomplete closure of the pathway of descent → thyroglossal cyst thyroglossal duct. Thyroglossal cysts
can be defined as an irregular neck
Vertebral level of thyroid cartilage? mass or a lump which develops from
C4 cells and tissues left over after the
formation of the thyroid gland during
Why thyroid moves up with deglutition? developmental stages.
As the thyroid gland present within the pretracheal fascia which is attached to
the thyroid cartilage and hyoid bone. When the digastric muscle contract it pulls the hyoid bone upward which pulls the
thyroid cartilage which pulls the pretracheal fascia with its contents.
Show the veins draining the thyroid?

Show the artery supplying the thyroid?
Thyrohyoid
Inferior thyroid a.
Left subclavian Right recurrent Thyrocervical trunk

artery laryngeal nerve
Inferior thyroid
veins
Commonly injured nerves during thyroidectomy?

• ELN (close to the superior thyroid artery)
• RLN (close to the inferior thyroid artery)
• Cervical sympathetic chain (lateral ligature of the inferior thyroid artery trunk causing ischemia induced neural
damage)
Type of thyroid cancer which spreads via the lymphatic route?

Papillary thyroid cancer is the only type to which spread via the lymphatic route
Cell origin of medullary carcinoma?

Parafollicular C cells
Late complications of thyroidectomy?

• Hypothyroidism
• Hypocalcemia
Parathyroid
Location?
On the posterior aspect of the thyroid gland 2 on each side
Hormone secretion?
Parathormone which plays a role in calcium homeostasis
Embryology?
• Inferior parathyroid from the 3rd branchial arch with the thymus
• Superior parathyroid from the 4th branchial arch
Blood supply?
Inferior thyroid artery
Larynx
Nerve supply?
• Motor:
All laryngeal muscles are supplied by RLN except for cricothyroid muscle, which is supplied by the external
laryngeal nerve (ELN) (branch of SLN which is a branch of vagus)
• Sensory:
Above vocal cord: Internal laryngeal nerve (ILN) (branch of SLN which is a branch of vagus)
Below vocal cord: RLN (from vagus)
Attachments of vocal cords?

• Anterior: Thyroid cartilage
• Posterior: Arytenoid cartilage
• Lateral: Laryngeal muscle
• Medial: Free border
Muscles responsible opening vocal cords?

By the 2 posterior cricoarytenoid muscles by externally rotating the arytenoids
Muscles responsible for closing the larynx during swallowing?

By lateral cricoarytenoid muscle
Action of the lateral cricoarytenoid muscles Action of the posterior cricoarytenoid muscles
Muscles responsible for tensing vocal cords?

By the 2 cricothyroid muscles
Site of cricothyroidotomy?
Cricothyroid membrane (between thyroid and cricoid cartilage)
Inferior Laryngeal Nerve (Recurrent Laryngeal Nerve) (RLN)
Supply?
Supplies all laryngeal muscles except cricothyroid muscle (supplied by SLN)
Sensory innervation of the mucous membranes of the larynx below the vocal cords
Injury on one side (unilateral) during thyroidectomy may lead to? Branches of Superior laryngeal nerve
• Diplophonia, hoarseness of voice • External laryngeal nerve “motor”
• Dysphagia • Internal laryngeal nerve “sensory”
Damage to SLN
Bilateral injury may lead to? Semon’s Law • Abnormalities in pitch
• Partial (adducted cords): Respiratory compromise • Inability to sing with smooth change to
each higher note (glissando or pitch glide)
• Full (½ ab(ad)ducted): Aphonia, inability to speak or cough
Inferior vagal ganglion

Superior laryngeal nerve
Internal laryngeal nerve

Right vagus ne
External laryngeal nerve
Cricothyroid muscle
Right recurrent laryngeal Left recurrent laryngeal
Ligamentum arteriosum
Left pulmonary artery
Skull
Identify pterion?
Bones forming?
• Frontal
• Parietal
• Temporal
• Sphenoid
Clinical significance?
Middle meningeal artery runs behind, and injury
here may lead to extradural hematoma
Layers encountered on pterional burr hole procedure?

SCALP + temporalis muscle
• Skin
• Connective tissue
• Aponeurosis of occipitofrontalis muscle
• Loose areolar tissue.
• Temporalis muscle
• Periosteum
Layers of the scalp - SCALP
Identify coronal suture on XR?
Age cranial sutures ossify by?

18 to 24 months
If fused at birth?
Craniosynostosis
Mastoid bone develops by the which age?

2 years
What are diploic veins?

Veins found in the skull that drain the diploic
space to the dural venous sinus
Tear to which vessel might cause subdural

haematoma?
Cerebral vein and bridging veins
Type of temporomandibular joint?
Bi-arthrodial hinge joint (synovial)
Articulating surfaces of TMJ?

• Head of the mandible
• Mandibular (Articular) fossa of the temporal bone
• Articular tubercle (from squamous part of the temporal bone)
Temporomandibular joint. A. Mouth closed. B. Mouth open.
Movements of TMJ?
• Elevation
• Depression*
• Protrusion*
• Retraction
• Side to side
*Opening (protrusion + depression)
By DLGM: Digastric, Lateral pterygoid,
Geniohyoid, Mylohyoid
Movements of the temporomandibular joint
Muscles of mastication?
• Masseter
• Temporalis
• Lateral pterygoid
• Medial pterygoid
Muscles of opening the mouth?

DLGM
• Digastric
• Lateral pterygoid
• Geniohyoid
• Mylohyoid
Identify ethmoidal sinus on XR?
Foramina
Foramen Location Contents
• Otic ganglion • Accessory meningeal artery
Foramen ovale
• V3 (Mandibular nerve: 3rd branch • Lesser petrosal nerve
“OVALE”
of trigeminal) • Emissary veins
• Middle meningeal artery
Foramen spinosum
• Meningeal branch of the Mandibular nerve
Foramen rotundum • Maxillary nerve (V2)
•
Sphenoid bone
ICA* (passes along its superior surface but does not traverse it)
Foramen lacerum • Nerve of the pterygoid canal (Vidian n.) (deep petrosal + superficial greater petrosal)
• Artery of the pterygoid canal
• Optic nerve + 3 layers of dura → infection of meninges is seen as papilledema
Optic canal • Ophthalmic artery (end artery)
• Sympathetic nerves
Superior orbital • Lacrimal branch of ophthalmic (V1) • Nasociliary branch of ophthalmic (V1)
fissure • Frontal branch of ophthalmic (V1) • Inferior Division of oculomotor (III)
“Live Free Son To See • Superior ophthalmic vein • Abducens (VI)
No Ignorant-Ass • Trochlear (IV) • Inferior ophthalmic veins
Individuals”
(nerves: 3, 4, 51, 6)
• Superior division of oculomotor (III)
Carotid canal • Sympathetic plexus around arteries • Deep petrosal nerve
“SIDE” • Internal carotid artery • Emissary veins
Temporal bone
• Anterior: inferior petrosal sinus

• Intermediate: glossopharyngeal, vagus, and accessory nerves. (9, 10, 11)
Jugular foramen
• Posterior: sigmoid sinus (becoming the internal jugular vein) and some
meningeal branches from the occipital and ascending pharyngeal arteries.
Stylomastoid • Stylomastoid artery
foramen • Facial nerve
Vessels Nerves Tissues
Occipital
• Vertebral arteries • Spinal root of XI • Tectorial membranes

Foramen magnum
• Anterior spinal artery • Lower end of • Apical ligament of the
• Posterior spinal artery medulla dens
Foramen rotundum:
(middle cranial fossa/ Cribriform plate:
pterygopalatine fossa) (anterior cranial fossa/ nasal cavity)
• [V2] Maxillary division of • [I] Olfactory nerves
[V] (trigeminal nerve)
Optic canal:
Foramen ovale: (middle cranial fossa/ orbit)
(middle cranial fossa/ • [II] Optic nerve
infratemporal fossa) • Ophthalmic artery
• [V3] Mandibular division of
Superior orbital fissure:
Carotid canal: (middle cranial fossa/ orbit)
(middle cranial fossa/ neck) • [V1] Ophthalmic division of
• Internal carotid artery [V] (trigeminal nerve)
• [III] Oculomotor nerve
• [IV] Trochlear nerve
Foramen spinosum:
• [VI] Abducent nerve
(middle cranial fossa/
• Superior ophthalmic vein
infratemporal fossa)
Foramen lacerum:
Jugular foramen:
(filled with cartilage in life)
(posterior cranial fossa/ neck)
• [IX] Glossopharyngeal nerve
• [X] Vagus nerve
• [XI] Accessory nerve Internal acoustic meatus:
• Internal jugular vein (posterior cranial fossa/ear, and neck
via stylomastoid foramen)
• [VII] Facial nerve
• [VIII] Vestibulocochlear nerve
Foramen magnum:
• Labyrinthine artery and vein
• Spinal cord
• Vertebral arteries Hypoglossal canal:
Roots of accessory nerve [XI] pass from upper region (posterior cranial fossa/ neck)
of spinal cord through the foramen magnum into the • [XII] Hypoglossal nerve
cranial cavity and then leave the cranial cavity
though the jugular foramen
Foramen ovale:
• [V3] Mandibular division of
Carotid canal:
• Internal carotid artery
Foramen spinosum:
Hypoglossal canal:
• [XII] Hypoglossal nerve
Stylomastoid foramen:
• [VII] Facial nerve
Jugular foramen:
• [IX] Glossopharyngeal nerve
• [X] Vagus nerve
• [XI] Accessory nerve
• Internal jugular vein
Foramen magnum:
• Spinal cord
• Vertebral arteries
Identify What is the cranial nerve track on the clivus?
• Trigeminal impression for trigeminal Abducent nerve
ganglion?
• Squamous part of the temporal bone? Name of the juvenile structure that form the clivus?
• Tegmen tympani? Spheno-occipital synchondrosis
• Frontal crest?
Benign tumors of the posterior cranial fossa?
• Clivus?
• Hemangioblastoma
• Groove for the transverse sinus?
• Acoustic neuroma
• Internal occipital protuberance?
• Ependymoma
• Hypoglossal canal?
• Ependymoblastoma
Muscles attached to the styloid process?
• Styloglossus
• Stylohyoid
• Stylopharyngeus
Causes of lytic skull lesions?

• Lytic skeletal metastasis
• Multiple myeloma
• Paget’s disease
• Sarcoidosis
• Osteomyelitis
• Hemangioma
Identify middle cranial fossa? Boundaries of the posterior cranial fossa?
Boundaries? • Anterior: The apex of the petrous part of the
Anterior: temporal bone
• Lesser wing of sphenoid • Posterior: Occipital bone
• Anterior clinoid process • Lateral: Squamous + mastoid parts of the
Posterior: temporal bone
• Petrous part of temporal bone
• Dorsum sellae Bones forming posterior cranial fossa?
Laterally Occipital bone + temporal bone
• Squamous part of the temporal bone
Contents?
The temporal lobe
ANTERIOR CRANIAL FOSSA

MIDDLE CRANIAL FOSSA
POSTERIOR CRANIAL FOSSA
Cavernous Sinus
There are 2 cavernous sinuses each lying laterally on either side of the sella turcica.
Draining blood from? Drains blood to?

• Superior ophthalmic veins • Superior and inferior petrosal sinuses.
• Facial vein • IJV
• Emissary veins from pterygoid plexus. • Intercavernous sinus
• Sphenoparietal sinuses
Clinical significance?
Contents? Cavernous sinus thrombosis
“O TOM CAT” Due to infections from the dangerous area of the
Lateral wall (from top to bottom:) face (drained by ophthalmic and facial veins) may
components Oculomotor nerve (III) spread to the cavernous sinus as the draining veins
Trochlear nerve (IV) are valveless
Ophthalmic nerve (V1)
Maxillary nerve (V2) Signs of thrombosis?
Contents of (from medial to lateral:) • Painful swelling of the eye
the sinus Internal Carotid artery (and sympathetic plexus) • 3rd, 4th, 5th, 6th cranial palsies
Abducens nerve (VI) • Gradual loss of vision
Cavernous sinus syndrome is most

commonly caused by cavernous sinus
tumors. Diagnosis is based on signs of
pain, ophthalmoplegia, proptosis,
trigeminal nerve lesion (ophthalmic
branch) and Horner's syndrome.
Dural / Cranial Venous Sinuses
Paired Unpaired
Middle meningeal Superior sagittal
Sphenoparietal sinus Inferior sagittal
Superior petrosal sinus Straight
Sigmoid sinus Occipital
Cavernous sinus Anterior intercavernous
Transverse sinus Posterior intercavernous
Inferior petrosal sinus Basilar venous plexus
Petrosquamous
Dural venous sinus Tributaries

Superior sagittal sinus Parietal emissary veins, superior cerebral veins, scalp veins, cavernous sinus through
superior anastomotic veins, meningeal veins, veins of the frontal sinus, diploic veins.
Inferior sagittal sinus Veins draining the limbic lobe (cingulated gyrus), medial frontoparietal lobe and genu of
the corpus callosum, deep cerebral veins (incl. vein of Galen).
Straight sinus Superior cerebellar veins, few tributaries from falx cerebri.
Transverse sinus Inferior cerebellar veins, superior petrosal sinus, inferior cerebral veins, anastomotic
veins and diploic veins
Superior petrosal sinus Cerebellar, inferior cerebral and tympanic veins.
Sigmoid sinus Mastoid and condylar emissary vein, cerebellar veins and internal auditory vein
Sinus Drains into: Location

Sphenoparietal sinuses Cavernous sinuses Lesser wing of the sphenoid
Inferior sagittal sinus Straight sinus Inferior border of the falx cerebri
Superior sagittal sinus Superior border of the falx cerebri
Confluence of
Straight sinus Superior border of tentorium cerebelli
sinuses
Occipital sinus Inner surface of the occipital bone
Transverse sinus Transverse sulcus (groove on the inner aspect of occipital bone)
Superior petrosal sinus Sigmoid sinus Superior petrosal sulcus
Inferior petrosal sinus Inferior petrosal sulcus
Sigmoid sinus IJV Sigmoid sulcus (floor of the PCF)
What is the major vein draining the brain parenchyma?
Great Cerebral vein
Describe blood flow from the superior sagittal sinus to the IJV
See table
Describe the location of the straight sinus

Tentorium cerebelli and flax junction
Show transverse sinus and sigmoid sinus on skull bone model?

See pic
Identify temporalis muscle?
Blood supply?
Deep temporal arteries (anterior and posterior) from
maxillary artery
What supplies the scalp over the temporalis muscle?

Superficial temporal artery from ECA
Temporalis muscle
Facial Nerve (VII)
Intracranial course of facial nerve?
Origin between pons and medulla → IAM → facial canal (petrous part of temporal bone) → exit through the stylomastoid
foramen
Branches in the face?

Enters parotid gland and divides into 5 branches: “The Zebra Buggered My Cat”
• Temporal branch
• Zygomatic branch
• Buccal branch
• Marginal mandibular branch
• Cervical branch
Facial nerve [VII] on the face. A. Terminal branches. B. Branches before entering the parotid gland.
Cranial nerves that transmit parasympathetic fibers?

The only cranial nerves that transmit parasympathetic fibers are the Oculomotor (III), Facial (VII), Glossopharyngeal (IX),
and Vagus (X) nerves
Parotid Gland
Identify parotid gland?
Identify parotid duct? Surface anatomy?
The middle ⅓ of a line drawn between intertragic notch to the middle of the philtrum
Opening?
Crosses the masseter, pierces the buccinator and drains adjacent to the 2nd upper molar
tooth (Stensen's duct).
Structures passing • Facial nerve (most superficial structure)
through the gland? (“The Zebra Buggered My Cat” Temporal Zygomatic, Buccal, Mandibular, Cervical)
• External carotid artery
• Retromandibular vein
• Auriculotemporal nerve (from posterior trunk of V3)
• Deep parotid lymph nodes
Relations • Anterior: masseter, medial pterygoid, superficial temporal and maxillary artery, facial
nerve, stylomandibular ligament
• Posterior: posterior belly digastric muscle, sternocleidomastoid, stylohyoid, internal
carotid artery, mastoid process, styloid process
Arterial supply? Branches of external carotid artery
Venous drainage? Retromandibular vein (union of the superficial temporal and maxillary veins)
Lymphatic drainage? Deep and superficial parotid lymph nodes → upper deep cervical lymph nodes
Nerve innervation • Parasympathetic: Secretomotor (from otic ganglion)
Parasympathetic • Sympathetic: Superior cervical ganglion
ganglion? • Sensory: Greater auricular nerve
Maxillary artery and vein
Transverse facial artery and vein Superficial temporal artery and vein
Posterior auricular artery
Retromandibular vein
Buccinator
Marginal mandibular
branches
Cervical branches
Surface anatomy?
• Upper end: curved line from the tragus to the center of mastoid bone
• Anterior border: a line from the tragus of the ear to the center of the posterior border of the masseter then to
the point 2 cm below and behind the angle of the mandible
• Posterior border: straight line from the mastoid process to a point 2cm below and behind the angle of the
mandible
Parotid gland and duct, CN VII & XI,

cutaneous branches of cervical plexus
and internal jugular vein.
1) porion line;
2) zygomatic sutural line;
3) zone of location of the
(fronto)temporal nerve;
4) parotid gland;
5) zone of location (white) of the
parotid duct (green line): sits within
1.5 cm of the middle half of a line
passing from the lower tragus to the
chelion;
6) lower tragus–chelion line;
7) marginal mandibular nerve;
8) zone of emergence of the cutaneous
branches of the cervical plexus
(white), posterior to the middle third
of sternocleidomastoid;
9) zone of location of the accessory
nerve, from 3–10 cm below the tip
of the mastoid process to 1–10 cm
above the insertion of trapezius into
the clavicle;
10) hyoid bone;
11) thyroid cartilage (laryngeal
prominence);
12) cricothyroid ligament/membrane;
13) cricoid cartilage;
14) external jugular vein;
X (blue), angle of the mandible;
X (red), facial artery and anterior
border of masseter crossing the lower
border of the mandible;
X (orange), superficial temporal artery.
Type of parotid salivary secretions?

Serous
Parasympathetic stimulation produces a water-rich, serous saliva.
Sympathetic stimulation leads to the production of a low volume, enzyme-rich saliva.
Differential diagnosis of parotid lump?

• Infection (parotitis, mumps)
• Obstructed duct (calculus or external compression)
• Neoplasm (pleomorphic adenoma, Warthin’s tumor)
• Deep parotid lymph nodes
Frey syndrome?
Damage of the parasympathetic fibers from the auriculotemporal nerve resulting in excessive gustatory sweating in
response to salivary stimulus
Where to palpate facial artery?
Can be palpated as it crosses the inferior border of the mandible adjacent to the anterior border of the masseter
Submandibular duct opening?

Opens in the floor of the mouth on either side of the lingual frenulum
Submandibular gland type of secretion?

Mucous + serous
Nerves at risk of injury on submandibular gland excision?

• Lingual nerve (above)
• Hypoglossal nerve (below) → deviation of the tongue to the affected side on protrusion
• Marginal mandibular branch of facial nerve
Difference between UMNL and LMNL facial palsy?
In upper motor neuron lesion upper part of face will be spared (only lower part will be affected)
In lower motor neuron lesion both upper and lower part of face will be affected.
Regions drained by pre-auricular LNs?

• Upper half of the face
• Temporal region
• Auricle and external auditory
meatus
• Gums
Identify this picture?

Microscopic picture of malignant
melanoma lymph node metastasis
(note pigmented cells)
Tongue
Nerve supply?
Motor Innervation
All of the motor innervation is provided by Hypoglossal (XII) except for the palatoglossus muscle which is provided by
Vagus (X).
Sensory and taste Innervation

Area Sensory Innervation Gustatory (taste) Innervation
Posterior part of the root of tongue Vagus (X)
Posterior 1/3 Glossopharyngeal (IX)*
Anterior 2/3 Mandibular (V3) via Lingual Facial (VII) via Chorda tympani
*Supplies general sensation to the posterior third of the tongue and contributes to the gag reflex.
Sensory
Anterior two-thirds (oral)
• General sensation mandibular
nerve [V3] via lingual nerve Posterior one-third (pharyngeal)
• Special sensation (taste) facial • General and special (taste) sensation via
nerve [VII] via chorda tympani Glossopharyngeal nerve [IX]
glossopharyngeal nerve [IX] Chorda tympani (from [VII])
Lingual nerve
(from [V3])
Motor
Hypoglossal
nerve [XII]
Intrinsic muscle Deep lingual vein

Genioglossus Dorsal lingual vein
Lingual artery
Common carotid artery
Palatoglossus Internal jugular vein

vagus nerve [X]
Sternocleidomastoid branch of occipital artery
Extrinsic muscles of the tongue?

SHPG
• Styloglossus (XII)
• Hyoglossus (XII)
• Genioglossus (XII)
• Palatoglossus (X)
Muscle retracting the tongue?

Styloglossus
Nerve supply?
All by hypoglossal nerve except for the palatoglossus by vagus nerve
Ear Anatomy
Roof of the middle ear? Identify Internal auditory meatus (IAM)?

Tegmen tympani Structures passing through IAM?
• Facial nerve
How middle ear infections cross the skull? • Vestibulocochlear nerve
By direct erosion of tegmen tympani It may also
spread to mastoid air cells causing mastoiditis What can make irreversible damage to vestibulocochlear nerve?
Acoustic neuroma
Clinical picture of meningism?
• Photophobia Why patient with acoustic neuroma hear sounds loudly on
• Neck stiffness affected side?
• Fever Affection of facial nerve with paralysis of stapedius
Relations of the middle ear?

• Roof (Tegmental wall): Tegmen tympani; separates tympanic cavity from MCF
• Floor (Jugular wall): Thin bone separates tympanic cavity from superior bulb of IJN
• Anterior wall: Thin bone; separates tympanic cavity from ICA and at its upper part are openings into two canals
(auditory tube and canal for tensor tympani)
• Posterior wall (mastoid wall): Aditus to the mastoid antrum superiorly and pyramid inferiorly (for stapedius)
• Lateral wall (membranous wall): Tympanic membrane (doesn’t extend superiorly) and lateral wall of epitympanic
recess (superiorly)
• Medial wall: Lateral wall of the inner ear
Prominence of facial canal Tegmen tympani

Prominence of lat. Semicircular canal
Promontory
Tensor tympani muscle
Aditus to mastoid antrum
Round Internal carotid artery

window
Chorda tympani
Tympanic branch of glossopharyngeal nerve [IX]
Facial nerve
Internal jugular vein
Boundaries of the right middle ear
Brain
Subarachnoid Spaces / Cisterns

● Cisterna magna
● Prepontine cistern
● Suprasellar cistern
● Interpeduncular cistern
● Quadrigeminal cistern
● Ambient cistern
● Cerebellopontine cistern
● Premedullary cistern
● Sylvian cistern
Interpeduncular cistern
Prepontine cistern
Suprasellar cistern
Arnold Chiari malformations?
It is a condition affecting the brain. It consists of a downward displacement of the cerebellar tonsils through the foramen
magnum causing non-communicating hydrocephalus as a result of obstruction of cerebrospinal fluid (CSF) outflow.
Arnold-Chiari malformation. Midsagittal section showing

small posterior fossa contents, downward displacement of
the cerebellar vermis, and deformity of the medulla (arrows
indicate the approximate level of the foramen magnum).
Identify parasagittal hyperdense mass?
Meningioma
Where does it arise from? What is the patient will be presented by?
They arise from the arachnoid "cap" cells Monoparesis of the contralateral lower limb
of the arachnoid villi in the meninges
What area of the brain is affected?
What structures may it compress? Motor area 4
• Superior sagittal sinus
• Cerebral hemisphere What area of body is represented on medial side of
motor area?
What structures does it lie between? Lower limbs
Falx and cerebral hemisphere
What area is located in pre-central gyrus?
Identify corpus collosum and lateral ventricle Primary motor cortex
and Precentral gyrus on MRI
See before Which layer of meninges is meningioma attached to?
Dura
Type of contrast
Gadolinium
What is meant by ring enhancement?

Is an abnormal radiologic sing of MRI or CT scans obtained using
radiocontrast. On the image, there is an area of increased density,
surrounded by a bright rim from concentration of the enhancing
contrast dye. This enhancement may represent breakdown of the
blood-brain barrier and the development of an inflammatory capsule.
Differential diagnosis? MAGIC DR

• Metastasis
• Abscess
• Glioblastoma
• Infarct (subacute phase)
• Contusion
• Demyelinating disease
• Radiation necrosis or resolving hematoma
What is the aggressive form of glioma?

Glioblastoma multiforme (GBM)
CSF
Circulation of cerebrospinal fluid (CSF)?
The arrows show the pathway of cerebrospinal fluid flow from the choroid
plexuses in the lateral ventricles to the arachnoidal villi protruding into the
dural sinuses.
Lateral Ventricle Lateral Ventricle
Interventricular Interventricular
Foramen (Foramen of Foramen (Foramen of
Monroe) Monroe)
Third Ventricle
Aqueduct of Sylvius
(Cerebral Aueduct)
Fourth Ventricle
Foramen of Luschka Foramen of Magendie Foramen of Luschka

(Lateral Aperture) (Median Aperture) (Lateral Aperture)
Subarachnoid Space
Arachnoid Villi
Superior Sagittal Sinus
Circle of Willis
The two internal carotid arteries and two
vertebral arteries form an anastomosis known
as the Circle of Willis on the inferior surface of
the brain. Each half of the circle is formed by:
1. Anterior communicating artery
2. Anterior cerebral artery
3. Internal carotid artery
4. Posterior communicating artery
5. Posterior cerebral arteries and the
termination of the basilar artery
The circle and its branches supply; the corpus
striatum, internal capsule, diencephalon and
midbrain.
Vertebral arteries
• Enter the cranial cavity via foramen
magnum
• Lie in the subarachnoid space
• Ascend on anterior surface of medulla
oblongata
• Unite to form the basilar artery at the base
of the pons
Branches:
• Posterior spinal artery
• Anterior spinal artery
• Posterior inferior cerebellar artery
Basilar artery branches
• Anterior inferior cerebellar artery
• Labyrinthine artery
• Pontine arteries
• Superior cerebellar artery
• Posterior cerebral artery
Internal carotid arteries branches
• Posterior communicating artery
• Anterior cerebral artery
• Middle cerebral artery
• Anterior choroid artery
Entry of vertebral artery into the skull?
Vertebral artery enters the skull through the foramen magnum
Crosses transversely across the posterior arch of the atlas
Vertebral artery course?

Inside the skull, the 2 vertebral arteries pass upwards, forwards and medially in the subarachnoid space to reach the
anterior aspect of the medulla oblongata, then they unite together at the lower border of the pons to form the basilar
artery
What the vertebral artery and basilar artery supply in the brain?
The vertebrobasilar arterial system perfuse the medulla, cerebellum, pons, midbrain, thalamus, and occipital cortex
Which vein drain the dangerous area of the face?

Inferior ophthalmic vein
Where does the ICA enter the skull / Course of the internal carotid artery?
ICA enters the skull through the carotid canal in the petrous part of temporal bone
What branch gives off before ACA, MCA?

Ophthalmic artery
Berry aneurysm rupture?

Subarachnoid hemorrhage
Signs of MCA infarct?

• Hemiplegia of the lower ½ of the contralateral face
• Hemiplegia of the contralateral upper and lower extremities
• Aphasia if in the dominant hemisphere
Identify vessels on cerebral angiogram?
Carotid arteriogram
Internal Carotid Artery Occlusion: Cerebral Angiogram.

Note that the left internal carotid artery (ICA) is completely occluded. The entire right hemisphere is being perfused from
the contralateral side. Thus, with an intact circle of Willis, some patients can be completely asymptomatic from a carotid
occlusion.
Right internal carotid artery injection - AP view. Left common carotid artery injection, AP view.
Identify optic nerve, ICA, optic chiasm, oculomotor and abducent nerves?
Identify falx cerebelli and tentorium cerebelli?
Anterior attachment of tentorium cerebelli?

Superior angle of the petrous part of the temporal bone
Blood vessel supplying the inner table of temporal bone

Middle meningeal artery
If there is a tumor in the precentral gyrus, what is the bone to penetrate?

Parietal bone
Relationship between ICP and oculomotor?

Increase in ICP → oculomotor nerve palsy → dilated pupil (see ASSCC)
What are false localizing signs?

Neurological signs have been described as “false localizing” if they reflect
dysfunction distant or remote from the expected anatomical locus of
pathology. They occur in two major contexts: as a consequence of raised Internal carotid artery
ICP, and with spinal cord lesions. E.g.: abducent nerve palsy due to ↑ ICP
Muscles supplied by oculomotor nerve?
• Levator palpebrae superioris
• Superior rectus
• Inferior rectus
• Medial rectus
• Sympathetic fibres to Muller’s muscle
• Inferior oblique
• Sphincter pupillae
Paralysis of oculomotor nerve leads to?

The eye will be displaced outward and downward
• Outward because the lateral rectus
(innervated by Abducens [VI]) maintains
muscle tone in comparison to the paralyzed
medial rectus.
• Downwards, because the superior oblique
(innervated by Trochlear [IV]) is un-antagonized
by the paralyzed superior rectus, inferior
rectus and inferior oblique.
The affected individual will also have a ptosis and
mydriasis
SO4 LR6
Superior oblique innervated by 4th (trochlear)
Lateral rectus innervated by 6th (abducent)
What is the exact structure on which the oculomotor

nerve is pressed against?
Petrous part of the temporal bone (attached border of
tentorium cerebelli)
Structures passing through superior orbital fissure?

See before (foramina)
A. Action of individual muscles (anatomical action).

B. Movement of eye when testing specific muscle (clinical testing).
ANATOMY
ABDOMEN MRCS Part B Notes by Mo
Abdominal aortic branches ...................................................................................................................................................... 2

Abdominal Aortic Aneurysm .................................................................................................................................................... 3
Coeliac trunk ............................................................................................................................................................................. 4
Superior Mesenteric Vessels .................................................................................................................................................... 6
Inferior Mesenteric Vessels ...................................................................................................................................................... 8
IVC ............................................................................................................................................................................................ 10
Liver ......................................................................................................................................................................................... 12
Gallbladder .............................................................................................................................................................................. 13
Pancreas .................................................................................................................................................................................. 14
Spleen ...................................................................................................................................................................................... 18
Esophagus................................................................................................................................................................................ 20
Stomach ................................................................................................................................................................................... 22
Duodenum ............................................................................................................................................................................... 24
Appendix .................................................................................................................................................................................. 26
Diaphragm ............................................................................................................................................................................... 28
External Oblique Muscle ......................................................................................................................................................... 30
Internal Oblique Muscle ......................................................................................................................................................... 30
Inguinal Canal .......................................................................................................................................................................... 32
Urinary bladder ....................................................................................................................................................................... 34
ANATOMY ABDOMEN MO’s MRCS B NOTES (Previously called Reda’s Notes) 1

Abdominal aortic branches
'Prostitutes Cause Sagging Swollen Red Testicles [in men] Living In Sin':
Branches Level Paired Type
Inferior Phrenic T12 (Upper border) Yes Parietal
Coeliac T12 No Visceral
Superior mesenteric L1 No Visceral
Middle Suprarenal L1 Yes Visceral
Renal L1-L2 Yes Visceral
Testicular (in men) Gonadal L2 Yes Visceral
Lumbar L1-L4 Yes Parietal
Inferior mesenteric L3 No Visceral
Median Sacral L4 No Parietal
Common iliac L4 Yes Terminal
Identify branches on mesenteric

angiogram?
A. Abdominal aorta
B. Rt. common iliac
C. Lt. Common iliac
D. Lt. Renal a.
E. Rt. renal a.
F. splenic a.
G. common hepatic
H. SMA
I. gastroduodenal a
J. Lt. Hepatic a.
K. Rt. hepatic a.
L. IMA
Anterior relations?
• Celiac trunk and branches
• Body of the pancreas
• SMA
• 3rd part of duodenum
• Root of mesentery
• Splenic vein
• Left renal vein
Surface markings of transpyloric plane?

Located halfway between the jugular
notch and the upper border of the
pubic symphysis
Types of Aneurysms
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY ABDOMEN

Abdominal Aortic Aneurysm
Identify AAA on CT angiography
Saccular Infrarenal AAA
Define aneurysm:
Abnormal dilatation of the wall of an artery.
Pathogenesis:
Median cystic necrosis (true aneurysm), post- traumatic (false
aneurysm)
Causes (risk factors):

• HTN secondary to atherosclerosis secondary to smoking
• Marfan syndrome
• Syphilis
• Bicuspid aortic valve
Dissecting aneurysm:
Separation of the layers of the arterial wall with propagation of
dissection proximally and distally
Complications:
o Hemorrhage due to rupture
o Ascending aorta---> acute MI
o Arch of aorta ---> stroke

Coeliac trunk
The coeliac axis has three main branches. “Left Hand Side (LHS)”
Left Gastric Common Hepatic Splenic
• Right Gastric • Pancreatic
• Gastroduodenal • Short Gastric
• Hepatic proper (gives right and left hepatic) • Left Gastroepiploic
• Cystic (occasionally).

Superior Mesenteric Vessels
Identify branches supplying GIT?

Inferior Mesenteric Vessels

IVC

IVC Tributaries?
Level Vein I Like To Rise So High” Identify right and left gonadal veins?
T8 Hepatic vein • Iliacs
Inferior phrenic vein • Lumbar Anterior relations of renal veins?
Pierces diaphragm • Testicular • Rt. side:
L1 Suprarenal veins • Renal o 2nd part of duodenum
Renal vein • Suprarenal • Lt. side
L2 Gonadal vein • Hepatic veins o Body of Pancreas
L1-5 Lumbar veins
o SMA
L5 Common iliac vein
o Splenic vein
Formation of IVC

Liver

Body of GB Hepatic duct
Fundus of GB
Neck of GB Quadrate lobe
Fissure for
ligamentum teres
Left lobe
Right lobe
Porta hepatis
Cystic duct
Bile duct
Portal vein
Fissure for
Caudate lobe ligamentum
Hepatic artery
venosum
What are the first 2 organs injured in stab epigastrium? Ligaments supporting?
• Liver (left lobe) • Falciform ligament (to the diaphragm and
• Stomach AAW)
• Lesser omentum (to the stomach and 1st part
What demarcates left and right lobe? of duodenum)
Anatomical: • Right and left triangular ligament (to the
• Falciform ligament (anteriorly) diaphragm)
• Fissure for ligamentum teres and ligamentum • Upper and lower coronary ligament (to the
venosum (posteroinferiorly) diaphragm)
Surgical:
• A line passing from IVC to the fossa of GB
Gallbladder
Venous drainage?
Hepatic veins to IVC Surface marking of Gallbladder
At the angle between the 9th costal cartilage and the
What artery of the celiac trunk supplies both liver and lateral margin of the rectus sheath
stomach?
Hepatic artery (runs in the free border of lesser Why is there shoulder pain in cholecystitis?
omentum to porta hepatis) An inflamed gallbladder may irritate the diaphragm.
Roots of phrenic nerve that supply the diaphragm as
Porta hepatis structures? the same as the supraclavicular nerve supplying the
From anterior to posterior shoulder tip.
• Right and left hepatic ducts
• Hepatic artery
• Portal vein

Pancreas
Parts?
Head, Neck, Body, and Tail
Production of islet cells?

• Alpha cells: glucagon
• Beta cells: insulin
• D cells: somatostatins
Ducts / Describe ductal drainage system of pancreas / Where do the pancreatic duct open?
• Main pancreatic duct (of Wirsung): drains head, body and tail → opens into major duodenal papilla.
• Accessory pancreatic duct (of Santorini): drains the uncinate process → opens into minor duodenal papilla.

Aorta
Inferior vena cava
Right kidney
Right kidney
Jejunum
Uncinate process
Superior
mesenteric vein Superior mesenteric artery

Blood supply?
3 sources
1. Superior pancreaticoduodenal aa (from gastroduodenal artery)
2. Inferior pancreaticoduodenal aa (from SMA)
3. Pancreatic branches (from splenic artery)
Vessels encountered during Whipple?

• Abdominal aorta
• SMA and SMV
• PV
• Left renal vein
• Splenic vein
• Superior and inferior pancreaticoduodenal arteries
Ligament connecting the tail of pancreas with the spleen?

Lienorenal (splenorenal) ligament
Peritoneal relation of pancreas?

All is retroperitoneal except for the tail
Vessel present behind body of pancreas?

Splenic artery
Vessel present behind neck?

Portal vein
Space present behind pancreas?

Lesser sac

Development of pancreas?
• Ventral bud: From the hepatic diverticulum and it gives rise to the lower part of the head and uncinate process.
• Dorsal bud: From the dorsal aspect of the duodenum and gives rise to upper part of the head, neck, body and
tail.

Spleen
Identify?
1,3,5,7,9,11 (odd numbers up to 11)
Blood supply? 1 inch thick, 3 inches wide, 5 inches long,
Arterial: Splenic artery (from the celiac trunk) weighs 7oz (150-200g), lies between the
Venous: Splenic vein → SMV → portal vein 9th and 11th ribs
Related ribs?
Opposite 9th,10th,11th ribs
Structure to warry during splenectomy?

Tail of the pancreas
Describe the course of splenic arteries?

Arises from the coeliac trunk → passes to the left above the upper border of the pancreas →
behind the stomach separated from it by the lesser sac → lien ligament → ends by giving up terminal branches inside
the hilum of the spleen
It supplies: pancreas, stomach, spleen

Esophagus
Begins?
At the lower border of cricoid cartilage(c6)
Blood supply?
Artery Vein Lymphatics Muscularis externa
Upper third Inferior thyroid Inferior thyroid Deep cervical Striated muscle
Mid third Aortic branches Azygos branches Mediastinal Smooth & striated muscle
Lower third Left gastric Left gastric Gastric Smooth muscle

Cell lining?
Stratified squamous epithelium
Barret's esophagus?
Columnar metaplasia with increased risk of developing adenocarcinoma
Achalasia?
Esophageal achalasia is an esophageal motility disorder involving the smooth muscle layer of the esophagus and the
lower esophageal sphincter (LES). It is characterized by incomplete LES relaxation, increased LES tone, and lack of
peristalsis of the esophagus
Microscopic picture of achalasia?

Hypertrophied musculature with absence of myenteric plexus
Lymphatic drainage?
See table
What makes an indent on the esophagus?

• Left bronchus
• Aortic arch
• Left atrium
Complications of perforated esophagus?

Mediastinitis
Constrictions of the esophagus

Structure Distance from incisors
Cricoid cartilage 15cm
Arch of the Aorta 22.5cm
Left principal bronchus 27cm
Diaphragmatic hiatus 40cm

Stomach

Parts?
• Fundus
• Body
• Pylorus
Blood supply?
Arterial Venous
• Left gastric artery from celiac trunk • Left gastric vein → portal vein
• Right gastric artery from hepatic artery • Right gastric vein → portal vein
• Left gastroepiploic from splenic artery • Left gastroepiploic → splenic vein
• Short gastric a. from splenic artery • Short gastric veins → splenic vein
• Right gastroepiploic from gastroduodenal from hepatic artery • Right gastroepiploic vein → SMV

Duodenum
Duodenum consists of 4 parts
Peritoneal relations / Which part of the duodenum lies intraperitoneal?

The first part of the duodenum lies within the peritoneum, but its other parts are retroperitoneal
Blood supply?
• Superior pancreaticoduodenal artery (from gastroduodenal)
• Inferior pancreaticoduodenal artery (from SMA)
• Branches from hepatic, right gastric, right gastroepiploic and supraduodenal arteries
Relations of the different parts of the duodenum?

First part:
• Superiorly: Epiploic foramen being divided from it by the portal vein and bile duct.
• Inferiorly: Head and neck of the pancreas.
• Anteriorly: Quadrate lobe of the liver and gallbladder.
• Posteriorly: Portal vein, gastroduodenal artery, and common bile duct (CBD).
Second part:
• Anteriorly: Gallbladder and right lobe of the liver, transverse colon, transverse mesocolon (commencement),
and coils of the small intestine.
• Posteriorly: Right kidney and right renal vessels, right edge of the inferior vena cava (IVC), and right psoas major
muscle.
• Medially: Head of the pancreas.
• Laterally: From below upward, ascending colon, right colic flexure, and right lobe of the liver.
Third part:
• Anteriorly: Root of the mesentery, superior mesenteric vessels, and coils of the jejunum.
• Posteriorly: Right psoas major, right ureter, IVC, abdominal aorta, and right gonadal vessels.
• Superiorly: Head of the pancreas with its uncinate process.
• Inferiorly: Coils of the jejunum.
Fourth part:
• Anteriorly: Transverse colon and transverse mesocolon.
• Posteriorly: Left psoas major muscle, left sympathetic chain, left gonadal vessels, and inferior mesenteric vein.
• Superiorly: Body of the pancreas.
• On to the left: Left kidney and left ureter.
• On to the right: Upper part of the root of mesentery.
Vessels present in front and behind the 3rd part of the duodenum?
Major duodenal papilla (papilla of Vater)?

It’s a well-marked conical projection on the posteromedial wall and situated 8-10 cm distal to the pylorus (2nd part of the
duodenum). It’s the opening of the junction of pancreatic duct and common bile duct (ampulla of Vater) into the
duodenum.

Appendix
Positions?
• Retrocecal
• Subcecal
• Pelvic
• Pre-ileal
• Post-ileal
Blood supply?
• Appendicular artery from the ileocolic artery
• Appendicular vein to SMV
Why appendicitis pain is referred to umbilicus?

Pain initially starts in the periumbilical region as visceral pain from the appendix is conveyed in nerve fibres
entering the spinal cord at the T10 level (the T10 dermatome covers the level of the umbilicus).
Irritation of the parietal peritoneum by an inflamed appendix later on causes localisation of pain to the RIF.
Arterial supply to the cecum and appendix
Positions of the appendix

Identify the following? (on a plastic model)
• Uterus
• Fallopian tubes
• Ovaries
• Douglas pouch (rectouterine pouch)
• Caecum
• Terminal ileum
• Appendix

Diaphragm
Openings?
T8 (8 letters) = Vena cava
T10 (10 letters) = Oesophagus
T12 (12 letters) = Aortic hiatus
Level T8 T10 T12
Location Central Tendon Right crus Behind median arcuate ligament
IVC Esophagus Aorta
Structures Right phrenic nerve Vagus nerves Azygous vein
Thoracic duct
Attachments?
Sternal part Costal part Vertebral part (crura and arcuate ligaments)
Xiphoid process Inner surface of • Right crus (L1, L2, L3)
of the sternum the lower six • Left crus (L1, L2)
costal cartilages • Median arcuate ligament (between the 2 crura)
Origin • Medial arcuate ligament (extends from the side of the
body of L1 to the tip of the transverse process of L2)
• Lateral arcuate ligament (extends from the tip of the
transverse process of L1 and is inserted into the lower
border of the 12th rib)
Insertion Central aponeurotic tendon
Actions Inspiration and forced expiration
Innervation Phrenic nerve (C3, C4, C5) – “3, 4, 5, keeps the diaphragm alive”
Blood Supply Inferior Phrenic artery

External Oblique Muscle
Origin Outer surfaces of the lowest eight ribs

Insertion • Anterior two thirds of the outer lip of the iliac crest.
• Linea alba*
• Pubic tubercle
• Pubic crest
• ASIS
Nerve supply Ventral rami of the lower six thoracic nerves (T7 – T12)
Direction of fibers Downwards, forwards and medially
Actions Contains the abdominal viscera, may contract to raise intra-abdominal pressure. Moves trunk to
one side.
Linea alba attaches to xiphoid process of the sternum and the pubic symphysis.
Internal Oblique Muscle
Origin • Thoracolumbar fascia

• Anterior 2/3 of the iliac crest
• Lateral 2/3 of the inguinal ligament
Insertion • Cartilages of the lower 3 ribs
• Conjoint tendon
• Pubic crest
• Linea alba
Nerve supply • Lower six thoracic nerves (T7 – T12)
• Iliohypogastric and ilioinguinal nerves

Muscles of the left side of the trunk. External oblique has been removed to show internal oblique, but its digitations from the ribs have been
preserved. The sheath of rectus abdominis has been opened and its anterior layer removed.

Inguinal Canal
Boundaries?
Mnemonic “MALT”
Roof (Superior wall) • Internal oblique Muscle
“2 Muscles” • Transversus abdominis Muscle
Anterior wall • External oblique Aponeurosis
“2 Aponeurosis” • Internal oblique Aponeurosis
Floor (Inferior wall) • External oblique aponeurosis
“2 Ligaments” • Inguinal Ligament
• Lacunar Ligament
Posterior wall • Transversalis fascia
“2 Ts” • Conjoint Tendon
Laterally • Internal ring
• Transversalis fascia
• Fibres of internal oblique
Medially • External ring
• Conjoint tendon
Anterior superior
iliac spine
Superficial
inguinal ring

Urinary bladder
Identify UB
Identify internal iliac artery?
Blood supply?
Arterial: Superior and inferior vesical arteries from the internal iliac
artery
Venous: To vesical venous plexus → internal iliac vein
Nerve supply to detrusor muscle?

• Sympathetic: inhibit contraction of the muscle (from L1, L2)
• Parasympathetic: stimulate contraction of the muscle (from
S2-S4)
Most common bladder cancer?

• TCC
• SCC
• Mixed
• Adenocarcinoma
C/P of bladder cancer?

Painless hematuria
Risk factors of bladder cancer?

• Aniline dyes
• Smoking
• β-naphthylamine
• Schistosoma haematobium Bladder. A) Superolateral view. B) The trigone. Anterior
view with the anterior part of the bladder cut away.
How does ureter enter the bladder?
At the base of the bladder at the corner of the trigone
Peritoneal relations of the bladder?

Covers the superior surface and the upper part of the posterior surface
Layers encountered during suprapubic catheterization?

• Skin
• Subcutaneus tissue
• Scarpa's fascia
• Linea alba
• Fascia transversalis
• Preperitoneal fat
Posterior relations of the bladder?

Male
• Rectovesical pouch
• Two vas deferens
• Terminal part of the 2 ureters
Female
• Vesicouterine pouch
• Terminal part of the 2 ureters
Ligaments that anchor the neck of the bladder

and pelvic part of the urethra to the pelvic bones.
A) In women. B) In men.

ANATOMY
THORAX MRCS Part B Notes by Mo
Heart .......................................................................................................................................................................................... 2
Lungs .......................................................................................................................................................................................... 8
Thoracic Inlet and Mediastinum ............................................................................................................................................ 12
Posterior mediastinum ........................................................................................................................................................... 14
Sympathetic Trunk .................................................................................................................................................................. 15
ANATOMY THORAX MO’s MRCS B NOTES (Previously called Reda’s Notes) 1

Heart
In A, the pericardium has been incised and

turned back (23) to display the anterior
surface of the heart. The pulmonary trunk
(17) leaves the right ventricle (22) in front
and to the left of the ascending aorta (3),
which is overlapped by the auricle (5) of
the right atrium (18). The superior vena
cava (25) is to the right of the aorta and
still largely covered by pericardium. The
anterior interventricular branch (2) of the
left coronary artery and the great cardiac
vein (7) lie in the interventricular groove
between the right and left ventricles (22
and 11), and the right coronary artery
(19) is in the atrioventricular groove
between the right ventricle (22) and right
atrium (18).
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY THORAX

Superior vena cava
Ascending aorta Pulmonary trunk
Left auricle
Anterior
interventricular branch
of left coronary artery
Great cardiac vein

Anterior
interventricular
groove
Left ventricle
Obtuse margin
Small cardiac vein
Inferior margin

Superior vena cava
Pulmonary trunk
Right auricle
Anterior semilunar cusp

Right semilunar cusp
Left semilunar cusp
Right atrium
Pulmonary valve
Conus arteriosus
Anterior cusp Septal papillary

Tricuspid Septal cusp muscle
valve Posterior cusp
Septomarginal
trabecula
Anterior papillary muscle Posterior papillary muscle
Trabeculae carneae

How many cusps have the pulmonary valve?
3
Vertebral level of the pulmonary valve?

T6
Where to auscultate pulmonary valve?

2nd ICS left parasternal edge

Tributaries of Azygos vein?
“Right Handed PM Loves Eating Burgers”
• Right superior intercostal vein
• Hemiazygos and accessory hemiazygos
• Pericardial veins
• Mediastinal veins
• Lower right posterior intercostal veins
• Esophageal veins
• Bronchial veins
Branches of ascending aorta?

Right and left coronary arteries arising from the aortic sinus opposite the aortic valve

Brachiocephalic trunk
Right brachiocephalic vein
Left brachiocephalic vein

Lungs
Identify structures passing through the hilum of lung?

• Pulmonary artery and vein (most anterior)
• Right and left main bronchus (most posterior)
• Bronchial artery and vein
• Lymph nodes
• Autonomic nerves
Pulmonary ligament?
Pleural fold that connects the mediastinal surface of the lung and the pericardium to allow expansion of pulmonary veins
with increased blood flow
Anterior border
vein
Posterior
border
Costal surface
surface
Inferior border
RIGHT LUNG (diaphragmatic surface) LEFT LUNG

Identify surface anatomy of the lung on the skeleton?
• Apex: curved line from the sternoclavicular joint to 3 cm above the junction between the medial ⅓ and the
middle ⅓ of clavicle
• Anterior border: Sternoclavicular joint to the xiphisternal joint behind the lateral border of the sternum (left lung
deviates laterally from the sternum at the 4th costal cartilage to form the cardiac notch)
• Inferior border: Line drawn between 6th rib MCL, 8th rib MAL, 10th rib vertebral column
• Posterior border: Transverse process of C7 – T10
• Hilum: Opposite T5, T6, T7
• Carina: At the level of T4
Superior lobe Superior lobe
Horizontal fissure
Middle lobe Costomediastinal recess
Rib VI
Inferior lobe Inferior lobe
Rib VII Costodiaphragmatic

recess
Rib X
Parietal pleura
Upper lobe
Rib V Oblique fissure

Rib VI
Lower lobe
Rib X
Parietal pleura

How many bronchopulmonary segments in each
lung?
10
What is the nerve relation anterior and post?

Phrenic nerve, sympathetic chain
Describe the course of a clot from deep veins of the

calf to pulmonary artery?
Popliteal vein → femoral vein → EIV → CIV → IVC
→ right atrium → AV valve → pulmonary valve →
pulmonary artery
Nerve supply of the intercostal muscles?

Intercostal nerves and their collateral branches
Branches of the aortic arch?
Bronchopulmonary segments of right and left lungs (medial view)
Subclavian steal syndrome?

Retrograde flow of blood flow down to the vertebral artery due to
stenoocclusive disease in the subclavian artery proximal to the
vertebral artery. This will lead to brainstem ischemia on arm
exercise
Thoracic outlet syndrome?

Compression of the neurovascular bundle (brachial plexus,
subclavian artery) between the scalenus medius and scalenus
anterior → neurological and vascular symptoms in the arm
Show on the skeleton where to put a chest tube?

5th ICS midaxillary line
Why bradycardia after chest tube insertion?

Due to irritation of the vagus nerve.

Thoracic Inlet and Mediastinum

Trachea Esophagus
Right common carotid artery
Left common carotid artery
Right internal jugular vein Left internal jugular vein

Right subclavian artery Left subclavian artery
Right subclavian vein Left subclavian vein
Left pulmonary artery

Superior vena cava
Left main bronchus
Pulmonary trunk
Thoracic aorta
Right main bronchus Esophagus Ascending aorta
Thyroid cartilage
Larynx
Cricoid cartilage
Inferior thyroid veins

Posterior mediastinum
Boundaries of posterior mediastinum?

Anterior Pericardium
Vertical part of the diaphragm
Posterior Lower 8 thoracic vertebrae
On each side Mediastinal pleura
Contents of posterior mediastinum?

Region Contents
• Esophagus
• Thoracic aorta
Mediastinum
• Azygos vein
Posterior
• Thoracic duct
• Vagus nerve
• Sympathetic nerve trunks
• Splanchnic nerves
• Superior vena cava
• Brachiocephalic veins
Superior mediastinum
• Arch of aorta
• Thoracic duct
• Trachea Middle
• Esophagus mediastinum
• Thymus
• Vagus nerve
• Left recurrent laryngeal nerve
• Phrenic nerve Posterior
• Thymic remnants mediastinum
Ant.
• Lymph nodes
• Fat
• Pericardium
mediastinum
• Heart
Middle
• Aortic root
• Arch of azygos vein
• Main bronchi
Sternal angle
Superior mediastinum
Inferior mediastinum

Sympathetic Trunk
Where preganglionic fibres come from?

The corresponding spinal nerves T1-L2
What connects it to the spinal nerves?

Ganglion + white ramus communicans + grey ramus communicans
How sympathetic nerves leave the sympathetic chain?

Through the spinal nerves forming plexuses around blood vessels (cardiac and pulmonary plexuses, greater splanchnic
nerve, lesser splanchnic nerve)
Paravertebral
sympathetic trunk Spinal cord
Spinal nerve

PATHOLOGY
MRCS Part B Notes by Mo
Infective Endocarditis (IE) ......................................................................................................................................................... 2

Aortic Stenosis ........................................................................................................................................................................... 6
Temporal Arteritis (Giant Cell Arteritis) (GCA) / Osteoporosis ............................................................................................... 8
Gangrene + Mesothelioma ..................................................................................................................................................... 12
Lung Cancer ............................................................................................................................................................................. 14
Tuberculosis (TB) ..................................................................................................................................................................... 16
Breast Cancer .......................................................................................................................................................................... 18
MEN 1 Syndrome .................................................................................................................................................................... 22
MEN 2 Syndrome .................................................................................................................................................................... 24
Parotid Tumors ........................................................................................................................................................................ 26
Nasopharyngeal Carcinoma.................................................................................................................................................... 32
Carcinoid Tumor ...................................................................................................................................................................... 34
Inflammatory Bowel Disease (IBD) ......................................................................................................................................... 35
Familial Adenomatous Polyposis (FAP) .................................................................................................................................. 41
GB Cancer + Pseudomembranous Colitis .............................................................................................................................. 43
Diverticulitis + Endometriosis ................................................................................................................................................. 45
Peptic Ulcer Disease + Hyperparathyroidism ........................................................................................................................ 49
Esophageal Carcinoma............................................................................................................................................................ 51
Gastric Carcinoma ................................................................................................................................................................... 53
Cancer Colon + Hemorrhoids + Myocardial Infarction ......................................................................................................... 55
Malignant Melanoma ............................................................................................................................................................. 59
Malignant Melanoma Metastasis........................................................................................................................................... 61
Basal Cell Carcinoma (BCC) ..................................................................................................................................................... 63
Sickle Cell Disease + Brain Tumor........................................................................................................................................... 65
Polycystic Kidney Disease (APKD) ........................................................................................................................................... 67
Testicular Teratoma ................................................................................................................................................................ 69
Prostate Cancer ....................................................................................................................................................................... 71
Abscess .................................................................................................................................................................................... 73
Osteomyelitis........................................................................................................................................................................... 75
Pathological Fractures ............................................................................................................................................................ 79
Polytrauma + Transfusion ....................................................................................................................................................... 81
Hepatitis C (HCV) ..................................................................................................................................................................... 83
Acute Pancreatitis ................................................................................................................................................................... 88
Summary of Definitions .......................................................................................................................................................... 90
1
PATHOLOGY MO’s MRCS B NOTES (Previously called Reda’s Notes) 1
Infective Endocarditis (IE)
Definition?
Inflammation of the endocardial surfaces of the heart including heart valves which is caused by certain microorganisms.
Types of endocarditis?
• Infective endocarditis: here microbes colonize the heart valves and form friable vegetations. The 2 types of IE
are acute and subacute. Diagnosis via Duke’s criteria
• Non-bacterial thrombotic endocarditis aka marantic endocarditis: this variant characteristically occurs in the
settings of cancers e.g. adenocarcinomas
• Libman sacks endocarditis: occurs in the settings of cancers e.g. adenocarcinoma
Major forms of vegetative endocarditis. The acute rheumatic fever phase of rheumatic heart disease (RHD) is marked by the appearance of
small, warty, inflammatory vegetations along the lines of valve closure; as the inflammation resolves, substantial scarring can result. Infective
endocarditis (IE) is characterized by large, irregular, often destructive masses that can extend from valve leaflets onto adjacent structures (e.g.,
chordae or myocardium). Nonbacterial thrombotic endocarditis (NBTE) typically manifests with small- to medium-sized, bland, nondestructive
vegetations at the line of valve closure. Libman-Sacks endocarditis (LSE) is characterized by small- to medium-sized inflammatory vegetations
that can be attached on either side of the valve leaflets; these heal with scarring.
Why rheumatic heart and valve replacement patients are more susceptible to IE?
Blood usually flows smoothly over valves, when these valves are damaged (as in RH) or in valve replacement, there will
be an increased chance for bacterial colonization on damaged tissues.
Pathophysiology of RHD?
• Acute rheumatic fever results from host immune responses to group A streptococcal antigens that cross-react
with host proteins. In particular, antibodies and CD4+ T cells directed against streptococcal M proteins can also
in some cases recognize cardiac self-antigens. Antibody binding can activate complement, as well as recruit Fc-
receptor bearing cells (neutrophils and macrophages); cytokine production by the stimulated T cells leads to
macrophage activation (e.g., within Aschoff bodies). Damage to heart tissue may thus be caused by a
combination of antibody- and T cell–mediated reactions
• Recurrent inflammation, progressive fibrosis, narrowing and stiffening of the valve leaflets with commissural
fusion, retraction of the leaflet edges, valve thickening, calcification leading to stenosis.
CD4+ TH1 cells (and sometimes CD8+ T cells, not shown) respond to tissue antigens by secreting cytokines that stimulate inflammation
and activate phagocytes, leading to tissue injury. CD4+ TH17 cells contribute to inflammation by recruiting neutrophils (and, to a lesser
extent, monocytes).
2
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) PATHOLOGY
Gross findings?
Acute phase: Valvular vegetations (verrucae) along the lines of closure, having little effect on cardiac function
Chronic phase: Commissural fibrosis, valve thickening, and calcification + shortened and fused chordae tendinea (fish
mouth shape)
Microscopic findings?
Aschoff bodies, a form of granulomatous inflammation which consists of a central zone of degenerating ECM infiltrated
by lymphocytes, plasma cells and Anitschkow cells (activated macrophages also termed as caterpillar cells due to wavy
nuclear outlines), found in all 3 layers of the heart – pericardium, myocardium or endocardium
What to see macroscopically?

• Aschoff nodules
• Fibrinoid necrosis
Rheumatic heart disease. (A) Acute rheumatic mitral valvulitis superimposed on chronic rheumatic heart disease. Small vegetations
(verrucae) are visible along the line of closure of the mitral valve leaflet (arrows). Previous episodes of rheumatic valvulitis have
caused fibrous thickening and fusion of the chordae tendineae. (B) Microscopic appearance of an Aschoff body in acute rheumatic
carditis; there is central necrosis associated with a circumscribed collection of mononuclear inflammatory cells, including some
activated macrophages with prominent nucleoli and central wavy (caterpillar) chromatin (arrows). (C and D) Mitral stenosis with
diffuse fibrous thickening and distortion of the valve leaflets, commissural fusion (arrows), and thickening and shortening of the
chordae tendineae. There is marked left atrial dilation as seen from above the valve (C). (D) Anterior leaflet of an opened rheumatic
mitral valve; note the neovascularization (arrow). (E) Surgically removed specimen of rheumatic aortic stenosis, demonstrating
thickening and distortion of the cusps with commissural fusion
Investigation to identify vegetations?

2D echo
What to look for in 2D echo?

1) Valvular regurgitation: A regurgitant jet >1 cm in length and peak velocity >2.5 m/s
2) Leaflet: Prolapse, Coaptation failure, Thickening (>4 mm), Reduced mobility, Nodules
3) Annular dilatation
4) Chordal elongation/rupture
5) Increased echogenicity of subvalvular apparatus
6) Pericardial effusion
7) Ventricular dilatation and dysfunction (almost always with significant regurgitation)
3
Common organisms?
• Viridans Strep. or Staph.
• Coagulase negative staph.
• Enterococci
• Hacek group of microorganisms (oropharyngeal commensals)
• (Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella
species.)
Diagnosis?
Dukes criteria
Selection Criteria (Diagnostic):
• 2 Major Criteria and 0 Minor Criteria
• 1 Major Criteria and 3 Minor Criteria
• 0 Major Criteria and 5 Minor Criteria IE-Infective endocarditis
Major Criteria
Blood cultures positive for endocarditis
Typical microorganisms consistent with IE from 2 separate blood cultures, microorganisms consistent with IE
from persistently positive blood cultures, single positive blood culture for Coxiella burnetii or antiphase I IgG
antibody titer >1:800.
Evidence of endocardial involvement
Echocardiogram positive for IE, abscess, new partial dehiscence of prosthetic valve, new valvular regurgitation.
Note: Worsening or changing of pre-existing murmur NOT sufficient.
Minor Criteria
Predisposition Fever
Heart condition or IV drug use Greater than or equal 38ᵒc
Vascular phenomena Immunologic phenomena
Major arterial emboli, septic pulmonary infarcts, Glomerulonephritis, Osler’s nodes, Roth’s spots, and
mycotic aneurysm, intracranial hemorrhage, rheumatoid factor.
conjunctival hemorrhages, and Janeway’s lesions.
Microbiological evidence Echocardiographic findings
Positive blood culture but does not meet a major consistent with endocarditis but do not meet a major
criterion as noted above or serological evidence of criterion as noted above
active infection with organism consistent with IE.
Causes and risk factors of IE?

• Acquired valvular heart disease with stenosis or • Cyanotic congenital heart defects
regurgitation • Colorectal cancer (Streptococcus bovis)
• Valve replacement • UTI (enterococci)
• Structural congenital heart disease, including • IVDA
surgically corrected, but excluding isolated ASD, • RHD
fully repaired VSD/PDA • HIV
• Previous IE • Malignancy
• HOCM (hypertrophic obstructive • DM
cardiomyopathy) • Alcohol
• Devices (Implantable cardioverter-defibrillators) • Tooth extractions.
Complications of IE?
Cardiac Non-cardiac
• AMI • GN
• Pericarditis (endocarditis-associated glomerulonephritis)
• Arrhythmia • AKI
• Valvular insufficiency • Stroke
• CCF (congestive cardiac failure) • Mesenteric/splenic abscess or infarct
• Sinus of Valsalva (aneurysm of the aortic sinus)
• Aneurysm
• Intra-cardiac abscess
• Arterial emboli
4
Signs in hand? Roths spot-sphincter haemorrhage in retina Signs and symptoms of IE FROM JANE
• Osler nodes: • Fever
Painful, raised, red lesions due to immune complex deposition • Roth's spots
• Janeway lesions: • Osler's nodes
Non-painful, nodular or macular red lesions due to septic emboli • Murmur
which deposit bacteria forming microabscesses • Janeway lesions
• Splinter hemorrhages: tiny blood clots under nails • Anemia
• Nail hemorrhage (splinter hge)
• Emboli
Janeway lesion on palm of a 36 year old male with staphylococcus Osler nodes on index finger. Note also the tiny splinter
endocarditis haemorrhages on fingernail also seen in end
Treatment?
IV antibiotics depending on culture and sensitivity for 6 weeks (IV ceftriaxone and vancomycin)
Restrictions
• Valves do not have specific blood supply so antibiotics cannot reach
• Organisms lie inside the vegetations
• Bacteria form a biofilm (glycocalyx covering) that shields them from antibiotics
If IE occurs in tricuspid valve in younger persons: → right sided heart failure
If no response to medical treatment?

Valve replacement or heart transplantation
Matching before heart transplantation?

HLA antigen
If not matched?
Type 1 → graft rejection
How to prevent graft rejections?

Immunosuppressant therapy
• Tacrolimus
• Mycophenolate
• Steroids
Side effects of long-term steroid?

• Opportunistic bacterial and viral infections such as EBV, CMV ---> leukemia, lymphoma
• Cushingoid features: obesity, muscle weakness, hirsutism, striae
• Cardiovascular: fluid retention, hypertension
• Endocrine: DM
• Musculoskeletal: osteoporosis, AVN, proximal myopathy
Mechanism of action of immunosuppressants? How do immunosuppressants work?

The four classes of immunosuppressive drugs
5
Class Examples Action
Corticosteroids Prednisone, methyl prednisone Anti-inflammatory; kills T cells
Cytotoxic drugs Cyclophosphamide, azathioprine, methotrexate, Blocks cell division nonspecifically
leflunomide, mycophenolate mofetil, brequinar
sodium,
Immunophilins Cyclosporin Blocks T cell responses
Lymphocyte-depleting Antilymphocyte globulin, monoclonal antibodies Kills T cells nonspecifically, kills
therapies activated T cells
After valve replacement why on warfarin?

To prevent thromboembolism
Mechanism of action of warfarin?

Vitamin K antagonist thus inhibiting clotting factors 2,7,9,10
How to monitor?
INR
Reversal?
• Vitamin k
• FFP
• PCC
Right sided vegetations = tricuspid valve IE = IV drug abuser
Prophylaxis against infective endocarditis

Antibiotic prophylaxis against infective endocarditis is not recommended routinely:
• for people undergoing dental procedures
• for people undergoing non-dental procedures at the following sites[2]:
o upper and lower gastrointestinal tract
o genitourinary tract; this includes urological, gynaecological and obstetric procedures, and childbirth
o upper and lower respiratory tract; this includes ear, nose and throat procedures and bronchoscopy.
Chlorhexidine mouthwash should not be offered as prophylaxis against infective endocarditis to people at risk of
infective endocarditis undergoing dental procedures.
Source: https://www.nice.org.uk/guidance/cg64
Aortic Stenosis
Also see questions from the previous (IE) station…
Clinical picture?
See Pre-Operative Aortic stenosis station, ASSCC
Causes?
• Post-inflammatory scarring (rheumatic heart
disease)
• Senile calcific aortic stenosis
• Calcification of congenitally deformed valve
Cause of sudden death in AS?

• MI
• Aortic dissection
Dystrophic calcification of the aortic valve. View looking down onto the
How stenosis occurs? unopened aortic valve in a heart with calcific aortic stenosis. It is
Lipid accumulation, inflammation, calcification → markedly narrowed (stenosis). The semilunar cusps are thickened and
valve thickening and stenosis fibrotic, and behind each cusp are irregular masses of piled-up
dystrophic calcification.
6
Pathophysiology?
• As the aortic valve progresses from sclerosis to stenosis, the left ventricle encounters chronic resistance to
systolic ejection (↑ afterload) → thickening of the left ventricular wall (hypertrophy)
• Effects of high left ventricular afterload include decreased left ventricular myocardial elasticity and coronary
blood flow and increased myocardial workload, oxygen consumption, and mortality.
• Late manifestations of LVH include a smaller left ventricular chamber size, which decreases preload and worsens
systolic dysfunction. The result is insufficient stroke vol ume, cardiac output, and ejection fraction. Finally,
backward transmission of increased left ventricular pressure to the lungs may cause pulmonary venous
hypertension and reactive vasoconstriction of the pulmonary vasculature.
Aortic valve endocarditis, after a while weakness in

arm, why?
Thromboembolism which lead to cerebrovascular
stroke
Which coagulation system will not be affected by

warfarin?
Intrinsic pathway
Define thrombus?
Thrombus is defined as solid material formed from the
constituents of blood in flowing blood
Surgical options for valve replacement

• Mechanical valve – a long-lasting valve made
of durable materials
• Tissue valve (which may include human or
animal donor tissue)
• Ross Procedure – “Borrowing” healthy valve
and moving it into position of the damaged
Calcific valvular degeneration. (A) Calcific aortic stenosis of a previously normal
aortic valve valve (viewed from above the valve). Nodular masses of calcium are heaped up
• TAVI/TAVR procedure – Transcatheter aortic within the sinuses of Valsalva (arrow). Note that the commissures are not fused,
valve replacement as in rheumatic aortic valve stenosis (B) Calcific aortic stenosis occurring on a
congenitally bicuspid valve. One cusp has a partial fusion at its center, called a
Alternative options include aortic valve balloon raphe (arrow). (C and D) Mitral calcification, with calcific nodules within the
valvuloplasty – the valve is widened using a balloon annulus (attachment margin) of the mitral leaflets (arrows). (C) Left atrial view.
(D) Section demonstrating the extension of calcification into the underlying
myocardium. Such involvement of adjacent structures near the interventricular
septum can impinge on the conduction system.
If metallic valve replacement was done and the patient developed IE, why the valve should be removed?
• The valve will be a septic focus
• The valve will be dehiscent
If we found microscopic branching hyphae on a

removed metallic valve, what’s the cause?
This is fungal infection:
• Candida
• Aspergillus
• Microsporum
• Trichophyton
• Epidermophyton
Mechanical valve Tissue valve
Mechanical vs Tissue valve?
Mechanical Tissue
Excellent durability (95% at 10 years) – low rate of reoperation Noiseless
Warfarin Do not need warfarin
Easy to insert Insertion maybe more difficult
Thrombo-embolism 1-2 % / patient / year Low risk of thrombo-embolism (0 – 1%)
Bleeding risk 2% / pt / yr Low risk of bleeding (0 – 1%)
7
Temporal Arteritis (Giant Cell Arteritis) (GCA) / Osteoporosis
What is GCA? SCENARIO:

Inflammatory disease of blood vessels (large and medium) of the 60 y old female with headache (temporal
head, mainly branches of ECA. pain) and skull tenderness on mastication
and transient loss of vision.
Which part of vessel is affected most?
Tunica medium Biopsy from the temporal artery revealed
giant cell arteritis (granulomatous
Describe the pathological changes in microscopic picture? panarteritis with mononuclear cell infiltrates)
Morphology
• Involved arterial segments develop intimal thickening (with occasional thromboses) that reduces the luminal
diameter.
• Classic lesions exhibit medial granulomatous inflammation centered on the internal elastic lamina that produce
elastic lamina fragmentation.
• There is an infiltrate of T cells (CD4+ > CD8+) and macrophages.
• Although multinucleated giant cells are seen in approximately 75% of adequately biopsied specimens,
granulomas and giant cells can be rare or absent
• Inflammatory lesions are only focally distributed along the vessel and long segments of relatively normal artery
may be interposed
Temporal (giant cell) arteritis. (A) Hematoxylin-eosin-stained section of a temporal artery showing giant cells near the
fragmented internal elastic membrane (arrow), along with medial and adventitial inflammation. (B) Elastic tissue stain
demonstrating focal destruction of the internal elastic membrane (arrow) and medial attenuation and scarring.
One simple blood test to prove?

ESR (elevated)
Most confirmatory test?

Temporal artery biopsy
Why blindness?
Ophthalmic artery involvement
8
Treatment?
Corticosteroids. Start prednisolone 60mg/d PO immediately or IV methylprednisolone if evolving visual loss or history of
amaurosis fugax. Typically a 2-year course.
One year later developed fracture NOF, why?

• AVN
• Osteoporosis
Why osteoporosis in this patient?

• Steroid therapy
• Post-menopausal
Pathological changes in osteoporosis?

• Histologically normal bone that is decreased in quantity.
• Postmenopausal osteoporosis the increase in osteoclast activity affects mainly bones or portions of bones that
have increased surface area, such as the cancellous compartment of vertebral bodies.
• The trabecular plates become perforated, thinned, and lose their interconnections, leading to progressive micro
fractures and eventual vertebral collapse
What is osteoporosis and what is its pathogenesis

Metabolic bone disease characterized by:
• Low bone mass
• Micro architectural deterioration of bone tissue
• Increase bone fragility
• Loss of bone matrix
Three main mechanisms:
• Inadequate peak bone mass
• Excessive bone resorption
• Inadequate formation of new bone during bone turnover
Mechanism by which corticosteroids cause osteoporosis?
• Direct inhibition of osteoblast formation
• Direct stimulation of bone resorption
• Inhibition of GIT calcium absorption
• Stimulation of renal calcium losses
• Inhibition of sex steroids
Causes of osteoporosis?
o Primary
• Idiopathic
• Postmenopausal
• Senile
o Secondary
Endocrine Disorders Gastrointestinal Miscellaneous
• Addison disease • Hepatic insufficiency • Anemia
• Diabetes, type 1 • Malabsorption • Homocystinuria
• Hyperparathyroidism • Malnutrition • Immobilization
• Hyperthyroidism • Vitamin C, D deficiencies • Osteogenesis imperfecta
• Hypothyroidism Drugs • Pulmonary disease
• Pituitary tumors • Alcohol
• Neoplasia • Anticoagulants
• Carcinomatosis • Anticonvulsants
• Multiple myeloma • Chemotherapy
• Corticosteroids
9
Other causes of pathological fracture?
• Skeletal metastasis
• Paget's disease
• Multiple myeloma
• Rickets
• Osteomalacia
• Osteogenesis imperfecta
• Radiotherapy
What’s multiple myeloma?

It’s a plasma cell neoplasm commonly associated with lytic bone lesions, hypercalcemia, renal failure, and acquired
immune abnormalities. It produces large amounts of IgG 55% or IgA 25%. It is the most common primary bone tumor in
elderly
Diagnosis?
• Punched-out lytic skull lesions on x-ray
• M spike on protein electrophoresis
• Ig light chains in urine (Bence Jones proteins)
• CRAB:
o HyperCalcemia (corrected calcium > 2.75 mmol/l, > 11 mg/dL)
o Renal insufficiency attributable to myeloma
o Anemia (hemoglobin < 10 g/dl)
o Bone lesions (lytic lesions or osteoporosis with compression fractures)
What is Bence Jones protein?

Are monoclonal globulin proteins or immunoglobulin light chain found in the urine. The proteins are produced by
neoplastic plasma cells. Bence Jones proteins are present in 2/3 of multiple myeloma cases.
Concerns if going to surgery?

Addisonian crisis
See Steroids station, ASSCC
How to prevent?
• Increase the patient steroid dose prior to surgery
• Convert to IV hydrocortisone
The patient went for THA, died in POD1 suddenly, cause?

Fat embolism
Cause of fat embolism?

• Long bone fracture (closed)
• Major Burns
• Acute pancreatitis
• DM
• Orthopedic surgery (intramedullary nailing, joint reconstruction)
• Decompression sickness
• CPBG (cardiopulmonary bypass graft)
How to manage?
Mainly supportive / prevention of complications like ARF, ARDS.
• Respiratory (O2/mechanical ventilation)
• Fluid and electrolytes balance
• General (DVT, sepsis, nutrition)
Specific unproven:
• Ethanol
• Dextran
• Heparin
10
11
Gangrene + Mesothelioma
Define gangrene? SCENARIO:

Gangrene (or gangrenous necrosis) is a type of necrosis caused by a worker, smoker, toe gangrene
critically insufficient blood supply
Define necrosis?
Accidental and unregulated form of cell death resulting from damage to cell membranes and loss of ion homeostasis
Types of cell death?

• Necrosis
• Apoptosis
Feature Necrosis Apoptosis

Cell size Enlarged (swelling) Reduced (shrinkage)
Nucleus Karyopyknosis → karyorrhexis → karyolysis Fragmentation into nucleosome-size
fragments
Plasma membrane Disrupted Intact; altered structure, especially
orientation of lipids
Cellular contents Enzymatic digestion; may leak out of cell Intact; may be released in apoptotic bodies
Adjacent inflammation Frequent No
Physiologic or Invariably pathologic (culmination of Often physiologic, means of eliminating
pathologic role irreversible cell injury) unwanted cells; may be pathologic after
some forms of cell injury, especially DNA
damage
Pathogenesis of necrosis?
Severe/prolonged ischemia: severe swelling of mitochondria, calcium influx into mitochondria and into the cell with
rupture of lysosomes and plasma membrane. Death by necrosis due the release of cytochrome C from mitochondria
12
Difference between dry and wet gangrene?
Feature Dry Gangrene Wet Gangrene
Site Commonly limbs More common in bowel
Mechanism Arterial occlusion More commonly venous obstruction
Macroscopy Organ dry, shrunken and black Part moist, soft, swollen, rotten and dark
Putrefaction Limited due to very little blood supply Marked due to stuffing of organ with blood
Line of demarcation Present at the junction between healthy and No clear cut line of demarcation
gangrenous part
Bacteria Bacteria fail to survive Numerous present
Prognosis Generally better duet to little septicemia Generally poor due to profound toxemia
What do you think is the cause of ischemia?

Atherosclerosis
Define atherosclerosis?
Pathological process of the vasculature in which an artery wall thickens as a result of accumulation of fatty
materials such as cholesterol
Risk factors?
• Smoking
• HTN
• DM
• Family history
• Increased LDL
Patient developed cough, one bedside test to do?

Sputum analysis
X-ray → pleural plaque

Pleural plaques, the most common manifestation of asbestos exposure, are well-circumscribed plaques of dense collagen
that are often calcified
Significance?
Increased malignancy risk of mesothelioma and lung adenocarcinoma
Give one classification of lung cancer?

Non-small cell lung cancer Small cell lung carcinoma /Oats cell carcinoma
These share common features of prognosis and Small cell lung carcinomas are comprised of cells with a
management. Paraneoplastic features and early disease neuro endocrine differentiation. The neuroendocrine
dissemination are less likely than with small cell lung hormones may be released from these cells with a wide
carcinoma. They comprise the following tumors: range of paraneoplastic associations. These tumors are
• Adenocarcinoma (40% cases) most common strongly associated with smoking and will typically arise in
lung cancer type encountered in never smokers. the larger airways. They disseminate early in the course
• Squamous cell carcinoma (25% cases) more slow of the disease and although they are usually
growing and are typically centrally located chemosensitive this seldom results in long lasting
• Large cell carcinoma (10% cases) remissions.
Now the patient is presented with Mets, poorly differentiated, how to tell its epithelial origin?
Immunohistochemistry
If the tumor was epidermal growth factor positive, what will be the chemotherapeutic agent?
Tyrosine kinase inhibitor (imatinib)
Types of necrosis
• Coagulative
• Liquefactive
• Caseous
• Fat
• Fibrinoid
• Gangrenous
13
Lung Cancer
What other lung cancers do you know? SCENARIO: 70-year-old male smoker,
Small cell and non-small cell See previous station (Gangrene + Mesothelioma) COPD with small cell lung cancer.
Histology report saying carcinoid
What are the signs of aggressiveness on the report? invading pleura and lymph nodes.
• Invading pleura
• Lymph nodes involved
Pathogenesis of clubbing?
Various hypotheses have been proposed over the years to explain the pathophysiology of digital clubbing.
• Some research found significantly higher plasma growth hormone levels in patients with lung carcinoma and
clubbing than patients without clubbing.
• Megakaryocyte or platelet clusters, lodged in the peripheral vasculature of the digits, release platelet-derived
growth factor (PDGF) and lead to the increased vascularity, permeability, and connective tissue changes that are
the hallmark of clubbing
Pancoast paraneoplastic syndrome, what hormones?

ACTH causing Cushing syndrome
Now the patient presents with metastasis, poorly differentiated, how to tell its epithelial origin?
FISH technique?
Fluorescence in situ hybridization (FISH) is a kind of cytogenetic technique which uses fluorescent probes binding parts of
the chromosome to show a high degree of sequence complementarity. Fluorescence microscopy can be used to find out
where the fluorescent probe bound to the chromosome See Breast Cancer station
If the tumor was epidermal growth factor positive, what will be the chemotherapeutic agent?
Tyrosine kinase inhibitor (imatinib)
6 month later he came with back pain. Why?

Bone metastasis
What other tumor metastasis to bone?

BLT with kosher pickle - See Spine Anatomy file
Define adenocarcinoma
Adenocarcinoma is cancer that forms in mucus-secreting glands throughout the body. The disease may develop in many
different places, but it is most prevalent in the following cancer
Define emphysema
Emphysema is a lung condition that causes shortness of breath. In people with emphysema, the air sacs in the lungs
(alveoli) are damaged. Over time, the inner walls of the air sacs weaken and rupture — creating larger air spaces instead
of many small ones.
Paraneoplastic syndromes? Give examples?

Definition: Symptom complexes that occur in patients with cancer and that cannot be readily explained by local or distant
spread of the tumor or by the elaboration of hormones indigenous to the tissue of origin of the tumor are referred to as
paraneoplastic syndromes.
• The most common paraneoplastic syndromes are hypercalcemia, Cushing syndrome, and nonbacterial
thrombotic endocarditis, and the neoplasms most often associated with these and other syndromes are lung
and breast cancers and hematologic malignancies.
• Paraneoplastic syndromes also may manifest as hypercoagulability, leading to venous thrombosis and
nonbacterial thrombotic endocarditis.
• Other manifestations are clubbing of the fingers and hypertrophic osteoarthropathy in patients with lung
carcinomas
Paraneoplastic syndrome -Agroup of r are disorder trigger by abnormal immune response to a cancerous tumour
nil poddo
14
a
Paraneoplastic Syndromes
Clinical syndrome Major Forms of Neoplasia Causal mechanism(s) / Agent(s)
Endocrinopathies
Cushing syndrome Small cell carcinoma of lung ACTH or ACTH or ACTH-like substance
ACTH-like substance
Pancreatic carcinoma
Neural tumors
Syndrome of inappropriate anti- Small cell carcinoma of lung; Anti-diuretic hormone or atrial
diuretic hormone secretion intracranial neoplasms natriuretic hormones
Hypercalcemia Squamous cell carcinoma of lung Parathyroid hormone–related
Breast carcinoma protein, TGF-α
Renal carcinoma
Adult T cell leukemia/lymphoma
Hypoglycemia Fibrosarcoma Insulin or insulin-like substance
Other mesenchymal sarcomas
Ovarian carcinoma
Polycythemia Renal carcinoma Erythropoietin
Cerebellar hemangioma
Hepatocellular carcinoma
Nerve and Muscle Syndrome
Myasthenia Bronchogenic carcinoma, thymoma Immunologic
Disorders of the central and Breast carcinoma, teratoma Immunologic
peripheral nervous systems
Dermatologic Disorders
Acanthosis nigricans Gastric carcinoma Immunologic; secretion of epidermal
Lung carcinoma growth factor
Uterine carcinoma
Dermatomyositis Bronchogenic and breast carcinoma Immunologic
Osseous, Articular, and Soft-Tissue Changes
Hypertrophic osteoarthropathy and Bronchogenic carcinoma Unknown
clubbing of the fingers
Vascular and Hematologic Changes
Venous thrombosis (Trousseau Pancreatic carcinoma Tumor products (mucins that activate
phenomenon) Bronchogenic carcinoma clotting)
Other cancers
Nonbacterial thrombotic endocarditis Advanced cancers Hypercoagulability
Anemia Thymoma Immunologic
Others
Nephrotic syndrome Various cancers Tumor antigens, immune complexes
Hormones in paraneoplastic syndrome?

Histologic type Paraneoplastic syndrome
Adenocarcinoma • Hypertrophic pulmonary osteoarthropathy
• Trousseau’s syndrome
Squamous cell carcinoma • Humoral hypercalcemia of malignancy (PTHrP)
• Pancoast syndrome
Small (oat) cell carcinoma • SIADH
• Lambert-Eaton myasthenic syndrome
• Cerebellar degeneration
15
Tuberculosis (TB)
Differential Diagnosis? SCENARIO: A young Indian lady came

• Hodgkin’s lymphoma (more in this age group and involves cervical back from a foreign travel with
lymph nodes more commonly) cervical lymphadenopathy (anterior
• TB triangle mass), loss of weight, night
sweating
Which labs you will send her sputum to?
Microbiology + Cytology labs
What are the tests of TB?

• Sputum examination (culture, Ziehl Neelsen stain)
• Mantoux test
• PCR to differentiate mycobacteria tuberculosis from other species
• QuantiFERON (interferon gamma assays)
• FNAC of lymph node
How to label the sputum specimens?

Category-B UN3373
Where to put it?

In a biohazard bag
Organism of TB?
• Mycobacterium tuberculosis
• Mycobacterium avium intracellulare (MAC) → disseminated infection in immunocompromised patients
• Mycobacterium bovis
What are the culture media for mycobacteria?

• Solid media: Lowenstein Jensen media, Middlebrook media
• Liquid media: BACTEC/MIGT (mycobacteria growth indicator tube)
How long to culture?

1-8 weeks
What type of protein deposition?

Amyloid
Given the FNAC result: (necrotic tissue, histiocytes, giant cells), interpret?
TB
What are giant cells?

Multinucleated cells comprising of macrophages often forming granuloma
e.g. Langerhans’ giant cells, Reed sternberg cells
Public health concern/ community concerns?

1- Notify the consultant in communicable disease control (CCDC)
2- Avoid working in the food factory
3- Use mask during sneezing or coughing
4- DOTS (Directly Observed Treatment, Short-course) anti-TB therapy
5- Contact tracing: the identification and diagnosis of persons who may have come into contact with an infected
person
What is your advice to contacts?

Counselling, screening and treatment of other family members.
What is a granuloma?
Organized collection of macrophages fusing to form Langerhans’ giant cells.
16
Other Causes of granuloma?
• Leprosy
• Schistosomiasis
• Sarcoidosis
• Crohn’s
• Rheumatoid arthritis
The sequence of events in primary pulmonary tuberculosis, commencing with inhalation of virulent Mycobacterium tuberculosis
organisms and culminating with the development of cell-mediated immunity to the organism. A, Events occurring during early
infection, before activation of T-cell–mediated immunity. B, The initiation and consequences of T-cell–mediated immunity. The
development of resistance to the organism is accompanied by the appearance of a positive tuberculin test.
17
Breast Cancer
[mammogram+ pathology report]
What can you recognize in mammogram?

Speculated mass + microcalcifications
What other tests to do?

Tissue biopsy (TRU-cut, FNAC)
FNAC done showed C4 lesion what this mean?

• C1 – inadequate sample
• C2 – benign
• C3 – equivocal
• C4 – suspicious
• C5 – malignant
Excision, you are given a pathology report.

What to report/look for?
• Type of cancer
• Number of positive lymph nodes
• Margins status
• HER2 receptors status – poor prognosis
• ER/PR receptor status – good prognosis
• Ki 67 proliferation index – how progressive the cancer is? i.e. the
higher its % the higher the progression of the cancer
What is the most common site of breast cancer?

Most common site is upper outer quadrant as it has more glandular tissue
What’s the most common type of breast cancer?

Invasive duct carcinoma
Anatomic origins of common breast lesions.
18
HER2?
Oncogene, biomarker, transmembrane Human Epidermal growth factor Receptor 2 and it is overexpressed in 15% of
breast cancer cases and associated with bad prognosis.
Test: IHC, FISH. IHC-immunohistochemical/immunoperoxidase stain,,FiSH-fluroscence in situ hybridization
How to test for HER2

Immunohistochemistry (IHC) measures the amount of HER2 protein in the cancer cells.
Fluorescence in situ hybridization (FISH) looks at the number of copies of the HER2 gene in the cancer cells.
Identification of HER2-positive breast cancer. HER2 protein overexpression is virtually always caused by amplification of the region of
chromosome 17q that contains the HER2 gene. The increase in HER2 gene copy number is detected by fluorescence in situ
hybridization (FISH) using a HER2-specific probe (red signal), which is typically co-hybridized to tumor cell nuclei with a second probe
specific for the centromeric region of chromosome 17 (green signal), allowing the chromosome 17 copy number to be determined.
Alternatively, HER2 protein overexpression in tumor cells can be detected by immunohistochemical staining with antibodies specific for
HER2. Red signal-gene,,green-chromosome
What is HER positive?

HER2-positive breast cancer is a breast cancer that tests positive for a protein called human epidermal growth factor
receptor 2 (HER2), which promotes the growth of cancer cells.
They're less likely to be sensitive to hormone therapy
HER2-positive breast cancers tend to grow faster and are more likely to spread and come back.
Treatments that specifically target HER2 are very effective. (e.g. Lapatinib, Neratinib, Pertuzumab, Trastuzumab)
Why is it important to know if HER positive or negative?

For treatment choice (see above) and for prognosis
Herceptin (trastuzumab) and how it works at cellular level?

Trastuzumab, (Herceptin) is a monoclonal antibody that interferes with the HER2/neu receptor, which are embedded in
the cell membrane and communicate molecular signals from outside the cell to inside the cell, and turn genes on and off.
The HER (human epidermal growth factor receptor) protein, binds to human EGF and stimulates cell proliferation,
leading to inhibition of MAPK and PI3K-Akt.
Herceptin: (trastuzumab) mode of action?

Causes antibody mediated destruction of cells overproducing HER2, taken 3 times weekly for 12 months.
19
What else in management?
• Radiotherapy
• Chemotherapy
• Hormonal therapy:
o Premenopausal: Tamoxifen (20mg /d) for 5 years – blocks estrogen receptor
o Postmenopausal: Aromatase inhibitors (anastrozole) to prevent peripheral conversion to estrogen
Who should be involved in care of this patient?

Radiologist, surgeon, oncologist, pathologist.
Patient going for an implant and flap, what single microbiological screening test would you do for this patient?
MRSA screen
What if positive?
Patient is a carrier and will require decolonization – According to trust protocol Please note the
Nose: Mupirocin 2% (Bactroban Nasal®) nasal ointment TDS for 5 days difference in treatment
Skin: Once daily wash with Chlorhexidine 4% (Hibiscrub®) for 5 days between MRSA infection
Hair: Wash with Chlorhexidine 4% (Hibiscrub®) on day 1 and day 5 and MRSA carrier
Now has breast erythema and discharge from nipple, what single microbiological test would you do now?
Cultures and sensitivity
What is the causative organism?

Staph. aureus
How would you treat her?

• Broad spectrum antibiotic (after discussion with microbiologist and according to trust policy) most likely
Flucloxacillin
• Wound care
Patient has redness around nipple, why?

• Eczema
• Paget disease -Dx-Punch Biopsy
Pathophysiology of Paget disease?

It is caused by the extension of DCIS (ductal
carcinoma in situ) up the lactiferous ducts and
into the contiguous skin of the nipple,
producing a unilateral crusting exudate over the
nipple and areolar skin.
Unlike Paget disease of the vulva, Paget disease
of the nipple stems from in situ extension of an
underlying carcinoma.
why mammo not before 40?

-breast become more dence in later age
-brest has more glandular tissue below
age,more dence and more fat contain in
later age.
Paget disease of the nipple. Ductal carcinoma in situ arising within the
ductal system of the breast can extend up the lactiferous ducts and into the
skin of the nipple without crossing the basement membrane. The malignant
cells disrupt the normally tight squamous epithelial cell barrier, allowing
extracellular fluid to seep out and form an oozing scaly crust.
20
21
MEN 1 Syndrome /wermer syndrome
Define hyperplasia? SCENARIO:

Increase in the number of cells in tissue or organ in response to a stimulus Man with parathyroidectomy,
pancreatic mass
How many parathyroid glands are mostly affected?
The 4 glands
Microscopic picture of hyperplasia?

• Microscopically, the most common pattern seen is that of chief cell hyperplasia, which may involve the glands in
a diffuse or multinodular pattern.
• Less commonly, the constituent cells contain abundant water-clear cells (“water-clear cell hyperplasia”).
• In many instances there are islands of oxyphils, and poorly developed, delicate fibrous strands may envelop the
nodules.
The patient developed stupor, confusion and hypoglycemia (1.2 mmol/l), why do you think that happened?
Insulinoma
What cell derived from?

β-cell of islets of Langerhans’
What other causes of unresponsive hypoglycemia do you know?

• Abnormal insulin sensitivity,
• Diffuse liver disease,
• Inherited glycogenoses,
• Ectopic production of insulin by certain retroperitoneal fibromas and fibrosarcomas
Clinical picture of Insulinoma?

• Confusion
• Stupor
• Loss of consciousness (blood glucose 2.5 mmol/L or less)
These episodes are precipitated by fasting or exercise
Promptly relieved by feeding or parenteral administration of glucose.
Biochemical diagnosis:
• High circulating levels of insulin (<10 μU/mL)
• High insulin-to-glucose ratio
What do you suspect as another pathology in this patient?

Pituitary adenoma (MEN 1)
.
What are the 3 gene mutations in Insulinoma?
1- MEN1, which causes familial MEN syndrome, type 1, also is mutated in a number of sporadic neuroendocrine
tumors
2- Loss-of-function mutations in tumor suppressor genes such PTEN and TSC2 (which results in activation of the
oncogenic mammalian TOR (mTOR) signaling pathway
3- Inactivating mutations in two genes, alpha-thalassemia/mental retardation syndrome, X-linked (ATRX) and
death-domain associated protein (DAXX), which have multiple cellular functions, including telomere
maintenance.
What is two hit hypothesis?

Like all genes, tumor suppressor genes may undergo a variety of mutations; however, most loss-of-function mutations
that occur in tumor suppressor genes are recessive in nature. Thus, in order for a particular cell to become cancerous,
both of the cell's tumor suppressor genes must be mutated. This idea is known as the "two hit" hypothesis
What is telomere?
A telomere is a region of repetitive nucleotide sequences at each end of a chromosome, which protects the end of the
chromosome from deterioration or from fusion with neighboring chromosomes
What is apoptosis?
Programmed cell death
22
See Gangrene / Mesothelioma station
23
MEN 2 Syndrome
Single best test to diagnose? SCENARIO:

FNAC Female with thyroid nodule,
elevated calcitonin levels
Pathology report: FNAC showed malignant cell features, amyloid deposits,
immunohistochemistry stains positive with calcitonin, stains negative for thyroxine
What is the type of cancer?

Medullary thyroid cancer
Why?
• Amyloid deposits
• Calcitonin positive on IHC -immunohisto chemistry stain.
Cell source?
Parafollicular C cells
What is IHC in simple words?

It is a method of localizing specific antigens in tissues or cells based on antigen antibody recognition
How does it work?

The antibodies are usually linked to an enzyme or a fluorescent dye. When the antibodies bind to the antigen in
the tissue sample, the enzyme or dye is activated, and the antigen can then be seen under a microscope.
What is the type of Ag- Ab reaction in IHC?

Complement fixation
Another pathology report showing size, number of positive lymph nodes (2-6)
Do TNM
Tumor
Tx Primary cannot be assessed
T0 No evidence of primary
T1 Limited to thyroid, 1 cm or less
T2 Limited to thyroid > 1 cm but < 4 cm
T3 Limited to thyroid > 4 cm
T4 Extending beyond capsule, any size
Notes
Nx Cannot be assessed
N0 No regional lymph node metastases
N1 Regional node metastases
M status
Mx Cannot be assessed
M0 No metastases
M1 Metastases present
Stage Under 45 years Over 45 years

I Any T, any N, M0 T1, N0, M0
II Any T, any N, M1 T2, N0, M0 or T3, N0, M0
II T4, N0, M0 or any T, N1, M0
IV Any T, any N, M1
If the patient developed hypertension, what do you think she might have?
Pheochromocytoma
24
How can you diagnose pheochromocytoma?
Plasma:
• Free metanephrine
• Catecholamines
• Catecholamines stimulation test
Urine:
• Fractionated metanephrine
• Total metanephrine
• Catecholamines
• VMA
Imaging:
• Ultrasound
• CT
• MRI
• MIBG scintigraphy
• PET/CT
If this condition was familial, what other condition you suspect?

Parathyroid hyperplasia
Types of MEN syndromes? Oncogene mutation? Mode of inheritance?

The table below summarizes the three main types of MEN:
MEN type I MEN type IIa MEN type IIb
Mnemonic 'three P's': • Hyperparathyroidism (usually Same as MEN IIa with addition of:
• Parathyroid (95%): Parathyroid adenoma hyperplasia) • Marfanoid body habitus
• Pituitary (70%): Prolactinoma/ACTH/Growth • Pheochromocytoma • Mucosal neuromas
Hormone secreting adenoma • Medullary thyroid cancer
• Pancreas (50%): Islet cell tumors/Zollinger
Ellison syndrome
also: Adrenal (adenoma) and thyroid
(adenoma)
Most common presentation = hypercalcemia

MENIN gene (chromosome 11) RET oncogene (chromosome 10) RET oncogene (chromosome 10)
Autosomal Dominant Autosomal Dominant Autosomal Dominant
Treatment of medullary thyroid cancer?

Total thyroidectomy with block neck dissection
25
Parotid Tumors
SCENARIO – 1:
65-year-old man with a 2-month history of unilateral 4 cm parotid swelling without facial nerve problem
See Parotid Gland, Head & Neck Anatomy

See Head & Neck Surgery file, Part A Notes
What is the most common parotid benign swelling?
Pleomorphic adenoma
What is the meaning of pleomorphic?

Remarkable histologic diversity
Describe pleomorphic adenoma appearance?

Benign tumors that consist of a mixture of ductal (epithelial) and myoepithelial cells, and therefore they show both
epithelial and mesenchymal differentiation
What are the causes of bilateral swelling?

Local Systemic Drugs
• Mumps • Sarcoidosis • High oestrogen OCP
• Parotitis • TB • Thiouracil
• Sialectasis • Alcoholism/liver cirrhosis • Isoprenaline
• Sjogren’s • Cushing’s
• Neoplasia • Bulimia Nervosa
What are the causes of unilateral parotid swelling?

• Duct obstruction – salivary calculus, external ductal compression
• Neoplasia – benign or malignant
• Infective mumps (although bilateral swelling is more common), parotitis
Types of parotid neoplasm?

Benign (85%) Malignant (15%)
Pleomorphic adenoma (mixed) (50%) Mucoepidermoid carcinoma (15%)
Warthin tumor (5% - 10%) Adenocarcinoma (NOS) (10%)
Oncocytoma (1%) Acinic cell carcinoma (5%)
Other adenomas (5% - 10%) Adenoid cystic carcinoma (5%)
Basal cell adenoma Malignant mixed tumor (3%-5%)
Canalicular adenoma Squamous cell carcinoma (1%) Pleomorphic adenoma.Low-power view
showing a welldemarcated tumor with
Ductal papillomas Other carcinomas (2%)
adjacent, deeply staining, normal salivary
gland parenchyma.
What are the clinical signs of malignant parotid tumour?
• Facial nerve affection
• Rapid increase in size
• Fixity to underlying tissue
• Invasion of the skin
• Skin ulcer
• Presence of associated nodes
What are the characteristics of malignant neoplasms?

• More rapid increase in size
• Less differentiation (or lack of differentiation, called anaplasia)
• Tendency to invade surrounding tissues (not respect tissue boundaries)
• Ability to metastasize to distant tissues
Pleomorphic adenoma. High-power view
showing epithelial cells as well as
myoepithelial cells within chondroid
matrix material.
26
Features of malignant cells? Cytologic features of malignant neoplasms
• Invasion: Malignant cells do not respect tissue boundaries, and • Increased nuclear size (with increased
can be seen infiltrating or invading into surrounding structures nuclear/cytoplasmic ratio--N/C ratio).
• Increased mitotic rate: Malignant cells will often have increased • Variation in nuclear or cell size
numbers of mitoses. (pleomorphism).
• Differentiation and anaplasia: Normal cells are usually • Lack of differentiation (anaplasia).
structured in a particular way that corresponds with their • loss of normal tissue architecture (loss
function. This is known as differentiation. Malignant cells may of polarity)
become less differentiated as part of their path to malignancy. • Increased nuclear DNA content with
This is known as anaplasia. Well differentiated malignant cells subsequent dark staining on H and E
show features similar to the parent tissue. For example, well slides (hyperchromatism).
differentiated adenocarcinoma cells will tend to form gland-like
• Prominent nucleoli or irregular
structures; well differentiated squamous cell carcinomas may
chomatin distribution within nuclei.
show intercellular bridging or keratin formation. Poorly
• Increased mitotic rate (especially
differentiated cells have lost most of their resemblance to the
irregular or bizarre mitoses).
parent tissue, which may be difficult to identify without special
• Giant cells some malignant cells may
staining techniques. Anaplastic cells have no resemblance to
coalese into so-called giant cell
their parent tissue, and usually indicate a very aggressive
• Ischemic necrosis (from tumor cells
malignancy.
outgrowing their blood supply)
Anaplastic Features
o Loss of normal tissue architecture: Normal cells are
usually arranged in an orderly fashion. Epithelial cells often have polarity, with their nuclei at a
specific location. Malignant cells lose this architecture and are arranged haphazardly
o Pleomorphism: Malignant cells may show a range of shapes and sizes, in contrast to regularly sized
normal cells. The nuclei of malignant cells are often very large (often larger than the entirety of a
normal cell) and may contain prominent nucleoli.
o Hyperchromatic nuclei: The nuclei of malignant cells typically stain a much darker colour than their
normal counterparts.
o High nuclear-cytoplasmic ratio: The nuclei of malignant cells often take up a large part of the cell
compared with normal cell nuclei
o Giant cells: Some malignant cells may coalesce into so-called giant cells, which might contain the
genetic material of several smaller cells.
Anaplasia?
Lack of differentiation (loss of similarity to the mother cell indicate very aggressive tumor)
Single best test to differentiate between benign and malignant cells?

FNAC
Difference between cytology and histology?

Cytology is the study of cellular structure and function
Histology is the study of tissue under the microscope
How to differentiate between carcinoma and lymphoma?

IHC - See Breast Cancer station and MEN2 syndrome station
How to rule out malignancy intraoperative?

Frozen section – See Peptic Ulcer Disease + Hyperparathyroidism station
FNAC findings
• If you find Langerhans giant cell + lymphocytes + necrotic material → granuloma (TB)
• If you find Brown pigmented cell + epithelioid cells → malignant melanoma
• If you find Reed Sternberg cell + lymphoid cell + blast cell → lymphoma
27
FNAC done and you have needle stick injury, what you will do?
• The wound should be allowed to bleed under running water and wash with soap
• Assess incident risk
• Assess source patient
o Take history if he has a possibility of any blood borne infection, take a blood sample from the patient if
high risk after consent.
• I would file an incident report and speak to occupational health for advice.
• Documentation
Source: https://www.bmj.com/content/351/bmj.h3733
28
What are the postoperative complications of Sweat glands
parotidectomy?
• 7th CN palsy
• Frey’s Syndrome
Sympathetic
• Salivary fistula
• Greater auricular nerve damage -numbness to Sensory
earlobe Parasympathetic
What is Frey’s Syndrome?

Auriculotemporal syndrome: post-operative A Parotid
phenomena following salivary gland surgery resulting in
gustatory sweating and facial flushing due to Sweat glands
reinnervation of postganglionic fibers to sweat gland and
cutaneous blood vessels Mixed
Sympathetic
After 10 years from resection patient develop neck
swelling, cause?
Parasympathetic Parotid
Possible recurrence with metastasis Mixed bed
B
What is the definition of a high sensitivity test?
Frey's syndrome. A, Normal anatomy. B, Mixing of fibers dt surgery.
Sensitivity is the ability of a test to correctly classify an
individual as ′diseased′ (true positive rate)
High sensitivity = low number of false negatives
What is the definition of a high specificity test?

Specificity is the ability of a test to correctly classify an individual as disease-free (true negative rate).
High specificity = low number of false positives
Screening Test Statistics

Disease present Disease absent
Test positive TP FP
Test negative FN TN
TP = true positive; FP = false positive; TN = true negative; FN = false negative
Sensitivity TP / (TP + FN ) Proportion of patients with the condition who have a

positive test result
Specificity TN / (TN + FP) Proportion of patients without the condition who have a
negative test result
Positive predictive value TP / (TP + FP) The chance that the patient has the condition if the
diagnostic test is positive
Negative predictive value TN / (TN + FN) The chance that the patient does not have the condition
if the diagnostic test is negative
Likelihood ratio for a sensitivity / (1 - specificity) How much the odds of the disease increase when a test
positive test result is positive
Likelihood ratio for a (1 - sensitivity) / specificity How much the odds of the disease decrease when a test
negative test result is negative
Positive and negative predictive values are prevalence dependent. Likelihood ratios are not prevalence dependent
29
SCENARIO – 2:
55 years old female with Mastectomy done 5 years back and parotidectomy for pleomorphic adenoma 10 years back.
Now presented by neck swelling (supra-clavicular LN swelling)
What is the relation between breast cancer and pleomorphic adenoma?

Genetic (BRCA1 and BRCA2)
Investigation?
FNAC or Tru-Cut® biopsy
What is the advantage of FNAC over Tru-Cut biopsy?

FNAC Tru-Cut
• Cost effective • Avoid unnecessary excisional biopsy
Advantage
• Simple • More reliable

• Quick result • Grading and typing of factor
• Less invasive • Relatively easy
• False -ve • More invasive than FNAC
Disadvantage
• Diagnosis is based on purely cytological evaluation • Expensive

• Insufficient sample • Scar
• Inability to differentiate invasive from in situ
carcinoma
Fine needle aspiration cytology

(FNAC) is an operator dependent
procedure that may or may not be
image guided and essentially
involves passing a needle through
a lesion whilst suction is applied to
a syringe. The material thus
obtained is expressed onto a slide
and sent for cytological
assessment.
Tissue samples may also be

obtained by both core and tru cut
biopsy. A core biopsy is obtained
by use of a spring-loaded gun with
a needle passing quickly through
the lesion of interest. A tru cut
biopsy achieves the same objective
but the needle moved by hand.
FNAC Needle biopsy
What test to be done in FNAC?

IHC, receptor status - See Breast Cancer station and MEN2 syndrome station
What is the meaning of pleomorphic? Ans-Nuclear,cytoplasmic ratio almost equal.

Describe pleomorphic adenoma appearance?
After 10 years from resection patient develop neck swelling what this indicate? recurrence,carcinoma
What other things do you consider? What is DD?

• Lymphoma
• Carotid body tumor
• Carcinoma
If the metastasis from the erodes carotid artery it doesn’t stop bleeding, why?
Because of high blood flow
30
Define metastasis:
Survival and growth of cells at a site distant from their primary
origin
List 5 pathological steps by which carcinoma spreads?

• Direct or continuous extension
• Penetration into lymphatic, blood vessels or body
cavities
• Transport of the tumour cells into the circulation
• Arrest in the capillary beds of secondary sites
• Growth of the disseminated tumour cells in
secondary sites
The metastatic cascade. Sequential steps involved in the

hematogenous spread of a tumor.
Main routs of spread of malignant tumor?

• Lymphatic (permeation and lymph emboli)
• Hematogenous
• Trans-celomic (along body cavity to peritoneal
surface)
How or what is the mechanism of lymphatic spread?

• As the cancer cells and the tumor -associated
macrophages secrets growth factors such as VEGF-C
and VEGV-D to induce lymph-angiogenesis in primary
Invasion of the ECM initiates the metastatic cascade and is an
active process that can be resolved into several steps tumor and in draining sentinel LN, thereby promoting
• “Loosening up” of tumor cell–tumor cell interactions LN metastasis
• Degradation of ECM • Also, primary tumors release immunomodulatory
• Attachment to novel ECM components molecules like exosomes which lead to
• Migration and invasion of tumor cells immunosuppression
31
Nasopharyngeal Carcinoma
Define carcinoma?
Carcinoma is a type of cancer that develops from epithelial cells.
What are the differences between Benign and malignant cells?

Benign and malignant tumors can be distinguished from one another based on the degree of differentiation, rate of
growth, local invasiveness, and distant spread.
• Benign tumors resemble the tissue of origin and are well differentiated; malignant tumors are poorly or
completely undifferentiated (anaplastic).
• Benign tumors are slow-growing, whereas malignant tumors generally grow faster.
• Benign tumors are well circumscribed and have a capsule; malignant tumors are poorly circumscribed and
invade the surrounding normal tissues.
• Benign tumors remain localized to the site of origin, whereas malignant tumors are locally invasive and
metastasize to distant sites.
What is the mechanism of radiotherapy?

Ionizing radiation works by damaging the DNA of
cancerous (base damage, single and double-strand
breaks, and crosslinks between DNA and protein)
tissue leading to cellular death.
What is the SI units of radiotherapy?

• Coulomb/kg: Exposure
• Gray (Gy): Dose
• Sievert (Sv): Dose equivalent
• Becquerel: Activity
Risk factors for nasopharyngeal carcinoma?

• Gender: twice as often in males as it is in
females.
• Ethnicity and race: most common in
southern China (including Hong Kong),
Singapore, Vietnam, Malaysia, and the
Philippines. It is also fairly common in
Northwest Canada and Greenland.
• Diet: consumption of salted fish
containing carcinogenic volatile
nitrosamines -produced when smoked
• Infection with the Epstein-Barr virus Effects of ionizing radiation on DNA and its consequences. The effects on DNA
• Genetic factors can be direct, or most importantly, indirect, through free radical formation.
• Family history
• Tobacco and alcohol use Gray
It is defined as the absorption of one joule of
Patient had an oral lesion, swab showing hyphae? radiation energy per kilogram of matter
Candida
Sievert
The sievert takes into account the relative
What are the risk factors for that patient for oral candidiasis? biological effectiveness (RBE) of ionizing
• As a complication of radiotherapy or chemotherapy radiation, since each form of such radiation—
• Being a diabetic e.g., X-rays, gamma rays, neutrons—has a
slightly different effect on living tissue.
What are the routes of spread of nasopharyngeal carcinoma? Accordingly, one sievert is generally defined as
the amount of radiation roughly equivalent in
• Lymphatic spread
biological effectiveness to one gray
• Local invasion
Becquerel
One becquerel is defined as the activity of a
quantity of radioactive material in which one
nucleus decays per second. The becquerel is
therefore equivalent to an inverse second, s−1.
32
Where to spread locally?
What are the common lymph node tumors?

• Lymphoma (Hodgkins and Non-Hodgkins)
• Leukemia
• Metastatic
How will you investigate for metastasis in lymph nodes?

• Tissue biopsy: FNAC, Excisional biopsy, sentinel biopsy for histopathological assessment with or without
immunohistochemistry
• Imaging modalities: ranging from ultrasound scan, CT scan, MRI and PET-CT
33
Carcinoid Tumor
SCENARIO:
Middle aged man with RIF pain, surgery was done, revealed dilated appendix (looks like -mass), histopathology
revealed appendicular abscess plus 6mm appendicular mass involving the mucosa and the muscularis layers
Define abscess?
Abscess is focal collection of pus that may be caused by seeding of pyogenic organisms into a tissue or by secondary
infections of necrotic foci.
Structure of the abscess?

Abscess typically has a central, largely necrotic region rimmed by a layer of preserved neutrophils, with a surrounding
zone of dilated vessels and fibroblast proliferation indicative of attempted repair
How neutrophils migrate to the site of inflammation?

See Diverticulitis + Endometriosis station
The neutrophils first roll, then become activated and adhere to endothelium, then transmigrate across the endothelium,
pierce the basement membrane, and migrate toward chemoattractants emanating from the source of injury.
Blood tests to identify the inflammation?

• ESR, CRP
• White blood cells count
What is carcinoid tumor?

Slow-growing type of neuroendocrine tumor originating in the cells of the neuroendocrine system.
Where it is most commonly found?

Small intestine, appendix (terminal third) and they can also be found in the rectum, stomach and lung
Cells arising from?

Enterochromaffin (EC) cells (also known as Kulchitsky cells) in the crypts of Lieberkuhn
What does it release?

Notably: serotonin (5-HT), bradykinins, prostaglandins, tachykinins, substance P and histamine
Clinical presentation?
• Periodic abdominal pain
• Manifestations of carcinoid syndrome:
o Cutaneous flushing
o Diarrhea and malabsorption
o Cardiac manifestations: Valvular heart lesions, fibrosis of the endocardium
o Wheezing or asthma like syndrome: Due to bronchial constriction
How does it spread?

Cells produce a significant amount of beta-catenin, which enables the tumor cell adhesion, thus promoting metastasis.
Most common metastatic site?

The liver
Why a person with heavy metastasis in liver has symptoms than with primary tumor?
That's because most of the blood circulation from the gastrointestinal tract must pass through the liver before it reaches
the rest of the body. The liver has strong enzymes that break down and neutralize most of the excess serotonin and
other substances produced by the carcinoid tumors, preventing them from reaching tissues where they can cause
symptoms. When carcinoid tumors metastasize to the liver, the substances they overproduce can more easily reach the
bloodstream, and reach tissues where they can cause symptoms.
Diagnosis of carcinoid syndrome?

• Chromogranin A (CgA) Testing in the blood (protein secreted from carcinoid tumor cells)
• 5-Hydroxyindoleacetic Acid (5-HIAA) Testing in 24 h urine (byproduct of serotonin)
• Pathological diagnosis: immunohistochemistry stains positive for chromogranin B
34
Inflammatory Bowel Disease (IBD)
What is ulcerative colitis? SCENARIO: A Lady known to have

Inflammatory bowel disease affecting the colon in the form of colitis with
ulcerative colitis and on surveillance
characteristic ulcers
colonoscopy is found to have a lesion
Pathogenesis? less than 1cm in sigmoid colon.
Idiopathic
Colonoscopy done with biopsy showing tubular dysplasia in one part, adenocarcinoma in other part showing a picture of a
tumor eroding through the muscularis layer + 1/4 positive node
What will you offer this lady? Total colectomy

Why? The whole colon is susceptible
If there is liver Mets, how will this affect TNM staging?

M1
Microscopic features of Crohn’s?

See table below
Microscopic features of UC?

See table below
Complications?
• Intestinal obstruction
• Fistula formation
• Abscess
• Toxic megacolon
• Malabsorption
• Malignancy
• Gall stones (due to inhibition of enterohepatic circulation so bile salts will not be absorbed leading to increased
amount of cholesterol)
Extraintestinal manifestation of
Why is the patient having diarrhea? inflammatory bowel disease: A PIE SAC
• Malabsorption • Aphthous ulcers
• Infection • Pyoderma gangrenosum
• Increased motility • Iritis
• Erythema nodosum
Why you need endoscopic surveillance? • Sclerosing cholangitis
For risk of colon cancer • Arthritis
• Clubbing
Renal stone formation in Crohn’s?
Increased intestinal fat (due to malabsorption) → binds to calcium → leaving oxalates (hyperoxaluria)
Had resection of terminal ileum but diarrhea continued, possible cause?

Relapse of Crohn’s or malabsorption
Management of Crohn’s
Stoma → ischemia, what to do? Medical
Inform consultant, patient relatives, consider refashioning • Advice from gastroenterology
• Steroid, antibiotics, 5-aminosalicylic
Type of vitamin deficiency? acid, immunomodulators
A, D, E, K deficiency Conservative
• Dietary control (low residue diet)
Other investigations? Surgery for
• Stool analysis • Refractory disease
• Barium follow through • Intestinal obstruction
• Prothrombin concentration: to detect vit. K def. • Toxic megacolon
• Calcium oxalate levels • Abscess, fistula, perforation,
• Full blood count: macrocytic anemia hemorrhage, cancer
35
Crohn's disease Ulcerative colitis
Common Site Terminal ileum Rectum
Distribution Mouth to anus Rectum and colon (back-wash ileitis)
Macroscopic • Cobblestone appearance • Pseudopolyps
changes and • Aphthoid ulceration • Extensive ulceration
gross features • Linear fissures • Contact bleeding
• Thickened bowel wall
• Creeping fat
Depth of disease Transmural inflammation Superficial inflammation
Dist. pattern Patchy, skip lesions Continuous
Histological Granulomas (non caseating epithelioid cell aggregates Crypt abscesses, Inflammatory cells in
and with Langhans' giant cells) the lamina propria
microscopic
features Active colitis Active colitis
• Cryptitis • Cryptitis
• Crypt abscess formation • Crypt abscess formation
• Mucosal ulceration • Mucosal ulceration
• Inflammatory pseudo polyps • Inflammatory pseudo polyps
• Inflammation involves all wall layers
(Transmural)
Chronic colitis Chronic colitis
• Increased lymphoplasmacytic lamina propria • Increased lymphoplasmacytic lamina
infiltrate propria infiltrate
• Paneth cell metaplasia – left colon • Paneth cell metaplasia in left colon
• Pseudopyloric gland and gastric surface • Architectural distortion
(foveolar) metaplasia o Branched, dilated irregular
• Paneth cell hyperplasia – small bowel and crypts
right colon o Crypts don’t reach the
muscularis mucosa
Extraintestinal Uncommon More common

Manifestations
Cancer Risk Slightly 1-3% 5-25%
36
Describe adenoma carcinoma sequence?
Stepwise accumulation of mutations of oncogenes and tumor suppressor genes:
1- Loss of APC (tumor suppressor gene) → hyperplasia
2- K-RAS (oncogene) mutation → dysplasia
3- Loss of p 53 (tumor suppressor gene) → adenocarcinoma
Molecular model for the evolution of colorectal cancers through the adenoma-carcinoma sequence. Although APC mutation is an early
event and loss of TP53 occurs late in the process of tumorigenesis, the timing for the other changes may be variable. Note also that
individual tumors may not have all of the changes listed. Top right, cells that gain oncogene signaling without loss of TP53 eventually
enter oncogene-induced senescence. LOH, loss-of-heterozygosity.
How proto-oncogenes and tumor suppressor genes

act?
Genes that promote autonomous cell growth in
cancer cells are called oncogenes, and their
unmutated cellular counter-parts are called proto-
oncogenes. Oncogenes are created by mutations in
proto-oncogenes and encode proteins called
oncoproteins that have the ability to promote cell
growth in the absence of normal growth-promoting
signals. Oncoproteins resemble the normal products
of proto-oncogenes but bear mutations that are
often inactivate internal regulatory elements;
consequently, their activity in cells does not depend
on external signals. Cells expressing oncoproteins
are thus freed from the normal checkpoints and
controls that limit growth, and as a result proliferate
excessively
• Proto-oncogenes: normal cellular genes
whose products promote cell proliferation
• Oncogenes: mutated or overexpressed
versions of proto-oncogenes that function
autonomously, having lost dependence on
normal growth promoting signals
• Tumor suppressor genes (p53, APC):
normal genes whose absence can lead to
development of cancer, they act as
gatekeepers: inhibit proliferation or
promote the death of cells with damaged
DNA
Growth factor signaling pathways in cancer. Growth factor receptors,

RAS, PI3K, MYC, and D cyclins are oncoproteins that are activated by
mutations in various cancers. GAPs apply brakes to RAS activation,
and PTEN serves the same function for PI3K.
37
Function of KRAS?
The KRAS gene provides instructions for making a protein called K-Ras that is part of a signaling pathway known as the
RAS/MAPK pathway. The protein relays signal from outside the cell to the cell's nucleus. These signals instruct the cell to
grow and divide (proliferate) or to mature and take on specialized functions (differentiate). The K-Ras protein is a
GTPase, which means it converts a molecule called GTP into another molecule called GDP. In this way the K-Ras protein
acts like a switch that is turned on and off by the GTP and GDP molecules. To transmit signals, it must be turned on by
attaching (binding) to a molecule of GTP. The K-Ras protein is turned off (inactivated) when it converts the GTP to GDP.
When the protein is bound to GDP, it does not relay signals to the cell's nucleus.
Intrinsic and Extrinsic Pathways of apoptosis

Intrinsic and extrinsic pathways of apoptosis
and mechanisms used by tumor cells to evade
cell death. (1) Loss of p53, leading to reduced
function of pro-apoptotic factors such as BAX.
(2) Reduced egress of cytochrome c from
mitochondria as a result of upregulation of
anti-apoptotic factors such as BCL2, BCL-XL,
and MCL-1. (3) Loss of apoptotic peptidase
activating factor 1 (APAF1). (4) Upregulation
of inhibitors of apoptosis (IAP). (5) Reduced
CD95 level. (6) Inactivation of death-induced
signaling complex. FADD, Fas-associated via
death domain.
38
Function of P53?
DNA damage and other stress signals may trigger the increase of p53 proteins, which have three major functions: growth
arrest, DNA repair and apoptosis (cell death). The growth arrest stops the progression of cell cycle, preventing replication
of damaged DNA. During the growth arrest, p53 may activate the transcription of proteins involved in DNA repair.
Apoptosis is the "last resort" to avoid proliferation of cells containing abnormal DNA.
The role of p53 in maintaining the integrity of the genome. Activation of normal p53 by DNA-damaging agents or by hypoxia leads to
cell cycle arrest in G1 and induction of DNA repair by transcriptional upregulation of the cyclin-dependent kinase inhibitor CDKN1A
(encoding the cyclin-dependent kinase inhibitor p21) and the GADD45 genes. Successful repair of DNA allows cells to proceed with the
cell cycle; if DNA repair fails, p53 triggers either apoptosis or senescence. In cells with loss or mutations of the p53 gene, DNA damage
does not induce cell cycle arrest or DNA repair, and genetically damaged cells proliferate, giving rise eventually to malignant
neoplasms.
39
WNT-winless related integration site
Function of APC?
Encodes a factor that negatively regulates the WNT pathway in colonic epithelium by promoting the formation of a
complex that degrades β-catenin
The role of APC in regulating the stability and function of β-catenin. APC and β-catenin are components of the WNT signaling
pathway. A, In resting colonic epithelial cells (not exposed to WNT), β-catenin forms a macromolecular complex containing the APC
protein. This complex leads to the destruction of β-catenin, and intracellular levels of β-catenin are low. B, When normal colonic
epithelial cells are stimulated by WNT molecules, the destruction complex is deactivated, β-catenin degradation does not occur, and
cytoplasmic levels increase. β-catenin translocates to the nucleus, where it binds to TCF, a transcription factor that activates genes
involved in cell cycle progression. C, When APC is mutated or absent, as frequently occurs in colonic polyps and cancers, the
destruction of β-catenin cannot occur. β-catenin translocates to the nucleus and coactivates genes that promote entry into the cell
cycle, and cells behave as if they are under constant stimulation by the WNT pathway.
What is TNF
It is a cytokine involved in systemic
inflammation and in making up the acute
phase reaction
Role of TNF in IBD?

TNF and other immune mediated signals
direct epithelia to increase tight junctions
permeability which increase the flux of
luminal bacterial components which
activates innate and adaptive immune
responses
What drugs antagonize TNF?

• Infliximab
• Adalimumab
• Certolizumab
Mechanism of action of these drugs?

Monoclonal IgG1 antibody to TNF- α
Why are they used in treatment of UC?

They are called (biologics), used mainly in
steroid refractory UC cases and for
treatment of extra intestinal
manifestations A model of pathogenesis of inflammatory bowel disease (IBD). Aspects of both
Crohn disease and ulcerative colitis are shown.
40
Familial Adenomatous Polyposis (FAP)
SCENARIO: A young lady with endometriosis concerned that her father died of a cancer at an early stage. She had a
colonoscopy just now
Identify a picture of FAP?

Multiple polyps the largest one is about 7mm and
ulcerated
Definition of FAP?
Autosomal dominant condition characterized by loss
of APC tumor suppressor gene on the long arm of
chromosome 5 leading to development of hundreds
of tubular adenomas with 100% risk of cancer by the
age of 40
Function of APC tumor suppressor gene?

Encodes a factor that negatively regulates the WNT
pathway in colonic epithelium by promoting the
formation of a complex that degrades β-catenin
(see previous station…)
Classification of polyps?
• Non-neoplastic:
o Hamartomatous
o Metaplastic
• Inflammatory:
o Pseudopolyps
o Ulcerative colitis
• Neoplastic:
o Villous (40%)
o Tubulovillous (20%)
o Tubular (5%)
What does the malignant potential of adenomas depend on?

• Type of adenoma
• Diameter of adenoma:
o < 1 cm → 5%
o 2 cm → 20 %
• Degree of dysplasia
Extracolonic manifestations in the related gardener syndrome?

• Mandibular osteoma
• Desmoid tumors
• Sebaceous cyst
Management?
Prophylactic near total colectomy by the age of 25
If the patient has a 2yo child, what is your advice?

Colonoscopic screening by the age of 12
Define endometriosis?
Endometriosis is defined by the presence of “ectopic” endometrial tissue at a site outside of the uterus
41
Definitions
Dysplasia?
Disordered cellular development characterized by increased mitosis, pleomorphism without the ability to invade
the basement membrane
Severe dysplasia = carcinoma in situ
Abscess? Collection of pus surrounded by granulation or fibrous tissue
Pus? collection of neutrophils plus dead or dying micro organisms
Ulcer? a lesion in the mucous membrane or the skin resulting from the gradual disintegration of surface
epithelial cells
Secondary intention? secondary healing by reepithelization and contraction
Life style modifications to reduce risk of cancer colon?

• Fibre-rich diet
• Limit alcohol
• Reduce fat intake
• Stop smoking
42
GB Cancer + Pseudomembranous Colitis
What is the commonest type of malignant neoplasm of the SCENARIO:

gall bladder? Cholecystectomy + surgical site infection
Adenocarcinoma Histology report describes malignant gall bladder
neoplasm
Causes of GB cancer?
• Cholelithiasis; gall stones
• Chronic cholecystitis
Risk factors?
• Age > 70 yrs
• Female sex
• Family history
• Ethnicity (Mexicans/native American)
• Smoking
• Gall stones (most common)
• GB polyp >1 cm
• Porcelain GB
• Chronic infection by S. typhus [salmonell]
• ABPJ
• Choledochal cyst
• Obesity
Where does GB cancer spread to first?

Direct invasion to liver (segment 4/5)
Spread?
• Porta hepatis lymph nodes
• Liver (segment V)
• CBD
• Stomach
• Duodenum
Pathology?
Adenocarcinoma
SSI in POD3 with yellowish and smelly discharge, cause?

• Local sepsis, most likely to be bacterial
• Actinobacillus (sulphur granules)
What is the most common organism causing surgical site infection?

Staph. aureus
Name three organisms likely to be associated with necrotizing fasciitis?

• Group A streptococcus (Strep. Pyogenes)
• Staph. aureus
• Clostridium perfringens
• Bacteroides fragilis
• MRSA
43
Diagnosis?
• Cellulitis
• Crepitus
• Laboratory: LRINEC (laboratory risk indicator for necrotizing fasciitis)
Score >= 6 → necrotizing fasciitis is highly considered
Ix Value Points
CRP ≥15 mg/dL (150 mg/L) 4
< 15 0
White blood cell count
15 - 25 1
(x10,000/µL)
> 25 2
> 13.5 0
Hemoglobin (g/dL) 11 – 13.5 1
< 11 2
Na+ (mEq/L) < 135 2
Creatinine > 141 µmol/L (>1.6 mg/dL) 2
Glucose > 10 mmol/L (>180 mg/dL) 1
Pathology?
Extensive necrosis with thrombosis of blood vessels
Management?
ccrlsp-care of critically ill surgical pt
• Hemodynamic support according to CCrISP protocol
• Surgical debridement
• Antibiotics according to culture and sensitivity
Who to involve in care?

• ITU specialist
• Plastic surgeon
Patient responds to treatment and is improving but 9 days later patient develops bloody diarrhea, cause?
• Pseudomembranous colitis
• Ischemic colitis
• Hospital acquired infective gastroenteritis, norovirus
• Inflammatory bowel disease
Pathogenesis of PMC?
Pseudomembranous colitis is often triggered by antibiotic therapy that disrupts the normal microbiota and allows C.
difficile to colonize and grow. The organism releases toxins that disrupt epithelial function. The associated inflammatory
response includes characteristic volcano-like eruptions of neutrophils from colonic crypts that spread to form
mucopurulent pseudomembranes.
44
Diverticulitis + Endometriosis
SCENARIO:
Patient with LIF pain + peritonism → ruptured diverticulitis
Hartman's procedure was done
Histopathology revealed diverticulitis + endometriosis
Pathophysiology of diverticulosis?
• Congenital
• Acquired (Constipation + Ageing)
Colonic diverticula result from the unique structure of the colonic muscularis propria and elevated intraluminal
pressure in the sigmoid colon. Where nerves, arterial vasa recta, and their connective tissue sheaths penetrate the
inner circular muscle coat, focal discontinuities in the muscle wall are created. In other parts of the intestine these
gaps are reinforced by the external longitudinal layer of the muscularis propria, but, in the colon, this muscle layer is
gathered into the three bands termed taeniae coli. Increased intraluminal pressure is probably due to exaggerated
peristaltic contractions, with spasmodic sequestration of bowel segments, and may be enhanced by diets low in fiber,
which reduce stool bulk, particularly in the sigmoid colon.
Complications? colon lining-simple columner epithelium

• Infections
• Diverticulitis
life span of Neutrophil=2-5 days
• Perforation, paracolic abscess, focal peritonitis
• Fistula (colovesical, vaginocolic, ileocolic)
• Bleeding
• I.O
Cause of diverticulitis in diverticular disease?

Obstruction of diverticula leads to inflammatory changes, producing diverticulitis and peridiverticulitis. Because the wall
of the diverticulum is supported only by the muscularis mucosa and a thin layer of subserosal adipose tissue,
inflammation and increased pressure within an obstructed diverticulum can lead to perforation.
Classification for perforated diverticulitis?

Hinchey classification
I Pericolic abscess
IIa Distant abscess amenable to percutaneous drainage
IIb Complex abscess associated with fistula not amenable to percutaneous drainage
III Generalized purulent peritonitis
IV Fecal peritonitis
Management of diverticulitis? Terminology

Conservative (for uncomplicated diverticulitis) • Diverticulosis—the presence of
• Fluids diverticula that are asymptomatic
• NPO • Diverticular disease—diverticula
• Antibiotics associated with symptoms
• CT guided percutaneous drainage of collection should be considered • Diverticulitis—evidence of diverticular
inflammation (fever, tachycardia) with
Surgery (perforations): staged procedure:
or without localised symptoms and
• Diverting colostomy signs
• Hartmann • Complicated diverticulitis—
• Resection anastomoses perforation*, abscess, fistula,
stricture/obstruction
Investigations?
• FBC
• Urine
• CXR and AXR
• Rigid sigmoidoscopy
• Barium enema
• CT abdomen
45
How neutrophils migrate to the site of infection? (see diagram and text below)
(1) Margination and rolling along the vessel wall
(2) Firm adhesion to the endothelium
(3) Transmigration between endothelial cells
(4) Migration in interstitial tissues toward a chemoattractant stimulus
The multistep process of leukocyte migration through blood vessels, shown here for neutrophils. The leukocytes first
roll, then become activated and adhere to endothelium, then transmigrate across the endothelium, pierce the
basement membrane, and migrate toward chemoattractants emanating from the source of injury.
Different molecules play predominant roles in different steps of this process: selectins in rolling; chemokines (usually
displayed bound to proteoglycans) in activating the neutrophils to increase avidity of integrins; integrins in firm
adhesion; and CD31 (PECAM-1) in transmigration. ICAM-1, Intercellular adhesion molecule 1; PECAM-1 (CD31),
platelet endothelial cell adhesion molecule-1; TNF, tumor necrosis factor.
How did endometriosis get to the colon?

Theories are as follows:
• The regurgitation theory: proposes that
endometrial tissue implants at ectopic sites via
retrograde flow of menstrual endometrium.
Retrograde menstruation through the fallopian
tubes occurs regularly even in normal women
and can explain the distribution of
endometriosis within the peritoneal cavity.
• The benign metastases theory: holds that
endometrial tissue from the uterus can “spread”
to distant sites (e.g., bone, lung, and brain) via
blood vessels and lymphatic channels.
metaplastic• The metaplastic theory: suggests that
colon=transcoe endometrium arises directly from coelomic
epithelium (mesothelium of pelvis or abdomen),
lomic spread from which the müllerian ducts and ultimately
the endometrium itself originate during
embryonic development. In addition,
mesonephric remnants may undergo
endometrial differentiation and give rise to
ectopic endometrial tissue. Pathogenesis of endometriosis
• The extrauterine stem/progenitor cell theory:
is a recent idea that proposes that
stem/progenitor cells from the bone marrow
differentiate into endometrial tissue.
46
Intraperitoneal picture?
Burn powder, dark blue, black, chocolate cysts
Describe epithelium of uterus?

Simple columnar supported by thick vascular stroma. The endometrium is the inner epithelial layer, along with its
mucous membrane. It has a basal layer and a functional layer; the functional layer thickens and then is sloughed during
the menstrual cycle.
Is endometriosis can increase the risk of cancer?

Yes, especially ovarian cancer (3.5-fold risk increase) 3-5 fold
Why endometriosis causes pain?

Because of intrapelvic bleeding and periuterine adhesions
Few days later developed LIF collection why?

Retained collection (pelvic abcess)
What antibiotics to give?

• Amoxicillin clavulanic (1.2 g BD for 7 days) to cover gram +ve organisms
• Gentamycin (80 mg BD for 3 days) to cover gram -ve organisms
• Clindamycin (600 mg BD for 5 days) to cover anaerobes
47
48
Peptic Ulcer Disease + Hyperparathyroidism
SCENARIO: Patient with gastric ulcer → hematemeses → OGD → peptic ulcer, biopsy was taken. Hypercalcemia
Define an ulcer?
An ulcer is a local defect of the mucous membrane or the skin due to gradual disintegration of the surface epithelial cells
OR
Breach of the continuity of skin, epithelium or mucous membrane caused by sloughing out of inflamed necrotic tissue.
Risk factors of PUD?

• H-pylori infection
• NSAIDs
• Smoking
What is H. pylori?
Gram negative microaerophilic spiral bacteria found in the stomach
CLO test (campylobacter like organism):

It depends on urease production by H. pylori
A gastric mucosal biopsy is taken during gastroscopy and is placed in a medium containing urea and an indicator such as
phenol red, urease production by H-pylori converts urea to ammonia which increase pH changing the colour (yellow to
red) → positive test
How H. pylori can survive in acidic medium?

H. pylori survives in acidic conditions by producing urease, which catalyzes hydrolysis of urea to yield ammonia thus
elevating the pH of its environment.
How does H. pylori cause gastritis?

H. pylori produce certain proteases and phospholipases and these together with toxic ammonia produced from
breakdown of urea, damage gastric mucosa and cause inflammation
Mechanism by which H-pylori can colonize the stomach?

1- Flagella, which allow the bacteria to be motile in viscous mucus
2- Urease, which generates ammonia from endogenous urea, thereby elevating local gastric pH around the
organisms and protecting the bacteria from the acidic pH of the stomach
3- Adhesins, which enhance bacterial adherence to surface foveolar cells
4- Toxins, such as that encoded by cytotoxin-associated gene A (CagA), that may be involved in ulcer or cancer
development by poorly defined mechanisms
These factors allow H. pylori to create an imbalance between gastroduodenal mucosal defenses and damaging forces that
overcome those defenses.
Type of gastric cancer that can be caused by H. pylori?

• Adenocarcinoma
• MALT (Mucosal associated lymphoid tissue tumor)
Eradication of H. pylori?
7 days twice daily of
Full dose of PPI + metronidazole 400 mg + clarithromycin 250mg, or
Full dose of PPI + amoxicillin 1g + clarithromycin 500mg
Mechanism of action of PPI

PPI binds irreversibly to H+/K+ ATPase enzyme (proton pump) on gastric parietal cells and blocks secretion of H+, which
combine with CI- in the stomach lumen to form HCL.
See ASSCC (Gastric Ulcer Station)
Action of HCL?
• Activated pepsinogen to pepsin which help in proteolysis
• Antimicrobial
49
How can NSAIDs causes PUD?
• Topical irritant effect on the epithelium
• Impairment of the barrier properties of the mucosa
• Suppression of gastric PG synthesis (inhibitors of cyclooxygenase)
• Reduction of gastric mucosal blood flow
• Interference with the repair of superficial injury
Other causes of hematemesis in this patient?

Hypercalcemia → increased gastrin release → increased HCl production
Common causes of hypercalcemia?

• Malignancy
• Hyperparathyroidism (PTH adenoma)
• Renal failure
Cause of UTI in this patient?

Renal stones
How to localise parathyroid glands?

• Sestamibi scan (pre-operative)
• Frozen section (intra-operative)
What is frozen section?

It’s a pathological laboratory procedure to perform rapid microscopic analysis of a specimen.
How the specimen is fixed?

The surgical specimen is placed on a metal tissue disc which is then secured in a chuck and frozen rapidly to about -20 to
-30 °C. The specimen is embedded in a gel like medium called OCT and consisting of poly ethylene glycol and polyvinyl
alcohol. Subsequently, it is cut frozen with the microtome portion of the cryostat, the section is picked up on a glass slide
and stained (usually with hematoxylin and eosin, the H&E stain).
Why we cannot use paraffin based histopathology intraoperatively?

As it takes a week for paraffin to embed through the tissues
Epithelium of gastric mucosa in antrum?

Simple columnar with mucosal and goblet cells
What immune endocrine diseases and malignancy associated with helicobacter infections?
• Hashimoto's thyroiditis
• MALT
How many platelets present in packed RBC’s?

No platelets in packed RBC’s
After removing 4 parathyroid glands…

You are given the following histopathology report:
1 gland 0.2 g chief cells
3 glands ranging from 0.08 to 0.09 g oxyphilic cells and fat cells
What’s your interpretation?
Parathyroid adenoma in one gland with involution to the other glands
Histology of parathyroid adenoma?

• Uniform, polygonal chief cells with small, centrally placed nuclei.
• A few nests of larger oxyphil cells are present as well. Uncommonly, adenomas are composed entirely of this
cell type (oxyphil adenomas).
• A rim of compressed, non-neoplastic parathyroid tissue, generally separated by a fibrous capsule, is often visible
at the edge of the adenoma
Microscopic picture of parathyroid hyperplasia?

See MEN station
50
Where to find parathyroid gland if you do not see them in the normal position?
The superior mediastinum
(As the thymus originates from the third branchial arch, it occasionally drags the inferior glands down to the
mediastinum)
Treatment of parathyroid adenoma?

Excision
Types of hyperparathyroidism?
Disease type Hormone profile Clinical features Cause
Primary • PTH (↑) • May be asymptomatic if mild Most cases due to solitary
hyperparathyroidism • Ca2+ (↑) • Recurrent abdominal pain adenoma (80%), multifocal
• Phosphate (↓) (pancreatitis, renal colic) disease occurs in 10-15% and
• Urine Ca2+: creatinine • Changes to emotional or parathyroid carcinoma in 1%
clearance ratio > 0.01 cognitive state or less
Secondary • PTH (↑) • May have few symptoms Parathyroid gland hyperplasia
hyperparathyroidism • Ca2+ (↓ or normal) • Eventually may develop bone occurs as a result of low
• Phosphate (↑) disease, osteitis fibrosa cystica calcium, almost always in a
• Vitamin D levels (↓) and soft tissue calcifications setting of chronic renal failure
Tertiary • PTH (↑) • Metastatic calcification Occurs as a result of ongoing
hyperparathyroidism • Ca2+ (Normal or ↑) • Bone pain and / or fracture hyperplasia of the parathyroid
• Phosphate levels (↓ or • Nephrolithiasis glands after correction of
Normal) • Pancreatitis underlying renal disorder,
• Vitamin D (Normal or ↓) hyperplasia of all 4 glands is
• ALP (↑) usually the cause
Treatment of hypercalcemia?
• Hydration
• Forced diuresis
• Bisphosphonates: IV pamidronate
• Calcitonin
Esophageal Carcinoma
What is the normal esophagus lining? SCENARIO:

Non keratinized stratified squamous epithelium Patient, smoker with dysphagia
Hx of GERD and loss of weight
What is the most probable diagnosis? (20 pounds)
Cancer esophagus
What the etiological factors of cancer esophagus in this patient?

• Chronic GERD
• Smoker
What is the effect of prolonged GERD?

Chronic GERD leads to the development of Barret’s esophagus with increased risk of developing adenocarcinoma
Which test to do for this patient?

Endoscopy plus EUS with FNAC
What is the obtained cells will tell you?

• Stage
• Grade
• Immunohistochemistry
What is the stain used in immunohistochemistry?

Cytokeratin
Pathology report showed Barret’s esophagus Columnar metaplasia of the stratified squamous epithelium of the
esophagus Type of lining: columnar epithelium Type of cancer: adenocarcinoma. Staging: TNM [T2, N1]
51
T status
Tis High-grade dysplasia
T1 Invasion into the lamina
propria, muscularis mucosae,
or submucosa
T2 Invasion into muscularis
propria
T3 Invasion into adventitia
T4a Invades resectable adjacent
structures (pleura,
pericardium, diaphragm)
T4b Invades unresectable
adjacent structures (aorta,
vertebral body, trachea)
N status
N0 No regional lymph node
metastases
N1 1 to 2 positive regional lymph
nodes
N2 3 to 6 positive regional lymph
nodes
N3 7 or more positive regional
If patient develops pleural effusion, what are the possible causes? lymph nodes
• Spread of cancer cells to pleura M status
• Lung metastases M0 No distant metastases
• Obstruction of the thoracic duct M1 Distant metastases
Histologic grade
What pathological test to do? G1 Well differentiated
Effusion cytology G2 Moderately differentiated
G3 Poorly differentiated
How to treat? G4 Undifferentiated
Palliative treatments
• Thoracentesis,
• Indwelling pleural catheters (IPCs),
• Pleurodesis,
• Pleuroperitoneal shunting (PPS).
Developed enlargement of a supraclavicular lymph node, what test/investigation to do?

FNAC
Features under the microscope: metastatic adenocarcinoma with tumor cells having hyperchromatic eccentric nuclei and
intracytoplasmic vacuolation
Investigations of MI?
• ECG
• Troponin
• CK-MB
What is troponin?
Troponin-ICT
A complex of three regulatory proteins (troponin C, troponin I, and troponin T) that is integral to muscle contraction
Where is it found?
Cardiac muscle (myocardium) and skeletal muscle
52
Gastric Carcinoma
On entering you are given a histopath report showing SCENARIO:

o Signet ring carcinoma Patient with LIF pain + gastric cancer
o Positive LN Surgery was done (gastrectomy with splenectomy)
o Margin Positive Pathology report inside
o Spleen involved
2 major risk factors for gastric cancer? WHO classification

• H. pylori infection • Papillary adenocarcinoma
• Chronic atrophic gastritis • Tubular adenocarcinoma
• Intestinal metaplasia • Mucinous adenocarcinoma
• Pernicious anemia • Signet-ring cell carcinoma and other poorly
• Adenomatous polyps more than 2 cm cohesive carcinoma
• Previous gastric surgery • Mixed carcinoma
• HNPCC o Adenosquamous carcinoma
• FAP o Squamous cell carcinoma
o Hepatoid adenocarcinoma
Pathogenesis? o Carcinoma with lymphoid stroma
Gastric cancer is believed to develop by a sequence of o Choriocarcinoma
pathological changes o Carcinosarcoma
Normal mucosa → Chronic gastritis → Intestinal metaplasia → o Parietal cell carcinoma
Dysplasia → Intramucosal carcinoma → Invasive gastric o Malignant rhabdoid tumor
carcinoma o Mucoepidermoid carcinoma
o Paneth cell carcinoma
Discuss pathology report with the family in 4 simple lines? o Undifferentiated carcinoma
• This is cancer of the stomach o Mixed adeno-neuroendocrine carcinoma
• With incomplete resection o Endodermal sinus tumor
• With high possibility of recurrence o Embryonal carcinoma
• The patient will require further resection and o Pure gastric yolk sac tumor
chemotherapy o Oncocytic adenocarcinoma
What is the commonest histological type of gastric cancer?

Adenocarcinoma 95%
Classification?
The WHO classification: 5 main types
• Tubular adenocarcinoma – This is made up of different sized small branching tubes (tubules).
• Papillary adenocarcinoma – This tumor grows outward from the stomach wall and contains finger-like
growths that stick out into the stomach cavity. The cells tend to look and behave much like normal cells.
• Mucinous adenocarcinoma – There is a lot of mucin (the main substance in mucus) outside of the cancer
cells.
• Poorly cohesive carcinomas (including signet ring cell carcinoma and others) – These are arranged into
clumps of cancerous cells.
• Mixed carcinoma – This contains a mix of types of adenocarcinomas of the stomach.
The classification is based on the predominant histologic pattern of the carcinoma which often co-exists with less
dominant elements of other histologic patterns. Tubular adenocarcinoma is the most common histologic type of
early gastric carcinoma
The Lauren classification divides adenocarcinoma of the stomach into 2 main types:
• Intestinal type – Tumor cells are well differentiated, grow slowly and tend to form glands. This type is found
more often in men than in women and occurs more often in older people.
• Diffuse type – tumor cells are poorly differentiated, behave aggressively and tend to scatter throughout the
stomach (rather than form glands). This type spreads to other parts of the body (metastasizes) much
quicker than intestinal type tumors. The diffuse type occurs equally among men and women and tends to
develop at a younger age than the intestinal type.
53
7-10 days later the patient had axillary vein thrombosis, what predisposes to that?
• Hypercoagulable state in malignancy
• Venous stasis from Virchow LN
6 months later came with ascites, deranged liver functions, hepatic metastasis Mention 2 pathological tests to do?
• Ascites tap and cytology
• Liver biopsy from metastasis
• FNAC from the left supraclavicular lymph node
• Tumor marker: CA72-4
Treatment of this patient?

• Feeding jejunostomy
• Palliation of ascites by repeated tapping
• Pain relief using opioids
• Palliative chemotherapy
Mechanism of malignant ascites in cirrhotic liver?

• Oncotic pressure is high
• Interstitial pressure is increased
See ASSCC (Esophageal Varices and Hematemesis station)
Borrmann classification system for gastric cancer?

Macroscopic appearance of the lesion:
• Polypoid growth
• Fungating growth
• Ulcerating growth
• Diffusely infiltrating growth (linitis plastica)
Which para-neoplastic conditions associated with gastric cancer?

• Acanthosis nigricans
• Dermatomyositis.
What are the procedure specific complications of total gastrectomy?

Early
• Anastomotic leak
• Pancreatitis
• Cholecystitis
• Hemorrhage
• Infection.
Late
• Dumping syndrome
• Vitamin B12 deficiency (lack of intrinsic factor)
• Metabolic bone disease
• Recurrence of malignancy
What is dumping syndrome?

Loss of the reservoir function of the stomach (e.g. following gastrectomy) results in the rapid transit of highly osmotically
active substances into the duodenum following meals and may cause ‘dumping syndrome’.
Early dumping: 30–60 minutes following a meal, rapid transit of the hyperosmolar gastric contents into the small bowel
results in a fluid shift from the intravascular compartment to the gastric lumen and small bowel distension, colicky
abdominal pain, diarrhoea and vasomotor symptoms, such as tachycardia and postural hypotension.
Late dumping: 1–3 hours following meals. Rapid transit of carbohydrate into the small bowel results in sudden
absorption of high levels of glucose and compensatory hyperinsulinemia, resulting in subsequent hypoglycaemia.
54
Cancer Colon + Hemorrhoids + Myocardial Infarction
SCENARIO: PR bleeding diagnosed as hemorrhoids, colonoscopy done revealed adenocarcinoma with melanosis coli,
biopsied, histopathology revealed lesion up to muscularis layer
Dukes’ staging?
What is hemorrhoids?
Swollen or inflamed anal cushions
Pathogenesis of hemorrhoids?
• The anal cushions function normally when they are fixed to their proper sites within the anal canal by
fibromuscular ligaments, which are the anal remnants of the longitudinal layer of the muscularis propria from
the rectum (Treitz's ligaments).
• When these submucosal fibres fragment (as by prolonged and repeated downward stress related to straining
during defecation), the anal cushions are no longer restrained from engorging excessively with blood and may
result in bleeding and prolapse.
Pathogenesis of thrombosed hemorrhoids?

• Acute thrombosis results from sudden raised pressure causing rupture of the vascular plexus leading to a blood
clot at the anal verge.
• Any activity requiring excessive abdominal straining such as over-exercising can cause this
Why coronary arteries get thrombosed?

Due to coronary artery atherosclerosis
Define melanosis coli?

It is a disorder of pigmentation of the wall of the colon, often identified at the time of colonoscopy. It is benign and may
have no significant correlation with disease.
Define adenoma?
The term adenoma is generally applied to benign epithelial neoplasms producing gland patterns and to neoplasms
derived from glands but not necessarily exhibiting glandular patterns.
55
How coronary arteries get atherosclerosis?
• Endothelial injury—and resultant endothelial
dysfunction—leading to increased
permeability, leukocyte adhesion, and
thrombosis
• Accumulation of lipoproteins (mainly oxidized
LDL and cholesterol crystals) in the vessel
wall
• Platelet adhesion
• Monocyte adhesion to the endothelium,
migration into the intima, and differentiation
into macrophages and foam cells
• Lipid accumulation within macrophages,
which release inflammatory cytokines
• Smooth muscle cell recruitment due to
factors released from activated platelets,
macrophages, and vascular wall cells
• Smooth muscle cell proliferation and ECM
production
Risk factors of atherosclerosis?

Non-modifiable (Constitutional)
• Genetic abnormalities
• Family History
• Increasing age
• Male gender
Modifiable
• Hyperlipidemia
• Hypertension
• Cigarette smoking
• Diabetes
• Inflammation
What is the function of thrombus?

A thrombus is a healthy response to injury intended to
prevent bleeding
How it is formed?
The following sequence of events takes place:
• An atheromatous plaque is suddenly
disrupted by intra-plaque hemorrhage or
mechanical forces, exposing sub-endothelial
collagen and necrotic plaque contents to the
blood.
• Platelets adhere, aggregate, and are
activated, releasing thromboxane A2,
adenosine diphosphate (ADP), and
serotonin—causing further platelet
aggregation and vaso-spasm.
• Activation of coagulation by exposure of
tissue factor and other mechanisms adds to
the growing thrombus.
• Within minutes, the thrombus can evolve to
completely occlude the coronary artery
lumen.
Response to injury in atherogenesis: 1, Normal. 2, Endothelial injury
with monocyte and platelet adhesion. 3, Monocyte and smooth muscle
cell migration into the intima, with macrophage activation. 4,
Macrophage and smooth muscle cell uptake of modified lipids and
further activation. 5, Intimal smooth muscle cell proliferation with ECM
elaboration, forming a well-developed plaque.
56
The natural history, morphologic features, main pathogenic events, and clinical complications of atherosclerosis
Mechanism of myocardial infarction?

• Within seconds of vascular obstruction, aerobic glycolysis ceases, leading to a drop in adenosine triphosphate
(ATP) and accumulation of potentially noxious metabolites (e.g., lactic acid) in the cardiac myocytes
• The functional consequence is a rapid loss of contractility, which occurs within a minute or so of the onset of
ischemia. Ultrastructural changes (including myofibrillar relaxation, glycogen depletion, cell and mitochondrial
swelling) also become rapidly apparent.
• These early changes are potentially reversible. Only severe ischemia lasting at least 20 to 40 minutes causes
irreversible damage and myocyte death leading to coagulation necrosis
57
58
Malignant Melanoma
Definition? SCENARIO:
Malignant neoplasm of melanocytes (melanin producing cells), mainly Skin lesion, you are given a pathology report
arising in skin.
Other sites: nasal cavities, retina, gastrointestinal mucosa
Skin conditions associated with melanoma?

• Xeroderma pigmentosa
• Albinism
• Giant congenital pigmented naevus Key=Nevus/Nevi
• Fitzpatrick skin type 1
• Dysplastic naevus, multiple nevi
Other risk factors of malignant melanoma?

• Hutchinson’s melanotic freckles
• Immunocompromised patients
• Past history of melanoma
• Red hair, sun exposure
Comment on the pathology report?

• Size
• Breslow thickness: measured in mm. From the top of stratum granulosum to the deepest point of tumour
involvement
• Depth of invasion (Clark’s levels)
• Ulceration, mitoses, lymphovascular invasion
• Immunohistochemistry staining
How to differentiate melanoma from SCC?

Melanoma SCC
Arise from the lower layer of the epidermis from any Arise from upper and mid layer of epidermis with keratin
part of the body pearl formation usually on sun exposed areas BCC-Prarly Colour
Needs intermittent sun exposure Nonmelanoma need continuous sun exposure
Arise from lower most layers of epidermis Arise from superficial layers
Develops in younger people Older people
Anywhere in body Sun exposed areas
Appears as red bump, scaly patch or non-healing sore Asymmetrical mole with irregular border and multicolored
Incidence more common Less common
Metastasis less common More common
Better prognosis Poorer prognosis
59
Difference between BCC and SCC?
Basal cell carcinoma Squamous cell carcinoma
Spreads less commonly Spreads more commonly than BCCs
Found deep within skin layers of thick skin Found near body orifices and in the oral cavity
Occupies basement membrane Occupies outer layer of skin
Most common form of NMSC Less common but more dangerous
96% of victims 40 years or more Almost all victims are 40 years or older
Red, pale, or pearly in color Thickened, red, spot, may bleed, crust or ulcerate
Keratin pearl fomation
Poor prognostic factors?

• Increased tumor thickness (Breslow thickness)
• Increased depth of invasion ,
• Type of melanoma: nodular, amelanotic melanoma
• Presence of ulceration
• Presence of lymphatic or perineural invasion
• Presence of regional or distant metastasis
• Male, old age
Genes responsible for familial MM?

CDKN2A and CDK4, MC1R, BRCA2 gene BRAF most important
Lesion excised, Breslow thickness 1.5 mm, margins 0.5 mm, what to do?
Re-excision
Management?
Excision + Safety margin
Size of the safety margin is based on the Breslow thickness
• <0.76mm thickness= 1 cm margin
• 0.76-1mm thickness= 2 cm margin
• 1mm= 3 cm margin
What to do to ensure adequate margins?

• Frozen section
• Mohs microsurgery
Post excision the patient developed regional lymphadenopathy, management?

• FNAC
• Whole body CT
60
Post excision the patient developed painful swelling of the arm + dyspnea, cause?
• Axillary vein thrombosis → pulmonary embolism
How to treat DVT?

• Acute treatment with parenteral anticoagulation (LMWH, fondaparinux).
• Maintaining patients on anticoagulation for at least 6 months is the standard of practice.
• Warfarin, to keep INR 2-3, standard doses range between 1–10 mg per day for 6 months
• Catheter-directed thrombolysis (CDTL) if clot is less than 14 days in duration or acute phlegmasia cerulea
dolens inpatients with no contraindications to thrombolytic therapy. A clot present for more than 14 days
leads to thrombus organization that limits the effectiveness of thrombolysis. Use tPA continuous infusion of
0.5–1 mg per hour for at least 8 hours (an initial bolus, every 6–8 hours monitor fibrinogen levels, which
should be kept above 100 mg/dL to avoid depletion. Fibrinogen levels below 100 mg/dL can cause
hemorrhagic complication. Upon termination of the procedure, the patients are systemically anticoagulated
with warfarin for 6 month
• Indications for SVC filter placement are failure or contraindication to therapeutic anticoagulation or for
presurgical prophylaxis in the setting of substantial thromboembolic risk factors
Risk factors for thrombosis?

Virchow's triad:
• Hypercoagulable state
• Venous stasis
• Endothelial injury
Management (suspecting PE)?

• CTPA -CT pulmonary angiography
• SC LMWH if the patient is hemodynamically
stable
• Thrombolysis or embolectomy (massive
embolism)
Malignant Melanoma Metastasis
DD? SCENARIO: A patient known to have

Inguinal lymph nodes receive lymphatic drainage from the lower hypothyroidism with a hard swelling in
extremities and skin of the lower abdomen, genitals, and perineum. her right inguinal region, her GP sent
Infections associated with inguinal lymph node: her for biopsy
• Cellulitis of the lower extremities
• Venereal infections - Syphilis, chancroid, herpes simplex virus
infection, lymphogranuloma venereum
Malignancies associated with inguinal lymph nodes:
• Lymphomas
• Metastatic melanomas from lower extremity primary site
• Squamous cell carcinomas from genital primary site
Results of histopath. Revealed malignant melanoma, what are types of malignant melanoma?
Melanomas are divided into 5 main types, depending on their location, shape and whether they grow outward or
downward into the dermis:
• Lentigo maligna: usually occur on the faces of elderly people
• Superficial spreading or flat melanoma: grows outwards at first to form an irregular pattern on the skin with an
uneven color
• Desmoplastic melanoma: is a rare malignant melanoma marked by non-pigmented lesions on sun-exposed
areas of the body
• Acral melanoma: occurs on the palms of the hand, soles of the feet, or nail beds
• Nodular melanomas: are lumpy and often blue-black in color and may grow faster and spread downwards
What is Epitheloid Melanoma?

Melanoma cells can be categorized into 2 major types: epithelioid and spindle cells.
Epithelioid cells are large and round with abundant eosinophilic cytoplasm, prominent vesicular nuclei and large nucleoli.
They most commonly arise in superficial spreading and nodular melanomas.
61
What is a satellite lesion?
It is a form of local spread of malignant melanoma by contiguity and continuity leading to pigment spreading to the
surrounding area. They are found within 2 cm of the primary tumor.
How can you know the phenotype of the tumor?

Recent histopathological studies of lymph node in metastatic melanoma other than IHC?
Genetic mutation studies (BRAF gene)
Genetic subtypes
These molecular subtypes are based on the distinct genetic changes of the melanoma cells (mutations).
These genetic changes include:
• BRAF mutations: The most common genetic change in melanoma is found in the BRAF gene, which is mutated in
about 50% of cutaneous melanomas.
• NRAS mutations: NRAS is mutated in the tumors of around 20% of patients with melanoma
• NF-1 mutations: NF-1 mutations are present in the tumors of around 10% to 15% of patients with melanoma
• KIT mutations: These mutations occur more commonly I melanomas that develop from mucus membranes,
melanomas o the hands or feet, or melanomas that occur in chronically sun-damaged skin, such as lentigo
maligna melanoma.
Where would you examine this lady?

• Primary sites: whole lower limb including nail beds and soles
• Metastatic sites: chest, abdomen and brain
How would you to treat this lady?

Excision of the primary lesion with safety margin plus block inguinal lymph node dissection plus radiotherapy
Post-operative the wound is red and swollen, culture was done revealed diplococci
Examples of gram-negative diplococci?
• Neisseria sp.
• Moraxella catarrhalis
• Acinetobacter
• Haemophilus
• Brucella
Examples of gram-positive diplococci?
• Streptococcus pneumoniae
• Enterococcus.
Next the patient got toxemia with rapidly spreading infection, what do you think?
Necrotizing fasciitis
What is SIRS?
Systemic Inflammatory response syndrome
Manifestations of SIRS include, two or more of the following:
• Body temperature less than 36 °C (96.8 °F) or greater than 38 °C (100.4 °F)
• Heart rate greater than 90 bpm
• Tachypnea (high respiratory rate), with greater than 20 breaths per minute; or, an arterial partial pressure of
carbon dioxide less than 4.3 kPa (32 mmHg)
• White blood cell count less than 4000 cells/mm³ (4 x 109 cells/L) or greater than 12,000 cells/mm³ (12 x 109
cells/L); or the presence of greater than 10% immature neutrophils (band forms). Band forms greater than 3% is
called bandemia or a "left-shift."
• Hyperglycemia (blood glucose > 6.66 mmol/L i.e. 120 mg/dL) in absence of diabetes mellitus
• Altered mental state
What happens to lung in SIRS?

ARDS
Define ARDS? See Burn / ARDS station in ASSCC
Diffuse alveolar damage and lung capillary endothelial injury
62
Basal Cell Carcinoma (BCC)
Describe the lesion?

SCENARIO: Lump over arm. Excision biopsy done,
Pearly papule with a central ulcer, with granulation tissue on base shown report BCC with depth of invasion, deep
and with rolled in (inverted) edges with surrounding margin involvement
telangiectasia -[widened venule]
Why the surrounding skin is red? -due to widened venule

Due to the presence of dilated subepidermal blood vessels
(telangiectasia)
Most probable diagnosis?

BCC
Differential Diagnosis?
• BCC
• SCC
• TB
• Actinic keratosis
• Seborrheic keratosis
• Verruca vulgaris
Natural Hx of BCC?
• Indolent with slow progression
• Locally destructive but limited
potential to metastasize (never
metastasize)
How lymph node spread occurs?

• Permeation
• Embolization
What is your concern in pathology report?

Deep margin involvement
How would you manage a pt with deep margin involvement?

Re-excision
Treatment options for basal cell carcinoma?

• Surgical
o Curettage and Electrodessication: scraping away the tumor and stopping bleeding with cautery
o Excision with primary closure: flaps, grafts, and secondary intention healing. Excision margin of 4 mm
around the tumor is recommended where possible
o Cryotherapy (with liquid nitrogen), but can't obtain tissue biopsy
o Mohs micrographic surgery – Serial tangential horizontal sections are taken and examined histologically
until all margins are clear
• Radiotherapy
• Topical
o Topical photodynamic therapy - δ-aminolevulinic acid made up in a 20% emulsion and applied topically.
Tumor tissue absorbing this porphyrin metabolite becomes photosensitive with its conversion to
protoporphyrin IX and subject to photo destruction when exposed to light, usually in the wavelength
range 620-670 nm
o Topical fluorouracil 5%
o Topical imiquimod 5%
How to prevent recurrence of deep margin involvement during re-operation?

If recurrent, go for Mohs micrographic surgery (frozen section)
Skin graft placed for pt and subsequently had graft failure. Cause for graft failure?
Wound infection
63
Common organism?
S. aureus.
Wound C&S grew MRSA, what is MRSA?

Methicillin-resistant Staphylococcus aureus.
How would you manage this pt with MRSA wound infection?

If abscess, I&D
Outpatient
• Oral Antibiotics as clindamycin, amoxicillin plus tetracycline or tmp/smx, linezolid*
Inpatient:
• Vancomycin Dose to target trough level 7-14days
• Linezolid 600 mg twice daily, PO or IV 7-14
• Daptomycin 4 mg/kg once daily 7-14
• Telavancin 10 mg/kg once daily 7-14
• Clindamycin 600 mg IV or 300 mg PO 3times daily
Decolonization with mupirocin nasal or chlorhexidine for body decolonization
Infection control of MRSA:

Measures apply to all patients, regardless of MRSA status:
• High standards of hand decontamination are required to minimize the risk of cross infection
• Hands should be decontaminated before and after every patient contact
• Handwashing should be with liquid soap and water
• Alcohol hand rub may be used as an alternative
• Maintain high standards of aseptic technique
• Maintain high standards of ward cleanliness
• All linen should be handled in accordance with Trust Laundry Policy
• All waste should be disposed of in accordance with Trust Policy
• Re-usable equipment must be decontaminated before use on another patient.
Trust
• Decontamination and Disinfection Guidelines should be followed
• Antibiotics should be used in accordance with Trust Antibiotic Guidelines
• Minimize inter-ward transfer of patients
• Avoid overcrowding of patients
• Maintain adequate and appropriately skilled nursing and other staff levels
The following additional precautions should be used for all MRSA positive patients:
• Place patient in a single room
• If a side room is unavailable, may be managed in ward bays next to a sink following agreement
with the Infection Control Team
• If a number of MRSA positive patients are present, these may be managed in a cohort. This should
only occur following discussion with the Infection Control Team
• Wear gloves and disposable plastic aprons when handling the patient or having contact with their
immediate environment
• All waste should be regarded as clinical waste and to be disposed of in yellow waste bags
• All linen to be treated as contaminated/infected and to be disposed of in an inner red alginate bag
or alginate seamed/stitched bag placed within a white plastic outer
• Gowns may be required where extensive contact with the patient is anticipated
After excision, the patient developed regional lymphadenopathy? FNAC was done and revealed (lymphocytes, PMNL,
histiocytes, cells with an bilobed nuclei) Interpret?
Reed-Sternberg cells: (owl eye appearance) → Hodgkin’s lymphoma
Mechanism of lymphatic spread?

Malignant tumors release growth factors such as VEGF-C to induce lymphatic vessel expansion (lymph angiogenesis) in
primary tumors and in draining sentinel LNs, thereby promoting LN metastasis
64
Sickle Cell Disease + Brain Tumor
haemoglobinopathy-abnonal haemoglobulin chain
What is sickle cell disease? SCENARIO:
Sickle cell disease is a common hereditary hemoglobinopathy caused by a point A lady known to have sickle
mutation in β-globin that promotes the polymerization of deoxygenated cell disease, had head injury.
hemoglobin, leading to red cell distortion, hemolytic anemia, microvascular CT was done and a temporal
obstruction, and ischemic tissue damage. mass of 3.8 cm was
HbS is produced by the substitution of valine for glutamic acid at the sixth amino acid accidentally discovered
residue of β-globin. In homozygotes, all HbA is replaced by HbS, whereas in
heterozygotes, only about half is replaced.
Complications?
• Vaso-occlusive crisis: triggered by infection,
dehydration, acidosis, affecting the bones
(painful bone crisis as in hand-foot
syndrome), lungs (acute chest syndrome),
brain (stroke and retinopathy), spleen
(autosplenectomy) sequestration-occupy
• Sequestration crisis: in children, massive
entrapment of sickle cell in the spleen will
lead to rapid splenic enlargement and
hypovolemic shock
• Aplastic crisis: due to infection of red cell
progenitors by parvo-virus
• Chronic tissue hypoxia: organ damage
(spleen, heart, kidney, lungs)
• Increased susceptibility of infection with
encapsulated organisms
Mechanism of autosplenectomy?
In early childhood, the spleen is enlarged up to
500 gm by red pulp congestion, which is caused by
the trapping of sickled red cells in the cords and
sinuses. With time, however, the chronic
erythrostasis leads to splenic infarction, fibrosis,
and progressive shrinkage, so that by adolescence
or early adulthood only a small nubbin of Fibrous
splenic tissue is left; this process is called
autosplenectomy
What are the surgical relevance of sickle cell disease?

• Gall stones
• Autosplenectomy
• Avascular bone necrosis
• Osteomyelitis
• Pulmonary hypertension
• Heart failure
Why the patient is immunocompromised?

Because of autosplenectomy with increased susceptibility of infection with encapsulated organisms
Most common organisms causing infection after splenectomy

• Streptococcus pneumoniae Streptococcus,Meningococcus,Haemophilus
• Haemophilus influenzae
• Neisseria meningitidis
65
Most common brain tumor in elderly?
High-grade:
• Gliomas and glioblastoma multiforme.
• Medulloblastoma.
Low-grade:
• Meningiomas.
• Acoustic neuromas.
• Neurofibroma.
• Pituitary tumors.
• Pineal tumors.
• Craniopharyngiomas.
Secondaries
Manifestations of brain tumors?

The presentation will depend on location and rate of growth but includes features of a space occupying lesion and raised
intracranial pressure (ICP):
• Headache, which is typically worse in the mornings.
• Nausea and vomiting.
• Seizures.
• Progressive focal neurological deficits, for e.g. diplopia associated with a cranial nerve defect, visual field
defects, neurological deficits affecting the upper and/or lower limb.
• Cognitive or behavioral symptoms.
• Symptoms relating to location of mass, for e.g. frontal lobe lesions associated with personality changes,
disinhibition and parietal lobe lesions might be associated with dysarthria.
• Papilledema (absence of papilledema does not exclude a brain tumor).
What if the tumor is left untreated?

Death
Biopsy showed squamous cells?

Metastatic SCC
Possible primary sources?

SCC of skin, lung, esophagus, nasopharynx, cervix
Post biopsy had wound infection, common organisms?

Staph aureus
Wound discharge showed glucose, cause?

CSF communication
66
Polycystic Kidney Disease (APKD)
SCENARIO:
Patient with ADPK going for bilateral nephrectomy due to intractable abdominal pain.
You are shown this picture
Describe gross pathology?

Enlargement of the kidney with multiple cyst formations
Mode of inheritance?
Autosomal dominant condition due to mutations in 2 genes: PKD1,
PKD2
Pathogenesis of cyst formation?

The cells of the renal tubules divide repeatedly until causing an out-
pocketing of the tubular wall with the formation of a saccular cyst
that fills with fluid derived from glomerular filtrate that enters from
the afferent tubule segment. Progressive expansion eventually
causes most of the emerging cysts to separate from the parent
tubule, leaving an isolated sac that fills with fluid by transepithelial
secretion. This isolated cyst expands relentlessly as a result of
continued proliferation of the mural epithelium together with the
transepithelial secretion of sodium chloride and water into the
lumen
Possible mechanisms of cyst formation in cystic kidney diseases
Other organs in the abdomen causing cyst formation?

• Liver
• Ovaries
• Pancreas
• Spleen
67
Complications?
• Renal failure
• Infection
• Hypertension
Other pathology associated with PCKD?

• Liver cysts
• Pancreatic cyst
• Brain aneurysms
• Mitral valve prolapse
Associated lesion in the brain?

Cerebral aneurysm
Why there is pain?

Weight of the organ dragging upon its pedicle or stretching of renal capsule by cysts.
What other symptoms?

• Pain
• Irregular abdominal mass
• Hematuria
• Infection
• Hypertension
• Uremia
Other differentials?
• Simple cyst
• Acquired cystic kidney disease
• VHL
• Medullary sponge kidney
• Tuberous sclerosis
Type of matching before transplant?

ABO blood matching
HLA matching: Human Leucocyte Antigens. HLA-A, HLA-B and HLA-DR are the most important. They are proteins located
on the surface of WBC.
Types of graft rejections?

Type of rejection Key features
Hyperacute Occurs within minutes of clamp release
Due to pre formed antibodies*
Immediate loss of graft occurs
Accelerated acute Occurs in first few days following surgery
Involved both cellular and antibody mediated injury
Pre-sensitisation of the donor is a common cause
Acute Traditionally the most common type of rejection
Seen days to weeks after surgery
Predominantly a cell mediated process mediated by lymphocytes
Organ biopsy demonstrates cellular infiltrates and graft cell apoptosis
Chronic Increasingly common problem
Typically; graft atrophy and atherosclerosis are seen. Fibrosis often occurs as a late event
* Episodes of hyperacute rejection are typically due to preformed antibodies. ABO mismatch is the best example.
However, IgG anti HLA Class I antibodies are another potential cause. These events are now seen less commonly because
the cross matching process generally takes this possibility into account
What types of malignancy occur with immunosuppression?

Malignancy: this is 5 times greater than the normal population. Most commonly squamous cell carcinoma of skin, cervix,
basal cell carcinoma’s, lymphoma and Kaposi’s sarcoma.
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Testicular Teratoma
On ultrasound, groin mass turned out to be undescended testis with solid SCENARIO:
and cystic components (i.e. suspicious of cancer) 35y man with left groin mass,
Tissue diagnosis and you are given the following a pathology report: examination revealed a single palpable
Teratoma testis
Positive margins
Lymphovascular invasion
T4, Nx (i.e. nodal disease can’t be assessed), Mx (metastatic disease can’t be assessed)
Define cryptorchidism?
Cryptorchidism is a complete or partial failure of the intra-abdominal testes to descend into the scrotal sac and is
associated with testicular dysfunction and an increased risk of testicular cancer.
Etiology / Risk factors of cryptorchidism

• Family history
• Low birth weight, premature birth
• High abdominal pressure (gastroschisis)
• Down syndrome
How does undescended testis contribute to increased risk of testicular cancer?

The cryptorchid testis carries a 3 to 5-fold higher risk for testicular cancer, which arises from foci of intratubular germ cell
neoplasia within the atrophic tubules
Other complications?
Infertility, inguinal hernia, testicular torsion
What will be your management?

• CT abdomen and pelvis
• Staging
• Discuss in MDT
• Orchiectomy + chemotherapy
• If nodal disease → RPLND (Retroperitoneal Lymph Node Dissection)
Role of orchiopexy?
Reduces risk of infertility and cancer, testicle can be checked at new location (for ca)
Types of germ cell tumors?

• Seminomatous tumors
o Seminoma
o Spermatocytic seminoma
• Nonseminomatous tumors
o Embryonal carcinoma
o Yolk sac (endodermal sinus) tumor
o Choriocarcinoma
• Teratoma
• Sex Cord-Stromal tumors
o Leydig cell tumor
o Sertoli cell tumor
Discuss pathology report with family in 3 simple lines?

• This is cancer in the testis
• With incomplete resection
• With lymphatic spread
Where teratoma spread to first?

To the para-aortic lymph nodes
Where does it spread to next?

Locoregional
69
Serological markers / Blood tests?
Biologic markers include
• HCG
• AFP
• Lactate dehydrogenase
Which HCG?
B-HCG
Other conditions where HCG is elevated?
Pregnancy
Value of serum markers is fourfold

• In the evaluation of testicular masses
• In the staging of testicular germ cell tumors. For example, after orchiectomy, persistent elevation of HCG or AFP
concentrations indicates stage II disease even if the lymph nodes appear of normal size by imaging studies.
• In assessing tumor burden
• In monitoring the response to therapy. After eradication of tumors there is a rapid fall in serum AFP and HCG.
With serial measurements it is often possible to predict recurrence before the patients become symptomatic or
develop any other clinical signs of relapse.
Post-operative developed hematoma, mention stages of hematoma resolution?

• Lysis of the clot by macrophages (about 1 week)
• Growth of fibroblasts from into the hematoma (2 weeks)
.
After few months developed small pneumothorax, what’s the cause?
Lung metastasis
Define metastasis?
Survival and growth of cells at a site distant from their primary origin
One year later the patient came with para-aortic lymph node compressing renal artery and vein + SOB + PE
Why PE in this patient?
• Venous stasis
• Hypercoagulable state
Why hypercoagulable state?
Tumor cells to produce and secrete procoagulant/fibrinolytic substance which activate coagulation cascade
stimulation of tissue factor production by host cell.
Which part of Virchow's triad is missing here?

Endothelial injury
What is choriocarcinoma and what is its tumor marker?

Choriocarcinoma is a highly malignant form of testicular tumor.
Histologically the tumors contain two cell types, syncytiotrophoblast and cytotrophoblast
Tumor marker is B-HCG
What is the common tumor in this age group?

Seminoma
(Non–Hodgkin lymphoma is the most common testicular tumor in men older than 60 years.)
What is the cell origin of seminoma?

Most testicular germ cell tumors originate from a precursor lesion called intratubular germ cell neoplasia (ITGCN)
Histopath showed papillary thyroid tissue and GIT adenocarcinoma, why?

Teratoma has the 3 germ cell lines (mesoderm, endoderm, ectoderm)
70
Prostate Cancer
SCENARIO: A man with BPH, poor urine stream, low back pain
DRE was done and a firm, round prostate was felt, what’s your diagnosis
BPH
Cause of prostate enlargement?

Androgen
Investigations
• PSA
• MSU analysis
• U&Es
How to take a prostate biopsy?

TRUS guided from: mid lobe parasagittal plane at the apex, the mid gland, and the base bilaterally.
Why multiple biopsies?

• Prostatic cancer can be focal, so it’s important to take samples from different sites Focal=Central
• There is often only a scant amount of tissue available for histologic examination in needle biopsies
• Malignant glands may be admixed with numerous benign glands
• Moreover, the histologic findings pointing to malignancy may be subtle (leading to underdiagnoses),
• There are also benign mimickers of cancer that can lead to a misdiagnosis of cancer
How to differentiate between rectum and prostate cells in a needle biopsy?

• Using immunohistochemical marker (α-methylacyl-coenzyme A-racemase) (AMACR)
• CEA (in rectal cells)
What are the gene mutations involved in pathogenesis of prostate cancer?

The most common acquired genetic lesions in prostatic carcinomas areTPRSS2-ETS fusion genes and mutations or
deletions that activate the PI3K/AKT signaling pathway.
“Patient went to radical prostatectomy, PSA is 7 three months later”
How can you judge the success of radical prostatectomy?

Fall in the level of PSA below detectable levels within 4-6 weeks
High PSA after prostatectomy → recurrence should be considered
Why PSA is not reliable?

• PSA is organ specific, but not cancer specific.
• Although serum levels of PSA are elevated to a lesser extent in BPH than in prostatic carcinomas, there is
considerable overlap.
• Other factors such as prostatitis, infarction of nodular hyperplasia, instrumentation of the prostate, and
ejaculation also increase serum PSA levels
71
What is the grading system?
Gleason score
It grades prostate tumors from 2 – 10,
10 being the most abnormal and
therefore the most likely to spread.
The pathologist allocates a number
from 1 - 5 for the most common
histological pattern in the specimen,
then does the same for the second
most common pattern.
The sum of these two numbers gives
the Gleason score
One test to exclude bony metastasis?

Alkaline phosphatase
What kind of metastases?

Sclerotic
Why?
Due to increased bone
deposition due to increased
osteoblastic activity
Post-operative, developed fever, dusky red urine, why?

Post-operative, patient is confused and has a raised white cell count, why?
UTI
Which of the blood components will rise? Types of bone metastases

WBC's - neutrophils Bone metastases are typically characterized as ‘lytic’,
‘sclerotic’ or ‘mixed’, according to the radiographic
Most common organisms? and/or pathologic appearance of the lesions.
E-coli
One year after surgery, PSA is 3 ng/ml

PSA is only secreted by prostatic tissues. If all prostatic tissue was removed, PSA should not be present
What is the rational in treating prostate cancer by bilateral orchidectomy?

Androgen deprivation
The growth and survival of prostate cancer cells depends on androgens, which bind to the androgen receptor (AR) and
induce the expression of pro-growth and pro-survival genes.
What are the cells producing testosterone?

Leydig cells
Lobes of the prostate
72
Abscess
Definition? SCENARIO:
Focal collection of pus that may be caused by seeding of pyogenic organisms into a Patient with forearm abscess
tissue or by secondary infections of necrotic foci.
What tissue is the wall of an abscess characteristically

composed of?
Granulation tissue. This used to be called the “pyogenic
membrane”, but it is not a true membrane and is not
itself pyogenic.
What is present inside an abscess?

Central, largely necrotic region rimmed by a layer of
preserved neutrophils, with a surrounding zone of
dilated vessels and fibroblast proliferation indicative of
attempted repair.
What is pus?
Pus is the product of acute inflammation composed of
cellular and fluid, exudative phases.
Organisms causing abscess? The abscess contains neutrophils and cellular debris and is
• Bacterial: Staph aureus, Streptococcus surrounded by congested blood vessels.
pyogenes
• Non-bacterial: Fungal, viral, parasitic
pus colour=green-pseudomonus,sulphar granules-
One simple test to detect the cause of abscess? actinomycosis,
Gram stain ,Culture and sensitivity yellow-staph aureus
What is the cause of fever in abscess?
Fever is produced in response to substances called pyrogens (TNF, IL-1) that act by stimulating prostaglandin synthesis in
the vascular and perivascular cells of the hypothalamus.
Major roles of cytokines in acute inflammation.
73
Define cellulitis?
A spreading bacterial infection of the skin affects the dermis and subcutaneous fat, characterized by redness, warmth,
swelling, and pain
What is the difference between abscess and cellulitis?

Abscess Cellulitis
Caused by Staphylococcus aureus Group A Streptococci
Causative organism Organism secretes coagulase enzyme Fibrinolysin
Hyaluronidase
Inflammation Localized Diffuse
Necrosis Central zone of necrosis Extensive necrosis
Pus Rapid formation, thick and yellow Slow formation, thin and contains RBCs
When to give Antibiotic in abscess?

Antibiotics are indicated if the abscess is not localised (e.g. evidence of cellulitis) or the cavity is not left open to drain
freely
What are giant cells?

These are multinucleated cells derived from the fusion of multiple activated macrophages to form granuloma
Most common cause of granuloma formation?

Tuberculosis
Causative agent?
Mycobacterium T.B
Type of stain?
Ziehl–Neelsen stain (Acid fast stain)
What changes you see in lymph node affected with

inflammation?
Reactive follicular hyperplasia
Typical tuberculous granuloma showing an area of central necrosis

surrounded by multiple Langhans-type giant cells, epithelioid cells,
and lymphocytes.
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Osteomyelitis
SCENARIO: Patient with previous tibial fracture fixation 3 years ago and presenting with redness and swelling of knee
Common organisms causing osteomyelitis?

Age group Most common organisms
Newborns (< 4 m) S. aureus, Enterobacter species, and group A and B Streptococcus species
Children (4 m to 4 y) S. aureus, group A Streptococcus species, Kingella kingae, and Enterobacter species
Children, adolescents S. aureus (80%), group A Streptococcus species, H. influenzae, and Enterobacter species
(4 y to adult)
Adult S. aureus and occasionally Enterobacter or Streptococcus species
Sickle Cell Anemia S. aureus is typically most common, but Salmonella species is pathognomonic
Patients
About Osteomyelitis
Osteomyelitis can be classified on the basis of patient age (pediatric or adult), causative organism, pathogenesis
(contiguous spread, traumatic, hematogenous), anatomic location, or duration of symptoms (acute, subacute,
chronic). These variables can be used individually or in combination for categorization. There are also a number of
named classification systems that focus on various clinical aspects of osteomyelitis, but no one system is universally
accepted. The most commonly used classification system for adult osteomyelitis is the Cierny–Mader staging system
Cierny Classification of Osteomyelitis

(describes anatomic involvement, host, treatment, prognosis)
Anatomic Location
Stage I Medullary
Stage 2 Superficial
Stage 3 Localized
Stage 4 Diffuse
Host Type
Type A Normal
Type B Compromised
Type C Treatment is worse to patient than infection
Exogenous: most common osteomyelitis in adults

• Acute osteomyelitis from open fracture or bone exposed at surgery
• Chronic osteomyelitis from neglected wounds: diabetic feet, decubitus ulcers
Hematogenous: most common osteomyelitis in children
• Bloodborne organisms of sepsis (often positive blood cultures before antibiotics given)
• Pediatric—immature immune system
o Metaphysis or epiphysis of long bones
o Lower extremity more often than upper
o Boys more often than girls
• Adults—immunocompromised—vertebrae most common adult hematogenous site
o Dialysis patient—rib and spine osteomyelitis
o IV drug abuser—medial or lateral clavicle osteomyelitis
o Elderly, IV drug abuser, transplant patients
Subacute osteomyelitis: Brodie abscess

Residual of acute osteomyelitis versus hematogenous seeding of growth plate trauma
75
Pathogenesis of osteomyelitis?
1- Invasions and Inflammation
2- Suppuration
3- Necrosis (sequestration)
4- New bone formation
5- Resolution
76
What is abscess? See previous stations (Carcinoid station and Abscess station)
Is a localized painful collection of pus in tissues, organs, or confined spaces usually because of an infection by a pyogenic
organism. It is surrounded by granulation tissue called pyogenic membrane, however it is not a true membrane and is
not itself pyogenic.
What is pus?
Thick, yellowish liquid that is formed as part of an inflammatory response typically associated with an infection and is
composed of exudate chiefly containing dead white blood cells (as neutrophils), tissue debris, and pathogenic
microorganisms (as bacteria)
Pathogenesis of pus formation?

Microbial invasions → acute inflammation with vascular congestion and exudation of fluids with infiltration of PMN cells
Fate of abscess
• Resolution
• Rupture
• Spread - sepsis
• Chronic abscess formation
Definition of sequestrum?
Dead bone that has become separated during the process of necrosis from normal or sound bone. It is a complication
(sequela) of osteomyelitis
Definition of involucrum?
Reactive woven or lamellar bone depositions forming a shell of living tissue around a sequestrum
Or Thick sheath of periosteal new bone surrounding a sequestrum.
Why pus may burst through the bone?

• Due to increased intraosseous pressure due to increased osmolarity which occurs due tissue breakdown
• Due to formation of a large rounded cloacal opening in the involucrum. So, pus will escape through the
involucrum and the surrounding soft tissue to the skin surface within a sinus tract
Why the fixing plate should be removed?

• It has become a septic focus
• Formation of biofilm - less sensitive to antibiotics
• Implant might be loose
SCC developed in the sinus, why?

Due to chronic irritation
In chronic osteomyelitis what is the sequence of events by which the draining sinus can develop SCC
Chronic irritation → hyperplasia → dysplasia → carcinoma
Name of protein deposition in chronic OM?

Amyloid AA
Treatment?
• Antibiotic therapy:
o Blood cultures are taken and high-dose intravenous antibiotics, active against Staphylococcus
aureus, Streptococci and Gram-negative rods such as Escherichia coli are given.
o Cephalosporins, co-amoxiclav or a combination of Flucloxacillin and Gentamicin may be used.
• Supportive treatment for pain and dehydration
• Splintage of the limb
• Surgical drainage: if there is no response to antibiotics for 2 days
77
Differential diagnosis of swollen knee?
• OA and overuse syndrome
• Septic arthritis, infections (gonorrhea, Lyme disease, TB, brucellosis)
• Gout
• Pseudogout (Ca+2 pyrophosphate deposition disease)
• Hemarthrosis
• Tumors
• Trauma (ligamentous injury, fractures, patellar dislocation, meniscus injury, etc.)
• Polyarthritis (RA, Reiter’s syndrome, Juvenile rheumatoid arthritis)
Single bedside test to do?

Aspiration
Tests to be done on the aspirate?

• Urgent gram stain
• Cytology, chemical analysis, crystals
• CS (culture & sensitivity)
Types of crystals in gouty arthritides?

Characteristic Gout Pseudogout
Crystal composition Monosodium urate Calcium pyrophosphate
Crystal shape Needle-shaped Rhomboid-shaped
Birefringent Negative Positive
Most common site 1st MTPJ Knee
Radiography “Rat-bite” erosions White lines of chondrocalcinosis
1st line treatment NSAIDs
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Pathological Fractures
What is pathological fracture? SCENARIO:

Bone fracture which occurs without adequate trauma and is caused by a Young female was cycling
preexistent pathological bone lesion. developed pain in her thigh
soon as she put her foot on the
Causes? ground. X-ray showed fracture
• Neoplastic: malignant tumors shaft femur with hypodense
o Primary (multiple myeloma) shadow
o Metastatic
• Non-neoplastic:
o Osteoporosis
o Osteomyelitis
o Osteomalacia
o Osteogenesis imperfecta
o Paget’s disease
o Bone cyst
o Radiotherapy
Mention 5 possible primary sites for metastasis?

• Breast
• Prostate
BPLTK
• Lung
• Thyroid
• Kidney
What are other sites of ectopic thyroid tissues other than head and neck and thorax?
Ovarian and testicular teratoma
Fixation was done, how to check malignancy?

Bone biopsy
Pathology report: typical bland appearance (follicular cells), what is the probable location primary tumor?
Thyroid gland
We have done FNAC of the thyroid but unable to differentiate cancer, why?
Malignancy is determined by capsular and vascular invasion which need histology rather than a cytology to confirm
What investigations to do to confirm thyroid metastasis?

Radioactive iodine scan
79
Which thyroid cancer will show no response to iodine uptake?
Medullary thyroid cancer as its origin is from parafollicular C cells so it is not of a follicular origin
If a patient is O +ve, what test to do prior to blood transfusion?

• ABO
• RH group cross matching
If the patient is telling you his group, you will still do cross matching and why?
Yes, to determine if the recipient has pre-formed antibodies against any antigens on the donor's cells
Complications of incompatible blood transfusion?

• Acute hemolytic reactions
• Febrile non- hemolytic transfusion reaction
• Delayed hemolytic transfusion reactions
• Transfusion related acute lung injury
Define hemolysis
Rupture (lysis) of RBCs and release of their contents (cytoplasm) in the surrounding fluid (blood, plasma)
80
Polytrauma + Transfusion
Define DIC? SCENARIO:

It is a pathological consumptive coagulopathy due to activation of the coagulation A patient who is known to
and fibrinolytic systems, activation of the latter leads to formation of micro thrombi have hepatitis C → trauma →
in many organs with the consumption of the clotting factors and platelets. blood loss
Characterized by: Splenectomy was done and
• Widespread hemorrhage patient received blood
• Thrombocytopenia, decreased fibrinogen, increased FDPs transfusion
Patient develops DIC
Functions of the platelets?
Platelets contribute to the hemostatic process in two different ways. First, through their adhesive and cohesive functions
that lead to the formation of a hemostatic plug. Second, they can activate coagulation mechanisms
What is the precursor of platelets? How platelets are formed from bone marrow?
From megakaryocytes
Stages of hemostasis
See ASSCC, Ruptured AAA/Hypothermia station
Why this patient has bleeding tendency?

Because of the liver affection
What are very late manifestations of HCV?

• Cirrhosis
• HCC
What activates intrinsic and extrinsic pathways?

• Intrinsic pathway is activated by vessel injury which will lead to activation of factor 12
• Extrinsic pathway is activated by tissue thromboplastin released by the damaged cells
• APTT tests for intrinsic pathway
• PT tests for extrinsic pathway and the common pathway
Hypersensitivity reactions:
The Gell and Coombs classification divides hypersensitivity reactions into 4 types
Type I Type II Type III Type IV
Description Anaphylactic Cytotoxic Immune complex Delayed type
Mediator IgE IgG, IgM IgG, Ig A, IgM T-cells
Antigen Exogenous Cell surface Soluble Tissues
Response time Minutes Hours Hours 2-3 days
Examples Asthma Autoimmune hemolytic anaemia Serum sickness Graft versus host disease
Hay fever Pemphigus SLE Contact dermatitis
Goodpasture's Aspergillosis
Which blood product will you give? Mnemonic for the reactions and the mediators involved ACID EGG-T
Packed RBC's ACID EGG T (mediators)
• Type 1 Anaphylactic • IgE
Percentage of white blood cells in packed • Type 2 Cytotoxic • IgG
RBC's? • Type 3 Immune complex • IgG
<5x10^6 cells/L (Leukoreduced Packed RBC's) • Type 4 Delayed type • T cells
- LPRC
What’s the life span of RBC's?

120 days
What tests to do before blood transfusion:

• ABO
• RH
81
What is GXM: A group and save is the sample processing. It
Group cross matching: to test donor red cells against recipient serum to consists of a blood group and an antibody
detect any potential incompatibility through which antibodies in recipient screen to determine the patient’s group and
cause hemolysis to donor cells whether or not they have atypical red cell
antibodies in their blood. If atypical
Antigen in cross matching? antibodies are present the laboratory will do
additional work to identify them.
ABO
A crossmatch is when the laboratory actually
What are the stages of bone healing? provides red cells products for the patient. It
1. Hematoma formation (mass of clotted blood) at fracture site. is not possible for the laboratory to provide
Tissue in fracture site swells, very painful, obvious inflammation, crossmatched blood without having
and bone cells are dying. processed a group and save sample first.
2. Fibrocartilaginous callus develops over a 3 to 4-week period.
This process involves
• Capillary growth in the hematoma
• Phagocytic cells invading and cleaning-up debris in injury site
• Fibroblasts and osteoblasts migrating into site and beginning reconstruction of bone
Note that the fibrocartilaginous callus serves to splint the fracture.
3. Bony callus begins forming after 3 to 4 weeks after injury and is prominent 2 to 3 months following the injury.
Continued migration and multiplying of osteoblasts and osteocytes result in the fibrocartilaginous callus turning
into a bony callus.
4. Remodeling. Any excess material of the bony callus is removed and compact bone is laid down in order to
reconstruct the shaft. Remodeling is the final stage.
Effects of prolonged immobility on bone?

Loss of bone density and increased risk of osteoporosis
Infected implant, why you should remove?

Septic focus
What the 1st test to do?

Wound swab for culture and sensitivity
What is PVL Staph aureus?

Panton-Valentine leukocidin (PVL) is a cytotoxin produced by Staphylococcus aureus that causes leukocyte destruction
and tissue necrosis.
It is one of the β-pore-forming toxins. The presence of PVL is associated with increased virulence of certain strains
(isolates) of Staphylococcus aureus. It is present in the majority of community-associated Methicillin Resistant
Staphylococcus aureus
What is the effect of this cytotoxin?

PVL creates pores in the membranes of infected cells and is the cause of necrotic lesions involving the skin or
mucosa, including necrotic hemorrhagic pneumonia.
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Hepatitis C (HCV)
Hepatitis C? SCENARIO:
Is inflammation that disrupts hepatocytes and small bile ductules that is caused by virus 55-year-old lady, IVDU with
C via parenteral transmission (e.g., IVDA, unprotected intercourse, needle stick) left lower limb venous ulcer
risk from transfusion is almost nonexistent due to screening of blood
Hepatitis C virus?
Is a single-stranded RNA virus from family flaviviruses
Hepatitis virus causes acute hepatitis, which may progress to chronic hepatitis
• Acute hepatitis presents as jaundice (mixed CB and UCB) with dark urine (due to CB), fever, malaise, nausea, and
elevated liver enzymes (ALT > AST)
• Chronic hepatitis is characterized by symptoms that last > 6 months. With a risk of progression to cirrhosis &
HCC
The leading causes of chronic liver failure
What is the pathological sequence in HCV worldwide include chronic hepatitis B, chronic
1. Acute Hepatitis hepatitis C, nonalcoholic fatty liver disease, and
2. Chronic Hepatitis alcoholic liver disease.
3. Liver cirrhosis & portal hypertension
4. Liver cell failure
5. HCC /Ca
Most common risk factors for HCV infection?

• Intravenous drug abuse
• Multiple sex partners
• Having had surgery within the last 6 months
• Needle stick injury
• Multiple contacts with an HCV-infected
individual
• Employment in the medical or dental field
Cirrhosis
End-stage liver damage characterized by disruption of
the normal hepatic parenchyma by bands of fibrosis
and regenerative nodules of hepatocytes
Clinical features & Pathological sequence?

• Portal hypertension
o Ascites
o Congestive
splenomegaly/hypersplenism
o Portosystemic shunts (esophageal
varices, hemorrhoids, and caput
medusae)
o Hepatorenal syndrome (rapidly
developing renal failure secondary to
cirrhosis)
• Decreased detoxification
o Mental status changes, asterixis, and
eventual coma (due to raised serum
ammonia)
o Gynecomastia, spider angiomas and
palmar erythema due to hyperestrinism
o Jaundice
• Decreased protein synthesis
o Hypoalbuminemia and edema Major clinical consequences of portal hypertension in the setting of
o Coagulopathy due to decreased cirrhosis, shown for the male. In women, oligomenorrhea, amenorrhea,
synthesis of clotting factors. and sterility as a result of hypogonadism are frequent.
• Hepatocellular carcinoma
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The most common cause of cirrhosis in the UK?
Chronic Alcoholism
Alcoholic liver disease. The interrelationships

among hepatic steatosis, alcoholic hepatitis,
and alcoholic cirrhosis are shown, along with
depictions of key morphologic features. It
should be noted that steatosis, alcoholic
hepatitis, and steatofibrosis may also
develop independently. In particular some
patients present initially with cirrhosis
without any of the other forms of alcoholic
liver disease.
The most common cause of death in cirrhosis?

Rupture esophageal varices
Necrosis:
Necrosis is a form of cell death in which cellular
membranes fall apart, and cellular enzymes leak
out and ultimately digest the cell
Divided into several types based on gross features
• Coagulative necrosis: ischemic infarction
of any organ except the brain
• Liquefactive necrosis: Brain infarction,
Abscess, Pancreatitis
• Gangrenous necrosis: dry gangrene, wet
gangrene
• Caseous necrosis: TB
• Fat necrosis: Traumatic in breast,
Enzymatic in Pancreatitis
• Fibrinoid necrosis: Hypertension
See Gangrene + Mesothelioma station
What is the type of necrosis in HCV?

Coagulative
Mechanisms of fibrosis. Persistent tissue injury leads to chronic

inflammation and loss of tissue architecture. Cytokines produced by
macrophages and other leukocytes stimulate the migration and
proliferation of fibroblasts and myofibroblasts and the deposition of
collagen and other extracellular matrix proteins. The net result is
replacement of normal tissue by fibrosis.
84
Types of Candida? Candida albicans is the most
• Oral common disease-causing
• Vaginal fungus. It is a normal
• Cutaneous inhabitant of the oral cavity,
• Invasive gastrointestinal tract, and
Oral candida albicans is the most common type (oral thrush) it can grow as yeast, vagina in many individuals.
pseudohyphae, or true hyphae Systemic candidiasis (with
associated pneumonia) is a
disease restricted to
immunocompromised patients
that has protean
manifestations.
In tissue sections, C. albicans

demonstrates yeastlike forms
(blastoconidia), pseudohyphae,
and true hyphae
Pseudohyphae
Are an important diagnostic
clue and represent budding
yeast cells joined end to end at
constrictions, thus simulating
true fungal hyphae.
The organisms may be visible
with routine H&E stains, but a
variety of special “fungal”
stains (Gomori
The morphology of fungal infections. (A) Candida organism has pseudohyphae and budding
methenamine-silver, periodic
yeasts (silver stain). (B) Invasive aspergillosis (gross appearance) of the lung in a hematopoietic
acid–Schiff) commonly are used
stem cell transplant recipient. (C) Gomori methenamine-silver (GMS) stain shows septate
hyphae with acute-angle branching, consistent with Aspergillus. (D) Cryptococcosis of the lung to better highlight the
in a patient with AIDS. The organisms are somewhat variable in size. pathogens.
85
What are the stages and classification of venous leg ulcers?
CEAP classification
• C0 – No visible or palpable signs of venous disease
• C1 – Telangiectasias or reticular veins
• C2 – Varicose veins
• C3 – Edema
• C4a – Milder skin changes due to venous disorder (pigmentation, eczema)
• C4b – Severe skin changes due to venous disorder (dermatosclerosis, atrophie blanche)
• C5 – Healed ulcers
• C6 – Skin changes with active ulcers
Causes of inguinal lymphadenopathy?

Systemic
• Neoplastic
o Hodgkin’s and non-Hodgkin’s
lymphoma (common)
o Leukemia (uncommon
• Inflammatory
o Tuberculosis (uncommon)
o Sarcoid (uncommon)
Local causes
• Infective
o Non-specific reactive lymphadenopathy
form infection in groin or lower limb
(very common)
• Specific infections
o Cat scratch fever (very rare)
o Lymphogranuloma venereum (very
rare)
• Neoplastic
o Metastatic disease (from primary lesion
I lower limb, external genitalia, perianal
region)
o Malignant melanoma
86
What you will see microscopically in inguinal LN cut section in this patient?
Follicular hyperplasia
Chronic non-specific reactive lymphadenopathy (One of the three patterns depending on the is caused by stimuli that
causative agents) activate B cell follicles,
• Follicular hyperplasia e.g. RA, HIV
Predominantly B-cells response with germinal center hyperplasia which may be
associated with marginal zone hyperplasia. Follicles vary in size and shape (vs Paracortical hyperplasia
lymphoma). caused by stimuli that
o collagen vascular disease trigger T-cell–mediated
o systemic toxoplasmosis immune responses, e.g.
o syphilis EBV
• Paracortical (interfollicular) hyperplasia
Reactive changes within the T-cell region of LN with paracortical expansion caused by Sinus histiocytosis
o viral infection e.g. infectious mononucleosis (EBV) refers to an ↑ in the no.
o certain vaccination (e.g., smallpox) and size of the cells that
o immune reaction induced by certain drugs line lymphatic sinusoids.
• Sinus histiocytosis (reticular hyperplasia) It is nonspecific but may
Distension and prominence of lymphatic sinusoids, due to marked hypertrophy of be prominent in LNs
lining endothelial cells and an infiltrate of macrophages (histocytes). It is often draining cancers
encountered in
o LN draining cancers
o Immune response to tumor or its products
Paracortical hyperplasia, identified by the prominence of

postcapillary venules
Follicular Hyperplasia.
A, Low-power view showing marked differences in size of
germinal centers, their well-circumscribed character, and the fact
that they are surrounded by a well-defined mantle.
B, High-power view showing numerous “tingible body”
macrophages.
Sinus Hyperplasia. The cells present in the sinus represent an

admixture of histiocytes and sinus lining cells.
87
Acute Pancreatitis
See Acute Pancreatitis station, ASSCC SCENARIO:

What is amylase and what is its function? 50-year-old patient
complaining of epigastric pain.
• Group of proteins (digestive enzymes) found in saliva and pancreatic juice
Recent history of
• All are glycoside hydrolases and act on α 1,4-glygoside bond to convert starch
hospitalization for acute
into smaller carbohydrate molecules (oligosaccharides and disaccharides)
pancreatitis 3 weeks ago.
What is CRP and from where it produced?
• C-reactive protein (CRP) is a substance produced by the liver early in response to inflammation (acute phase
reactant)
• It is not very specific, it isn’t unique to one disease
• Can help to monitor disease progress and flares.
What is blood test to do in acute pancreatitis?

• Serum amylase
• Serum lipase (preferred over the amylase due to higher sensitivity)
• LDH
• CRP
• FBC ABG -lactate
What biochemical test to do?

• Electrolytes
• ABG
• Ca+2
• Albumin
The patient having a compression over stomach, what is that?

Pseudocyst
What non-bacterial organism can cause infection in this patient?

• Viruses (e.g. Mumps, Coxsackie B and hepatitis)
• Parasites (e.g. ascaris lumbricoides, fasciola hepatica, and hydatid disease)
• Bacteria (mycoplasma pneumonia and leptospirosis)
Patient’s haemoglobin is dropped, why?

• Rupture of splenic artery (GDA, PDA) pseudoaneurysm
• Haemorrhage
/Spleenic vein thrombosis
What non-surgical option to stop bleeding?
Interventional radiology
How does it work?

Using real-time imaging, the physician guides a catheter
through the artery and then releases clotting agents (coils,
particles, gel, or foam) into the blood vessel slowing the
blood flow and causing an internal injury to activate the
coagulation cascade.
88
Which part of coagulation will be activated?
Intrinsic pathway
What factors involved in intrinsic pathway?

(Factors XII, XI, IX, X)
89
Summary of Definitions
Atherosclerosis: Frozen section:

Pathological process of the vasculature in which an Is a pathological labora1ory procedure to perform rapid
artery wall thickens as a result of accumulation of fatty microscopic analysis of a specimen.
materials such as cholesterol.
Gangrene:
ARDS: A type of necrosis caused by a critically Insufficient
Diffuse alveolar damage and lung capillary endothelial blood supply.
Injury.
Giant cells:
Barret's esophagus: Multinucleated cells derived from the fusion of multiple
Columnar metaplasia of stratified squamous epithelium activated macrophages to form granuloma.
of the esophagus that increase risk of developing
adenocarcinoma. Group. cross matching (GXM):
To test donor red cells against recipient serum to detect
Bence Jones protein: any potential incompatibility through which antibodies
Monoclonal globulin proteins or IG light chain found in in recipient cause hemolysis to donor cells.
the urine, produced by neoplastic plasma cells.
Present in 2/3 of multiple myeloma cases. Hemorrhoids:
Swollen or inflamed anal cushions.
Breslow thickness:
Measured in mm. From the top of stratum granulosum HER-2:
to the deepest point of tumor involvement. Transmembrane epidermal growth factor and it is
overexpressed in 15% of breast cancer cases and
Carcinoma: associated with bad prognosis.
Is a type of cancer that develops from epithelial cells.
High sensitivity test:
Carcinoid tumor: The ability of a test to correctly identify those with the
Slow-growing type of neuroendocrine tumor originating disease (true positive rate).
in the cells of the neuroendocrine system.
High specificity test:
Cellulitis: The ability of the test to correctly identify those without
Spreading bacterial infection of the skin affects the the disease (true negative rate).
dermis and subcutaneous fat, characterized by redness,
warmth, swelling, and pain. Human Leucocyte Antigens:
Proteins located on surface of WBC.
Choriocarcinoma:
Is a highly malignant form of testicular tumor contain 2 Hyperplasia:
cell types, syncytiotrophoblasts & cytotrophoblasts. Increase in the No. of cells in tissue or organ in
response to a stimulus.
Contact tracing:
The Identification and diagnosis of persons who may Immunohistochemistry
have come into contact with an infected person. Method of localizing specific antigens in tissues or cells
based on antigen antibody recognition.
Cryptorchidism:
Complete or partial failure of the intra-abdominal testes Involucrum:
to descend into the scrotal sac and Is associated with Thickened new bone formed by periosteum enclosing
testicular dysfunction and an increased risk of testicular sequestrum which if infection of the bone persist will
cancer. lead to perforation of involucrum and sinus formation
to the skin through it pus will discharge and causing
DIC: establishment of chronic osteomyelitis.
Pathological consumptive coagulopathy characterized
by widespread hemorrhage, Thrombocytopenia, Malignant melanoma:
decreased fibrinogen, increased FDPs due to activation Malignant neoplasm of melanocytes.
of coagulation and fibrinolytic systems that leads to
formation of microthrombi in many organs with the
consumption of the clotting factors and platelets.
Mohs micrographic surgery:
One of surgical options for treatment of basal cell
carcinoma in which serial tangential horizontal sections
90
are taken and examined histologically until all margins
are clear. Pus
Thick, yellowish liquid that is formed as part of an
Metastasis: inflammatory response typically associated with an
Survival and growth of cells at a site distant from their infection and is composed of exudate chiefly containing
primary origin. dead white blood cells (as neutrophils), tissue debris,
and pathogenic microorganisms (as bacteria).
Multiple myeloma:
The most common primary bone tumor in elderly of Sickle cell disease:
plasma cell neoplasm commonly associated with lytic Common hereditary hemoglobinopathy caused by a
bone lesions, hypercalcemia, renal failure & acquired point mutation in 13-globin that promotes
Immune abnormalities. it produces large amounts of polymerization of deoxygenated hemoglobin, that leads
igG 55% or igA 25%. to replacement of glutamate with valine resulting
abnormal hemoglobin (HbS) that responsible for the
Necrosis: disease and causing red cell distortion, hemolytic
Accidental and unregulated form of cell death resulting anemia, microvascular obstruction & ischemic tissue
from damage to cell membranes and loss of ion damage.
homeostasis.
Telomere:
Pathological fracture: Region of repetitive nucleotide sequences at each end
Bone fracture which occurs without adequate trauma of a chromosome, which protects the end of
and is caused by a preexistent pathological bone lesion. chromosome from deterioration or from fusion with
neighboring chromosomes.
Panton Valentine leucocidin (PVL}:
Cytotoxic one of 13-pore-formlng toxins associated with Thrombus:
increased virulence of certain strains of Staphylococcus Solid material formed from the constituents of blood in
aureus. It is present in the majority of community flowing blood.
associated Methicillin resistant Staphylococcus aureus
(MRSA).
91
ASSCC
Burns + ARDS ........................................................................................................................................................................ 2

ARDS .................................................................................................................................................................................. 3
Head Injury / Extradural Hematoma .................................................................................................................................... 6
SDH.................................................................................................................................................................................... 9
Polytrauma ......................................................................................................................................................................... 10
Polytrauma with C-Spine Fracture ..................................................................................................................................... 14
Polytrauma With Pelvic Fracture ....................................................................................................................................... 18
Crush Injury / Compartment Syndrome and Rhabdomyolysis .......................................................................................... 22
Rhabdomyolysis .............................................................................................................................................................. 23
Esophageal Varices and Hematemesis ............................................................................................................................... 24
PUD / Perforated Gastric Ulcer .......................................................................................................................................... 28
Gastric Outlet Obstruction ................................................................................................................................................. 32
Obstructive Jaundice .......................................................................................................................................................... 34
Acute Pancreatitis............................................................................................................................................................... 38
Diverticular Abscess + Septic Shock ................................................................................................................................... 44
Bloody Diarrhea .................................................................................................................................................................. 46
Intestinal Obstruction......................................................................................................................................................... 48
Enterocutaneous Fistula..................................................................................................................................................... 50
Steroids ............................................................................................................................................................................... 52
Addisonian crisis: ............................................................................................................................................................ 53
Calcium Homeostasis ......................................................................................................................................................... 54
Hypothyroidism .................................................................................................................................................................. 58
Diabetes Mellitus ................................................................................................................................................................ 60
Hypotension in Pregnant Lady ........................................................................................................................................... 62
Pain Management .............................................................................................................................................................. 64
Post-Operative Fluid Management .................................................................................................................................... 68
Epidural ............................................................................................................................................................................... 72
Nutrition / Surgical Feeding Options .................................................................................................................................. 74
Pre-Operative Aortic Stenosis ............................................................................................................................................ 78
Atrial Fibrillation + Rupture Viscus ..................................................................................................................................... 80
Ruptured AAA / Hypothermia ............................................................................................................................................ 82
Pneumothorax + CV Line Insertion .................................................................................................................................... 86
Pulmonary Edema (Fluid Overload) ................................................................................................................................... 88
Respiratory Failure / Respiratory Acidosis ......................................................................................................................... 90
Renal Failure with Hyperkalemia ....................................................................................................................................... 92
Transurethral Resection of the Prostate (TURP) Syndrome .............................................................................................. 94
General Questions .............................................................................................................................................................. 98
ASSCC MO’s MRCS B NOTES (Previously called Reda’s Notes) 1

Burns + ARDS
Calculate the surface area of the burn? SCENARIO:
According to Wallace rule of nine's Burn victim. Before entering the station there is a diagram
Or Lund and Browder indicating affected areas, you need to calculate surface area
Management? ATLS
A. Airway:
• Look for signs of airway burns and inhalational injury as it may cause airway edema
• Consider intubation if there is airway edema
B. Breathing and ventilation:
• Ensure that adequate ventilation can be achieved as tracheal or pulmonary burns can impair effective gas
exchange, also full thickness chest burns can impede chest expansion
C. Circulation:
• 2 large bore cannulae and fluid resuscitation (any patient > 15% TBSA, any child > 10%)
Parkland formula
(Crystalloid only e.g. Hartman's solution / Ringers' lactate)
Total fluid requirement in 24 hours =
4ml x total burn surface area (%) x body weight (kg)
• 50% given in first 8 hours
• 50% given in next 16 hours
Resuscitation endpoint: Urine output of 0.5-1.0 ml/kg/hour in adults (increase rate of fluid to achieve this)
Points to note:
• Starting point of resuscitation is time of injury
• Deduct fluids already given
• Urinary catheter, consider CV line
Why not to give colloids in burn?

because of the increased capillary permeability occurring during the first 24 h, colloids will pass to the extravascular
space, exert an oncotic effect, and cause a paradoxical augmentation of the third space (interstitial space).
How do you assess the adequacy of fluid therapy?

A number of clinical parameters may be used
• Clinical measures of the cardiac index
o Peripheral warmth
o Capillary refill time
o Urine output
• Central venous pressure and its response to fluid challenges
• Core temperature, e.g. rectal temperature
• Hematocrit (Hct), which determines the plasma volume and the red cell mass. This is unreliable if there has
been a recent transfusion or hemolysis
What are you afraid of? Complications of burns?

• Burns shock’: hypovolemic shock due to plasma loss following loss of skin cover. Leads to hypotension,
tachycardia, increased systemic vascular resistance and a fall in the cardiac output
• Sepsis
• ARDS
• Renal failure (myoglobinuria)
• Constricting circumferential burns (ischemia in limbs / ventilators problems in chest- require escharotomy.
• Electrolyte disturbances: Hypo or hypernitremia, hyperkaliemia, hypocalcaemia
• Coagulopathy due to disseminated intravascular coagulation and hypothermia
• Hemolysis leading to hemoglobinuria and anaemia
How to tell if he has superficial or deep burn?

• Partial thickness: red/white, blistering, sensate
• Full thickness: white, leathery, desensate
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) ASSCC

ARDS
Definition?
Acute, diffuse, inflammatory form of lung injury (acute respiratory
failure) Characterized by:
1. Hypoxemia
2. Decreased lung compliance
3. Diffuse pulmonary infiltrates on CXR
4. Normal PAWP (< 18 mmHg)
5. PaO2/ FiO2 < 26.6
PaO2/ FiO2: The ratio of partial pressure arterial oxygen and

fraction of inspired oxygen, sometimes called the Carrico index,
is a comparison between the oxygen level in the blood and the
oxygen concentration that is breathed. This helps to determine
the degree of any problems with how the lungs transfer oxygen
to the blood.
Pathophysiology of ARDS?
Two phases are recognized in ALI / ARDS:
• An acute phase, characterized by
1) Widespread destruction of the capillary endothelium, extravasation of protein-rich fluid and interstitial
edema
2) Migration of neutrophils and extensive release of cytokines
3) The alveolar basement membrane is also damaged, and fluid seeps into the airspaces, stiffening the
lungs and causing ventilation/perfusion mismatch.
• A later reparative phase, characterized by
4) Fibroproliferation, and organization of lung tissue.
5) If resolution does not occur, disordered collagen deposition occurs leading to extensive lung scarring.
The normal alveolus (left side) compared with the injured alveolus in the early phase of acute lung injury and acute
respiratory distress syndrome.

Causes / Conditions associated with development of Acute Respiratory Distress Syndrome?
Infection Chemical Injury
• Sepsis* • Heroin or methadone overdose
• Diffuse pulmonary infections* • Acetylsalicylic acid
o Viral, Mycoplasma, and Pneumocystis • Barbiturate overdose
pneumonia; miliary tuberculosis • Paraquat
• Gastric aspiration* Inhaled Irritants
Physical/Injury • Oxygen toxicity
• Mechanical trauma, including head injuries* • Smoke
• Pulmonary contusions • Irritant gases and chemicals
• Near-drowning Cardiopulmonary Bypass
• Fractures with fat embolism Pancreatitis
• Burns Hematologic Conditions
• Ionizing radiation • Transfusion associated lung injury (TRALI)
Hypersensitivity Reactions • Disseminated intravascular coagulation
• Organic solvents Uremia
• Drugs
*More than 50% of cases of ARDS are associate with these 4 conditions
What is Berlin criteria?

The new Berlin definition for ARDS categorizes it as being mild, moderate, or severe:
ARDS Severity PaO2/FiO2* Mortality**
Mild 200 - 300 27%
Moderate 100 - 200 32%
Severe < 100 45%
*on PEEP 5+; **observed in cohort
Management of ARDS? (Ventilation, Steroids, Fluids, Nutrition)

Admit to ITU, give supportive therapy and treat the underlying cause.
• Respiratory support:
o Positive end-expiratory pressure (PEEP) of 5-15 cm H2O to prevent premature alveolar closure.
Although PEEP helps with oxygenation, it does so at the expense of cardiac output.
o Prone positioning: This has been found to significantly improve oxygenation (up to 65%).
• Steroids:
o Low dose steroids are associated with improved mortality and morbidity outcomes
• Sepsis
o Identify organism(s) and treat accordingly. If clinically septic, but no organisms cultured, use empirical
broad-spectrum antibiotics, but avoid nephrotoxic antibiotics.
• Hemodynamic management
o Fluids should be replaced, but with care not to overload. Assessment may be made by measuring blood
pressure and urine output. Finer assessment may be necessary using a Swan Ganz catheter to measure
the pulmonary capillary wedge pressure.
o If there is evidence of circulatory failure despite adequate hydration - such as fall in cardiac or urine
output - then consider low dose dopamine as a renal arterial dilator, and dobutamine for its positive
inotropic action. If there is fluid overload, consider frusemide 40-120 mg per 24 hours IV
• Other supportive care
o Nutritional support - enteral feeding is better than parenteral feeding.
o Venous thromboembolism prevention with low molecular weight heparin.
o Gastric ulcer prevention with prophylactic medications.
What are the long-term sequelae of ARDS?

• Impaired gas exchange with refractor hypoxemia
o V/Q mismatch ventillation/perfusion mismatch
o Physiological shunting
• Decreased lung compliance
o Stiff, poorly or non-aerated regions of lung
• Pulmonary hypertension

Wallace rule of nines

Head Injury / Extradural Hematoma
CT features SCENARIO:
• Biconvex shape, hyperdense RTA → GCS 15 → 2 episodes of vomiting
• Midline shift → amnesic events → GCS 8
• Compression on the ventricles
When to consider CT brain for trauma?

High Risk Criteria
• GCS < 15 at 2h post-injury
• Suspected open or depressed skull fracture
• Any sign of basilar skull fracture
o Hemotympanum
o Raccoon Eyes
o Battle's Sign
o CSF oto-/rhinorrhea
• ≥ 2 episodes of vomiting
• Age ≥ 65
• Any head injury in anticoagulated patient
Medium Risk Criteria

• Retrograde Amnesia to the Event ≥ 30 minutes Conditions where ICP-monitoring is used.
• "Dangerous" Mechanism • Traumatic head injury
o Pedestrian struck by motor vehicle • Intracerebral hemorrhage
o Occupant ejected from motor vehicle • Subarachnoid hemorrhage
o Fall from > 3 feet or > 5 stairs • Hydrocephalus
• Malignant infarction
Normal value of ICP? • Cerebral edema
7 to 15 mmHg (supine) and -10 (standing) • CNS infections
• Hepatic encephalopathy
Ways to measure?
Method Advantages Disadvantages
Intraventricular catheter • ‘Gold standard’ • Most invasive method
• Allows drainage of CSF to lower ICP • High infection rate
• Re-zeroing (calibration) possible • May be difficult to insert
• Simultaneous CSF drainage and ICP
monitoring not possible
Intraparenchymal probe • Low infection rate • Measures local pressure
• Drift of zero over time
Subarachnoid probe • Low infection rate • Limited accuracy
• No brain penetration • High failure rate
• Periodic flushing necessary
Epidural probe • Low infection rate • Limited accuracy
• Easy to insert • Relatively delicate
• No penetration of dura
Lumbar CSF pressure • Extracranial procedure • Inaccurate reflection of ICP
• May be dangerous when brain edema is
present
Tympanic membrane • Non-invasive • Insufficient precision
displacement
Transcranial Doppler • Non-invasive • Limited precision
What is the danger of lumbar puncture in increased ICP?

Herniation and coning

What is the Cushing reflex?
Physiologic nervous system response (mixed vagal and sympathetic stimulation) to an elevated ICP that results in
Cushing’s triad. It leads to hypertension, which ensures an adequate CPP. There is also a resultant bradycardia.
cpp-cerebral perfusion pressure
Pathophysiology of increased ICP?
(Monro - Kellie doctrine / hypothesis)
• The skull is fixed box containing 3 components
o Brain (80%), blood (10%), CSF (10%)
• ICP/volume relationship is governed by these 3 components
• Increase in volume in one component may result in compensatory decrease in the volume of another
component in order to prevent rise in ICP (compensation)
• However, once the ICP has reached around 25 mmHg, small increases in brain volume can lead to marked
elevations in ICP; this is due to failure of intracranial compliance (decompensation) leading to brain herniation
Lucid interval?
A temporary improvement in a patient condition after traumatic brain injury after which the condition deteriorates with
rapid decline of consciousness
During this period, blood accumulates in the extradural space leading to an increase in ICP leading to
cerebral edema
CPP = Mean arterial pressure - Intra cranial pressure

𝟏
MAP = Diastolic + (Systolic - Diastolic pressure)
𝟑
MAP auto-regulation range is between 50 - 150 mmHg to maintain a constant cerebral blood flow in cases of traumatic
brain injury, this will be disruption of MAP autoregulation →cerebral ischemia

Clinical picture of increased ICP?
• Headache
• Nausea, vomiting
• Papilledema
• Fall in GCS
o Pressure symptoms (hematoma)
o Ischemia (loss of autoregulation of MAP)
• Dilated pupil (oculomotor nerve palsy)
• Defect in lateral gaze (abducent nerve palsy)
• Cushing's triad (not to be confused with Cushing
reflex)
o Increased systolic blood pressure &
widened pulse pressure
o Bradycardia
o Irregular respiratory pattern
Management?
• ABC
Diagrammatic summary of the factors affecting overall cerebral
• Intubation blood flow.
Indications for intubation?

• GCS ≤ 8
• Risk of raised ICP due to agitation (i.e. sedation required)
• Inability to control/protect the airway or loss of protective laryngeal reflexes. A fall of 2 or more points in the
motor component of the GCS
• In order to optimize oxygenation and ventilation
• Seizures
• Bleeding into mouth/airway
• Bilateral fractured mandible, severe facial injuries
Management of raised ICP?

Improving venous drainage from the brain
• Elevation of the head of the bed to 30
• Good neck alignment – head in the neutral position
• Ensuring ties holding the endotracheal tube in place do not compress the neck veins. Alternatively tape the tube
using ‘trouser-legs’.
• Where possible immobilize the patient’s cervical spine with sandbags and tape rather than restrictive neck
collars
Reducing cerebral edema
• Use mannitol (an osmotic diuretic) 0.5-1g/kg (= 5-10ml/kg of 10% or 2.5-5ml/kg of 20% mannitol). Some unit
use small aliquots of hypertonic saline as an alternative
• Use frusemide (a loop diuretic) 0.5-1mg/kg
• Maintain serum Na+ in the range 140-145mmol/l
Reduction of the cerebral metabolic rate for oxygen:
• Close temperature regulation. Avoid hyperthermia, but do not actively induce hypothermia.
• Use of sedation and anaesthetic drugs. Ensure that the patient is appropriately sedated and has received
adequate analgesia.
• If the patient has a witnessed seizure loading with an anticonvulsant, usually phenytoin 18mg/kg, should be
considered.
• In cases of intractable raised ICP, a thiopentone infusion can be used to reduce the cerebral metabolic rate to a
basal level. This is identified on EEG monitoring as ‘burst suppression’.
Reducing intracranial blood volume
• Hyperventilation can be used to reduce the PaCO2 as a temporary measure, but cerebral ischemia may result if
this is prolonged.
• The final resort if ICP remains raised is to perform a decompressive craniectomy.
Reducing CSF volume
In a neurosurgical centre, use of an external ventricular drain (EVD) allows drainage of CSF to relieve raised ICP

SDH
CT brain, what does it show?
SCENARIO:
Lens / crescent shape hyperdense lesion. Right subdural hemorrhage
80-year-old woman who fell down
(SDH). In A&E eyes open to pain,
What does loss of grey-white matter suggest?
makes incomprehensible sounds, and
Many studies have shown that injury to gray matter, areas of the brain that withdraws to painful stimulus.
contains nerve cell bodies, can cause long-lasting cognitive disability.
What is “GCS”, and what is her GCS?

Glasgow Coma Scale is a neurological scale which aims to give a reliable and objective way of recording the conscious
state of a person for initial as well as subsequent assessment. Her GCS: 2+2+4=8
• Spontaneous
Eye • To speech
opening • To pain
• None
• Orientated
• Confused
Verbal
• Words
response
• Sounds
• None
• Obeys commands
• Localizes to pain
• Withdraws from pain
Motor
• Abnormal flexion to pain (decorticate
response
posture)
• Extending to pain
• None
Management of Acute SDH?

Urgent surgical evacuation of hematoma for
• Acute SDH, +/- coma, with neurologic deterioration (signs of increased intracranial pressure) since time of injury
with potential for recovery
• Clot thickness 10mm or midline shift > 5mm on initial brain CT regardless of GCS
Nonsurgical managed patients should be nursed in ICU with ICP monitoring and serial head CT scans. Next scan at 6-8h.
If there are signs of neurologic deterioration or persistently increased ICP (> 20mmHg), urgent surgical evacuation within
2-4h of deterioration
Tracheostomy tube advantage?

• Easier cleaning of the mouth and face
• Less likely to aspirate
• Less dead space
• Better tolerated on the long term (more comfort, no gagging, doesn’t need sedation)
• May help weaning from the ventilator
• May allow swallowing and the ability to eat and drink

Polytrauma
Management of airway and breathing according to ATLS protocol SCENARIO:
(primary survey) RTA
A. Airway and cervical spine control:

Assessment:
• Speaking to the patient if can speak → secure airway
• If cannot speak:
o (look): in the mouth for FB or in the face for maxillofacial injuries
o (feel): the breath on your cheek
o (listen): to abnormal breath sounds stridor or hoarseness
Management:
• Chin lift or jaw thrust
• Remove any FB in the mouth
• Oro/nasopharyngeal airway
• Cricothyroidotomy
• Tracheostomy
• Endotracheal intubation
• Immobilize the cervical spine by hard collar or sandbag or tape
B. Breathing:
Assessment:
• Inspection:
o Any obvious chest injuries
o Open wounds, flail segment
o Count R.R
o Symmetrical chest wall movement
• Palpation:
o Central trachea
o Surgical emphysema
• Percussion and auscultation:
o For obvious hemo or pneumothorax
Management:
• High flow O2 via non-rebreather mask
• Needle thoracostomy or chest tube
• Occlusive dressing for open pneumothorax
Comment on this CXR?

Pneumothorax + rib fracture + surgical emphysema
How will you manage this?

Urgent needle thoracostomy in the 4th or 5th
intercostal space anterior to the midaxillary
line*, then chest tube insertion
*
ATLS 10th Edition

C. Now, patient is shocked, how will you manage the circulation?
Assessment:
• Pulse rate and character
• Blood pressure
• Class of hemorrhagic shock
Parameter Class I Class II Class III Class IV
Blood loss ml <750ml 750-1500ml 1500-2000ml >2000ml
Blood loss % <15% 15-30% 30-40% >40%
Pulse rate <100 >100 >120 >140
Blood pressure Normal Normal Decreased Decreased
Respiratory rate 14-20 20-30 30-40 >35
Urine output >30ml 20-30ml 5-15ml <5ml
Symptoms Normal Anxious Confused Lethargic
Base deficit 0 to -2 mEq/L -2 to -6 mEq/L -6 to -10 mEq/L -10 mEg/L or less
Need for blood Monitor Possible Yes Massive Transfusion
products protocol
Management:
• Stop any obvious source of bleeding
• Gain venous access by 2 large bore
cannulae
• Take blood for FBC, glucose, U&E
• Cross match for 4 units of blood
• Commence IV fluid resuscitation
with 1L of crystalloids
• Consider blood transfusion if no
response to fluids
How will you monitor the response?

• Heart rate
• Blood pressure
• Capillary refill time
• Urine output
• Mental status
Comment on this CT?

There is a liver tear
Management of liver tear?

Conservative:
• Blood transfusion, monitoring of the hemodynamic status of the patient
Surgical
• Damage control: perihepatic packing
• Repair
• Resection
Was CT a good investigation of this patient?

No, patient is hemodynamically unstable, FAST was the investigation of choice
The four classic areas that are examined for free fluid are the perihepatic space (also called Morison's pouch or the
hepatorenal recess), perisplenic space, pericardium, and the pelvis.

Grades of liver tear?
AAST (American Association for the Surgery of Trauma) liver injury scale
Grade I • hematoma: subcapsular, <10% surface area
• laceration: capsular tear, <1 cm parenchymal depth
Grade II • hematoma: subcapsular, 10-50% surface area
• hematoma: intraparenchymal <10 cm diameter
• laceration: capsular tear 1-3 cm parenchymal depth, <10 cm length
Grade III • hematoma: subcapsular, >50% surface area of ruptured subcapsular or parenchymal hematoma
• hematoma: intraparenchymal >10 cm or expanding
• laceration: capsular tear >3 cm parenchymal depth
Grade IV • laceration: parenchymal disruption involving 25-75% hepatic lobe or involves 1-3 Couinaud segments
Grade V • laceration: parenchymal disruption involving >75% of hepatic lobe or involves >3 Couinaud segments
(within one lobe)
• vascular: juxtahepatic venous injuries (retrohepatic vena cava / central major hepatic veins)
Grade VI • vascular: hepatic avulsion
World Society of Emergency Surgery (WSES) has presented the following classifications utilizing the AAST grading system
Grade I (minor hepatic injury): AAST grade I-II hemodynamically stable either blunt or penetrating lesions.
Grade II (moderate hepatic injury): AAST grade III hemodynamically stable either blunt or penetrating lesions.
Grade III (severe hepatic injury): AAST grade IV-VI hemodynamically stable either blunt or penetrating lesions.
Grade IV (severe hepatic injury): AAST grade I-VI hemodynamically unstable either blunt or penetrating lesions.

Polytrauma with C-Spine Fracture
SCENARIO:
Management?
26-year-old male cyclist, involved in RTA
According to ATLS protocol (as before)
with spine and chest trauma and
hemorrhagic shock secondary to
A - Airway and cervical spine control:
hemothorax
Assessment is based on the principle of: Look, Listen and Feel.
• Look for
o Presence of accessory muscles of respiration (neck, shoulders, chest and abdomen) being used
o Presence of obvious foreign bodies in the airway
o Facial/airway injury and the ‘see-saw’ pattern of complete airway obstruction (NB. central cyanosis
is a late sign)
• Listen
o For the presence of inspiratory stridor, as this indicates upper airway obstruction (laryngeal level
and above).
o Also take note of grunting, gurgling (liquid or semi-solid foreign matter in the upper airways) and
snoring sounds (indicating the pharynx is partially occluded by the tongue or palate).
o Expiratory wheeze suggests lower airways obstruction. Crowing indicates laryngeal spasm
• Feel
o Chest wall movements and airflow at the nose and mouth (for 10 seconds)
• Cervical spine control:
o Semirigid neck collar, sandbag and tape (triple immobilization) plus spinal board immobilization
Management of airway:
• Simple measures:
o Basic airway maneuvers: these include chin lift and jaw thrust, which open up the airway and
permit the use of rigid suction devices (Yankauer sucker) to clear secretions and forceps (Magill) to
remove solid debris
o Basic airway adjuncts: these include nasopharyngeal and oropharyngeal airways. If a patient
tolerates an oropharyngeal, then it is prudent to request an anesthetic review as the airway is at
risk of imminent collapse
• Complex measures:
o Endotracheal intubation: this requires anesthetic expertise and can be achieved through the
mouth (orotracheal) or the nose (nasotracheal) intubation
o Surgical airway: this requires a cut down through tissues (cricothyroidotomy, tracheostomy)
B - Breathing and ventilation:

Assessment:
• Look: (evidence of respiratory distress)
o Tachypnea
o Use of accessory muscles of respiration
o Abnormal/asymmetrical chest wall movement
o Cyanosis (late finding)
• Listen: (signs of partial airway obstruction or compromise)
o Asymmetrical or absent breath sounds
o Additional sounds (e.g., sounds indicative of hemothorax)
• Feel: (air or fluid)
o Hyperresonance to percussion
o Dullness to percussion
o Crepitations
Management:
• Maintain a patient’s oxygenation, oxygenated inspired air is best provided via a tight-fitting oxygen
reservoir face mask with a flow rate of greater than 10 L/min. Other methods (e.g., nasal catheter, nasal
cannula, and non-rebreathing mask) can improve inspired oxygen concentration.
• Tube thoracostomy in pneumothorax
• Needle or finger decompression followed by tube thoracostomy in tension pneumothorax
• 3-way occlusive dressing followed by tube thoracostomy in open pneumothorax

After inserting a chest tube, air column is not moving, why?
• Improper placement (not inside pleural cavity)
• Blockage (tissue or blood clots)
C - Circulation:
Assessment:
• Level of Consciousness: When circulating blood volume is reduced, cerebral perfusion may be critically
impaired, resulting in an altered level of consciousness.
• Skin Perfusion: This sign can be helpful in evaluating injured hypovolemic patients. A patient with pink skin,
especially in the face and extremities, rarely has critical hypovolemia after injury. Conversely, a patient with
hypovolemia may have ashen, gray facial skin and pale extremities.
• Pulse: A rapid, thready pulse is typically a sign of hypovolemia. Assess a central pulse (e.g., femoral or
carotid artery) bilaterally for quality, rate, and regularity. Absent central pulses that cannot be attributed to
local factors signify the need for immediate resuscitative action.
Management:
• Definitive bleeding control: any source of external bleeding has to be controlled
• Appropriate replacement of intravascular volume:
o Vascular access must be established; typically, two large-bore peripheral venous catheters are
placed to administer fluid, blood, and plasma
o Blood samples for baseline hematologic studies are obtained including blood gases and/or lactate
level are obtained to assess the degree of shock
o Initiate IV fluid therapy with crystalloids: bolus of 1 L of an isotonic solution may be required to
achieve an appropriate response in an adult patient. If a patient is unresponsive to initial
crystalloid therapy, he or she should receive a blood transfusion.
• Insert urinary catheter to measure UOP and monitor fluid response
• Monitor the patient response to fluid therapy by the clinical parameters of blood pressure, pulse rate and
urine output
Classes of hemorrhagic shock?

(see before)
Define shock: (see Septic Shock station)

A state of cellular and tissue hypoxia due to reduced oxygen delivery and/or increased oxygen consumption or
inadequate oxygen utilization.
Types of shock / classify shock?

• Distributive
o Septic shock
o Systemic inflammatory response syndrome (SIRS)
o Neurogenic shock
o Anaphylactic shock
o Drug and toxin-induced shock
o Endocrine shock
• Cardiogenic
o Cardiomyopathic
o Arrhythmic
o Mechanical
• Hypovolemic
o Hemorrhagic
o Non-hemorrhagic
• Obstructive
o Pulmonary vascular
o Mechanical
• Combined

Difference between spinal shock and neurogenic shock?
Spinal shock Neurogenic shock
Definition Immediate temporary loss of total power, Sudden loss of the sympathetic
sensation and reflexes below the level of injury nervous system signals
BP Hypotension
Pulse Bradycardia
Bulbocavernos reflex Absent Variable
Motor Flaccid paralysis Variable
Time 48 – 72 hours immediate after SCI
Mechanism Peripheral neurons become temporarily Disruption of autonomic pathways →
unresponsive to brain stimuli loss of sympathetic tone and
vasodilation
Agents given in neurogenic shock?

Phenylephrine hydrochloride, dopamine, or norepinephrine (Vasopressors)
D - Disability
• As soon as the patient’s cardiopulmonary status is managed, perform a rapid, focused neurological examination.
This consists primarily of determining the patient’s…
o GCS score
o Pupillary light response
o Focal neurological deficit.
E - Exposure
• Logroll maneuver is performed to evaluate the patient’s spine
and any posterior chest injuries
One person is assigned to restrict motion of the head and
neck. Other individuals positioned on the same side of the
patient’s torso manually prevent segmental rotation, flexion,
extension, lateral bending, or sagging of the chest or
abdomen while transferring the patient. Another person is
responsible for moving the patient’s legs, and a fourth person
removes the spine board and examines the back.
Identify the problem in CT scan?

C3 cervical spine fracture with possible cord compression
Spinal cord syndromes?

• Central cord syndrome:
o Characterized by a disproportionately greater loss of motor strength in the upper extremities than in
the lower extremities, with varying degrees of sensory loss.
o Occurs after a hyperextension injury in a patient with preexisting cervical canal stenosis.
o The prognosis for recovery in central cord injuries is somewhat better than with other incomplete
injuries.
• Anterior cord syndrome:
o Characterized by paraplegia and a bilateral loss of pain and temperature sensation. However, sensation
from the intact dorsal column (i.e., position, vibration, and deep pressure sense) is preserved
o Results from injury to the motor and sensory pathways in the anterior part of the cord mostly after
cord ischemia
o This syndrome has the poorest prognosis in recovery of the incomplete injuries
• Brown Sequard syndrome:
o Ipsilateral motor loss (corticospinal tract) and loss of position sense (dorsal column), associated with
contralateral loss of pain and temperature sensation beginning one to two levels below the level of
injury (spinothalamic tract)
o Results from hemi-section of the cord, usually due to a penetrating trauma
o Some recovery can be achieved

Four-Person Logroll. At least four people are needed for logrolling a patient to remove a spine board and/or examine the back.
A. One person stands at the patient’s head to control the head and c-spine, and two are along the patient’s sides to control the body
and extremities. B. As the patient is rolled, three people maintain alignment of the spine while C. the fourth person removes the board
and examines the back. D. Once the board is removed, three people return the patient to the supine position while maintaining
alignment of the spine.
Clinical Assessment of Spinal Cord Tracts

Tract Location in Spinal Cord Function Method of Testing
Corticospinal In the anterior and lateral Controls motor power on the By voluntary muscle
tract segments of the cord same side of the body contractions or involuntary
response to painful stimuli
Spinothalamic In the anterolateral aspect of Transmits pain and By pinprick
tract the cord temperature sensation from
the opposite side of the body
Dorsal In the posteromedial aspect of Carries position sense By position sense in the toes
columns the cord (proprioception), vibration and fingers or vibration sense
sense, and some light-touch using a tuning fork
sensation from the same side of
the body

Polytrauma With Pelvic Fracture
What other injuries would you suspect and how will you manage the
SCENARIO:
condition?
A 28-year-old motor-cyclist has
• Rupture bladder / urethra fractured his femur and tibia treated
• Renal injury along with ecchymosis in the flanks,
• Vascular injury tenderness and pain in the lower
Since the patient has an RTA, I will follow the ATLS protocol with ABCDE abdomen with blood at the urethral
approach. meatus. The patient is pale,
hypotensive and tachycardic.
What is the first thing you will do?
I will clear his airway and immobilize C-spine.
Breathing is fine, what will you do in circulation?

• Assess / check
o Pulse rate and character
o Blood pressure
o Capillary refill time
o Pallor and peripheral temperature
• ECG: this may initially just be rhythm lead
• Gain IV access with 2 large bore cannulae into the antecubital fossae, taking blood for FBC, U&Es, LFTs, glucose,
ABG’s, lactate, coag and X-match for at least 4 units of bloods.
• Start fluid resuscitation with 1L of warmed crystalloid and move on to looking for any obvious source of bleeding
in the chest, abdomen, pelvis, long bones or floor (the 5 areas discussed in ATLS) and order FAST.
• If there was any question of a pelvic injury I would put on a pelvic binder and it would be appropriate to ask for
a trauma series of c-spine, chest and pelvic XR at this stage, as long as they don’t get in the way of resuscitation.
Describe the finding of the X-ray Pelvis?

This X-ray shows a pelvic fracture with an increased pubic diastasis distance along with a sacroiliac joint disruption.
What are the types of pelvic fracture?

The four patterns of force leading to pelvic fractures include
• AP compression
• Lateral compression
• Vertical shear
• Complex (combination) pattern.
Given that the patient has hypovolemic shock what % blood loss would you expect?
Due to his pelvic, femur and tibia fractures Grade 4 shock i.e. >40% as they have decreased BP but they have a pulse
>140 beats per minute.
How would you manage the hypovolemic shock?

Crystalloid and blood urgently, with urgent control of the bleeding e.g. pelvic binder/external fixation for pelvic injuries,
stabilization of long bone fractures, laparotomy to control intraabdominal bleeding (if suspected)
How will you monitor the response?

Heart rate, Blood pressure, Capillary refill time, Urine output, mental status
What does blood on the urethral meatus signify?

Urethral trauma (membranous urethra)
What other urinary organ is most commonly injured in a pelvic fracture?

Urinary bladder
How will you confirm the diagnosis?

• Anterograde cystourethrogram.
• Retrograde urethrogram.

What are the contraindications to Foley’s
catheterization?
• Pelvic fracture.
• Blood on the meatus (Urethral trauma)
• Perineal hematoma.
• Bleeding tendency.
• Pre-existing infection around the glans
or the meatus.
• High riding prostate on DRE.
• Meatal stenosis.
How will you manage and who will you involve?

Urologist for suprapubic catheterization.
What other types of urinary catheters do you

know?
• Condom catheter.
• Straight catheter.
• Coudé tip catheter.
• Silicon catheter.
• 3-way catheter for continuous bladder
irrigation.
• Suprapubic catheter.
• Nélaton’s catheter for irrigation of clots.
Advantages and disadvantages of whole-body CT

Advantages
• Polytrauma patients
o Early diagnosis
o Improves survival rates
• Rule out or determine extent of/location
of disease, trauma or other medical
condition
Disadvantages
• High radiation exposure
• Not cost effective
Cause of narrow pulse pressure?

Pulse pressure = Systolic - Diastolic
In hypovolemia, decrease in circulating blood
volume will increase SVR to maintain BP
(COP×SVR). Increase in vasomotor tone will raise
diastolic pressure.
So Systolic is decreased due to volume loss and
diastolic is increased due to high SVR
Net result... narrow pulse pressure
Pelvic ring injuries - Young and Burgess (based on injury mechanism)

How will you manage pelvic fracture? (see BOAST 3 guidelines) (https://www.boa.ac.uk/standards-guidance/boasts.html)
• When there is a suspected active bleeding from a pelvic fracture, apply a pelvic binder in the correct position.
This should be applied pre-hospital if possible
• IV Tranexamic Acid as soon as possible
• Suspected pelvic fractures from high-energy trauma should have a CT scan with IV contrast including head,
chest, abdomen and pelvis on admission. This should include a head to toe scanogram.
• Active bleeding from the pelvis in patients who do not respond to resuscitation can be managed by surgical
packing of the pelvis or interventional radiology with selective embolization of active arterial bleeding vessels.
• External fixation should be considered for temporary mechanical stabilization when early definitive surgery
cannot be performed.
• In displaced vertical shear fractures, traction should be considered when early definitive surgery cannot be
performed
• Potential injury to the bladder or urethra should be suspected, diagnosed and managed according to The
Management of Urological Trauma Associated with Pelvic Fractures BOAST.
• Open pelvic fractures associated with wounds to the lower abdomen, groin, buttocks, perineum, anus (including
sphincters) and rectum require urgent assessment by a consultant general or colorectal surgeon and wound
debridement as per the Open Fractures BOAST.
• Reconstruction of the pelvic ring should occur within 72 hours of the stabilization of the patient’s physiological
state if associated injuries allow.
Pelvic Fractures and Hemorrhagic Shock Management Algorithm


Crush Injury / Compartment Syndrome and Rhabdomyolysis
What are the complications?
SCENARIO:
• Compartment syndrome
28yo male, leg crushed for a few hours,
• Rhabdomyolysis left unobserved on orthopedic ward
Bloods: AKI
Clinical picture of compartment syndrome? /Disproportionate Urine dipstick: blood
• Worsening pain: this may be out of proportion to the injury
• Paresthesia: especially loss of two-point tactile discrimination
• Clinical signs:
o Tense and swollen compartments
o Sensory loss
o Pain on passive stretching
• Loss of regional pulses, which is a late sign
How to diagnose compartment syndrome in a patient with altered sensorium or sensorimotor deficit?
This can be achieved by:
• Measurement of intercompartmental pressure, tissue pressures of greater than 30 mmHg suggest decreased
capillary blood flow, which can result in muscle and nerve damage from anoxia
• Blood pressure: The lower the systemic pressure, the lower the compartment pressure that causes a
compartment syndrome.
Normal compartment pressure?

(0-15 mmHg). If > 30 = indication of fasciotomy
Treatment?
Emergency fasciotomy
e.g. In lower leg (4 compartment fasciotomies through 2 incisions as an emergency procedure)
Cross-section of lower leg showing compartments, neurovascular structures and approaches for fasciotomy
What will you say to patient when you consent for fasciotomies?
Explain operation, complications (permanent nerve damage, permanent muscle damage, permanent scarring, loss of
affected limb, infection, kidney failure, and in rare cases death can occur).
Acute renal failure: (why)?

• Nephrotic effect of myoglobulin precipitating in renal tubules
• Decrease extracellular volume → vasoconstriction
• Renal tubular ischemia and necrosis
• Myoglobulin, uric acid → obstructive cast formation

Myoglobin?
O2 binding protein found in muscles
Rhabdomyolysis
Definition
The release of potentially toxic muscle cell components into the systemic circulation
Causes?
• Blunt trauma to skeletal muscle, e.g. crush injury
• Massive burns
• Hypothermia or hyperthermia
• Ischemic reperfusion injury, e.g. clamp on an artery during surgery
• Prolonged immobilization on a hard surface
• Strenuous and prolonged spontaneous exercise, e.g. marathon running
• Drugs, e.g. statins, fibrates, alcohol
Labs of rhabdomyolysis?
• Increased creatine kinase (CK) > 5 times the normal
• Increased lactate, LDH, creatinine
• Electrolyte disturbances:
o Hyperkaliemia (and metabolic acidosis with an ↑ anion gap)
o Hypocalcemia
o Hyperphosphatasemia
o Hyperuricemia
• Myoglobinuria suggested by positive dipstick to blood in the absence of hemoglobinuria (red cells on
microscopy)
Management?
• ABC
• Fluid resuscitation: ensure good hydration to support urine output >300 ml/h using IV crystalloid until
myoglobinuria has ceased.
• Diuretics, e.g. mannitol, may also be used
• Alkalinization of urine: NaHCO3 to prevent renal damage
• Treat electrolyte disturbances (hyperkalemia)
• Monitor ECG, electrolytes, UOP, CK (6-12h), LDH, urine myoglobulin, compartment pressure.

Esophageal Varices and Hematemesis
What are your concerns regarding this patient? SCENARIO:
• On-going bleeding resulting in hypovolemia, as patient has cirrhosis and 45-year-old man admitted to SAU
clotting abnormalities with history of hematemesis.
• Likelihood of complications such as O/E Jaundice and ascites
o Hepatic encephalopathy PMH: ETOH abuse
o AKI After a 2nd episode of
o Hepatorenal syndrome hematemesis he becomes
confused. ↓BP, ↑ HR (shock)
Differentials? Lab results are available.
• Bleeding esophageal varices due to portal HTN caused by cirrhotic liver
• Mallory-Weiss tear
• Boerhaave’s syndrome
• Bleeding peptic ulcer
How will you manage this patient?

• Active resuscitation, reduction of portal venous pressure and measures to avoid hepatic encephalopathy
o High flow oxygen
o Venous access
o Immediate cross matching, 2-4 units of blood after discussing with hematologists
o Fresh blood transfusion, FFP, Platelets
o Close monitoring (Pulse Blood Pressure Hourly urine output Central venous pressure)
• Assessment of coagulation status:
o Prothrombin time
o Platelet count
• Control of bleeding:
o Tamponade (Minnesota tube) if bleeding uncontrolled
o Pharmacological measures (e.g. vasopressin / octreotide)
o Urgent endoscopy: Endoscopic banding or injection sclerotherapy
Endoscopic band ligation: not more than 6 bands per session
Cause of thrombocytopenia in this case?

• Hypersplenism
• DIC
• Hemodilution
• Chronic low platelet production
What are the indications for platelet transfusion?

Ongoing coagulopathy with continued bleeding

Blood findings in alcoholic patients? Features of FBC to suggest ETOH abuse?
• Low platelets due to toxic effect on bone marrow, impaired hematopoiesis (also affecting RBCs and WBCs)
• Raised mean corpuscular volume (MCV), anemia (megaloblastic and hemolytic)
• Elevated liver enzymes (serum GGT, AST, ALT and ferritin)
Sites of portosystemic anastomosis:
Which varices are usually bleeding?

Varices in the submucosa of the lower esophagus are the common source of major bleeding
Pathogenesis of portal HTN in chronic alcoholism:

• Cirrhosis resulting from chronic liver disease and is characterized by liver cell damage, fibrosis and nodular
regeneration. The fibrosis obstructs portal venous return and portal hypertension develops.
• Arteriovenous shunts within the liver also contribute to the hypertension.
Surgical treatment options / Therapeutic maneuvers to reduce portal venous pressure apart from drugs?
• Portosystemic shunts (splenorenal shunts - TIPSS: a metal stent is inserted via the transjugular route using a
guidewire passed through the hepatic vein to the intrahepatic branches of the portal vein.)
• Stapled esophageal transection: The gastric vein and short gastric veins are ligated, and the distal esophagus is
transected and re-anastomose just above the cardia using a stapling gun
• Orthotopic liver transplantation (OLT) - Treatment of choice in patients with advanced liver disease

How alcohol causes cirrhosis?
• Changes in lipid metabolism
• Decreased export of lipoproteins
• Cell injury caused by reactive oxygen species and cytokines
What are the hepatic changes as a consequence of excessive alcohol consumption?

• Fatty change
• Alcoholic hepatitis with liver cell damage
• Cirrhosis
• Hepatocellular carcinoma
How is alcohol metabolized by the liver?

• Microsomal ethanol oxidizing system (MEOS) enzymes
• Alcohol dehydrogenase
• Catalase reaction
All of these reactions metabolize ethyl alcohol to acetic acid
Mechanism of ascites?
• Increased formation of hepatic and splanchnic lymph
• Hypoalbuminemia
• Retention of salt and water due to increased aldosterone and antidiuretic hormone levels
Cause of confusion in this patient

Hepatic encephalopathy
Patient with macrocytic anemia, what could be the cause?

Nutrition deficiency (vitamin B12 deficiency) with chronic alcoholism
How vitamin B12 deficiency causes macrocytic anemia?

Vitamin B12 is important in DNA synthesis. When DNA synthesis is impaired, the cell cycle cannot progress from the G2
growth stage to the mitosis (M) stage. This leads to continuing cell growth without division, which presents as
macrocytosis
If the patient is to go for liver transplant, what will you tell his family?
• Counseling regarding patient condition, proposed treatment options, outcome of treatment,
• Lifestyle modifications, abstinence from alcohol 6 months later
• ABO matching
• Immunosuppression

Sengstaken Blakemore tube?
Double balloon tamponade
Ports?
• Port for gastric ballon
• Port for esophageal ballon
• Port for gastric suction
Modification:
Esophageal suction port to help suction of esophageal
contents (Minnesota tube)
Sengstaken-Blakemore tube (3 lumen) replaced by Minnesota
tube (4 lumen) as allows aspiration of both gastric and
esophageal contents, not just gastric contents
If there is no modification?
Insert NG tube Minnesota tube
Indications for Sengstaken tube placement?

Acute life-threatening bleeding from esophageal or gastric varices…
• that does not respond to medical therapy (including endoscopic hemostasis and vasoconstrictor therapy)
• when endoscopic hemostasis and vasoconstrictor therapy are unavailable
Technique? (see video)

• Position the patient and elevate the head of the bed to 45
• Anesthetize the posterior pharynx and nostrils with topical anesthetic
• Coat the balloons with lubricating jelly
• Pass the tube from the nostrils to at least 50 cm mark
• Suction from the gastric and esophageal ports
• When the gastric ballon is correctly positioned in the stomach, inflate the ballon with 500 ml of air and clamp,
the port, pull the tube back until resistance is felt against diaphragm
• Inflate the esophageal ballon by the sphygmomanometer to 30-45 mmHg and clamp the port
• When bleeding is controlled, reduce the esophageal ballon by 5 mmHg every 3 hours until 25mmHg is reached
without bleeding then keep the tube for 12-24 hours
• Deflate the esophageal ballon for 5 min/6 hours to prevent esophageal necrosis

PUD / Perforated Gastric Ulcer
SCENARIO:
Middle aged man, OA, NSAIDs, peritonism
The most likely diagnosis?

Perforated gastric ulcer or duodenal ulcer
Comment on CXR?
Air under diaphragm
Moderate amount of subdiaphragmatic air on the right side.
Risk factors of perforation?

• NSAID's
• H. pylori
• Steroids
• Previous peptic ulcers
• Malignancy
How can NSAID's causes peptic ulceration?

• Topical irritant effect of these drugs on the epithelium,
• Impairment of the barrier properties of the mucosa
• Suppression of gastric prostaglandin synthesis, (inhibition of cyclooxygenase)
• Reduction of gastric mucosal blood flow
• Interference with the repair of superficial injury.
Management options?
Omental patch repair, good peritoneal toilet, intraabdominal drain
In perforated gastric ulcers, we will take a biopsy to rule out malignancy
Post- operative medications?

Long term PPI

Mechanism of action of PPI?
The PPI binds irreversibly to a hydrogen/potassium ATPase enzyme (proton pump) on gastric parietal cells and blocks the
secretion of hydrogen ions, which combine with chloride ions in the stomach lumen to form HCL
Pharmacologist’s view of gastric secretion and its regulation: the basis for therapy of acid-peptic disorders. Shown are the interactions
among neural input and a variety of enteroendocrine cells: an ECL cell that secretes histamine, a ganglion cell of the ENS, a G cell that
secretes gastrin, a parietal cell that secretes acid, and a superficial epithelial cell that secretes mucus and bicarbonate. Physiological
pathways, shown in solid black, may be stimulatory (+) or inhibitory (−). 1 and 3 indicate possible inputs from postganglionic cholinergic
fibers; 2 shows neural input from the vagus nerve. Physiological agonists and their respective membrane receptors include ACh and its
muscarinic (M) and nicotinic (N) receptors; GRP and its receptor, the BB2 bombesin receptor; gastrin and its receptor, the CCK2; HIST
and the H2 receptor; and PGE2 and the EP3 receptor. A red line with a T bar indicates sites of pharmacological antagonism. A light blue
dashed arrow indicates a drug action that mimics or enhances a physiological pathway. Shown in red are drugs used to treat acid-
peptic disorders. NSAIDs can induce ulcers via inhibition of cyclooxygenase. Not shown is a physiological pathway that reduces acid
secretion: a D cell that secretes SST, which inhibits G-cell release of gastrin.
Actions of HCL?
• Activates pepsinogen to pepsin which help in proteolysis
• Antimicrobial
• Stimulates small intestinal mucosa to release CCK and secretin
• Promotes absorption of calcium and iron in the small intestine

Phases of gastric secretions?
1. Cephalic phase (smell / taste of food)
• 30% acid produced
• Vagal cholinergic stimulation causing secretion of HCL and gastrin release from G cells
2. Gastric phase (distension of stomach)
• Stomach distension / low H+ / peptides causes Gastrin release
3. Intestinal phase (food in duodenum)
• High acidity / distension / hypertonic solutions in the duodenum inhibits gastric acid secretion via
enterogastrones (CCK, secretin) and neural reflexes.

Priority of the operation according to NCEPOD intervention classification?
The National Confidential Enquiry into Patient Outcome and Death intervention classification
Target time Expected
Code Category Description Example Scenarios Typical procedures
to theatre location
1 Immediate Immediate (A) Within Next Ruptured aortic Repair of ruptured
lifesaving or (B) minutes of available aneurysm aortic aneurysm
limb or organ- decision to operating Major trauma to Laparotomy/
saving operate theatre – abdomen or thorax thoracotomy for
intervention. “break-in” to Fracture with major control of
Resuscitation existing lists neurovascular deficit hemorrhage
simultaneous with if required Compartment Fasciotomy
surgical syndrome Coronary
treatment. Acute myocardial angioplasty
infraction (AMI)
2 Urgent Acute onset or Within Day time Compound fracture Debridement plus
deterioration of hours of “emergency” Perforated bowel fixation of fracture
conditions that decision to list or Out- with peritonitis Laparotomy for
threaten life, limb operate and of-hours Critical organ or limb perforation
or organ survival; normally emergency ischemia Coronary
fixation of once theatre Acute coronary angioplasty
fractures; relief of resuscitation (including at syndromes (ACS)
distressing completed night) Perforating eye
symptoms. injuries
3 Expedited Stable patient Within days Elective list Tendon and nerve Repair of tendon
requiring early of decision which has injuries and nerve injuries
intervention for a to operate “spare” Stable & non-septic Excision of tumor
condition that is capacity or patients for wide with potential to
not an immediate Day time range of surgical bleed or obstruct
threat to life, limb “emergency” procedures Coronary
or organ survival list (not at Retinal detachment angioplasty
night)
4 Elective Surgical Planned Elective Encompasses all Elective AAA repair
procedure theatre list conditions not Laparoscopic
planned or booked & classified as cholecystectomy
booked in planned immediate, urgent or Varicose vein
advance of prior to expedited. surgery
routine admission admission Joint replacement
to hospital Coronary
angioplasty

Gastric Outlet Obstruction
SCENARIO:
Lady with vomiting and epigastric fullness. Hyponatremia and pH of 7.5
Causes of this clinical picture?

• Benign: pyloric stenosis secondary to chronic peptic ulceration
• Malignant: (gastric or pancreatic) carcinoma
ABG
Metabolic alkalosis
Biochemical abnormalities
Hypochloremic hypokalemic metabolic alkalosis
• Hypochloremia due to loss of chloride in the
vomitus
• Hypokalemia due to increased aldosterone in
response to hypovolemia
Why bicarbonate is increased?

• There will be increased uptake of bicarbonates
in renal tubules in response to loss of chloride
in order to maintain electrochemical neutrality
• Reduction of pancreatic juice secretion (due to
loss of acid load in the duodenum) →
retention of bicarbonate-rich pancreatic juice
Why hyponatremia?
In metabolic alkalosis, kidneys excrete more NaHCO3 to reduce blood alkalinity → hyponatremia
Why paradoxical aciduria?

Hyponatremia → stimulation of angiotensin aldosterone system → more Na+ and H2O reabsorption in exchange of H+ and
K+ → hypokalemia and the urine becomes acidic due to the presence of H+
Management?
Normal saline 0.9% + K+ supplementation
Clinical picture of hyponatremia?

• Confusion
• Agitation
• Fits
• Reduced GCS

Causes of hyponatremia?
• Depletional:
o Diarrhea
o Diuretics
o Burns
• Dilutional:
o Heart failure
o Post-operative over administration of 5% glucose
• Endocrine:
o Addison's disease
o Hypothyroidism
• Pseudohyponatremia:
o Multiple myeloma
• SIADH

Obstructive Jaundice
What type of jaundice from the blood results? SCENARIO:
Obstructive or post-hepatic jaundice You’re asked to see a 45-year-old
female patient complaining of 2-day
In what form does bilirubin circulate within the plasma? history of epigastric pain, nausea,
As free bilirubin and conjugated to glucuronic acid vomiting, diarrhea. She has dark urine.
O/E she is jaundiced and has mild
Why clotting deranged? epigastric tenderness.
Liver synthesize most of the clotting factors. Labs:
In severe liver damage and biliary obstruction there will be decreased Increases ALT, AST, ALP, GGT.
absorption of vitamin K. Vitamin K required to activate factors 2,7,9,10. Urobilinogen undetectable in urine
Which clotting studies may be abnormal?

This will lead to increased prothrombin time or INR Normal bilirubin level: 3-30 μmol/L
Apparent jaundice ---> 35 μmol/L
How to correct clotting abnormality?
• IV vitamin K
• Fresh frozen plasma
• Prothrombin complex concentrates
• Consult hematologist
Alkaline phosphatase?
• Enzyme located in the epithelium
Digestion of fats
of bile canaliculi
• Present also in bone and placental
tissue
• Increases in cholestasis to a far greater extent than ALT, AST
• ALT, AST present in hepatocytes and their increase is suggestive for liver damage rather than obstructive
jaundice.
• ALT > AST in liver pathology
Other investigation you want to do?

Abdominal ultrasound
What finding on abdominal USS will confirm diagnosis of obstructive jaundice?

Dilatation of intra- or extrahepatic bile ducts
If you find a CBD stone?

ERCP
Function of bile?
Emulsification of fat into micelles thus provides a greatly increased surface area for the action of the enzyme pancreatic
lipase
How do bile salts help in emulsification of fat?

Bile salt anions are hydrophilic on one side and hydrophobic on the other side; consequently, they tend to aggregate
around droplets of lipids (triglycerides and phospholipids) to form micelles, with the hydrophobic sides towards the fat
and hydrophilic sides facing outwards. The hydrophilic sides are negatively charged, and this charge prevents fat droplets
coated with bile from re-aggregating into larger fat particles.
Constituents of bile?
• Water.
• Cholesterol.
• Lecithin (a phospholipid)
• Bile pigments (bilirubin & biliverdin)
• Bile salts and bile acids (sodium glycocholate & sodium taurocholate)
• Small amounts of copper and other excreted metals.

What is bilirubin conjugated to?
In the liver, conjugates with glucuronic acid by the
enzyme glucuronyl transferase
Bilirubin metabolism?
• Conjugated bilirubin goes into the bile and
thus out into the small intestine. Though most
bile acid is resorbed in the terminal ileum to
participate in enterohepatic circulation,
conjugated bilirubin is not absorbed and
instead passes into the colon
• There, colonic bacteria disconjugate and
metabolize the bilirubin into colorless
urobilinogen, which can be oxidized to form
stercobilin, these give stool its characteristic
brown color
• 10% of the urobilinogen is reabsorbed into the
enterohepatic circulation to be re-excreted in
the bile: some of this is instead processed by
the kidneys, coloring the urine yellow.
What is urobilinogen? How it is formed? How do they

circulate?
It is a byproduct of bilirubin metabolism formed in the
intestine by gut flora.
Some are excreted in the feces after oxidation
(stercobilinogen) and some are reabsorbed into the
portal circulation again. Some of the reabsorbed
urobilinogen is again excreted by the liver but small
amounts enter the systemic circulation and are excreted
in urine.
Enterohepatic circulation?
Reabsorption of bile salts from the terminal ileum and
return them back to the liver (95%)
Why in this case is urobilinogen not detectable in urine?

Because there is an obstruction to the flow of the bile
and bilirubin does not reach the gut. Bilirubin metabolism and elimination. 1, Normal bilirubin production
(0.2 to 0.3 g/day) is derived primarily from the breakdown of
Complications of reduction of bile salts in small senescent circulating red cells, with a minor contribution from
degradation of tissue heme-containing proteins. 2, Extrahepatic
intestine?
bilirubin is bound to serum albumin and delivered to the liver. 3 and 4,
• Steatorrhea due to malabsorption of fat Hepatocellular uptake (3) and glucuronidation (4) by
• Poof absorption of fat-soluble vitamins (ADEK) glucuronosyltransferase in the hepatocytes generate bilirubin
monoglucuronides and diglucuronides, which are water-soluble and
If the patient had fever, pain, chills? readily excreted into bile. 5, Gut bacteria deconjugate the bilirubin and
Ascending cholangitis degrade it to colorless urobilinogens. The urobilinogens and the
residue of intact pigments are excreted in the feces, with some
reabsorption and reexcretion into bile.
What is the sepsis 6? how treat sepsis?
1. Administer high-flow oxygen, aim to keep > 94% unless COPD
2. Take blood cultures and consider infective source. CXR and urinalysis for all adults.
3. Administer intravenous antibiotics according to trust protocol
4. Give intravenous fluid resuscitation
5. Check serial lactate and Hb
6. Commence hourly urine output measurement. Urinary catheter needed.
(See Sepsis Six PDF file in ‘Resources Folder’)

Causes of jaundice?
Pre-Hepatic Hepatocellular Post-Hepatic
• Hemolytic anaemia • Alcoholic liver disease • Gallstones
o Sickle cell anaemia • Viral hepatitis • Sclerosing cholangitis
o G6PD • Medication • Cholangiocarcinoma
o Hereditary spherocytosis • Hereditary haemochromatosis • Strictures
• Gilbert’s syndrome or Crigler- • Autoimmune hepatitis • Drug-induced cholestasis
Najjar syndrome • Primary biliary cirrhosis • Pancreatic cancer
• Hepatocellular carcinoma • Abdominal masses


Acute Pancreatitis
Differentials? SCENARIO:
1 • Acute relapsing pancreatitis 45-year-old male diagnosed and
4 • Acute cholecystitis managed for acute pancreatitis 2 weeks
3 • Ascending cholangitis ago. Now presents with tachycardia,
2 • Pancreatic pseudocyst tachypnea and SOB
The patient is tachypneic, why?

• Abdominal pain
• Pressure by pseudo cyst
• ARDS
Scoring systems?
• Glasgow criteria: PANCREAS
• PaO2 < 8 kPa (normal: 10-13 kPa) <60%
• Age > 55
• Neutrophils > 15,000
• Calcium < 2 mmol [after 48h]
• Renal (urea) > 16 mmol/L (normal: (2.5-6.7))
• Enzymes (LDH) > 600 (after48h)
• Albumin < 32 g/L (after 48h)
• Sugar (glucose) > 10 mmol/L
(at least 3 of the above = severe episode = ITU admission)
• Ranson's criteria:
Estimates mortality of patients with pancreatitis, based on initial and 48-hour lab values.
Criteria at time of patient admission to hospital
• A Age > 55
• N WBC > 16,000
• S Glucose > 11 mmol/L (> 200 mg/DL)
• AST > 250 IU/L
• E LDH > 350 IU/L
Criteria after 48 hours of admission
• Hct drops 10% or greater haematocrit
• Fluid sequestration > 6L fluid loss
• Calcium < 2.0 mmol/L (< 8 mg/dL)
• PO2 < 60 mmHg (< 8 kPa)
• BUN rises more than 1.98 mmol/L (> 5 mg/dL) after IV fluid hydration
• Base deficit > 4 mmol/L
Prognostic implications of Ranson’s Criteria
• 0-2 points: Mortality is 1%
• 7-11 points: Mortality almost 100%
• Balthazar CT scoring system:

A. Normal pancreas
B. Enlargement of pancreas
C. Inflammatory changes in pancreas and peripancreatic fat
D. Ill-defined single peripancreatic fluid collection
E. Two or more poorly defined peripancreatic fluid collections
• APACHE II
(Acute Physiologic Assessment and Chronic Health Evaluation)
Is serum amylase important in scoring systems?

No

What can be the cause of normal amylase in pancreatitis? NB
(too early or too late) Serum amylase determinations are
It returns back to normal levels 48h after the onset of the attack, it routinely available, but they are not specific
Relate doesn't correlate with the severity of pancreatitis, it is not specific for for pancreatitis. Preferably, the amylase P
pancreatitis level should be measured, which is
somewhat more specific to pancreatic
Which enzymes to check apart from amylase and lipase? pathology. Elevations can occur in patients
LDH (lactate dehydrogenase) with small intestinal obstruction,
mesenteric ischemia, tubo-ovarian disease,
Pathophysiology of hypocalcemia? renal insufficiency, or macroamylasemia.
• In early phase: Rarely, elevations may reflect parotitis. The
Autodigestion of mesenteric fat by pancreatic enzymes and serum half-life of amylase is short, and
release of free fatty acids (chelate calcium), which form elevations generally return to the reference
calcium salts, transient hypoparathyroidism, and ranges within a few days.
hypomagnesaemia.
• Later stages: Lipase has a slightly longer half-life and its
Due to complication by sepsis, which will lead to increased abnormalities may support the diagnosis if
circulating catecholamines which will cause a shift of a delay occurs between the pain episode
circulating calcium into the intracellular compartment leading and the time the patient seeks medical
to relative hypocalcemia. attention. Elevated lipase levels are more
specific to the pancreas than elevated
Pathophysiology of hyperglycemia? amylase levels.
2 • Pancreatic enzymes destroy B cells of islets of Langerhans →
increase in serum glucose
1• Stress response
Management of nutrition? first reffered to nutrionnist team

• TPN is usually needed in severe cases
• Recently, there is growing trend towards early institution of enteral feeding with a naso jejunal tube
• Take into account:
o Premorbid nutritional status
o Current nutritional needs
o Estimated return to normal feeding
Complications?
1.• Local 7 • Hematological (DIC) 3• Metabolic
o Pseudocyst 8 • Hepatobiliary o Hypocalcemia
o Abscess o Jaundice o Hypoalbuminemia
o Ascites o Portal vein thrombosis o Hypoxemia
o Necrotizing pancreatitis o Strictures o Hypomagnesemia
o Fat necrosis 2 • Systemic o Hyperglycemia
o Splenic vein thrombosis o Hypovolemic shock 4• Respiratory
o Phlegmon o Hemorrhagic pancreatitis o ARDS
5 • GI (Grey Turner sign, Cullen’s o Pleural effusion
o Ileus sign) • Death
o Bleed o SIRS
6 • Renal (acute renal failure) o MOF
Treatment of splenic vein thrombosis

LMWH
Multidisciplinary approach that may include a gastroenterologist/hepatologist, a hematologist, and an interventional
radiologist and/or a surgeon.

Functions of the pancreas?
Endocrine: cells of islets of Langerhans
• Alpha → glucagon
• B cells → insulin
• Delta cells → somatostatins
• PP cells → pancreatic polypeptide
Exocrine: pancreatic enzymes (digestion of fat, carbohydrates, proteins)
• Enterokinase (trypsinogen → trypsin)
• Lipase
• Amylase
Causes of acute pancreatitis?

• Gall bladder stone • Hypercalcemia
• Alcoholism • Viral infection (mumps)
• Abdominal trauma • Drugs (thiazide diuretics)
• Post ERCP • Idiopathic
• Hyperparathyroidism
Pathogenesis?
• Duct obstruction: reflux of bile into the pancreatic ducts causing injury; increased intra-ductal pressure may
damage pancreatic acini, lead to leakage of pancreatic enzymes with further damage to pancreas.
• Direct acinar damage: due to viruses, bacteria, drugs or trauma.
• Protease release causes widespread destruction of pancreas and increases further enzyme release with
consequent further damage.
• Lipase causes fat necrosis, resulting in characteristic yellowish-white flecks on the pancreas, mesentery and
omentum, often with calcium deposition (fat necrosis).
• Elastase destroys blood vessels, leading to hemorrhage within the pancreas and hemorrhagic exudate into the
peritoneum.
• Hemorrhage (extensive) may lead to acute hemorrhagic pancreatitis.
Three proposed pathways in the pathogenesis of acute pancreatitis.

Identify CT?
Identification of liver, spleen, pancreas, aorta, vertebrae and
stomach.
Identification of massive pseudocyst
CT findings in acute pancreatitis?

• Edema
• Fat strandings
• Collection
• Necrosis
• Abscess
• Pseudocyst
Management?
ABCDE and fluids, history to establish cause, physical Early management of sever acute pancreatitis
examination, ABG, bloods, USG, ICU transfer Admission to HDU/ICU
• CV line for: Analgesia
o Rehydration (because of the fluid Aggressive fluid rehydration
sequestration and 3rd space loss) Supplemental oxygen
o Monitoring Invasive monitoring of vital signs, central venous
o TPN pressure, urine output, blood gases
• Pain management Frequent monitoring of haematological and
• Nasogastric tube, urinary catheter biochemical parameters (including liver and renal
• Octreotide (somatostatins) to decrease pancreatic function, clotting, serum calcium, blood glucose)
secretions Nasogastric drainage (only initially)
• Antibiotics Antibiotics if cholangitis suspected; prophylactic
• IV PPi to prevent stress ulcers and erosive bleeding antibiotics can be considered
CT scan essential if organ failure, clinical deterioration
Role of corticosteroids in pancreatitis? or signs of sepsis develop
Corticosteroids suppress the release of inflammatory ERCP within 72 hours for severe gallstone pancreatitis
cytokines in AP. or signs of cholangitis
Corticosteroid therapy can benefit SAP (severe acute Supportive therapy for organ failure if it develops
pancreatitis) patients by reducing the length of hospital stay, (inotropes, ventilatory support, haemofiltration, etc.)
the need for surgical intervention and the mortality rate If nutritional support is required, consider enteral
(nasogastric) feeding
Antibiotics to use in acute pancreatitis?
Carbapenem and Quinolone (penetrating pancreas)
Management of pain?
Pethidine/meperidine is the drug of choice (no morphine / no NSAIDs). According to WHO analgesic ladder: paracetamol first
• Pain medication begins with non-opioids (like----------------------------------------------
acetaminophen, ibuprofen, or both). Paracetamol
• If non-opioids do not relieve pain, mild opioids (codeine) are given.
• If mild opioids do not relieve pain, strong opioids, PCA and epidural analgesia.

Definition of pseudocyst?
Collection of amylase-rich fluid enclosed in a wall of fibrous or granulation tissue
It requires 4 weeks or more from the onset of the attack
Location? It is most frequently located in the lesser peritoneal sac in proximity to the pancreas.
Symptoms? Presentation?
• Epigastric swelling
• Dyspepsia
• Vomiting
• Mild fever
Complications of pancreatic pseudocyst?

Process Outcome
Infection • Abscess
• Systemic sepsis
Rupture
Into the gut • Gastrointestinal bleeding
• Internal fistula
Into the peritoneum • Peritonitis
Enlargement
Pressure effects • Obstructive jaundice from biliary compression
• Bowel obstruction
Pain
Erosion into a vessel • Hemorrhage into the cyst
• Hemoperitoneum
Difference between true pancreatic cyst and pseudocyst?

A pseudocyst isn’t closed and doesn’t have a lining of epithelial cells separating it from the nearby tissue.
Management of pseudocyst?
• Up to 40% of acute pseudocysts will resolve within approximately one week. Supportive treatment is all
that is required in this time.
• Should the cyst fail to resolve after 2 months, become infected, or is greater than 6cm in diameter,
cystogastrostomy or cystojejunostomy is required. The former entails: entering the anterior wall of the
stomach, fashioning a large hole through the posterior wall into the pseudocyst, securing stomach and
pseudocyst with a circumferential stitch. The pseudocyst then drains into the stomach.
How does paracetamol overdose cause liver injury?

Toxic metabolite NAPQI is neutralized by glutathione, when excess acetaminophen is taken, not all NAPQI is
neutralized and it accumulates in liver and effects vital functions.
Diagnosis of pseudocyst?
USG, CT, MRCP and cyst fluid analysis:
CEA and CEA-125 (low in pseudocysts and elevated in tumors)
Fluid viscosity (low in pseudocysts and elevated in tumors)
Amylase (usually high in pseudocysts and low in tumors)


Diverticular Abscess + Septic Shock
Differential Diagnosis? SCENARIO:
• Diverticulitis Old lady, critically ill, with LIF pain and
• Sigmoid volvulus tenderness
• Gastroenteritis
• Acute constipation
• Pelvic tumor
• Ureteric colic
Interpret ABG, FBC?

• Metabolic acidosis with partial compensation
• Increased total leucocyte count
Define shock?
Shock is circulatory failure resulting in inadequate organ perfusion, e.g. cannot meet the metabolic demands
Different types of positive feedback that can lead to progression of shock.
What kind of shock this patient having?

Septic shock
Define septic shock?

This is the presence of sepsis associated with hypotension (systolic BP <90 mmHg) or hypoperfusion resulting in organ
dysfunction despite adequate fluid resuscitation (or the requirement for inotropes), e.g. persisting lactic acidosis,
decreased urine output and altered GCS

Basic principles of management of septic shock?
• Circulatory support: to maintain the cardiac index and oxygen delivery to the tissues
o Use IV fluids, e.g. colloids and crystalloids such as 0.9% saline
o Inotropes may be required to increase the systemic vascular resistance
• Respiratory support:
o Non-invasive or invasive ventilation may be required for the management of ARDS and respiratory
failure
• Renal support: to ensure that the urine output is >0.5 ml/kg/h
o Dopamine or a furosemide infusion may be required to support the failing kidney
o Cardiac support helps maintain the renal perfusion pressure
o Renal replacement therapies may also be required
• Nutritional support: may be enteral or parenteral. Enteral nutrition helps maintain mucosal integrity and reduce
bacterial translocation
• Antimicrobials:
o During the early phases there is empirical use of broad spectrum antibiotics and surveillance of
infection, but in the latter stages, agents are targeted to grown microbiological sensitivities from
general, e.g. blood, and local sources
CT confirmed the presence of diverticular abscess, what are the management options?
1. Open drainage:
• Advantages:
o Proper drainage with peritoneal toilet
o Has the ability to make a stoma if needed
• Disadvantages:
o Liability of wound infection
o General increase in morbidity
2. Image guided aspiration:
• Advantages:
o No wound infection
o Less hospital stay
o Possibility of leaving peg-tail catheter for repeated drainage and administration of antibiotics
• Disadvantages:
o Less adequate drainage
o Doesn’t have the ability to make a stoma

Bloody Diarrhea
Labs SCENARIO:
FBC: Hb: 8.7 g, platelets: 666000, WBCs: 12000 55 y old abdominal pain, bloody
Hyponatremia, hypokalemia, ↑ CRP diarrhea, hypotensive, tachycardiac,
creatinine: 109, urea: 9 feverish, admitted, fluid
resuscitation done, 10 episodes of
What type of anemia? bloody diarrhea, stopped after 6 hours
normocytic normochromic
Microcytic hypochromic anemia
Why platelets are elevated?

• Secondary to acute inflammation (acute phase reactants)
• Dehydration
Abdominal x-ray:
Dilatation of the ascending and transverse colon, with narrowing of the descending colon with thumbprinting sign
(Thumbprinting is a radiographic sign of large bowel wall thickening, usually caused by edema, related to an infective or
inflammatory process (colitis). The normal haustra become thickened at regular intervals appearing like thumbprints
projecting into the aerated lumen.)
Thumbprinting sign
DD of bloody diarrhea?
• Ulcerative colitis and Crohn’s disease (IBD)
• Ischaemic colitis
• Amoebic colitis
• Bacillary dysentery
• Carcinoma colon
• Infectious colitis by Clostridium difficile, Campylobacter jejuni
Why not transfuse blood?

• State of sepsis
• Not indicated as Hb is not below 7g
Why there is hyponatremia and hypokalemia?

Due to losses from diarrhea

How else would you investigate the patient?
• ESR, CRP
• Stool analysis and culture
• CEA
• Antibodies for UC, Crohn’s
• Colonoscopy (later stage)
How will monitor the patient response?

• Clinically: fever settles, diarrhea stops
• Lab: ↓ CRP, ↓ TLC
Indications of urgent surgical management?

• Toxic megacolon refractory to medical management
• Fulminant attack refractory to medical management
• Uncontrolled colonic bleeding
• Perforation (free or walled off)
• Obstruction and stricture with suspicion for cancer
Surgical management?
Pan-proctocolectomy with ileostomy

Intestinal Obstruction
SCENARIO:
60-year-old patient has abdominal pain and distention on the wards. The nurse called you as surgical trainee and
asked you to come and see patient because the patient has become confused.
What do you see in this radiograph?

Dilated small bowels denoting intestinal
obstruction
Differential diagnosis?
Adhesions, volvulus, colorectal carcinoma,
complicated diverticulitis, impacted stool.
How to scan him?

Beside x-ray, US, CT
How will you manage this patient?

I will assess and manage this patient
according to CCrISP as he is critically ill
A. Airway assessment and treatment
B. Breathing assessment and
treatment
C. Circulation assessment and
treatment
D. Dysfunction of CNS
E. Exposure of patient for full
assessment and treatment
How to assess circulation?

• Heart rate
• Level of consciousness
• Urine output
• blood pressure
• Capillary refill
• CVP
• Clinical parameters, i.e. dry tongue, pallor, skin turgor
If capillary refill 4 seconds, what do you think?

Delayed, so patient in hypoxia and dehydrated
How to know that patient is hypoxic?

Pulse oximeter, ABG
What you expect in ABG?

Metabolic acidosis (compensated or partially compensated)
Hemoglobin dropped from 13 gm to 9 gm, what may be the causes?

Blood loss, Overhydration causing dilution of hemoglobin
What are the factors affecting tissue oxygenation? (asking about the equation)
Oxygen delivery may be calculated:
DO2 = CO x CaO2 x 10.
(Where CO is the cardiac output, CaO2 is arterial O2 content)
The formula may include the cardiac index (CI) = COP / body surface area.
How O2 is carried to blood?

By hemoglobin

Factors influence the affinity of hemoglobin for oxygen?
• The partial pressure of CO2
• pH, independent of CO2
• The concentration of 2,3-DPG inside the erythrocytes
• The presence of unusual hemoglobin species
• Temperature
Mnemonic for right shift of the oxygen

dissociation curve: CADET face RIGHT
• C O2
• A cidosis
• 2,3-DPG
• E xercise
• T emperature
Shifts to Left = Lower oxygen delivery Shifts to Right = Raised oxygen delivery
• low [H+] (alkali) • raised [H+] (acidic)
• low pCO2 • raised pCO2
• low 2,3-DPG • raised 2,3-DPG (diphosphoglycerate)
• low temperature • raised temperature
• HbF, methaemoglobin, carboxyhaemoglobin
Now the patient has regained consciousness, what next?
Full Patient
Stable Daily management plan
Assessment
Chart review Decide and Plan
History and Diagnosis Specific
Unstable Definitive care
Examination required investigations
In CBC, MCV is low, what is this meaning?

In such age, patient has microcytic hypochromic anemia (iron deficiency anemia)
How to investigate this?

Total iron binding capacity, serum ferritin, occult blood in stool

Enterocutaneous Fistula
Definition?
Abnormal communication lined by granulation tissue between the skin and gastrointestinal tract
Classifications?
May be classified according to
• Congenital / Acquired
• Etiology (infection, inflammation, malignancy, RT)
• Internal / External
• Simple / Complex
• Anatomy (EE, EC, colovaginal, vesicocolic)
• Physiology (high / low output)
Predisposing factors?
• Intestinal anastomosis
• Crohn's disease
• Infection
• Cancer
• Irradiation
• Ischemia
Complications of ECF?
• Sepsis
• Malnutrition
• Fluid and electrolyte imbalance
What brings the patient to OT within first 24 hrs?

• Distal obstruction
• Intraabdominal sepsis
Signs of Intraabdominal sepsis?

Nausea, vomiting, swinging pyrexia, abdominal tenderness, rigidity, tachycardia, hypotension.
Management? SNAP
• Sepsis control
• Nutritional support – a period of parenteral nutrition may be required
• Anatomical assessment
• Adequate fluid and electrolyte replacement
• Protect skin to prevent excoriation
• Planned surgery
o Management of fistulas requires an MDT approach following initial resuscitation and stabilization with an ABCDE
approach, which is particularly pertinent in patients with high-output fistulas
o For nutritional support, one would liaise with a dietician asking him to recommend a TPN regimen that adequately
meets the patient's calorific needs.
o To ensure adequate fluid and electrolyte replacement, one would arrange bloods tests with the U&Es guiding
electrolyte replacement, and WCC and CRP acting as a measure of inflammation or infection.
o Imaging such as an MRI, CT or US scan of the abdomen can exclude an underlying collection or abscess.
o With conservative management, 60% of fistulae will close spontaneously when sepsis is controlled and distal
obstruction is relieved.
o Surgical management is normally delayed until after a trial of conservative measures has been undertaken; however,
peritonitis with ongoing sepsis will require more urgent surgical intervention. In general terms the aim of surgery is to
excise the fistula tract with resection of the bowel involved and anastomosis or exteriorization of the remaining
bowel, followed by delayed anastomosis.

Factors preventing spontaneous healing?
• Distal obstruction
• Malignancy
• Infection
• Radiation
• Crohn's
• Malnutrition
• High output
Imaging?
• CT abdomen and pelvis with contrast
• Fistulogram
o To delineate the track length
o Locating the fistula
o Locating any distal obstruction
Fluid management?
High output fistula: TPN
Nutritional assessment are normally performed by a dietician. It is based on a patient’s body weight and ho unwell they
are. The energy requirement is 25-30 kcal/kg/day for a normal person and 45-55 kcal/kg/day for a patient following
extensive trauma. In addition, the protein, fats, glucose, electrolytes and fluids are calculated and adjusted based on
regular blood tests

Steroids
What is a steroid? SCENARIO:
Organic compound that contains a characteristic arrangement of 4 RA patient on steroids / immunomodulators
cycloalkane rings that are joined together.
Layers of adrenal cortex?

GFR
• Zona glomerulosa: aldosterone /Mineralocorticoid
• Zona fasciculata: cortisol/glucocorticoid
• Zona reticularis: sex hormones
Actions of aldosterone? (mineralocorticoid)

• Na+ reabsorption and K+ excretion in
DCT and collecting ducts
• Water balance: salt and water retention
• Acid base balance: metabolic alkalosis
(excretion of K+)
Actions of cortisol?
• Anti-insulin effect: increase blood
glucose
• Stimulate gluconeogenesis: increase
blood glucose
• Stimulate protein synthesis in the liver
• Stimulate lipolysis
• Metabolic effect as aldosterone
• Anti-inflammatory effect
• Immunosuppressive effect
• Control body stress response
Draw the hypothalamic Pituitary Adrenal axis? Advice to patients starting steroids?
• They should not stop the drug suddenly. The
drug should be tapered off slowly
• Make doctors aware that they are on
steroids if they are admitted to hospital or
prior to surgery (carry steroid card, wear
medic alert bracelet)
• There is increased possibility for infection,
delayed wound healing
• Steroids may lead to osteoporosis with
increased risk of fractures
• Steroids may lead to weight gain
• Steroids increase blood sugar, if diabetic you
will encounter poor glycemic control, if not
you can develop diabetes
• Steroids can lead to muscle weakness
• Steroids can lead to mood or behaviour
changes
• Steroids increase the risk of peptic ulcers; do
not take NSAID's
Mechanism for regulation of glucocorticoid secretion. ACTH,

adrenocorticotropic hormone; CRF, corticotropin-releasing factor.

Addisonian crisis:
Definition?
It is acute reduction of the circulating steroids
• Primary: Addison’s disease: adrenal supply of cortisol cannot meet the body requirements
• Secondary to
o Trauma .meningococcal infection
o Surgery
o Infection
o Exogenous steroids are suddenly stopped rather than being tapered off
Cardinal features?
• Abdominal pain
• Nausea, vomiting
• Unexplained shock
• Hyponatremia, hyperkalemia
Management?
• CCRISP protocol [CCrlSP-care of critically ill surgical patient]
• ABC protocol
• IV steroids – immediate bolus of 100mg hydrocortisone IV or IM, followed by continuous intravenous infusion of
200mg over 24h
• IV fluids – rapid IV infusion of 1000cc of isotonic saline infusion within the first hour, followed by further IV
rehydration as required
• Adjust metabolic disturbances
Prevention? [HPA-hypothalamic pituitary axis]

• Increase the patient steroid dose prior to surgery
<5mg day • Convert to IV steroids.
< 10 mg day Assume normal HPA response Additional steroid cover not required
25 mg hydrocortisone at induction 100mg
Patients currently
>5mg day Minor surgery

taking steroids
Moderate surgery Usual pre-operative steroids

mg
+ 25mg hydrocortisone at induction 100
> 10 mg day + 100mg day for 24 h 200mg
Major surgery Usual pre-operative steroids
+ 25mg hydrocortisone at induction 100mg
+ 100mg day for 48 – 72h 200mg
NB:
Cortisol Increases Liver and Plasma Proteins. Coincidentally with the effect of glucocorticoids to reduce proteins
elsewhere in the body, the liver proteins are increased. Furthermore, the plasma proteins (which are produced by
the liver and then released into the blood) are also increased. These increases are exceptions to the protein
depletion that occurs elsewhere in the body.

Calcium Homeostasis
Causes of post-thyroidectomy hypocalcemia? SCENARIO:
• Removal of parathyroid glands Post thyroidectomy hypocalcemia
• Ischemia of parathyroid glands Ca+2 1.8 → POD4: 0.7
. Normal Ca=2-2.5 mmo l/L
How calcium is transported in the blood?
• 50% unbound and ionized
• 45% bound to plasma proteins
• 5% is associated with anions such as citrate and lactate
Physiologic role of calcium in the body?

• Physiologic processes
o Neuromuscular transmission
o Smooth and skeletal muscle contraction
o Cardiac automaticity
o Nerve function
o Cell division and movement
o Certain oxidative processes
• Co-factor for many steps during blood coagulation Distribution of ionized calcium (Ca++), diffusible but
un-ionized calcium complexed to anions, and non-
• Involved in the action of other intracellular messengers, e.g.
diffusible protein bound calcium in blood plasma.
CAMP, and thus mediates the cellular response to numerous
hormones, including epinephrine, glucagon,
ADH, secretin.
• Calcium binding proteins e.g. troponin, Metabolism of Ca+=
calmodulin
• Mineralization of bone
Hormones involved in Ca+2 homeostasis?

• PTH: (increases calcium)
o Bone: increases the synthesis of enzymes
increase that break down bone matrix to release
osteoclast calcium and phosphate into the circulation.
It also stimulates osteolytic and
osteoclastic activity, leading to progressive
bone reabsorption
o Renal: increases renal phosphate excretion
while reducing renal calcium loss. It also
stimulates 1-α hydroxylase activity in the
kidney, increasing 1,25 dihydroxy-vitamin
D 3 (calcitriol), thus indirectly increasing
calcium absorption
• Vitamin D3: (calcitriol)
o Bone: calcitriol increases both serum
calcium and the calcification of bone
Osteoblast matrix. It stimulates osteoblastic
proliferation and protein synthesis
o Renal: it promotes calcium and phosphate
reabsorption
Effects of PTH and 1,25-dihydroxycholecalciferol on whole body calcium
o Gastrointestinal: it enhances gut
homeostasis. A reduction in plasma calcium stimulates parathyroid
absorption of calcium and phosphate hormone secretion. PTH in turn causes calcium conservation and
• Calcitonin: production of 1,25-dihydroxycholecalciferol in the kidneys, the latter of
decrease o Bone: inhibits bone resorption through which increases calcium uptake in the intestine. PTH also releases calcium
Osteoclast inhibition of osteoclastic activity if serum from the readily exchangeable pool in the bone. All of these actions act to
calcium >2.6 mmol/L restore normal plasma calcium.
activity o Renal: stimulates the excretion of sodium,
chloride, calcium and phosphate

Summary of calcium homeostasis: The actions of the three principal hormones that regulate the plasma concentration of Ca+2
PTH increases plasma Ca+2 by mobilizing this ion from bone. It increases Ca+2 reabsorption in the kidney, but this may be offset
by the increase in filtered Ca2+. It also increases the formation of 1,25-dihydroxycholecalciferol. 1,25-Dihydroxycholecalciferol
increases Ca+2 absorption from the intestine and increases Ca+2 reabsorption in the kidneys. Calcitonin inhibits bone resorption
and increases the amount of Ca+2 in the urine.
How vitamin D3 is formed?
Signs of hypocalcemia?
• Neurological: irritability manifest as peripheral and circumoral
paresthesiae
• Muscular: cramps
• Tetany: spasms
• Chvostek's sign: twitching of the facial muscles on tapping of
the facial nerve anterior to the tragus
Carpopedal• Trousseau's sign: tetanic spasm of the hand upon tapping the
spasm median nerve following blood pressure cuff-induced arm
ischemia
Which muscle are you worried about in tetany?

Laryngeal muscle for the fear of laryngospasm Hypocalcemic tetany in the hand, called carpopedal
spasm.
How to treat hypocalcemic tetany?
• Commencement of cardiac monitoring Signs & Symptoms: CATS go Numb
• Fluid Resuscitation Give 10 ml of 10% calcium gluconate IV, followed • Convulsions
by 10–40 ml in a saline infusion over 4–8 hours • Arrhythmias
• Tetany
• Spasms and stridor
• Numbness in the fingers
Calcium
Normal – 2.5 mmol/L
• 99% bone (as hydroxyapatite)
• 1% body fluids (cellular, extracellular, blood)
o Free Ca+2 (ionized) (50%)
o Bound to protein (un-ionized) (40%) – non-diffusible
o Bound to ions (un-ionized) (10%) – diffusible
Acidosis increases the amount of ionized calcium via osteoclastic activity on bone, Alkalosis leads to increased binding and
decrease Ca (hypocalcemia)
Vitamin D3
Calcitriol, also called 1,25-dihydroxycholecalciferol, or 1alpha,25-dihydroxyvitamin D3, 1,25-dihydroxyvitamin D3 and other
variants, is the hormonally active metabolite of vitamin D which has three hydroxyl groups. It can be abbreviated 1α,25-(OH)2D3 or
simply 1,25(OH)2D.

Vitamin D metabolism. Vitamin D is produced from 7-dehydrocholesterol in the skin or is ingested in the diet. It is converted in the liver
into 25(OH) D, and in kidney into 1,25(OH)2D (1,25-dihydroxyvitamin D), the active form of the vitamin. 1,25(OH)2D stimulates the
expression of RANKL, an important regulator of osteoclast maturation and function, on osteoblasts, and enhances the intestinal
absorption of calcium and phosphorus in the intestine. DBP, Vitamin D–binding protein (α1-globulin); FGF23, fibroblast growth factor
23.


Hypothyroidism
What’s the most probable based on the labs and clinical picture?
SCENARIO:
primary Hypothyroidism A 65-year-old woman presents with
long standing goiter, she also
Draw the hypothalamic pituitary thyroid axis?
describes general malaise and chronic
fatigue.
Labs: low T3 and low T4 with high
TSH, anemia
Difference between T3 and T4?

• T3 is more biologically active, less
protein binding capacity
• T4 is in vitro inactive, more protein
binding capacity
Synthesis of T3 and T4? [TOP-thyroid per oxidase]

• Iodide ions enter the thyroid
follicular cell by active pumping
• Iodide is converted to iodine by TOP
• Iodine combines with tyrosine
forming: monoiodotyrosine (MIT)
and diiodotyrosine (DIT)
• MIT + DIT = T3 (tri iodotyrosine)
• DIT + DIT = T4 (tetra iodotyrosine)
TPO/TOP
Iodide-------------Iodine
Type of anemia in this case? Iodine+Tyrosine=MIT
Macrocytic anemia = pernicious anemia MIT+MIT=DIT
(lack of absorption of vit. B12 due to anti parietal cell antibodies leading to lack of intrinsic factor)
Causes of hypothyroidism?
Primary hypothyroidism:
• Iatrogenic
o Surgery
o Radioiodine therapy
o Drugs
• Autoimmune (Hashimoto’s)
• Iodine deficiency
• Idiopathic
• Genetic defects in thyroid development
• Thyroid hormone resistance syndrome (THRB) (rare)
• Congenital biosynthetic defect (dyshormonogenetic goiter) (rare)
• Transient thyroiditis (De Quervain’s thyroiditis)
• Infiltrative (amyloidosis, sarcoidosis)
Secondary
• Pituitary failure (rare)
• Hypothalamic failure (rare)
Signs of hypothyroidism?
• Weight gain
• Memory loss
• Cold intolerance
• Constipation
• Myxedema
• Bradycardia
• Muscle weakness
• Pretibial edema
A patient with myxedema

If this patient has hypothyroidism as a result of hypopituitarism, how will the TFTs be different
• ↓ T3 and T4
• ↓ TSH
Disorder TSH T4
Euthyroid ↔ ↔
Primary hypothyroidism ↑ ↓ Primary atrophic hypothyroidism
Secondary hypothyroidism ↓ ↓ Replacement steroid therapy is required prior to
thyroxine
Primary hyperthyroidism 1ry is the term used when the pathology is within thyroid
↓ ↑
Thyrotoxicosis1 (e.g. Graves' disease) In T3 thyrotoxicosis the free T4 will be normal
Secondary hyperthyroidism ↑ ↑ 2ry is when the thyroid is ++ by excessive TSH
Sick euthyroid syndrome2 ↓3 ↓ Common in hospital inpatients
Poor compliance with thyroxine ↑ ↔/ ↑
Steroid therapy ↓ ↔
1
although the term thyrotoxicosis has been used synonymously with hyperthyroidism, some experts have tried to
differentiate the two terms.
hyperthyroidism - excess synthesis and secretion of thyroid hormones from the thyroid gland
thyrotoxicosis - excessive amounts of circulating thyroid hormones, but includes extrathyroidal sources of thyroid
hormone or by a release of preformed thyroid hormones into the circulation
2
now referred to as non-thyroidal illness
3
TSH may be normal in some cases, although a common pattern is ↓ Total and Free T3 with normal levels of T4 and TSH
Patient with hypothyroidism not compliant to medications comes for an emergency surgery, what are the risks?
• Pre-operative
o Anemia
o Increase risk of ischemic heart disease
• Intra-operative
o Bradycardia
o Hypotension
o Hypothermia
Which may lead to coagulopathy and airway compromise
• Post-operative
o Delayed recovery from anesthesia
o Confusion
o Myxedema coma
o Poor wound healing

• Endocrinologist
• Anaesthesia consultant
• Surgical consultant
How to increase patient compliance with the treatment?

• Discuss with patient the reason for non-compliance, social or psychological reasons
• Communication with GP and family member
• Medical follow-up
• Simple regime,
o Make the dose single not divided
o To make the dose of replacement in the early morning
• Emphasize that relapse is inevitable if therapy is interrupted

Diabetes Mellitus
SCENARIO: 65-year-old with type II DM, on oral medications. Presented with perianal abscess and went for I&D
What are the types of DM and describe the pathogenesis of each?

The vast majority of cases of diabetes fall into one of two broad classes:
• Type 1 diabetes (T1DM): is characterized by an absolute deficiency of insulin secretion caused by pancreatic
beta cell destruction, usually resulting from an autoimmune attack. Type 1 diabetes accounts for approximately
10% of all cases.
• Type 2 diabetes (T2DM): is caused by a combination of peripheral resistance to insulin action and an inadequate
compensatory response of insulin secretion by the pancreatic beta cells (relative insulin deficiency).
Approximately 80% to 90% of patients have type 2 diabetes.
What is the function of insulin and what are other hormones affecting blood glucose level?
The principal metabolic function of insulin is to increase the rate of glucose transport into certain cells in the body
Carbohydrates:
• Increases the uptake of glucose into various tissues
• Stimulates glycogenesis in many tissues, but especially the liver
• Stimulates hepatic generation of glucose-6-phosphate from glucose
Proteins:
• Enhances the uptake of amino acids into peripheral tissues
• Stimulates protein synthesis –for this reason, insulin can be regarded as one of the growth hormones
Fats:
• Stimulates lipid uptake into cells
• Enhances oxidation of lipids once inside cells
• Also causes fat deposition by stimulating lipogenesis in adipocytes and in the liver

Other hormones affecting blood glucose level: (all of them increase blood glucose level)
• Glucagon
• Catacholamines: epinephrine and norepinephrine
• Glucocorticoids: most important being cortisol
• Somatotrophin: a pituitary hormone
Precautions for diabetic patient going for surgery? How to prevent intraoperative hypoglycemia?
• Patients with diabetes must be prioritized in the operating list
• Routine overnight admission is not necessary
• Starvation time should be no more than one missed meal
• Analgesia and anti-emetics should be used to enable early return to diet and usual insulin regime
• Insulin infusions should only be used if a patient is expected to miss more than one meal
• 0.45% sodium chloride with 5% glucose and 0.15% or 0.3% KCl is the recommended IV fluid
• Capillary blood glucose should be measure hourly during and after the any surgical procedure
• The WHO surgical safety checklist should identify all diabetic patients
• The target blood glucose should be 6-10 mmol/ L (acceptable range 4-12 mmol/ L).
Immediate and late post-operative complications?

Immediate:
• Hyper or hypoglycemia
• Dehydration with electrolytes imbalances
• Hyperglycemic hyperosmolar syndrome
• DKA
Late:
• Infection
• Sepsis
• Impaired wound healing
Post-operatively, who you will involve in care of this patient?

Endocrinologist
What do you think this patient might need if his DM not well controlled on oral medications?
Conversion to insulin therapy

Hypotension in Pregnant Lady
Benefits and risks of this patient undergoing this operation? SCENARIO:
Benefits: 34 weeks pregnant undergoing open
• Control of infection which may lead to sepsis and induction of cholecystectomy for necrotizing
pre- term labor cholecystitis, BP is decreasing, HR is
Risks: decreasing, reversed Trendelenburg
• Pre-term labor position, combined GA, epidural, the
• IUFD operation is taking longer duration than
• DVT (long duration) expected

• Neonatologist (in case of pre-term labor)
• Obstetrician
• ITU registrar
• Anaesthetist
Where to manage this case postoperative?

Obstetric HDU
Why blood pressure is decreasing?

• Compression of IVC by the uterus which will decrease the venous return which will decrease preload thus
decreasing the cardiac output
• Reversed Trendelenburg position
• Sepsis from necrotizing cholecystitis
Simple measure to increase BP?

Repositioning to lateral, pulls the gravid uterus to the left side (away from IVC). Raise patient’s leg → ↑VR
Pre-load?
• It is the end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions
Or
• The amount of myocardium that has been stretched at the end of diastole
Shock?
Shock is circulatory failure resulting in inadequate organ perfusion, e.g. cannot meet the metabolic demands.
What will be the body response to decreased blood pressure?

The autonomic response is due to decreased venous return (preload) which causes a drop in cardiac output and arterial
pressure by the Frank–Starling mechanism
• Reflexes:
o Baroreceptor: stimulates sympathetic activity producing a compensatory tachycardia, increased stroke
volume and peripheral vessel constriction (↑ SVR). This increases the cardiac output and maintains
blood pressure.
• Hormones:
o Catecholamines: the adrenal medulla is stimulated by pain and injury and releases hormones to cause
peripheral vessel constriction, e.g. noradrenaline (↑ SVR)
o Mineralocorticoids: the adrenal cortex releases hormones to stimulate salt and water retention, e.g.
cortisol to increase the blood pressure
The reduction in the circulating volume, and increased sympathetic activity, stimulates renin release
from the macula densa of the juxtaglomerular apparatus of the kidney, e.g. renin–angiotensin–
aldosterone (RAA) cascade. A resultant increase in salt and water retention helps to restore circulating
volume over several hours.
What is the physiological response to standing up?

Standing up leads to pooling of blood in the peripheries and hence decreases VR to the heart. By Starling’s law, this
results in a temporary reduction in CO. As BP = SVR * CO, this leads to a reduction in BP. This fall in BP is sensed by the
baroreceptors in the aortic arch and carotid sinus, leading to a reflex constriction of the arterioles and capillaries. This
increase in SVR results in a normalization of the blood pressure. Sympathetic stimulation caused by the fall in CO also
results in a reflex tachycardia. In addition, the increase in sympathetic drive causes an increase in contractility.

Baroreceptors?
• Mechanoreceptors located in the carotid sinus and in the aortic arch.
• Their function is to sense pressure changes by responding to change in the tension of the arterial wall.
• Supplied by sinus nerve of Hering, which is a branch of cranial nerve IX (glossopharyngeal nerve).
Factors affecting venous return?

• Muscle contraction: Contraction of limb muscle (walking, running, swimming) promotes venous return by the
muscle pump mechanism.
• Decreased venous compliance: Sympathetic activation of veins decreases venous compliance, increases central
venous pressure and promotes venous return indirectly by augmenting cardiac output through the Frank-
Starling mechanism, which increases the total blood flow through the circulatory system.
• Respiratory activity: During respiratory inspiration, the venous return increases because of a decrease in right
atrial pressure.
• Vena cava compression: An increase in the resistance of the vena cava, as occurs when the thoracic vena cava
becomes compressed during a Valsalva maneuver or during late pregnancy, decreases return.
• Gravity decreases venous return
Can you name some devices used in mechanical DVT prophylaxis may be used to improve circulatory parameters in this
patient?
Intermittent pneumatic compression devices, TEDS (thromboembolic deterrent stockings)
What can be done to improve the preload of this patient?

Fluids, inotropic and vasopressor agents
Actions of inotropes?
• Adrenergic agonists: adrenaline, noradrenaline, isoprenaline increase the systemic vascular resistance (SVR)
through vasoconstriction, heart rate, stroke volume and resultant cardiac output to increase the systolic blood
pressure
• Dopaminergic agents: (with some adrenergic activity): dopamine, dobutamine, dopexamine increase the heart
rate, stroke volume and resultant cardiac output and contractility to increase the blood pressure, but depending
on dose, decrease the SVR to produce vasodilatation

Pain Management
Define pain? SCENARIO:
Unpleasant Sensory and emotional experience associated with actual or Patient with severe post-operative pain.
potential tissue damage. Drug chart: received only Panadol and
Arcoxia (selective COX2 inhibitor)
What to do after seeing this drug chart?
• Investigate why PRN medications were not given
• File an incident report
How will you manage this patient after this drug chart?
Immediate management:
In the critically ill patient in pain, patient assessment is vital. It should follow the same CCrISP system of assessment as in
any other circumstance.
A. Airway: Start at the beginning by checking that the patient has a patent airway.
B. Breathing: Check the respiratory rate, pattern and depth of breathing. Is your patient’s respiratory function
impaired by inadequate analgesia? Can he or she cough and expectorate properly to avoid problems later?
C. Circulation: Tachycardia should not automatically be assumed to be caused by pain–there is commonly an
underlying cause. A persistent tachycardia or hypertension caused by inadequate analgesia may potentiate the
development of myocardial ischemia, particularly in the patient who is already hypoxemic.
D. Disability: It is important to assess whether the method of analgesia is contributing to the patient’s clinical
deterioration. Particular attention should be paid to the patient’s level of consciousness as decreasing conscious
level is an early indicator of opioid toxicity.
Full patient assessment:
• Chart review: If pain relief is felt to be contributing to the patient’s deterioration, the drug charts should be
reviewed with the following questions in mind:
o Is effective analgesia prescribed?
o Is effective analgesia being given?
o Is the treatment appropriate for this patient?
• History and systemic examination
• Investigations: serial ABG analysis and chest X-rays
• Decide and plan: If pain relief is adequate and the patient is improving then continue and review. If pain relief is
inadequate determine why:
o Is it due to failure of the method of analgesia?
o Is it due to incorrect implementation of the method chosen?
o Is it due to the development of a surgical complication?
• Liaise with acute pain multi-disciplinary team (acute pain services): multidisciplinary acute pain team consisting
of surgeons, anesthetists, nursing staff and pharmacists.
Side effects of opioids?

Adverse Effects with Acute Use Adverse Effects with Chronic Use
• Respiratory depression • Hypogonadism
• Nausea / vomiting • Immunosuppression
• Pruritus • Increased feeding
• Urticaria • Increased growth hormone
• Secretion • Withdrawal effects
• Constipation • Tolerance, dependence
• Urinary retention • Abuse, addiction
• Delirium • Hyperalgesia
• Sedation • Impairment while driving
• Myoclonus
• Seizures

Pain intensity escalation and management
Pain intensity Management
Mild Paracetamol or NSAID
Mild-to-moderate Combination analgesic ± NSAID
Moderate Oral opioid OR combination analgesic ± NSAID
Moderate-to-severe Oral opioid + paracetamol ± NSAID
Severe Parenteral opioid (IV, IM or SC) + paracetamol ± NSAID OR epidural (local anaesthetic ± opioid)
Combination analgesics are a mixture of weak oral opioid and paracetamol
What is the pain pathway?

Pain is transmitted via fast A-delta fibers (sharp pain) and slower C fibers (dull pain) to lateral spinothalamic tract then to
the thalamus
Ascending tracts carrying sensory information from peripheral receptors to the cerebral cortex. A) Dorsal column pathway mediates
touch, vibratory sense, and proprioception. Sensory fibers ascend ipsilaterally via the spinal dorsal columns to medullary gracilus and
cuneate nuclei; from there the fibers cross the midline and ascend in the medial lemniscus to the contralateral thalamic ventral
posterior lateral (VPL) and then to the primary somatosensory cortex. B) Ventrolateral spinothalamic tract mediates pain and
temperature. These sensory fibers terminate in the dorsal horn and projections from there cross the midline and ascend in the
ventrolateral quadrant of the spinal cord to the VPL and then to the primary somatosensory cortex.

Patient controlled analgesia: (PCA)
• It's a syringe pump connected IV to allow the patient to self-administer boluses of morphine
• Overdosage is avoided by limiting both the size of the bolus and the frequency of administration
• A lock-out time is set within which pressing the button again will not result in a bolus of analgesia
• One-way valve preventing backflow of opiates into the infusion chamber which may lead to over dose when
redelivered
Normal dose of morphine (PCA)?

0.5-2 mg bolus
Problems?
• Patient has to be alert and oriented to be able to use it
• Can break down, run out of battery
• Sleep disturbance
• Not suitable for patients who are confused or who are unable to press the demand button for physical reasons.
• Limits patient mobility
Complications of pain?
• CVS:
o Increased HR, BP, and myocardial consumption → MI
o DVT from immobility
• GIT:
o Delayed gastric emptying
o Reduced bowel motility
o Paralytic ileus
• Respiratory:
o Limit chest movements leading to atelectasis, retained secretions, pneumonia
How would you manage his pain initially?

After ABCDE assessment, I will assess the severity of the pain with one of the pain scales then I will consult the Pain Team
if available, if no pain team l will give analgesics according to the WHO analgesic ladder with the regular assessment.
• Non-pharmacological methods: Preoperative explanation and education, relaxation therapy, hypnosis, cold or
heat, splinting of wounds, Transcutaneous Electrical Nerve Stimulation (TENS).
• Pharmacological methods: Simple analgesia (paracetamol), NSAIDs, Opiates, LA (epidural & local infiltration).
Give examples of the opioids in common use. Which agents are synthetic and which ones are non-synthetic?
• Non-synthetic: morphine, codeine (10% of this is metabolized to Morphine)
• Semi-synthetic: diamorphine, dihydrocodeine.
• Synthetic: pethidine, fentanyl.
Why is codeine bad?

• Drowsiness, constipation, itching, nausea, vomiting, dry mouth, miosis, orthostatic hypotension, urinary
retention, euphoria, dysphoria, and coughing.
• Rare anaphylaxis, seizure, acute pancreatitis, and respiratory depression.
• CYP2D6 (cytochrome P450 enzyme) converts codeine into morphine in the liver. Some Patients (Ultra-rapid
Metabolizers) who have high level of CYP2D6 resulting in rapid formation of morphine in them causing life-
threatening intoxication, including respiratory depression requiring intubation, can develop over a matter of
days. Other patients (10%) lack this enzyme, they lose the analgesic effect of codeine (poor metabolizers), but
suffer its side effects

What is the mechanism of action of Paracetamol?
Mechanism of action of paracetamol (acetaminophen) is not completely understood. But it’s generally considered to be
a weak inhibitor of the synthesis of prostaglandins (PGs). However, the in vivo effects of paracetamol are similar to those
of the selective cyclooxygenase-2 (COX-2) inhibitors
Manage paracetamol toxicity?

• Gastric decontamination:
o Gastric lavage, within 60 minutes of ingestion.
o Activated charcoal: 30 minutes to 2 hours of ingestion,
• Acetylcysteine (N-acetylcysteine): Antidote replenishing body stores of the antioxidant glutathione.
• Liver transplant in acute liver failure
Pain scoring systems?

Verbal descriptor scale Is your pain: 0, absent; 1, mild; 2, discomforting; 3, distressing; 4, excruciating
Verbal Numerical rating scale Which number describes your pain: 0, no pain; 10, worst imaginable
Visual Analogue Scale (VAS) No pain to Worst imaginable
Wong-Baker FACES® For children
Functional assessment Can you move? Can you cough?
WILDA: Word to describe, Intensity, Location, Duration, Aggravating/alleviating factors
Examples of Visual Analog Scales (VAS), can also be numbered
Wong-Baker FACES® Pain Rating Scale

Post-Operative Fluid Management
Explain the fluid chart / what is the cause of low UOP? SCENARIO:
Persistent hypotension and tachycardia with 2 fluid challenges and nothing 48-year-old lady presented by
in between. The patient has reduced intravascular volume maybe due to persistent hypotension and tachycardia
inadequate fluid replacement in the peri-operative period. post-operative THR/Hartman’s
procedure, transferred to the ward
Is that adequate? 3pm, hypotensive and tachycardiac
No 70/30 at 2am
Fluid chart: 2X250 ml bolus with small
How would you manage this case? improvement initially
In view of response to previous fluid challenges, I will do more fluid
challenges (250ml bolus or 10ml/kg) and monitor the response SCENARIO:
You are called to surgical HDU to review
Why would you give fluid challenge rather than speeding up the drip? a 60-year-old man who underwent
Because fluid challenge is both diagnostic and therapeutic. Giving fluid anterior abdominoperoneal resection
slowly doesn’t stretch the left ventricle (explain Starling’s law), speeding for the rectum under GA 12-hours-ago.
the drip up doesn’t give information regarding the patient’s CVS response The nursing staff are concerned about
and may not resuscitate the patient quickly. the UOP. Physical examination is
unremarkable. The examiner will give
Formula of fluid challenge? you a fluid balance chart and obs chart.
250ml bolus or 10-20ml/kg, and monitor the fluid responsiveness
The patient is on 2 hours monitoring, is that adequate?

No, he should be monitored hourly
How to manage this patient after fluid challenge / for the remainder of your shift?
• Regular review of the clinical signs for example capillary refill time
• Repeat fluid challenge if necessary
• Maintain high index of suspicion for other problems such as occult hemorrhage
• Leave instructions for nursing staff you contact me if they're concerned
Assuming the patient becomes more hemodynamically unstable and you have given him more fluid. How to assess the
cardiovascular function and patient’s response to therapy?
• Minimally invasive cardiovascular monitoring (arterial line)
o Lithium dilution cardiac output monitoring (LiDCO)
o Pulse contour analysis (PiCCO)
• Transesophageal Doppler
• CVP monitoring (less frequently)
Who to notify, when?

I will notify my consultant when no response to multiple fluid challenges
How blood pressure is calculated?

Blood pressure (BP) is the product of the cardiac output (CO) and the systemic vascular resistance (SVR). The CO is the
product of the heart rate (HR) and stroke volume (SV)
How to increase blood pressure?

Inotropic support and fluids to increase CO, vasopressor agents to increase SVR
Hormonal response to surgery and trauma / What hormones will be secreted to preserve circulation?
Increased Decreased No Change
Growth hormone Insulin Thyroid stimulating hormone
Cortisol Testosterone Luteinizing hormone
Renin Estrogen Follicle stimulating hormone
Adrenocorticotrophic hormone (ACTH)
Aldosterone
Prolactin
Antidiuretic hormone
Glucagon

Where is ADH (vasopressin) produced and what factors stimulate its secretion?
Produced in the hypothalamus then transported, stored and released from the posterior pituitary
Factors stimulating its secretion
• Reduce circulating volume
• Increased plasma osmolarity
• Angiotensin II
Where in the kidney does ADH act?

Collecting duct
Action of ADH
1. Increases the reabsorption of solute-free water by the collecting duct.
2. NaCl reabsorption by the thick ascending limb of Henle thus increasing the concentration of the interstitium
around the loop of Henle, this enhances the nephron’s ability to reabsorb water.
Formation of a concentrated urine when antidiuretic

hormone (ADH) levels are high. Note that the fluid
leaving the loop of Henle is dilute but becomes
concentrated as water is absorbed from the distal
tubules and collecting tubules. With high ADH levels, the
osmolarity of the urine is about the same as the
osmolarity of the renal medullary interstitial fluid in the
papilla, which is about 1200 mOsm/L. (Numerical values
are in milliosmoles per liter.)
By what mechanism does ADH facilitate reuptake of water from the tubular fluid?
It stimulates water reabsorption by insertion of aquaporins (proteins) or “water channels” into the membranes of
collecting ducts. These channels transport solute-free water through tubular cells and back into blood.
Why does the water cross from the tubular fluid into the medulla?
Because of the high osmotic gradient between the tubular fluid and medullary tissue
What is the process by which the medullary tissue becomes hypertonic? / What are the mechanisms by which the kidneys
increase osmolarity in the renal medulla?
Countercurrent multiplier mechanism:
• The descending limb of the loop of Henle is permeable to water but impermeable to solutes, thus water moves
across the tubular wall into the medullary space, making the filtrate hypertonic
• Sodium is actively transported out of the thick ascending limb which is impermeable to water. This creates an
osmotic pressure drawing water from the descending limb into the hyperosmolar medullary space, making the
filtrate hypertonic.
• The countercurrent flow within the descending and ascending limb thus increases, or multiplies the osmotic
gradient between tubular fluid and interstitial space.
It is an efficient way of concentrating the urine over a relatively short distance along the nephron with minimal
energy expenditure
How does aldosterone act to maintain circulating volume?

Stimulates the reuptake of Na+ by acting on the receptor at the junction between DCT and collecting duct.

Actions of renin angiotensin aldosterone system
(RAAS):
Actions of Angiotensin II
• Arteriolar constriction and a rise in systolic
and diastolic blood pressure.
• Acts directly on the adrenal cortex to
increase the secretion of aldosterone.
• Direct effect on the renal tubules to
increase Na+ reabsorption.
• Facilitation of the release of norepinephrine
by a direct action on postganglionic
sympathetic neurons
• Contraction of mesangial cells with a
resultant decrease in GFR
• Acts on the brain to ↓ the sensitivity of the
baroreflex, and this potentiates the pressor
effect of angiotensin II.
• Acts on the brain to increase water intake
and increase the secretion of vasopressin
and ACTH. It does not penetrate the blood-
brain barrier, but it triggers these responses
by acting on the circumventricular organs

Epidural
Differentials?
1. High epidural block SCENARIO:
2. Distributive shock 2ry to epidural Lobectomy using thoracic epidural, now
3. Paralysis of intercostal muscles has hypotension, bradycardia,
4. Paralysis of diaphragm desaturation (SpO2 92%), upper limb
5. Hemothorax or pneumothorax parasthesia, oliguria
6. Post-operative hypovolemic shock
Why patient having bradycardia?

High epidural block → blocking of the cardioaccelerator fibres (sympathetic fibres) from T1-T5 → unopposed
parasympathetic action of the vagus nerve
Management plan?
• Call the operating consultant and anesthesia consultant
• Sit the patient upright
• 100% O2
• Stop any injections in the epidural catheter
• Rule out any concomitant hypovolemic shock
• Epinephrine, phenylephrine, metaraminol (inotropic agents)
• Atropine (chronotropic agent)
Factors affecting epidural efficiency?

• Level of injection
• Dosage
• Type of medications
• Vasoconstrictors
• Posture
• Age, height, weight
Why epidural in this case?

• Longer surgery
• Post-operative analgesia
• Improves outcomes
What levels used for which surgeries?

• T4: Upper abdomen
• T6: Intestinal, gynecology, urology (TUR)
• T10: Vaginal delivery, hip surgery
• L1: Thigh, lower leg
• L2: Foot and ankle
• S2-5: Perineal and anal surgery
How to test the level of the block?

Using temperature sensation (ice packs)
What else besides ice packs?

Ethyl chloride spray
Why we use temperature sensation?

Because of the arrangements of fibers, the motor fibers are the last to be affected
Why temperature not pin-prink?

Painful, bleeding, possible infection

How to differentiate high epidural block from hypovolemic shock?
Epidural Hypovolemia
• Warm and pink peripheries (due to vasodilatation) • Cold, clammy peripheries
• Bradycardia • Tachycardia
Systemic effects of Epidural analgesia?

• Hypotension: due to block of the sympathetic outflow causing peripheral vasodilatation
• Reduced CO due to a reduction in the VR
• Attenuation of the surgical stress response
• Reduction of FRC
• Reduction of post-operative DVT: due to a number of causes including the concomitant use of IV fluids used to
support the arterial pressure.
Who would you involve besides anaesthetist?

Operating consultant
What signs and symptoms would tell you patient is getting worse?
• ↓ BP
• ↓ HR
• ↓ O2 Saturation
• Paresthesia
• Oliguria
What would tell you he’s getting better?

Nutrition / Surgical Feeding Options
SCENARIO 1:
A critically burnt ill patient is in ITU and requires nutrition. In this station you will be asked the physiology of nutrition
and its clinical application.
SCENARIO 2:
Lady with Crohn’s went for ileocecal resection. On POD4 there was anastomotic leakage, defunctioning ileostomy
was done
“This is an AP chest radiograph of an adult male/female. The

chest x-ray view is adequate and the NG tube cannot be seen
“This is an AP chest radiograph of an adult male/female. The
bisecting the carina and is above the midline to the level of the
chest x-ray view is adequate and the NG tube can be seen
diaphragm. The tip of the nasogastric tube is also not visible
bisecting the carina and remaining in the midline to the level of
below the diaphragm. I can confirm that this tube is not in a safe
the diaphragm. The tip of the nasogastric tube is visible below the
position to commence feeding”
diaphragm and is at least 10cm beyond the gastro-oesophageal
junction. I can confirm that this tube is in a safe position to
How to confirm correctly placed NG tube?
commence feeding”
According to NICE guidelines (CG32)
• Measuring the pH of aspirate using pH indicator
strips/paper
• Radiography (chest x-ray)
Methods which should be NOT be used for confirming NG tube position include
• Auscultation of air insufflated through the feeding tube (‘whoosh’ test)
• Testing the acidity/alkalinity of aspirate using blue litmus paper
• Interpreting the absence of respiratory distress as an indicator of correct positioning
• Monitoring bubbling at the end of the tube
• Observing the appearance of NG tube aspirate

What does AXR show?
Small bowel dilatation (stack-of-coins appearance)
What may be the cause in this patient?

Stricture due to Crohn’s
Feeding options? Methods of feeding?

• Parenteral e.g. TPN, PPN
• Non-parenteral (enteral)
Types of enteral (non-parenteral) feeding?

• Oral
• Nasogastric
• Naso duodenal
• Naso jejunal
• Percutaneous endoscopic gastrostomy (PEG)
• Jejunostomy
Advantages and disadvantages of naso-jejunal tube?

Advantages
• Bypass the Stomach
o less liability to pneumonia
o Avoids gastric phase of stimulation
o Doesn’t stimulate pancreatic secretions
o Feed delivered directly to the intestine
thus maintaining mucosal integrity
Disadvantages
• Needs endoscopic guidance for placement
• Smaller in diameter (more prone to kinking)
Complications of enteral feeding?

Tube related:
• Kinking
• Misplacement
• Injury
• Migration
• Blockage
• Infection (sinusitis)
• Aspiration pneumonia
Feed related:
• Diarrhea
SBO showing stack-of-coins appearance due to the plicae circulares
• Nausea
that extend across the entire bowel in contrast to the haustra of the
• Vomiting colon
• Aspiration
• Refeeding syndrome
• Fluid & electrolyte imbalance
• Deranged liver functions
Complications of parenteral feeding?

(see below, complications of TPN)
What is refeeding syndrome and cause behind it?

It is a metabolic disturbance which occur on feeding a person following a period of starvation. The metabolic
consequences include:
• Hypophosphataemia
• Hypokalaemia
• Hypomagnesaemia
• Abnormal fluid balance
See part A notes Post-op management and Critical Care Chapter

Patients at high risk for refeeding syndrome?
If one or more of the following: If two or more of the following:
• BMI < 16 kg/m2 • BMI < 18.5 kg/m2
• Unintentional weight loss >15% over 3-6 months • Unintentional weight loss > 10% over 3-6 months
• Little nutritional intake > 10 days • Little nutritional intake > 5 days
• Hypokalaemia, Hypophosphataemia or • History of: alcohol abuse, drug therapy including
hypomagnesaemia prior to feeding (unless high) insulin, chemotherapy, diuretics and antacids
How to prevent refeeding syndrome?

• Start at up to 10 kcal/kg/day increasing to full needs over 4-7 days
• Start immediately before and during feeding: oral thiamine 200-300mg/day, vitamin B co strong 1 tds and
supplements
• Give K+ (2-4 mmol/kg/day), phosphate (0.3-0.6 mmol/kg/day), magnesium (0.2-0.4 mmol/kg/day)
Signs of malnutrition? Patients identified as being malnourished?

Patients identified as being malnourished
• BMI < 18.5 kg/m2
• Unintentional weight loss of > 10% over 3-6/12
• BMI < 20 kg/m2 and unintentional weight loss of > 5% over 3-6/12
AT RISK of malnutrition
• Eaten nothing or little > 5 days, who are likely to eat little for a further 5 days
• Poor absorptive capacity
• High nutrient losses
• High metabolism
Indications of TPN:
General critical illness:
• Severe malnutrition (> 10 % weight loss)
• Multiple trauma
• Sepsis with MOF
• Severe burns
Gut problems:
• Short bowel syndrome (short gut)
• Enterocutaneous fistula
• Bowel obstruction
• IBD
• Radiation enteritis
Routes of TPN administration?

Central line or PICC
Types of electrolytes in TPN?

• Sodium chloride
• Calcium chloride
• Potassium chloride
• Magnesium chloride
Components? / TPN ratio of CHO, protein & fat?

Water, carbohydrates (50%), lipids (30%), proteins, vitamins, nitrogen, trace elements
How it is given?
• In a central line because of high osmolarity (must be < 900 mOsm/L)

Complications?
Line related:
• Infection; sepsis, thrombophlebitis
• Thrombosis
• Pneumothorax
• Hemothorax
Feed related:
• Fluid overload, overfeeding
• Electrolyte imbalance, Hyperchloremic metabolic acidosis (if there is an excess of chloride)
• Hyperlipidemia
• Hyperammoniemia, e.g. if there is liver disease, or a deficiency of L-glutamine and arginine
• Essential fatty acid deficiency
• Hypo and hyperglycemia
• Ventilatory problems due to excess production of CO2 if too much glucose is used in the mixture. In the
ventilated critically ill patient, the amount of glucose given in 24 hours may have to be restricted to 5g/kg
• The most potent risk is that of the re-feeding syndrome, particularly in the chronically malnourished.
• Gut atrophy: due to the absence of trophic signals released in response to luminal nutrients, during regular
feeding which will lead to bacterial translocation
Nutrition Monitoring?
NICE Guidelines
• Weight: daily if fluid balance concerns, otherwise weekly reducing to monthly
• BMI: at start of feeding and then monthly
• If weight cannot be obtained: monthly mid arm circumference or triceps skin fold thickness
• Daily electrolytes until levels stable. Then once or twice a week.
• Weekly glucose, phosphate, magnesium, LFTs, Ca, albumin, FBC, MCV levels if stable, 2-4 weekly Zn, Folate, B12
and Cu levels if stable
• 3-6 monthly iron and ferritin levels, manganese (if on home parenteral regime)
• 6 monthly vitamin D
• Bone densitometry initially on starting home parenteral nutrition then every 2 years
From which sources may the energy requirements be satisfied? How much energy does each of these provide?
The predominant sources of energy are from carbohydrates and lipid, but protein catabolism also yields energy
• Fats provide 9.3 kcal/g of energy
• Glucose provides 4.1 kcal/g of energy
• Protein provides 4.1 kcal/g of energy
What are the disadvantages of using glucose as the main energy source?
The problems of glucose are
• Glucose intolerance: as part of the stress response, critically unwell patients are often in a state of
hyperglycemia and glucose intolerance. Therefore, if glucose is the only source of energy, patients will not
receive their required daily amount due to poor utilization of their energy source
• Fatty liver: the excess glucose occurring as a consequence of the above is converted to lipid in the liver, leading
to fatty change. This may derange the liver function tests
• Respiratory failure: the extra CO2 released upon oxidation of the glucose may lead to respiratory failure and
increased ventilatory requirements
• Relying solely on glucose may lead to a deficiency of the essential fatty acids.
Therefore, ∼ 50% of the total energy requirement must be provided by fat.

Pre-Operative Aortic Stenosis
Pathophysiology of aortic stenosis, what are the problems you might face? SCENARIO:
Patient has a fixed cardiac output → limited coronary blood supply → Elective TURBT, patient has history of
cannot respond to decreased afterload which may occur with anesthesia
aortic stenosis
or blood loss
How to calculate coronary perfusion pressure?

Coronary perfusion pressure = systemic diastolic arterial pressure - LVED pressure
Clinical picture of aortic stenosis? Split S2:

Symptoms: It is caused when the closure of the
• Syncope aortic valve (A2) and the closure of the
• Anginal pain pulmonary valve (P2) are not
synchronized during inspiration. In a
• Dyspnea
healthy person, A2 is followed by P2.
• Paroxysmal nocturnal dyspnea
Paradoxical splitting:
• Orthopnea
Reverse of normal physiology, splitting
Signs:
of second heart sounds during
• Pulsus alternans
expiration, singular during inspiration
Reduced/Low • Narrow pulse pressure
• Paradoxical splitting of S2
• Ejection Systolic murmur (right 2nd IC space on right sternal border)
Examiner will give you ECG, ID?

+ve lead 1, +ve lead aVL
-ve lead 2, -ve lead aVF
Left axis deviation = left ventricular hypertrophy
How to calculate HR based on this ECG?

300 / no. of large squares between two R-R intervals
What are the complications of aortic stenosis?

• LVH
• HTN
• CHF
• VT, VF
• Angina
Investigations?
2D echocardiography
What to do?
• Inform the consultant and the anaesthetist
• Cancel the operation
• Call the operating theatre to cancel listing
• Explain to the patient
• Discuss in MDT

If this patient had a bladder cancer, will you proceed to bladder surgery or valve surgery first?
This will depend on the severity of aortic stenosis:
Normal aortic valve surface area is 2.5-3.5 cm2
< 1cm2 = severe stenosis = transvalvular gradient > 40 mmhg
If the operation was cancelled, what are you worried about?

Spread of cancer
If you proceed to surgery?

Preoperative antibiotics for prophylaxis against infective endocarditis (according to NICE guidelines)

Atrial Fibrillation + Rupture Viscus
SCENARIO: Elderly gentleman has abdominal pain, looks confused. CXR and ECG inside the cubicle.
You are shown a CXR + ECG
What are the items to be commented on a chest x-ray?

‘Pam Found Peter’s Rubber In A CHEST’
Patient details Check that it is the correct patient's film, noting their name, hospital number, age, sex & ethnic
background.
Film details Check the date & orientation of the film & describe the projection.
(date, The preferred projection for the CXR is posterior-anterior (PA). X-rays travel in a posterior-anterior
orientation, direction. The plate is positioned close to the front of the patient with their arms elevated around
additional info) the plate, thus removing the scapulae shadows from the film
An anterior-posterior radiograph (AP) is taken when the patient is too unwell or unable to stand.
The plate is behind the patient & the x-rays travel in an anterior-posterior direction, thus
magnifying mediastinal structures. The scapulae overlie the chest
Look for additional markers to indicate how the film has been taken e.g. supine, portable or semi-
erect.
Penetration The vertebral end-plates of the mid-thoracic vertebrae should be just visible behind the heart.
Rotation The medial ends of the clavicles should be equidistant from the spinous processes of the vertebrae.
Inflation Count 6-8 anterior ribs in the mid-clavicular line.
Air Check for air under the diaphragm, pneumothoraces & subcutaneous emphysema.
CHEST Examine both lungs (remember they extend behind the heart & diaphragms) & follow their
contours, paying attention to the apices & costophrenic angles. Look for asymmetry & compare
each side. Check that the domes of the diaphragm & heart borders are not obscured by adjacent
lung pathology. Check for pleural effusions.
Cardiac & Follow the structures of the cardiomediastinal contour. The heart borders should be easily traced &
Vessels distinct. The cardiothoracic ratio should not be >50% (a measurement from the widest diameter of
the heart to the widest diameter of the thoracic cage).
Hila The left hilum is normally slightly higher than the right hilum. There is increased density at the hila
with soft tissue masses, commonly lymphadenopathy e.g. lymphoma, sarcoid & TB.
External devices Chest drain, CVP line, ECG leads, ETT, foreign body, NGT, oxygen mask & tubing, pacemakers,
/ objects penetrating object, pulmonary artery catheter, sternotomy wires, valve replacement etc.
Skeleton & Soft Review the bones & soft tissues, checking for rib fractures & bony metastases. Follow the outline of
tissues both scapulae & evaluate both breast shadows in females.
Trachea Check the trachea is central; it will be deviated towards a collapsed lung or tumor. It will be
deviated away from a tension pneumothorax or large pleural effusion.
Identify the pathology in CXR?

Air under the diaphragm

Identify the pathology in ECG?
AF
Why?
• Irregular rhythm
• There are no p waves
Count the heart rate in ECG?

Since the HR is irregular:
Count the number of QRS in 30 blocks (6 seconds) and multiply it by 10 (or number of QRS in 10-second strip x 6)
Why it is different from HR recorded by the automatic machine?

Because automatic machine cannot measure irregularity (because AF causes inadequate heart contraction resulting in a
small volume pulse)
What is the cause of AF in this patient?

• Hypokalemia
• Sepsis
Management of AF?
1. Cardioversion: chemical (amiodarone), DC shock
Give 300 mg of amiodarone in a large vein over 10–20 minutes and repeat the shock, followed by 900 mg over
24 hours
2. Anticoagulation: unfractionated heparin 70 units/kg as a bolus then 15 units/kg/h till adjusting APTT to 40-60
seconds
Differentials of perforated viscus?

• Ruptured diverticulum
• Perforated DU
• Ischemic bowel
• Necrotizing enterocolitis
Other causes of abdominal pain in this age group?

MI
How to consent in such case?

Since the patient is confused, I will proceed for the operation for the patient’s best interest with signatures from 2
consultants on the consent.

Ruptured AAA / Hypothermia
On entering the station, you are given a chart (shows hypothermia) SCENARIO:
Define perioperative hypothermia? 66-year-old woman undergoing
Perioperative hypothermia: Under anesthesia hypothermia is defined as a laparotomy for rupture AAA. Prolonged
core temperature less than 36°C.
surgery and blood loss of about 4L.
Core temperature has dropped to 35°C.
How to measure core temp?
Oral, axillary, tympanic membrane, rectal, esophageal
Risk factors?
• Major surgery
• Exposed surgery
• Massive blood transfusion
• Combined general and regional anesthesia
• Preoperative temp less than 36°C
Etiological factors for perioperative hypothermia?

• Increased heat loss through radiation to cold objects in theatre
• Increased heat loss through evaporation from body surfaces and open cavities.
• Increased heat loss by direct transfer of heat to operating table and cold infusion fluids (conduction)
• Massive blood transfusion
• Blood loss (hypovolemic shock)
• Anesthesia
o Cooling effect of cold anesthetic gases.
o Hypothalamic function altered by anesthetic agents decreasing heat production.
o Abolished behavioral responses (shivering).
o Reduced muscle activity.
o Reduced metabolic heat production.
Mechanisms/Ways of heat loss?

• Radiation (50%)
• Evaporation
• Conduction
• Convection
In this case
Conduction - direct transfer of heat to
operating table and cold infusion fluids
Convection - by warming of the cool air
around the patient
Evaporation - open abdominal wound
Radiation - by radiation to other cold bodies
in the theatre, compounded by
vasodilatation caused by anesthesia.
Give one potential intraoperative problem that may arise as a result of hypothermia in this patient?
Coagulopathy, cardiac arrhythmia and myocardial ischemia
Complications of hypothermia?
• Cardiovascular: decreased cardiac output (anaesthetized), arrhythmias, vasoconstriction, ECG abnormalities
(increased PR interval, wide QRS complex)
• Respiratory: increased pulmonary vascular resistance and V/Q mismatch, decreased ventilator drive. Increased
gas solubility
• Renal: decreased renal blood flow and glomerular filtration rate, cold diuresis.
• Hematological: reduced platelet function and coagulation, increased fibrinolysis, increased hematocrit, left shift
of oxygen dissociation curve.
• Metabolic: reduced basal metabolic rate, metabolic acidosis, insulin resistance, hyperglycemia.
• Gastrointestinal / hepatic: reduced gut motility.
• Neurological: reduced cerebral blood flow, impaired conscious state leading to coma.

How to prevent these complications?
NICE guidelines: (see: https://www.nice.org.uk/guidance/cg65/chapter/Recommendations)
• Avoid prolonged fasting
• Do not do induction unless core body temp is 36 .0°C
• Avoid prolonged surgery
• Theatre temp. Is maintained at 21°C
• Bair Hugger™ System (patient warming device)
• Warm IV and irrigation fluids are used
• Patient exposed only as needed
• Postoperative the patient should not leave the recovery room to the ward until core temp is above 36 .0°C
Types of blankets used in hypothermia

• Space blankets
• Blizzard blankets
• Wool blankets
• Heat pockets
Space blanket 3M® Bair Hugger™
Definition of DIC?
It is a pathological consumptive coagulopathy due to activation of the coagulation and fibrinolytic systems, activation of
the latter leads to formation of micro thrombi in many organs with the consumption of the clotting factors and platelets.
Characterized by:
• Widespread hemorrhage
• Thrombocytopenia, decreased fibrinogen, increased FDPs
Pathophysiology of disseminated intravascular coagulation.

Cause of DIC in this patient?
Severe hemorrhage, massive blood transfusion, hypothermia
Treatment of DIC?
FFP, platelets, cryoprecipitates
What else can assist in correcting this patient’s bleeding?

• Actively warm the patient (fluid warmer, Bair Hugger®)
• Consider agents such as tranexamic acid

Hematology consultant
Anesthesia consultant
Indications of platelet transfusion?

Platelet loss, consumption, dysfunction, any cause of thrombocytopenia, e.g. <50 × 10 9, disseminated intravascular
coagulation (DIC) and post-cardiopulmonary bypass.
Shelf life?
5 days
Stages of hemostasis?
1. Vasoconstriction: smooth muscle contraction by local reflexes, thromboxane A2, serotonin released from
activated platelets
2. Platelet activation: adherence, aggregation, plug
3. Coagulation: intrinsic and extrinsic pathway → fibrinogen → fibrin
Summary of reactions involved in

hemostasis. Injury to a blood vessel
exposes collagen and
thromboplastin, recruiting platelets
to the site of injury to form a
temporary plug. Platelets release 5-
hydroxytryptamine, among other
factors, resulting in smooth muscle
contraction and vasoconstriction.
Activation of the clotting cascade in
response to collagen and
thromboplastin activates thrombin,
which converts circulating
fibrinogen to fibrin monomers.
Fibrin monomers polymerize and
are cross-linked and accumulate
with platelets at the site of injury to
form the definitive clot.
How does vascular surgery interfere with each of these 3 phases?

• If surgeon removes section of vessel, vascular contraction will be impaired
• Formation of platelet plug will be impaired by thrombocytopenia and hemodilution
• Fibrin formation will be reduced because clotting factors will be diluted by massive fluid transfusions
Which factors will be deficient in stored blood?

Factor V and VIII

Measures to reduce blood loss intra-operative / Intra-operative measures to reduce need for transfusion apart from
prevention of hypothermia?
• Cell salvage, autologous transfusion
• Hypotensive technique.
• Good hemostasis
What is Autologous blood transfusion?

Recovering blood lost during surgery and re-infusing it into the patient.
What is massive blood transfusion?

Replacement of more than 50% of the patient's blood volume in 12-24 hours
Complications of massive blood transfusion?

• Fluid overload
• Hypothermia
• Electrolyte disturbances: hyperkalemia due to K+ leakage from the stored RBC's, Acid base disturbance
• Hypocalcemia due to chelation of Ca+2 by citrate
• ARDS (TRALI) (Transfusion Related Acute Lung Injury)
• Thrombocytopenia: stored blood has decreased number of functioning platelets
• Coagulopathy: stored blood rapidly loses functions of the labile factors V and VIIIc
• Multi-organ failure
Early post-operative complications of AAA repair?

• Organ failure • Stroke
• Continued hemorrhage • Abdominal compartment syndrome
• Limb ischemia • Bowel ischemia
• MI • Spinal cord ischemia
Coagulation pathways (for reference only)

Pneumothorax + CV Line Insertion
System for reading CXR?
The ABCDE mnemonic is a useful one when trying to ensure that the SCENARIO:
examination of a chest x ray is a systematic one. Iatrogenic pneumothorax following CVP
• Airway line insertion
• Bone
• Cardiac
• Diaphragm
• Equal (lung) Fields
• Gastric bubble
• Hilum and mediastinum
I also have to add the T which stands for Technicals. (see before)
You will be given a CXR, interpret?

Simple/Tension pneumothorax
Is this adequate CXR?

No, cannot see the costophrenic angles
Types of pneumothorax?
Open vs Closed
Simple vs Tension
Primary vs secondary
Difference between tension and simple pneumothorax?

In Tension pneumothorax:
• Trachea and mediastinum is shifted to the opposite side
• Tachycardia, hypoxia
• Emergency situation requiring urgent needle thoracostomy in 4th or 5th ICS anterior to the midaxillary line then
tube thoracostomy in the 5th ICS midaxillary line
• There is continuous entry of air through a one-way valve
Safe triangle of insertion of chest tube?

• Ant: Lateral border of pectoralis major
• Post: Mid-axillary line or anterior border of latissimus dorsi
• Inf: A line drawn from the nipple line backwards
Indications of central line insertion?

• Monitoring of fluid balance and fluid resuscitation
• TPN
• Certain fluids and medications (K+ rich fluids)
• Failed peripheral venous access
• Hemodialysis
• Transvenous cardiac pacing
. centrally acting inatropes
Complications of central venous line insertion? The safe ‘triangle’ is not really a triangle, as the axilla
• Infection cuts off the point of the triangle. Draw a line along
• Thrombosis (DVT), Air embolism the lateral border of pectoralis major, a line along
• Arrhythmias the anterior border of latissimus dorsi, and a line
• Injury superior to the horizontal level of the nipple. The
apex of the triangle is the axilla.
o Perforation of right atrium → cardiac tamponade
o Pneumothorax
o Arterial puncture: hemorrhage, pseudoaneurysm, hemothorax
o Left IJV cannulation: damage of the thoracic duct → chylothorax

NICE guidelines for insertion?
• Insertion under ultrasound guidance
• Post procedure radiograph for:
o Position of the radiopaque tip in SVC just superior to its entry in RA (Right Atrium)
o Pneumothorax
Technique for insertion of central venous line? (IJV)

• Anatomical landmarks: mastoid process, carotid pulse and the depression between the two heads of
sternocleidomastoid immediately above the clavicle.
• Locate:
o Clavicle
o 2 heads of sternomastoid
• In the center of the triangle formed by the previous land marks, palpate the carotid artery and insert the needle
lateral to it.
• The needle is directed at 30ᵒ angle towards the patient in the coronal plane aiming towards the ipsilateral nipple
• Aspirate as the needle advances, once the blood is aspirated, cannulate the vein with Seldinger technique
• Suture the line in place [Rt IJV-12-14cm,Left IJV-14-15cm]
Removal technique?
Head down to prevent air embolism
Indications of removal?
• Cessation of cardiac support through inotrope
• Resolution of acute problem
• Line sepsis
• Discharge home
Sites for inserting a central venous line?

• IJV
• Subclavian vein
• Femoral vein
• PICC (peripherally inserted central catheter)
landmark IJV?
Lateral to carotid artery, between 2 heads of SCM. Insert direction of ipsilateral nipple.
Organism causing infection?

Staph. epidermidis
How to prevent line infection?

• Perform hand hygiene
• Apply appropriate skin antiseptic
• Ensure that the skin prep agent has completely dried before inserting the central line
• Use all five maximal sterile barrier precautions:
o Sterile gloves
o Sterile gown
o Cap
o Mask
o Large sterile drape
• Once the central line is in place:
o Follow recommended central line maintenance practices
o Wash my hands with soap and water or an alcohol-based hand rub before and after touching the line
o Remove a central line as soon as it is no longer needed. The sooner a catheter is removed, the less
likely the chance of infection.

Pulmonary Edema (Fluid Overload)
SCENARIO:
Post-operative patient. Fluid chart + vitals chart inside the station. Patient has taken crystalloids + colloids about 7
liters, 4 liters of them are normal saline, now he is tachycardiac, hypertensive, desaturated, oliguric.
What are your expected physical findings?

• Congested neck veins
• Puffiness of face
• Lung crepitations
• Confusion
Interpret this CXR?

Pulmonary edema, loss of cardiophrenic angle, cardiomegaly
Chest x-ray findings in pulmonary edema?

A. Alveolar edema (bat wing or butterfly)
B. Kerley B lines
C. Cardiomegaly
D. Dilated prominent upper lobe vessels
Why this patient is on high risk of MI?

Tachycardia leads to ↓ diastole time which ↓ coronary filling
Also it ↑ cardiac load
What is the minimal UOP?

In adults, the minimum acceptable urine output is
0.5 ml/kg/h
Can you explain why the patient is oliguric?

• The most common cause is due to the
physiological stress response to surgery
in the first 24–36 hours post-operatively.
This is due to circulating glucocorticoids
and mineralocorticoids inducing salt and
water retention.
• Surgical trauma and various anaesthetic gases also stimulate the release of vasopressin from the posterior
pituitary, stimulating post-operative solute-free water retention.
• Congestive heart failure with low renal perfusion
Explain what are the fluids given to this patient?

Crystalloids and colloids
Amount of Na+ in 0.9 % saline: 150 mmol/L
Amount of Na+ in Hartman's solution: 131 mmol/L
How to manage Fluid overload?

• Lasix
• Morphine
• Oxygen
• Nitroprusside
• Aminophylline
• Rotating Tourniquet
• Inotropic agents.
Daily requirement of Na+ and K+?

• Na+: 1-2 mEq/kg
• K+: 0.5 - 1 mEq/kg

What can be done to prevent this from happening again?
• Insert a CV line, monitoring the central venous line
• Monitoring UOP
• Report to the hospital incident reporting system
• Better training of junior staff.
Management?
• CCrISP, ABC
• Stop all IV fluids
• Commence high flow O2
• IV frusemide
• GTN infusion if systolic BP > 100
• Liaise with ITU registrar [Liaise-communicate]
• Request CXR
• Request ABG, electrolytes
• Request ECG
• Ventilatory support: [CPAP-Continuous Positive Pressure Ventillation]
o Consider non-invasive ventilation in severe APO (CPAP preferred for cardiogenic pulmonary edema)
• Medical management:
o Preload reduction – nitrates e.g. GTN (caution in hypotension), diuretic, IV morphine sulphate
o After load reduction – ACE inhibitor e.g. enalapril 1.25mg IV or captopril 25mg sublingual; ARB
o Ionotropic support – Dobutamine ideal for cardiogenic shock; Dopamine (5- 10mcg/kg/min for
stimulation of β-receptors)

Respiratory Failure / Respiratory Acidosis
How CO2 is transported in the blood? SCENARIO:

1. Bicarbonate (70%): Post-op morphine overdose → dyspnea.
2. Carbaminohemoglobin (20%): between the CO2 and proteins or Received 60% O2
peptides most of which with the globin portion of Hb.
3. Dissolved CO2 (10%)
Examiner will give you a pen and paper and

tell you to write the equation. [CA-C arbonic
𝑪𝑨 𝒊𝒏 𝑹𝑩𝑪 anhydrous]
𝐇𝟐 𝐎 + 𝐂𝑶𝟐 ⇔ 𝑯𝟐 𝑪𝑶−
𝟑 ⇔ 𝑯+ + 𝑯𝑪𝑶−
𝟑
-
HCO3 → diffuses out to the plasma
H+ → binds to Hb
Cl- → diffuses into the RBC
Chloride shift?
Chloride diffuses into the red cell to
maintain cellular balance, as HCO3- moves
out
Examiner will give you an ABG, interpret?

↓ pH, ↑ PCO2, normal bicarb
Therefore, uncompensated respiratory
acidosis
Cause?
Morphine overdose (depresses CNS)
Why still no metabolic compensation?

Kidney takes time to react
Why is bicarb normal?

In acute respiratory acidosis, compensation occurs in
2 steps
• The initial response is cellular buffering that
occurs over minutes to hours. Cellular
buffering elevates plasma bicarbonate
(HCO3−) only slightly, approximately 1
mEq/L for each 10-mm Hg increase in
PaCO2.
• The second step is renal compensation that
occurs over 3–5 days. With renal
compensation, renal excretion of carbonic
acid is increased and bicarbonate
reabsorption is increased.
Type A and type B intercalated cells of the collecting tubule. Type A cells
contain hydrogen-ATPase and hydrogen-potassium- ATPase in the
luminal membrane and secrete hydrogen ions while reabsorbing
bicarbonate and potassium ions in acidosis. In type B cells the hydrogen-
ATPase and hydrogen-potassium-ATPase transporters are located in the
basolateral membrane and reabsorb hydrogen ions while secreting
bicarbonate and potassium ions in alkalosis.

What type of respiratory failure is that?
Type 2 (hypercapnia)
Types of respiratory failure and what are their causes?

Type 1
Ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of
blood to the lungs.
• Pneumonia
• Bronchitis
• PE
• Pneumothorax
Type 2
Caused by inadequate alveolar ventilation; both O2/CO2 are affected.
Defined as the buildup of carbon dioxide levels (PaCO2) that has been generated by the body but cannot be eliminated.
The underlying causes include:
• Increased airways resistance (COPD, asthma, suffocation)
• Reduced breathing effort (drug effects, brain stem lesion, extreme obesity)
• A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis)
• Neuromuscular problems
• Deformed (kyphoscoliosis)
Response mechanisms to hypercarbia?

Elevation in CO2 leads to central acidosis, which stimulates central chemoreceptors and leads to increased respiratory
rate in order to blow off extra CO2.
How morphine act?

By binding to mu receptors on the respiratory center causing respiratory depression
Look at ABG, what do you think of PaO2?

Normal
Why PaO2 is in normal range?

Because FiO2 is 0.6 = 60%
Where to manage this patient?

ITU
Management? (ITU)
• ABC, managed according to CCrISP protocol [CCrlSP-Care of critically ill surgical patient]
• Ensure adequate oxygenation by humidified O2
• Ensure adequate ventilation either noninvasive or invasive (intubation and invasive respiratory support or CPAP)
• Management of the underlying cause
• Morphine antagonist: (Naloxone)
Dose of Naloxone?
0.4 -2 mg IV initially and repeat every 2-3 min if no response, to a maximum of 10 mg
Side effects:
Nausea, vomiting, sweating, tachycardia, abdominal cramps, pulmonary edema, cardiac arrest
ITU admission is indicated for multi-organ mechanical support:

• Respiratory: mechanical ventilation, non-invasive ventilation
• Renal: continuous hemofiltration, intermittent hemodialysis.
• Cardiac: advanced cardiac output monitoring, inotropic support.
• Neurological: intracranial pressure monitoring.

Renal Failure with Hyperkalemia
Bloods: K+= 8, Na+ = 121, creatinine = 700 SCENARIO:
78y, dementia, renal impairment,
Interpretation of labs? history of recurrent UTI, baseline
AKI due to creatinine 250, now developed UTI,
• Obstructive uropathy nausea, vomiting
• Pre-renal due to decreased oral fluid intake due to dementia
This patient had urinary catheter inserted, drained 1500 ml, then 4 L/day, why?
This is the diuretic phase of AKI, which occurs after correction of the cause
Pathophysiology of poly uric phase?

Due to recovery of the glomeruli first with no improvement in distal tubules which will lead to increase in GFR
(increased UOP with dehydration)
Why are uremic patients anaemic?

Uremic patients may develop a normocytic, normochromic anaemia for a number of reasons:
• Deficiency of erythropoietin (most important cause)
• Presence of circulating bone marrow toxins
• Bone marrow fibrosis during osteitis fibrosa cystica
• Increased red cell fragility caused by uremic toxins
Functions of potassium?
Potassium is essential for maintaining proper fluid balance, nerve impulse function, muscle function, cardiac (heart
muscle) function.
Homeostasis of K+?
There are a number of influential factors on serum potassium:
• Gastrointestinal
o Diet: The Western diet may contain 20–100 mmol of potassium daily
• Endocrine:
o Aldosterone: this mineralocorticoid, produced by the zona glomerulosa of the adrenal gland, stimulates
sodium reabsorption in the distal convoluted tubule and cortical collecting duct, through an active
exchange with potassium. It promotes its excretion
o Insulin: stimulates potassium uptake into cells, reducing the serum level
• Renal:
o Acid–base balance: potassium and H+ are exchanged at the cell membrane, producing reciprocal
changes in concentration, e.g. acidosis leads to hyperkalemia. Similarly, alkalosis can lead to
hypokaliemia. Also, renal reabsorption of one causes excretion of the other
o Tubular fluid flow rate: increased flow promotes potassium secretion, one method by which diuretics
may cause hypokaliemia
Action of K+ on the cardiac muscle?

Excess K+ causes the heart to be dilated, flaccid and decreases the heart rate and can block the conduction of cardiac
impulse
Mechanism?
High K depolarizes the resting membrane potential causing it to be less negative which will decrease the
intensity of action potential making the contraction weaker.
What use does knowledge of the cardiac effects of potassium have for surgical practice?
Potassium-rich cardioplegic solutions are used to arrest the heart in diastole to permit cardiac surgery once
cardiopulmonary bypass has been established.
Manifestations of hypokalemia?
• Muscular weakness and cramps
• Lethargy and confusion
• Atrial and ventricular arrhythmias
• Paralytic ileus

Manifestations of hyperkalemia?
• CVS:
o Wide QRS
o Peaked T wave
o Dysrhythmia
o Hypotension
o Sudden death
• MSK:
o Muscle cramps
o Muscle weakness
o Flaccid paralysis
• GIT:
o Anorexia
o Nausea, vomiting
o Diarrhea
o Hyperactive bowel sounds
o Abdominal pain
What is the emergency management of hyperkalemia?

• Immediate ABCDE assessment,
• Implement Continuous cardiac monitoring
• Stop all potassium-containing intravenous fluids, including Hartmann's
• Calcium gluconate (10 ml of 10%) is given IV over 10 min, which provides a short-term cardioprotective effect
but does not decease the serum potassium
• Give 5–10 U of insulin in 50 ml of 50% dextrose IV over 30 minutes, which increases cellular uptake of potassium
• Sodium bicarbonate (50 mmol IV over 5–10 min followed by IV infusion of 1.26% or 1.4% solution at 100 ml/h)
• Hemodialysis might be needed if the potassium is persistently high or if there is severe acidosis (pH <7.20).
• Salbutamol (5–10 g/min by intravenous infusion, or nebulized)
• Calcium arsonium (15 g PO or 30 g PR) can be given to provide longer term potassium depletion
Ethical issues of dialysis of 77y old man with dementia?

• The patient will be unable to give a consent, so i will proceed for dialysis for the patient best interest with two
consultant signatures
• Also I have to involve the staff of his residentiary house, special nurse

Transurethral Resection of the Prostate (TURP) Syndrome
Possible causes / Differential diagnosis? SCENARIO:
• TURP syndrome 74-year-old man underwent TURP under spinal
• Blood loss anesthesia. Procedure took a long time, there was
• Sepsis significant blood loss. Post-op patient is confused,
• MI / Heart failure / Cerebrovascular disease agitated, hypoxic and hypotensive. No new drugs or
• Effects of anesthesia and sedation fluids have been giving since theatre.
• Hyponatremia
Look at the investigations (Hyponatremia, low

Hb and low hematocrit). Why low Hb & HCT?
Maybe dilutional
Mechanisms of hyponatremia?
• ↑ total body water
• ↓ in total body Na+
What is the most likely diagnosis?

TURP
Clinical picture?
• Restlessness
• Confusion
• Blurred vision
• Initial HTN followed by hypotension
• HF
• Pulmonary edema
Causes of hyponatremia in patients TURP /

Definition of TURP syndrome?
Effects of isotonic (A), hypertonic (B), and hypotonic (C) solutions on cell volume.
Dilutional hypotonic hypervolemia due to the
use of glycine rich hypotonic irrigation solution
which will be absorbed/metabolized leading to severe dilutional hyponatremia
(glycine is used instead of saline because isotonic solutions limit diathermy use)
How will you treat this patient with hyponatremia and low BP?
• Hyponatremia here is dilutional, therefore will be treated with diuretic
• Colloids or isotonic crystalloids (Hypertonic saline will cause more sodium overload)
Which diuretics will you use?

Osmotic diuretics (mannitol) to remove water and conserve sodium.
Can also use loop diuretics (furosemide)
Action of furosemide?
Site of action: thick ascending limb of loop of Henle
Mechanism: inhibit Na/K pump thus preventing NaCl absorption, so the distal convoluted tubules tries to preserve Na+
and lose K+
Other diuretics and their mechanism of action?

• Osmotic diuretics: mannitol (osmosis) – large molecules which increase the osmotic pressure in the tubules
resulting in water secretion
• Thiazide diuretics: DCT (inhibit Na reabsorption)
• K+ sparing diuretics: spironolactone (aldosterone antagonist) acts on DCT on Na/K pumps
• Amiloride (binds to Na+ channel at DCT)

Site of action Diuretic Carrier or channel inhibited % of filtered sodium excreted
Ascending limb of loop of Henle Frusemide Na+/K+ 2Cl- carrier Up to 25%
Distal tubule and connecting segment Thiazides Na+ Cl- carrier Between 3 and 5%
Cortical collecting tubule Spironolactone Na+/K+ ATPase pump Between 1 and 2%
Causes of confusion?
• Hyponatremia: cerebral edema
• Hypoxia
• High ammonia: glycine is broken down to ammonia in the liver (glycine toxicity)
Cause of hypoxia?
Pulmonary edema (water overload reduced plasma osmolarity. As a result, there is a shift of fluid out of the plasma into
the tissue)
Where will you manage this patient and why?

HDU, because of significant physiological deterioration which will require monitoring and treatment
What other problems should anticipate in this patient?

• Cardiac arrhythmia because of acute changes in sodium concentration and extracellular osmolarity
• Seizures due to combination of hyponatremia and cerebral edema
• Glycine toxicity
Management?
• ABC according to CCrISP protocol [CCrlSP-care of critically ill surgical patient]
• Stop the operation if ongoing and prevent father irrigation by hypotonic fluid
• Consider intubation according to the consciousness level
• Order ABG and electrolytes
• Correct hypothermia using Bair Hugger®, infusion of warm fluids
• Furosemide to correct fluid overload
• Refer to HDU
• Replacement of sodium but not more than 10 mmol/ day

For transurethral resection of the prostate the
resectoscope is inserted transurethrally. Electric
current is passed through a diathermy loop at the
end of the instrument. The surgeon moves this
back and forth to create a cavity using diathermy
to cauterize as they go. The resultant chips are
washed out of the bladder intermittently
throughout the procedure. A visual image of the
operative field is transmitted through lenses
running in the middle of the resectoscope. Around
this lens, irrigating fluid is instilled and flows out,
washing blood away from the operative field. The
procedure is complete when an adequate channel
has been created through the prostate.


General Questions
Inotrope: drug increases cardiac contractility
Vasopressor: drug increases vasoconstriction, MAP
Both are acting through autonomic nervous system
Receptors acting on
• Adrenergic alpha 1 receptor: (vessel wall, heart) → vasoconstriction, inotropic
• Adrenergic beta 1 receptor: (heart) → inotropic, chronotropic, minimal vasoconstriction
• Adrenergic beta 2 receptors: (vessel wall) → vasodilatation
• D1, D2 receptors: (kidneys) → diuresis
Indications?
• Hypotension refractory to fluid resuscitation
• Low cardiac output states
• Low SVR
Definition of shock?
Inadequate tissue perfusion to meet metabolic requirement
SIRS:
Criteria: (2 or more)
• Temp. > 38 c or < 36
• RR > 20
• PaCO2 < 4.3
• Pulse > 90/min.
• WBC's > 11 or < 4
Sepsis?
SIRS + documented infection
Septic shock?
Sepsis with organ hypo perfusion leading to
organ dysfunction despite fluid replacement
Which inotrope to be used in septic shock?

• Noradrenaline (alpha 1 effect) Splanchnic-viscera
• Dopamine (D1, D2, alpha effect)
How would you monitor?

1. Maintain MAP = 65 mmHg to maintain
end organ perfusion:
o Maintain UOP
o Optimize intra-abdominal
perfusion pressure
2. Monitor blood pressure and heart rate
3. Central venous pressure monitoring
MAP:
Average blood pressure during a single cardiac
Cardiac output is equal to venous return and is the sum of tissue and organ
cycle blood flows. Except when the heart is severely weakened and unable to
(CO x SVR) + CVP adequately pump the venous return, cardiac output (total tissue blood flow) is
determined mainly by the metabolic needs of the tissues and organs of the
Preload? body.
The amount of the myocardium that has been
stretched at the end of diastole

Starling law of the heart?
The force of the myocardial contraction is directly proportional to the myocardial fiber length, so the stroke volume of
the heart (SV) = the volume of blood ejected from the heart during systole is directly proportional to the end diastolic
volume (EDV) = the volume of the blood entering the heart during diastole
Effect of changes in myocardial

contractility on the Frank-
Starling curve. The curve shifts
downward and to the right as
contractility is decreased. The
major factors influencing
contractility are summarized on
the right. The dashed lines
indicate portions of the
ventricular function curves
where maximum contractility
has been exceeded; that is, they
identify points on the
“descending limb” of the Frank-
Starling curve. EDV, end-
diastolic volume.
Control of blood pressure?

Through baroreceptors located in the aortic arch and carotid sinus
BP = CO x SVR
• When blood pressure increases: stretching of baroreceptors → reflex reduction in the vasoconstriction and
reduction in heart rate → decrease in SVR, CO → decrease in BP
• When blood pressure decreases: baroreceptors are less stretched → increase in vasoconstriction and increase
in heart rate → increase in SVR, CO → increase in BP
HDU admission criteria

• Patients requiring support for a single failing organ system
• Patient does not require advanced respiratory support
• Patients requiring more detailed monitoring that can not be provided on the ward
• Postoperative patients who require post-op monitoring for more than a few hours
• Patients being stepped down from ITU
ITU admission criteria?

• Patients requiring or likely to require advanced respiratory support (endotracheal intubation and mechanical
ventilation)
• Patients requiring support for 2 or more failing organ systems
• Patients with a severe chronic impairment of one or more organ system who now require support for an acute
reversible failure of another organ system
• Patients requiring 1:1 nursing care
• Respiratory: ventilation, CPAP
• Renal: hemodialysis
• Cardiac: inotropic support
• Neurological: ICP monitoring

PROCEDURAL
SKILLS
CONTENTS
Ordering A Theatre List ........................................................................................................................................................ 2

Cannulation of an ATLS Patient ............................................................................................................................................ 6
Taking a Blood Culture from an HIV Patient ........................................................................................................................ 7
FNAC ..................................................................................................................................................................................... 8
Debridement of a Contaminated Wound ............................................................................................................................ 9
Suturing of a Wound .......................................................................................................................................................... 10
Knot Tying ........................................................................................................................................................................... 12
Excision of a Nevus ............................................................................................................................................................. 14
Abscess Drainage ................................................................................................................................................................ 17
Scrubbing ............................................................................................................................................................................ 18
Male Catheterization .......................................................................................................................................................... 20
Chest Drain Insertion .......................................................................................................................................................... 24
Airway Management in ATLS Patient ................................................................................................................................. 26
STEPS FOR ALL PROCEDURAL SKILLS
1. Introduce yourself
“Hello, I am Dr … on of the surgical doctors.”
2. Confirm patient’s name and age
“Could you please confirm your name and date of birth for me?”
“Could I check your name, please?”
3. Explain the procedure
“Today I’m going to …”
4. Gain consent
“Is that alright?”
“Can I proceed?”
“Are you okay with that?”
5. WHO checklist (patient, side and procedure)
6. Prepare your equipment
7. Procedure
8. Disposal
9. Patient instructions
10. Documentation
PROCEDURAL SKILLS MO’s MRCS B NOTES (Previously called Reda’s Notes) 1

Ordering A Theatre List
Patient Name Hospital ID DoB Sex Operation Notes

Todd Smalls 67839202 23/03/34 M Right inguinal hernia repair COPD
Sarah Jarvis 40229385 12/12/45 F Laparotomy for diverticular abscess drainage Diabetic on insulin
Alexa Malton 74830204 04/02/54 F Left carpal tunnel decompression MRSA
John Yip 40555403 06/08/73 M Laparoscopic cholecystectomy Nil
Order
1) Strangulated inguinal hernia (COPD patient with a pacemaker)
2) Diverticular abscess (allergic to penicillin and iodine)
3) BKA (IDDM, MRSA and AF)
General principles
• Patients with diabetes go early in the list
This prevents complications of hypoglycemia and allows early return to normal glycemic control. Peri and
postoperative normoglycemia is essential in order to reduce rates of surgical site infections.
• Patients with latex allergies should be considered to be first in the list:
Natural rubber allergies require a clean theatre and time must be given for previous latex “dust” to settle before
starting the case. All latex products must be removed form theatre or clearly labelled.
• Children should be operated on early.
This minimizes distress to the child and the parents.
• Procedure under local anesthesia (minor point)
Some surgeons would put local anaesthetic cases first or last as a professional courtesy to their anaesthetic
colleagues. However, it is also practical to place small local anaesthetic cases between major cases to allow the
anaesthetist to recover the last patient and anaesthetize the next to optimize theatre time.
• Major procedures should be considered to be early in the list
Major procedures and patients for cancer resection should not be cancelled due to time constraints. It is often
best to put these cases first or early on the list.
• Patients with infection go last in the list.
MRSA and C. difficile must go last on a list to prevent cross contamination between patients. If possible, order a
list according to USA NRCS guidelines (Clean, Clean* contaminated, Contaminated, Dirty).
• Clinical Priority
It is important to appreciate the difference in operative priority between emergency and elective procedures.
Life* or limb* threatening conditions must go first on an emergency list.
QUESTIONS
Types of anesthesia in each case on the list?

Discuss with anesthetist
• Inguinal hernia: Regional (spinal) anesthesia because of COPD
• Other cases: GA
What are the current guidelines for perioperative glycemic control in the diabetic patient?
• Patients with diabetes must be prioritized in the operating list.
• Routine overnight admission is not necessary.
• Starvation time should be no more than one missed meal.
• Analgesia and anti-emetics should be used to enable early return to diet and usual insulin regime.
• Insulin infusions should only be used if a patient is expected to miss more than one meal.
• 0.45% sodium chloride with 5% glucose and 0.15% or 0.3% KCl is the recommended IV fluid.
• Capillary blood glucose should be measure hourly during and after the any surgical procedure.
• The target blood glucose should be 6* 10 mmol/L (acceptable range 4 - 12 mmol/L).
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) PROCEDURAL SKILLS

What precautions should be taken in a patient with a pacemaker?
Preoperatively:
• The patient should undergo a pacemaker check where a “passport” containing information on the device
model, date of implant, and reason for implant should be available.
• They should have had a recent review by their pacemaker follow up clinic with information regarding degree of
pacing dependency, extent of any heart failure and any particular safety advice communicated to the
anaesthetic and surgical team.
Intraoperatively:
• The use of monopolar should be strictly limited, and not used near the pacemaker device. Where its use is
unavoidable, it should be limited to short bursts. The return electrode should be placed so that the current
pathway is as far away from the pacemaker as possible.
• The theatre should have cardiopulmonary resuscitation and temporary pacing equipment available.
• The patient’s ECG should be monitored throughout from before induction
What is the difference between bipolar and monopolar diathermy?

• In monopolar diathermy current passes from the active electrode through the tissues being operated on to an
electrode plate on the patient. The current is disseminated thought a larger surface area of at least 70 cm2 than
it originated in, therefore preventing a heating effect at the plate electrode.
• In bipolar diathermy, current passes between the two tips of the active electrodes, therefore only passing
though tissue that lies between the tips. There is no plate electrode
What complications are patients with COPD at risk from?

Patients with COPD have a several fold increase (2.7 - 4.7x) in postoperative complications including atelectasis,
pneumonia, and respiratory failure.
How can you reduce these?

• The risk of pulmonary complications can be reduced though smoking cessation at least 4 - 8 weeks before
surgery and early mobilization following surgery.
• Pre and postoperative respiratory physiotherapy to provide deep breathing exercises, intermittent positive
pressure breathing, and incentive spirometry can help reduce complications.
• Postoperatively, adequate pain relief and an upright position in bed should aim to ensure the patient is able to
cough and that the diaphragm is not splinted.
How would you manage warfarin?

It depends on her current risk;
• If the patient has recently been started on warfarin for AF and the AF is the source of an emboli that has led to
vascular problems in the leg to be operated on, then I would place him in the high-risk thromboembolic
category.
• I would take advice from a consultant hematologist. They might advise that he stop warfarin 4 days before
surgery and commence subcutaneous low molecular weight heparin. This would be withheld the evening before
surgery, and then restarted from 6h after surgery once hemostasis had been achieved.
• I would ensure the INR had fallen to below 1.4 before operating.
General guidelines (you should always check local policy and ask the advice of a hematologist)
• Low Thromboembolic risk
o Stop warfarin 5 days pre-op.
o Restart warfarin post-op as soon as oral fluids are tolerated
• High thromboembolic risk
o Stop warfarin 4 days pre-op and start low molecular weight heparin (LMWH) at therapeutic dose
o Stop the LMWH 12-18h pre-op
o Restart LMWH 6hpost-op (assuming hemostatics is achieved)
o Restart warfarin when oral fluids are tolerated
o Stop LMWH when INR is in range again

What to use in case of iodine allergy?
Chlorhexidine based antiseptic instead
Which antispectic will be used in patient with MRSA?

According to hospital protocol and infection control guidelines
Chlorhexidine instead of
What prophylactic antibiotic in patient with penicillin allergy?

Cefazolin, vancomycin
Colostomy preparation?
• Stoma site marking should be done prior to surgery
• Stoma has to be made within the rectus abdominis muscle, below the belt line, on a flat surface, and easily
visualized by the patient (in this case will be on LIF) , avoid skin creases, bony prominences, scars, drain site
• Involve a stoma nurse and stoma specialist
What antiseptics can be used for skin preparation?

The two main antiseptic agents used for pre-operative skin preparation are:
• Chlorhexidine gluconate (CHG)
• Iodophors (povidone iodine; PI)
They are available in either an aqueous or alcohol-based form. There is limited evidence to suggest that one agent is
better than another.
The new WHO guidelines on prevention of surgical site infections recommend chlorhexidine-alcohol rather than aqueous
povidone-iodine or povidone-iodine with alcohol for surgical skin preparation.

The National Confidential Enquiry into Patient Outcome and Death intervention classification
Target time Expected
Code Category Description Example Scenarios Typical procedures
to theatre location
1 Immediate Immediate (A) Within Next Ruptured aortic Repair of ruptured
lifesaving or (B) minutes of available aneurysm aortic aneurysm
limb or organ- decision to operating Major trauma to Laparotomy/
saving operate theatre – abdomen or thorax thoracotomy for
intervention. “break-in” to Fracture with major control of
Resuscitation existing lists neurovascular deficit hemorrhage
simultaneous with if required Compartment Fasciotomy
surgical syndrome Coronary
treatment. Acute myocardial angioplasty
infraction (AMI)
2 Urgent Acute onset or Within Day time Compound fracture Debridement plus
deterioration of hours of “emergency” Perforated bowel fixation of fracture
conditions that decision to list or Out- with peritonitis Laparotomy for
threaten life, limb operate and of-hours Critical organ or limb perforation
or organ survival; normally emergency ischemia Coronary
fixation of once theatre Acute coronary angioplasty
fractures; relief of resuscitation (including at syndromes (ACS)
distressing completed night) Perforating eye
symptoms. injuries
3 Expedited Stable patient Within days Elective list Tendon and nerve Repair of tendon
requiring early of decision which has injuries and nerve injuries
intervention for a to operate “spare” Stable & non-septic Excision of tumor
condition that is capacity or patients for wide with potential to
not an immediate Day time range of surgical bleed or obstruct
threat to life, limb “emergency” procedures Coronary
or organ survival list (not at Retinal detachment angioplasty
night)
4 Elective Surgical Planned Elective Encompasses all Elective AAA repair
procedure theatre list conditions not Laparoscopic
planned or booked & classified as cholecystectomy
booked in planned immediate, urgent or Varicose vein
advance of prior to expedited. surgery
routine admission admission Joint replacement
to hospital Coronary
angioplasty

Cannulation of an ATLS Patient
Preparations
• Tell the examiner that you would wash your hands prior to setting up your equipment.
• Choose an appropriately sized cannula as indicated by the clinical situation
Color Size Flow Rate Situation
Blue 22G 25 ml/min Slow IV fluids and IV medications in patients with difficult veins
Pink 20G 65 ml/min Maintenance IV fluids and IV medications
Green 18G 110 ml/min Non-urgent blood transfusion / injection of contrast for imaging
Grey 16G 210 ml/min Shocked patients, massive blood loss
Orange / 14G 315 ml/min Shocked patients requiring urgent resuscitation, massive blood loss
Brown requiring urgent blood volume replacement
• Prepare 10mL of 0.9% normal saline flush in a 10mL syringe.
• Introduce yourself and include your full name and grade.
• Ask to check the patient’s identity, “Can I just check you are…. and what is your date of birth?”
• Explain what you are about to do, why and what the complications are.
• The patient must give verbal or implied consent for the procedure.
• Position yourself and the patient and select an appropriate vein. It can often be helpful to allow the patient’s
arm to hang over the side of the bed in order to distend the veins or offer to warm the patient’s hands.
• In general, the veins on the dorsum of the hand should be used and the antecubital fossa should be reserved for
trauma or emergency situations.
Procedure:
• Apply the tourniquet and offer to don two pairs of gloves
for high risk patients.
• Sterilize the skin with an alcohol wipe and allow it to dry.
• Do not re-palpate.
• Check the cannula, apply skin traction and insert cannula
until flashback is seen.
• Flatten off the angle of your approach and advance while
removing the needle.
• Place the needle in the sharps bin.
• If a blood sample is required, it can be taken from the
cannula at this point using a syringe or vacutainer.
• Release the tourniquet and occlude the vein above the
level of cannulation.
• Position the hub on the end of the cannula. Flush with
10ml normal saline ensuring that no resistance is felt.
• Apply the appropriate cannula dressing with the time and
date of insertion written on it.
• Dispose of all equipment into a yellow bag.
• Wash your hands.
• Offer to document date, time and site of insertion in the A The closely fitting cannula is smoothly chamfered distally
onto the needle. B The needle enters the vessel; then hold it
patient notes. steady. C Advance the cannula over the needle. D Withdraw
the needle, leaving the cannula in place.
watch video…
QUESTIONS
What the fluid regimen will you administer?

1 liter of crystalloids over 15 min

Taking a Blood Culture from an HIV Patient
• Wash your hands, introduce yourself and gain permission to take blood.
• Prepare your equipment;
o Gloves
o 2% chlorhexidine 70% isopropyl alcohol wipe
o Tourniquet
o Winged Vacuette® blood collecting set or a needle and syringe
o Sterile gauze
o An aerobic and an anaerobic culture bottle
o A microbiology request form
• Wash your hands again
• Wear an apron, eye protection and gloves
• Once you have chosen vein, make sure you clean thoroughly with the chlorhexidine wipe, and then do not touch the
area again before venepuncture. Allow the skin to dry.
• Flip the tops off the two culture bottles and clean with a fresh chlorhexidine wipe. Allow to dry.
• Insert the bottles into the collection port, or the needle and syringe into the bottle depending on what equipment is
available,
• Inoculate the aerobic bottle first, then the anaerobic bottle, and rotate 180ᵒ to ensure the blood mixes evenly.
• Label the bottles with the demographics, time and date,
• Complete the request form. Send for microscopy, sensitivity and culture.
• Thank the patient and wash your hands.
QUESTIONS
What is the rate of HIV transmission from a needle stick injury?

It is around 0.3% following a needle stick injury from an HIV positive patient
How does this compare to hepatitis B and C transmission?

• Before vaccination the risk of transmission following a needlestick injury from a patient with hepatitis B was
around 30%, but has been reduced significantly by the hepatitis vaccination, obligatory for at risk health care
workers, which is 90-95% effective.
• The risk of hepatitis C transmission is around 1.8%
What should you do if you get a needle stick injury?

• Clean the wound with soap and water.
• Report the incident to your occupational health department or A&E out of hours.
• Another doctor should approach the patient and ask permission to take some blood to test it for HIV, and viral
load, hepatitis B and C.
• They should also take a sample of blood from you for testing.
• Retest again at 6 weeks and 3 months for HIV, HBC and HCV antibodies, and for elevated liver enzymes, which
could indicate hepatitis.

FNAC
Stem
Patient had an excision of a malignant melanoma 6 months ago. Currently presenting with a cystic swelling over the
previous scar. Please do fine needle aspiration and prepare the specimen for cytological analysis.
For this technique we will use a 10ml syringe with a green needle and a vial of
heparinized saline.
• The first step is to draw up a little heparinized saline into the syringe. This is
then drawn up and down the syringe as shown.
• The saline is then expelled, leaving the needle and syringe flushed with
heparinized saline.
• In this specimen, there is a palpable lesion simulating cystic swelling. It is not
common practice to use local anaesthetic for this procedure, but this may be
required if the patient is particularly anxious. It is necessary to obtain some
cells for cytology.
• After cleaning the overlying skin, the needle is passed directly into the lesion.
• Once the tip of the needle is inside the lesion, the plunger is pulled back with
the thumb whilst keeping the syringe and needle in place with the other
fingers.
• Multiple passes are needed through the lesion to collect an adequate
sample.
• The needle is then removed, and you should have a small sample of aspirate
in the green portion of the needle.
• Using a pair of slides, pre-marked with the patient’s details, pass a small
amount of aspirate onto one slide as shown. The other slide is then passed
across the first to form two smears.
• One slide will then be air dried and the other sprayed with a fixing agent.
• The rest of the aspirate can be placed in a pot with some saline, to be spun
down for further analysis. (Cytospin container)
The principle of fine-needle

aspiration cytology. The action of a
syringe holder allows the syringe
and needle to be controlled with one
hand while the other steadies the
lump. Squeezing the handle of the
syringe holder draws out the piston
and exerts a suction effect through
the attached needle.

Debridement of a Contaminated Wound
• Firstly, dirt and debris must be gently removed to expose any underlying tissue damage. It is important to use a swab
on an artery forcep to keep your fingers away from the tissue, as there may be sharp materials concealed in the
wound.
• Use a systematic approach, starting at the centre of the wound and working out to the periphery. Gently sweeping
the debris away shows that there is a lot of dirt in this wound. After an initial washout, forceps may be used to
inspect the wound.
• Any foreign bodies should be removed using the forceps; this should prevent any ongoing infection.
• Deep within this wound, there is a damaged tendon which will need to be repaired at a later stage. Working
systematically around the wound, in an anticlockwise fashion, any devitalized tissue should be identified and
removed.
• The next step is to irrigate the wound with saline. It is the pulsed pressure of the fluid that is important for clearing
the tissues.
• A swab is then used to gently mop out and clear the wound. Any deeper areas of damage should also be irrigated to
ensure that the wound is clear.
• Areas of devitalized tissue must be removed. In general, it is better to remove too much tissue that too little.
• Once the wound is clear, it is important to insert a pack. In this case, a saline wick is gently inserted to hold the
wound open and the tail is trimmed to allow easy removal.
QUESTIONS
When is tetanus toxoid / tetanus immunoglobulin indicated?

There are specific guidelines on tetanus prophylaxis for each hospital but in general wound are considered high risk if
they:
• Are contaminated with farmyard material such as soil or manure.
• Involve the axilla or feet.
• Penetrate into the deep tissues. Are animal or human bites.
• Have large amounts of devitalized tissue.
Status Low Risk High Risk

Full course with Booster < 10 years ago Nil Single Ig
Full course with booster > 10 years ago Booster Single Ig + Booster
No immunization / Unknown Full course of toxoid Single Ig + Full course of toxoid

Suturing of a Wound
You should also ask about the patient's tetanus status, whether they have any allergy and state that you would like to
arrange an X-ray of the limb to check for foreign bodies.
Equipment:
Due to time constraints, the correct equipment is usually provided for you and the patient is already prepared and
draped. However, be prepared to clean and drape the wound if asked.
Equipment that you may require includes:
• Sterile gloves and gown.
• Skin preparation solution (Iodine or Chlorhexidine in alcohol)
• Sterile drapes
• 10ml syringe.
• Needles (1 x 21 and 1 x 25 gauge needles)
• Local anaesthetic (1% Lignocaine).
• Toothed forceps.
• Skin suture.
• Suture scissors.
• Adherent dressing.
• Gauze swabs.
Preparation:
If the equipment is not already laid out for you and the patient is not prepared and draped, first open a wound care pack,
pour some antiseptic solution into the receptacle and open the relevant remaining equipment onto the sterile field. At
this point state the need to wash your hands before donning a pair of sterile gloves.
Local anaesthetic:
Firstly, state that you would like to check the local anaesthetic and its expiry date. Then attach the 21G needle to the
syringe and draw up the desired amount of anaesthetic. Discard this needle into a sharps bin and mount the 25G needle
onto the filled syringe. At this point, if not already done for you, clean the wound using the antiseptic solution and use
the drapes to create a surgical field. Administer the local anaesthetic appropriately around the wound, remembering to
warn the patient before introducing the needle. Introduce the needle in a smooth motion, pull back on the plunger to
ensure you that are not injecting into a vessel, and then slowly administer the local anaesthetic whilst withdrawing the
needle. Repeat this step until the surgical field is anaesthetized adequately. Discard the needle into a sharps bin and
state that you would now leave the anaesthetic to work for at least 5 minutes. Before starting to suture the wound,
always check that the local anaesthetic has taken effect, either using a needle or pinching with toothed forceps.
Closure:
It is most likely that the wound will be a clean, straight incision. If it is not, then state that you would like to debride the
unhealthy wound edges to turn a ‘traumatic wound’ into a ‘clean, surgical wound’ before closing. In this scenario, when
suturing a traumatic wound, it is advisable to use interrupted sutures to close rather than a continuous suture. This is
because if the wound became infected, then not only could the wound discharge between the interrupted sutures, but
individual sutures could be removed to allow drainage, without opening up the whole wound. A suitable suture in this
scenario would be a nonabsorbable, monofilament suture material such as 4.0 Nylon. After suturing, finish by applying a
simple adherent dressing to the wound.
Post-operative instructions & follow up

Once you have finished the procedure, the first thing you should do is discard your sharps into a sharps bin, which will be
provided in the station. At this point the patient may ask you a few questions regarding postop instructions, but you will
appear far more professional if you offer this information without being prompted. Explain that the patient will go home
with some simple analgesia, and that they must seek medical attention if they are concerned about any of the following
signs/ symptoms:
• Increased pain.
• Redness.
• Discharge/blood through the dressing.
• Malodor
• Systemic symptoms (fever/nausea/malaise).
Give the patient the appropriate followup information with regards to when and where the sutures must be removed.

Position of the needle in the holder:
(a) correct;
(b) incorrect— needle holder liable to flatten
the needle;
(c) incorrect— needle held by the bendable
hollow section;
(d) incorrect— needle at an angle.
QUESTIONS
Xylocaine dose (lidocaine 1%)?

3mg/kg (up to 20 ml of 1% concentration)
(see abscess drainage station…)
Lidocaine + Adrenaline?
7 mg/kg
Mechanism of action?
Blocks Na+ channels thus preventing depolarization
If allergic to xylocaine, what to give?

Bupivacaine
Dose of bupivacaine?
0.25% concentration: Inject up to the maximum dose of 175 mg (up to 7ml of 0.25% concentration)
Can the dose of bupivacaine be increased if used with adrenaline?

No
What are the side effects of bupivacaine?

Common: Arrhythmias; dizziness; hypertension; hypotension; nausea; paraesthesia; urinary retention; vomiting
Uncommon: Neurotoxicity
Risk of infection?
• In this scenario, the patient would need at least a single dose of antibiotic.
• If there was a delay in presentation, two further doses would be required post closure.
For the type of antibiotic prescribed, you should follow hospital/ department guidelines where available. In this clinical
scenario a broad-spectrum antibiotic such as Co-amoxiclav is appropriate.

Knot Tying
Tie a braided nonabsorbable simple reef knot

The reef knot consists of two throws: the coming down and going up throw.
watch video…
The siting of sutures. As a rule of thumb, the distance of insertion from

the edge of the wound should correspond to the thickness of the tissue
Interrupted suture technique. being sutured (X). Each successive suture should be placed at twice this
distance apart (2X).
Perform a hemostatic suture for bleeding tissue using a nonabsorbable monofilament suture
You will need to use instruments for this part of station and demonstrate safe handling of the sharp needle.
watch video…
Tie an absorbable braided knot at depth

Though the throws are the same for a reef knot, your hands have to move in the vertical plane to tie at depth.
watch video…
Tying a knot in a cavity. Form the hitches on the surface, so

ensure the thread is sufficiently long.
When tightening a knot within a cavity, you must push

one end in with exactly the force with which you pull the
other end out. If not, you will displace the structure, or
pull off the ligature.

QUESTIONS
What other knots do you know?

• Surgeon's knot
• Granny knot
What is Vicryl is made up from?

Polyglactin
When Vicryl is absorbed?

Within 56–70 days.
How long it holds a tensile strength?

For two to three weeks
This is a true surgeon’s knot. The first half-hitch has
two ‘throws’ or turns. The second is a standard half-
Advantages of braided sutures? hitch; It should be finished off with a third half-hitch
• Greater tensile strength that forms a reef knot with the second half-hitch.
• Better flexibility
How to protect tissues while tying at depth?

• Obtain more light in the field
• Retraction of tissues outside
• Making the knot loose then securing it by pushing it
down by finger
Size of suture material

Metric (EurPh) Range of diameter (mm) USP (‘old’)
1 0.100–0.149 5–0
1.5 0.150–0.199 4–0
Reef knot. The left thread was passed behind the right
2 0.200–0.249 3–0 thread for the first half-hitch, then under it through
3 0.300–0.349 2–0 the loop and taken to the right. The right thread
3.5 0.350–0.399 0 emerges on the left. For the second hitch the new left
thread passes in front of the new right and passes
4 0.400–0.499 1
under it to emerge on the right.
5 0.500–0.599 2
Granny knot. Follow the path of the threads; for the

first half-hitch, the left thread was passed in front of
the right one, then underneath, to emerge in front on
the right side. For the second half-hitch, the new left
thread (the former right thread) is also passed in front
of the new right thread (the former left thread) and
emerges in front on the right.

Excision of a Nevus
• The best way to excise the lesion is using an elliptical incision. The
incision site should be measured to allow enough clearance on either
side of the lesion.
• The two points indicate ideal 2mm clearance margins. This distance is
then multiplied by three to indicate the length of the long axis of the
elliptical incision
• To create this incision, it is most effective to hold the blade in a pencil
grip. Whilst holding the skin taught with your other hand, start the
incision using the belly of the blade. Move the blade along
perpendicular to the skin, smoothly along the line of the ellipse.
• At the edge, it is important to make sure that it forms a smooth V
shape to allow excision of the lesion. Make sure that you have cut
through all of the skin and then proceed to remove the lesion,
dissecting through the subcuticular plane.
• Take care to dissect along the line of the ellipse and not cut into the
skin edge.
• Complete the excision with a smooth V shape, keeping the blade
perpendicular at all times. The lesion is then removed.
• It is now necessary to close this ellipse.
• Sometimes you may find that there is a lot of tension in the mid portion
of the ellipse. In these circumstances, it is helpful to undermine the
subcutaneous tissue away from the skin edges
• To close this ellipse, the best method is to place the first sutures at the
distal edges, then gradually work towards the centre. If you try to start
the closure at the widest part of the wound, you may find it difficult to
bring the edges together.
• Postoperative instructions & follow up Once you have finished the
procedure, the first thing you should do is discard your sharps into a
sharps bin, which will be provided in the station. At this point, the
patient may ask you a few questions regarding post* op instructions,
but you will appear far more professional if you offer this information
without being prompted. Explain that the patient will go home with
some simple analgesia, and that they must seek medical attention if
there are any worrying signs/ symptoms (increased pain, redness,
discharge/ blood through dressing etc.). Give the patient the
appropriate follow* up information with regards to when and where
the sutures must be removed, and that a further clinic appointment
will be posted to them once the results are available from histology
(within 2 weeks)
Elliptical excision of lesions of the skin or attached

to the skin. Above is shown the elliptical shape
enclosing the lesion. It is preferably parallel to the
skin tension lines. Below this is shown the
horizontal defect resulting after removing a
superficial skin lesion, with the specimen below it.
Below this is shown the defect resulting from the
excision of a lesion extending into the
subcutaneous tissues, with below it, the boat-
shaped specimen. At the bottom is shown the
Your wrist and little finger rest on the base, forming a steadying defect following the excision of a possible or likely
bridge while you hold the scalpel to make a precise incision. malignant melanoma, and the specimen with
vertical walls extending down to the deep fascia.

(a) Correct and (b) incorrect way to hold a scalpel.
(a) Correct proportions—3:1 ratio, and (b) incorrect proportions for an ellipse.
Correct incision technique: (a) ‘pen’ grip; (b) 45° cutting angle; (c) perpendicular wound edge.
Incorrect incision technique: scalpel held at an angle to the perpendicular.

Langer's lines Ellipse Incision
They correspond to the natural orientation of collagen
fibers in the dermis and are generally parallel to the
orientation of the underlying muscle fibers.
Langer’s lines. These depict the orientation of the dermal

collagen fibres.
Ellipse excision: (1-3) from one apex, and (4-

6) from the other apex.

Abscess Drainage
• The first step is to make a generous incision at this point. This will result in an immediate release of pus, which
should be cleared away using swabs.
• We are left with a cavity which still contains pus and an overlying linear skin incision.
• It is vital to ensure that the skin incision cannot close over. This can be achieved firstly by making a generous skin
incision. Usually, an elliptical incision should be made
• At this point, a swab is taken, placed in a container and sent for culture and sensitivity tests at the bacteriology lab.
• The next stage is to express the remaining pus using two handed pressure and plentiful swabs to clear away the
exudate. We are now left with a cavity and an overlying cruciate incision. It is sometimes necessary to excise the
edges of necrotic skin tissue further.
• A finger is then inserted into the cavity to break down any loculi, leaving one continuous space. If necessary, the
cavity can be irrigated with saline using either a bladder tipped or standard syringe. On occasion, 3% hydrogen
peroxide can be used to help clean out the cavity.
• A pack must then be inserted into the cavity to keep the ostium open and to absorb any further exudate. Either a
saline wick or an alginate dressing can be used. The pack is loosely inserted, and the wick trimmed, leaving a small
tail to aid subsequent removal.
• The wick will remain in place for about 24 hours and will then be replaced by an alginate dressing.
• When removing the pack, make sure that it is moist, as pulling out a dry dressing will disturb the granulation tissue
forming at the base of the cavity.
• If an alginate dressing is used from the outset, it is important to trim this to match the size of the cavity, as a larger
dressing may cause maceration of the surrounding normal tissue.
QUESTIONS
Trade name and function of alginate dressing?

Sorbsan®, Kaltostat®
Alginate dressings are highly absorbent and suitable for use on exuding wounds, and for the promotion of autolytic
debridement of debris in very moist wounds. Alginate dressings also act as a hemostatic, but caution is needed because
blood clots can cause the dressing to adhere to the wound surface. Alginate dressings should not be used if bleeding is
heavy and extreme caution is needed if used for tumors with friable tissue.
Dose of local anesthetic?

Agent Dose plain Dose with adrenaline
Lignocaine 3mg/Kg 7mg/Kg
Bupivacaine 2mg/Kg 2mg/Kg
Prilocaine 6mg/Kg 9mg/Kg
These are a guide only as actual doses depend on site of administration, tissue vascularity and co-morbidities.
Maximum total local anesthetic doses

• Lignocaine 1% plain - 3mg/kg - 200mg (20ml)
• Lignocaine 1% with 1 in 200,000 adrenaline - 7mg/kg - 500mg (50ml)
• Bupivacaine 0.5% - 2mg/kg- 150mg (30ml)
Maximum doses are based on ideal body weight
1% contains 10mg/ml, 0.5% contains 5mg/ml
Why did you do that incision?

Langer’s lines (see before)
It is vital to ensure that the skin incision cannot close over (see above)
What are the advices you give to the patient?

• You will need daily wound dressings initially, usually carried out by your practice nurse at the GP surgery
• Healing of abscesses can be very slow and drainage wounds may take up to 8 weeks to heal completely.
• If you develop a temperature, increased redness, throbbing or drainage at the site of the operation, please
contact your GP. (also warn about DVT signs and symptoms)
• You can eat and drink as normal. A high protein diet is advised to help the healing process.
• You will also be given a leaflet containing all the important information

Scrubbing
Pre-scrub
• Mention you would be in scrubs with appropriate footwear and a scrub cap.
• Remove any watches or rings (make sure you are not wearing nail varnish!)
• Expose hands and forearms to elbows
• Put out a gown and appropriately sized gloves
• Put on a face mask
• Put a nailbrush on the sink
Scrub
• Scrub time: 5 mins for first scrub of the day and 3 mins for each subsequent scrub (look at a clock!)
• Always hold hands at a higher level than elbows
• Initial pre-scrub – apply surgical detergent, work up a lather then wash hands and forearms to elbow and rinse
from finger* tip to elbow
• Then apply more scrub solution to hands
• Clean each nail under running water with nail stick
• Scrub each nail against palm of opposite hand
• Scrub each finger on all 4 sides - 5 strokes/side
• Scrub back of hand and palm from base of fingers to wrist
• Small overlapping circles are used to scrub from wrist to 2 inches above elbow
• Rinse hands and forearms from fingertip to elbow
Drying
• Lift one of the drying towels up and away from the sterile field
• Dry fingers and hand then dry remainder of the forearm
• Drop towel into bin
• Lift the other towel and dry the other hand and forearm
Gowning and gloving:

• With one hand, pick up the gown and hold by the neck and allow to unfold with arm holes facing.
• Slide arms into sleeves and your assistant will secure at the back
• “Gloving” is performed by the closed or open method
• Hand your assistant the belt tie and turn around to then secure waist belt.

Male Catheterization
General
• Introduce yourself
• Patient Identification
Consent (Explanation, Risks and benefits)

• Explain the procedure in layman’s terms. Indication for procedure. Risks, if not performed. Alternatives. What
the procedure entitles. Complications. Failure (need for alternatives). False passage. Hematuria. Pain (bladder
spasm). Occasional need for monitoring urine output post catheterization (diuresis).
Safety
• Patient history (previous catheterization)
• Allergies
• Contraindications
Equipment
A second examiner may act as an assistant and offer to get a trolley ready for you.
• Basic catheter pack.
• Kidney dish, gallipot, gauze and sterile drape.
• Skin preparation solution (sterile water is acceptable).
• 2 pairs of sterile gloves.
• Appropriate urinary catheter (14 Ch is probably the most appropriate; ensure that it is not a female catheter as
these are shorter).
• 10ml syringe + 10ml water (not saline) if not supplied with catheter.
• Instillagel (anaesthetic, antiseptic lubricant) –minimum 10ml.
• Appropriate catheter bag (large ‘night’ bag or a urometer).
Positioning:
Patient should be as flat as possible to perform the procedure.
Procedure
• Wash your hands
• Prepare your equipment, open catheter, Instillagel® and gloves sterile field with a non-touch technique.
• Pour saline into sterile pot
• Place catheter drainage bag at the end of the bed
• Obtain adequate exposure.
• Cleanse hands with an alcohol-based agent and first pair of sterile gloves.
• Drape the patient
• Use one hand to retract the foreskin using a gauze (as a sling) and clean the foreskin, glans and meatus
(separate swabs for each, using forceps if available).
• Insert Instillagel® into the urethra and wait for 3-5 minutes.
• Change to 2nd pair of sterile gloves.
• Place the kidney dish or collecting dish between the patient’s legs.
• Remove packaging on the tip of the catheter and advance the catheter with the penis held pointing to the
ceiling with gentle traction.
• Pass the catheter all the way to the hilt and wait for urine to drain.
• After urine has started to drain, inflate the balloon with the appropriate amount of sterile water (usually 10mL,
but some such as 3-way catheters require 30mL) and withdraw the catheter gently.
• Replace the foreskin if present.
• Dry and cover the patient before asking them to redress.
• Dispose of the equipment in the appropriate bin.
• Measure the amount of urine draining after an adequate period of time (5 - 10 minutes) and obtain a CSU for
microscopy, culture and sensitivity.
• Document the procedure in the notes

Drape the patient and place a collecting vessel Clean the penis
Insert Instillagel® (sterile gel containing local anesthetic) Advance the catheter tip from its sleeve
Wait for urine to flow into the collecting vessel Inflate the balloon using 10ml of saline

QUESTIONS
What is a catheter?
• It is surgical apparatus. It is a sterile hollow tube that is inserted into the body.
• It may be self-retaining by balloon tip or fixed to skin to prevent dislodgment
• Uses
o to drain “UC”
o or insert into vessel to infuse drugs and fluid
o or as a channel for monitoring device “CVL”
If unable to pass catheter?

• Use adequate LA and Gel
• Consider different size catheter. Larger size maybe easier to insert in BPH – more stiff, easy to push
• Consider coudé tip catheter
• Do USS
• Call urology
Commonest cause of anuria?

Blocked catheter
Other causes
• Urethral stricture
• BPH
• Bladder outlet obstruction or Bladder neck obstruction or bladder stone
• ARF
• Hypovolemia
Commonest cause of blockage?

Gel
What would you do if no urine drains after catheterization?

• Reevaluate presence of urine in bladder by percussing the suprapubic region if you haven't done this already.
• Apply suprapubic pressure.
• Aspirate with a syringe.
• Nothing should be introduced until you see urine
If still no urine
• Consider hypovolemia, give fluid challenge (500 ml / 15 min)
• If no hypovolemia from fluid chart → take out the IC
Why?
• False passage
• Catheter tip in urethral not bladder
• Not a true palpable bladder: suprapubic mass
You insert the catheter; it drains no urine and you therefore remove it. You then examine this patient’s abdomen and
there is a suprapubic mass. What is your differential diagnosis?
• Bladder was not catheterized appropriately
• Malignancy from bladder, prostate or colon
• Pelvic collection, abscess
• Mesenteric cyst
• Large iliac aneurysm

If still anuria with normal US and normal fluid chart?
ARF causes
Pre-renal (decreased renal perfusion)
• Hge
• Dehydration
• Burns
• Sepsis
Renal (nephrotoxic drugs)
• NSAIDs
• ACE - acute cortical necrosis
• Aminoglycosides
• Contrast
Post-renal
• Ureteric & lower urinary tract obstruction
Complications of catheterization?
• Allergies
• Infection UTI, urethritis, pyelonephritis
• Urethral injury

Chest Drain Insertion
Equipment
• Sterile gloves and gown.
• Skin preparation solution (iodine or chlorhexidine in alcohol).
• Sterile drapes.
• 10ml Syringe. Needles (21–25 gauge).
• Gauze swabs. Local anaesthetic (1% or 2% lignocaine).
• Scalpel and No. 11 blade.
• Suture material (1 silk).
• Large hemostat or Spencer* Wells Clamp for blunt dissection.
• Large bore chest tube (24 to 30 French).
• Connecting tubing.
• Closed drainage system (underwater seal).
• Occlusive dressing (sleek tape).
Positioning
• Patients should be supine with 30 o of head up if possible and the bed slightly rotated towards the side of
insertion.
• The patient’s arm should be placed behind their head to expose the axillary area.
• It is essential that the patient undergoes regular hemodynamic observations and pulse oximetry during the
procedure.
Site
• Although variations have been suggested, the 'safe triangle' for insertion of a chest drain has the following
borders:
o Posterior margin Mid-axillary line (some literature states the anterior border of latissimus dorsi to be
the posterior margin but if this is taken as a landmark, then the insertion point will be in the mid-
axillary line where the long thoracic nerve lies).
o Anterior Margin: Lateral border of pectoralis major.
o Inferior margin: 5th intercostal space (above 6th rib).
o Apex: Below the axilla.
• Ideal placement should be just anterior to the midaxillary line within this triangle to avoid damage to the long
thoracic nerve of Bell.
• Blunt dissection should be over the superior aspect of the inferior rib in order to avoid damage to the
intercostal neurovascular bundle.
Anaesthesia
Lignocaine or similar is infiltrated to the skin and periosteum of the superior margin of the inferior rib. There is no
evidence that local anaesthetic with adrenaline reduces the risk of iatrogenic hemothorax. The skin is tested before any
incision is made. Despite local anaesthetic the procedure is poorly tolerated by patients and concomitant anxiolytics or
opiates are recommended by the BTS.
Insertion
• Make a skin incision parallel and just above the rib below, slightly longer than the tube diameter (1 French is ⅓
mm).
• Use a large hemostat or clamp to blunt dissect through the parietal pleura before doing a finger sweep.
• A small clamp can be attached to the end of the tube through one of the holes to guide placement.
• Aim the tube apically for pneumothoraces and basally for hemothoraces.
• Watch for tube fogging to confirm appropriate placement.
• Suture the drain in place with a stay suture and pass a horizontal mattress closing suture but leave this untied.
The end of the closing suture can be covered in sleek or a transparent adhesive dressing with the drain to stop it
coming loose.
Drainage
• A unidirectional closed drainage system such as the underwater seal drain is most commonly used. Connection
tubing is used between the chest tube and underwater drain.
• Before the procedure is completed it is essential to ensure that the fluid within the tube is moving with
respiration (“swinging” or bubbling).
• Post Procedure It is essential to obtain a chest x-ray to ensure appropriate tube placement.

QUESTIONS
Indications for contacting thoracic surgeons?

• A persistent pneumothorax despite drainage may suggest a bronchial tear.
• Hemothorax
• More than 1,500 mL of blood immediately evacuated by tube thoracostomy.
• Persistent bleeding 150 mL/h to 200 mL/h for 2 hours to 4 hours.
• Persistent blood transfusion is required to maintain hemodynamic stability.
Insertion of chest drain: (a) triangle of safety; (b) penetration of the skin, muscle and pleura; (c) blunt dissection of the parietal pleura;
(d) suture placement; (e) gauging the distance of insertion; (f) digital examination along the tract into the pleural space; (g) withdrawal
of central trochar and positioning of drain; (h) underwater seal chest drain bottle.

Airway Management in ATLS Patient
How is the airway assessed clinically?

Assessment is based on the principle of: Look, Listen and Feel.
• Look:
For the presence of accessory muscles of respiration (neck, shoulders, chest and abdomen) being used,
presence of obvious foreign bodies in the airway, facial/airway injury (i.e. Le Forte fractures) and the ‘seesaw’
pattern of complete airway obstruction (NB. central cyanosis is a late sign)
• Listen:
For the presence of inspiratory stridor, as this indicates upper airways obstruction (laryngeal level and above).
Also take note of grunting, gurgling (liquid or semi-solid foreign matter in the upper airways) and snoring sounds
(indicating the pharynx is partially occluded by the tongue or palate). Expiratory wheeze suggests lower airways
obstruction. Crowing indicates laryngeal spasm
• Feel:
For chest wall movements and airflow at the nose and mouth (for 10 seconds)
What techniques of airway management will you do?

Simple measures:
• Basic airway maneuvers: these include chin lift and jaw thrust
o Chin lift:
The fingers of one hand are placed under the mandible in the midline and then lifted upwards to
bring the chin forward
o Jaw thrust:
The angles of the mandible are identified on both sides, the index and middle fingers are placed
behind it and a steady upwards and forwards pulling pressure is applied to lift the mandible (this is
painful, and if a patient tolerates it, consider an anaesthetic review). Finally, the thumbs are used
to slightly open the mouth by downward displacement of the chin
• Basic airway adjuncts: this includes oropharyngeal airway
o Oropharyngeal airway: open the mouth employing basic airway maneuvers. Suction out debris and
insert it upside down (curved side pointing to the palate). Rotate it 180° between the hard and soft
palate and seat the flattened section between the gums and teeth. OPA should be measured so
that it stretches from the corner of the mouth to the angle of the mandible
• Cervical spine control:
Neck collar, sandbag and tape (triple immobilization)
o With the patient in neutral alignment, use your fingers to measure the distance from the top of
the shoulder to the bottom of the chin
o Find the sizing line on the collar and match the collar size to the patient
o Adjust and lock both sides of the adjustable collar by pressing the two lock tabs
o Apply the collar while manually maintaining neutral head alignment; ensuring the chin support is
well under the chin
o Head immobilization with adhesive tape and lateral head support (sand bag)
• Ventilations are delivered at 8 to10 per minute (1 ventilation every 6-8 seconds)
Jaw thrust and chin lift Measuring the oropharyngeal airway

Complex measures:
• Endotracheal intubation: this requires anaesthetic expertise and can be achieved through the mouth
(orotracheal) or the nose (nasotracheal) intubation
• Surgical airway: this requires a cut down through tissues in the neck and can be achieved in three ways
There are three types of surgical airway:
o Needle cricothyroidotomy (and jet insufflations of oxygen)
o Cricothyroidotomy
o Tracheostomy, which may be performed in the emergency or elective setting
What are the indications for a surgical airway?

• Failed intubation, e.g. due to edema
• Traumatic fracture of the larynx
In which anatomic location are the surgical airways sited?

• Both types of cricothyroidotomy are performed through the median cricothyroid ligament. This is the thickened
anterior portion of the cricothyroid membrane that runs between the cricoid and thyroid cartilages.
• A tracheostomy may be placed from the 2nd to 5th tracheal rings
Methods of oxygen delivery

• Nasal cannula
• Simple mask
• Venturi mask
• Non-rebreather mask
Simple Oxygen Mask Non-rebreather Mask
Nasal cannula Venturi mask

EXAMINATION
KNEE EXAMINATION ............................................................................................................................................................................2

HIP EXAMINATION ...............................................................................................................................................................................6
ANKLE EXAMINATION ........................................................................................................................................................................10
Shoulder Examination ........................................................................................................................................................................12
HAND EXAMINATION .........................................................................................................................................................................18
SPINE AND PERIPHERAL NEUROLOGICAL EXAMINATION .................................................................................................................24
FOOT DROP – COMMON PERONEAL NERVE INJURY ........................................................................................................................30
CARDIOVASCULAR EXAMINATION.....................................................................................................................................................34
RESPIRATORY EXAMINATION ............................................................................................................................................................40
CRANIAL NERVE EXAMINATION.........................................................................................................................................................42
CEREBELLAR EXAMINATION ..............................................................................................................................................................48
VARICOSE VEINS ................................................................................................................................................................................50
PERIPHERAL LOWER LIMB ARTERIAL EXAMINATION ........................................................................................................................52
THYROID .............................................................................................................................................................................................54
PAROTID .............................................................................................................................................................................................58
SUBMANDIBULAR GLAND..................................................................................................................................................................59
POST-OPERATIVE ANASTMOTIC LEAKAGE - CCrISP...........................................................................................................................60
ABDOMINAL EXAMINATION ..............................................................................................................................................................62
ACUTE DIVERTICULITIS ......................................................................................................................................................................64
ACUTE CHOLECYSTITIS .......................................................................................................................................................................68
ACUTE APPENDICITIS .........................................................................................................................................................................70
GENERALIZED LYMPHADENOPATHY..................................................................................................................................................71
PARAUMBLICAL HERNIA AND INCISIONAL HERNIA...........................................................................................................................74
INGUINOSCROTAL EXAMINATION .....................................................................................................................................................75
BREAST EXAMINATION ......................................................................................................................................................................79
CHEST PAIN / PULMONARY EMBOLISM ............................................................................................................................................83
ARTERIOVENOUS FISTULA .................................................................................................................................................................85
SUPERFICIAL LUMP / LIPOMA............................................................................................................................................................87
EXAMINATION STEPS SUMMARY / CHECKLIST ..................................................................................................................................89
STEPS FOR ALL EXAMINATIONS (WIPE)

1. Wash hands
2. Introduce yourself, confirm patient’s name
3. Explain Procedure, Ensure Privacy / chaperone (if necessary), Permission (consent)
4. Exposure
5. Reposition
Don’t forget to ask about existing pain before palpation
EXAMINATION MO’s MRCS B NOTES (Previously called Reda’s Notes) 1

KNEE EXAMINATION
Stem Probable findings after examination

Osteoarthritis • Crepitus felt with active and passive movements of the knee joint
• ↓ ROM
Sports injury • Antalgic gait • Locked knee (in flexion)
(non-contact) • Tenderness over the lateral aspect of the knee • + ve Varus stress test
on palpation • + ve McMurray’s test
❶LOOK ❹SPECIAL TESTS

(standing position) 1) Posterior sag sign (PCL)
• Alignment
• Flexion and Hyperextension (from the side)
• Deformities (valgus and varus)
• Scars
• Swelling: pre-patellar / infra-patellar
• Muscle wasting
• Erythema
• Asymmetry
• Baker’s Cyst in popliteal fossa
• Accessories for e.g. walking stick / crutches
• Observe gait: Ask the patient whether he/she uses
any walking aids, then ask him/her to walk across the
room
❷FEEL
(supine position) 2) Anterior and posterior drawer tests
• Ask the patient if there are any areas of localized pain The patient should be supine with knees flexed to 90°.
• Assess temperature The feet are stabilized in a neutral position and the
• Measure quadriceps circumference and compare (10 examiner sits at the forefeet of the patient. Grasp the
cm above patella) knee with both hands; the tip of your thumbs should
be just below the joint line. Then pull the tibia forward.
• Effusion
The amount of anterior translation of tibia and quality
o Cross Fluctuation
of end point is assessed.
o Patellar tap test (large-moderate effusions)
o Milking test
• Palpation
Palpate the following with the knee flexed at 90°:
o Patella – palpate the borders for tenderness /
effusion
o Tibial tuberosity
o Head of the fibula – irregularities / tenderness
o Tibial & Femoral joint lines – irregularities /
tenderness
o Collateral ligaments – both the medial and lateral
o Popliteal fossa – feel for any obvious collection of
fluid (e.g. a Baker’s cyst)
❸MOVE ROM-Rupture of membrane

• ROM: test active and passive flexion and extension
and feel crepitus
• Muscle testing
o Quadriceps
o Hamstrings
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) EXAMINATION

3) Lachman's test (ACL) 5) McMurray’s test (medial and lateral menisci)
The patient is in a supine position. The examiner Patient in supine position flexes the knee as far as
grasps the thigh with one hand and with the other possible. One hand supports the knee in such a way
hand grasps the tibia at the level of the tibial tubercle that the thumb and index finger are on the medial and
and brings the knee to 30° of flexion. The hand on the lateral joint lines respectively. The other hand grasps
thigh stabilizes it. The hand holding the tibia pulls it the foot. To test the medial meniscus, external
forward and the amount of anterior translation of rotation force is applied to the foot, with varus stress
tibia on the femur is measured. to the knee joint to close the medial compartment and
then the knee is passively extended. To test the lateral
meniscus, internal rotation force is applied to the foot,
with valgus stress to the knee joint in order to close
the lateral compartment and then the knee is
passively extended
4) Valgus (MCL) and varus (LCL) stress tests: (MCL)

The patient is relaxed in a supine position. The
examiner holds the leg in his axilla, with the knee in
20° of flexion. With both hands, the tibia is held firmly
in such a way that the thumbs are on either side of the
patellar tendon and the index fingers are placed on
the femoral attachments of the medial and lateral
femoral condyles (Figure 6.29). Then valgus force (for
MCL) and varus force (for LCL) is applied and the
amount of opening is noted.

DISCUSSION
Male patient had a non-contact sporting injury where he twisted his knee. On examination he has an antalgic gait, . His range of
passive movement was not affected, but active movement was limited by pain. He did not have localised joint tenderness. Varus
stress test and McMurray’s test were positive, fitting with lateral collateral ligament and meniscal tear.
Example presentation for 2nd stem

“I’ve examined this patient presenting after a sports injury to his left knee. On inspection, there were no visible swellings, visible
scars, muscle wasting, nor asymmetry. The patient had a limping gait.”
“On palpation, temperature was equal on both sides. There was some tenderness over the lateral aspect of the left knee. No
discrepancy regarding quadriceps circumference in both limbs. The patient didn’t have knee effusions.”
“On testing active and passive movements of the left knee joint, the patient had decreased ROM especially on extension with no
palpable crepitus.”
“Patient had a positive varus stress test, which may indicate the presence of LCL injury. Positive McMurry’s test which may indicate
the presence of lateral meniscal injury as well.”
What is your differential diagnosis?

• Medial collateral ligament tear
• Cruciate injuries
• Combination injuries
• Bony injuries
What investigations would you perform?

Initially I would arrange a weight bearing X-ray of the knee. However, the most important investigation would be a knee MRI.
What to look for in MRI?

• Increased internal signal intensity in the meniscus.
• Abnormal meniscus shape
Management:
Nonoperative
• Rest (with weight bearing as tolerated or with crutches) Ice
• Compression bandaging
• Elevation of the affected limb to minimize acute swelling and inflammation.
Operative:
• Repair or partial meniscectomy
X ray of OA:
There are four main radiographic signs in osteoarthritis:
• Narrowing of the joint space
• Subchondral sclerosis
• Cyst formation
• Osteophyte formation
How is osteoarthritis of the knee managed?

Conservative
• Maintain or achieve a healthy weight i.e. aim to decrease weight, and therefore force, going through a joint
• Regular exercise, with particular attention to strengthening the muscles around the joint. For example, in OA of the knee,
cycling is beneficial
• Analgesia: care to be taken with NSAID's with relation to gastric irritation
• Heat application to the joint may offer relief
• Physiotherapy
• Intra-articular steroids
Surgical
• Arthroscopy and arthrocentesis
• Realignment osteotomy
• Total or partial knee replacement

SUMMARY
Position
Standing (look) then lying on bed (feel, move)
Exposure
Hip to ankle
Discussion
I examined this patient presenting with knee pain…
Gait +/- walking aid & antalgic gait

Skin No scars or erythema
LOOK
Muscle No muscle wasting

Swelling (including back) No swelling, effusion, bursae or baker cyst
Asymmetry No asymmetry
Deformity No visible deformity
Temperature Normal skin temperature

Tenderness Tender lateral aspect of joint (LCL, meniscus)
FEEL
Effusion No effusion
Quadriceps circumference Equal quadriceps circumference bilaterally
Range of motion No limitation of movement (+/- limited flexion and crepitus in OA), (+/- limited extension
MOVE
“locking” in meniscus)
Hyperextension No hyperextension
Cruciate ligaments Intact anterior and posterior cruciate ligaments

TESTS
Collateral ligaments Intact bilaterally (+ve varus stress test in LCL)

Menisci No meniscal injury (+ve McMurray test in meniscal injury)

HIP EXAMINATION

Hip Osteoarthritis Scar, +ve Trendlenbury gait and test, +Thomas test, ↓ RoM
❶LOOK
• Patient Standing
o Facing the patient
▪ Position of shoulders / trunk
▪ Position of ASIS
o Side
▪ Lumbar spine
▪ Buttocks
o Behind
▪ Is the spine straight?
▪ Gait (Antalgic, Trendelenburg, etc.)
o Trendelenburg sign
In a normal individual, the pelvis is pulled up by
the abductors of the weight bearing leg. The
pelvis drops on the unsupported side if the weight
bearing hip is unstable. The patient has to lurch
toward the weight bearing side to shift the center
of gravity over the foot and avoid falling. This is
called Trendelenburg lurch.
To perform the test, face the patient. To assess
the left hip, place your right hand against the left
shoulder (to prevent lurching) and offer your left
hand to give support. Ask the patient to lift his
right leg (opposite leg to the test side) by bending
the knee. In a positive test, the examiner feels
pressure on his supporting hand as the patient
tries to prevent himself from falling over.
• Patient Supine
o Skin, Scars, Swelling
o Wasting
o Limb attitude
Weakness of abductors of the left hip o Limb length
▪ Galeazzi test (differentiates between tibial
and femoral length discrepancy)

❷FEEL ❹SPECIAL TESTS
• ASIS 1) Thomas’ test (test for flexion deformity of the hips)
• Pubic symphysis With the patient in a supine position, the examiner
• GT places his hand under the lumbar spine. Then the
patient is asked to flex both hips as far as possible. The
• Length Measurement
lumbar lordosis is now eliminated, and the examiner
o Apparent (Xiphisternum to the medial malleolus)
feels the lumbar spine pressing on his hand, which is
o True (ASIS to medial malleolus)
under the lumbar spine. The patient is asked to hold
one knee fully flexed with both hands to maintain the
❸MOVE flexion at the hip joint. The other leg is now brought
• Range of movement down to the table. If a flexion deformity is present, the
o Flexion leg cannot reach the table and the angle between the
o Abduction posterior aspect of the thigh and the examination
o Adduction table is read as the angle of flexion deformity
o Rotation
▪ Sectoral sign
o Extension
• Muscle testing
o Iliopsoas
o Gluteus maximus
o Gluteus medius
o Adductors
2) FABER / Patrick’s test
To complete my examination, I would assess the neurovascular

status of the lower limbs and examine the joint above and
below (knee and spine.)

DISCUSSION
Male patient who presents with right sided hip pain. I note that he has an antalgic gait and a scar overlying the left hip suggesting
a previous operation. Positive findings include reduced range of movement in hip flexion, extension and internal and external
rotation on the right. Trendelenburg and Thomas’ test were negative and there was no discrepancy with respect to true or
apparent leg length.
Example presentation
“On inspection, I noted a scar on the right hip joint indicating previous hip surgery. There was no gluteal or quadriceps wasting. No
pelvic tilt. Lumbar lordosis was normal. The patient had Trendelenburg gait. Trendelenburg test was positive, indicating right
superior gluteal nerve injury. “
“On palpating the joint there was no tenderness nor any leg length discrepancy. Thomas test was positive on the left side indicating
fixed flexion deformity. “
“On testing the active and passive movements of the left hip, there was decreased RoM with no crepitus.”
“My main diagnosis would be superior gluteal nerve injury on the right side, with left hip OA causing positive flexion deformity.”

My top differential for this patient with hip pain and reduced range of movement is osteoarthritis.
Other arthritides should be considered. These include
• Rheumatoid arthritis
• Pseudogout, gout
• Inflammatory or infective arthritis
• Reactive arthritis
How would you investigate and manage this patient?

I would take routine bloods, paying particular attention to raised inflammatory markers, which would alert me to possible
infection, and order hip and knee X-rays. If required, an MRI of the affected joint could also be ordered but may be unnecessary.
If this patient had osteoarthritis, then management is aimed at alleviating pain and improving the patient’s functional status. Non-
operative measures include weight loss, exercise, physical and occupational therapy. Simple analgesia such as regular
paracetamol and prn NSAID can be prescribed. More invasive measures such as a corticosteroid injection can be considered, but
ultimately the patient may need surgery in the form of an arthroplasty.

SUMMARY
Position
Standing (look) then lying on bed (feel, move)
Exposure
Lower limbs
Discussion
I examined this patient presenting with hip pain…
Gait Trendelenburg gait, +/- walking aid

Skin No erythema, (+ scar on lateral side for previous operation)
LOOK
Swelling No swelling
Asymmetry No pelvic tilt
Deformity No visible deformity
Trendelenburg test Positive Trendelenburg test (sagging of non-operated side)

Tenderness No tenderness (+/- tender anterior part of OA side)
FEEL
Leg length discrepancy Equal bilateral leg length
Range of motion No limitation of movement (extension in OA side not done due to fixed flexion deformity)
MOVE
Thomas test Positive on non-operated side (fixed flexion deformity)

TESTS
FABER test

ANKLE EXAMINATION

• Antalgic gait, • Restrictive ROM,
Soccer player, sprained ankle
• Tenderness over the lateral malleolus • Positive talar tilt test
❶LOOK
• Gait *
o Is the patient demonstrating a normal heel strike
/ toe off gait?
o Is each step of normal height? – increased
stepping height is noted in foot drop
o Is the gait smooth & symmetrical?
• Swelling / erythema of the foot or ankle – may
suggest injury / inflammatory arthritis / infection
• Scars – suggestive of previous injury / surgery
❷FEEL
Ask the patient to lay on a bed.
• Assess temperature & compare between legs – ↑
temperature may indicate inflammatory pathology • Anterior drawer test (assesses the integrity of the
• Assess pulses in both feet – posterior tibial & dorsalis anterior talofibular ligament).
pedis Patient sitting on the edge of the table with the foot
• Palpate the achilles tendon – assess for thickening or relaxed. Hold the heel while the other hand stabilizes
swelling the leg just above the ankle joint. Dorsiflex and planter
• Palpate the joints / bones flex the ankle to make sure the ankle joint is relaxed.
o Work distal to proximal – assess for tenderness / Then pull the heel forward and feel the amount of
swelling / irregularity translation. If the difference between anterior
o Squeeze MTP joints – observe patient’s face for translation of the normal and the injured side is more
discomfort than 5 mm, the anterior talofibular ligament is likely
o Tarsal joint Ankle joint to be injured.
o Medial / lateral* malleoli
o Proximal fibula
❸MOVE *
Assess each of the following movements actively and
passively (feeling for crepitus).
• Foot plantarflexion – “push your feet downwards, like
pushing a car pedal” – 30-40°
• Foot dorsiflexion – “point your feet towards your
head” – 12-18°
• Foot inversion – grasp ankle with one hand & heel
with the other – turn sole towards midline – passive
assessment only
• Foot eversion – grasp ankle with one hand & heel
• Talar tilt test * (assess anterior and posterior
with the other – turn sole away from midline –
talofibular ligaments, calcaneofibular ligament and
passive assessment only
deltoid ligaments)
Patient sitting with the knee flexed to 90°
❹SPECIAL TESTS o ATFL: plantarflex the foot and perform
• Thompson / Simmonds’ test (for rupture of the inversion
achilles tendon) o PTFL: dorsiflex the foot and perform
Patient in prone position with the feet off the end of inversion
the table or kneeling on a chair with the feet off the o CFL: foot in anatomical position and perform
end of the chair. Then squeeze the calf on the normal inversion
side and note the amount of plantar flexion. The o Deltoid complex: foot in anatomical position
absence of plantar flexion on the injured side indicates and perform eversion
a rupture of the Achilles tendon. Test is considered positive if there is increased
motion or pain on eversion/inversion

Talar tilt test
DISCUSSION
I examined this patient complaining of pain after twisting his ankle playing football. On inspection the patient had antalgic gait.
There were no visible scars or swelling. No local rise in temperature. Distal pulses were normal in both limbs. Achillis tendon was
intact on palpation. There was tenderness over the right lateral malleolus.
On testing active and passive movements of the ankle joint, the patient had limited ROM on the right side due to pain.
On doing special tests, Simmonds’ test was negative, anterior drawer test was negative indicating and intact ATFL. Talar tilt test
was positive on inversion indicating the presence of a possible CFL injury
Differentials?
• Ankle ligament sprain (lateral collateral ligaments)
• Fracture lateral malleolus
• Base of 5th MT
• Cuboid
• Cuneiforms
Management?
X-ray on ankle joint
X-ray showed undisplaced fracture of fibula with swelling of the ankle, management?
• Backslap and analgesia
• Rest and elevation to reduce edema
SUMMARY
Position Exposure
Standing (look) then lying on bed (feel, move) knee to ankle
Gait Antalgic gait & +/- walking aid Range of motion Limited ROM in active and
MOVE
Skin No scars or erythema passive movements

LOOK
Swelling No swelling, effusion

Asymmetry No asymmetry Simmonds’ test Intact achilles tendon
Deformity No visible deformity Anterior drawer test Intact ATFL
TESTS
Talar tilt test Intact deltoid ligament,

Temperature Normal skin temperature possible injury to
FEEL
Tenderness Tender lateral malleolus or LCL calcaneofibular ligament

Pulse Intact pulse

SHOULDER EXAMINATION

Examine the shoulder Painful restricted movement all directions, especially external rotation
❶LOOK ❸MOVE
Front Side Behind ① RANGE OF MOVEMENT
• Alignment and • ACJ • Trapezius • Forward flexion
shoulder height • Deltoid • Deltoid This occurs in the sagittal plane. Whilst the patient is
• Scars • Acromion • Scapula sitting or standing, ask him to lift the arm as far as
• Swelling possible. Normal range: 160–180°
• Deformity / Wasting If forward flexion limited
o Trapezius → arthritis
o Deltoid → adhesive capsulitis
o ACJ → rotator cuff tear
o Clavicle
o SCJ
❷FEEL
• SCJ Sterno Clavicular joint
Start your palpation in the middle of the clavicle and move
medially toward the joint. The SCJ is 1.5cm to 2 cm lateral
to the middle of the sternal notch.
• Clavicle
• ACJ
Follow the clavicle laterally to its end. Usually one can feel
the articulation between the acromion and the clavicle
• Acromion
• Coracoid
This can be felt 2 cm inferior to the junction between the
middle and lateral thirds of the clavicle.
• CC ligament
• Abduction
As the name suggests, it runs between the coracoid and
This occurs in the coronal plane. While the patient is
the lateral end of the clavicle. It is important to check it
sitting or standing, ask him to lift the arm sideways as
for tenderness once you have palpated the acromion
far as he can. Normal RoM: 160–180°
The GHJ account for 0–90° of abduction. The last 60°
occurs entirely at the scapulothoracic joint. Note the
degree of abduction when the pain is elicited.
Pain only between 60–120° (Painful arc)
→ impingement
→ rotator cuff tear
Pain in terminal degrees of abduction
→ ACJ pathology
If the patient cannot initiate abduction
→ weakness of deltoid
Coracoclavicular ligament → massive rotator cuff tear
• Trapezius
• Biceps tendon
Hold the arm in 10° of internal rotation and run your
thumb just distal to the anterior edge of the acromion
Tenderness in the area 1–4 cm distal to the anterior edge
of the acromion is considered as biceps tendinitis

• Adduction The patient is asked to reach up his back with the back
Ask the patient to put the hand over the opposite of his hand. The vertebral level reached is noted and
shoulder. Pain in this movement is usually due to ACJ compared with the other side. This is a complex
pathology movement of internal rotation and extension of the
shoulder
Normal level: T7–T9 (Inferior angle of scapula @ T7)
• External rotation
Ask the patient (sitting or standing) to bend the elbow
to 90° of fl exion, while keeping it by the side and
externally rotating the forearm
Normal range of movement: 45–90°
Increased passive external rotation
→ Massive rotator cuff tear involving SC
Decreased external rotation
→ Adhesive capsulitis
→ Glenohumeral arthritis
→ Posterior dislocation (Rowe’s sign)
• Internal rotation

② MUSCLE TESTING o Napoleon belly press test
• Rhomboid – not done Ask the patient to push his hands on the abdomen
• Latissimus Dorsi – not done firmly and bring the elbows forward. In weakness of
• Deltoid – not done the subscapularis (positive test), the patient is
o Anterior fibers – not done unable to bring the elbows forward
o Middle fibers – not done
o Posterior fibers – not done
• Pectoralis major – not done
• Trapezius
Stand behind the patient and ask him to shrug his
shoulders.
• Supraspinatus
o Jobe’s / empty can test
Stand facing the patient. Place the patient’s arm in
30° of abduction and 30° of forward elevation (in the
plane of the scapula) with thumb facing down
(position of emptying a can). You then apply
resistance, while asking the patient to maintain the
position.
• Serratus Anterior
Stand behind the patient and ask him to push against the
wall
• Subscapularis

• Infraspinatus & Teres Minor ❹SPECIAL TESTS
o Lag test / external rotation Subacromial Impingement tests (Pick only 1 to do)
These two muscles are tested together. Ask the 1- Neer sign
patient (sitting or standing) to bend the elbow to 90° While the patient is sitting or standing, you passively
of flexion and keep it by his side. elevate the patient’s internally rotated arm in the
Then ask the patient to externally rotate the forearm plane of the scapula (about 30° from the coronal
while you apply resistance to the distal forearm plane)
2- Hawkins’ test
Ask the patient, sitting or standing, to forward flex the
shoulder to 90° and keep the forearm parallel to the
floor. You hold the patient’s arm and internally rotate
it further
3- Neer test – not done
4- Horn Blower’s test – not done
Instability tests

1- Drawer tests ACJ pathology
Before testing, ask the patient if the shoulder feels 1- O’Brien test (with thumbs down)
unstable and in which direction
While standing behind the patient, use one hand to
stabilize the shoulder girdle by holding on to the
scapula with your thumb and coracoid with your index
finger and, with the other hand, hold on to the
humeral head. For the anterior drawer test, apply an
anterior translational force and for the posterior
drawer test apply a posterior translational force
2- Scarf test
Ask the patient to put the hand over the opposite
shoulder while holding the elbow at the level of the
2- Anterior and posterior apprehension tests – not done shoulder. Then you apply force to the patient’s elbow
Labral tests / Biceps / SLAP tests

1- O’Brien test
Patient is standing or sitting.. The arm is forward
flexed to 90° and internally rotated so that the thumb
is facing downward, apply downward force and ask
the patient to resist. Repeat the test with the palm
facing upward
Pain produced deep in the shoulder joint with
palm up → Labral tear
Pain produced on top of the shoulder with
thumb down → ACJ pathology.
2- Speed’s test – not done
3- Yergason’s test – not done

DISCUSSION
What are the causes of painful abduction? Differential diagnosis of painful shoulder?
See before • Intrinsic shoulder pain:
o Rotator cuff disorders:
What are the rotator cuff muscles? ▪ Rotator cuff tears.
See Upper Limb Anatomy ▪ Subacromial pain (Impingement, subacromial
bursitis, tendonitis or tendinopathy)
What is the pathology of frozen shoulder? ▪ Calcific tendonitis.
Primary adhesive capsulitis (AC), is also known as frozen o Glenohumeral disorders:
shoulder is an idiopathic, insidious painful condition of the ▪ Arthritis.
shoulder persisting more than 3 months. This inflammatory ▪ Adhesive capsulitis ('frozen shoulder')
condition that causes fibrosis of the glenohumeral joint o Acromioclavicular disorders.
capsule is accompanied by gradually progressive stiffness and ▪ ACJ disruption (e.g. trauma)
significant restriction of range of motion (typically external ▪ OA or osteolysis of ACJ
rotation). o Labral tears
o Biceps tendonitis.
Stages o Infection, septic arthritis
• Stage 1 – Freezing (6 weeks – 9 months) o Shoulder instability - associated with hypermobility
Slow onset of pain. ↓ range of motion including subluxation or dislocation
• Stage 2 – Frozen (4-6 months) o Fractures
Pain may improve but stiffness ↑ • Extrinsic shoulder pain:
• Stage 3 – Thawing (5 months – 2 years) o Referred pain
Gradual ↑ RoM ▪ Neck pain
▪ Myocardial ischaemia
Diagnosis ▪ Referred diaphragmatic pain (e.g. gallbladder
Clinical in presence of a normal x-ray appearance disease, subphrenic abscess).
o Polymyalgia rheumatica.
Risk factors of primary adhesive capsulitis o Malignancy: apical lung cancers, metastases.
• Diabetes mellitus (with a prevalence up to
20%)
• Stroke
• Thyroid disorder
• Previous shoulder injury
• Dupuytren disease
• Parkinson disease
• Cancer
• Complex regional pain syndrome
Can also be secondary typically following trauma or injuries to

the shoulder. Common injuries include rotator cuff tears,
fractures, surgery, or immobilization.

HAND EXAMINATION

Carpal Tunnel Syndrome • Motor and sensory affection of (median n. distribution) • +ve Tinel’s and Phalen’s tests
Dupuytren disease • Deformity • Nodular thickening of the palm
❶LOOK ❷FEEL
Dorsum Dorsum
• Inspect hand posture – asymmetry / abnormalities • Assess and compare temp using the back of your hand:
• Scars or swellings o Forearm
• Skin colour: o Wrist
o Erythema – e.g. cellulitis (erythema) / palmar o MCP joints
erythema • Gently squeeze across the metacarpophalangeal (MCP)
o Pallor – e.g. peripheral vascular disease / anaemia joints – observe for non-verbal signs of discomfort –
• Deformities tenderness may indicate inflammatory arthropathy
o Bouchard’s nodes (PIP) / Heberden’s nodes (DIP) – • Bimanually palpate the joints of the hand (MCP / PIP / DIP
OA / CMC) – assess and compare for tenderness /
o Swan neck deformity – distal interphalangeal (DIP) irregularities / warmth
joint hyperflexion with proximal interphalangeal o Metatarsophalangeal (MCP) joint
(PIP) joint hyperextension – RA o Proximal interphalangeal (PIP) joint
o Z-thumb – hyperextension of the interphalangeal o Distal interphalangeal (DIP) joint
joint, in addition to fixed flexion and o Carpometacarpal (CMC) joint of the thumb
o Subluxation of the metacarpophalangeal (MCP) joint (squaring of the joint is associated with OA)
– RA • Palpate the anatomical snuffbox – tenderness may
o Boutonnières deformity – PIP flexion with DIP suggest scaphoid fracture
hyperextension – RA • Bimanually palpate the patient’s wrists
• Skin changes Elbows
o Skin thinning or bruising – long term steroid use • Palpate the patient’s arm along the ulnar border to the
o Rashes – e.g. psoriatic plaques elbow, note any rheumatoid nodules or psoriatic plaques
• Muscle wasting – may indicate chronic joint pathology or (extensor surface)
motor neurone lesions
• Nail changes: ❸MOVE
• Nail fold vasculitis – small areas of infarction • Assess movements actively first. Then assess movements
• Pitting and onycholysis – associated with psoriasis passively, feeling for crepitus and noting any pain.
Palms o Finger extension – “open your fist and splay your
• Inspect hand posture – asymmetry / abnormalities (e.g. fingers”
clawed hand) o Finger flexion – “make a fist”
• Scars – e.g. carpal tunnel release surgery o Wrist extension – “put palms of your hands together
• Swellings and extend wrists fully”
• Skin colour: o Wrist flexion – “put backs of your hands together
o Erythema – e.g. cellulitis (erythema) / palmar and flex wrists fully”
erythema • Test separately for both sets of flexor tendons:
o Pallor – e.g. peripheral vascular disease / anaemia o Flexor digitorum profundus: stabilize the PIPJ and
• Deformity – Dupuytren’s contracture ask the patient to flex at the DIPJ
• Nodular thickening of the palm, especially ring and little o Flexor digitorum superficialis, isolate the finger
finger – Dupuytren’s contracture being examined by holding the other fingers in
• Thenar/ hypothenar wasting – isolated wasting of the extension, then ask the patient to flex at the PIPJ
thenar eminence is suggestive of carpal tunnel syndrome • Assess all movements of the thumb –flexion, extension,
• Elbows – psoriatic plaques or rheumatoid nodules abduction, adduction and opposition NB: To simply check
for extension of the thumb, ask the patient to place
his/her hand palm down on the table and see if he/she
are able to raise his/her thumb off the table. Feel for
integrity of the Extensor Pollicis Longus tendon.
• Function
o Power grip – “squeeze my fingers with your hands”
o Pincer grip – “place your thumb and index finger
together and don’t let me separate them”
o Pick up small object or undo a shirt button – “can
you pick up this small coin out of my hand?”

❹NERVE AND MUSCLE EXAMINATION • Tinel’s test
Motor The patient’s wrist is supported on the table. With the tip
• Median Nerve: of the middle finger, the examiner taps the median nerve
o Test the function of abductor pollicis brevis; with between the tendons of PL and FCR. The test is considered
patient’s palm facing up, stabilize the rest of positive if the patient complains of pain or a shooting
patient’s hand on the table and ask them to point electric current sensation down the hand
with the thumb to the ceiling.
• Ulnar Nerve:
o Palmar interossei –adduct the fingers
o Dorsal interossei –abduct the fingers
o Froment’s sign: ask the patient to grasp a piece of
paper between the index finger and the thumb. You
then try to pull the paper away. If there is an ulnar
nerve lesion, the distal phalanx of the thumb flexes
(due to action of the unaffected flexor pollicis
longus) to compensate for the weak muscle
(adductor pollicis) that is supplied by the ulnar
nerve. This is a positive Froment’s sign
• Radial nerve:
o Ask the patient to extend the fingers and wrist .
against resistance. • Phalen’s test (If the examination findings are suggestive
Sensory of CTS this test may be used to further support the
• Volar aspect of index finger (Median nerve and C6) diagnosis)
• Volar tip of middle finger (C7) Ask the patient to hold their wrist in complete and forced
• Volar tip of little finger (Ulnar nerve and C8) flexion (pushing the dorsal surfaces of both hands
• First dorsal web space (Radial nerve) together) for 60 seconds. If the patient’s symptoms of
carpal tunnel syndrome are reproduced then the test is
❺SPECIAL TESTS positive (e.g. burning, tingling or numb sensation over the
• Modified Durkan’s test thumb
The examiner exerts direct compression over the median
nerve between the tendons of PL and FCR at the wrist
joint with his index finger for a minute. If compression of
the median nerve produces numbness or tingling of the
fingers, then irritation of the nerve is suspected.
To complete my examination
• Perform a full neurovascular examination of the upper
limbs
• Examine the elbow joint.

DISCUSSION – CARPAL TUNNEL
Sensory deficit is present on the palmar aspect of the first three digits and radial one half of the fourth digit.
Motor examination: Wasting and weakness of the median-innervated hand muscles (LOAF muscles) can be detectable.
Positive Phalen’s and Tinel’s tests
Differential diagnosis
• CTS
• Cervical disc disease
• Diabetic neuropathy
Risk factors
The following have been associated with higher risk of CTS.
• Increasing age.
• Female sex.
• Increased body mass index (BMI).
• Square-shaped wrist, short stature, dominant hand.
• Race (white).
• Strong family susceptibility.
• Wrist fracture (Colles).
• Acute, severe flexion / extension injury of wrist.
• Space-occupying lesions within the carpal tunnel (e.g., flexor tenosynovitis, ganglions, hemorrhage, aneurysms,
anomalous muscles, various tumors, edema).
• Diabetes.
• Thyroid disorders (usually myxoedema).
• Rheumatoid arthritis and other inflammatory arthritides of the wrist.
• Recent menopause (including post-oophorectomy).
• Renal dialysis.
• Acromegaly.
• Amyloidosis.
• Repeated activity involving severe force and extreme posture of the wrist / vibrating activity.
Investigations
• Electrophysiologic studies including electromyography (EMG) and nerve conductions studies (NCS) are the first-line
investigations in suggested CTS.
• MRI scan can exclude underlying causes in the carpal tunnel.
• laboratory: blood glucose, thyroid functions
Treatment
• Treatment of underlying disease, if any.
• Conservative management of mild to moderate disease (EMG and NCS) includes: –Splinting the wrist at night time for a
minimum of three weeks –Steroid injection into the carpal tunnel –Non- steroidal anti-inflammatory drugs (NSAIDs) and /
or diuretics
• Surgical treatment is indicated for severe disease, or when conservative management fails and includes carpal tunnel
release.

DISCUSSION – DEPUYTREN DISEASE
Dupuytren’s contracture
Dupuytren disease is a benign fibroproliferative disorder of unclear etiology.
Typically begins as a nodule in the palmar fascia and progresses insidiously to
form diseased cords and finally digital flexion contractures involving the MCP
and/or PIP joints
Dupuytren diathesis
Early disease onset and rapid progression of joint contractures,
often bilateral and including more radial digits.
Risk factors
• White men, Northern European descent
• Tobacco
• Alcohol
• Diabetes
• Epilepsy
• Chronic pulmonary disease
• Tuberculosis
• HIV
Pathophysiology
• Cytokine-mediated (transforming growth factor [TGF]-β) transformation of normal fibroblasts into myofibroblasts
• Myofibroblast contractile properties are abnormal and exaggerated.
• Increase in ratio of type III to type I collagen
Treatment
• Non-operative
o Splinting
o Steroid injection
o Collagenase injection (derived from Clostridium histolyticum) as an alternative to surgery has become more
widespread in the hand surgery community
• Operative
Indications include inability to place hand flat on tabletop (Hueston test), MCP flexion contracture greater than 30 degrees, or
any PIP flexion contracture
o Open limited fasciectomy (procedure of choice)
o Percutaneous cord release under local anesthetic with a large-gauge needle is an alternative to formal open surgery
Most common complication after operative treatment is recurrence, with long-term rates as high as 50%
Multiple digit surgery using the “modified Bruner” approach

SUMMARY
Position
Hands on pillow
Exposure
Elbow to hand
Discussion
I examined this patient presenting with hand pain and paresthesia
Carpal Tunnel Dupuytren Contracture

Skin No scars or erythema Skin thickening over the palmar aspect
Swelling No swelling Nodular thickening / lump
LOOK
Asymmetry No asymmetry Asymmetrical

Deformity No visible deformity Flexion deformity of the fingers
Nails No abnormality
Elbow No visible nodules

FEEL
Tenderness No tenderness
Range of motion No limitation of movement Unable to extend fingers

MOVE
Motor Intact motor functions Unable to extend fingers

NEURO
Sensory Paresthesia over the lateral 3½ fingers Normal sensation
Durkan’s test Positive Durkan’s test

TESTS
Tinel test Positive Tinel sign

Phalen test Positive Phalen test


SPINE AND PERIPHERAL NEUROLOGICAL EXAMINATION
Stem Scenario Probable findings after examination

Patient presenting with LBP
1
Examine this patient Signs and symptoms of L4/5 disc prolapse
2 Patient with lower limb claudication, ABPI normal
① SPINE EXAMINATION ❹SPECIAL TESTS

Don’t forget to expose the patient 1) Straight Leg-Raising Test (SLR)* / Lasègue’s test* /
Lazarević’s sign*
❶LOOK (all normal) A test to identify lumbar nerve root irritation. With
General: both legs relaxed and knees extended, the examiner
• Walking aids will lift one leg straight up supporting the heel with
• Gait the palm of the hand. Test is considered positive if
Behind pain radiates below the knee joint.
Once positive, slowly decrease in angle of leg elevation
• Scars
until pain disappears. At this time, dorsiflex the foot
• Muscle wasting
and symptoms will redevelop confirming the nerve
• Scoliosis
tension (Lasègue’s test). This test is important if the
• Abnormal hair growth
patient’s symptoms exacerbates in 30–70° of leg
Side
elevation. Pain generated over 70° of leg elevation in
• Cervical lordosis most cases is not a radicular pain.
• Thoracic kyphosis
• Lumbar lordosis
Front
• Posture of the head and neck
• Symmetry of shoulders
❷FEEL
• Spinous processes*
• Sacroiliac joints
• Paraspinal muscles
❸MOVE
Assess active movements
• Cervical spine (not done): flexion, extension, lateral
flexion, rotation
• Thoracic spine (not done): rotation
• Lumbar spine: flexion, extension, lateral flexion

2) Femoral nerve stretch (negative) 3) Schober’s test (negative)
This is to assess the compression on L2, L3 or L4 nerve (Assess the amount of lumbar flexion) (ankylosing
roots. While the patient prone and knee flexed to 90°, spondylitis)
the examiner lifts the patient’s thigh to extend the hip. Identify position of the posterior superior iliac spine
Reproduction of radicular pain in anterior thigh is (PSIS) – “dimples of Venus”. Mark the skin in the
positive midline 5cm below PSIS and 10 cm above. Ask the
Radicular-radiating
patient to touch their toes (full lumbar flexion).
Measure the distance between the two lines (started
at 15cm) Normally the distance between the two
marks should increase to >20cm. Reduced range of
motion can indicate conditions such as ankylosing
spondylitis.

② PERIPHERAL NEUROLOGICAL EXAMINATION
TOPCARS
TONE (normal tone, no clonus)

• Leg roll (from the knee)
Roll the patient’s leg and watch the foot – it should flop independently of the leg
• Leg lift (from the knee)
Briskly lift leg off the bed at the knee joint – the heel should remain in contact with the bed
• Ankle clonus
Clonus is a repetitive, rhythmic contraction of a muscle when attempting to hold it in a stretched state. It is a strong, deep
tendon reflex that occurs when the CNS fails to inhibit it. With the patient seated on the edge of the examination table,
the examiner holds the foot and does an active dorsiflexion in a quick stroke. If positive, the foot contracts more than
three times in a rhythmic plantar flexion which is called clonus. Fewer than three contractures are considered normal.
POWER
Hip
• Flexion (L2) – “raise your leg off the bed and stop me from pushing it down”
Knee
• Extension (L3)
Ankle
• Dorsiflexion (L4) – “point your foot towards your head and don’t let me push it down”
• Plantar flexion (S1) – “press against my hand with the sole of your foot”
Big toe *
• Hallux extension (L 5) – “don’t let me push your big toe down”
CO-ORDINATION
• Heel to shin test (see cerebellar examination station)
“Run your heel down the other leg from the knee and repeat in a smooth motion”
REFLEXES
• Knee jerk (L3, L4)
• Ankle jerk (L5, S1)
SENSATIONS * (diminished sensations over L5 nerve root, i.e. dorsum of the foot)
• Light touch (dorsal column) – test individual dermatomes
• Pin-prick (spinothalamic tract)

SUMMARY
Position
Standing (Look, Feel, Move), then lying on bed
Exposure
Back and lower limbs
Discussion
I examined this patient presenting with low back pain
Skin Normal gait ± walking aid

Spine inspection No Shoulder asymmetry
No abnormal curvatures
LOOK
No scars
No deformities
No muscle wasting
No abnormal hair
There is lower back tenderness

FEEL
Tenderness
No tenderness on palpation of paraspinal muscles or sacroiliac joints
Range of motion No limitation of movement in flexion, extension, or lateral flexion

MOVE
Schober test No limitation in forward flexion
SLR / Lasègue’s test Positive on affected side

TESTS
Femoral stretch test Negative bilaterally
Power All normal except for big toe extension

NEUROLOGICAL
Decreased sensations over anterolateral part of leg and dorsum of foot for both light touch
Sensory
and pin prick sensations
Reflexes Normal reflexes with -ve Babinski sign
Tone Normal tone, no clonus
Co-ordination Normal co-ordination

DISCUSSION
I examined the peripheral neurology of the lower limbs of this patient with back pain. His gait was normal, he had a positive
Lasègue’s sign on the right, with normal tone, power, co-ordination and reflexes throughout both lower limbs. He had impaired
sensation over the L5 dermatome on the right leg, to both light touch and pin prick.
“I examined this patient presented by LBP.”
“On examining his spine, there was no were signs of previous scars, muscle wasting or scoliosis. The patient had normal cervical
lordosis, thoracic kyphosis and lumbar lordosis.”
“On palpating his spine there was some tenderness over the spinous process of L5 and S1 with no tenderness over the paraspinal
muscles.”
“On testing the active movement of the spine, the patient had some pain on active flexion and active extension. The patient is
having positive SLR on his right lower limb, indicating the presence of sciatic nerve impingement, especially on the right side. The
patient had negative femoral stretch test and negative Schober’s test.” Impingement-.conflict
“On doing peripheral lower limb neurological examination, the patient had normal tone with no clonus.”
“On testing his muscle power, the patient had weak hallux extension, normal coordination, normal reflexes but impaired sensation
over L5 nerve root distribution”
Differentials?
Disc herniation between L4-5 impinging on the L5 spinal nerve.
I also have to consider
• Spinal canal stenosis
• DM (peripheral neuropathy)
• Vitamin B12 deficiency (subacute combined degeneration of the cord)
• Drug therapy (e.g. anti-retroviral, thalidomide, phenytoin)
• Heavy metal/chemical exposure (lead, arsenic, mercury)
• Carcinoma (most likely spinal metastases)
• Tabes dorsalis (syphilitics myelopathy).
Imaging?
• X-ray lumbosacral spine
• MRI lumbosacral spine
Treatment?
• Conservative
• Surgical
o Discectomy
o Laminectomy


FOOT DROP – COMMON PERONEAL NERVE INJURY

Patient had radio-frequency ablation / EVLT for right lower
Signs and symptoms of common peroneal nerve injury
limb varicose veins and now complaining of numbness
① FOOT EXAMINATION
❶INSPECTION
While standing, look for:
• Scars (stab avulsions scars will be demonstrated over the leg)
• Swelling and erythema, which may be present after trauma and may suggest
compartment syndrome – negative
• Muscle wasting (anterior and lateral compartments) – negative
• Fasciculations (may suggest motor neuron lesion) – negative
• Gait * (the actor will demonstrate high stepping gait on the affected side; the foot
hangs with the toes pointing down, causing the toes to drag on the ground while
walking, requiring the patient to lift the leg higher than normal when walking)
• Ask the patient to walk on the heels * (difficulty on the affected side)
❷PALPATION
• Palpate the course of the common peroneal nerve for local tenderness
• Tinel’s sign: lightly tap over the nerve at the fibular head; tingling or “pins and
needles” in the nerve distribution indicates a lesion here
• Check the popliteal space for masses
Foot is dragged or lifted high and

② PERIPHERAL LOWER LIMB NEUROLOGICAL EXAMINATION
slapped on to the floor. Unable to walk
on the heels. Caused by foot drop
TONE (normal tone, no clonus) owing to lower motor neurone lesion
Ask the patient to keep their legs fully relaxed and “floppy” throughout your assessment.
• Leg roll, leg lift and ankle clonus (see before)
POWER
(weak ankle dorsiflexion, weak eversion)
Assess one side at a time and compare like for like. Remember to stabilize the joint whilst testing power.
Hip
• Flexion (L2) – “raise your leg off the bed and stop me from pushing it down”
• Extension – “stop me from lifting your leg off the bed”
• Abduction – “push your legs out”
• Adduction – “squeeze your legs in”
Knee
• Extension (L3) – “kick out your leg”
• Flexion – “bend your knee and stop me from straightening it”
Ankle
• Dorsiflexion (L4) – “keep your legs flat on the bed…cock your foot up towards your face…don’t let me push it down “
• Plantarflexion (S1) – “push down like on a pedal”
• Inversion – “push your foot in against my hand”
• Eversion – “push your foot out against my hand”
Big toe
• Extension (L5) – “don’t let me push your big toe down”
CO-ORDINATION
• Heel to shin test (see cerebellar examination station)
“Run your heel down the other leg from the knee and repeat in a smooth motion”

REFLEXES SENSATIONS
(decreased ankle reflex with negative Babinski sign) (diminished sensations over the dorsum of the foot and the
• Knee jerk (L3/4) anterolateral aspect of the lower leg)
• Ankle jerk (L5/S1) • Light touch sensation
• Plantar reflex (S1) Assesses dorsal/posterior columns. The patient’s
Run a blunt object along the lateral edge of the sole eyes should be closed for this assessment.
of the foot, moving towards the little toe, then Touch the patient’s sternum with the cotton wool
medially under the toes. Observe the great toe. wisp to confirm they can feel it. Ask the patient to
Normal result = Flexion of the great toe and flexion say “yes” when they are touched. Using a wisp of
of the other toes cotton wool, gently touch the skin (don’t stroke).
Abnormal (Babinski sign) = Extension of the great Assess each of the dermatomes of the lower limbs.
toe and spread of the other toes – upper motor Compare left to right, by asking the patient if it
neuron lesion feels the same on both sides.
• Pin-prick sensation
Assesses spinothalamic tracts.
Repeat the previous assessment steps, but this
time using the sharp end of a neurotip.
To complete the examination:

• Spine examination
• Hip, knee and ankle examination
SUMMARY
Position
Standing then lying down
Exposure
Hip to foot
Discussion
Gait High steppage gait with difficulty in heel walking

INSPECTION
Scar There is a scar over the leg

Muscle No muscle wasting or fasciculations
Swelling No swelling
Tenderness There is no tenderness over the course of the common peroneal nerve
PALPATION
Popliteal fossa No swelling in the popliteal fossa

Tinel sign Tinel sign is negative
Power All normal except for weak ankle dorsiflexion and eversion
NEUROLOGICAL
Decreased sensations over anterolateral part of leg and dorsum of foot for both light touch
Sensory
and pin prick sensations
Reflexes Normal reflexes with -ve Babinski sign
Tone Normal tone, no clonus
Co-ordination Normal co-ordination

DISCUSSION
“I examined this patient presented by numbness after EVLT. “On inspection, I observed the presence of multiple small scars, most
probably from previous surgeries for varicose veins. There was no lower limb swelling, muscle wasting nor fasciculations. Patient
has a stepping gait and difficulty on heel walking on his right side.”
“On palpation there was some tenderness over the course of the common peroneal nerve with positive Tinel sign and no masses
were felt in the popliteal fossa.”
“On doing peripheral lower limb neurological examination the patient had normal tone with no clonus. Also, the patient had
normal power in his lower limb except for weak ankle dorsiflexion and weak eversion of the right ankle. He had normal
coordination and normal reflexes with negative Babinski sign. The patient had diminished sensation diminished sensations over the
dorsum of the foot and the anterolateral aspect of the right lower leg”
“My main differential diagnosis would be foot drop”
Foot drop causes?

• Common peroneal nerve injury due to
o Radio-frequency ablation
o Fracture head/neck of fibula
o Prolonged tight plaster cast
o Fracture dislocation of the knee
Clinical picture
o Weakness of foot dorsiflexion (tibialis anterior muscle),
o Weakness in toe extension (extensor digitorum longus muscle and extensor hallucis longus muscle),
o Weakness in foot eversion (peroneus longus and brevis muscles),
o Sensory loss in dorsum of foot.
o Sensory loss of the anterolateral aspect of the lower leg
• Sciatic nerve injury involving common peroneal division due to
o Fracture dislocation of the hip
o Fracture femur
o Hip surgery
• L4, L5 disc herniation with L5 nerve root compression (weak hip abduction)
• Central causes
o Motor neuron disease
o Multiple sclerosis, stroke
o Brain tumor
o Parkinsonism
Clinical picture
o Positive Babinski sign
o Hyperactive tendon reflexes
• Other causes
o DM
o Vitamin B12 deficiency
o Alcohol misuse
Investigations?
• Electrodiagnostic studies (EMG/NCS)
• MRI lumbar spine
• Blood analysis for a possible metabolic cause like diabetes or alcoholism
Treatment?
• Consider an ankle foot orthosis to support the foot while walking and to reduce risk of falling.
• Consider physiotherapy for specific muscle training if weakness is severe.
• Surgical treatment:
o Exploration
o Decompression
o Repair
o Tendon transfer


CARDIOVASCULAR EXAMINATION
Stem Patient going for an elective hernia repair… Findings

• Young patient
1 Mitral Regurgitation* • Pansystolic murmur (heard over the Apex i.e. 5th intercostal space
MCL)
• Old age
2 Aortic Stenosis • Ejection systolic murmur (heard over the aortic area i.e. right 2nd
intercostal space parasternal line)
• Midline sternotomy scar
3 Valve Replacement
• Metallic click (on auscultation)
• Left infraclavicular scar
4 Pacemaker*
• Otherwise, normal CVS examination
• Usually old patient
• Midline sternotomy scar
5 Valve Replacement + Mitral Regurgitation*
• Metallic click
• Pansystolic murmur
*Most common in Cairo exam
• Palpate for:
❶INSPECTION AND PALPATION o Apex beat (5th ICS midclavicular line)
• General:
o Walking aids
o O2
o Medications
o Observation chart
o ECG
o Midline sternotomy scar
• Hands:
o Signs of IE (negative) for e.g. splinter
hemorrhages, Janeway lesions
o Tar staining
o Capillary refill
o Palpate the radial pulse (rate, rhythm, radio-
radial delay, collapsing pulse)
o Clubbing
• Blood pressure measurement o Heaves (using both hands for RVH or LVH)
• Neck:
o JVP assessment
o Palpate the carotid pulse
• Face: malar flush
• Eye
o Mucous membranes
o Corneal arcus
o Xanthelasma
• Mouth:
o Oral hygiene
o Central cyanosis
• Chest (don’t forget posterior and lateral aspects):
o Scars (sternotomy, thoracotomy,
infraclavicular)
o Visible apex pulsations
o Thrills (palpable murmurs)

❷AUSCULTATION o Lean forward & listen over aortic area during
(Put your left hand on the carotid pulse to time systole and expiration – aortic murmurs are louder
diastole) (stenosis & regurgitation)
• Mitral area: 5th ICS midclavicular line
Pan systolic murmur radiating to the axilla
• Tricuspid area: 4th ICS left parasternal edge
• Pulmonary area: 2nd ICS left parasternal edge
• Aortic area: 2nd ICS right parasternal edge
Ejection systolic murmurs radiating to the
carotids
• Accentuation maneuvers (these maneuvers cause
particular murmurs to become louder DURING
expiration)
o Roll onto left side & listen to mitral area with
bell during expiration – mitral murmurs
(stenosis & regurgitation) • Metallic heart sounds:
o One metallic click corresponding to S1 =
mitral valve replacement
o Two metallic clicks corresponding to S2 =
aortic valve replacement
• Carotid bruits
• Lung bases
❸CHECK LOWER LIMB

• Edema
• Vein graft harvest scars
Tricuspid valve
Auscultation position for Auscultation position for

tricuspid valve mitral valve

DISCUSSION
Male patient who I assessed in preadmission clinic. On examination of his cardiovascular system from the end of the bed I noted a
midline sternotomy scar. There were no peripheral stigmata of cardiovascular disease, he was hemodynamically stable with a
narrow pulse pressure of 120/100 millimeters of mercury, and slow rising pulse. On closer inspection of his chest, there was an
old midline sternotomy scar; the apex beat was not displaced. On auscultation I heard a metallic second heart sound, but no
murmur. There were no signs of heart failure; however, I noted abdominal bruising, perhaps consistent with the use of
subcutaneous heparin injections, and a vein harvest scar over the right great saphenous area. His signs are consistent with a CABG
and metallic aortic valve replacement for which he is on anticoagulation. I am slightly concerned that he has signs of aortic
stenosis - a slow rising pulse and narrow pulse pressure although I did not hear a murmur - despite the valve replacement,
therefore I would investigate this thoroughly.
Example presentation for MR station:

“I have done CVS examination on this patient who is being prepared for an elective hernia repair. “
“On general examination, the patient looks comfortable, no walking aids, no surrounding oxygen cylinders or medications noticed.”
“On inspecting his eyes, no corneal ulcers were found, arcus or xanthelasma. No malar flush, good oral hygiene. No central
cyanosis, or congested neck veins”
“On palpating the carotid pulse there was no palpable thrill. On inspecting his hands, there were no signs of IE, no tar staining, the
capillary refill time was within normal range. His radial pulse was 75 with regular rhythm, no radio-radial delay and no water-
hammer pulse. His BP was 120/60. The patient does not have any obvious chest scars His apical pulsation was felt in the 5th ICS left
MCL. There were no palpable heaves but there was a palpable thrill over the apex”
“On auscultation the patient had a pansystolic murmur heard over the mitral area, which was propagating to the left axilla and
was accentuated when the patient was lying on this left lateral position. No basal crepitation heard over the lungs or carotid bruit.”
“There was no edema in the lower limbs and no signs of harvest scars.”
“So, my main diagnosis would be mitral regurgitation due to the heard pansystolic murmur”
What investigations would you order preoperatively?

This patient appears well but would require a baseline ECG and echo preoperatively. In addition, he would require bloods
including an INR as he is on warfarin.
How would you manage this patient’s anticoagulation?

General guidelines (you should always check local policy and ask the advice of a hematologist)
• Low Thromboembolic risk
o Stop warfarin 5 days pre-op.
o Restart warfarin post-op as soon as oral fluids are tolerated
• High thromboembolic risk
o Stop warfarin 4 days pre-op and start low molecular weight heparin (LMWH) at therapeutic dose
o Stop the LMWH 12-18h pre-op
o Restart LMWH 6hpost-op (assuming hemostatics is achieved)
o Restart warfarin when oral fluids are tolerated
o Stop LMWH when INR is in range again
The patient presents with fever 5 days postoperatively…?

Might have infective endocarditis

Causes of valve lesions?
Mitral Valve Disease Aortic Valve Disease
Mitral Stenosis Aortic Stenosis
• Postinflammatory scarring (rheumatic heart disease) • Postinflammatory scarring (rheumatic heart disease)
• Senile calcific aortic stenosis
• Calcification of congenitally deformed valve
Mitral Regurgitation Aortic Regurgitation
• Abnormalities of leaflets and commissures • Intrinsic valvular disease
o Postinflammatory scarring o Postinflammatory scarring (rheumatic heart
o IE disease)
o Mitral valve prolapse o IE
o “Fen-phen” – induced valvular fibrosis • Aortic disease
• Abnormalities of tensor apparatus o Degenerative aortic dilation
o Rupture of papillary muscle o Syphilitic aortitis
o Papillary muscle dysfunction (fibrosis) o Ankylosing spondylitis
o Rupture of chordae tendineae o RA
• Abnormalities of left ventricular cavity and / or annulus o Marfan syndrome
o Left ventricular enlargement (myocarditis,
dilated cardiomyopathy)
o Calcification of mitral ring
Interpretation of ECG
Note the pacemaker spikes, no P waves
Indications of pacemaker?
• Symptomatic sinus bradycardia
• SA node disease
• Symptomatic AV node disease
• Hypertrophic obstructive cardiomyopathy (HOCM)
• Dilated cardiomyopathy (DCM)
• Long QT syndrome
Who would you inform about the pacemaker?

An anaesthetist, ideally the consultant who will be doing the case. I would ensure it is clearly documented in the notes.
What precautions would you take?

• I would arrange a pre and postoperative pacemaker check and contact their pacemaker follow-up clinic to inform them
of the operation and ask for advice.
• During the operation I would avoid using a monopolar diathermy or limit its use to short bursts only.
• The return electrode should be placed so that the pathway between the diathermy electrode and return electrode is as
far away from the pacemaker and leads as possible
• I’d ensure that appropriate resuscitation equipment was available

SUMMARY
Position
Semi-sitting
Exposure
Chest and abdomen
Discussion
I examined this patient presenting wit …
General • No walking aids

• No O2 mask
• No drugs (Warfarin in Valve replacement)
Hands • No signs of IE
• No tar stains
• No clubbing
• Normal cap refill
INSPECTION AND PALPATION
• Radial pulse is… regular, no RR delay, no collapsing pulse

BP • Not done - “Ideally I’d also measure the blood pressure”
Neck • Neck veins are not congested
• Carotid pulses are equal bilaterally with no palpable thrill (+ve thrill in AS)
Face • No malar flush
Eyes • No mucous membrane pallor
• No xanthelasma
• No corneal arcus
Mouth • Proper oral hygiene
• No central cyanosis
Chest • Scars: No scars / midline sternotomy scar (valve replacement) / left infraclavicular scar (pacemaker)
• Apex beats: Apex beats are felt in the 5th IC space MCL / displaced (AS)
• Heaves: No heaves / LV heaves (AS)
• Thrill: No thrill / thrill at 2nd IC space right parasternal (AS) / thrill at apex (MR)
Mitral regurgitation Aortic stenosis Valve replacement Valve replacement + MR

Audible pansystolic murmur Audible ejection systolic Audible metallic click of Audible metallic click of
AUSCULTATION
over the apex, propagated murmur over 2nd IC space prosthetic valve valve replacement with
to axilla and accentuated in right parasternal, pansystolic murmur over
the left lateral position propagated to the carotid the apex, propagating to
and accentuated on leaning the axilla and accentuated
forward in the left lateral position
No carotid bruits
No basal crepitations
Scars No scars
LL
Tenderness No edema


RESPIRATORY EXAMINATION

• Tar staining • On percussion: hyperresonance
COPD patient going for
• Clubbing • On Auscultation: harsh bronchial breathing with wheezes
an elective hernia repair
• Barrel shaped chest
❶INSPECTION AND PALPATION ❷PERCUSSION

• General: Start with supraclavicular then medial ⅓ of the clavicle
o O2 Note that you need to percuss the anterior and lateral aspect of
o Medications the chest and posterior chest (can be done later)
o SOB
o Ask to take a deep breath and cough
o RR
• Mouth: central cyanosis
• Lymph nodes: cervical
• Trachea: central or not
• Hand:
o Tar staining*
o Clubbing*
o Radial pulse
• Chest:
o Scars for thoracotomy:
“Can you put your hand on your hips and bend your
elbows forward for me please?” ❸AUSCULTATION
o Barrel shaped From the same levels of percussion, ask patient to take deep
o Chest expansion: breaths in and out through their mouth.
Place your hands on the patient’s chest, inferior to the • Assess equality
nipples. Wrap your fingers around either side of the • Assess quality
chest. Bring your thumbs together in the midline, so o Vesicular (normal)
that they touch. Ask patient to take a deep breath. o Bronchial* (harsh sounding) – consolidation
Observe movement of your thumbs, they should move • Assess volume – quiet breath sounds suggest reduced
apart equally. If one of your thumbs moves less, this air entry – consolidation / collapse / fluid
suggests reduced expansion on that side. Reduced • Added sounds
expansion can be caused by lung collapse / pneumonia. o Wheeze* – asthma / COPD
o Coarse crackles – pneumonia / fluid
o Fine crackles – pulmonary fibrosis
• Vocal resonance (normal):
Ask patient to say “99” repeatedly and auscultate the
chest again
Increased volume over an area suggests increased
tissue density – consolidation / fluid / tumor
❹BACK OF THE CHEST

Repeat
• Chest expansion
• Percussion and auscultation
• Vocal resonance

DISCUSSION
“I’ve done respiratory examination of this patient who is being prepared for an elective hernia repair. “
“I didn’t notice any bedside medications or surrounding oxygen cylinders. The patient had some SoB while sitting down. “
“On inspecting his mouth there was no sign of central signs of cyanosis. No enlarged cervical LN, his trachea was central. On
inspecting his hand, I found that patient has tar stains and clubbing. His PR was about 90bpm RR was 20. On examining his chest, I
didn’t notice any obvious scars, chest expansion was equal on both sides. He had a barrel-shaped chest (↑ AP diameter). “
“On percussion, there was hyperresonance. “
“On auscultation there was equal air entry on both sides with harsh bronchial breathing and the presence of expiratory wheeze,
vocal resonance was normal on both sides. Examination of the back of the chest was done which revealed the same findings.”

Main diagnosis is COPD in a smoker of this age. However, asthma is also a possibility.
Who would you inform about this?

I would inform an anaesthetist, ideally the consultant who will be doing the case, otherwise the coordinating anaesthetic
consultant and the operating surgeon.
What further investigations would you arrange?

• A chest X-ray to rule out a preop pneumonia or underlying malignancy
• Spirometry and respiratory function tests
• A baseline ABG to identify preoperative paO2 and PaCO2
How could you try to reduce the risks in a patient with COPD about to undergo an operation?
• I would ask the GP to optimize medication before the operation and refer to a respiratory medic if necessary.
• Any infection should be treated before the operation.
• The patient should be encouraged to stop smoking
• I would arrange chest physio before and after surgery to encourage excretion of excess mucus
• In addition, I would inform HDU in case more intensive care is required post operatively
• Use open surgery, not laparoscopic because of CO2 pneumoperitoneum
• Use regional anesthesia instead of general anesthesia
Tobacco ‘tar’-stained finger.
Clubbing. Anterior view and lateral view.

CRANIAL NERVE EXAMINATION
Stem Scenario Probable findings after examination

• Bitemporal hemianopia
1 Referred by his GP for persistent headache
∆ most probable pituitary adenoma
Head trauma due RTA • Left conductive hearing loss
2
Please do ear examination and related CNs (V, VIII) ∆ most probably hematotympanum due to # skull base
• Anosmia
Female with anosmia, visual defects, memory • Decrease visual acuity
3 defects • Defective lateral gaze
Please do CN examination and memory test • Decrease AMTS
∆ most probably anterior cranial fossa lesion / tumor
Olfactory nerve • Visual fields Stem 1

With eyes closed, ask patient to identify various scents – e.g. Visual inattention (visual neglect):
coffee, vinegar o Ask patient to focus on your face and not to move
their head or eyes during the assessment.
Optic nerve o Hold both arms out, with one hand in the upper right
• Visual acuity Stem 3 and the other in the upper left quadrant of your visual
o Patient stands 6 meters away from the Snellen chart. If field.
patient normally uses distance glasses, ensure they o Remind the patient to keep their head still & their eyes
wear them for the assessment. fixed on your face.
o Ask the patient to cover one eye & read to the lowest o Move one of your fingers (on only one hand) and ask
line they can manage. the patient to point at the hand on which the finger is
o Visual acuity is recorded as chart distance (numerator) moving.
over number of lowest line read (denominator). o Move the finger on the left and right hand individually
o Record the lowest line the patient was able to read in whichever order you prefer.
(e.g. 6/6 which is equivalent to 20/20) o Then move the finger of both hands simultaneously.
o If patient only reports a finger on one of the hands
• Colour vision (not done)
moving (whilst both are moving simultaneously), it
• Pupils
suggests the presence of visual neglect.
o Direct reflex– shine torch into eye – look for pupillary
o Repeat the process with your hands in the lower
constriction in that eye
quadrants of vision.
o Consensual reflex – shine torch into eye – look for
Confrontation:
pupillary constriction in opposite eye
o Ask the patient to cover their left eye with their left
o Swinging light test– move light in from side of each eye
hand.
rapidly – relative afferent pupillary defect (RAPD)
o You should cover your right eye and be staring directly
o Accommodation reflex:
at the patient (mirror the patient).
▪ Ask patient to focus on a distant point (clock on a
o Ask patient to focus on your face & not move their
wall / light switch).
head or eyes during the assessment.
▪ Place your finger/object approximately 15cm in
o Ask the patient to tell you when they can see your
front of the eyes.
fingertip wiggling.
▪ Ask the patient to switch from looking at the distant
o Outstretch your arms, ensuring they are situated at
object to the nearby finger / object.
equal distance between yourself & the patient.
▪ Observe the pupils, you should see constriction &
o Position your fingertip at the outer border of one of
convergence bilaterally.
the quadrants of your visual field.
• Fundoscopy Stem 3 (not done – no mydriatics or dim light)
o Slowly bring your fingertip inwards, towards the centre
o Assess for red reflex
of your visual field until the patient sees it.
o Position yourself at a distance of around 30cm from
o Repeat this process for each quadrant – at 10 o’clock
the patient’s eyes.
/2 o’clock / 4 o’clock / 8 o’clock.
o Looking through the ophthalmoscope observe for a
o If you are able to see your fingertip but the patient
reddish / orange reflection in the pupil.
cannot, this would suggest a reduced visual field.
o An absent red reflex may indicate the presence of
o Map out any visual field defects you detect.
cataract, or in rare circumstances neuroblastoma.
o Repeat the same assessment process on the other eye.
o Move in closer and examine the eye with the
funduscope. Begin medially and assess:
▪ optic disc – colour / contour / cupping
▪ retinal vessels – cotton wool spots / AV nipping /
neovascularization
▪ macula – ask to look directly into the light – drusen
noted in macular degeneration

Oculomotor, Trochlear, Abducent (eye movement) Trigeminal nerve
Eye movements: • Sensory: close your eyes, use a cotton wool
• Ask the patient to keep their head still & follow your o Ophthalmic: forehead
finger with their eyes. o Maxillary: cheek bones
• Move your finger through the various axis of eye o Mandibular: jaw angles
movement (“H” shape). pin prick sensations not done
• Ask the patient to report any double vision. • Motor: muscles of mastication
• Observe for restriction of eye movement o Close and open your jaw against resistance
o Clench your teeth and feel temporalis and
masseter
• Reflexes: (not done)
o Corneal reflex
o Jaw jerk (not done)
Facial nerve
• Temporal (“Raise your eyebrows”)
• Zygomatic (“Close your eyes tightly”)
• Buccal (“Puff out your cheeks”)
• Marginal mandibular (“Show me your teeth”)
• Cervical (“Tense your neck muscles”)
• Chorda tympani (“Any change in taste sensations?”)
_-
A. Action of individual muscles (anatomical action).

B. Movement of eye when testing specific muscle (clinical testing).
NB: The superior oblique, acting in isolation, turns the eye
down and out. However, if was tested clinically by asking the
patient to look down and out its action could be mimicked by
the combined action of inferior and lateral recti. This is
particularly so as the inferior rectus acts most effectively when
the eye is abducted (looking laterally). Therefore, by asking the
patient to look down and in these muscles are excluded and
the problem is solved. Essentially, we are testing the ability of
the superior oblique to look downwards.

Vestibulocochleare nerve • Weber test:
Equilibrium Tap a 512HZ tuning fork & place in the midline of the
• March on spot forehead. Ask the patient where they can hear the
Hearing sound
• Whisper a number and ask the patient to repeat
• Rinne test:
The base of a vibrating 512Hz tuning fork is first placed
on the mastoid process and then after the sound is no
longer appreciated the vibrating top is held one inch
from the external auditory meatus. Patient is asked
then if he can still hear the sound
o Air conduction > Bone conduction
▪ Normal (Rinne’s positive)
▪ Neural deafness (both air & bone
conduction reduced equally)
o Bone conduction > Air conduction
▪ Conductive deafness (Rinne’s
negative)
Normal = sound is heard equally in both ears

Neural deafness = sound is heard louder on the side of
the intact ear Conductive deafness = sound is heard
louder on the side of the affected ear
Glossopharyngeal + Vagus
• Open your mouth and say AAH (look for any deviation
of uvula and soft palate)
• Ask the patient to cough (assess adduction of both
vocal cords by vagus nerve)
• Gag reflex (not done)
Spinal accessory
• Trapezius (shrug shoulder against resistance)
• Sternomastoid (turn head against resistance)
Hypoglossal nerve:
• Protrude your tongue (deviation towards the affected
side)
Left hypoglossal nerve lesion

DISCUSSION
Example presentation for bitemporal hemianopia station

“I’ve done CN examination except those that were not needed to be done. The examination revealed that all the CNs are intact
except while examining the optic nerve, I found that the patient has visual field defects affecting the lateral half in both of his eyes,
which means that the patient has bitemporal hemianopia. “
Where might the lesion be to cause these symptoms?

A bitemporal hemianopia is suggestive of a lesion affecting the optic chiasm, where the more medial fibres cross over to the
contralateral eye. This may be either a lesion of the optic chiasm itself or a mass pressing on it (e.g. pituitary tumor, pineal body
tumor or thalamic tumor). If a mass arises from above the chiasm (e.g. pituitary craniopharyngioma), the initial symptoms may be
of a bitemporal inferior quadrantanopia, progressing to a bitemporal hemianopia. Conversely, masses arising below the chiasm
may present at first with bitemporal superior quadrantanopia.
What else might you expect if a pituitary tumor were the cause of this lady's bitemporal hemianopia?
The other signs and symptoms of a pituitary tumor can be general or specific to hormone production
• General: Raised intracranial pressure may cause papilledema (as seen on fundoscopy) or headaches.
• Specific: Hyperpituitarism: this depends on the type of hormone secreted. The most common are growth hormone and
prolactin from pituitary adenomas. The former causes acromegaly and the latter hyperprolactinemia.
o Signs of acromegaly
▪ Prognathism
▪ Prominent brow
▪ Macroglossia
▪ Thickening of the skin
▪ Enlargement of hands and feet
▪ Hyperhidrosis,
▪ Carpal tunnel syndrome
o Signs of hyperprolactinemia
▪ Increased lactation
▪ Loss of libido
▪ Erectile dysfunction in males
▪ Amenorrhoea and infertility (anovulatory) in females

Management?
Investigations:
• Hormone assays
• MRI
• CT (disadvantages: poor soft tissue visualization, need for contrast)
Treatment:
• Anti-prolactin (bromocryptine)
• Surgery (trans-sphenoidal, trans-frontal)
Stem 2 Questions
Cause of conductive hearing loss in this patient? After fitting the otoscope, you found this picture, what’s your
Hemotympanum secondary to skull base fracture comment on this picture?
Hemotympanum
What cranial nerves to examine together?
Vestibulocochlear and facial (they exit together from IAM)
How to fit otoscope?

• Pull the pinna upwards & backwards – to straighten
the external auditory meatus
• Position otoscope at the external auditory meatus
• Otoscope should be held in your right hand for the
patient’s right ear and vice versa
• Hold the otoscope like a pencil and rest your hand
against the patient’s cheek for stability
• Advance the otoscope under direct vision
• Look for any wax, swelling, erythema, discharge or
foreign bodies
• Examine the tympanic membrane:
o Colour – pearly grey & translucent
(normal) / erythematous (inflammation)
o Erythema or bulging of the membrane? – Identify structures on otoscopic view?
inspect for a fluid level e.g. otitis media
o Perforation of the membrane? – note the
size of the perforation
o Light reflex present? – absence /
distortion may indicate ↑ inner ear
pressure e.g. otitis media
o Scarring of the membrane? –
tympanosclerosis – can result in significant
hearing loss
• Withdraw the otoscope carefully
Management?
• ATLS protocol
• CT brain
• Audiometry
• ENT review

Stem 3 Questions
Anterior cranial fossa tumor…?
Do AMTS (Abbreviated mental test scoring)
• How old are you?
• What time is it to the nearest hour?
• Can you remember this address? 24 West St. I will ask you this at the end
• What year is it?
• What is the name of this place?
• What is my job? And what is the job of this person (e.g. a nurse)?
• What is your date of birth?
• When did WW2 end?
• Who is the current prime minister?
• Can you count backwards from 20-1?
• What was that address I asked you to remember?
A score less than 6/10 suggests dementia / delirium
What do you want to look for in fundoscopy?

Ophthalmoscopy serves to identify:
• Papilledema suggestive of sustained raised intracranial pressure (e.g. caused by a tumor or hydrocephalus). This may be
absent in the context of acutely raised intracranial pressure, or there may be atrophic changes in longstanding chronic
disease.
• Hemorrhage into the vitreous humor (Terson's syndrome) or other intraocular hemorrhage secondary to a subarachnoid
hemorrhage.
Differential diagnosis of anterior cranial fossa tumor?

• Meningioma
• Olfactory neuroblastoma
• Sinonasal malignancies
Management?
• CT scan
• MRI with gadolinium
• Stereotactic biopsy
• Involve neuro-oncology MDT
• Treatment is by surgical resection and proton beam radiotherapy
SUMMARY
Nerve 1 2 3 Findings
Olfactory ✔ Bilateral anosmia
Optic ✔ Visual acuity: bilateral decreased acuity to 20/50 on Snellen chart
✔ Field: Defective temporal field on both sides (bitemporal hemianopia)
✔ ✔ Pupils: normal direct, consensual & accomodation reflexes
Not done Colour vision
✔ Fundoscopy: offer only to do and possibilities will be discussed (optic disc cupping)
Oculomotor, Trochlear, ✔ Free in all directions
Abducent ✔ Defective lateral gaze (abducent)
Trigeminal ✔ ✔ Normal findings
Not done Pin prick sensation, jaw jerk & corneal reflexes
Facial ✔ ✔ ✔ Normal findings
Vestibulocochlear ✔ ✔ Normal findings
✔ Unilateral conductive hearing loss
Glossopharyngeal, ✔ ✔ Normal findings
Vagus Not done Gag reflex
Accessory ✔ ✔ Normal findings
Hypoglossal ✔ ✔ Normal findings
AMTS ✔ Score < 6/10 suggesting dementia

CEREBELLAR EXAMINATION

Patient with posterior cranial fossa tumor • DANISH: Dysdiadochokinesia, Ataxic gait, Nystagmus,
Please examine the patient (cerebellum and CN 9, 10, 11 and 12) Intention tremors, Staccato speech, Hypotonia
❶Gait* ❹Co-ordination
• Stance – a broad based gait is noted in cerebellar disease • Finger to nose test *
• Stability – can be staggering and often slow & unsteady – o Ask patient to touch their nose with the tip of their
can appear similar to a drunk person walking index finger, then touch your finger tip. Position your
• Tandem (‘Heel to toe’) walking – Ask patient to walk in a finger so that the patient has to fully outstretch their
straight line with their heels to their toes. This is a very
sensitive test and will exaggerate any unsteadiness.
• Romberg’s test – ask patient to put their feet together,
keep their hands by their side and close their eyes (be
ready to support them in case they are unsteady!). This is
a test of proprioception – a positive Romberg’s test
indicates that the unsteadiness is due to a sensory ataxia
(damage to dorsal columns of spinal cord) rather than a
cerebellar ataxia.
❷Head
• Speech (staccato)*: say British constitution
• Nystagmus: follow my fingers by your eyes
❸Arms
• Pronator drift *
o Ask patient to close eyes & place arms outstretched
forwards with palms facing up. Observe the hands /
arm for signs of pronation / movement.
o A slow upward drift in one arm is suggestive of a
lesion in the ipsilateral cerebellum.
• Rebound phenomenon *
o Whilst the patient’s arms are still outstretched and
their eyes closed, ask the patient to keep their arms in
that position as you press down on their arm. Release
your hand. arm to reach it. Ask them to continue to do this finger
o Positive test if patient’s arm shoots up above the to nose motion as fast as they can manage. Move
position it originally was (this is suggestive of your finger, just before the patient is about to leave
cerebellar disease). their nose, to create a moving target.
• Tone o An inability to perform this test accurately (past
o Support the patient’s arm by holding their hand & pointing/dysmetria) may suggest cerebellar
elbow. Ask the patient to relax and allow you to fully pathology.
control their arm. Move the arm’s muscle groups
through their full range of movements. • Intentional tremors *
o Is the motion smooth or is there some resistance? o “Touch and hold this pen”
• Reflexes • Dysdiadochokinesia *
o Assess the patient’s upper limb reflexes, comparing o Demonstrate patting the palm of your hand with the
left to right. Biceps (C5, C6), Triceps (C7), Supinator back/palm of your other hand to the patient. Ask the
(C6) patient to mimic this rapid alternating movement.
o In cerebellar disease, there is often mild hyporeflexia. Then have the patient repeat this movement on their
other hand.
o An inability to perform this rapidly alternating
movement (very slow/irregular) suggests cerebellar
ataxia.

❺Legs • Co-ordination (heel to shin)
Patient lying down
• Tone: leg roll, leg lift (from the knee)
• Reflexes: (knee, ankle) should show hyporeflexia
To complete my examination, I would do: full neurological

examination including:
• Cranial nerves
• Upper and lower limbs
DISCUSSION
Example presentation: Posterior fossa tumors?

“I’ve done neurological examination of this patient who has • cerebellar astrocytoma
a posterior cranial fossa tumor. I started by examining the • Primary neuroectodermal tumors
gait, the patient had a broad-based gait with unsteadiness • Medulloblastoma
(ataxic gait) and inability to do tandem gait. Romberg’s test • Ependymoma and ependymoblastoma
was negative.” • Choroid plexus papilloma and carcinoma
“The patient had staccato speech with no nystagmus.” • Dermoid tumors
“On examining his upper limbs, the patient had positive • Hemangioblastoma
pronator drift with positive rebound. The patient had
• Metastatic tumors
hypotonia / normal tone with normal reflexes with
• Brainstem gliomas
dysmetria, dysdiadochokinesia and intention tremors. “
“On examining his lower limbs, the patient had normal tone,
Management?
normal reflexes with incoordination.”
Investigations:
“Examination the last 4 cranial nerves revealed normal
findings” • Plain x-ray skull: It may show calcification.
• MRI brain (enhanced) with gadolinium
Patient has (DANISH): Dysdiadochokinesia, Ataxic gait, • CT brain: CT scan of the posterior fossa is inferior
Nystagmus, Intention tremors, Staccato speech, Hypotonia to MRI in diagnostic value because of the artifact
My main diagnosis will be cerebellar ataxia due to posterior produced from the surrounding thick bone.
fossa tumor, other differentials include: However, CT scan is helpful for postoperative
• Cerebellar metastases due to lung or breast cancer follow-up.
• Head trauma • CT (whole body) to detect primary tumors
• cerebrovascular stroke • Guided biopsy
• TIA Treatment: Excision
• MS

VARICOSE VEINS

Patient presented by right/left lower limb varicose veins
Symptoms and signs of varicose veins
Please examine this patient
❶INSPECTION 1) Brodie-Trendelenburg test / Single tourniquet test

Inspect with the patient standing up. Ensure that the patient (The Trendelenburg test is used to determine the site of
is adequately exposed (from lower abdomen to feet) whilst valvular incompetence in a patient with varicose veins.)
dignity maintained. Ask the patient to lie down. Elevate the leg and empty
Inspect from all sides, easier done by kneeling in front of the the veins by massaging distal to proximal. Using a
patient then asking the patient to turn around. Look for: tourniquet (or fingers), occlude the superficial veins in
• Varicosities the upper thigh. Ask the patient to stand. If the
• Skin changes and ulceration from chronic tourniquet prevents the veins from re-filling rapidly, the
varicosities and their complications especially the site of the incompetent valve must be above this level
medial “gaiter” area i.e. at the saphenofemoral junction. If the veins re-fill,
• Lipodermatosclerosis Inflammation of layer of fat the communication must be lower down.
• Venous eczema Observing the same protocol, proceed down the leg
under the skin '. until the tourniquet controls re-filling. As necessary, test:
• Hemosiderin staining
• Atrophie blanche (white patches found in areas of • above the knee - to assess the mid-thigh
healed ulceration) perforator
• Edema • below the knee - to assess competence
between the short saphenous vein and
• Scars from previous surgery, including avulsion
popliteal vein
scars
If re-filling cannot be controlled, the communication is
• Saphena varix in the groin
probably by one or more distal perforating veins.
❷PALPATION 2) Perthes’ maneuver
• Feel at the saphenofemoral junction (4cm below This maneuver is used to distinguish antegrade flow
and lateral to the pubic tubercle) for a saphena from retrograde flow in superficial varicosities.
varix. If a swelling is present, check for a palpable Antegrade flow is an indicator of collateral flow around
thrill and a cough impulse which indicates an a deep venous obstruction. A tourniquet is applied to a
incompetent valve between the superficial and varicose leg in such a way that the superficial veins are
deep systems compressed without pressure being applied to the deep
• Feel down the leg over the course of the long vessels. The patient is then asked to stand repeatedly on
saphenous and then short saphenous veins for tiptoe, activating the calf muscles. Normally this would
tenderness along the veins which may indicate empty the varicosities but, in the presence of deep vein
perforator incompetence. obstruction, they would paradoxically become
congested.
❸SPECIAL TESTS
Two tests have classically been used to assess valvular ❹HAND HELD DOPPLER ASSESSMENT **
competency (Trendelenburg's test) and deep venous Hold the Doppler probe at a 45° angle to the skin at the level
patency (Perthes' test). They have been superseded to a of the saphenofemoral junction and the squeeze the
large extent by other non-invasive investigations but may patient’s calf. In a patient with a competent saphenofemoral
still be relevant in a primary care setting. The Royal College junction you will hear a short “swoosh” as you squeeze, but
of Surgeons in England expects its membership candidates this ceases as soon as you let go of the calf. If, however, the
to abandon Trendelenburg's, Perthes' and tap testing in saphenofemoral junction is incompetent, there is a more
favor of hand-held Doppler assessment but that they should prolonged “swoosh” of blood as it regurgitates back down
understand the principles behind the techniques. though the incompetent valve.
Do not confuse Trendelenburg Test with Multiple
To complete my examination, I would examine the arterial
Tourniquet Test
system and the abdomen
Trendelenburg test is to apply one tourniquet below
(for e.g. SFJ). If during the tourniquet is applied, there is
filling of varicose vein (which you had just emptied
before the test), it means the patient’s perforating vein
is incompetent, blood flow from deep vein to
superficial vein. If after applied, no filling, and when you
release the tourniquet and there is filling, it means the
SFJ above your tourniquet is incompetent and cause
downward flow of blood because of the gravity.

DISCUSSION
“I’ve examined this patient presenting with right lower limb varicose veins,
on inspection the varicosities appeared to be on the distribution of the GSV
with multiple visible incompetent perforators all over the right lower limb
above and below the knee. There was no visible saphena varix and the
patient had multiple transverse scars above and below the knee most
probably due to previous varicose vein surgery. There were no signs of
chronic venous insufficiency.”
“On palpation the varicosities were not tender and there wasn’t any
palpable saphena varix. On Trendelenburg test, I noticed that the SFJ was
incompetent. Multiple tourniquet test was not possible due to the
availability of only one tourniquet. Perthes’ test was not done.”
“On hand held doppler examination, there appeared to be SFJ
incompetence.”
“My main diagnosis would be primary varicose veins of the right lower limb
with incompetent SFJ”
On closer inspection of the legs, she has obvious varicosities bilaterally.

There were no ulcers, but I noted venous eczema, lipodermatosclerosis and
hemosiderin deposition reflecting chronic venous insufficiency. Doppler
assessment demonstrated incompetence at the saphenofemoral junction.
What further investigations would you arrange?

Venous duplex: Duplex ultrasound scan to determine the site of valvular
incompetence, ensure patency of the deep venous system
What are her management options?

Depends on symptoms and effect on quality of life.
Conservative:
• Graduated compression stockings
• Leg elevation
• Exercise and avoidance of prolonged sitting or standing.
Invasive, non-operative:
• Foam sclerotherapy
• Radiofrequency
• Photocoagulation (Laser) ablation (under local anaesthesia).
Invasive, operative (under general anesthesia):
Varicose vein surgery is reserved for symptomatic patients with skin
complications. It can involve ligation of the vein (long or short
saphenous) near the site of incompetence and excision (for the long
saphenous) by stripping through small skin incisions to reduce the risk
of recurrence. Varicose veins can be avulsed through small stab
incisions (phlebectomies), followed by compression bandaging.

PERIPHERAL LOWER LIMB ARTERIAL EXAMINATION

Patient referred from his GP, complaining from claudication in • Symptoms and signs of peripheral vascular disease
his lower limb. Please do arterial examination and ABPI
❶INSPECTION
(with the patient lying on the couch)
NB: Arterial ulcers typically have a
General:
“punched out” appearance and
• Inspect the hands looking for nicotine staining, tendon xanthomata, nail fold infarcts
are generally found around
and splinter hemorrhages and nail changes
pressure areas, i.e., lateral and
• Look at the skin and hair for changes suggestive of arterial disease, i.e., thin/shiny
medial malleoli, tips of the toes,
skin and hair loss.
head of the 1st and 5th
Specific:
metatarsals, the heel and the
• Look at the legs for Colour of the legs do they appear pale, cyanosed or red? interdigital clefts –so remember
• Scars suggestive of previous surgery (e.g., femoro-distal bypass) or amputated digits to look between toes and under
• Signs of venous insufficiency such as lipodermatosclerosis, venous eczema and the heel. (May often be confused
atrophy blanche with neuropathic ulceration;
• Venous guttering seen when veins collapse in limbs with peripheral vascular disease venous ulceration commonly
and appear as shallow grooves occurs around the gaiter region
• Ulceration comment on the location, shape depth and size of the ulcer (medial side) of the leg)
• Gangrene
❷PALPATION
• Compare the temperature on both legs using the • Palpate the pulses on both legs:
dorsum of your hand. o Femoral –felt in the mid-inguinal point, halfway
• Check the capillary refill time in toes of both feet. between the pubic symphysis and ASIS.
• Buerger’s test o Popliteal –felt deep in the midline of the popliteal
With the patient lying supine, ask if they have any pain or fossa with the knee flexed to ~30 degrees
restriction in hip movements. Then lift both legs slowly o Posterior tibial –felt posterior to medial
(ideally in about 10ᵒ increments and waiting for 10 seconds malleolus, ⅔rd of the way between the medial
at each stage) and evaluate the angle at which the leg malleolus and the insertion of the Achilles tendon
becomes pale or white. This is known as Buerger’s angle. In o Dorsalis pedis felt in the 1st webspace, just lateral
normal subjects it should be greater than 90ᵒ (even if the to the extensor hallucis longus tendon on the
limb is flexed further at the hip, there should be no colour dorsal surface of the foot (dorsiflexion of the
change in the limb). In patients with peripheral vascular hallux may aid palpation)
disease, the limb may go pale as it is lifted and reaches a o Remember also to check the radial pulse and
certain angle. If the angle is less than 25-30ᵒ, it suggests assess for radio-femoral delay.
severe ischemia. If you can’t feel distal pulses, you must use hand held
Once you have established Buerger’s angle, sit the patient up doppler
and swing the legs over the side of the couch. Watch for the
foot to re-perfuse –in normal subjects there should be no
colour change but in patients with peripheral vascular
disease, you will observe the legs becoming a dusky
crimson/purple colour, which is caused by reactive
hyperemia. This represents a positive Buerger’s test.

❸AUSCULTATION
For bruits (using the cone of stethoscope)
• Femoral bruits (midpoint of medial aspect of thigh)
• Iliac bruits (midpoint of inguinal canal)
❹ABPI
(Ankle Systolic Pressure/Brachial Systolic Pressure)
The ABPI gives an indication of the severity of peripheral vascular
disease where present
A normal ABPI is >1.0
• 0.7 –1 = mild disease (i.e., patient may present with intermittent
claudication)
• 0.5 –0.7 = moderate disease (i.e., likely to have rest pain)
• < 0.5 –0.3 (or absolute pressure < 50mmHg) = severe disease (i.e.
critical ischemia)
Complete the examination, I would like to

• Perform a complete neurological examination of the lower limbs
• Perform a full cardiovascular examination
• Perform a vascular examination of the upper limbs
• Feel the abdomen for any evidence of an aortic aneurysm and
auscultate for renal and aortic bruits.
DISCUSSION
A male/female patient who presents with leg pain on walking. He seemed generally stable, but I noticed a toe amputation on the
right. On closer examination he had difficult to palpate dorsalis pedis and posterior tibial pulses on the right, ABPI was 0.9 on the
left and 0.5 on the right, consistent with claudication in the right leg. My main differential would be atherosclerotic or diabetic
peripheral vascular disease.
“On general inspection, the patient didn’t have any signs of peripheral vascular disease. On local inspection of his legs, I noticed
that the patient had a pale right foot, with shiny skin and loss of hair. The patient didn’t have any scars on his lower limb. The
patient had an ulcer on the medial malleolus, it was 2x1 cm with punched out edges. The patient didn’t have venous guttering or
any signs of gangrene. On palpation, the right leg temperature was slightly decreased compared to the other side. The patient had
increased capillary refill time on the right compared to the left. The patient had a Buerger’s angle of about 45ᵒ on the right side
and a positive Buerger’s test. The patient had intact normal pulses on the left side, but on the right side the dorsalis pedis and
tibialis posterior arteries were not felt despite having normal femoral and popliteal pulses. I tried using the hand held doppler to for
the distal pulses, but I couldn’t manage to hear them either. On auscultation, there were no audible bruits on the femoral or iliac
arteries on both sides. I tried to measure the ABPI, but I couldn’t complete it because of the time limit.”
“My main differential diagnosis would be atherosclerotic / diabetic peripheral arterial disease on the right side.”
Investigations?
Imaging: Lab:
• Arterial duplex • Blood glucose level
• CT angiography • Lipid profile (LDL)
• MR angiography
Treatment?
• The patient should have an assessment of their risk factors and be actively discouraged from smoking, have their
cholesterol, blood pressure and blood sugar control optimized and be considered for an antiplatelet agent.
• The patient will probably need surgical or endovascular intervention. Options include endovascular stenting of a
stenosed portion of an artery, surgical bypass or amputation of the affected part of the limb.
• Conservative treatment alone is only an option if the patient were unfit or unwilling to have surgery.
Critical limb ischemia?

Critical ischemia can be defined by the presence of ischaemic pain at rest, or tissue loss in the form of gangrene or ulcers. It is
consistent with an ABPI of < 0.4.

THYROID

Patient with neck swelling • Simple multinodular goitre
① GENERAL ❷PALPATION
② HAND Tell the patient that you will examine him from behind
• Radial pulse
• Dry skin / acropathy / palmar erythema
• Tremors: Ask the patient to place their arms straight out
in front of them. Place a piece of paper across the backs
of their hands. Observe for a tremor
• Feel the lump: Tenderness, Temperature, Surface

(irregular), Edge (well-defined), Consistency (firm), Fixity
(mobile – not fixed to the underlying structures of the
overlying skin), Pulsatility (not-pulsatile)
• Feel below the lump – can you get below the swelling? If
not, retrosternal extension
③ FACE / EYES • Lymph nodes: submental, submandibular, preauricular,
• Exophthalmos: examine from above postauricular, occipital, posterior cervical, anterior
• Lid lag: Hold your finger high & ask the patient to follow it cervical, pretracheal, supraclavicular
with their eyes (head still). Move your finger downwards. • Swallow water – while palpating the gland
Observe the upper eyelid as the patient follows your finger • Protrude tongue – while palpating the gland
downwards • Trachea – from the front
• Eye movement: Ask the patient to keep their head still &
follow your finger with their eyes. Move your finger ❸PERCUSSION
through the various axis of eye movement (“H” shape). • Sternum (resonant – if dull, retrosternal extension)
Observe for restriction of eye movements & ask the
patient to report any double vision or pain ❹AUSCULTATION
• Bruits – with the bell of the stethoscope (negative)
④ NECK
❶INSPECTION
• Lump
• 6s: Site, Size, Shape, Symmetry, overlying Skin, Scars
• Neck veins
• Protrude tongue
• Swallow water
⑤ OTHERS
• Pretibial myxoedema (expose the patient)
• Reflexes (ankle or biceps reflex instead)
• Proximal myopathy: Ask patient to stand from a sitting
position with arms crossed. An inability to do this suggests
proximal muscle wasting

DISCUSSION
“I examined this patient presenting with a neck swelling. On inspection, there was a swelling in the anterior neck. The swelling was
midline. It was about 3 x 4 cm, oval in shape and not symmetrical. There were no signs of inflammation on the overlying skin. No
signs of previous surgery or scars. The patient didn’t have any congested neck veins. The swelling was mobile on deglutition but not
mobile on tongue protrusion.” “On palpation there was no local rise in temperature. The lump was not tender, the surface was
irregular with well-defined edges and a frim consistency. The swelling was mobile from side to side and was not fixed to the
underlying structures or the overlying skin. I could feel below the lump which means that there’s no retrosternal extension. The
trachea was central and there was no cervical lymphadenopathy.” “On percussing the sternum, the note was resonant which,
again, means that there’s no retrosternal extension.” “No bruits were heard on auscultation.” “On testing the thyroid functional
status, the patient appeared to be euthyroid.”
• Simple multinodular goiter
• Thyroid neoplasm
• Toxic nodular goiter
How would you manage this patient?

I would perform a triple assessment, taking a history as well as my examination, arrange an ultrasound and a fine needle
aspiration or a biopsy. Also, I have to check thyroid functions
If the patient come back with pain on swallowing, difficulty in breathing few months later, does it change your management?
Yes, these are obstructive symptoms requiring thyroidectomy
Her FNA comes back showing a follicular cell tumor. The report says “unable to differentiate carcinoma from adenoma”. Why is
this?
Follicular carcinomas are differentiated from follicular adenomas as they invade the tumor capsule or surrounding vessels.
Therefore, histology rather than simply cytology is needed.
What is the next step in the patient's management following this histological result?
This lady needs to be discussed in the MDT and worked up for a total or hemithyroidectomy
5-year survival rate of follicular carcinoma?

More than 90%

Classification of thyroid disease
Simple goitre Diffuse Physiological
(euthyroid) hyperplastic Pubertal
Pregnancy
Multinodular goitre
Toxic Diffuse (Graves’ disease)
Multinodular
Toxic adenoma
Neoplastic Benign
Malignant
Inflammatory Autoimmune Chronic lymphocytic thyroiditis
Hashimoto’s disease
Granulomatous De Quervain’s thyroiditis
Fibrosing Riedel’s thyroiditis
Infective Acute (bacterial thyroiditis, viral thyroiditis, ‘subacute thyroiditis’)
Chronic (tuberculous, syphilitic)
Other Amyloid
Principles of treatment of thyrotoxicosis

1. Antithyroid drugs
Those in common use are carbimazole and propylthiouracil. Antithyroid drugs are used to restore the patient to a euthyroid
state and to maintain this for a prolonged period in the hope that a permanent remission will occur, i.e. that production of
thyroid-stimulating antibodies (TSH-RAb) will diminish or cease. Antithyroid drugs cannot cure a toxic nodule. The overactive
thyroid tissue is autonomous and recurrence of the hyperthyroidism is certain when the drug is discontinued.
• Advantages: No surgery and no use of radioactive materials.
• Disadvantages: Treatment is prolonged and the failure rate is at least 50%. The duration of treatment may be
tailored to the severity of the toxicity, with milder cases being treated for only 6 months and severe cases for 2 years
before stopping therapy.
2. Surgery
In diffuse toxic goitre and toxic nodular goitre with overactive internodular tissue, surgery cures by reducing the mass of
overactive tissue by reducing the thyroid below a critical mass. After subtotal thyroidectomy the patient should return to a
euthyroid state, albeit after a variable period of hypothyroidism. There are however, the long-term risks of recurrence and
eventual thyroid failure. In contrast total/ near total thyroidectomy accepts immediate thyroid failure and lifelong thyroxine
replacement to eliminate the risk of recurrence and simplify follow-up. Operation may result in a reduction in TSH-RAb. In the
autonomous toxic nodule, and in toxic nodular goitre with overactive autonomous toxic nodules, surgery cures by removing
all the overactive thyroid tissue; this allows the suppressed normal tissue to function again.
• Advantages: The goitre is removed, the cure is rapid and the cure rate is high if surgery has been adequate.
• Disadvantages: Recurrence of thyrotoxicosis occurs in at least 5% of cases when subtotal thyroidectomy is carried
out. There is a risk of permanent hypoparathyroidism and nerve injury. Young women tend to have a poorer
cosmetic result from the scar. Every operation carries a risk, but with suitable preparation and an experienced
surgeon the mortality is negligible and the morbidity low.
3. Radioiodine
Radioiodine destroys thyroid cells and, as in thyroidectomy, reduces the mass of functioning thyroid tissue to below a critical
level.
• Advantages: No surgery and no prolonged drug therapy.
• Disadvantages: Isotope facilities must be available. The patient must be quarantined while radiation levels are high
and avoid pregnancy and close physical contact, particularly with children. Eye signs may be aggravated.

SUMMARY
Position Surface Nodular surface

Sitting Edge Well defined edges
Consistency Firm in consistency
Site Front of neck in midline Temperature Skin overlying has normal temperature
Size About 3x4cm in size Tenderness The swelling is not tender
Shape Oval Trachea Trachea was central
PALPATION
Surface With irregular surface LN There are no palpable lymph nodes
INSPECTION
Scar No scars of previous operations Pulsatility The swelling is not pulsatile

Skin Overlying skin doesn’t show any signs of Fixity The swelling in mobile and not
inflammation attached to overlying or underlying
Neck veins Neck veins aren’t distended on both structures (partially overlapped by
sides sternomastoid muscle)
Swallowing The swelling is mobile with swallowing Get below I could get below the swelling
Tongue And not mobile with tongue protrusion Pulse And carotid pulses were equally felt
protrusion bilateral
On percussion On auscultation
The upper end of sternum is resonant denoting no retrosternal There are no audible bruits heard over the swelling
extension of the swelling
On examination of thyroid status:
Patient is in euthyroid status

PAROTID

Patient with neck swelling Parotid swelling
❶INSPECTION
• 6s: Site, Size, Shape, Symmetry, overlying Skin, Scars
• The contralateral side
• Facial nerve (see Cranial Nerves Examination station…)
o Raise your eyebrow
o Shut your eyes against resistance
o Blow out your cheek
o Show your teeth
o Tense your neck muscles
• Oral cavity: inspect the Stensen’s duct (at the level of the upper 2nd molar tooth)
❷PALPATION
Explain to the patient that you will examine him from behind
• Palpate the lump: (ask the patient to clench his teeth) surface, consistency, fixity, edges,
pulsatility
• Palpate contralateral side
• Lymph nodes (as before)
• Palpate the Stensen’s duct Bimanual palpation of the
• Bimanual examination parotid gland
• Palpate the contralateral side
DISCUSSION
“I examined this patient presenting with neck swelling. On inspection, the swelling appeared to be in the region of the parotid
gland, above the angle of the mandible, and elevating the lobule of the ear. The swelling was oval in shape and about 5 x 4 cm. The
overlying skin showed no signs of inflammation or scars. There was no swelling in the contralateral side. Facial nerve was intact.
On inspecting Stenson’s duct there were no signs of inflammation.”
“On palpation, there was no local rise in temperature. Swelling was non-tender with smooth/irregular surface, firm in consistency
and mobile from side to side with well-defined edges and non-pulsatile.”
“The patient didn’t have any cervical lymphadenopathy. Contralateral side was normal. On palpating Stenson’s duct, there were
swellings or stones. On bimanual examination, the deep lobe of the gland couldn’t be felt.”
“So, my main differential diagnosis would be benign neoplasm, malignant neoplasm which is unlikely but has to be considered,
inflammatory lesions and infection which is also unlikely here because there is no pain or tenderness.”
Differential diagnosis of parotid lump? Investigations?

• Benign neoplasm: • CT, MRI to assess the extent of local, bony, or
o Pleomorphic adenoma perineural invasion
o Warthin’s tumor • U/S
• Malignant neoplasm: • FNAC
o Mucoepidermoid carcinoma
o Adenoid cystic carcinoma Treatment?
o Adenocarcinoma Superficial parotidectomy
o Lymphoma
• Inflammatory:
o Sjögren syndrome
o Mikulicz’s syndrome
• Infective:
o Parotitis

SUBMANDIBULAR GLAND

Patient with neck swelling Submandibular gland swelling
❶INSPECTION ❷PALPATION
• 6s: Site, Size, Shape, Symmetry, overlying Skin, Scars Explain to the patient that you will examine him from behind
• The contralateral side • Palpate the lump: surface, edges, consistency, fixity,
• The oral cavity: Wharton duct on either side of the pulsatility
lingual frenulum • Wharton duct
• Marginal mandibular nerve: show your teeth • Lymph nodes
• Hypoglossal nerve: take out your tongue (deviation to • Bimanual
the affected side) • Lingual nerve: touch sensations to ant. 2/3 of the
tongue
• Palpate the contralateral side
A: Examination with the mouth open. B: Examination with the tongue touching the roof of the mouth.
DISCUSSION
Examination revealed a diffusely enlarged left / right submandibular gland, approximately 4cm in diameter. There was no
associated cervical lymphadenopathy and there was normal flow of clear saliva into the oral cavity. The neck examination was
otherwise normal.

• Submandibular sialolithiasis
• Submandibular neoplasm
How would you investigate this patient?

• Ultrasound
• Sialogram if a salivary stone is suspected
• X-ray
• CT scan
• FNA if a neoplasm is suspected
What are the treatment options?

• Conservative management
o Analgesia
o Oral antibiotics
o Good hydration
o Gland massage
• Sialogram can occasionally be therapeutic, as the injection of contrast can 'wash out' the gland
• If the stone is within the duct, then the duct can be laid open and the stone retrieved. The duct is then left open as
suturing would result in a stricture
• Sialendoscopy: stone retrieval via endoscopic techniques
• Submandibular gland excision

POST-OPERATIVE ANASTMOTIC LEAKAGE - CCrISP

POD6 (left hemicolectomy anastomotic leakage) CCRISP • SOB
approach (Patient is presented with shortness of breathing, • Generalized abdominal pain
left shoulder tip pain, abdominal lower midline covered scar
with dressing) - you will be presented with an obs chart, labs
and ECG)
Patient lying in bed, wearing a hospital gown. After exposing chest, abdomen, and lower limbs, you notice a lower midline
abdominal dressing. Patient has TEDS (thromboembolic deterrent stockings)
Note that the patient will simulate SOB, Note the nearby O2 mask.
Ask the patient if he is having any pain at the moment, the patient will point to his abdomen.
Tell the patient that you will examine his tummy and that you will be gentle and take verbal permission.
Start by light palpation of the RIF. Note: the patient will jump in pain simulating acute abdomen.
Tell the examiner that the patient is experiencing severe abdominal pain, so further abdominal examination cannot be continued,
and that you are going to start assessing the patient using the CCrISP protocol.
AIRWAY
• The patient was talking so his airway is patent
BREATHING:
• Look for any central cyanosis
• Look for chest wall movements, equal or not
• Palpate for chest expansion
• Percuss the anterior and lateral chest wall only
• Auscultate anterior and lateral chest walls
CIRCULATION
• Look for the neck veins
• Look for signs of dehydration (dry tongue, sunken eyes)
• Auscultate the heart
DISABILITY
(consciousness level)
• The patient is alert
EXPOSURE
• Offer to remove the dressing to expose the laparotomy wound
• Look and squeeze for the calves to rule out DVT and PE
CHARTS
• EWS charts
o Rising temp.
o Rising PR
o Increasing O2 requirements)
• FBC
o Leucocytosis
• ECG
o AF

DISCUSSION
I examined this patient presented by SOB, left shoulder tip pain. On general inspection, the patient is obviously having SOB and
generalized abdominal pain. I started by doing light palpation on his RIF, which showed that the patient was having severe
abdominal tenderness, so this patient looked critically ill and therefore i started assessing the patient according to the CCRISP.
his airway is patent
Breathing: no central cyanosis, equal chest walls movements, percussion note was normal, equal air entry with no added sounds
Circulation: no congested neck veins, no signs of dehydration, normal heart sounds
The patient was alert.
There was no swelling or pain in his calves.
His charts showed: rising temperature, rising PR, increasing O2 requirements.
FBC showed leukocytosis, ECG showed AF.
So, my main diagnosis for that case is generalized peritonitis secondary to anastomotic leakage which caused the patient to have
sepsis. Shoulder tip pain in such case may be due to the presence of intraabdominal collection causing irritation of the diaphragm.
Management?
• NBM
• Urinary catheter to monitor output
• NG tube for suction and bowel rest
• May refer the patient to HDU to insert a central line and monitor
• Fluid resuscitation by crystalloids
• IV antibiotics
• Bloods: ABG, U&E
• Chest x-ray to rule out any respiratory problem
• CTPA to rule out PE
• Abdominal ultrasound to detect any abdominal collections
• CT with Gastrografin enema to identify the leaking anastomosis
• This patient will need urgent laparotomy; Hartman's procedure plus good peritoneal toilet plus drainage

ABDOMINAL EXAMINATION

Acute cases: 1 Acute diverticulitis • LIF tenderness, otherwise normal
(you will be (severe left side abdominal pain in patient • Note: do not do deep palpation on LIF
presented with a long-standing history of constipation)
with 2 Acute cholecystitis • Positive Murphy sign, otherwise normal examination
observational (Right hypochondrial pain for 4 days) Note: do not do percussions on the liver
charts, lab 3 Acute appendicitis • RIF pain
data and (RIF pain in a young lady) • Positive rebound
ECG) • Rovsing
• Obturator sign
Psoas sign
Chronic 4 Generalized Lymphadenopathy •
cases 5 Paraumbilical hernia •
6 Incisional hernia •

SUMMARY
.
Exposure
Chest, abdomen, groins
Diverticulitis Cholecystitis Appendicitis Paraumbilical & Incisional hernia

No jaundice or pallor
No signs of dehydration
General No enlarged cervical lymph nodes
No skin changes over the trunk
No asterixis, no clubbing or nail changes
No swelling There is a swelling in the peri-
umbilical region (elsewhere over the
abdomen in incisional hernia)
Increasing in size on
coughing
Local Inspection No scars Scar of previous operation (in
incisional hernia)
No abdominal distention
No scratch marks
No skin changes
No visible pulsations
No palpable masses There is a palpable mass in the peri-
Light palpation Tender LIF Tender Rt Tender RIF umbilical region
hypochondrium (superior/inferior/right/left) to the
No palpable masses umbilicus (or over the scar of previous
Don’t palpate LIF Don’t palpate right Elicit Rebound operation in incisional hernia)
hypochondrium tenderness The swelling is not tender, shows
Deep palpation expansile impulse on cough, doughy
in consistency, reducible
Defect size is X cm
Liver is not enlarged
Spleen is not enlarged
Palpation and
Kidneys show not tender renal angle
Percussion
No palpable pulsatile masses
No abdominal collection by percussion
Murphy sign Rebound tenderness
Rovsing
Special signs
Obturator
Psoas
Normal bowel sounds
Auscultation
No audible bruits over aorta, renal, iliac arteries

ACUTE DIVERTICULITIS
Perform classic abdominal examination ② LOCAL EXAMINATION

Look at the patient’s charts ❶INSPECTION
• Fever • Scratch marks
• Mild tachycardia • Swelling
• Distension
① GENERAL EXAMINATION • Caput medusae
From the end of the bed • Skin changes (bruising, signs of weight loss)
• Does the patient look comfortable? • Scars Striae
• How is the general appearance and nutritional • Any visible pulsations
status? • Ask the patient to cough or lift his/ her head off the
• Is there any obvious pallor or jaundice? bed to reveal any herniae or signs of peritonism (the
• THE HANDS patient will experience pain in LIF)
o Nails
o Anaemia ❷PALPATION
o Clubbing (Crohn’s disease, Ulcerative colitis,
• Kneel down at the patient’s right side
Cirrhosis)
• Ask the patient if there is any generalized pain or
o Leukonychia (Caused by hypoproteinemia
localized pain
associated with liver disease)
• Palpate all nine distinct areas of the abdomen
o Koilonychia (Spoon shaped nails seen in iron
starting furthest from you, unless the patient
deficiency anaemia)
indicates an area of pain, in which case palpate this
o Asterixis (liver flap), seen in decompensated
area last. Look at patient’s face for signs of pain while
liver disease.
palpating. Palpate the abdomen with flattened
• THE FACE
fingers. Start by superficial palpation of the 9
o Eyes
quadrants then by deep palpation and feel the
o Anaemia (pale conjunctiva)
presence of any masses
o Jaundice
o Mouth Dentition
o Ulcers (Inflammatory bowel disease, herpes
simplex)
o Tongue Dehydration- red, beefy (B12
deficiency)
o Angular stomatitis Caused by iron, folate
and vitamin B/ C deficiency Also seen in
herpes simplex and oral candidiasis
o Hepatic Fetor
• THE ARMS & TRUNK
o Spider Navi are found along the distribution
of the Superior Vena Cava (i.e., above the
nipple line) and are associated with
estrogen excess
o Purpura
o Petechiae can be caused by low platelets or
raised prothrombin time
o Gynecomastia
o Signs of pruritus – scratch marks
• SUPRACLAVICULAR LYMPH NODES Regions of the abdomen. RH, right hypochondrium; RF,
o Virchow’s Node in the left supraclavicular right flank or lumbar region; RIF, right iliac fossa; E,
fossa can be enlarged in gastric cancer. epigastrium; UR, umbilical region; H, hypogastrium or
suprapubic region; LH, left hypochondrium; LF, left flank
or lumbar region; LIF, left iliac fossa.
• Liver: (do percussion of liver after palpation)

Start in the right iliac fossa, asking the patient to take • Kidneys:
deep breaths in and out. Move your hand upwards ‘Ballot’ the kidneys using both hands
towards the costal margin during inspiration until
you feel a liver edge on expiration.
If the liver is palpable check the:
o Size (record enlargement in cm below costal
margin)
o Texture (soft / firm / hard / nodular)
o Edge (smooth / irregular) An irregular liver
edge suggests metastases
• Murphy’s test: (in cholecystitis station)

With your hand in the position of the gallbladder,
fingers pointing up, ask the patient to take a deep
breath in and out. Pain on expiration as the
gallbladder comes to rest against your fingertips is a
positive Murphy’s test.
• Spleen: (do percussion spleen after palpation)
Start palpating in the right iliac fossa, using the same
breathing technique as for liver palpation. However,
this time move gradually towards the left upper
quadrant. Note the size, texture and edge of the
spleen.
• Abdominal aorta:
Palpate in the region of the lower epigastrium/ upper
umbilical area, slightly towards the left of the mid-
line, deeply for a pulsatile mass. Note the
approximate diameter by using both hands to feel
the lateral edges of the mass.

❸PERCUSSION ❹AUSCULTATION
• Upper liver border • Over the left iliac fossa for bowel sounds
• Spleen • Over the liver for a bruit
• Bladder • Over the aorta (left of the umbilicus), iliac vessels
• Ascites (mid-inguinal point) and the renal arteries for bruits
Start by percussing in the midline towards either
flank and note any change in pitch from resonant to Say you would like to
dull, indicating fluid. If there is dullness, keep your • Feel the hernial orifices
finger on this area and ask the patient to roll onto • Examine external genitalia (e.g., for testicular
his/ her side so that the dull area is now superior. atrophy in chronic liver disease)
Percuss again and note any change in pitch back to • Perform a rectal examination
resonance. If present, this is shifting dullness. • Examine the lower limbs for peripheral edema

DISCUSSION
Patient presented by LIF pain and long-standing history of constipation. On general look, the patient seemed to be in pain. On
inspection of the hands, there was no clubbing, nail changes or liver flaps. No jaundice or signs dehydration. On inspecting the
arms and trunks, there were no spider naevi, gynecomastia, purpurea, pruritis or scratch marks. He doesn’t have any enlarged
supraclavicular LN.
On local inspection of his abdomen, there were no scratch marks, visible swellings or visible pulsations. The patient had some LIF
pain and tenderness on coughing and lifting his head of the bed.
On palpation, the patient didn’t have any palpable swellings over his abdomen in all 9 quadrants. But on light palpation over the
LIF there was tenderness. The patient didn’t’ have any liver or splenic enlargement. On ballottement of his kidneys, there was no
palpable swelling or tenderness. The patient didn’t have any palpable pulsatile abdominal masses.
On percussion, the patient didn’t seem to have any fluid collection.
On auscultation, the patient had normal bowel sounds with no audible bruits.
By looking at his charts, the patient has fever, tachycardia and an increased respiratory rate.
Differential diagnosis of LIF pain?

• Diverticulitis
• Constipation
• Irritable bowel syndrome
• Pelvic inflammatory disease
• Rectal carcinoma
• Ulcerative colitis
• Ectopic pregnancy
Investigations
• Complete labs
o FBC, inflammatory markers, liver functions, U&Es, ABG
• Imaging
o Abdominal USS
o CT Abdomen
If CT shows only sigmoid wall thickening with one locule of gas seen, what will be your management?
• Antibiotics:
o Co-Amoxiclav
o Garamycin
o Clindamycin
• Bowel rest
• DVT prophylaxis
If no response to antibiotics, what will you do?

• Percutaneous drainage
• Hartman's procedure

ACUTE CHOLECYSTITIS
Perform classic abdominal examination as before
Read the patient charts

• Fever
• Undetectable urobilinogen in urine
• Increased liver enzymes
DISCUSSION
Differentials?
Tokyo Consensus Guidelines for severity grading of acute
• Acute cholecystitis
cholecystitis.
• Ascending cholangitis
Grade III (severe) acute cholecystitis
• Appendicitis
Associated with dysfunction of any one of the following
• Perforated peptic ulcer organs/systems:
• Acute pancreatitis 1. Cardiovascular Hypertension requiring treatment
• Acute Pyelonephritis dysfunction with dopamine ≤5 μg/kg/min, or
• Myocardial infarction any dose of norepinephrine
• Lower lobe pneumonia (noradrenaline)
• Renal pathology 2. Neurological dysfunction Decreased level of consciousness
3. Respiratory dysfunction PaO2/FiO2 ratio <300
Charcot’s triad? (See part A, Hepatobiliary and 4. Renal dysfunction Oliguria; creatinine >2.0 mg/dL
pancreatic surgery) 5. Hepatic dysfunction Prothrombin time (PT-INR) >1.5
• Jaundice 6. Haematological Platelet count <100 000/mm3
• Fever, usually with rigors dysfunction
• Abdominal pain (RUQ) Grade II (moderate) acute cholecystitis
Associated with any one of the following conditions:
Investigations? 1. 1 Elevated white cell count (>18 000/mm3)
• Liver function tests 2. 2 Palpable tender mass in the right upper abdominal quadrant
• Urea and electrolytes 3. 3 Duration of complaints >72 hours
• Full blood count 4. 4 Marked local inflammation (gangrenous cholecystitis,
• CRP pericholecystic abscess, hepatic abscess, biliary peritonitis,
• Abdominal ultrasound emphysematous cholecystitis)
• MRCP Grade I (mild) acute cholecystitis
Does not meet the criteria of grade II or grade III acute cholecystitis.
What to see in USS? Grade I can also be defined as acute cholecystitis in a healthy person
• Presence of stones with no organ dysfunction and mild inflammatory changes in the
• Gallbladder wall thickening (greater than 4 – gallbladder, making cholecystectomy a safe and low-risk operative
5mm) or edema (double wall sign) procedure
• Sonographic Murphy’s sign
• Pericholecystic fluid
The sonogram only
• Common bile duct dilatation
shows gallstones
within the
Dilated CBD, what are you going to do? gallbladder but no
ERCP both diagnostic and therapeutic evidence of
cholecystitis (ie,
Management? gallbladder wall
Hospital admission + supportive care thickening,
pericholecystic fluid,
• IV hydration
common bile duct
• Correction of electrolyte abnormalities dilatation,
• Analgesia (NSAIDS adjusted for age and renal sonographic
function, Opioids if NSAIDS contraindicated) Murphy sign).
• NBM, if vomiting → NG tube
• IV Abx
Surgical treatment
• Cholecystectomy in 5 days if conservative
treatment fails

Abx?
Depends if the patient is high-risk or low risk. After discussion with microbiology and according to trust guidelines
Single-agent regimen
• Piperacillin-tazobactam 4.5gm IV QDS
Combination regiment with metronidazole
• Cefepime or Ceftazidime 2gm IV TDS
• + Metronidazole 500mg IV/PO TDS

ACUTE APPENDICITIS
Examine the patient charts

• Fever
• Mild tachycardia
• Leucocytosis
Special signs
• Rovsing's sign
Pressure in the LIF causes pain in the RIF with appendicitis
• Obturator sign
Ipsilateral hip and knee are flexed; internal rotation of the hip (heel moves outwards) stretches obturator internus, which
causes pain if in contact with an inflamed appendix
• Psoas sign
Inflammatory processes in the retroperitoneum irritate the psoas muscle, causing ipsilateral hip flexion, Straightening the
leg causes further pain.
DISCUSSION
Differentials?
• Acute appendicitis
• Leaking duodenal ulcer
• Pelvic inflammatory disease
• Salpingitis
• Ureteric colic
• Inflamed Meckel’s diverticulum
• Ectopic pregnancy
• Crohn's disease
• Complicated ovarian cyst
Investigations?
• Urine analysis
• Urea and electrolytes
• Full blood count
• Abdominal ultrasound
• CT abdomen and pelvis
Treatment?
Appendectomy (open / laparoscopic)
What will you do if you encountered blood in the peritoneal cavity while doing appendectomy?
• I will call for an obstetric surgeon (may be ruptured ectopic pregnancy)
• I will order group and save
• I will have to perform appendectomy eventually

GENERALIZED LYMPHADENOPATHY
Perform classic abdominal examination as before + examination of lymph nodes
Distribution of palpable lymph glands.
Palpation of the cervical glands.

(A) Examine the glands of the anterior triangle from behind, using both hands.
(B) Examine for the scalene nodes from behind with your index finger in the angle between the sternocleidomastoid muscle and the clavicle.
(C) Examine glands in the posterior triangle from the front.

Palpation of the axillary, epitrochlear and inguinal glands.
(A) Examination for right axillary lymphadenopathy.
(B) Examination of the left epitrochlear glands.
(C) Examination of the left inguinal glands.
DISCUSSION
Generalized Lymphadenopathy? Lymph nodes may be palpable in normal people,

• Lymphadenopathy found in more than two distinct anatomic especially in the submandibular, axilla and groin
regions. regions
• More likely to result from serious infections, autoimmune
disease, and disseminated malignancies. Specific testing is Lymphadenopathy =
usually required. enlargement of the lymph nodes
• Generalized adenopathy infrequently occurs in patients with
neoplasms, but it is occasionally seen in patients with leukemias Generalized =
and lymphomas, or advanced disseminated metastatic solid more than two non-contiguous lymph node groups
tumors.
Etiology
• Viral • Protozoal
o Common upper respiratory infections. o Toxoplasmosis, leishmaniasis, American
o Infectious mononucleosis, trypanosomiasis (also known as Chagas'
cytomegalovirus (CMV). disease).
o Rubella, varicella, measles. o African trypanosomiasis (sleeping
o HIV. sickness).
o Hepatitis A and hepatitis B. • Fungal
o Roseola infantum - human herpesvirus o Coccidioidomycosis.
type 6 (HHV-6). • Autoimmune disorders and hypersensitivity states
o Dengue. o Juvenile idiopathic arthritis.
o Adenovirus. o Systemic lupus erythematosus (SLE).
• Bacterial o Drug reactions (e.g. phenytoin,
o Septicaemia. allopurinol, primidone).
o Typhoid fever. o Serum sickness.
o TB. • Storage diseases
o Syphilis. o Gaucher's disease.
o Plague. o Niemann-Pick disease.
o Lyme disease. • Neoplastic and proliferative disorders
o Tularaemia. o Acute leukaemias.
o Brucellosis. o Lymphomas (Hodgkin's, non-Hodgkin's).
o Neuroblastoma.
o Histiocytoses.

Investigations
Depends on history and examination and likely cause of
lymphadenopathy. Investigations may not be required in cases of
obvious cause and quick resolution with or without treatment.
• FBC, blood film and ESR, plasma viscosity or CRP
(according to local policy).
• LFTs: liver infiltration.
• Infection swabs from primary infection site for C&S.
• Further investigations
Depends on the individual presentation but may include:
o Viral titres – e.g. Epstein-Barr virus, HIV, hepatitis.
o Investigations for tuberculosis, syphilis serology,
toxoplasma screen.
o Blood cultures.
o Autoantibody screen: SLE, rheumatoid arthritis.
o CXR: sarcoidosis, TB, primary or secondary
malignancy.
o Ultrasonography may be helpful in evaluating the
extent of lymph node involvement.
o CT scan/MRI scan: e.g. nodal distribution, staging
of lymphoma.
o Fine-needle aspiration.
o Newer imaging modalities such as 18F-
fluorodeoxyglucose positron emission tomography
(18F-FDG PET) and magnetic resonance
lymphography are increasingly being used in the
diagnosis and monitoring of lymphomas and other
conditions involving generalised
lymphadenopathies.
Excisional biopsy is regarded as the diagnostic method of choice
Lymph node regions
Lymphoma staging?
Ann Arbor staging system
• stage I: involvement of a single lymph node region or of a single extralymphatic organ or site
• stage II: involvement of two or more lymph node regions on the same side of the diaphragm or localized involvement of
an extralymphatic organ or site
• stage III: involvement of lymph node regions or structures on both sides of the diaphragm
• stage IV: diffuse or disseminated involvement of one or more extralymphatic organs, or either:
o isolated extralymphatic organ involvement without adjacent regional lymph node involvement, but with disease
in distant sites
o involvement of the liver, bone marrow, pleura or cerebrospinal fluid

PARAUMBLICAL HERNIA AND INCISIONAL HERNIA
❶INSPECTION
• Describe any scars and look for other scars, stomas, etc.
• Ask the patient to lift their head off the bed and look for bulging of the hernia or the scar
❷PALPATION
• Enquire about tenderness and palpate the hernia, commenting on any defect you can feel
• Ask the patient to cough and demonstrate weakness in the scar or abdominal wall, feeling for bulging of abdominal
contents against your hand
• Try to determine the size of the defect
• If there is a midline longitudinal abdominal bulging with no scar, consider divarication of the recti.
❸AUSCULTATION
• Listen for bowel sounds
DISCUSSION
Treatment?
Open or laparoscopic mesh repair is
possible. At open surgery, the mesh can be
inserted as an onlay, inlay, sublay or
intraperitoneal position (underlay)

INGUINOSCROTAL EXAMINATION

Inguinal hernia • Lump
Direct / Indirect (most probably) o Inguinal (bubonocele / inguinoscrotal
o Expansile impulse on coughing
o Reducible
• Positive DIR (if oblique hernia)
• Scrotal neck (full / empty)
• Swelling separable from the testis
• ± Bowel sounds on auscultation
Hydrocele • Lump purely scrotal
• Empty scrotal neck
• Swelling not separable
• Transilluminable
Patient standing during examination Expose the patient from umbilicus to feet.
❶INSPECTION
• Inspect the lump ❹TESTS
6S (Site, Size, Shape, Symmetry, Skin, Scars) • Perform deep inguinal ring (DIR) test – not
o Inguinal / inguinoscrotal: hernia significant if inguinoscrotal swelling is evident
o Purely scrotal: hydrocele • Transillumination
• Ask about pain
• Ask the patient to cough
o Inguinal / inguinoscrotal → visible impulse on
cough
❷PALPATION
• Check for temperature using the back of your hand
• Lump
o Palpate the lump: ask the patient to cough (if
hydrocele, there will be no expansile impulse on
coughing)
o Identify ASIS, pubic tubercle: show the position
of the lump in relation to the inguinal ligament
o Ask the patient to reduce the lump / hernia A – Hydrocele marked by a fluctuant painless scrotal swelling
• Scrotum B – Transillumination
o Inspect the scrotum from all sides, lift the
scrotum and inspect the base
o Examine scrotal neck
▪ Empty
 if mass is above the neck → inguinal
hernia / bubonocele
 if mass is only below the neck →
hydrocele
▪ Full → inguinoscrotal hernia
o Testicle, Epididymis, Vas Deferens
o Testis separable from swelling or not
▪ Separable → hernia
▪ Inseparable → hydrocele
• Contralateral side
• Lymph nodes
❸AUSCULTATION
• Auscultate the lump (may reveal the presence of
intestinal sounds)

DISCUSSION
Management of inguinal hernia? What are the differentials for a scrotal swelling?
Surgical repair (herniorrhaphy) Common differentials include:
Usually done in the elective setting • Hernia e.g. an inguinal or femoral hernia
• Open • Lymph nodes
Associated with postoperative pain and • Varicocele
numbness because of the large inguinal • Swelling related to the testes
incision. o Hydrocele
o Bassini method o epididymal cyst
old method – direct suturing o lipoma of the cord
o Open mesh repair o testicular tumor
▪ Open flat mesh (OFM) • Infection
▪ Open preperitoneal o Orchitis
mesh (OPPM) o Epididymitis
▪ Open plug and mesh • Testicular torsion
repair (OPM) • Spermatocele
• Laparoscopic
o Transabdominal preperitoneal
(TAPP) repair
involves access to the hernia
through the peritoneal cavity
o Totally extraperitoneal (TEP)
is the newer laparoscopic
technique, in which the hernia site
is accessed via the preperitoneal
plane without entering the
peritoneal cavity
Definition of Hydrocele? What is a hydrocele?

Accumulation of fluid within the tunica vaginalis
Types and causes

Type Cause
Communicating •Persistence of the processus vaginalis allows peritoneal fluid to communicate freely with the
hydrocele scrotal portion of the processus.
• They are congenital but may first present in older boys and men as a result of increased intra-
abdominal pressure
Non-communicating • Due to imbalance between secretion and reabsorption of fluid
hydrocele • Can occur secondary to minor trauma, testicular torsion, epididymitis, varicocele operation or
following a repair of a hydrocele.
Hydrocele of the cord The processus vaginalis closes segmentally, trapping fluid within the spermatic cord
Abdomino-scrotal Rare; a large hydrocele lies across the internal ring, with both inguino-scrotal and intra-abdominal
hydrocele lobes.
Can also be divided into primary (idiopathic) and secondary (e.g. trauma, tumor, epididymo-orchitis, lymphatic obstruction etc.)
A congenital, simple hydrocele

usually disappears within the first
1-2 years of life. Causes in older
boys and men include trauma,
epididymo-orchitis, testicular
torsion, hernia, varicocele, and
testicular tumour. Hydroceles in
older boys and men may also be
due to generalised oedema, such
as nephrotic syndrome or heart
Another classification for hydroceles (a) Vaginal hydrocoele (very common);
failure.
(b) ‘infantile’ hydrocoele; (c) congenital hydrocoele; (d) hydrocoele of the cord.

Investigations
Investigations are not required for simple hydroceles but are essential if there is any doubt in the diagnosis or any suggestion of
an underlying cause. EXCLUDE TUMOR
• Ultrasound can help to determine if any underlying pathology is present. Spermatoceles can be clearly distinguished.
• Diagnostic aspirations should be avoided, as they may lead to the spread of malignant cells.
• Serum alpha-fetoprotein and human chorionic gonadotrophin levels help to exclude malignant teratomas or other germ
cell tumours.
Management
Non-operative
• Many hydroceles in infancy resolve before the age of 2 years and so observation and non-intervention are usually
appropriate for hydroceles in infants unless there is suspicion of an associated inguinal hernia or underlying testicular
pathology.
• Asymptomatic adults with isolated noncommunicating hydroceles can be observed indefinitely or until they become
symptomatic
Surgical treatment
Congenital hydrocoeles are treated by herniotomy if they do not resolve spontaneously
Established acquired hydrocoeles often have thick walls. There are three main surgical techniques
• Plication
Lord’s operation is suitable when the sac is reasonably thin-walled. There is minimal dissection and the risk of haematoma
is reduced.
• Eversion
The sac is opened and everted behind the testis, with placement of the testis in a pouch prepared by dissection in the
fascial planes of the scrotum (Jaboulay’s procedure)
• Excision.
Unless great care is taken to stop bleeding after excision of the wall, haemorrhage from the cut edge is liable to cause a
large scrotal haematoma. This approach is not recommended.
Jaboulay’s procedure. The hydrocoele sac is Lord’s operation. A series of interrupted absorbable sutures
everted and anchored with sutures. is used to plicate the redundant tunica vaginalis. When
these are tied, the tunica bunches at its attachment to the
testis.

BREAST EXAMINATION

Gynecomastia Normal findings
50-year-old man, alcoholic, drinks 30 units/week, 20
cigarettes/day, having abdominal distention, bilateral breast
enlargement since long time, do breast examination
Position
Ask the patient to sit upright, ideally on the side of the bed.
Ask the patient to uncover the breasts at this point.
❶INSPECTION Hands on hips:

Hands on thighs / arms by side: Ask patient to place hands on their hips and push
• Position the patient with their hands on their thighs inwards (to tense pectoralis major) / lean forward
relaxed. • Repeat inspection.
• Scars – small scars (lumpectomy) / large diagonal • Observe for any masses once again:
scars (mastectomy) If a mass is noted, observe to see if the mass moves
• Asymmetry – healthy breasts are often with the pectoralis muscle. This is known as
asymmetrical tethering and suggests invasive malignancy
• Masses – note the size and position- look for
overlying skin changes Hands above head:
• Skin changes: Ask patient to place both hands behind their head.
o Erythema – infection / superficial • Inspect the breast tissue for any evidence of:
malignancy o Masses
o Puckering – may indicate an underlying o Asymmetry
malignant mass o Dimpling / puckering
o Peau d’orange – cutaneous edema – Ask the patient to now lean forwards, keeping their
inflammatory breast cancer hands behind their head.
• Nipple changes: • Repeat inspection of the breast tissue as above.
o Retraction – congenital / underlying tumor This position will exacerbate any skin dimpling /
/ ductal ectasia puckering which may relate to an underlying
o Discharge – may indicate infection or mass.
malignancy
o Scale – may indicate Eczema or Paget’s
disease
Positions for inspecting the breasts. (A) Hands resting on thighs. (B) Hands pressed on to hips. (C) Arms above head. (D) Leaning forward with
breasts pendulous.

❷PALPATION Nipple:
Patient lying 45ᵒ on couch • Ask the patient to squeeze the nipple to
Breast: demonstrate the presence of discharge
• Examine the “normal” asymptomatic breast first. • Yellow / green discharge – suggestive of infection
Ensure to warm your hands before touching the • Bloody discharge – more suspicious of malignancy –
patient. e.g. papilloma
• Position the patient laid on the bed at a 45-degree
angle. Axilla:
• Ask the patient to place their hand on the side being • Have the patient sit on the edge of the bed facing you.
examined behind their head. • Support the patient’s arm on the side being examined
with your forearm.
• If you’re examining the right axilla, use your right arm to
support the patient’s (vice versa for left).
• Palpate the axilla with your free hand, ensuring to cover
all areas of the axilla:
o Medial / lateral / anterior / posterior walls
o Apex of the axilla
o Note any lymphadenopathy – malignancy /
infection
Other lymph nodes:

• Finally perform a general lymph node examination
of the following areas:
• Cervical
• Supraclavicular
• Infraclavicular
• Parasternal
To complete my examination:
• Complete abdominal examination to detect liver
• Use the flat of your fingers to compress the breast enlargement (liver cirrhosis)
tissue against the chest wall, feeling for any masses. • Testicular examination to rule out testicular
• Use a systematic approach to ensure all areas of the enlargement (tumor), or atrophy
breast are examined: • External genitalia examination to rule out
o Clock face method – examine each “hour” hypogonadism
of the breast • Check thyroid status to rule out hyperthyroidism
o Spiral method – start at the nipple and • Check signs of liver failure
work outwards in a concentric circular • Check signs of renal failure
motion • Visual field examination to rule out prolactinoma
Axillary tail: • Chest examination to rule out bronchial carcinoma
Palpate the axillary tail of breast tissue

DISCUSSION
Causes of bilateral gynecomastia?

• Liver cirrhosis due to alcoholism (the main probable cause
in this patient) as a result of failure of the liver to
metabolize estrogens
• Bronchial carcinoma
• Pituitary tumors (prolactinoma)
• Hyperthyroidism
• Testicular tumors
• Renal failure
• Hypogonadism
• Drug related
• Senility
Drug-induced gynaecomastia caused by cimetidine.
Laboratory studies?
• A serum chemistry panel may be helpful in evaluating for renal or liver disease.
• Free or total testosterone, luteinizing hormone (LH), estradiol, and dehydroepiandrosterone sulfate levels are used to
evaluate a patient with possible feminization syndrome.
• thyroid-stimulating hormone (TSH) and free thyroxine levels if hyperthyroidism is suspected.
• Serum prolactin levels, if pituitary tumors were suspected
• Testicular tumor markers
Imaging studies?
• Mammogram if 1 or more features of breast cancer are apparent upon clinical examination.
• This can be followed by fine-needle aspiration or breast biopsy, as the case merits.
• Testicular ultrasonogram if the serum estradiol level is elevated and the clinical examination findings suggest the
possibility of a testicular neoplasm.
• Abdominal ultrasound to detect liver cirrhosis
• Chest x ray to rule out chest malignancies
Treatment?
• Treatment of the underlying cause
• Surgical:
o Reduction mammoplasty
o Mastectomy with preservation of the areola and nipple can be performed


CHEST PAIN / PULMONARY EMBOLISM
Stem Chest Pain on… Findings

1 POD8 after elective hip replacement • Symptoms and signs of PE
2 POD8 after abdominal surgery*
* Do not confuse with POD6 anastomotic leak station
This is a potentially unwell patient. Therefore, you should approach him in an ABC manner
A
• You know his airway is patent as he is talking to you
B
• Inspect chest for respiratory movement, is it equal?
• Look for central cyanosis, use of accessory muscles,
• Feel for chest expansion, tracheal position
• Percuss* the chest for dullness / hyper-resonance, test vocal fremitus
• Listen* for bilateral air entry, crackles of consolidation or pulmonary edema
* Percussion and auscultation on posterior chest as well
C
• Inspect for cyanosis, and look at the JVP
• Feel the pulse, making note of any rhythm abnormalities and tachycardia, and peripheries (cold and poorly perfused v
hot and septic)
• Auscultate the heart – muffled heart sounds could indicate tamponade, a murmur could suggest a significant valve lesion
D
• GCS / AVPU
E
• Make a point of checking the calves for a DVT
• Check the drug chart for SC heparin and TEDS – have they been signed for
• Check the fluid chart to ensure they are not overloaded

DISCUSSION
This patient presented with acute pleuritic chest pain and shortness of breath 8 days after a hip operation. I note from their drug
chart that they have missed two doses of their subcutaneous heparin.
He is hemodynamically stable but had saturations of 88% on 2L. This improved with high flow oxygen. They also had a swollen left
calf. Otherwise examination showed a clear chest with good bilateral air entry and a normal percussion note making a pneumonia
and pneumothorax unlikely. An MI is possible but less likely due to the nature of the pain, however I am awaiting an ECG and
troponin. My top differential is a pulmonary embolus.
• Pulmonary embolism
• Myocardial infarction
What investigation would you arrange now?

• Assuming renal function was within acceptable limits I would arrange a CTPA to exclude a PE
• Chest x-ray
• D- dimer
• ABG: respiratory alkalosis
• ECG
o Right ventricular strain pattern – T wave inversions in the right precordial leads (V1-4) ± the inferior leads (II, III,
aVF).
o Right axis deviation
o S1, Q3, T3 pattern – deep S wave in lead I, Q wave in III, inverted T wave in III
What is the management of a pulmonary embolism?

Management follows the usual ALS sequence of securing the airway before moving on to breathing where high flow oxygen is
essential and then circulation. Assuming this was all done, the management can be spilt into massive PE and non-massive PE.
Massive PE is characterized by hemodynamic compromise and may require thrombolysis. I would put out a crash call if the patient
presented in this way to get urgent help.
If the patient is stable, treatment initially with a therapeutic dose of subcutaneous heparin, followed by warfarin is warranted. I
would involve the appropriate medical team to follow this patient up.
If you were scrubbed in the theatre and have been updated with the patient condition, what will you do?
I will put a crash call immediately

ARTERIOVENOUS FISTULA

Brachiocephalic fistula with distal ischemia Dialysis associated steal syndrome (DASS)
Patient known to have chronic kidney disease and has had an • Ischemic changes on inspection
AV fistula for renal dialysis. The patient had blue discoloration • Radial pulse (diminished, augmentation on compression)
of his hand and upper limb overnight. Examine his upper limb
Position: Put the patient's hands and place his palms upward ❷PALPATION
on a white pillow if available • Tenderness: Not tender
Exposure: Expose hand, forearm, shoulder and chest • Temperature: Warm
• Pulses: All upper limb pulses must be evaluated, if any not
❶INSPECTION palpable use handheld doppler
• Fistula • Pulsatility:
o Site: Anterior aspect of forearm (antecubital fossa) The pulse in the fistula may be best appreciated using
o Size: 3 x 1 cm the fingers (not the palm or thumb) and should be
o Shape: Oval evaluated along the length of the fistula from the
o Skin overlying: Brown pigmentation Erythema arteriovenous anastomosis through the venous
o Surface: Regular outflow. Very little pulse should be detected with
o Scars: there is an overlying scar, any aneurysmal palpation of the fistula.
dilatations (localized bulging zone) Normal: not pulsatile, soft and compressible
o Aneurysms: comment on the presence of Outflow stenosis: Hyperpulsatile, Water-hammer
▪ Thin/shiny overlying skin pulse
▪ Ulcers Inflow stenosis: Hypopulsatile, feeble, flat
▪ Depigmentation • Thrill:
• Upper Extremity Best evaluated using the palm of the hand, rather
o Arm elevation test: (for venous outflow obstruction) than the fingers. The normal hemodialysis
If the arm is elevated to a level above that of the arteriovenous fistula is characterized by a soft,
heart, the normal AV fistula will collapse. Even if continuous, diffuse thrill that is palpable over the
the patient has a large "mega-fistula," it will at course of the fistula and most prominent over the
least become flaccid. However, if a venous stenosis arteriovenous anastomosis. It should have both a
is present, that portion of the AV fistula distal to systolic and diastolic component.
the lesion will remain distended while the proximal Normal: diffuse, systolic and diastolic, continuous
portion collapses. If the entire fistula collapses Outflow stenosis: localized, systolic only, discontinuous
when the patient's arm is elevated, one can Inflow stenosis: diffuse, systolic only, weak
conclude that the outflow of the fistula is normal. • Augmentation test:
o Central venous outflow obstruction When the normal fistula is occluded a short distance
▪ Venous collateralization over the chest / pectoral from the arteriovenous anastomosis, the arterial pulse
region or shoulder at the wrist should be increased or augmented.
▪ Entire upper limb edema Direction of flow:
o Hematoma The direction of flow can be easily determined by
o Signs of ischemia (Steal syndrome) occluding the fistula with the tip of the finger and
▪ Pallor palpating on each side of the occlusion point for a pulse.
▪ Bluish discoloration The side without a pulse is the downstream (i.e. in the
▪ Ulcers direction of flow) side
▪ Gangrene
❸AUSCULTATION
• Bruits
The bruit over a well-functioning fistula has a low-pitched,
soft, machinery- like rumbling sound and, like the thrill,
has both a systolic and diastolic component. The bruit is
also more accentuated at the arterial anastomosis.
Normal: low-pitched, soft, systolic + diastolic
Outflow obst: high-pitched, loud
• Heart murmurs (for IE)

❹EXAMINATION TO DETECT EXTREMITY ISCHEMIA 2) Ischemic monomelic neuropathy:
Two clinical variants of ischemia are recognized, both with Characterized by ischemic changes that are confined
characteristic findings on physical examination to the nerves of the hand and spare other tissues
• Paresthesias; and numbness in the hand,
1) Dialysis ischemic steal syndrome: • Diffuse motor weakness or paralysis:
• Hands appear pale or cyanotic and feels cool to the touch o Poor wrist extension (radial nerve)
• The radial pulse is generally diminished or absent o Poor function of the intrinsic hand
• Compression of the fistula augments the distal pulse and musculature (ulnar nerve)
may temporarily relieve painful symptom o Poor thumb opposition (median nerve)
• Using a Doppler to listen to the bruit over the distal artery are typically present.
frequently aids in this examination. The sound is • The hand is warm, and often a palpable radial
significantly augmented when the fistula is occluded. pulse or audible doppler signal is present.
• With chronic ischemia, ulceration and gangrene at the
fingertips may be present
DISCUSSION
Dialysis associated steal syndrome (DASS)
Investigations?
• Arterial duplex study
• CT angiography
Treatment options
• Restriction of fistula flow through banding, or modulation through surgical revision.
• Ligation of the fistula and creation of a more proximal fistula in the same or the contralateral limb

SUPERFICIAL LUMP / LIPOMA
❶INSPECTION • Compressibility
• 6S Swelling on pressure reduces in size only partially but
o Site will not disappear completely and on releasing the
o Size pressure swelling again comes back to its original size
o Shape and shape immediately.
o Surface – smooth, irregular • Pulsations, thrills, and bruits
o Skin changes, inflammation Two fingers are placed over the swelling
o Scars • Fluctuation, Paget’s test
Positive fluctuation signifies presence of fluid
❷PALPATION
• Size
Size is measured using tape (vertical in cm X
horizontal in cm)
• Temperature
• Tenderness
• Edge / Margins
Edge of the swelling is examined using pulp of the
index finger. Erosion of the margin into the deeper
plane like bone is also checked. Dermoid cyst
commonly shows erosion into the bone. In lipoma
margin slips away from the finger—slip sign
o Well-delineated or ill-defined
o Regular or irregular
o Sharp or rounded
• Fixity to skin
o Mobility of the skin over the swelling is
checked or skin over the swelling is pinched
to confirm whether skin is free or attached
to swelling underneath
• Fixity to deeper structures
o If swelling is freely mobile it could be in
subcutaneous plane
o If swelling is adherent to muscle underneath,
Typical slip sign is positive in lipoma.
then when muscle is contracted against
• Surface of the swelling resistance mobility of the swelling is
With palmar surface of the fingers restricted but it becomes more prominent.
e.g. smooth, nodular, irregular When muscles relaxes swelling will be
mobile
• Consistency
o If swelling is arising from the muscle or deep
e.g. soft / firm / hard
to muscle then size of the swelling decreases
• Reducibility
(less prominent) when muscle is contracted.
When swelling is pressed gets reduced completely and
Again mobility which is present initially will
disappears is said to be reducible swelling
disappear completely during contraction of
the muscle

• Transillumination ❸AUSCULTATION
o In a darkened room, press the lighted end of It is done to look for bruit over the swelling
a pen torch on to one side of the swelling. A
cystic swelling will light up if the fluid is ❹ASSESS REGIONAL LYMPH NODES
translucent. See Generalized Lymphadenopathy station
DISCUSSION
What is your differential diagnosis? Where you can't find lipoma?

• Lipoma Palms, soles, brain , tongue
• Sebaceous cyst
• Abscess Investigations?
• Soft tissue tumor • Ultrasound
• Bone tumor • CT / MRI
• Vascular malformation • Biopsy; FNAC, Excisional
Definition of lipoma? Treatment

Lipoma a benign tumor of fat, it’s the most common soft Excision / Liposuction assisted lipoma removal
tissue tumor of adulthood. These tumors are subclassified
according to morphologic and/or characteristic molecular Lipoma in COPD, anesthetic?
features as conventional lipoma, fibrolipoma, angiolipoma, • Local anesthetic if small
spindle cell lipoma and myelolipoma. Nerve block or regional if large
Dangerous lipomas?
• Mucosa of intestines
• Thecal or spinal cord
• Vocal cords

EXAMINATION STEPS SUMMARY / CHECKLIST
KNEE HAND
LOOK (standing position) LOOK
• Front, back and behind • Dorsum, palmar and elbow
• Gait FEEL
FEEL (supine position) • Temperature
• Temperature • Palpation incl. arm, snuffbox
• Effusion MOVE
• Quadriceps circumference • ROM, incl. PIP and DIP joints
• Palpation (in flexion) • Function: grip, dexterity
MOVE NERVES
• ROM: active and passive, feel crepitus SPECIAL TESTS
• Muscle testing • Modified Durkan’s
SPECIAL TESTS • Tinel’s
• Posterior sag sign • Phalen’s
• Drawer tests
• Lachman's test SPINE
• Varus and valgus stress LOOK (standing)
• McMurray’s • Front, back, behind
• Gait
HIP FEEL (sp, paraspinal, SIJ)
LOOK MOVE (lumbar spine only)
(standing) SPECIAL TESTS
• Front, back and behind • Schober’s test
• Gait • SLR, Lasegue
• Trendelenburg sign • Femoral nerve stretch
FEEL (supine) PERIPHERAL NEUROLOGICAL EXAM
• Temperature • Tone (leg roll, lift, ankle clonus)
• Palpation • Power
• Leg length, Galeazzi • Co-ordination
MOVE • Reflexes
• ROM, feel crepitus • Sensation
• Muscle testing
SPECIAL TESTS FOOT
• Thomas’ INSPECTION (standing)
• FABER • Front, back, behind
• Gait
ANKLE PALPATION (supine)
LOOK (standing) • Course of common peroneal
• Inspection • Popliteal space
• Gait • Tinel’s sign
FEEL PERIPHERAL NEUROLOGICAL EXAM
• Temperature • Tone (leg roll, lift, ankle clonus)
• Palpation including proximal fibula and Achillis • Power
• Pulses • Co-ordination
MOVE • Reflexes
• ROM, power • Sensation
SPECIAL TESTS
• Anterior Drawer
• Talar tilt

CVS CN
INSPECTION AND PALPATION I (smell sensation)
• General II
• Hand • Visual acuity
o Inspection • Pupils: light, accomodation
o Cap refill • Visual fields
o Pulse, collapsing pulse III, IV, VI
• BP • Eye movements (“H” shape)
• Neck V
o Carotid • Sensory
o JVP, reflex • Motor: clench teeth, jaw against resistance
• Face, eye, mouth VII
• Chest • Eyebrows, eyes, cheeks, teeth, neck, taste.
o Inspection VIII
o Palpate apex, heaves, thrills • March on spot
• Whisper
AUSCULTATION • Rinne, Weber
• Diaphragm and bell IX, X
• Accentuation maneuvers • Uvula deviation (“aaah”)
• Carotid bruits • Cough
• Back (lung bases) XI
LOWER LIMB • Trapezius
• Sternocleidomastoid
RESPIRATORY XII
INSPECTION AND PALPATION • Tongue deviation
• General
• Hand CEREBELLAR
o Inspection GAIT
o Cap refill HEAD
o Pulse • Speech
• Neck • Nystagmus
o Carotid • Finger to nose
o JVP, reflex ARMS
o Lymph nodes • Pronator drift
o Trachea • Rebound phenomenon
• Face, eye, mouth • Intentional tremors
• Chest • Dysdiadochokinesia
• Tone, reflexes
o Inspection
LEGS
o Palpate (expansion)
• Heel to shin
PERCUSSION
• Tone, reflexes
AUSCULTATION (incl. vocal resonance)
BACK (repeat expansion, percussion and
auscultation)

VARICOSE VEINS THYROID
INSPECTION (standing) GENERAL
• Kneel and examine front, side HANDS
PALPATION • Acropathy, dry skin, erythema
• SFJ, incl. thrill and cough impulse • Tremors
• Short and long saphenous • Pulse
SPECIAL TESTS FACE / EYES
• Trendelenburg • Lid lag
• Multiple tourniquet • Eye movement
• Perthes’ • Exophthalmos
DOPPLER NECK
• Inspection
PERIPHERAL LL ARTERIAL o Neck veins
INSPECTION (supine) o Gland (6S)
• Hands o Swallowing, tongue
• Legs, feet • Palpation
PALPATION o Gland
o Swallow / protrude
• Temperature
o Trachea
• Cap refill
o LN
• Pulses
• Percussion
• Buerger’s test
• Auscultation
AUSCULTATION (femoral, iliac bruits)
OTHERS
ABPI
• Reflexes
• Pretibial myxedema
ARTERIOVENOUS FISTULA
• Proximal myopathy
INSPECTION
• Fistula PAROTID
• Signs of ischemia
INSPECTION
• Shoulder, chest
• 6S, contralateral side
PALPATION
• Facial nerve
• Tenderness
• Oral cavity, Stenson’s duct
• Temperature
PALPATION
• Pulsatility, Thrill
• Augmentation test
• LN
• Arm elevation test
• Bimanual, Stenson’s duct
• UL pulses
AUSCULTATION
SUBMANDIBULAR
• Bruits
INSPECTION
• Heart murmurs
• Facial nerve
• Oral cavity, Wharton’s duct
PALPATION
• LN
• Bimanual, Wharton’s duct
NERVES
• Marginal mandibular
• Hypoglossal
• Lingual

BREAST CHEST PAIN / SOB
INSPECTION (sitting) A
• Hands on thighs B
• Hands on hips • Chest inspection, palpation percussion and
• Hands above head auscultation
PALPATION (45ᵒ) • Listen to heart
• Breast • Back
• Nipple • Trachea
• Axillary tail C
• Axilla • Carotid, JVP
• Other LN • Central cyanosis, Dehydration
• Pulse and peripheries
ABDOMEN D
GENERAL E
HAND
• Inspection
• Asterixis
FACE, EYE, MOUTH
NECK LN (from behind)
ABDOMEN
• Inspection
• Palpation (kneel besides patient)
o Liver, spleen, kidneys
o Murphy’s test (cholecystitis)
o Rovsing’s, obturator, psoas signs
(appendicitis)
• Percussion
o Liver, spleen, bladder, ascites
• Auscultation
o Bowel sounds (LIF)
o Liver
o Aorta, iliac, renal vessels
INGUINOSCROTAL
INSPECTION
• Lump
• Cough
• Scrotum
PALPATION
• Lump
• Cough
• Other side
• ASIS, pubic tubercle, ing ligament
• Reducibility
• Deep inguinal ring test
• Scrotum
o Scrotal neck
o Testis separable or not
o Transillumination
AUSCULTATION

HISTORY
CONTENTS
Example Station .................................................................................................................................................................... 3

Knee pain: (OA)..................................................................................................................................................................... 4
Back pain (Functional Back Pain) / Cauda Equina ................................................................................................................ 4
Lower Limb Claudication ...................................................................................................................................................... 5
Hematuria (Bladder Cancer)................................................................................................................................................. 8
Urine retention: (BPH) .......................................................................................................................................................... 9
Preoperative Confusion / Dementia .................................................................................................................................... 9
Bleeding Per Rectum .......................................................................................................................................................... 12
Dysphagia ........................................................................................................................................................................... 14
Change in Bowel Habits (IBD) ............................................................................................................................................. 16
Thyroid status (Female with Hyperthyroidism) ................................................................................................................. 17
Abdominal Pain (IBS) .......................................................................................................................................................... 18
Abdominal Pain (Acute Pancreatitis).................................................................................................................................. 19
Abdominal Pain (Chronic Pancreatitis)............................................................................................................................... 20
Anxious Patient (SOB) In Pre-admission clinic ................................................................................................................... 21
Headache (Subarachnoid Hemorrhage)............................................................................................................................. 22
Seizures (Brain Tumor) Right Arm Seizures........................................................................................................................ 24
Unilateral tonsillar enlargement: (Neoplastic) ................................................................................................................... 26
Depression: (Reactive Depression Post-operative on Discharging)................................................................................... 27
Impotence .......................................................................................................................................................................... 28
Chest Pain (PE).................................................................................................................................................................... 30
Inguinal Hernia ................................................................................................................................................................... 31
Groin Swelling (Infected Femoral Pseudoaneurysm) ........................................................................................................ 32
HISTORY MO’s MRCS B NOTES (Previously called Reda’s Notes) 1

History taking template / scheme
Introduction
↓
Presenting complaint
↓
Patient comfort (if necessary)
↓
Elaboration of presenting complaint
↓ ↓ ↓ ↓ ↓
Pain Incident Recurrent symptom Depression Confusion / Delirium
o SOCRATES (fall, seizure, etc.) o Since when? /Duration o AMTS (0 – 10)
o Before o How many / often? /number of episodes 1. Place
o During o When for each episode? /Duration of each 2. Time
o After o Elaborate most recent 3. Year
episodes 4. DoB (Date of Birth)
episode?
5. Age
o Elaborate first episode?
6. Identify
o Progression? 7. Queen
8. WWII [World War 2]
↓ ↓ ↓
9. Address
• 8 questions 10. Count
Q1) Previous episodes o MMSE (0 – 30)
Q2) Recent health* + specific / associating symptoms
(if not already asked when elaborating complaint)
It’s important here to exclude your ΔΔ **
Q3) Past medical conditions*
Q4) Medications* /Drug
Q5) Allergies
Q6) Previous hospital admissions
Q7) Previous surgeries
Q8) Family history
• Personal Hx
1) Smoking
2) Alcohol
3) Diet
4) Physical activity
• Social Hx (4F)
1) Family
2) Friends***
3) Finances / Job / History of Travel
4) Forensics ***
+/- ICE
o Ideas
o Concerns
o Expectations
* Remember to follow-up open questions with closed questions specific to the case or your provisional diagnosis
** Always exclude malignancy in any station, ask about constitutional symptoms; weigh loss, tiredness, etc.
*** For psych / depression stations
****
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) HISTORY

Example Station
Introduction
• “Hello, my name is Dr. …, I’m one of the ….”
• “Could you confirm your name for me please? “
Presenting complaint
• “So, John, how can I help you today?”
• “Can you tell me what brought you to the hospital?”
Elaboration
• “Could you tell me more about this ….?” (Open Question)
• Closed Questions (for e.g SOCRATES)
-Site o S – Could you tell me where is this pain exactly?
-Onset
-Nature o O – When did it start?
-Description o O – How did it start
o C – Could you describe this pain for me please?
-Radiation
o R – Does it go anywhere? Do you feel this pain anywhere else?
-Aggravating/reliving factor
o E – Does anything increase the pain? Does anything make the pain better?
-Score o S – Could you score this pain for me please on a scale of 1 to 10? 1 being the lowest and 10 being the
highest.
• “Do you have any other symptoms” (Ask about any other presenting complaints before moving on to PMH)
8 Questions
Q1) “Has this happened to you before?”
“Is this the first time this has happened to you?”
“Any previous problems with your knee/back/etc?”
“Any previous episodes…?”
Q2) “How has your health been recently?”
“Have you been feeling well in yourself lately”?
“Any weight loss?” (always exclude malignancy – ask about other features as well… e.g, general tiredness, SOB)
“(Specific questions about associated symptoms and your differential diagnosis)”
Q3) “Where you diagnosed with any medical condition in the past” (Open Question)
“Any diabetes/high blood pressure/etc” (You can then specifically ask a closed question if relevant)
Q4) “Do you take any regular medication?”
Q5) “Do you have any allergies”
Q6) “Were you ever admitted to the hospital before?”
Q7) “Have you had any surgeries in the past?”
Q8) “Has anyone in your family ever been diagnosed with any medical condition?”
Personal Hx
• “Do you smoke?” (If yes, ask about details)
“How much do you smoke?” “Since when?”
• “Do you drink alcohol?”
• “Tell me about your diet” “Do you eat healthy food”
• “Tell me about your level of activity” “Do you exercise often?”
Social Hx
• “Who do you have at home with you?” “
“Who do you live with?”
• “What do you do for a living?”

Knee pain: (OA)
Normal history taking scheme…
Stem: Footballer, had right
Differential Diagnosis knee injury 30 years ago, had
• Traumatic knee operation that he has no
o Ligaments - Do you experience giving away when walking? (Q2) idea about, developed
o Menisci - Do you experience locking of your knee? (Q2) worsening right knee pain 4
• Infection months ago
o Fever (Q2)
o Swelling, redness, hotness (Q2)
• Inflammatory
o Stiffness – Have you noticed any stiffness in your joint(s) when you wake up in the morning? How long
does that last for? (Q2)
• Spine Pathology
o Back pain (Q2)
o Do you have any numbness / weakness? (neurology) (Q2)
• Extra-intestinal IBS
o Rashes – Have you noticed any rashes anywhere on your body? (Q2)
o Enteropathy – Have you had any diarrhea? (Q2)
o Uveitis/iritis – Have you had painful or red eyes? (Q2)
o Spondyloarthropathy – Have you had any back pain? (Q2)
DISCUSSION
Mr... is a ... year-old gentleman who has been referred with increasing pain from his right knee. This started
approximately … years ago and has been increasing in severity over the past 4 months. He is experiencing a dull constant
ache that is increased on exertion and at the end of the day. However, the joint does not swell, lock or become unsteady
on walking. The pain is limiting his daily routine. The patient has a past history of knee trauma and surgery
My main differentials will be:
• OA (traumatic)
• RA
• Meniscal injury
• Referred pain from hip or spine pathology
Investigations?
Knee x-ray (standing and weight bearing), AP and lateral views
Treatment:
Conservative
• Maintain or achieve a healthy weight i.e. aim to decrease weight, and therefore force, going through a joint
• Regular exercise, with particular attention to strengthening the muscles around the joint.
• Analgesia: care to be taken with NSAIDs with relation to gastric irritation
• Heat application to the joint may offer relief
• Physiotherapy
• Intra-articular steroids
Surgical:
• Arthroscopy and arthrocentesis
• Realignment osteotomy
• Total or partial knee replacement
Causes of failure of TKR

• Aseptic loosening
• Infection
• Wear
• Periprosthetic fractures
Will the patient be likely to play soccer in 9 months?

No
Back pain (Functional Back Pain) / Cauda Equina
Stem Scenario Diagnosis

Female with a 5-year history of back pain, worse in the last 3 years, MRI 4 years Mechanical back pain
1 ago showed mild degenerative change, no neurological symptoms, no trauma,
disabled husband, work commitment.
Cauda equina compression /
2 Male with leg weakness, urine and fecal incontinence, erectile dysfunction
syndrome
Differential Diagnosis
• Intervertebral disc protrusion, prolapse or herniation. – weakness, numbness
• Spinal canal stenosis – weakness, numbness
• Cauda equina syndrome / compression – Have you had any problems with your waterworks? Bowels? Have you
had any difficulty in gaining an erection?
• Spinal metastasis, malignancy – constitutional symptoms
• Spondylitis, Ankylosing spondylitis – stiffness
• Infection / TB – night sweats, weight loss, feeling unwell, fever, etc
• Spondylolysis / Spondylolisthesis
• Spondylosis / OA
• Non-spinal causes of back pain (AAA, fibromyalgia, pancreatitis, renal calculi)
DISCUSSION
Diagnosis?
• My main differential diagnosis will be functional back pain (mechanical lower-back pain)
o Localised pain that worsens with movement and changes in posture
o History of heavy lifting
o History of previous similar episodes over several years
o No features of systemic illness, nor neurological symptoms
Cauda Equina syndrome?

Cauda equina syndrome is a rare and severe type of spinal stenosis causing compression of the cauda equina roots.
Symptoms include:
• Bladder and bowel dysfunction
• Bilateral sciatica
• Numbness around genitals / anus
Investigations?
• A full examination is required, particularly looking for perianal sensory loss and anal tone. I would carefully
check for a reduction in power and decreased reflexes. Back examination and lower-limb neurological
examination
• Bloods: FBC, LFTs, U&Es, CRP and ESR
• X-ray
• Urgent MRI scan if cord compression or cauda equina is suspected. MRI is not needed if the history suggests
uncomplicated mechanical back pain
• Consider DEXA scan if a crush fracture is suspected
• Consider chest X-ray and QuantiFERON-TB Gold (QFT) if TB suspected
Management?
Simple back pain (including prolapsed intervertebral disc):
• Advise to stay active and avoid prolonged bed rest Physiotherapy, regular analgesia and consider short-course
muscle relaxants
• Serious pathology or red-flag symptoms: Cord compression –dexamethasone and urgent surgery; radiotherapy
in malignancy
• Cauda equina syndrome – urgent surgery
• Refer to social worker
Lower Limb Claudication

• Vascular
o Pain increases in cold weather (SOCRATES)
o Pain going uphill (SOCRATES)
o Skin changes (thin skin, tissue loss, ulcer, color changes, temperature) (Q2)
o Pain after exercise, relieved by rest (Q2)
• Neurological (Disc, spinal canal stenosis)
o Pain relieved by bending forward or going downhill (SOCRATES)
o Back pain (Q2)
o Tingling or numbness (Q2)
o Weakness in lower limb (Q2)
o Problems with pee or poo (Q2)
• DVT
o Calf pain(Q2)
o Calf swelling (Q2)
o Calf redness (Q2)
o Chest pain, SOB (Q2)
• Musculoskeletal injury
o History of trauma (Q2)
• OA

DISCUSSION
My main diagnosis will be chronic lower limb ischemia causing vascular claudication I will also consider:
• Spinal canal stenosis
• DVT
• Disc lesion causing spinal claudication
• Osteoarthritis
• Musculoskeletal injury
How to differentiate between spinal and vascular claudication?

Peripheral vascular disease
• Skin changes
• Temperature
• Claudication pain is a cramping pain in the calf, thigh or buttocks
• Brought on by exercise and relieved by rest
• Exacerbated by walking faster or uphill and by cold weather
• Risk factors/associated factors for atherosclerosis: Diabetes Hypercholesterolemia Stroke
• Rest pain may indicate critical limb ischemia
Spinal claudication
• Often relieved when walking up a hill
• Often has associated limb numbness
• Weakness
• Back pain
Sciatica
• Shooting pain down the back of a leg to the feet
• History of lower-back pain
Investigations?
• Full peripheral vascular, cardiovascular and neurological examination
• Assess gait and balance
• Arterial duplex
• CT angiography (if surgical intervention was needed)
• MR angiography
Treatment?
• Optimize blood sugar, cholesterol, blood pressure
• Antiplatelet agents: aspirin, clopidogrel
• Antilipemic agents: simvastatin
• Surgical treatment: endovascular stenting, surgical bypass, amputation

Hematuria (Bladder Cancer)
• Cancer (Bladder, Renal, Prostate cancer) – constitutional symptoms (Q2)
• Calculi (Renal, Ureteric, Bladder) – dysuria (Q2)
• Benign
o BPH – frequency, hesitancy, poor stream, drippling, etc., see BPH station (Q2)
o UTI – fever feeling, unwell, etc (Q2)
o PKD – family history – (Q8)
• General
o Bleeding disorder – (Q3)
o Blood thinner – (Q5)
o Instrumentation – (Q6)
o Trauma – history of trauma (Q2)
Don’t forget to ask about…

• Back pain (Q2)
• Beetroot and certain medications (Q5)
• Job (Social)
DISCUSSION
Mr. … is a … year-old male, presented by painless hematuria one month ago, with associated weight loss over the last …,
there is no any abdominal or loin pain, there is no problems in urine stream, he is concerned about the possibility of
having cancer
Differentials?
• My main ∆∆ will be bladder cancer, renal cell carcinoma considering (his hemorrhage, weight loss, occupation)
• Stone kidney, bladder, ureter
• Infection
• Trauma
• Bleeding tendency
Types of Bladder cancer?

• Transitional (Urothelial) cell carcinomas (90% of bladder cancers in developed countries)
• Squamous cell carcinoma – associated with chronic bladder irritation and infection, risk factor: schistosomiasis
• Adenocarcinoma: rare
• Small-cell carcinoma
Investigations?
• Urine dipstick to confirm hematuria, assess infection, send a sample for cytology
• Bloods: FBC, U&E, clotting screen, PSA
• Cystoscopy and biopsy
• U/S, CT
Treatment
Depends on the stage and the grade of the tumor
• Surgical:
o TURBT, often followed by instillation of chemotherapy or vaccine‑based therapy into the bladder.
Cystoscopy as a follow-up
o Radical cystectomy
• Non-surgical: Chemotherapy and radiotherapy and immunotherapy
Why does patient have trouble passing urine?

• Bleeding → clot → retention
• Obstruction from the cancer itself

Urine retention: (BPH)
BPH
• Urgency: Do you have to rush to the loo?
• Incontinence: Are you able to hold your urine?
• Hesitancy: When you go to the loo, do you have to wait until your urine starts to go?
• Frequency: Do you go to the loo more often?
• Drippling: Does a bit of urine drop and stain your underwear soon after going to the loo?
• Poor stream: Does it take longer to empty your bladder?
• Nocturia: Do you have to wake at night to go to the loo?
• Incomplete evacuation: Do you have a feeling of not emptying your bladder completely?

• Bone pain?
• Problems with erections
• Neurological symptoms
• Drug history: patient takes nasal sprays containing phenylephrine (α agonist) which may counteract the effect of
tamsulosin (α blocker)
DISCUSSION
Mr. … is a … year-old male, presenting with difficulty in initiating urination, slow stream, hesitancy, urgency and
increased frequency. He does not have dysuria, hematuria, bone pains, weight loss or neurological symptoms.
Differentials? If the patient is taking phenylephrine will that affect

• Benign prostatic hyperplasia your management? What about salbutamol?
• Overactive bladder Salbutamol (selective β2 agonist) will not affect our
• Prostatic cancer management.
• Obstructive bladder pathology (malignancy or But phenylephrine (α agonist) will affect / antagonize
calculi) effect of tamsulosin
Investigations? Causes of increased PSA?

• Full clinical examination including DRE • Age
• Urinary frequency-volume chart, International • BPH
prostate scoring system (IPSS) • Prostatitis or prostate infection
• Bloods: • UTI
o CBC • Perineal trauma
o PSA • Sexual activity
o U&E • Prostate cancer
• Urine analysis
• Imaging: What to do if the PSA is increased?
o Abdominal USS
o Transrectal USS (TRUS) What is free PSA?
Amount of PSA that is floating freely in the
Treatment? bloodstream, without being bound to a protein
Medical:
• Tamsulosin (1-α adrenergic blocker) Prostate cancer is associated with a lower percentage of
• Finasteride (5-α reductase inhibitor) free PSA in the serum as compared with benign conditions
Surgical:
• TURP The percentage of free PSA (free/total PSA ratio [f/t PSA])
has been used to improve the sensitivity of cancer
How do these medications act? detection when total PSA is in the normal range (<4
• Tamsulosin – Alpha Blocker ng/mL) and to increase the specificity of cancer detection
when total PSA in the "gray zone" (4.1 to 10 ng/mL). In
works by relaxing bladder and prostate
this latter group, the lower the value of f/t PSA, the
muscles
greater the likelihood that an elevated PSA represents
• Finasteride – 5-Alpha Reductase Inhibitor
cancer and not BPH.
causes prostate to shrink prevents growth
Preoperative Confusion / Dementia

Introduction…
“Would you mind if I asked you some questions to test your memory?”
Abbreviated mental test scoring:

1. What is the name of this place? / Do you know where you are right now?
2. What time is it to the nearest hour? / What time of day is it, roughly?
3. What year is it?
4. What is your date of birth? / Can you tell me your date of birth?
5. How old are you?
6. What is my job? And what is the job of this person (e.g. a nurse)?
7. Can you count backwards from 20-1?
Can you remember this address? 24 West St. I will ask you this at the end
8. When did WW2 end?
9. Who is the current prime minister? or What’s the name of the Queen?
10. What was that address I asked you to remember?
AMTS score < 6 suggests dementia or delirium
To complete my assessment of the patient i will do MMSE (mini mental state examination)
MMSE: A 30-point questionnaire that is used to measure cognitive impairment.
MMSE
Questions Max Score
“What is the year? Season? Month? Date? Day of the week?” 5
“Where are we now: Country? County? Town/City? Hospital? Floor?” 5
Examiner names three objects (e.g. apple, table, penny) and asks the patient to repeat
3
(1 point for each correct. THEN the patient learns the 3 names repeating until correct).
Subtract 7 from 100, then repeat from result. Continue five times: 100, 93, 86, 79, 65.
5
(Alternative: spell “WORLD” backwards: DLROW).
Ask for the names of the three objects learned earlier 3
Name two objects (e.g. pen, watch). 2
Repeat “No ifs, ands, or buts”. 1
Give a three-stage command. Score 1 for each stage.
3
(e.g. “Take a paper in your hand, fold it in half, and put it on the floor.”).
Ask the patient to read and obey a written command on a piece of paper.
1
The written instruction is: “Close your eyes”.
Ask the patient to write a sentence. Score 1 if it is sensible and has subject and a verb. 1
“Please copy this picture.” (The examiner gives the patient a blank piece of paper and asks him/her to
draw the symbol below. All 10 angles must be present and two must intersect.)
24-30: no cognitive impairment

18-23: mild cognitive impairment
0-17: severe cognitive impairment

DISCUSSION
The patient has acute confusion with het AMTS SCORE of 2/10 Which suggests delirium or dementia

• Hypoxemia / hypercarbia
• Hypoglycemia / hyperglycemia
• Hypotension and hypoperfusion
• Dehydration
• Electrolyte disturbance (sodium, calcium, magnesium, phosphorus)
• Infection / Sepsis (pneumonia, urinary tract infection_
• Alcohol and drug toxicity or withdrawal
• Medication / Vitamin deficiencies (Wernicke’s)
• CNS lesion, injury, infection (CVA, subdural hematoma, meningitis, encephalitis)
• Endocrinopathies (thyroid, adrenal)
• Cardiac disease (myocardial infarction, congestive heart failure, arrhythmia)
• Hyperthermia or hypothermia
Management
• Observations:
o Early Warning Scores can be useful
o BP / Pulse – ↓BP ↑Pulse may indicate sepsis / dehydration
o Temperature, respiratory rate and oxygen saturation are all important diagnostic clues.
• CT head:
o Ischaemic stroke
o Intracranial bleeds (from trauma or spontaneous)
o Space occupying lesions
• Bloods:
o FBC – white cells for signs of infection, anaemia, increased MCV (macrocytic anaemia can be caused by
B12 or folate deficiency which can have a variety of origins: leukemias, alcohol use, lack of intake, lack
of absorption (i.e. post-gastrectomy), pernicious anaemia; hypothyroidism, liver disease.)
o U&E – deranged electrolytes can cause confusion (consider sodium, but relative to what is normal for
the patient).
o LFTs – confusion can be caused by liver failure, malnutrition or be based on the background of alcohol
abuse.
o INR – can be useful to know if the patient is on Warfarin & you are concerned about intracranial
bleeding
o TFTs – confusion is more common in hypothyroid states.
o Calcium – Hypercalcemia often causes confusion/delirium – Bones, moans, psychotic groans
o B12 + folate / hematinics – macrocytic anaemia, and B12/folate deficiency can compound confusion
o Glucose – hypoglycaemia is a common cause of confusion
• CXR – As part of a sepsis screen to identify infection source –? Pneumonia
• Blood cultures if appropriate – as part of sepsis screen
• Urine dipstick/culture – UTI is a very common cause of delirium in the elderly History: take history from the
patient (if possible), from the notes, from her relatives
Fitness for the operation?

Not fit for giving a consent, as she cannot retain information and she cannot make an informed decision
Should the operation go ahead?

No. The operation is non-urgent. Therefore, it can be postponed until the cause of the confusion has resolved. I would
talk to my consultant and the anaesthetist in charge of the case to inform them of the confusion and ask their advice
before cancelling it.
If the cause of confusion was only senile dementia, how you will consent for the operation?
As the patient lack capacity, consent should be recorded using consent form 4 with 2 consultant signatures

Bleeding Per Rectum

• Color of blood
• Amount of blood
• Blood clots, mucous, etc.
• Pain, frequency
• Cancer colon
o Constitutional manifestations (anorexia, weight loss, tiredness) (Q2)
o Disturbed bowel habits (Q2) – POSITIVE
o Mucous/slime discharge or blood (Q2) – POSITIVE
o Family history (Q8) – POSITIVE
• IBD
o Abdominal pain (Q2)
o Extra-intestinal manifestations
▪ Joint pain, back pain (Q2)
▪ Skin changes (Q2)
▪ Eye changes (Q2)
o Mucous discharge (Q2)
• Local causes (fissure, piles, etc.)
o Swelling, itching, pain (Q2)
• Bleeding tendency
o Bleeding from any other sites (Q2)
o Blood thinners (Q5)
• Upper GI bleeding
o Vomiting (Q2)
o Heartburn (Q2)
o Reflux, acid taste (Q2)
• Gastroenteritis
o Fever (Q2)
o History of travel (Social)
o Tenesmus (Q2)

DISCUSSION

The weight loss, the change in bowel habit and PR bleeding are concerning. My main differential is colorectal cancer,
which would need thorough investigation. Other differentials for PR bleeding include
• Hemorrhoids
• Inflammatory bowel disease
• Angiodysplasia
• Diverticular disease
• Benign polyp
• Anal fissure
It may also be secondary to medication or a hematological condition.
What is the most important investigation to carry out?

As I am suspecting colorectal cancer, the most important investigation is a colonoscopy +/- biopsy to examine the whole
colon.
If immediately available in clinic, a rigid sigmoidoscopy may be carried out in the first instance
Other investigations:
• Hematology:
o FBC: anaemia, leukocytosis (infective colitis, inflammatory bowel disease, ischaemic colitis), low
platelets (bleeding disorder)
o Clotting screen
o Group and save / cross match for transfusion.
• Biochemistry:
o U&Es, LFTs (hepatic failure with variceal bleed, malignancy)
• ABG: Raised lactate (ischemia), metabolic acidosis.
• ECG: Mesenteric ischemia, atrial fibrillation (emboli).
• Endoscopy:
o OGD (to exclude upper gastrointestinal cause)
o Sigmoidoscopy / proctoscopy (hemorrhoids, anorectal lesion, distal colitis, rectal ulcer)
o Colonoscopy (malignancy, diverticular disease, colitis, angiodysplasia).
• Radiology:
o Mesenteric angiography (CT or invasive) / Technetium scan / Labelled red cell scan, if source not
identified by endoscopy (looking for angiodysplasia / Meckel’s diverticulum).
o AXR (obstruction, toxic megacolon of inflammatory bowel disease)
o US scan / CT (if suspected malignancy, for liver metastases and staging).
• Microbiology:
o Stool cultures (infective colitis).

Dysphagia

• Solids or liquids? –Do you have difficulty swallowing solids, fluids or both?
• Timing –Is it there all the time or does it come and go?
• Onset –When did this start? Progression –Has it worsened over time?
• Pain –Is there any pain when swallowing? Any chest pain?
• Cancer Esophagus
o Have you had any unintentional weight loss? If so, how much have you lost and over how long?
o Have you vomited at all? If so, was there any blood?
• Achalasia
o Dysphagia more to liquids
• GORD / Dyspepsia
o Do you ever taste acid at the back of your mouth?
o Heartburn? Pain in your tummy?
o Vomiting
• Pharyngeal pouch
o Have you noticed having bad-smelling breath recently?
o Do you ever notice gurgling or a wet voice after swallowing?
o Regurgitation of food while lying down?
• Goiter
o Neck swelling, Do you ever feel a lump in your throat?
• Neuro / Bulbar palsy
o Have you noticed any weakness anywhere? Any problems walking?
• Autoimmune, myasthenia, scleroderma
o Do you suffer with painfully cold hands?
o Dry eyes or mouth?
• Esophagitis
o Painful swallowing

DISCUSSION
Considering difficulty in swallowing, weight loss, heavy smoking, alcohol drinking, hematemesis my main diagnosis will be
esophageal carcinoma causing mechanical obstruction of the esophagus
I also have to consider:
• Lung cancer, pharyngeal pouch, retrosternal goiter (compression from outside)
• Esophageal web, Plummer-Vinson syndrome
• Achalasia (motility disorder) Differential diagnosis
• Myasthenia gravis Mechanical
• Esophageal carcinoma
Investigations: • Gastric carcinoma
• Full clinical examination checking for lymphadenopathy • Pharyngeal pouch (regurgitation of
• Bloods –FBC, U&Es, LFTs and clotting and bone profile food when lying down / on pillow)
• Chest X-ray • Stricture
• Esophageal manometry: achalasia, GORD o Corrosive burn
• Barium swallow o GORD
• Endoscopy and biopsy
• Esophageal endoluminal US, also for staging of carcinoma. Motility
• Videofluoroscopy –assessing for aspiration • Achalasia cardia (liquid > solid)
• Staging CT scan, depending on what the previous • Esophageal spasm (intermittent)
investigations reveal • Bulbar palsy (difficulty initiating
swallowing)
Treatment • Myasthenia gravis (difficulty in
• Operable cases: swallowing ↑ as the day progresses)
o Esophagectomy + chemoradiotherapy
• Non-operable cases:
Palliation:
o Self-expanding metallic stent
o Palliative chemotherapy and radiotherapy
o Feeding jejunostomy

Change in Bowel Habits (IBD)
• Specify –When you say constipation/diarrhoea, what do you mean exactly? Do you mean you are going
more/less often, or the consistency has changed?
• What about before?
• Onset
• Character (watery, semi-solid or solid?)
• Blood or mucus in the stools
• Color
• Dark, foul-smelling stools?
• Associated features: Bloating, Pain, Weight loss, Exhaustion, Lasting urge (Tenesmus),
• Swallowing/upper-GIT symptoms –Any vomiting? (If so, ask about hematemesis), Heartburn
• Extra-intestinal features IBD – Have you had any mouth ulcers? Fever? Painful red eye? Joint or back pain?
• Foreign travel – Have you been abroad anywhere recently?
• Timing – How many times a day do you go to the toilet to pass feces now? How often do you normally go? What
are your stools normally like? Have you ever suffered from the opposite? (i.e. constipation/diarrhoea)
• Exacerbating/relieving factors –Does anything relieve the constipation/diarrhoea? Does anything make it
worse?
• Severity –How badly is this affecting your day-to-day life
DISCUSSION
Considering weight loss, diarrhea, PR bleeding, mucous discharge, extra-intestinal manifestations, my main diagnosis will
be Crohn’s disease or ulcerative colitis
I will also consider:
• Infective gastroenteritis
• Colorectal cancer
• Diverticular disease
Investigations?
• Abdominal examination including DRE
• Routine bloods: FBC, U&E, CRP, LFTs, calcium, magnesium, phosphate, coagulation screen, - group and save.
(Looking for raised inflammatory markers, dehydration, electrolyte disturbance secondary to diarrhoea, albumin
as a guide of nutritional status, coagulation defects.)
• Stool sample
• Fecal occult blood test
• Abdominal Radiograph - assess for toxic megacolon
• CT or MRI abdomen and pelvis if concerning features on examination and for pre-operative planning if surgery is
indicated
• Colonoscopy
Treatment?
• Conservative:
o Dietary control (low residue diet)
• Medical:
o Mesalazine
o Prednisolone
o Immunomodulators (infliximab)
• Surgical:
In toxic megacolon, IO, malignant transformation, fistulation, refractory cases

Thyroid status (Female with Hyperthyroidism)
Associated features:
Compressive symptoms:
• Changes in voice
• Difficulty in swallowing
• Difficulty in breathing
Toxic symptoms:
• Changes in vision or difference in eyes
• Diarrhea
• Menstruation (do you menstruate regularly)
• Sleep disturbances
• Hot or cold intolerance
• Weight loss
• Mood or behavioral changes
• Appetite
DISCUSSION
Mrs. ... Is ... year-old woman, previously fit and well, presents with a lump in her neck, the lump has grown over the past
... years, in addition she has symptoms indicating hyperthyroidism such as … She has also compressive symptoms such as
… My main differentials will be:
• Toxic MNG
• Simple MNG
• Thyroid neoplasm
• Thyroiditis
Management?
Triple assessment:
• Full clinical examination
• Ultrasound imaging
• FNAC
Other investigations:
• Radioisotope scan
• TSH, T4
Possible causes of sudden enlargement?

• Hemorrhage inside a cyst
• Malignancy
o Papillary carcinoma
o Follicular carcinoma
o Medullary carcinoma
Treatment?
Medical: Antithyroid drugs
Radioactive iodine
Surgical: Thyroidectomy (hemi, near total or total) with such compressive symptoms
What possible complications of surgery do you advise this patient about?

• Risk of RLN injury: hoarseness of voice, aphonia, stridor and possibility of tracheostomy
• Risk of hypocalcemia
• Lifelong thyroxine replacement

Abdominal Pain (IBS)
Female referred by her GP for chronic calculous cholecystitis

• Pain increases with fatty meal? (-ve)
• Yellowish discoloration of your eyes? (-ve)
• Discoloration of your urine or stool? (-ve)
• Pain referred to right shoulder? (-ve)
• Is the pain relieved by passing stool or flatus? (+ve)
• Bloating? (+ve)
• Change of bowel habits (+ve)
• Social history / stress? (+ve)
Differential diagnosis
• IBS
• IBD
• Biliary Colic
• Gastritis
• Cancer colon
DISCUSSION
Mrs. .... is a … year-old woman, presented by abdominal pain, the pain is colicky in nature, it is not related to meals, she
experiences it in the middle of her abdomen, has no special timing, no aggravating or relieving factors. Ir associated with
disturbed bowel habits, she also has some social stress
My main diagnosis will br IBS, I will also consider
• IBD
• Colon cancer,
• Chronic calculous cholecystitis
Investigations?
• Abdominal ultrasound
• AXR
• Colonoscope
• Stool analysis
• FBC
Treatment
• Fiber diet
• Antispasmodics
• Antidepressants
• Refer patient to a social worker

Abdominal Pain (Acute Pancreatitis)
Stem:
45-year-old female, presenting with acute onset epigastric pain. Known smoker and alcoholic. History of previous
gastric ulcer (used to take PPI)
45-year-old male/female, alcoholic, vomiting and collapse at a party

Upper and central abdominal pain, sudden, dull aching, radiating to the back

o Site (epigastric)
o Referred to the back
o Difficulty in leaning backwards
o Diarrhea and repeated vomiting
• Acute cholecystitis (-ve)
o Jaundice, yellowish discoloration of eyes or stools
o Fatty meal intolerance
o Fever
• Gastritis / Perforated peptic ulcer (-ve)
o Hematemesis
o Heart burn
• MI (-ve)
o Chest pain
o SOB
o Palpitations
o Referred pain
DISCUSSION
See questions from Applied Knowledge Section
What’s the immediate investigations?

• ECG
• Cardiac enzymes
Differenital diagnosis?
• MI
• Acute cholecystitis
• Gastritis, Perforated peptic ulcer
Management?

Abdominal Pain (Chronic Pancreatitis)
Old station, unlikely to face in the exam…

40-year-old divorced male with chronic epigastric pain radiating to the back for the past year, with steatorrhea. Drinks 5
pints of beer per day, previously admitted for acute pancreatitis. Takes 30 mg of morphine / day to numb the pain,
depressed
DISCUSSION
Differentials?
• Chronic pancreatitis (epigastric pain, steatorrhea, previous attack of acute pancreatitis, alcoholic)
• Pancreatic pseudocyst
• PUD
What do you think about the history of taking 30 mg of morphine, what should be the normal dose?
15-30 mg /4hours as needed
Investigations:
• Secretin stimulation test
• Serum amylase and lipase (elevated)
• Serum trypsinogen
• CT scan (pancreatic calcifications)
• MRCP: identify the presence of biliary obstruction and the state of the pancreatic duct
• Endoscopic ultrasound
Treatment:
Medical treatment of chronic pancreatitis:
• Treat the addiction:
o Help the patient to stop alcohol consumption and tobacco smoking
o Involve a dependency counsellor or a psychologist
• Alleviate abdominal pain:
o Eliminate obstructive factors (duodenum, bile duct, pancreatic duct)
o Escalate analgesia in a stepwise fashion
o Refer to a pain management specialist
o For intractable pain, consider CT/EUS-guided coeliac axis block
• Nutritional and digestive measures:
o Diet: low in fat and high in protein and carbohydrates
o Pancreatic enzyme supplementation with meals
o Correct malabsorption of the fat-soluble vitamins (A, D, E, K) and vitamin B12
o Medium-chain triglycerides in patients with severe fat malabsorption (they are directly absorbed by the
small intestine without the need for digestion)
o Reducing gastric secretions may help treat diabetes mellitus
• Treat DM
The role of surgery is to overcome obstruction and remove mass lesions

Anxious Patient (SOB) In Pre-admission clinic
Stem:
Lady planning for cholecystectomy, SOB for few minutes, increasing in frequency 6 weeks after being scheduled for
operation

• Cough
• Have you noticed any blood?
• Wheeze – “Do you get wheezy? Is it worse at any time of the day?”
• Fever
• Constitutional, weight loss?
• Chest pain? If so, SOCRATES
• Palpitations
• Anxiety – If relevant, do you only get breathless when you are anxious?
Exclude
• MI / Heart failure (paroxysmal dyspnea? Increase SOB on lying flat?)
• PE (recent surgery? recent flight? calf swelling? haemoptysis? SOB?)
• Chest infection
• Bronchogenic carcinoma
DISCUSSION
The SOB described does not fit with cardiac or pleuritic chest problem, and the patient tells me that she has been
investigated and ruled out. My top differential would therefore be anxiety related to her impending operation.
I will also consider: anginal pain, pneumonia, pleurisy.
Management?
• I should contact the GP to get hold of all the notes regarding investigation of the patient’s chest pain.
• I would examine the patient and ensure that we repeat the patient’s bloods, ECG, CXR and get a baseline ABG
on room air.
• I would want to ensure she had a recent echo and angiogram and discuss these with a cardiologist.
• I would reassure the patient that she is going to be well looked after and ask her if there’s anything we could do
to allay her fears.
• I would also suggest that we involve her close relatives or friends so that she has an adequate support network
in place before and after the operation
Can the operation go ahead?

Since we have no documented evidence that there is no cardiac or respiratory illness, the operation should go ahead
FEV1?
Volume that has been exhaled at the end of the first second of forced expiration (measurement shows the amount of air
a person can forcefully exhale in one second of the FVC test)
FVC?
The amount of air which can be forcibly exhaled from the lungs after taking the deepest breath possible
FEV1/FVC ratio?
Represents the proportion of a person's vital capacity that they are able to expire in the first second of forced expiration
In obstructive lung disease, the FEV1 is reduced due to an obstruction of air escaping from the lungs. Thus, the FEV1/FVC
ratio will be reduced
In restrictive lung disease, the FEV1 and FVC are equally reduced due to fibrosis or other lung pathology (not obstructive
pathology). Thus, the FEV1/FVC ratio should be approximately normal

Headache (Subarachnoid Hemorrhage)
Normal history taking scheme… Possible symptoms

Headache (occipital, sudden onset,
Differential Diagnosis severe)
• SAH Neck stiffness
o Injury or trauma Sickness
o Are you sensitive to light? Photophobia
o Meningism (see below) Visual problems (blurry vision,
• Infection, meningitis, encephalitis double vision)
o Have you been feeling ill or had a fever?
o Do you have any neck stiffness? Weakness to one side of the body
o Have you noticed a rash anywhere? Speech problems
• Brain tumor Facial problems
o Have you ever had seizures or blacked out? Have you ever lost
consciousness? Loss of consciousness
o Have you had any arm or leg weakness? Fits / convulsions
o Any other sensory disturbance?
o Any visual disturbances?
• Migraine
• Visual problems
o Any eye pain? Visual disturbances? Nausea or vomiting
• Trauma
o Have you banged your head, had a fall recently?

• Timing – When can you remember this starting? Was it continuous or intermittent? How long do they last?
When was the last time you had a headache?
• Past medical history: Polycystic kidney (relevant history)
• Family history: My aunt died suddenly of an aneurysm in the brain

DISCUSSION
My main differential is a subarachnoid hemorrhage, but I would also consider other causes of an acute severe headache
including:
• Meningitis
• Encephalitis
• Migraine
• Increased ICP due to brain tumor
• GCA
Management?
I would manage him in an ABC manner, ensuring that he is stable and arrange appropriate bloods and a plain CT head.
Investigations?
• CT brain
• CSF tapping
Treatment?
• I would refer this patient to a neurosurgical unit.
• Bed rest, 3L of IV fluids /24h.
• Oral nimodipine 60mg every 4 hours, and laxatives
• Attempt to coil the aneurysm is made
• Burr holes
• Craniotomy
• Discuss in neurovascular MDT

Seizures (Brain Tumor) Right Arm Seizures

• Before (aura)
• During (loss of consciousness, eye rolling, tongue biting, incontinence)
• After (weakness, parasthesia, speech problems)
• Brain Tumor
o ICP – vomiting, headache, weakness
• Infections, encephalitis, meningitis
o Fever, meningism, neck stiffness, photophobia
• Traumatic
o History of trauma
• Epilepsy
o Past history of epilepsy or fits
• TIA, Strokes
o Weakness
o Speech disturbance
• Metabolic
o ETOH excess
o Hypoglycemia
o Hypoxia
• Sleep disorder
o Change in sleep pattern
• Migraine
o Headache
• Psychological

DISCUSSION
Investigations?
• Blood glucose
• CBCD
• Electrolytes, BUN, creatinine, calcium, magnesium, anion gap, lactate, prolactin (will be elevated after seizure,
sometimes used if not sure if event was a seizure)
• ABG, U/A, LP
• CT head if trauma, suspected intracranial hemorrhage, suspected structural lesion in first time seizure,
prolonged altered mental status, focal neurological deficit, anticoagulated patient, HIV/Cancer patients
• If infection – may require full septic w/u (LP, cultures, etc.)
• EEG – most likely to be done as an outpatient
• MRI – in consultation with neurology
Treatment?
If the patient is seizing
• Move to safe place
• Turn to side (recovery position) if possible
• Observation for specific activity and progression and duration Prepare to assess/monitor once seizure
subsides (ABC’s) Consider treatment if patient is in status
Postictal
• Seizure precautions ABC’s and monitors, O2
• Benzodiazepines may be used to prevent further seizures. Consider anticonvulsant therapy
• Phenytoin (Dilantin®) 300-600mg PO TDS
• Phenobarbital 60-200mg PO daily
• Valproic acid (Epival®) 15-60mg/kg daily divided BD or TDS
• Carbamazepine (Tegretol®) 400-1200mg daily divided TDS/QDS
Status epilepticus (≥ 30 min of active seizing or no recovery/consciousness between)
• IV line
• O2
• Monitors
• Consider intubation
• Benzodiazepines (diazepam 10-20mg IV, or lorazepam 4-8mg IV)
• Phenytoin 18-20mg/kg IV @ 25mg/min
Stereotactic biopsy and resection or debulking of brain tumors

Unilateral tonsillar enlargement: (Neoplastic)

• Rapid increase in size, respiratory difficulties
• Change in voice
• New onset snoring
• Dysphagia
• Odynophagia Painful swallowing
• Neck swelling
• Night fever
• Manifestations of infection
• Abdominal swelling (hepatosplenomegaly in glandular fever)
• Constitutional symptoms (weight loss, etc.)
DISCUSSION
Mr. … is a year-old male, previously fit and well gentleman, presents with a 2-month history of an enlarging left tonsil. He
has lost approximately half a stone in weight and has increasing discomfort on swallowing, with no other symptoms.
Differentials?
• Neoplastic:
o Lymphoma (non-Hodgkin’s)
o SCC
• Infective:
o Acute infection: peritonsillar abscess
o Chronic infection: mycobacteria, fungi, actinomycosis, infection mononucleosis (glandular fever)
• Asymmetric anatomical positions
Investigations?
• Bloods
o FBC: looking for raised WCC associated with infection
o U&Es: looking for renal impairment if patient has had decreased oral intake
o LFT’s: derangement may indicate glandular fever or metastasis
• Tonsillectomy for biopsy
• Biopsy with flow cytometry
• CT or PET-CT to rule out lymphoma
• Panendoscopy: examination of the upper aerodigestive tract (pharynx, larynx, upper trachea and esophagus).
• Monospot test (detecting glandular fever)
Treatment?
• Staging: MRI neck, CT neck, U/S liver
• Discuss in MDT
• Block neck dissection (radical, modified radical, selective)
• Radiotherapy

Depression: (Reactive Depression Post-operative on Discharging)
Developing a rapport:
• “How have you been feeling recently?”
Screening for core symptoms:
Screen for core symptoms of depression – feelings of depression, anhedonia and fatigue. “In the past days during your
hospital stay have you…”
• Felt down, depressed or hopeless?
• Found that you no longer enjoy, or find little pleasure in life? Been feeling overly tired?
Sleep cycle:
• “How has your sleep pattern been recently?”
• “Have you had any difficulties in getting to sleep?”
• “Do you find you wake up early, and find it difficult to get back to sleep?”
Mood:
• “Are there any particular times of day that you notice your mood is worse?”
• “Does your mood vary throughout the day?”
• “Do you find that your mood gradually worsens throughout a day?”
Appetite:
• “Have you noticed a change in your appetite?”
• “What is your diet like at the moment?”
• “What are you eating in a typical day?”
Libido:
• “Have you noticed a change in your libido?”
• “Since you have been feeling this way, have you noticed a difference in your sex drive?”
Past psychiatric history, previous episodes of depression or dysthymia:
• “Have you ever felt like this before?”
• “Have you ever had any other periods of feeling particularly low?”
• “In the past, have you had any problems with your mental health?”
• “Have you had any counselling for any issues before?”
• “Have you ever been admitted to hospital because of your mental health?” If so, obtain details – time, method of
admission, result.
DISCUSSION
Management?
Mild:
• Regular exercise
• Advice on sleep hygiene (regular sleep times, appropriate environment)
• Psychosocial therapy –CBT
Moderate to severe:
• Regular exercise, advice on sleep hygiene,
• CBT
• Medication –SSRIs
• High-intensity psychosocial intervention (CBT or interpersonal therapy)
• Immediate and considerable high risk to themselves or others: Admit to psychiatric ward (use Mental
Health Act if necessary)

Impotence

• Difficulty obtaining an erection?
• Is the erection suitable for penetration?
• Can the penetration be maintained until partner has achieved orgasm?
• Does ejaculation occur and if yes, is it premature?
• Do both partners experience sexual satisfaction?
• Experience nocturnal/morning erections?
• Is there associated pain/discomfort - if yes, where?
• Penile curvature?
• Sexual History questions
• Psychological history:
o Any episodes of ↓ mood, insomnia, lethargy, moodiness? loss of libido
o Problems/ tension in sexual relationship?
o Any stress from work/ other sources?
o Any symptoms or signs of depression –insomnia, lethargy, low mood.
o Difficulties within a relationship.
o Family or social pressures.
o Any changes to sexual desire.
o Any anxiety related to performance.
• Any systemic features: SOB, ↑°c, night sweats, Kg ↓, loss of appetite?
• Cardiovascular: Chest pain, SOB, orthopnea, palpitations, dizziness, ankle swelling
• Respiratory: SOB, exercise tolerance, PND, wheeze, chest pain, cough, hemoptyses, hoarseness SOB=Shortness of breath
• Gastrointestinal: Change in appetite/diet, Kg loss, dysphagia, odynophagia, change in bowels
• Urogenital: abdominal pain, micturition, dysuria, urgency, polyuria, hematuria
• CNS & PNS: fits, faints, headache, LoC, tremor, m. weakness, paralysis, sensory changes
• MSK: muscle/bone/joint pain, deformity, swelling, stiffness, limb weakness
• Metabolic system: change in BMI/ appetite, alteration in build/ appearance
• Past Medical History
o Any history of pelvic surgery/ trauma, previous prostate surgery, irradiation to prostate, CV RFx?
• Thyroid dysfunction, Hypertension, Rheumatic, Epilepsy, Asthma, Diabetes, Stroke, MI, Jaundice
• Specific drugs: Antihypertensives, anti-ulcer (e.g. PPI), lipid lowering, 5α-reductase inhibitors, antidepressants,
anti- ψ, testosterone anabolic steroids
International index of erectile function

1. How often were you able to get an erection during sexual activity?
2. How often were you able to get an erection during sexual activity?
3. When you attempted intercourse, how often were you able to penetrate (enter) your partner?
4. During sexual intercourse, how often were you able to maintain your erection after you had penetrated
(entered) your partner?
5. During sexual intercourse, how difficult was it to maintain your erection to completion of intercourse?
6. How many times have you attempted sexual intercourse?
7. When you attempted sexual intercourse, how often was it satisfactory for you?
8. How much have you enjoyed sexual intercourse?
9. When you had sexual stimulation or intercourse, how often did you ejaculate?
10. When you had sexual stimulation or intercourse, how often did you have the feeling of orgasm or climax?
11. How often have you felt sexual desire?
12. How would you rate your level of sexual desire?
13. How satisfied have you been with your overall sex life?
14. How satisfied have you been with your sexual relationship with your partner?
15. How do you rate your confidence that you could get and keep an erection?

DISCUSSION
Differentials?
• Atherosclerotic vascular disease (smoker)
• Drug induced (antihypertensive drugs; Atenolol)
• Psychological
Investigations?
• Hematology:
o FBC, ESR, hematinics, clotting screen, group & save.
o Glycated hemoglobin (cardiovascular risk assessment).
o Biochemistry: U&Es, LFTs, CRP, lipid profile.
o Prostate specific antigen (if relevant history).
o Serum free testosterone.
o Serum prolactin.
o Serum FSH / LH.
o ACTH (synanche) stimulation test.
• Urinalysis: Microscopy to exclude a genitourinary cause.
• Radiology:
o Duplex ultrasonography to assess vascular function of the penis.
o Ultrasonography of the testes to exclude any abnormality.
o Transrectal ultrasonography to exclude any pelvic or prostatic abnormality.
o Angiography: It can be useful for planning vascular procedures / reconstruction, particularly following
trauma.
• Injection of prostaglandin E1: This outpatient investigation includes the injection of prostaglandin E1 directly
into the corpora cavernosa and to assess rigidity after ten minutes. While it can help to evaluate the
vasculature, a positive result may still be found with mild vascular disease. It can also be utilized to assess penile
deformities to aid planning of surgical correction.
Treatment?
• Risk factor modification by controlling lipidemia and diabetes, weight loss, smoking cessation, increase exercise.
• CBT, solve social issues
• CVS specialist to change BP medication
• Phosphodiesterase-5 inhibitor therapy (sildenafil)
• Intercavernous injection therapy (alprostadil)
• Placement of a penile prosthesis which may take the form of either a semirigid or inflatable implant.

Chest Pain (PE)

• Associated symptoms
• Breathlessness –Do you get breathless?
• Orthopnea –Do you ever get breathless when lying flat? How many pillows do you sleep with at night?
• Paroxysmal nocturnal dyspnea –Do you ever wake up gasping for breath?
• Cough –Have you noticed a cough? Do you bring anything up? Any blood?
• Musculoskeletal –Is the pain worse on movement? Does it hurt to press on the area?
• Do you have any lower limb pain or swelling?
DISCUSSION
Diagnosis?
Considering pleuritic chest pain, acute onset of SOB, hemoptysis, my main diagnosis will be pulmonary embolism
I will also consider:
• Pneumonia
• Basal atelectasis
• MI
Investigations?
• CTPA
• V/Q scan
• CXR
• ECG
• ABG
• Duplex LL
Treatment?
• ABC PROTOCOL
• Non-massive: heparin until APTT 50-60 sec.
• Massive: thrombolysis/ embolectomy

Inguinal Hernia

• Is the bulge always present or does it appear and disappear?
• Is there pain on the swelling? (uncomplicated hernia is classically painless)
• Is there change in the overlying skin, wound or sore over the bulge? Is there discharge?
o Change in overlying skin and discharge may suggest strangulation or inflammation
• Ask for other GIT symptoms
o Is there straining at defecation?
o Is there abdominal mass or distension?
• Meds / Supplements
• Sexual Hx
Exclude
• Abscess
• LN
• Femoral pseudoaneurysm
Review of other systems:

All other systems must be reviewed starting from the nervous system. But the clinician should pay attention to symptoms
of chronic obstructive airway disease and obstructive uropathy such as chronic cough and straining at micturition
respectively
DISCUSSION
ICE: Ideas, Concerns, Expectations
How does a hernia happen?

With straining like you do, there will be muscle tearing, and some gut will protrude through the defect
Could it be better?
It usually needs a surgical operation for repair, the operation may be in open fashion or key hole surgery
Where to get back to work?

Few weeks
Indications of laparoscopic repair?

• Recurrent
• Bilateral
Steps of hernia repair?

Groin Swelling (Infected Femoral Pseudoaneurysm)
Stem:
Patient referred from his GP due to the presence of groin abscess

• Injection: “Did you have any recent injection or trauma in your groin?”
• Pulsatility: “Do you feel that this swelling is having pulses?”
• Ischemic manifestations: “Do you feel any limb pain or coldness or colour changes or limb swelling?”
• Neurologic manifestations: “Do you have any limb numbness?”
DISCUSSION
Differential diagnosis?
• Infected femoral pseudo aneurysm
• Groin abscess
• Infected hematoma
• Inguinal lymphadenopathy
Investigations?
• Duplex ultrasonography
• CT angiography
Treatment?
Ligation of the involved artery with delayed revascularization.

COMMUNICATION
Phone Call
CONTENTS
Self-discharge (DAMA) ......................................................................................................................................................... 2
Consent for OGD, dilatation and biopsy .............................................................................................................................. 3
Anxious Parent (1) Spleen .................................................................................................................................................... 4
Anxious Parent (2) Perforated Appendix ............................................................................................................................. 5
Angry Patient (1) Arthroscopy .............................................................................................................................................. 6
Angry Patient / Wife (2) CT Machine ................................................................................................................................... 8
Counseling a Patient Before Stopping Warfarin .................................................................................................................. 9
TKR ...................................................................................................................................................................................... 10
Consent Colonoscopy ......................................................................................................................................................... 12
Jehovah’s Witness .............................................................................................................................................................. 14
COMM. PERSON MO’s MRCS B NOTES (Previously called Reda’s Notes) 1

Self-discharge (DAMA)
Young pt who/ RTA / suffered a large splenic hematoma. Observed for 48h, remained well, but planned by consultant
for further observation KIV, splenectomy if hematoma ruptures. Pt wants to AOR discharge because he has an
important interview the next day. Also facing financial difficulties because of wife’s new diagnosis of cancer…
You Hello Mr. ……, I am …… one of the surgical doctors, I have been told that you want to leave the hospital,
can I ask you first why?
Patient …
You Ok, I understand that staying in hospitals is frustrating and disappointing but you have to know that
people are only kept in hospitals when absolutely necessary.
Patient …
You First let me explain your case, you have what we call (splenic hematoma) which means a collection of
blood around the capsule of your spleen (spleen is an organ which is present right here in the upper left
side of your tummy), this was due to fracture to your ribs. Your hemoglobin dropped also by 1 gram which
gives the possibility of continued bleeding which may lead to serious deterioration and danger to your life.
Patient …
You I definitely understand your situation but you have to look also for your own health. If something bad
happened to you, your wife's condition will be worse as nobody will look after her. I can arrange with our
social workers to find a way to give help to your wife until your condition improves.
Patient …
You Ok Mr. ……, can you repeat for me what I have told you about your condition so as to be able to know if
you understand me right or not.
Patient …
You Mr. …… as I cannot discharge you medically, you will have to sign a legal document stating the exact
details of your case and that the continued admission was medically advised and that the potential
sequences have been explained and that you take the responsibility of any adverse outcomes.
Patient …
You Ok, if you felt that your state is deteriorating like feeling drowsy or having unbearable tummy pain, I
suggest that you should attend to the A&E department immediately and ask them to contact me or the
SHO in charge directly.
Patient …
You Mr. ……, you have decided to self-discharge and you are going to sign the appropriate documents, so I am
going to sum up what we have been through. You know that you have a splenic hematoma and that the
medical advice is to keep you in hospital. You understand the risks of not being in hospital which include
becoming more unwell and possible even may lead to a danger to your life. You have accepted the
responsibility of those risks.
Also we have discussed what signs to look for out and that you will return to hospital if you were more
unwell
If you have any other questions, please ask me. Thank you
Patient …
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) COMM. PERSON

Consent for OGD, dilatation and biopsy
60-year-old, history of smoking, alcohol presents with dysphagia. Your consultant has gone off for a meeting and you
are tasked to consent for OGD, biopsy and dilatation under GA.
You Hello Mr. ……, I am …… one of the surgical doctors, I have been asked to talk to you about an investigation
we would like to arrange for you. Can I ask you what do you know so far about this?
Patient …
You Ok, this is what we call esophagogastroduodenoscopy which can be abbreviated to OGD. The camera is
called the endoscope which will be inserted through your mouth down your food pipe then to your
stomach then along the first part of your small bowel. This camera will relay the image to a TV screen so
we can have a look inside. We shall also make a widening of the narrow part of your food pipe which was
discovered previously on the barium image. We may also take some samples from the lining of your food
pipe which may help us in figuring out your case. This will typically be under sedation which will make you
slight drowsy and feel no pain.
Patient …
You No procedure is without risks. The possible risk may include:

• Damage to your teeth from the introduction of the scope
• Infection such as chest infection
• Bleeding from the sites of tissue samples
• The most serious risk is cutting through your food pipe wall which may need a surgical operation
for repair
Patient …
You Listing those risks doesn't mean that they will essentially happen. My advice is to accept doing this
investigation as it is very crucial in determination of your case. Also you have to know that only skilled and
experienced surgeons are the only allowed to perform such procedures.
Patient …
You This is most probably due to the narrowing present inside your food pipe which hinders your regular
secretions to flow downwards smoothly
Patient …
You Still early to confirm that, we will have to wait until the results of this investigation appear and probably
we may need to do further investigations to figure it out
Patient …
You It usually appears within 2 weeks’ time, I can understand your apprehension and will make sure to contact
you once it is available
(close the consultation and ask if any other questions)
Don’t forget general advice, no driving, etc.

Anxious Parent (1) Spleen
Son with splenic rupture, Father approved operation. Mother appears later crying, demands to speak to consultant.
You Hello, I am …… one of the surgical doctors, I apologize that you have not been contacted before. I will tell
you everything about your child condition but let me know first what do you know so far about what
happened?
Mother …
You Mrs. …... your child apparently fell off his climbing frame and probably seriously harmed himself. I
apologize that you couldn't see him before taken to the theater but the case was an emergency and we
could not wait until you arrive.
Mother …
You Unfortunately, the scan we have made when he came in suggested that he had a ruptured spleen (which
is an organ present inside his tummy in the upper left side) and he is now being operated on to fix that
Mother …
You A ruptured spleen is definitely a serious condition, that's why he was taken urgently to the theater. You
have to know that he is now in very good and experienced hands, however his condition remains serious
to the extent that may affect his life.
Mother …
You His father told us that your child was playing at garden when he suddenly called out in pain as he had
fallen from a height. He noticed a big bruise on the left side of his chest so he called an ambulance.
Mother …
You I will have to share this information. In any case like yours we have to make extra precautions to ensure
that your child is going to be safe. We will take some standard procedures like finding out about your child
situation at home. Also we will need to involve a child protection consultant. We routinely involve child
protection services to make sure that anything we do will be in your child best interest
Mother …
You The spleen has some functions in the body's defense mechanism, so if his spleen is going to be removed,
he will need to be vaccinated after that to protect him against potential infections he may get. Also it will
be recommended to receive lifelong protective antibiotics.
Mother …
You You have to make sure that our first priority is your child medical care. We will ensure that he will make a
good recovery. We will not discharge him until we have undertaken full clinical examination and make
sure that his GP is aware about any concerns.
Mother ….
You Again if you need to ask me about anything, please let the nurses call me, thank you

Anxious Parent (2) Perforated Appendix
You are the SHO on call for emergency general surgical admissions. A 10-year-old girl has just been admitted as an
emergency with peritonitis. She has been unwell for 2 days and very unwell for one day. The child is extremely ill. A
perforated appendix is suspected and she is being resuscitated by your registrar before being taken to the operating
theatre. Your consultant, Mr. Mann is on his way in from home, and will perform the operation. You have been
instructed to see the child’s father, and explain the situation. You did not have an opportunity to see the child yourself
before she was taken to theatre.
You Hello Mr./Mrs. ……, I am …… one of the surgical doctors, I was told to speak with you about your child
condition. Can you first tell me what do you know so far?
Parent …
You First, you don't have to feel guilty because this could happen anyway. Your daughter was brought by your
neighbor complaining of tummy pain. Our initial investigation revealed the suspicion of acute
appendicitis. She was managed by our registrar and received some IV fluids and antibiotics. We are now
waiting for the consultant who will operate upon her
Parent …
You We are suspecting acute appendicitis as this is common condition and also her signs and symptoms
denotes this. But we cannot be certain 100% until we open and see
Parent …
You In children specifically there is less fat inside the abdomen, so perforation can be particularly dangerous.
In such case your child may go to a higher care area
Parent …
You A small horizontal wound will leave a little scar, but we may need to expand the wound and this may be
disfiguring
Parent …
You Yes, probably severe infection can block the reproductive tubes in young girls, so future sub fertility may
happen
(close the consultation and thank the mother)

Angry Patient (1) Arthroscopy
Post-Traumatic Meniscus Injury, Arthroscopy cancelled twice before and now again due to an emergency case.
Patient is frustrated.
In preparation bay: Write all the dates on paper, as they may not be in order.
You Good morning Mr. ……, my name is Dr. ……, I am the orthopedic trainee covering for my consultant
Patient …
You I understand that you have come today for your knee operation
Patient …
You Mr. ......, I am very sorry to say that but unfortunately my consultant has been called away for an
emergency case and we will be unable to carry out your case today
Patient …
You Again I do apologize. I can see that your knee has been really troubling you. It would’ve been good to have
been able to have it done today. I understand your frustration as I see from your notes that you were
postponed once before. However surgical emergencies have to be prioritized and this is why my
consultant was called away. I am really sorry for that.
Patient …
You Sorry, as I told you, he is busy now with that emergency case and he will be unable to pick up my call
Patient …
You Mr. ……., It is your right to choose your doctor but I am afraid that also will be time consuming as the new
consultant will study your case from the start
Patient …
You I am sorry but I am not authorized to do such operations without supervision
Patient …
You I am sorry but I cannot give you the next available date just now. We will call you once we put in a date.
But I promise I will mention your circumstances and emphasize the importance of having you listed in the
next possible session.
Patient …
You I am sorry sir, but if such an emergency should rise again, it will need to be prioritized
Patient …
You I can write a letter to your employer explaining the medical reason of why you will not be able to carry out
your job as a post man for now and that you will need more sick-leave as your procedure has been
postponed. Even if you want I can call him for you
Patient …
You Well, there will be some wearing and tearing. However, you should remain active with non-weight
bearing exercises such as swimming to keep the muscles around your knee strong. I can also refer you to
a physiotherapist who will recommend some good exercises to strengthen your knee
Patient …
You I can prescribe a different type of pain killer. You should stop diclofenac as it increases the risks of
stomach ulcers
Patient …
You Again accept my sincerest apologies

Extra questions
Patient I am not happy and I want to file a complaint
You
Patient How will the arthroscopy procedure be done, can you explain to me?
You
Patient When can I walk again after the suregery? Will I have to stay in overnight?
You

Angry Patient / Wife (2) CT Machine
Patient referred from GP for ascites. Peritoneal tap was done and showed malignant cells on cytology. Tumor markers
sent (pending). Planned for CT AP today, but CT broke down. Engineer sent for, coming tomorrow, CT will only be up
next week. Radiologist offered to do U/S abdomen today. Consultant was supposed to speak to wife, but had to go to
EOT. Registrar wrote in notes that if patient develops SOB, can consider therapeutic tap.
Task: Update patient’s wife
You Hello Mrs. ……, I am …… one of the surgical doctors, I am very sorry that you have been waiting for too
long to see Mr. Mann.
Patient …
You No, I am not, I am very sorry he has been called for an emergency. I am here to see what is wrong and talk
to you about what i can do for you. I will definitely tell Mr. Mann that you were here and I can arrange
another appointment for you to meet him.
Patient …
You I know that is a very tough situation. I know that he came in couple of days ago after having some tummy
swelling for 6 weeks and he was sent to do a CT scan. But unfortunately we are currently experiencing
some problems with our CT machine.
Patient …
You First, let me tell you why we request this investigation. We know that he had a tummy swelling due to
accumulation of fluids inside. Some of these fluids were taken for analysis which showed the presence of
cancer cells. What we need to know from this investigation is what is the kind of this cancer and where it
is coming from and how much it has spread.
Patient …
You As a temporary alternative, we can do an ultrasound scan (like the jelly scan of the pregnant women)
which will give us an idea about his liver and whether it contains any suspicious spots or not, also it will
give us an idea about the amount of fluids. Another alternative also is MRI scan which can be equally
helpful as CT, but we have to take Mr. Mann’s opinion on that. Our last option is that we may transfer him
to another hospital to do the scan.
Patient …
You I am so sorry, I agree that we may be a small hospital and probably don’t have much resources available
to us but we routinely do all the required investigations for such patients within a 2 weeks’ time frame.
So, we will not leave him to suffer if we found that he needs to be moved to somewhere else.
Patient …
You Well, to tell somebody that he is having cancer, I have to be ready to answer questions like where it
comes from, what its stage is, what are the options of treatment. For your husband, the only thing that
we have in hand is the fluids analysis which tells that there is cancer.
Patient …
You We do operations for cancers that we only think it may improve. In your husband's case, the presence of
tummy fluids gives an impression of an advanced cancer. In cases like this, it will be unkind to put the
patient in pain with only little benefit and little hope of improving.
Patient …
You Yes, this is due to the presence of large amounts of fluid inside his tummy pushing his lungs so he cannot
breathe well. I will discuss with Mr. Mann if we can withdraw some of the fluid from his tummy. Also,
there are certain medications which can help him to get rid of these fluids.
Patient …
You (Summarize again, apologize at the end, ask for any other concerns, close the consultation, thank the
patient.)

Counseling a Patient Before Stopping Warfarin
Recurrent inguinal hernia (past surgery 30 years ago), legally blind (walking stick ,dark glasses) from cataracts.
Patient had mechanical heart valve replacement and is on warfarin since. Planned for operation so should stop
warfarin. Anxious and afraid to stop warfarin. Already talked to consultant in clinic, but still has some concerns.
You Hello Mr. ……, I am …… one of the surgical doctors in this department, I have been told that you’re having
some concerns regarding stopping your warfarin pills, can you tell me more about your apprehension
towards this?
Patient …
You First let me explain what is warfarin and how it acts. Warfarin is a medication that thins the blood by
preventing the production of certain chemicals. It is prescribed for patients to prevent or treat the
formation of clots in the blood. In your case you have been prescribed by warfarin to prevent formation of
clots over your artificial valve. As we are going to operate upon you, we will have to stop this blood
thinning effect of warfarin for the fear that it might cause bleeding during or after the operation. The
problem here is that warfarin has a long duration of action, so to eliminate its action we have to stop it 5
days before your surgery. But we cannot leave you without protection for this period, so to keep you safe
from formation in clots in the blood, you will be given another injectable drug which is called (heparin)
that will be equivalent in effect to warfarin but has a shorter duration of action, so it can be stopped only
for 12 hours before surgery.
Patient …
You Both of them are providing the same required blood thinning effect that will protect you from formation
of clots over your artificial valve, but the difference is that warfarin has a long duration of action which
means it will be acting up to 5 days of its stoppage while the injectable heparin is having only 12 hours of
action. So as I told you it can be stopped shortly before your surgery
Patient …
You After your surgery is finished and if we are satisfied that there will be no more bleeding, we will continue
giving you this injectable heparin together with your warfarin tablets till we get sure through some blood
investigations that the blood thinning effect of warfarin is regained. Then we will stop injectable heparin.
Patient …
You Yes, during this period in which we are stopping warfarin and started injectable heparin you will stay in
hospital. This will be about 5 days prior to your surgery.
Patient …
You You should not stop your diazepam tablets till the morning of surgery but only with a small sip of water
Patient …
You (Summarize, ask the patient if he still has some concerns or if there are any other reasons he doesn’t want
to stop warfarin. Close the consultation, thank the patient)

TKR
Patient is going for an elective total knee replacement. Please council the patient and address his/her concerns.
You Hello Mr. ……, I am …… one of the surgical doctors, I have been asked to talk to you about your knee
operation. Is there anything specific you would like to know?
Patient How long does the operation take?
You The operation itself usually takes a couple of hours but there is also anesthetic time and recovery time
Patient Are there any complications to this procedure?
You No surgical procedure is without risks. Some of the complications include

• Bleeding: it is common to have a small amount of bleeding from the wound after surgery.
• Stiffness: You will be shown exercises to improve movement in your knee and will have physiotherapy
as an outpatient.
• Pain: This operation is designed to remove arthritic pain caused by the knee joint. Initially after the
operation you are likely to have pain due to the surgical procedure however the nursing staff will
provide you with pain relief to manage this.
• Clicking and clunking in the knee
• There is also a risk of infection and blood clots forming in your leg.
Patient What methods will be taken to help prevent blood clots
You The most important factors in helping to reduce blood clots are keeping well hydrated and mobile. It’s
very important that you walk or exercise your legs whenever possible, even if you are in bed or in a chair.
You may need a pair of anti-embolism stockings and we will prescribe you some blood thinners as well.
Patient Can I have breakfast on the morning of the surgery.
You Please do not eat anything at least 6 hours before the procedure. You are allowed to drink clear fluids up
to two hours before the surgery.
Patient Will I be put to sleep during the procedure?
You Your anesthetist will come to see you before your operation to discuss the type of anesthetic that you will
have, this may be a general anesthetic or spinal.
Patient How long will I need to stay in the hospital after surgery
You It depends on your recovery and your progress with the physios. The average length of stay is around 3
days after surgery, but it differs from patient to patient.
To ensure you are ready to go home we need to check the following:
• You must be able to walk safely around the ward with either crutches or walking sticks by yourself
• You must have managed a set of stairs or a step safely (depending on what you have at home)
• You need to be able to get on and off a bed, toilet and chair by yourself
• Your wound needs to be showing signs of healing
• Your blood results and x-ray of your new joint must be satisfactory
• Your pain needs to be under control
• You need to be medically fit
• You must achieve a minimum bend of 75 degrees in your knee
Patient When will I need a hospital follow-up?
You This will depend on the consultant who is doing the operation. But we usually have follow-ups in the out-
patient department at 6 weeks and 6 months after your surgery. Your GP or DN will also assess your
wound at 2 weeks after the operation.
Patient When can I return to work?

You The medical staff will be able tell you when you can return to work. This will depend, largely, on what you
do for a living.
Patient How soon will I be able to walk after my surgery
You The physiotherapists will try to get you back on your feet as soon as possible, hopefully on the 1st day
following your surgery.
Patient Will I be able to go swimming after my operation?
You We advise that your wound needs to be fully healed before you go into the pool. You also need to be
confident with your walking so that you can manage to walk safely on the wet pool side.
Patient When can I start driving again?
You You should not drive for a minimum of six weeks until you are confident that you can safely do so.
Patient How soon can I travel after my operation?
You Flying is not recommended for at least three months after your operation due to the risk of blood clots.
For any other long-distance travel (car, train, coach), make sure you are able to walk around regularly.
Take care when travelling on a bus or when getting into a car with a high step
Patient Thank you
You (Summarize)
(Advice, Safety Netting, Warning signs and general advice)
It is absolutely normal to have swelling in the knee and leg after the operation for up to 3 months. There
also maybe some healing redness around the wound in the first six weeks. It is also normal for your knee
to be hot to touch for up to one year after the surgery.
We will also provide you with an information booklet that contains all the important info that you may
need.

Consent Colonoscopy
You have been asked by your consultant to consent Mr. Mead, a 59-year-old, for a colonoscopy. When you read
through the clinic notes, you see that he has been suffering with PR bleeding and weight loss over the past 2 months.
You Hello Mr. Mead, I am Mr. Roberts’ SHO and I have been asked to talk to you about an Ix. he would like to
arrange for you. Can I just start by asking you what you understand so far?
Patient Sure, no problem. From what I gather, Mr. Roberts wants to use a camera to have a look into my bowel to
see where the bleeding’s coming from.
You Yes, that’s right. The camera test is called a colonoscopy. It is a camera, known as an endoscope (2 pence
size), which is inserted through the back passage and into the large bowel. {draw a quick diagram}. The
camera then relays the image onto a TV screen so we can have a look inside and see what may be causing
your symptoms. It is a very accurate way of looking at the lining of the bowel to see if there is any disease,
also need to take some tissue samples from the lining of bowel to help us with our diagnosis…. Normally
this doesn’t hurt. Does that make sense so far?...... You will be given laxatives to clear your bowels out to
allow us to see clearly. You will be awake for the procedure but receive sedation medication through a
vein on back of your hand …which means you will not mind the procedure / remember it clearly, drowsy
after the procedure and can’t drive so it is important to arrange transport home afterwards. During the
procedure you may feel as if you are passing wind as air is passed into the bowel, you shouldn’t feel
embarrassed. The operator may ask you to move around onto your side or back at certain times. The
reason for a colonoscopy is because a change in your bowel habit can sometimes mean there is
something happening on the inside of your bowel. We need to find out about this as early as possible as
the earlier we find out someone has a medical problem the earlier it can be treated… Does it sound good?
Patient Yes, it does, it doesn’t sound particularly pleasant! Will I be awake for the procedure?
You You will be awake for the procedure but receive sedation medication through a vein on back of your hand
which means you will not mind the procedure / remember it clearly
Patient Are there any alternatives to having this done?
You Yes, a Barium enema is an alternative, which involves the insertion of contrast solution into the back
passage and X rays are then taken. However, this does not provide as much detail as an endoscopic
investigation and we cannot take tissue samples for analysis.
Patient Oh right, I better have the colonoscopy then. Are there any risks?
You No procedure is without risk. The risks are:

• Sedation (midazolam, fentanyl) – Breathing/ blood pressure problems: respiratory depression,
hypotension, bradycardia, allergy, nausea, vomiting (closed monitoring required)
• Bleeding from the site of the tissue sampling. Usually this stops on its own and if it doesn’t it can be
treated with cauterization or injection treatment. (1 in 200)
• Perforation or a tear in the bowel lining which nearly always needs an operation to repair. (1 in 1000)
• Incomplete procedures (scope can't reach caecum due to bowel material)
Patient Can I eat and drink as normal beforehand?
You So that we can have a good clear view of the bowel, you will need to be on a low fibre diet and drink
plenty of fluids 2 days prior to the procedure. The day before, you should have clear fluids only including
black tea/coffee with sugar, glucose drinks, clear soups. You will also need to take a laxative which will
explain when to take it on the label.
Patient Should I take my BP tablets in the morning?
You Yes, take your regular medications in the mornings.
Patient What about my Aspirin? My GP gave it to me as a precaution because I have high blood pressure and my
father died of a heart attack

You Because of the risk of increased bleeding, you will have to stop your aspirin 7 days before the procedure.
You can restart it immediately after the procedure. Do you have any other questions?
Patient Yes, just one more. How long will it take to get the Results of the tissue sample?
You The results of the tissue biopsy take 2 weeks. You will be seen in the outpatient clinic following the
procedure to discuss the findings of the investigation.
Explain bowel preparation methods. Inform him when to be NBM and to take his regular medications.
Summarize if necessary and keep checking that he understands the information
Offer information leaflet.
Preparation:
• 4 days before – Stop iron, constipating drugs / bulking agents.
• 2 days before – Eat only Eggs, cheese, white bread, butter, NO meats, fish, fruits, vegetables,
• 1 day before – breakfast with above, then clear liquids (tea, coffee, fruit juice), 3 pm – 45 ml fleet with half
glass water, then 2 glass water (same at 9 pm).
• Day of investigation - NBM.
Tell the patient that he needs to sign a consent form and not to drink Alcohol afterwards.

Jehovah’s Witness
Mr. Ungwe, 67-year-old male scheduled for craniotomy (highly vascular brain tumor), Need 4 units of blood for
crossmatch, he has previously stated that does not want a blood transfusion. Explain the operation Mr. Ungwe is
going to have including the possibility of a transfusion.
You Hello Mr. Ungwe, I’m one of the surgical SHOs, I wanted to discuss the operation you're due to have if
that's ok? Can I start by finding out what you know?
(Rapport / Open question …let him talk …set the scene)
Patient I know I am going to have an operation to take out a brain tumor. If it goes well, please God, I will be
cured. I understand there are risks"
You Yes. We are planing an operation to take the tumor out of your head…. It is a risky operation mainly
because the tumor can bleed a lot. Therefore, I wanted to get your permission to crossmatch and store
some blood so that it is available if the need arose. Would that be okay?
Patient (refuses)
What are the risks if I don't?
You The tumor is a vascular tumor, which means that it can bleed a lot. We will do our best to avoid this but
bleeding can be unavoidable sometimes. The risks if we can't stop the bleeding are that we have to
abandon the operation before the tumor is completely removed. It could also cause a serious stroke, and
there is an increased risk that you could die.
Patient (Understands this but still refuses a blood transfusion.)
How would you check the patient has capacity to make this decision?
I would ask them to relay the information and the risks of refusing a transfusion back to me. Patients have capacity to
refuse treatment even lifesaving treatment if they can understand, retain and weigh up the information, and are able to
communicate their decision by any means.
Who would you inform of this decision?

I would discuss the refusal of a blood transfusion with the consultant neurosurgeon, anaesthetist, and liaise with theatre
staff.
Should the operation be considered safe without a transfusion what precautions can be taken to reduce the
risk?
Preoperatively: check the baseline Hb; if low it may be worth postponing the operation and establishing a higher baseline
Hb. I would discuss the case with a hematologist and consider EPO, Tranexamic acid to increase the preoperative Hb. I
would consider starting IVF to ensure good hydration in the run up to the operation.
Intraoperatively: a quick operation by an experienced consultant is preferable, with focus on hemostasis. We could use a
cell salvager to allow blood lost to be replaced in an autologous transfusion. Good communication between the
anaesthetic and surgical team is important to ensure that blood loss is anticipated and treated quickly with fluid
replacement.
Postoperatively: I would ensure adequate hydration, recheck the Hb immediately after the operation, then again in the
evening and morning after. I would hand this patient to the on call surgical team and clearly document the refusal of
transfusion under any circumstances in the notes.
How would you close the consultation?

I would close by summarizing our discussion and documenting it in the notes. For instance, we have been through some
of the risks of the operation, and discussed why we would recommend that you have blood available for a transfusion.
“You have decided to refuse a transfusion, even in the event that it is needed to save your life. As you understand all of
the risks, we will respect your decision and I will make sure everyone involved in your care is aware of it. I have told you
that we will take extra precautions to minimize the risk of significant blood loss, and you are happy with these
precautions. Do you have any further questions?"

COMMUNICATION
Phone Call MRCS Part B Notes by Mo
CONTENTS
Postoperative Oliguria / Oliguria POD-1 .............................................................................................................................. 2
CBD Injury / Bile Leakage After Laparoscopic Interval Cholecystectomy ............................................................................ 4
Refer A Poly-Traumatized Patient to A Cardiothoracic Consultant ..................................................................................... 6
Mastectomy POD-2 Discharge Against Medical Advice ....................................................................................................... 7
Update The Trauma Head About a Trauma Case ................................................................................................................ 8
Perforated Viscus ............................................................................................................................................................... 10
Acute Limb Ischemia .......................................................................................................................................................... 11
COMM. PHONE CALL MO’s MRCS B NOTES (Previously called Reda’s Notes) 1
Postoperative Oliguria / Oliguria POD-1
Stem: low urine output (POD-1) by ward nurses. You are MO on call seeing this patient. Please see the notes and
summarize the events and come out with a management plan to update the surgeon in charge of her. Came to this
room with temperature, BP, HR chart (looks different from local charts) Essentially, patient has tachycardia, low-
grade temperature, mild hypotension and a narrow PP. Urine output is 10-20 ml/hr for last 8 hrs. Received only
1100mls of NS for POD1. Notes documented that catheter is not blocked. Operation notes stated some blood loss but
transfused 2 pints. Last Hb 12. Last TWC 14, High urea and borderline high creatinine. Results given can be quite
misleading if you don’t check the dates to find out the sequence of events. (E.g. they attached a pre-op renal panel at
the back of the case notes, which appeared normal, but somewhere in the case notes it was documented with the
latest renal penal results, which showed the above changes mentioned).
Stem: Call consultant about post op pt with low urine output. Pt had an elective low anterior resection / primary
anastomosis. In the end pt was under-loaded. Pt only had 800ml over 2 days and pt was NBM. Basically do as you
would in real life, remember SBAR. I volunteered to transfer pt to HDU for monitoring, KIV insert CVC.
Stem: Scenario was an elective left hemicolectomy for cecal tumor, with liver biopsy for suspected metastasis,
currently post-op D1, having persistent tachycardia 120 and hypotension SBP 90-100 post op, temp 37.5. postop
bloods unremarkable except drop in Hb from 12 to 10, Cr 116, Urea 16. ECG normal - no MI/PE. CXR clear, pt
documented as having benign abdomen, appears dehydrated, I/O in negative 150mls balance, GW nurses said there
is no urine output in IDC, asked to call consultant on call, as consultant in-charge is on leave. Likely AKI secondary to
dehydration, no abdomen signs at all, told him would hydrate and serial abdominal exams and update again and case
finished, 3 days post left hemicolectomy with anastomosis with oliguria, no signs of SIRS on ABG and observation
chart.
Stem: POD 1 post-left hemicolectomy for sigmoid adenocarcinoma with liver biopsy for suspicious liver nodule. Intra-
operatively had slipped clamp with blood loss. Now anuric, IDC already flushed. Hb slight drop, renal panel shows AKI
with raised Ur and Cr. Have to speak to on-call consultant regarding low urine output. Introduce yourself, pt’s primary
consultant and pt / SBAR, (after right hemicolectomy for cecal tumor)
Hello, I’m …… (SHO, ST1, CT2) working for Mr. …... I am calling to speak to Mr. …… to ask him an advice about a patient
who underwent right hemicolectomy for cecal tumor, he has been oliguric now. Could I check that I am speaking to ……?
Who is the consultant of the case?

Mr. …… (need to pick up this info in prep station)
Summarize your case?

Mr. …… is …… years old, he had a right hemicolectomy done 24h ago for cecal tumor, his urine output in the last 8 hours
is about (10-20 ml), I checked the urinary catheter which was not blocked. He is tachycardiac, has low grade fever, with
mild hypotension, his abdomen is lax. His bloods show that his Hb dropped from 12 to 10, urea is moderately raised and
creatinine is borderline high.
What do you think the cause is?

I think the patient is dehydrated, he received only 1100 ml of normal saline for POD1. Also on checking the operative
notes, there was a blood loss but he received 2 units of blood
Plans of action?
I will start fluid resuscitation by giving 1 liter of normal saline over 1 hour and will continually monitor the patient in the
ward. I will repeat bloods tomorrow morning, if no response to fluid challenge overnight, I will transfer the patient to
HDU to insert a central line and monitor. If bloods show Hb is still dropping, I will start blood transfusion
Do you think that the patient is bleeding?

May be, but I will monitor the vital signs continuously, I will do serial abdominal examinations. If I find any signs of
bleeding I will let you know
Do you think it is anastomotic leak?

For now, the patient is not toxic, his abdomen is lax, but I will do serial abdominal examinations and prepare for
abdominal ultrasound and will let you know if the patient becomes peritonitic
Do you need me to come back?

I will start fluid challenge, will update you subsequently
2 MO’s MRCS B NOTES (Previously Reda’s called Notes) COMM. PHONE CALL
Does he require HDU transfer?
Does he require operation now?
If HDU is full, who are you going to speak to?
Causes of shock in this patient?
Do you want me to see…?
What do to do, fluid challenge him? Dose?

30 ml/kg (1-2L) of crystalloids (250-500ml in 15 minutes)
Do you want to transfer him?
CBD Injury / Bile Leakage After Laparoscopic Interval Cholecystectomy
Interval cholecystectomy POD2, Op uneventful, 2 clips to CBD 2 clips to cystic artery, but since yesterday worsening
Abdomen pain with tachycardia, US: free fluid in abdomen no CBD dilatation. Labs: TW 18 and CRP 50, bilirubin raised
(something like that). Your consultant thinks there is bile leak from CBD injury, wants you to transfer to HPB
consultant Prof Archibald Rose at regional centre. His reg picks up. Reg not too happy that your labs are from
yesterday and nothing was done now you are calling at 4pm on a Friday.
Refer a patient with a possible CBD injury post lap chole (POD-4) to the local liver unit.
POD-1 jaundiced, labs show high bilirubin, slightly tachycardia, consultant went for nonemergency meeting, US shows
free fluid peritoneal cavity, ERCP services decided to close for staff shortage, POD-2 documentation for morning
rounds are best, no vitals, nothing… call for Transfer
Hello, I’m …… (SHO, ST1, CT2) working for Mr. …... in …… hospital. I am calling to speak to Mr. …… the hepatobiliary
consultant to ask him for advice about a patient, can I check that I’m speaking to Mr. ……?

Mrs. Smith is a 50-year-old lady, previously fit and well who underwent laparoscopic cholecystectomy 4 days ago. She
has been complaining of abdominal pain since. Today we noticed bile in her abdominal drain.
Clinically, he is tachycardiac, pyrexic, slightly jaundiced, has generalized abdominal pain, but his abdomen is lax. Her
bloods from 2 days ago show elevated bilirubin, elevated TLC and increased CRP. We have arranged for an abdominal
ultrasound which showed free intra-abdominal collection. We think that this patient has had a bile leakage and we were
hoping to transfer her to your specialist care for definitive treatment.
What are the possible sources of bile leakage?

May be due to:
• Cystic duct stump leakage due to slipped clips or retained CBD stone
• CBD injury
• Accessory cystic duct
• Leakage from the liver bed
Why do you think her CRP is up? Is there an infection?

As the CRP is an acute phase protein, it is likely to be raised due to the operation. The trend is showing it to be
decreasing, and in this patient the pattern of symptoms fits with a bile leak.
When were those bloods taken?

Unfortunately, the last set of bloods were taken 2 days ago. I apologize that I don't have a more recent set available, but
I'll make sure they are sent as soon as I am off the phone.
What will be your management?

• I started fluid resuscitation and antibiotics
• I will order new set of bloods when I am off the phone
• We need to make an ERCP to delineate the source of leakage and probably to put a stent, but this is not
available in our hospital now.
What does ERCP stand for and what does it involve?

Endoscopic Retrograde Cholangiopancreatography. It is an X-ray examination of the common bile duct and the
pancreatic duct. It involves an operator passes a flexible telescope down the esophagus into the duodenum. Dye is
injected through the ampulla of Vater (hepatopancreatic ampulla) to allow the bile ducts, pancreatic duct, gallbladder
and hepatic ducts to be visualized when an X-ray is taken. A bile leak will be shown by extravasation of dye into the
abdomen.
Is this urgent?
Yes, for the fear of developing biliary peritonitis
Do you need to arrange with anyone?

Yes, with the bed manager of both hospitals to discuss creating bed whether by facilitating discharge or repartitioning of
patients
What is billary peritonitis?
Peritoneal inflammation caused by leakage of bile into the peritoneal cavity, which may be caused by gallbladder
perforation, biliary trauma (thoracoabdominal or iatrogenic trauma), spontaneous perforation of the extrahepatic bile
ducts or peptic ulcers.
There are no beds available at this hospital at the moment. How do you think we should proceed?
I will alert the bed managers in both hospitals of the urgency of the transfer and ask if they have any way of creating a
bed for this patient, for instance, by facilitating the discharge or repatriation of a patient.
Left hepatic artery
An endoscopic retrograde cholangiopancreatogram
Refer A Poly-Traumatized Patient to A Cardiothoracic Consultant
Young motorcyclist, RTA, wearing full leathers and helmet at time of injury, documented by registrar that ST1 should
call for transfer to CTVS before going to see the patient, noted in patient’s bag an appointment card for a diabetic
clinic this coming Tuesday, GCS 14, PR 120, HR 100/80, Temp. 37. C/O right sides chest pain. 4L crystalloids given so
far, requested 6 units of blood for standby. Noted left thigh swollen, no open wounds - no Thomas or traction yet.
CXR: widened mediastinum, B/L pleural effusions, AXR: psoas shadow not seen, dilated small bowel loops, Left femur
XR: shaft fracture, CT: Not available for next 3 hours as it is being serviced. Registrar also documented insertion of
chest tube on the right. Swinging fluid with 200mls of blood-stained fluid, Hb 8, otherwise FBC normal, UECr/LFT
normal, CRP raised very minimally, pH 7.32, PaO2 10kPa, PaCO2 6.0kPa, HCO3 19.
Hello, I’m …… (SHO, ST1, CT2) working for Mr. …… in …… hospital. I’m calling to speak to Mr. …… the cardiothoracic
consultant to ask him to accept a referral of a poly-traumatized patient with a widened mediastinum on the chest x ray.
Could I check that I am speaking to Mr. ……

A man aged …… came to us on motorcycle RTA. On examination, his GCS was 14, his pulse rate was 120 bpm, his BP was
100/80, he has a swollen left thigh.
We did a CXR which revealed a widened mediastinum with bilateral hemothorax, we put a chest drain which drained
200cc of fresh blood. We could not do a CT scan as the machine is being serviced for the next 3 hours.
His AXR showed absent psoas shadow. X-ray femur showed fracture of the shaft.
His bloods: Hb 8.9, PH 7.32, with low HCO3. The patient is known to be diabetic.
We started fluid resuscitation by 4 liters of crystalloids and we cross matched 6 units of blood but not yet transfused.
What will you do for the cervical spine?

I will support it using a hard collar, sandbag and tape (triple immobilization).
What will you do for the leg?

I will use a Thomas splint
What will you do for the blood pressure?

We started fluid resuscitation and cross matched for blood, but we should not let the blood pressure rise for the fear of
increased hemorrhage
Why is the patient having metabolic acidosis?

Patient has a closed fracture of the femur, so compartment syndrome is a possible cause
The patient has a hemorrhagic shock
The patient may have diabetic ketoacidosis
What about the abdomen?

Absent psoas shadow denotes the presence of intra-abdominal collection, so he may require exploratory laparotomy.
What are his blood abnormalities?

Low Hgb
Who will accompany the case?

I will come with one of our anesthesia colleagues or ITU colleagues
Mastectomy POD-2 Discharge Against Medical Advice
78-year-old lady, with a background of COPD, mild LVF, underwent mastectomy and axillary LN clearance for breast
cancer. POD-2 she developed axillary discomfort with axillary swelling with SOB. Her daughter wants to take her
home.
The daughter of the patient whose notes you have, has arrived at the hospital. The patient was due to go home
tomorrow but some complications have arisen. Notwithstanding this the daughter wants to take her mother home
this afternoon to her house which is 60 miles away. She has persuaded her mother that this would be the best course
of action. You have spent the last 20 minutes trying, unsuccessfully, to persuade the daughter that discharge today is
not in the patient’s best interest especially to a house 60miles away.
The patient was keen to go home to her own bungalow, however in view of her complications she should stay in
hospital until she is better
The daughter is very determined and wants to have her own way and does not suffer fools gladly. She is convinced
that her mother will be fine going home with her today You have perceived that it would certainly be a lot more
convenient for the daughter because it will save her from coming to visit her mother in hospital or at her bungalow
She has convinced her mother that it will be best for her to go home with her today, although the patient would
almost certainly prefer go to her own house when she is well enough to go home. The daughter is a school teacher
and is out at work all day, as is her husband. They have two teenage daughters and a labrador so the house is busy
and noisy.
The patient has another daughter who lives near to the hospital, but she is a paranoid schizophrenic.
Call the consultant to update him about a POD-2 mastectomy patient whom her daughter wants to discharge against
medical advice.
Hello, I’m …… (SHO, ST1, CT2) working for Mr. …… in …… hospital. I am calling to inform you about a POD-2 patient who
underwent mastectomy with axillary clearance
Summarize your case

Mrs. Janice green, 78 years old. She had a mastectomy with axillary clearance 2 days ago for breast cancer, now she has
an axillary swelling and her wound suction drain has 90 ml of fresh blood, she also experiences SOB. The patient has also
a background of COPD and mild LVF. Now her daughter wants to take her home which is 60 miles away. I spent 20 min
trying unsuccessfully to persuade her daughter that discharge today will not be in the patient’s best interest
Has the PATIENT made their own decision or has she been bullied into making a decision to go home today?
I think the daughter has convinced her mother that it will be best for her to go home with her today, although the
patient would almost certainly prefer go to her own house when she is well enough to go home.
Is the patient alert and capable of making her own decisions?

Yes, she has the competence to make an informed decision
What do you think has happened to this patient?

In view of the fresh blood in the vacuum drain and the swelling in the axilla, there is a possibility of a reactionary
hemorrhage in the wound site.
Also I have to consider the presence of DVT and pulmonary embolism because of the SOB.
What will be your plan of action in the event of these complications?

As for hemorrhage, I’ll order an FBC to check the Hb to see if there was continued bleeding
A wound hematoma may require evacuation later on.
If I suspect DVT and PE, I would arrange for a CTPA and I’ll manage accordingly
So, what will you do if they were insisting to go home?

I will inform the patient and her daughter about the possible complications which may occur due to this premature
discharge especially because she lives 60 miles away. Also I’ll inform the patient that she will have to sign a legal
document stating that she wants to be discharged against medical advice and that she has full responsibility and that she
is aware of all the possible complications that might happen.
Also I’ll inform the patient about the warning signs and symptoms that she has to look out for, such as increasing
discharge from the wound or being more unwell and increasing shortness of breathing and that she has to seek advice
immediately in a nearby hospital or to come back here.
Update The Trauma Head About a Trauma Case
RTA, open fracture of the tibia and fibula, pulseless foot and abdominal collection
Stem: Motorbike rider, RTA by hit and run, unconscious initially but GCS 15 on arrival. Admitted. Ultrasound showed
free fluid in paracolic gutter. X-rays showed left open tibia and fibula fracture. Noted by nurse to suddenly have a cold,
pulseless limb. Please inform trauma consultant on call. Blood investigations on admission all normal, Raised CRP and
TW only. One prep station prior to this one - given case notes, no vitals chart, case notes had many entries (typed out)
from GS, radiologist etc.
Right tibia/fibula open #, antibiotics + ATT given, S/B GS, abrasions on left flank, abdomen soft, does not think needs
CT AP but ordered U/S - difficult exam, ?LHC free fluids, suggested CT AP , Pulses initially not mentioned, but nurses
later noted foot getting colder and paler, difficult to feel pulses , XRs showed tibia/fibula #s, right hand MC #s )
O/E Right hand swollen, abrasions left upper abdomen, open fracture left leg. Abdomen soft, non-tender. GCS 15.
X-rays: Right hand MC fracture, Left tibia/fibula fracture. CXR normal. GS registrar saw – No need for emergency
laparotomy for now, left leg became pale, DP/PT pulses not palpable. Worsening pain.
Bloods: Hgb ,UE, Cr, LFTs, PT/PTT normal. Tetanus and Abx given in A&E. 2L NS. given. GXM pending.
Call the trauma consultant
Hello, I’m …… (SHO, ST1, CT2). I am calling to speak to Mr. …… to update him about a trauma case. Could I check that I’m
speaking to Mr. ……?

21-year-old male came to A&E after an RTA. His GCS was 15 at time of examination. He is hemodynamically stable. He
has an open tibiofibular fracture on his left lower limb. Abdominal ultrasound shows free intra-abdominal collection. On
examination of the left distal pulses, there was no felt pulses on the left foot.
What is the most urgent?

The patient has an open fracture with an arterial damage on his left lower limb, urgent intervention is needed to avoid
ischemia and compartment syndrome.
Is the patient is wearing a c-collar?

(Info is not given in the notes)
I will definitely check for this
Is the patient dehydrated?

(Info is not given in the notes)
Again, I’m not sure. So I’ll definitely check for this
Plans of action?
• I will inform the orthopedic consultant and the vascular consultant
• I will reduce and immobilize the fracture
• I will order CT abdomen and pelvis
• I will order CT head and brain
What to do before sending him to the theatre?

IVF, analgesia, traction
What will you do for the wound?

Debridement of necrotic tissue.
What blood investigations will you send for?
Why are you calling me now?

May need overnight surgery.
How will you fix his fracture and why?

External fixation.
Initial stabilization of soft tissue and bony disruption in poly trauma patients (damage control orthopedics), They provide
unobstructed access to the relevant skeletal and soft tissue structures for their initial assessment and also for secondary
interventions needed to restore bony continuity and a functional soft tissue cover.
Why did GS ask for U/S when they felt abdomen was normal?
Abrasions, possible splenic injury
People I may need to call either pre- or intra-op?

• OT
• Anesthesia
• GS
• Vascular
• Plastics
Why Plastics?
Why GS?
Wound, Compartment syndrome, rule out intraabdominal injury.
Management of free fluid in abdomen?

Indication of emergency laparotomy.
Perforated Viscus
COPD + perforated viscus + ARF + metabolic acidosis.

Prep station, 73 y old lady brought by her daughter. Hx of COPD on steroids / relievers, seen in ED (Emergency) for
being "under the weather", unremarkable until she ate some food and suddenly had pain abdomen. Assessment
revealed suspected perforated viscus. Urgent Laparotomy was required.
Call ICU Registrar for Preoperative advice and request for ITU bed.
(Remember to write down his advice because he will make you repeat them at the end).
Pick up the phone and start speaking.
Hello, I am the surgical SHO …... working for Mr. …… at …... Hospital. I am calling to speak to the ITU registrar to ask
advice on an unwell patient who has been admitted today and is going to require a laparotomy. I would also like to
arrange an ITU bed postoperatively. Could I check who I am speaking to please?

Mrs... is a 73-year-old lady with a background of COPD, presented with a perforated viscus and has gone into acute renal
failure, with hypokalemia.
Her bloods tests: potassium …... creatinine ...... up from a baseline of ...…
ABG shows a metabolic acidosis, with a high lactate and high negative base excess.
Please could I have some advice on optimization before theatre and would it be possible to arrange an HDU bed
postoperatively?
What made you think of perforated viscous?

Physical examination showed signs of peritonism (abdominal tenderness).
Hemoglobin dropped 2 units.
CXR showed air under the diaphragm (or was clear, redo to look for free air)
U/S showed free fluids in abdomen.
What fluid-resuscitation will you do?

Crystalloids (rapid flush) then to colloids if poor response
I will also do cross matching for blood in view of the rapid Hb drop.
What preoperative arrangements do you suggest?

• ECG: to look for arrhythmias, AF, signs of hypokalemia
• Repeat CXR
• IDC insertion
• Antibiotics
• Check if the patient is on steroids, to give IV hydrocortisone
• I will keep the O2 saturation lower in the view of chronic COPD
• I will contact the anaesthetist to review the patient pre-operative
Criteria for ITU admission?

• 2 organ systems impaired with acute reversible causes
• Impaired respiratory system requiring mechanical ventilation
• 1:1 nurse patient ratio
• 1 organ system chronically impaired with a possible 2nd system being affected/impaired
What if I only have 1 ITU bed left and there is asthmatic young lady coming first?
I will continually monitor the patient in the recovery room until a bed is available.
Acute Limb Ischemia
Lady admitted for mild diverticulitis. Symptoms improving with IV antibiotics and fluids. Now complaining of sudden
acute right lower limb pain. ECG shows AF and premature ventricular complex. Sudden right acute limb ischemia. ABG
shows metabolic acidosis, hypokalemia. Arterial duplex showing acute ischemia
Lady admitted for mild diverticulitis. Irregular HR (?AF). Symptoms improving with IV Antibiotics and IV fluids.
Now complaining of acute right lower limb pain.
On examination, left lower limb pallor, pulseless, pain not responding to paracetamol
Bloods: Hypokalemia (GI losses, IV fluids)
ABG: Metabolic Acidosis (ischemia)
ECG: Premature ventricular complexes, AF
Arterial duplex: Acute ischemia.
Explain in SBAR format. (Situation, Background, Assessment, Recommendation)
Call the vascular consultant to refer a case of acute limb ischemia
Is it urgent, can we send it tomorrow morning instead?

Yes, it is urgent, patient has a critical limb ischemia, so early intervention is extremely needed for the fear of losing the
limb
Do you need cardiologist to review for PVC before transfer?

No, this can be assessed later on
What do you think of her presumed diagnosis of diverticulitis?

Now, in view of acute limb ischemia and AF, I have to consider the presence of mesentric ischemia as a cause of this
patient abdominal pain.
Appendicitis, cholecystitis, pancreatitis, mesentric ischemia, perforated viscous, infective colitis, IBS, ectopic pregnancy.
Do you want to scan the abdomen first?

We will need to scan her abdomen, but I think after the transfer
Could it be mesentric ischemia?

Yes, it could be, but for now the abdomen is soft and not tender, I will do serial abdominal examination and if we need
we may do CT Scan of the abdomen with contrast if the renal functions were normal
What imaging to do?

Arterial duplex and CT angiography
What to anticoagulate with and how?

Bolus of UFH 5000 IU, also LMWH
How to transfer (type of ambulance)?
Management plan?
• Correction of hypokalemia
• Correction of AF
• Anticoagulation
• Correction of metabolic acidosis
What will you tell her family?

I will tell them that the patient has developed acute reduction of circulation in her lower limb which may need an urgent
intervention and that is why we are going to transfer her to a vascular consultant.

Mo Reda Mrcs

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ANATOMY

SPINE & BACK MRCS Part B Notes by Mo

ANATOMY SPINE MO’s MRCS B NOTES (Previously called Reda’s Notes) 1

2 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY SPINE

Ligaments attached to the odontoid process?

Type of Atlanto axial joint?

4 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY SPINE

What is the first spinous process to be felt?

Demonstrate it on the subject?

Why we cannot feel the upper spinous processes?

Atypical cervical vertebrae and the atypical features?

ANATOMY SPINE MO’s MRCS B NOTES (Previously called Reda’s Notes) 5

ANATOMY SPINE MO’s MRCS B NOTES (Previously called Reda’s Notes) 7

8 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY SPINE

Level of the lumbar puncture?

Layers to pass through?

ANATOMY SPINE MO’s MRCS B NOTES (Previously called Reda’s Notes) 9

Movement on lumbar vertebrae?

Level of the spinal cord in newborn and adult?

Contents of the spinal canal below L2?

Location of the paravertebral venous plexus?

10 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY SPINE

How does spinal metastasis happen?

Batson venous plexus

ANATOMY SPINE MO’s MRCS B NOTES (Previously called Reda’s Notes) 11

Structures found at C6?

12 MO’s MRCS B NOTES (Previously Reda’s called Notes) ANATOMY SPINE

ANATOMY SPINE MO’s MRCS B NOTES (Previously called Reda’s Notes) 13

Terminal Cords Divisions Roots

Medial pectoral nerve

Lateral pectoral nerve

Long thoracic nerve

Medial cutaneous nerve of the arm

Where are parts of brachial plexus found?

Rotator cuff muscles?

Trapezius Levator scapulae

Cut edge of lateral head

Part Branch Course

Subclavius Pectoralis minor

Superior thoracic artery

Anterior circumflex humeral artery

Posterior circumflex humeral artery

Profunda brachii artery

Structures attached to the coracoid process?

Muscles inserted in bicipital groove?

Shoulder joint abduction?

Factors decreasing the stability of the shoulder

N.B Synovial Joints

Upper limb dermatomes?

1, 2 Buckle my shoe (Ankle).

Findings in nerve root compression

Muscles flexing the elbow joint?

Structures passing in spiral groove?

Clinical picture of radial nerve injury at the spiral groove?

Transverse humeral ligament

Short head of biceps

Separates the ulnar a.

Anterior View Posterior View

Abductor pollicis longus

Median nerve Ulnar nerve