ACUTE PANCREATITIS

Stem : 45 year old male, diagnosed and managed for acute pancreatitis 2
weeks back. Now presents with tachycardia, tachypnea and SOB.

Q. Shown CT scan with massive pseudocyst. Identify main organs(.Liver,

spleen, pancreas, aorta, vertebrae) (Stomach was squished till became a line
with a small black lining inside. Keep probing me till I said stomach lol)

Q. Main abnormality ? pseudocyst

Q. Functions of pancreas? Exo: pancreatic enzymes( digestion of

fat,carbohydrates,protien), enterokinase(trypsinogen-->trypsin), Endo: Alfa
(glucagon), beta(insulin), delta(somatostatin), PP

Q. D/D ? acute pancreatitis,acute cholecystitis,ascending cholangitis, perforated

viscous.
Q. Causes of acute pancreatitis? gallstone disease, chronic alcoholism,
infection, e.g. mumps, Coxsackie virus, typhoid, hypercalcaemia, e.g.
hyperparathyroidism, trauma, post-operative, e.g. after upper GI operations
where pancreas is handled, hyperlipidaemia, drugs: corticosteroids, oestrogen-
containing con-

traceptives, azathioprine, thiazide diuretic, hypothermia, vascular insufficiency,

e.g. shock, scorpion bites, iatrogenic, e.g. after ERCP.

Q. Pathogenesis? 1. 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.
2. Direct acinar damage: due to viruses, bacteria, drugs or trauma.
3. Protease release causes widespread destruction of pancreas and increases
further enzyme release with consequent further damage.
4. Lipase causes fat necrosis, resulting in characteristic yellowish-white flecks on
the pancreas, mesentery and omentum, often with calcium deposition (fat
necrosis).
5. Elastase destroys blood vessels, leading to haemorrhage within the pancreas
and haemorrhagic exudate into the peritoneum.
6. Haemorrhage (extensive) may lead to acute haemorrhagic pancreatitis.

Q. Glasgow criteria.? PANCREAS Pao2<8 kpa, Age > 55 , Neutrophils >

15,000 ,Ca. < 2 mmol , Renal ( urea) > 16 , Enzymes (LDH) >600,
Albumin<32g/L, Sugar(glucose) > 10 mmol( at least 3 of the above = severe
episode = ITU admission)

Q. Cause of Hypocalcemia ? fat saponification by pathologically released

pancreatic enzymes --->> FFA ---->> which chelate calcium . Others : ARF
causing hypocalcemia , deficiency of PTH due to pth gland destruction by
proteolytic enzymes.

Q. What scoring systems do you know?/To Risk Stratify ? Ransons,

APACHE- 2, Baltzhar CT scoring.

Q. Pick one with components. How does the score relate to mortality?
Ranson Criteria : On Admission : Age(>55), TLC( >16000), Glucose(>11),

LDH>350, AST>200. /. After 48 Hrs : Base deficit> 4, BUN > 5 mol/L , Ca. Low
< 2, Fluid sequestration >6 ltr, Hc fall>10%, O2 < 60 mm

Score 0-2: 2%, 3-4: 15%, 5-6 : 40%, 7-8 : 100% ( mortality)

Q. Balthazar CT scoring system? CT performed at 5-7 days after admission ,

can show edema, extra pancreatic changes, fluids collection, necrosis. 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.

Q. Causes of hyperglycaemia? Pancreatic enzymes destroy B- cells of tslets of

langerhans ---> increase in serum glucose and Stress hormones releases
glycogenolysis and glucogenesis.

Q. Which enzymes u test ? Amylase n Lipase.

Q. Is serum amylase is important in scoring systems? No

Q. 2 situations In acute pancreatitis where serum amylase normal ? too

early and too late .it returns back to normal after 48 hrs of attack,does not relate
to severity, top of chronic pancreatitis, hyperlipidemia.

Q. Patient is now tachypneic. WHY? Abdominal pain, Sympathetic overdrive

, Pressure by pseudo cyst, ARDS( V/Q mismatch due to ARDS and pleural
effusion) , splinting of diaphragmdue to large cyst, ARDS, sympathetic overdrive
as patient is not stable…all reasons.

Q.Radiological investigations will you do? US HBS first, CT criterion :

phlegmon, pancreatic necrosis,fat strandings,pancreatic abscess,pseudocyst

Q. Management of pancreatitis ? ABCDE and Fluids , HISTORY( establish

cause) , Physical exam, ABG, Bloods( FBC, LFT,Electrolytes , Urea, Albumin,
Glucose) , USG.. ICU transfer, CV line for : rehydration( because of the fluid
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sequestration and 3 rd space loss) and Monitoring and TPN( premorbid/current

needs/estimated return to normal ), pain management, NG tube , urinary
catheter/ NBM , Octreotides ( somatostatins) to decrease pancreatic secretions,
Antibiotics( broad spectrum ) , IV PPI to prevent stress ulcers and erosive
bleeding, ERCP n sphincterotomy.

Q. Complications of acute pancreatitis ? Death(10%), local (phlegmon,

pseudocyst, abscess, ascites, necrotising pancreatitis,fat necrosis , splenic vein
thrombosis), GI ( ileus, bleed) , hepatobiliary ( jaundice, portal vein thrombosis,
structure CBD ), Renal (ARF), Hematological ( DIC), Systemic ( hypvolemic
shock, hemorrhagic pancreatitis,ARDS,SIRS, MOF), Metabolic( hypocalcemia,
hypoalbuminemia, hypoxemia, hypomagnesia, hyperglycaemia), Respiratory
(ARDS, pleural effusion) , CVS(shock, arrhythmia)

Q. Nutrition in AP ? TPN is usually needed in severe cases

Recently , there is growing trend towards early institution of enteral feeding with a
nasojeujenal tube. Take into account : premorbid nutritional status, current
nutritional needs, estimated return to normal feeding

Q. Antibiotics to use in AP ? Carbapenam and Quinolone (penetrating

pancreas)

Q. How would you manage her pain? pethidine/ meperidine is drug of choice .
no morphine / no NSAIDS( WHO LADDER) ,Pain medication begins with
nonopioids (like acetaminophen, ibuprofen, or both).If nonopioids do not relieve
pain, mild opioids (codeine) are given.If mild opioids do not relieve pain, strong
opioids ( morphine) , PCA, Epidural Analgesia.

Q. Components of pseudocyst? Collection of amylase rich fluid ,necrotic

tissue, blood enclosed in wall of fibrous or granulation tissue ,bot the true
epithelium. Location: lesser sac.

Q. How long after will you suspect this? more than 4 weeks.

Q. What blood test to suspect? Persistent high amylase, high bilirubin ( CBD
obstruction)

Q. How they present? Epigastric swelling ,pain ,dyspepsia ,vomiting, fever

Q. Management ? Conservative initially ( NPO, TPN,avoid complications ,

Surgery : > 6 weeks, > 5 cm size, thick cystwall ---> internal drainage,
cystogastrostomy, cystoduodenostomy, cystojejunostomy and biopsy of wall to
rule out malignancy.

Q. Complications ? Rupture(bowel/ peritoneum), infection,bleeding(splenic

vessels), cholangitis,cbd obstruction,portal vein thrombosis.

Q. How does paracetamol overdose cause liver injury? Toxic metabolite

NAPQI is neutralised by glutathione, when excess acetaminophen is taken , not
all NAPQI neutralised and it accumulates in liver and effects vital functions.

Q. 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)

Q. What in blood results leads you to suspect pseudocyst? Amylase

PAIN
Stem: post operative pain , drug chart : had only panadol and arcoxia( selective
COX2 inhibitor)

Q. Define Pain ? Unpleasant Sensory and emotional experience associated with

actual/ potential tissue damage.

Q. 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.

Airway: Start at the beginning by checking that the patient has a patent airway.
Breathing: Check t RR, pattern and depth of breathing , respiratory function
impaired by inadequate analgesia? Cough and Expectorate ?

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
MI, particularly in the patient who is already hypoxaemic.

Disability : Assess whether the Method of analgesia is contributing to the

patient’s clinical deterioration. Particular attention to patient’s LOC, as
decreasing conscious level is an early indicator of opioid toxicity.
FULL PATIENT ASSESSMENT: 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 ( chart review) , Is effective analgesia prescribed? being
given? treatment appropriate ?, History and systemic examination, Investigations
like Serial ABG analysis and chest X-rays .

Decide and plan: If pain relief is adequate , patient is improving then continue
and review. If pain relief is inadequate determine why? Is it due to failure of the
method of analgesia? incorrect implementation of the method chosen?
development of a surgical complication ? Liase with acute pain MDT ( acute pain
services): consisting of surgeons, anaesthetists, nursing staff and pharmacists.

Q. S/E of opioids? Respiratory depression ( apnea)-Confusion,Hypotension,

Nausea and vomiting, Pin-point pupil- Itching, Constipation

Q. Drug chart: morphine not given…what u wanna give ?

Q. What is pain pathway ? Nociceptor --->Dorsal horn of spinal cord( via A

delta: sharp / C: slow fibres )----->lateral spinothalmic tract To Thalamus( via
second order neutron)------> Somatosensory cortex ( third order) .Ascending –
pain, Descending ( analgesic, hypothalamus,preiaueductal grey )

Q. Normal dose of morphine (PCA) ? 0.5-2 mg bolus

Q. What does this VAS mean (show0-10 VAS line with X somewhere to the
right of centre) …? Q. How much pain is this patient in? Moderate

Q. If you saw this drug chart, what would you tell the nurse? Drug chart was
strangely formatted, but seemed to show that both PRN drugs and regular drugs
hadn’t been given for a while.

Q. Different ways to assess pain? Verbal discriptor scale, Verbal neumeric

rating scale,VAS, Wong-Baker facial pain rating scale. WILDA: Word to
describe, Intensity, Location, Duration, Aggrevating/alleviating factors

Q. 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).

Q. What is the mechanism of action of Paracetamol? Mechanism of action of

paracetamol (acetaminophen) is not completelyunderstood. The main
mechanism proposed is THE Modulation of prostaglandin production in the CNS
by the inhibition of (COX), and recent findings suggest that it is highly selective
for COX-2. 1G of Paracetamol = 10mg of morphine (in action)

Q. How it's overdoses can cause liver failure??

Paracetamol is mostly converted to nontoxic metabolites by conjugation

with sulfate and glucuronide, with a small portion being oxidized via the
cytochrome P450 enzyme system to hepatotoxic metabolite , N-acetyl-p-
benzoquinoneimine NAPQI, this substance made harmless by conjugation to
glutathione.In overdoses glutathione depleted, leads to (NAPQI ) accumulation
and consequent liver injury and failure.

Q. Explain the WHO ladder : simple(PCM/ NSAIDS), weak opiates(codeine,

tramadol), strong opiates(morphine)

Q. What are the therapeutic effects of paracetamol? ( acetaminophen)?

This is an analgesic and anti-pyretic with minimal anti-inflammatory properties.

Q. What is Patient controlled analgesia: (PCA) ? it's a Electronically

controlled Infusion syringe pump connected i.v to allow the patient to self
adminster boluses of morphine(Overdosage is avoided by limiting both the size
of the bolus and the frequency of adminstration. A lock -out time is set within
which pressing the button again will not result in a bolus of analgesia. 1 way
valve preventing backflow of opiates into the infusion chamber which may lead to
over dose when redelivered

Q. Benefits? Faster pain sensation to pain relief time, hence better pain control,
Objective measure ( how much analgesia required), Reduced nursing input and
medication errors , Internal Safety mechanism to prevent opioid overdose , bcoz
of lock out time period , if patients administers too much they sleep n stop
pressing button.

Q. Complications/Poplems with PCA ? 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 handicapped patients, Limits patient mobility, S/E of opioids:
respiratory depression, sedation, nausea, vomiting, itching, urinary retention and

constipation. ...S/E of local anesthetics: hypotension, motor weakness,

numbness and urinary retention.

Q. Complications of pain ? CVS: increased HR, increased Bp, Increased

myocardial consumption-----> MI, GIT: delayed gastric empying, reduced bowel
motility,------> paralytic ileus, Resp. : Limit chest movements leading to
atelctasis, retained secretions , pneumonia, MSK: immobility leading to DVT,
Metabolic : hyperglycaemia, protien catabolism, Genitourinary: Urine
Retention, Neuroendocrine: Increased Glucagon and Adrenalin leads to
increase in Catabolic rate, Hyperglycemia, NA &H2O Retention and increase O2
consumption. Psychological: Anxiety, insomnia and fear..Others : poor wound
healing.

Q. 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 (Ultrarapid Metabolizers) who have high level of CYP2D6
resulting in rapid formation of morphine in them Life- threatening intoxication,
including respiratory depression requiring intubation, can develop over a matter
of days. Other pt (10%) lack this enzyme , they lose the analgesic effect of
codeine (poor metabolizers), but suffer it's side effects .

Q. What other modalities of analgesia are there? PCA, epidural

Q. Safety factors of PCAs? Lockout, measured dose, locked unit, non-return

valve on line

Q. In scoring system, what is the time interval to do the tests?

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Q. Why cannot give NSAIDS? Systemic side effects?

Coagulopathy: inhibition of platelet Tx A2 production leads to their reduced
ability to aggregate and form the primary platelet plug.

Bronchospasm: inhibition of COX leads to arachidonic acid being metabolized

down the pathway of leucotriene formation, which induces bronchospasm.
GI : Dyspepsia, Gastritis & peptic ulceration: direct stimulation of acid secretion
by the gastric parietal cells, with reduced bicarbonate and mucus production.
Renal: may precipitate AKI in pre-existing chronic kidney disease, dehydration,
hypotension or coexistent nephrotoxic pharmacological therapy, water retention.

Q. What other option if opioids not enough?pain mgmt team, anaesthetic

Q. Where would you manage the patient? ITU

Q. Is morphine effect on the sphincter spasm real or theoretical?

Q. 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.

Q. Manage paracetamol toxicity? Gastric decontamination: Gastric lavage,

within 60 minutes of ingestion. Activated charcoal: 30 minutes to 2 hours of
ingestion, Acetylcysteine(N-acetylcysteine): Antidote replenishing body stores of
the antioxidant glutathione. Liver transplant: acute liver failure
Minimum toxic doses of acetaminophen • Adults: 7.5-10 g
• Children: 150 mg/kg; 200 mg/kg in healthy children aged 1-6 years.

EPIDURAL BLOCK

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Stem : lobectomy / epidural T3 T4 level, now has hypotension , bradycardia

SpO2 92% desaturation, upper limb paraesthesia, oliguria

Q. Possible causes, what you would do ? (stop epidural immediately etc),

Q. Why would epidural cause this ? increased dose, incorrect positioning,

spinal level too high, etc. who would you involve(wanted someone in addition to
the anesthetist).

Q. What s/s would tell you patient is getting Worse ?

Q. What would tell you hes getting Better ?

Q .Why epidural in this case? What's so good ? Longer surgery and pain
relief after surgery . (because post op pain in a patient with lobectomy and h/o
copd would …. Described lung physio and path here)

Q. Recent evidence suggesting epidurals improve outcome ? yes

Q. What levels used for which surgeries ? T4: upper abdomen , T6: intestinal,
gyne, uro ( TUR), T10: vaginal delivery, hip sx, L1: thigh, lower leg, L2: foot,
ankle, S2-5: perineal, anal sx

Q. Why do we check temperature (I said arrangement of fibres, because motor

are last to be affected, seemed to accept it).

Q. Advantages? sleep v no sleep , CVS , respi effect?

Q. Why test pain temperature and not dorsal column in checking levels ?

Q. What would you do if suspect overdose /toxicity?

Q. Level of block depends on? (dose, duration, position)

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Q. Why patient having bradycharia ? why is higher/ T4 block dangerous?

High epidural block----> blocking of the cardioaccelerator fibres ( sympathetic
fibres) from T1-T5----> unopposed parasympathetic action of the vagus nerve

Q. Differentials? High epidural block , distributive shock secondary to epidural,

paralysis of intercostal muscles, paralysis of diaphragm, hemothorax or
pneumothorax, post operative hypovolemic shock .

Q. Management plan? (for all the different scenarios. remember to call

consultant of op as well as anaesthetist to review). call the operating consultant
and anaethesia consultant. Crash trolley, Sit the patient upright, 100% Oxygen ,
Stop any injections in the epidural catheter, Rule out any concomitant
hypovolemic shock, Epinehrine , phenylepherine, metaraminol ( inotroic agents),
atropine , dopamine.
Q. Factors affect the epidural efficacy? level of injection, Dosage,Type of
medications, Vasoconstrictors,Posture, Age, height , weight

Q. How to test level of the block ? Using temperature sensation ( ice packs)
Q. How to differntiate high epidural block from hypovolemic shock?
Eidural: warm and pink periphries ( due to vasodilatation), Bradychardia

Hypovolemia: cold ,clammy peripheries, Tachycardia

Q.Why test for temperature sensation rather than pain? Because

Temperature fibres conduct faster than pain.

Q. Systemic effects of Epidural analgaesia? 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 I.V fluids used to support the arterial pressure.

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SPINAL ANAESTHESIA
Spinal anaesthesia complicated by total spinal. Pt post TKR with spinal
anaesthesia. Few hrs after, BP crashed and HR low ,Impression:Total spinal
causing spinal shock.

Q .Types of spine anaesthesia ? Epidural and True spinal ( needle penetrates

duramater ) Marcain vs Lignocaine

Q. Management ? HD monitoring. Supportive with fluid support of BP till spinal

wears out. Possible need for adrenaline( Inotropes ) as pt requires both beta and
alpha receptors support.

Q.Types of inotrope ? Alpha, beta, mixed, dopaminergic. Explain using

preload, load and afterload module.

Q. Complications? Hypotension, headache, cardiac arrest, cauda equina, spinal

canal hematoma, epidural abscess

Q. Epidural versus Spinal ? E: epidural space/S: subarachnoid space, E:

around the injection site/ S: below the level, E: onset takes 25-30 minutes/ S: 5

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minutes, Injected drug volume larger in E, in dwelling catheter in

Pneumothorax/ Central line

Stem : Iatrogenic Pneumothorax following CVP line insertion.

Q. What are ur findings in this XR? Pneumothorax

Q. What type and why ? Simple , because No Tracheal deviation.

Q. Is this adequate CXR? no, cannot see costophrenic angles

Q. System for reading CXR ? ABCDE mnemonic

A-airway,B-bone, C-cardiac, D- diaphragm, E&F- equal (lung) fields, G- gastric

bubble, H- hilum and mediastinum (add the T which stands for technicals.)

Demographics: name, age,sex,hospital no.,previous X-ray.

Radiology: date, type(AP/PA,Standing/supine,Inspiration/Expiration).

Adequacy : Rotaion : medial borders clavicle to spinous process(distance) ,
Inspiration: 5-6 anterior ribs visible, Picture area : lung apex,costophrenic
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recess , Exposure : vertebral bodies visible through cardiac shadow.

Interpretation:(ABCD) : Airway (tracheal deviation, pneumothorax, effusion)
Breathing (lungs,consolidation,collapse,lesions) , Circulation (heart size, great
vessels, mediastinal shift) , Diaphragm (costophrenic angle,air below) , Extras(
bone, soft tissue)

Q. How to assess Breathing( post pneumothorax) ? RR, Rhythm, O2

saturation, Trachea ,Chest movements, Respiratory muscles use,
pattern,Inspect( skin colour, nailbeds) , percussion, auscultation

Q. Signs of Pneumothorax? Ipsilateral reduction of chestwall movements and

breath sounds, Tachypnea, Hypoxia, Hyperresonant chest( I/L) , Subcutaneous
Emphysema (occasionally) …..in Tension pneumothorax: additionally low BP,
high JVP, pulsus paradoxus, tracheal deviation, reduced GCS

Q. Types of pneumothorax ? Simple, tension, open

Q. Difference between tension and simple pnemothorax ?
Tension : Trachea is shifted oppsite side , tachycardia , hypoxia, Emergency
situation requiring urgent tube thoracostomy, Continuous entry of air through a
one way valve, Mediastinal shift and compression from the air in the pleural
space displaces the heart and great vessels, producing cardiovascular
compromise and shock
Simple : there is air in the pleural space, but no cardiovascular compromise
needle thoracostomy in the 2nd ICS , midclavicular line
Q. Safe triangle of insertion of chest tube ? Ant.: lateral border of pectoralis
major, Post. : mid-axillary line, Inf. : a line drawn from the nipple line backwards
Q. Indications of central line ? monitoring of fluid balance and fluid
resuscitation, TPN, certain fluids and medications ( K+ rich fluids), Failed
peripheral venous access, Hemodialysis, Transvenous cardiac pacing.
Q. Complications of central venous line insertion ? Pleural, venous, arteria,
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lymphatic, cardia, sepsis…..Infection + thrombosis( DVT), Air embolism, Arterial

puncture (hemorrhage, pseudoaneurysm, hemothorax), Pneumothorax, Left IJV
canulation: damage of the thoracic duct (chylothorax), Perforation of right atrium
----> cardiac tamponade, Arrythmias

Q. Immediate Complications ? Pneumothorax

Q. Causes/ Predisposing factors of Late CVP line infection?

Q. NICE guidlines for insertion ? insertion under ultrasound guidance,Post

procedure radiograph for: position of the radioopaque tip in SVC just superior to
its entry in RA, pneumothorax

Preprocedure checks : Lab (PT, Platlet count), Radio( CXR), Microbiology (

Sepsis) , Consent for Centre line and LA

Q. Technique for insertion of central venous line : ( IJV) ? Trendelenburgh

position : head down, feet up , Seldinger ( guidewire through introducing needle)
, locate: - clavicle - 2 heads of SCM , 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 30 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 with silk.

Surface marking IJV : ear lobule to medial end of clavicle.

Q. Removal technique? Head down to prevent air embolism

Q. Indications of removal? Cessation of cardiac support through initrope,

resolution of acute problem, line sepsis, discharge home
Q. Sites for inserting a central venous line? IJV, subclavian vein, femoral
vein(infection)

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Q. Organism causing infection ? staph. Epidermidis

Q. 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 5 maximal sterile barrier precautions:Sterile
gloves, Sterile gown,Cap,Mask, Large sterile drape. Once the central line is in
place:Follow recommended central line maintenance practices,Wash my hands
with soap and water or an alcohol-based handrub before and after touching the
line, 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.

Q. Investigations to do when SOB ? CXR, ABG,

Q. landmark IJV ? lateral to carotid artery, between 2 heads of SCM insert

direction of ipsilateral nipple .

Q. higher point you can insert into IJV?

Q. How do you manage this (pneumothorax)?

Q. Patient suddenly becomes SOB and hypoxic. What is happening? What

do you do? Where to insert needle? Tension pneumothorax. Needle
thoracocentesis, mid clavicular line, 2 nd ICS.

Q. Recommended way to insert jugular CVP ,NICE guidelines ? US guided

procedure, post procedure( CXR) : position of radio opaque tip in SVC, rule out
pneumothorax.

AAA / HYPOTHERMIA/ TRANSFUSION BLOOD

Q. Definition of perioperative hypothermia? core body temp less than 35

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Q. How to measure core temp? Oral, axillary, tympanic membrane, rectal

,oesphageal

Q.Causes of hypothermia in this patient ? Massive blood loss and transfusion,

resuscitation with unwarmed fluids, open surgery which was prolonged,Patient:
Hypovolemic Shock , Extrinsic: Massive blood transfusion, cold environment,
organs exposed during laprotomy

Q. Complications of hypothermia ? Why is it important to prevent

hypothermia? CVS–decreased CO (anaesthetised), arrhythmias,
vasoconstriction, ECG – increased PR interval, wide QRS complex, J wave ,
Respiratory –increased PVR and V/Q mismatch, decreased ventilator drive ,
Increased gas solubility, Renal –decreased RBF and GFR, cold diuresis.
Haematological –reduced platelet function and coagulation, increased
fibrinolysis, increased haematocrit, left shift of oxygen dissociation curve.,
Metabolic –reduced BMR , metabolic acidosis, insulin resistance,
hyperglycaemia. Gastrointestinal / hepatic –reduced gut motility. Neurological
–reduced CBF , impaired conscious state leading to coma.
Others : decreased drug metabolism leads to increased duration of drug

Q. Mechanisms/ Factors ? Mechanism: Conduction, Convection,

Evaporation(exposed viscera ) , Radiation (50%), Factors : cold anaesthetic
gases, decreased hypothalamic function and muscle relaxants, Anaesthetic
agents ( peripheral vasodilation) , Cold IV Fluids, Long Preoperatie Fasting
phase, Prolonged Immobility on OT table, Emergency Surgery, Shocked(
hypotension), Children, Massive blood transfusion.

Q. How do you reduce risk of hypothermia ? NICE: theatre temp at

21,Increase Ambient Pressure and Humidity, Warm irrigation I,v fluids/
Bloods/warm n humidify inspired gases, Least expose the patient , Cover the

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patient during transfer and induction, Insulate with wrap or warming blanket ,
Use Plastic bags for Exposed Visceras, Not leave the recovery room to ward until
core temp is 36 c, Use Forced -Air warming devices ( Bait Higgers)

Q. Consequence of Periop. Hypothermia? Increased Surgical Bleeding (slow

coagulation), MI and Arrhythmia, Delayed recovery from Anaesthesia, Excess
Sympathetic stimulation on waking , Negative Nitrogen Balance( protein
catabolism) , Impaired immunity, Wound Infection, Discomfort .

Q. Physiological complications of hypothermia ? Hypocalcaemia and

metabolic acidosis (secondary to reduced citrate and lactate metabolism)
Increased affinity of oxygen to haemoglobin,leading to hypoxia as the oxygen is
not delivered to tissues Platelet dysfunction Enzymatic dysfunction Cardiac
arrhythmias.

Q. Tell me why hypothermia is detrimental

Q. Ways that a patient loses heat intra operatively, preoperatively and post
operatively

Q. How to warm a patient intraoperatively and post operatively ?

Q .How to measure core body temperature ,I said Rectal, vesical and

PiCCO is an acronym for Pulse Contour Cardiac Output. It enables assessment of the patient's haemodynamic
PICCO, LiDCO ( seemed happy). status to guide fluid or vasoactive drugcatheter
therapy. ... PiCCO requires the insertion of a central venous pressure (CVP)
and a thermodilution arterial line.

LITHIUM DILUTION CARDIAC OUTPUT

Q .why surgery precipitate hypothermia? procedure heat loss, loss of

shivering, vasodilatation, cold IVF, cold gas of anesthesia machine, ways
of heat loss? how to avoid heat loss?

Q.How do you reduce blood loss in the above stem?

Q. What are the possible complications associated with a blood

transfusion? Complications may be broken down into Immunological, or Non-
immunological: -Immunological Acute haemolytic reaction (ABO incompatibility)
20



Febrile, non-haemolytic reaction Anaphylaxis Graft vs Host disease

Transfusion related lung injury -Non immunological Congestive cardiac failure
Hypothermia Electrolyte disturbance - ↑K ↓Ca Infections – eg prion

Q. What is Autologous blood transfusion? medical procedure involving

recovering blood lost during surgery and re-infusing it into the patient.

Q.What is Massive blood transfusion? Replacement of >1 blood volume in 24

hours or >50% of blood volume in 4 hours (adult blood volume is 70 mL/kg).

Q. Complications in massive blood transfusion? Volume overload, low

calcium, low temperature, low tissue oxygenation,low coagulation factors( 5,8),
Hyperkalemia due to K+ leakage from the stored RBC's, Hypocalcemia due to
chelation of ca+2 by citrate, ARDS( TRALI), Thromocytopenia ,Hypothermia

Q. Name 3 different blood components (PRBC, platelets, FFP, cryo, Blood -

packed/irradiated/leukodepleted).

Q. Give 3 indications of platelet transfusion? Haemorrhage in

thrombocytopenia, Consumptive Coagulopathy (DIC) ,Thrombocytopenia prior
to Invasive procedure.

Q. What is the shelf life of platelets ? 3 days /room temperature

Q.How are platelets transfused ? 4 hours or less,rapidly with short giving set
with no filter , Adult : 6 units, check 10 minutes to 1 hr after transfusion.

Q.intra-op complications

Q.risk factors in this patient

Q.how are you going to manage this patient ? (NICE GUIDELINES) , who
would you involve ?

Q.How do normal people generate heat ? Shivering

21



Q. Can the patient generate heat intraoperatively? No. paralytic given

Lab results: Low Hb, Low Plt, Raised PT / PTT, comment, what blood products
to give blood products. That’s why fresh blood is better.

Q. What clotting factors are stored blood products deficient in? - All

Q. How else can you reduce the use of blood products ?. Administering
volume expanders or intravenous fluids made with water, salt, sugar or starches
that help maintain the correct amount of fluid in the blood vessels. Volume
expanders may include crystalloids (e.g., normal saline or lactated Ringer's
solutions) or colloids (e.g. albumin or hetastarch). Applying cell saver or
intraoperative blood salvage techniques that use devices and methods to collect
blood from an active bleeding site and re-infusing that blood into the same
patient for the maintenance of blood volume.Implementing deliberate
intraoperative hypotensive anesthesia or lowering blood pressure during
surgery to reduce blood loss.Inducing hypothermia to lower a patient's body
temperature to decrease metabolic activity, heart rate and oxygen
consumption.Using acute normovolemic hemodilution (ANH) techniques or
blood conservation applications that are implemented by operating room
anesthesiologists. These techniques collecting, diluting and re-infusing a
patient's own blood.

Q. Mechanism of haemostasis ? Blood vessels vasoconstriction, platlet plug,

Blood coagulation ( fibrinogenà fibrin),Clot retraction, Fibrinolysis to dissolve clot

Q. What polymerizes fibrin ? thrombin

Q.How does vascular surgery inferfere with mechanisms of hemostasis?

22



Q. Complications of AAA? Rupture,Thrombosis (causing lower limb

ischaemia),Embolism,Fistulation to bowel (aorto-enteric), to vena cava, renal
vein,Pressure effects on adjacent organs, Death.

Q. Immediate post op complications of AAA ? Surgical : Malposition of graft,

arterial dissection, Endoleak,Rupture of Iliac arteries, Ischemia of Spinal cord,
kidney, liver, bowel. Delayed AAA rupture

Medical : ACS, Acute CCF, VTE, ARF

Q.How does a vessel stop bleeding after you transect it? Initially was ‘huh?’
don’t understand the question, but got led on to say the 3 factors he wanted,
vasoconstriction, platelets and clotting factors.

Q. Why AAA cannot stop ? again talk about above 3 factors, all cannot

Q .Management of ruptured AAA ? Assess and resuscitate patient

simultaneously – to stabilize patientABC protocol, 2 large-bore cannulae into
antecubital fossa veins – not central line Intravenous fluids judiciously – maintain
BP around 90–100 mmHg ,Intravenous analgesia, Urinary catheter – with a
urometer bag. Measure hourly urine outputs because this is the most sensitive
marker of tissue perfusion, Blood tests: FBC (full blood count), U Es (urea and
electrolytes), glucose, amylase, LFTs (liver function tests), clotting screen, Cross-
match 10 units of packed red blood cells 4 units of fresh frozen plasma (FFP),
Contact senior member of surgical team, If patient stable, CT to confirm
diagnosis, If any signs of being unstable, theatre, Contact anaesthetist and
theatre staff ahead. Book an intensive care bed Speak to the patient and
relatives .

23



DIC : 72 year old with a ruptured AAA has been taken to theatre . The patient
has lost 4L of blood and has a temperature of 34.8 °C. You organised for him
to have 3 units of blood in A&E and he is currently receiving a blood
transfusion in theatre. You are unsure as to how many units he has had in
total. Intra-operative blood results have just been sent: Hb 6.3g/dl, PLT 45 x
109, APTT 49s (2539), PT 18s (10-14), fibrinogen 0.8 g/L (1.5-4.0). The
patient is anaemic, thrombocytopenic, with a high APTT, PT and low fibrinogen.

young woman with hep c, had splenic injury, bloods show deranged coagulation
profile (all aptt, pt etc increased), severely hypotensive, high fever, etc –.asked
differentials,

Q. What does this blood picture suggest? DIC

Q. What is DIC? characterized by pathological activation of blood

coagulation, which results in generation and deposition of fibrin, leading to
microvascular thrombi in various organs. Subsequent consumption of
coagulation factors and platelets and activation of fibrinolysis secondary to
prolonged activation of coagulation can cause severe bleeding. I.e. It is a
pathological consumptive coagulopathy. Characterised by widespread
hemorrhage, Thrombocytopenia, decreased fibrinogen, increased FDPs

Q. Treatment of DIC ? FFP, platlets, cryoprecipitates

Q. Who to involve in care ? Hematology consultant
Q. Cause of DIC in this patient ? Severe hemorrhage, massive blood
transfusion, hypothermia
Q. What else is likely raised in the blood tests in this patient and why?
D-dimer. This is a breakdown product of fibrin and will be elevated due to
secondary activation of fibrinolysis.

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Q. What are other possible causes of DIC? Infectious – bacterial, viral or

fungal Malignancy – haematological, metastatic Trauma – burns, multiple
trauma, Transfusion – haemolytic reaction, Obstetric – placental abruption,
eclampsia Other – ventricular assist devices, shunts, liver failure

Q. Discussion on different types of blood products ? 1. Whole blood (rarely

used nowadays) as separated into its components .

2. Packed red cells (PRBC)– whole blood from which plasma has been removed
to Hc-70%. Shelf life – 42 days at 4 degree . Use in anemia without hypovolemia

3. RBCs suspended in SAG-M (sodium chloride, adenine, glucose and mannitol)

volume about 180-350ml, largely increases Hb by 1 g/dl, stored at 4 degrees
Celsius. ……….Has no coagulation factors, WBC die after ????

4. Platelets – given within 60 minutes used for low numbers or non- functioning
platelets. Shelf life 3 days( room temperature )

5. FFP – 200ml from 1 donor unit, stored at ( -30 ) degrees Celsius for 1 year(
shelf life ) , contains all coagulation factors but takes 30min to thaw out. Use in
major haemorrhage,liver disease, rapid reversal of warfarin

6. Cryoprecipitate- To create it FFP is centrifuged and the precipitate is collected. It is

often transfused as a four- to six-unit pool instead of as a single product. Unlike with
use of fresh frozen plasma, cross-matching (compatibility testing) is not strictly
necessary, but cryo is given as ABO compatible when possible. Factor 8 is important
constituent ( Antihemophilic factor) , also Van Willebrandt factor and Fibrinogen. ( use
in haemophilia .

Q. Stages of clotting? Vascular – vasoconstriction, Platlet phase – Platlets

clump together n adhere to injured blood vessel forming plug, Coagulation-
coagulation factors make clot , Clot Contraction phase, Fibdrinolysis – clots
break

25



Q . Patient has dyspnea and desaturation on POD 5 , What would you do

for patient ?

Q. What investigations to order ?1) D DIMER : FDP ( fibrinolytic pathway)

2.)Platelet below 15000, due to consumption with activation of clotting cascade.
3) Decreased Fibrinogen 4). Increased PT , APTT and 5) Reductions in
individual clotting factors.

Q . Explain picture? why does DIC happen? Triggering factors : 1) Infections

:gram – or anaerobic sepsis,or viral HIV,CMV, hepatitis 2) Trauma , 3) Burns ,
4)Hypothermia 5) malignancy 6) Massive transfusion 7) Obstetric causes –
amniotic fluid embolism,placental abruption 8) liver failure

Q. What does APTT test? Intrinsic/ Common System, all factors except 7

Q. What does PT test? Extrinsic / common pathway. Deficiencies of factor

1,2,5,7,10 will be detected.

Q. How is extrinsic/intrinsic pathway activated?

Q. What are platelets? Platelets have no cell nucleus: they are fragments of
cytoplasm that are derived from the megakaryocytes. . They gather at the site
and unless the interruption is physically too large, they plug the hole.

Q how do they work?. First, platelets attach to substances outside the

interrupted endothelium: adhesion. Second, they change shape, turn on
receptors and secrete chemical messengers: activation. Third, they connect to
each other through receptor bridges: aggregation.Formation of this platelet plug
(primary hemostasis) is associated with activation of the coagulation cascade
with resultant fibrin deposition and linking (secondary hemostasis). These
processes may overlap: the spectrum is from a predominantly platelet plug, or

26



"white clot" to a predominantly fibrin clot, or "red clot" or the more typical mixture.
The final result is the clot.

Q. Complications of hep C on liver? fibrosis, cirrhosis and malignancy.

Q. What are the risk factors in this patient ?hepatitis c, major trauma

Q. How would you manage ?. Treatment of DIC is centered around treating

the underlying condition. Transfusions of platelets or fresh frozen plasma can be
considered in cases of significant bleeding, or those with a planned invasive
procedure. The target goal of such transfusion depends on the clinical situation.
Cryoprecipitate can be considered in those with a low fibrinogen level.

Q. what is APTT , what does it mean what factors and what pathway
involved ? Deficiencies of factors VIII, IX, XI and XII and rarely von Willebrand
factor (if causing a low factor VIII level) may lead to a prolonged aPTT .
Intrinsic/Common pathway. Heparin treatment monitoring.( all factors except 7)

THYROID
Stem : Neck lump with lethargy and malaise / lady with low T4 , T3 , low Hb and
high TSH, high MCV , NOT compliant to medications.

Q.Interpret TFT, Whats ur Diagnosis?Hypothyroidism with anemia

Q. 6 features of hypothyroidism ? Weight gain, Memory loss,Cold

intolerannce, Constipation, Myxedema, Bradycardia ,Muscle weakness , anemia
,delayed reflexes.

Q.3 Causes of hypothyroidism ?primary :autoimmune ( hashimoto's-

microsomal autoantibodies),Iatrogenic ( thyroidectomy, irradiation),transient
thyroiditis ( Dequervian's thyroiditis) ,iodine deficiency, infiltrative ( amyldosis,

27



sarcoidosis), Drugs( lithium) ,Neoplasia, Secondary : Due to pituitary

(hypopituitarism ) or Hypothalamic disease(isolated TSH defciency)

Q. What are the TFTs if there is a pituitary cause of hypothyroidism?

Secondary hypothyroidism: both TSH and T-4 will be LOW !

Q. Patient with hypothyroidism not compliant to medication comes in for

Emergency surgery, what are the Risks? Risks of increased sensitivity to
medications, anaesthetic drugs, narcotics. Severe hypothyroidism is associated
with myocardial dysfunction,coagulation abnormality,electrolyte imbalance,
hypoglycaemia, rarely, myxedema coma after surgery

Q . How to improve compliance of medication ? Shared

decision making;Minimizing the discomfort of change; Motivational
interviewing;Behavior change counseling;Patient empowerment;Patient
support;Coping skills training. ONCE WEEKLY THROXINE TABLET !

Simplify regime, involve carer or family member, regular follow ups (Examiner
seemed to have wanted more)

Q . Blood tests show macrocytic anaemia, cause in this patient?

Associated autoimmune conditionn of pernicious anaemia causing Vit b 12

deficiency due to lack of intrinsic factor IF(antiparietal cell antibodies)
28



Q.patient with hypothyroidism not compliant to medications comes for an

emergency surgery, what are the risks ? myxedema coma, Delayed recovery
from anasthesia, Cardiac arrythmia, Involve endocrionolgist in care , anasthesia
consultant

Q. How to increase patient compliance with the treatment ? to make the

dose of replacement in the early morning, make the dose single not divided,
involve carer or a family member, regular follow up visits, emphasize that
relapse is inevitable if therapy is interrupted

Q .Lady with low T4 and High TSH , draw diagram to explain thyroxine
secretion, ie. Hypothalamus, pituitary, thyroid axis

Q.Difference between T3 and T4 ?

Q.How does T4 come about? Synthesis of T3 and T4:

1. Trapping: I- ions enters the thyroid follicular cell by active pumping .

2. Oxidation: Iodide is converted to I 2 by Thyroid peroxidase TPO.

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3. Iodination and Coupling : I 2 with tyrosine : MIT+ DIT= T3 ( triiodotyrosine),

DIT+DIT=T4 ( tetra)

4. Proteolysis of thyroglobulin 5. De iodination

Q. Where conversion of T3 to T4 take place ?. T4 is converted into the more

active T3 by the deiodinase system (D1, D2, D3) in multiple tissues and organs,
but especially in the liver, gut, skeletal muscle, brain and the thyroid gland itself.

Q. FBC : leucocytopenia and anemic. Macrocytic anemia, Likely cause?

pernicious anemia due to lack of intrinsic factor IF leading to vitamin B 12,
because of Antiparietal cell antibodies. Microcytic anemia is usually ascribed to
malabsorption of iron and loss of iron by menorrhagia. Macrocytic anemia is
caused by malabsorption of vitamin B12, folic acid, pernicious anemia and
inadequate nutrition.

Q.Likely cause of hypothyroidism ? autoimmune

Q .Lady low T4 and High TSH, draw diagram to explain?Axis HPA?

thyroxine secretion, ie. Hypothalamus, pituitary, thyroid

Q. Markers to do ? autoantibodies against IF and H/K ATPase.

Q. Symptoms if patient is supressed

Q. What would you expect in a patient with secondary hyperthyroidism?

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Q. What are the ddx of a patient with a goitre? Colloid nodule, Thyroid
adenoma, Nontoxic MNG, Toxic adenoma, Carcinoma, Thyroiditis.
Q..What to do for surgical patient with hypothyroidism? Which other
specialties to involve?

Sub clinical (Normal T4, high TSH) : proceed Sx

Mild-Moderate: postpone till euthyroid (elective), Thyroid hormone Replacement

therapy T4: 1.6 microgram/kg/50 mcg daily ( urgent)

Severe/Myxedema Coma : postpone (elective), call endocrinologist / T4 200

mcg load / 50 mcg daily and T3 2.5-10 mcg Q8 and Stress dose steroids
(urgent)

TFT, ECG and other baseline blood investigations after evaluating clinical
features of hypothyroidism,then I would report to consultants surgeon
regardingly. If it is subclinical (normal T4, high TSH) then I would like to proceed
for surgery after permission of consultant ,if it's mild to moderate then likely
postpone until euthyroid involve Endocrinologist,Cardiologist,Anaesthetist and
consultant surgeon.

NUTRITION
Stem : Lady with Crohns disease, had ileocecal resection , POD4 anastomotic
leak, so had defunctioning ileostomy . Plain Abdomen XRAY( preop) show:
Intestinal Obstruction

Q. What is ur Diagnosis?

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Q. What does AXR show? Coin appearance/ small bowel dilatation /obstruction

Q. Causes in this patient ? stricture due to crohn’ s disease

Q. Methods of feeding ?Enteral (Oral, NG, NJ,gastrost, PEG, PEJ)vs Parental

(TPN,PPN)

Q.. Routes of TPN administration ? (PICC, Central line)

Q. Besides glucose next highest energy source of TPN ? Fat

Q. What is Refeeding syndrome and cause behind it ?

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Q. What are types of non parenteral feeding options?

Q. Constituents of TPN ? Water,carbohydrates,proteins,lipids,vitamins and

trace elements n drugs( ranitidine n insulin). It's a mixture of hypertonic sugars
with fat emulsions,nitrogen, Vitamins n trace elements ( >50% carbohydrates , 30
-40% fat 1-2gm/kg body wt , Water 30-40ml/ kg/ day, Electrolytes
Na,K,Mg,Ca,Cl,P, vitamins A,D,E,K,B,C )

Q. Main source of carbohydrate in TPN? glucose

Q How do you give parenteral feeding? Peripheral/ central , Parenteral

nutrition is administered through a needle or catheter. This is placed in a large
vein that goes to the heart. It is usually used for 10 to 12 hours a day, five to
seven times a week. Most intravenous feedings are completed at home.

Monitoring: glucose – more than once daily,Urea,electrolytes,creatinine – once

daily, Albumin,ca,mg,p,LFT – twice weekly

Q. Indications for TPN) ? Anorexia : General critical illness, Severe

malnutrtion( > 10 % weight loss) ,Multiple trauma, Sepsis with MOF, Severe
burns, head injury, coma, Neurological disorders. Gut proplems:- ECF
(absolute indication ), Short bowel, IBD ,radiation enteritis, paralytic ileus,
TEF,Pancreatitis, intestinal atresia, obstruction ( tumours, stricture),
Hypercatabolic states

Q .What is enteral nutrition? Enteral nutrition generally refers to any method of

feeding that uses the gastrointestinal (GI) tract to deliver part or all of a person's
caloric requirements. It can include a normal oral diet, the use of liquid
supplements or delivery of part or all of the daily requirements by use of a tube .

Q. Assessment of nutrition status ? History,exam,anthropometric n

dyanamometric measure, biochemical ( albumin, LFT ), immune function

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Q. Signs of malnutrition ? low albumin n antibodies,poor wound healing

,acidosis,hyperkalemia,decreased cough reflex( pneumonia)

Q. Daily nitrogen req. ? 0.15 g/ kg ( healthy) , 0.3 g/kg (critically il)

Q. Enteral nutrition : Indications? Severe catabolic state like burns,

malnutrition presurgery, postop esophogastric surgery, unconscious patient(
head injury) , swallowing disorder( MND, post CVA) , upper GI
obstruction(esopheal stricture) , partial intestinal failure(ileus) Pscychological (
anorexia nervous a, depression)

Q. Advantages of enteral over TPN ? Safer, cheaper, fewer complications,

prevents atrophy of gut mucosa , prevents immunological barriers across gut
mucos(Ig A n intact endothelium )

Q. What is parenteral nutrition?. Delivery of nutrition via intravenous route

bypassing GI tract, to meet metabolic requirements of body in certain conditions
like catabolic state and nonfunctional GI tract

Q. Type of electrolytes in TPN? Na, K, Mg, Ca,P,Cl

Q. What is dextrose? Dextrose is a simple sugar ,made from corn and is

chemically identical to glucose, or blood sugar, used in baking products as a
sweetener,processed foods and corn syrup.

Q. What are sugars?sweet, short-chain, soluble carbohydrates, many of which

are used in food ,composed of C,H,O. Simple sugars are called
monosaccharides and include glucose (also known as dextrose), fructose, and
galactose, used as food is sucrose, a disaccharide. (In the body, sucrose
hydrolyses into fructose and glucose.) Other disaccharides include maltose and
lactose. Longer chains of sugars are called oligosaccharides.

34



Q. Complications of TPN? Mechanical: Blockage, Fracture, Migration,

Displacement, Pueumothorax, Central vein thrombosis, Air embolism,
Subclavian vessel injury , Cardiac arythmia , Peumothorax, Hydrothorax,
Hemothorax. Infections: Line sepsis , Exit skin site infection, IE, Metabolic –
glucose <>, high(TG,HCL) , hypercholermic acidosis, low (EFA,K,Mg,P),
deranged LFT, Ventilatory problems(high CO 2 due to glucose > 5 mg/ kg)

Q. Bowel mucosal atrophy, why/ how ? Absence of enteral feeding leads

to strophic changes in intestinal mucosa,bcoz local hormone release in
response of food stimulates release of enzymes responsible for integrity of
intestinal mucosa.

Q. What are complications? 1. Loss of cellular adhesions and development of

cellular channels . 2. Translocation of Bacteria across the bowelwall into
circulation is encouraged , which may lead to Sepsis and chances of SIRS.

Q. How to calculate? 1.Normal – 30 kcal/ kg ~ 2000 kcal (70kg)

2. Burns -basal requirement +replacement = 25-30 kcal/kg + 70kcal/kg/% burn (

up to 60 kcals/ kg

3. post surgery – 35 kcals/ kg ,increases by further 10% per degree increase in

temperature. 4. Sepsis – 40-45 kcal/kg

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Q. Methods of parenteral and enteral ? Enteral – Oral , NG, NJ, PEG, PEJ,
Surgical jejunostomy. , Parental – PPN,TPN

Q.What increases requirements? sepsis, post surgery,

Q. Complications of an ENTERAL feed ? Intubation – Fistulation, Wound

infection, Peritonitis, Displacement/catheter migration , Obstruction/blockage of
tube. Delivery of nutrient to GI tract – Aspiration, Pneumonia , Diarrhea,
Feed intolerance, colonisation of bacteria, overfeeding, refeeding syndrome.
Refeeding syndrome : within 4 days, fluid and electrolyte disorders, especially
hypophosphatemia, along with neurologic, pulmonary, cardiac, neuromuscular,
and hematologic complications ,. ----> hypophoshatemia, hypomagnesemia,
hypovalcemia, Irritation of gut lining n ulceration , nausea n vomiting , deranged
LFT

Q. How is TPN administered and why through a central line ?In a central
line because of high osmolarity ( must be < 900 mosm/L), Thickness of the fluid
and also causes phlebitis due to the high osmolarity .High osmolality of mixture
cause irritation to small vessels,hence central tunnelled subclavian vein is better.

Q. What happens to the gut after prolonged TPN ? Mucosal atrophy

Q .What is the implication of this? Translocation of bacteria to the blood

stream causing sepsis

Q. Disadvantages of using glucose as the main energy source?

1. Glucose intolerance : stress response, critically unwell patients are often

instate of hyperglycaemia and glucose intolerance. Therefore, if glucose is the
only source of energy, patients will not receive their required daily amount due to
poor utilisation of their energy source . 2. Fatty liver : the excess glucose
occurring as a consequence of the above is converted to lipid in the liver,

36



leading to fatty change, derange LFT . 3. Respiratory failure : the Extra CO 2

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 EFA. 50% of the total energy requirement must be by fat.

BURN N ARDS
Q. Calculate the surface area of the burn Wallace rule of nine's ?

Q. Management ? ATLS system of Trauma Care : ABCDE , Airway : look for

signs of airway burns and inhalational injury( facial burns, singed hair, cough,
sooty sputum ) as it may cause airway edema, Intubation of there airway edema
required. High flow O2.

Breathing and Ventilation as tracheal pulmonary burns can impair effective

gas exchange , also full thickness chest burns can impeded chest expansion

Circulation : 2 large bore cannulae and fluid resuscitation by crystalloids using

PARKLAND FORMULA > 15% TBSA( adult), child > 10%

37



Volume of crystalloids (ml) = 4 X % TBSA X patient weight-------------> divided

into 2 halfs : 1/2 in the first 8 hour, 1/2 in the subsequent 16 hour.

Deeper and more extensive burns may require a blood transfusion.

Mount Vernon formula : divides fluid administration into a number of discrete

time periods. The amount of f luid given in each period is the product of the
weight and the % burn divided by two. The first 24 h is divided into periods of
4,4,4,6,6 and 12h. Crystalloid or colloid may be used. None has a proven survival
benefit over the other. Consider C.V line and urinary catheter.

Renal support involves the maintenance of the renal perfusion pressure with i.v. f
luids. Given the added risk rhabdomyolysis, a urinary catheter should be
inserted, the urine output maintained 1 ml/kg/h, Analgesia: using i.v. opioids or
inhaled 70% nitrous oxide, Prevention of hypothermia with convection heaters
and a warm ambient temperature. This also helps to control the hypermetabolic
state, Stress ulcer prophylaxis is commenced, Prophylactic antibiotic use is
controversial, and should be used for proven sepsis. Surgery has a role in the
emergency management of constricting circumferential thoracic eschars that can
cause respiratory embarrassment. Nutritional supplementation (preferably by the
enteral route) should be commenced at an early stage.

Q.How to assess the adequacy of fluid therapy? Clinical measures CI

includes peripheral warmth,(CRT) , (UO) , ( CVP) and its response to fluid
challenge, Core Tmperature(rectal ) , Haematocrit (Hct), which determines the
plasma volume and the red cell mass.

Q. What do u fear of ? Complications of Burn ? Burns shock’: hypovolaemic

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

38



circumferential burns( ischemia in limbs / ventilators problems in chest- require

eschatotomy. Electrolyte disturbances: Hypo or hypernatraemia, hyperkalaemia,
hypocalcaemia, Coagulopathy due to disseminated intravascular
coagulation and hypothermia Haemolysis leading to haemoglobinuria and
anaemia
Q. Whole body burns ,tell if he has superficial or deep burn, why?
Determine thickness : Partial (red/white, blistering,sensate) versus full thickness
(white,leathery,desensate)

Burns are assessed by their extent on the body and their depth of skin
penetration.
Extent: described in terms of the percentage (%) BSA covered. As a rule of
thumb, the area covered by the patients’ palm is equivalent to 1%. Also by the
‘rule of nines’: anterior and posterior trunk 18%, head and arms 9%, legs
18% and genitalia 1%
Depth: may be superficial, partial or full-thickness: the clinical determinants of
the depth are : Presence of erythema: seen in superficial burns, Blisters,
Texture: leathery skin seen with full thickness burns, Sensation: burns are painful
in areas where there is no full thickness penetration
Q. Where do you want to manage this patient?burn unit

Q. Charcterised by / define/ what is ARDS ? 1.Severe acute lung injury 2.

Progressive and Refractive Hypoxemia 3. Diffuse bilateral pulmonary infiltrates(
CXR) 4. Non- cardiac causes( Normal PAWP) < 18 mmHg 5. Reduced Lung
compliance 6. V/Q mismatch

Q. Causes ? Direct( pulmonary) – inhalation injury, aspiration pneumonitis,

Near-drowning , chest trauma ,pneumonia, Indirect(Systemic) – sepsis, shock ,
burns ,polytrauma, head injury, acute pancreatitis, blood transfusion ( massive) ,
polytrauma, CABG, DIC( embolus)
39



Q. Management ? ABCDE , history, physical exam. Investigate Cause( initial

predesposing insult) , Oxygen therapy, early discuss with Anaesthetist and chest
physiotherapist for ventilators support. Keep lungs dry, fluids restriction, treat
complications early. Intubation ( high FiO2), Mechanical Ventilation : Low TV (
permissive hypercapnia ) , Moderate PEEP , Inverse I/E ratio ventilation, Prone
positioning,Physiotherapy, High frequency oscillation : low positive pressure with
high respiratory rates. , ECMO for profound refractory hypoxaemia, Steroids
.Haemodynamic management– use Inotropes to support , Inhaled nitric
oxide/prostacyclin – pulmonary vasodilation, reducing pulmonary hypertension
and improving gaseous exchange, Nutrition: Enteral nutrition after 48–72 hours
of ventilation

Q.. What is Berlin criteria?

Q. What labs to send?

Q. ITU CXR is taken, tell me the findings bilateral infiltrates on CXR. causes,
pulmonary oedema Vs. ARDS.

Q. Why this patient can have pulmonary oedema, why ARDS.Berlin Criteria
for ARDS. management of ARDS, what Abx?

Q .Define ARDS (Wanted pathological definition,not the pulmonary wedge

capillary pressure crap).

Q. Where will you admit if she has ARDS? ICU

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Q. What are the long term sequelae of ARDS?

1. Pulmonary function- mild impairment ( improved over 1 year)

2. Neurocognitive dysfunction 3. PTSD 4. Physical debiliation

Q. Pathophysiology : ARDS ?

Pathophysiology of ARDS: An acute phase, characterised by widespread

destruction of the capillary endothelium, extravasation of protein-rich fluid and
interstitial oedema with release of cytokines and migration of neutrophils; the
alveolar BM is also damaged, and fluid seeps into the airspaces, stiffening the
lungs and causing V/Q mismatch.
A later reparative phase, characterised by fibroproliferation, and organisation of

41



lung tissue. If resolution does not occur, disordered collagen deposition occurs
leading to extensive lung scarring.

Q.What happens to lung compliance? Decrease

Pulmonary edema ( fluid overload)

Stem: post-operative/ Fluid chart+vitals chart= taken crystalloids plus colloids
about 7 litres(4 litres NS ) , now he is tachycadiac, hypertensive,
desaturated, oliguria , B/L pulmonary infiltration, frusemide in liaison with
medicine ) interpret the vitals and input/ output chart.

Q. Read/ interpret the anaesthetic records, what can you tell about the
patient when he was discharged from anaesthesia recover? still
hypertensive and tachycardic

Q. Physical findings? Congested neck veins, Puffiness of face , Lung

Crepitations, Confusion

Q. Interpret this CXR? pulmonary edema ++, loss of cardiophrenic angle,

cardiomegaly.
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Q. Comment on the fluid status ? received 4 unit NaCl and 2 unit colloid in 12
hrs with poor urine output, likely fluid overload, too much electrolytes (sodium)
given as well (all crystalloids were normal saline)

Q. Resuscitation ?. What solution you would give ?.If used saline would
you use the same formula?? Said yes( seems accepted)

Q. How to manage Fluid overload ? Propped up, Lasix, Morphine, Oxygen,

Nitroprusside, Aminophyline, Rotating Tourniquet, Inotropic agents.

Management: ABC, Stop IV fluids, HighFlow Oxygen , I.v Frusemide, GTN

infusion(systolic B.P > 100) , Liaise with ITU registrar, Request CXR, ABG,
elctrolytes, ECG

Ventilatory support: consider non-invasive ventilation in severe APO (CPAP

preferred for cardiogenic pulmonary oedema) Medical management:
1.Preload reduction – nitrates e.g. GTN (caution in hypotension), diuretic, IV
morphine sulphate
2.After load reduction – ACE inhibitor e.g. enalapril 1.25mg IV or captopril 25mg
sublingual; ARB
3. Ionotropic support – Dobutamine ideal for cardiogenic shock; Dopamine (5-
10mcg/kg/min for stimulation of β-receptors)
Q. CXR findings in pulmonary edema ? A: alveolar edema ( bat wing or
butterfly), B: kerley B lines, C: cardiomegaly, D: dilated prominent upper lobe
vessels

Q. Why this patient is on high risk of MI ? Tachycardia decreases diastole

time which decrease coronary filling , also it increaes cardiac load.
Q. What is the minimal UOP? 0.5 ml/kg/h
Q. Why the patient is oliguric? 1. physiological stress (m/c) response to
surgery in the first 24–36 hours post-operatively, due to circulating

43



glucocorticoids and mineralocorticoids inducing salt and water retention.

2.Surgical trauma and various anaesthetic gases also stimulate the release of
vasopressin from the posterior pituitary, stimulating post-operative solute-free
water retention. 3. CHF with low renal perfusion.

Low urine output in fluid overload:

- Low CO -----decreased renal perfusion-----decreased urine output .
- During fluid overload, the LVEDV is high, this causes the interdigitation of actin
and myosin in cardiac muscles to no longer overlap , further worsening of the
fluid status decreases SV and hence CO.
- ↓ in the renal perfusion is detected by the juxtaglomerular apparatus, this
activates the RAAS, hence increasing fluid conservation
- ATN 2° ischaemia
- Post-op fluid conservation:Increased secretion of cortisol and aldosterone (both
mineralocorticoid activity), ADH secretion from posterior pituitary
Q. Explain what are the fluids given to this patient ? Crystalloids and
collids, Amount of Na in 0.9 % saline: 150 mmol/L, Na in Hartman's solution:
131 mmol/L

Q. Daily requirements ? Na: 1-2 mEq/kg , K : 0.5 - 1 mEq/kg

Q. Where to manage ? HDU

Q. What can be done to prevent this from happening again? Insert CVP
LINE ( monitor), U. Cath ( monitor urine output) , report to hospital incident
reporting system, quality control, inform people, better education, closer
monitoring in the immediate postop period, root cause analysis.

Q. management of cardiac failure.? Drugs u can use.

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Fluid management (post operative)

Stem: 48 year lady presented by persistent hypotension and tachycardia post
operative THR, transferred to the ward 3pm, hypotensive and tachycardiac,
worsening hypotension..70/30 at 2am. Fluid chart: 2X250 ml bolus with small
improvement initially

Q. Explain the fluid chart ? Persistent hypotension and tachycardia with 2 fluid
challenges and nothing in between !
Q. Is that adequate ? No

Q. How would you manage this case? In view of response to previous fluid
challenges, i will do more fluid challenges and monitor the response

Q. Formula of fluid challenge ? 500 ml crystalloids over 10-30 min. And

monitor the fluid responsiveness.

Q. The patient is on 2 hours monitoring , is that adequate? No, he should be

monitored hourly

Q. Whom to notify ,when? consultant , when no response to multiple fluid

challenges

Q. How blood pressure is calculated? product of (CO) and (SVR). The CO is

the product of the (HR) and (SV)
Q. How to incraese BP ? Inotropic support and fluids to increase CO,
vasopressor agents to increase SVR

Q.What are the 2 most likely causes of hypotension in this lady ?

Dehydration/Bleeding (stem said no bleeding, sighs)

Q. How is BP, CO, TPR related ? BP = CO x TPR

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Q. Options to monitor fluid balance status ? History( thirsty), PE( mucus Text

membrane, skin turgor, GCS, HR, BP, JVP, U.O. ) pulse oximetry, Bloods : RFT,
Hc.,Urine SG, ECG, CXR, Fluids chart( I/O)

Q. Conditions require increased maintenance fluids ? Pyrexia, ileus,

vomiting,stoma, fistula, pancreatitis

Q. Factors determine how much fluids? Preexisting fluid deficit, maintenance

fluids, ongoing losses.

Q. Fluids good for maintenance? NS with K, Hartmann

Q. What is the basal water requirement for an adult? 30–40 ml/kg/day.

Q. Composition of Hartmann’s solution , compare NS (0.9%)

Hartmann’s solution is composed of Sodium: 131 mmol/l,Potassium: 5 mmol/l
Chloride: 111 mmol/l, Bicarbonate: 29 mmol/l (provided as lactate, which is
metabolised to bicarbonate), It has an osmolality
Text of 280 mOsm/l
NS contains only sodium and chloride at a concentration of 150mmol/l. It is also
iso-osmolar with plasma with an osmolality of 300 mOsm/l (i.e. 150 150).

Q. What is the purpose of fluid therapy? To satisfy part or the entire basal
requirement of water and electrolytes, To replace f luid and electrolytes lost
beyond the basal requirements,To support the arterial pressure in cases of shock
by increasing the plasma volume and improving tissue perfusion. If given as
blood, to increase the oxygen carrying capacity of the blood

RESPIRATORY ACIDOSIS/MORPHINE TOXICITY

Q. Interpret the ABGs ? respiratory acidosis.

Q. Why is the bicarb normal ? In acute respiratory acidosis, compensation occurs

in 2 steps.
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Q. Why is the 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.

Q. Why does morphine cause this ? Depresses CNS

Q. How would you treat this patient ? naloxone

Q. How do kidneys regulate acid base balance? Under normal conditions,

the kidney's main role in acid-base balance is through the excretion
of acid in the form of hydrogen (H+) ions. The kidneys secrete excess
hydrogen ions primarily in the proximal tubule and reabsortion of bicarbonate.

Q. Types of resp 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)

Q. Describe how CO2 retention causes respiratory failure?

Q. Write Co2 bicarb equation along with its enzyme? H2O + CO2------CA----
>> H2CO3---(in RBC)----> H+ and HCO3- (H binds to Hb, HCO3 diffuses out
in plasma )

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Q. Where does it happen / where CA found ? RBC

Q. How CO2 is transported in the blood? carbaminogroup (20%): between the

co2 and proteins or peptides most of which with the globin portion of Hb,
dissolved co2 ( 10%) , bicarbonate ( 70% ) :

Q. Chloride shift ?chloride diffuses into RBC to maintain the balance, as HCO3
moves out of cell and Cl. moves into RBC to store electric neutrality ( RBC
membrane has HCO3-Cl carrier which passively facilitates diffusion. )

Q. How body sense hypercarbia ? chemoreceptors central, close to

respiratory centre in medulla

Q.Response mechanisms to hypercarbia ?elevation in CO 2 leads to central

acidosis,which stimulates central chemoreceptors and leads to increased
respiratory rate in order to blow off extra CO2.

Q. Why Pa02 normal range and why no metabolic compensation ?

Pa02 in ‘normal range’ because FI02 is 60% so Pa02 reference range needs to
be adjusted accordingly .No metabolic compensation because acute. Kidney
takes time to react. (3-4 days)

Q. I’d What is causing the respiratory acidosis?

Q. Why still no metabolic compansation? Kidney takes time to react

Q. What type of respiratory failure is that?Type 2 ( hypercapnia)

Q.how does morphine work ? Receptors? by binding to mu receptors in

respiratory centre causing respiratory depression.

Q. Where are the receptors? How do the center and receptors detect the
changes in the blood? Mu

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Q. Dose of naloxone? 0.4-2 mg i.v. Initially and repeat every 2-3 minutes, up
to maximum 10 mg

Q. What do I need to look out for ? Side effects: nausea, vomiting,sweating,

tachycardia, abdominal cramps, pulmonary Edema, cardiac arrest.

Q. Where will I monitor this patient? Management: (ITU), ABC,oxygenation by

humidified o2 , Ensure adequte ventilation either non- invasive or invasive
(Intubation and invasive respiratory support or CPAP) , Management of the
underlying cause, Morphine antagonist: ( NALOXONE) Dose : 0.4 -2 mg i.v
intially and repeat every 2-3 min. If no response to a maximum dose of 10 mg.

HEAD INJURY/EDH

Stem : RTA--> GCS 15---> 2 episodes Vomiting-----> amnesic events--> GCS 8.

CT : Biconvex shape, hyperdense ,Midline shift, Compression on the ventricles.

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Q. Normal value of ICP ? ( 7-15 ) mm.Hg ( supine) and (-10 in standing)

Q. Ways to measure ICP ? Invasive : External ventricular drain(EVD),ICP
tranducer, Subdural catheter, Non- invasive: Transcranial doppler can measure
MCA velocity and derive a pulsatility index correlating with ICP.
Q. Danger of LP in increased ICP? Herniation and conning

Q. Cushing triad ? Hypertension, bradycardia, dyspnea.

Q. What is the Cushing reflex? mixed vagal and sympathetic stimulation in

response to an elevated ICP. It leads to HT, which ensures an adequate CPP.
There is also a resultant bradycardia.

Q. Pathophysiology of increased ICP ? Monoro - Kellie hypothesis ? skull is

fixed box containing 3 components : Brain (80%), blood (10%), CSF ( 10% ),
ICP/ volume relationship is governed by these 3 components, Increase in volume
in one component may result in compansatory 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 .
Q. Lucid interval ? 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 increaes in ICP leading to cerebral edema.

CPP= MAP – ICP / MAP auto-regulation range : 50 - 150 mm.Hg to maintain a

constant CBF. In cases of traumatic brain injury , this will be disruption of MAP
autoregulation----> cerebral ischemia

Q. C/p of increased ICP ? headache ,Nausea, vomiting, Papiledema, Fall in

GCS , Pressure symptoms( hematoma), Ischemia( loss of autoregulation of

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MAP), dilated pupil ( occulomotor nerve palsy), Defect in lateral gaze ( abducent
nerve palsy) ,Cushing's triad : increased systolic BP, a widened PP, bradycardia
, irregular respiratory pattern.

Q. Managemnent ? ABC, Positioning : tilting the end of the bed 20–30° (head
up) and loosening of tracheal tapes and Neck collars to aid cerebral venous
drainage , Fluid restriction : to prevent cerebral oedema, e.g. a life-threatening
complication of managing (DKA), Diuretics : e.g. mannitol, which is an osmotic
diuretic given at a dose of 0.25–1.00 g/kg over 20–30 minutes. It rapidly
decreases ICP and is useful before hospital transfers , Controlled ventilation :
keeping the PaCO 2 (4.0- 4.5) kPa enables CO 2 to control the degree of
intracranial vasodilatation, Drainage : this can be done by direct tapping of CSF
from a ventricular catheter , Barbiturates : e.g. thiopentone, Surgery : a
decompressive craniectomy can be performed for malignant increases in ICP
refractory to optimal medical therapy.

Q.Asked why patient should have had a CT earlier ? Canadian CT rules,

patient had a few criteria

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Q. Why would the brain herniate ? Monroe kellie doctrine etc

Q. Cause of dilated pupils in raised ICP ? Herniation causing compression of

CN3 which carries the parasympathetic fibres, causing unopposed sympathetics
to the pupil and resultant dilatation.

Q. How to manage this patient if he was intubated to decrease risk of brain

injury ? Sedate patient to prevent straining, hyperventilate to maintain
normocarbia, hypothermia, position patient 30 degrees head up, judicious fluids
with monitoring, mannitol

Q.Why did the patient lose consciousness at first?

Q.Patient becomes hypertensive, bradycardic, irregular breathing, why and

what is that?

Q. What to do with raised ICP?

Q. Layers passed through when doing a burrhole over the pterion ? Skin,
subcutaneous tissue, temporal fascia, temporalis muscle, squamous part of
temporal bone , periosteum, outer n inner table, DAP layers, middle meningeal
artery.

Q. When I would consider intubating this patient (in addition to low GCS,
airway, pCO2 control, also wanted to hear “if I need to transport the patient to
another hospital”)

Q. Benefits of intubation ? after I said decrease pCO2, he prompted me “and

the other gas...?” Wanted to hear oxygenation to prevent HIE

CT brain of 80 yo woman who fell down (SDH). In A&;E eyes open to pain,
makes incomprehensible sounds, and withdraws to painful stimulus.

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Q. What does it show? Lense / crescent shape hyperdense lesion. Right SDH.

Q.What does loss of grey-white matter suggest? Many studies have shown
that injury to gray matter, areas of the brain that contains nerve cell bodies, can cause long-lasting
cognitive disability.

Q. What is “GCS”, and what is her GCS? GCS) 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. EVM :4/5/…. Her GCS : 2+2+4= 8

Q . Who will you involve in her care?

Q.Management: Acute SDH Urgent surgical evacuation of hematoma for 1.

acute SDH , +/- coma, with neurologic deterioration (signs of increased

intracranial pressure) since time of injury &potential for recovery 2. for clot
thickness n 10mm or midline shift &;gt;5mm on initial brain CT ,Nonsurgical
managed patients should be nursed in ICU with ICP monitoring & serial head CT

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scans. Next scan at 6-8 hrs. If with signs of neurologic deterioration or

persistently increased ICP >;20mmHg, urgent surgical evacuation within 2-
4hrsdeterioration

Q. Why would you choose to intubate ? if patient cannot maintain or protect

own airway (GCS 8 or less/ cannot swallow own secretions) , failure to
oxygenate (agitated, restless, spO2) or failure to ventilate (retaining Co2) ,
elderly with pneumonia in sepsis or burns with inhalational injury , Seizures,
Severe facial injuries( lefort, mandible fracture) , Ventilation insufficient ( pao2 <
80, paco2 > 50 ) , risk of hypoxia, aspirations.

Q. Trachy tube advantage ? Easier oral toilet, Less likely to aspirate, Less dead
space, Better tolerated long term ( not gagging /don’t need sedation), Easier to
wean n decannulate, Noninvasive positive pressure ventilation only for patients
who can protect their own airway /can swallow .

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

Assesment: speaking to the patient if can speak ----> secure airway,

Can not speak : (Look): in the mouth for FB or in the face for maxillofacial injuries
( listen) : abnormal breath sounds, stridor ,hoarsness, ( feel) : breath on your
cheek. Management: Chin lift / Jaw thrust, Remove any FB in the mouth, Oro-
naso pharyngeal airway,Cricothyrodotomy, Trachestomy,Endotracheal
entubation, Immobilise the cervical spine by hard collar ,sandbag , tape
2. Breathing:

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Inspection: Obvious chest injuries, Open wounds, flail segment, Count R.R,
symmetrical chest wall movement
Palpation: Trachea, Surgical emphysema

Percussion and auscultation : Hemo/ pneumothorax

Management: high flow o2 via non rebreath mask, needle thoractomy or chest
tube, Occlusive dressing for open pneumothorax
Q. Comment on this CXR ? Pneumothorax + rib fracture + surgical emphysema

Q. How will you manage this ? Urgent needle thoracostomy in the 2nd ICS
mid-clavicular line then chest tube insertion
Q. Now, patient is shocked , how will you manage the circulation?
Assesment: pulse rate and character- Blood pressure

Q. Class of hemrrhagic shock ? 4 classes :

Blood loss: ( ml) 750/ 750-1500/ 1500-2000/ > 2000

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Blood loss: % 15/ 15-30 /30-40 />40

Pulse: <100 /100-120/ 120-140/ >140

R.R: 12-20/ 20-30 /30-40/ >40

UOP: (ml/h) >30 /20-30 /5-15 /Anuric

Mental status : Slightly anxious/ Anxious /Confused/ Lethargic

Q. 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 i.v fluid resuscitation with 2litres of crysytalloid
- Consider blood transfusion if no response to fluids
Q. How will you monitor the response? Heart rate, Blood pressure, Capillary
refill time, Urine output, Mental status

Q. Comment on this CT ? There is a liver tear/ laceration

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Q. Management of liver tear ? Conservative : blood transfusion , monitoring of

the hemodynamic status , Surgical: damage control : perihepatic packing, repair,
resection. Blood GS, CXM

Q. Is CT was a good investigation of this patient? No , patient is

hemodynamically unstable , FAST was the investigation of choice

PULMONARY EMBOLISM
Stem : Chest pain and dyspnoea patient on the ward after a TKR,POD 1, walked
to toilet and developed sudden severe sharp left chest pain with dyspnoea

Q. DIFFERENTIALS ? Anxiety, Pleurisy, costochondritis, Pneumonia,

Bronchitis, MI, Pericarditis,CHF, Pulm. HT

Q. Investigations ? FBC/RP/CMP/trop I/D-dimer not useful as just post-op,

CXR, ECG, CT PA , Ventilation/ Perfusion scan,spiral CT, ABG ( V/Q mismatch :
hypoxia, hypocarbia.

Q. Management ?.This involves initial resuscitation, followed by medical or

surgical intervention. During CPR , a precordial thump may help to dislodge an
obstructing mass. Thrombolysis: with thrombolytic agents may be used in those
who are haemodynamically unstable following a large embolus, e.g.
streptokinase and urokinase can be infused directly into the pulmonary artery.
Following this, anticoagulation with heparin and warfarin is required. Pulmonary
embolectomy: this can be performed either as an open technique, or using a
catheter. These methods are also reserved for the haemodynamically unstable

Q. Asked whether I will give heparin/clexane? clexane – dose: 1.5mg/kg daily

or 1mg/kg BD

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Q. Ruptured divericulum with pelvic abscess and septcemia, mgmt? ABG,

investigations to do, open vs percutaneous drainage adv and disadv.

Q. Risk factors : DVT?Increased age, Venous stasis from

immobilisation:Prolonged bed rest, Recent surgery, Cardiac failure.
Polycythemia: causing increased blood viscosity
General medical illness: Malignancy, Dehydration, including the nephrotic
syndrome. General sepsis, Vessel injury: multiple/lower limb injury,
Haematological propensity: Protein C/protein S deficiency, Antithrombin III
deficiency, Factor V Leyden, Antiphospholipid antibodies, HRT, OCP

Q. How can pulmonary thromboembolism be prevented? Peri-operative use

of heparin: may be given subcutaneously or as an infusion, Thromboembolic
(TED) stockings, Intermittent pneumatic compression intra-operatively, Early
ambulation of patients, Transvenous intracaval device: such as umbrella and
wire f ilters, which inserted under local anaesthesia to prevent recurrent emboli.

Q. Pathophysiology of PE? There is pulmonary artery obstruction as the

embolus impacts in a vascular branch beyond the right ventricular outflow tract.
There is also the release of vasoacive mediators from activated platelets within
the thrombus. Both of these factors conspire to increase the pulmonary vascular
resistance and right ventricular afterload. This produces ventricular strain,
manifesting as tachycardia.
Reduced flow to lung units causes a V/Q mismatch and increased physiological
dead space. This may occur with a bronchospasm induced by circulating
mediators. Consequently, there is hypoxia, hypocarbia with tachypnoea.

Anastomoses leak

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Stem : Middle aged male, had low anterior resection 5 days back. Now having
persistent fever, tachycardia and difficulty breathing.

Q. What are possibilities ?

Q.Shows ABGs having picture of metabolic acidosis. Asks about

interpretation

Q.. Shows serum report having raised creatinine and potassium, asks
about causes?

Q .Show complete blood count. Asks what is SIRS. Which of SIRS factors
are positive in this patient. (All four were positive)

Q.How to manage hyperkalemia in this patient ? Cardiac monitor, calcium

gluconate/ calcium chloride (10%) I.v. , insulin with dextrose 5%, Ion exchange
resin therapy, Bicarbonate to correct metabolic acidosis, Hemodialyis (If K is very
high)

Q. Organism causing infection ? staph. Epidermidis

Q. How to prevent line infection ? Perform hand hygiene, use skin antiseptic,
Ensure that the skin prep agent has completely dried before inserting the central
line, Use all five maximal sterile barrier precautions: Sterile gloves,Sterile
gown,Cap,Mask,Large sterile drape.Once the central line is in place:Follow
recommended central line maintenance practices
Wash my hands with soap and water or an alcohol-based handrub before and
after touching the line Remove a central line as soon as it is no longer needed.
The sooner a catheter is removed, less infection

CALCIUM HOMEOSTASIS
Stem: Post thyroidectomy hypocalcemia.Calcium 1.8. POD-4 ( 0.7 )

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Normal – 2.5 mmol/L, 99%(bone-hydroxyapatite), only 1 % is FREE (0.9% is

intracellular and 0.1% is extracellular. Of this 1%, 40% is bound to albumin and
60% is free. Acidosis increases the amount of ionized calcium via osteoclastic
activity on bone, Alkalosis leads to increased binding and decrease ca.(
hypocalcemia)

Q. Causes for postthyroidectomy hypocalcemia ?. Inadvertent parathyroid

gland removal, Ischemia of parathyroid glands

Q. How is calcium Transported in body ? Which part is Active ? 50% --

unbound / ionised( Active ), 45%-- bound to plasma proteins and 5% with
anions (citrate,lactate) in circulation.

Q. What is calcium used for ? second messenger in cell signalling pathways,

muscle contraction, nerves functioning, blood clotting(coagulation), secretion of
hormones ( insulin), cell division , bone/teeth building.

Q. What is Vit D actions ?

Q. actions of parathyroid ? regulates serum calcium through its effects on

bone, kidney, and the intestine:

Bone: stimulates osteoclasts for bone resorption

Kidneys: 1. Reabsorption of Ca. in the DT and CD
2. Inhibition of the reabsorption of phosphate from the tubular fluid, 3. Increase
1- alpha hydroxylase activity
Intestine: Absorption of calcium in the intestine by increasing the production of
activated vitamin D

Q. Which muscle are you worried about in hypocalcemia tetany? (I really

didn’t get the correct answer for this one. I said diaphragm, intercostals. He just
shook his head. So I told him I didn’t know) Tetany is characterized by contraction

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of distal muscles of the hands (carpal spasm with extension of interphalangeal joints
and adduction and flexion of the metacarpophalangeal joints) and feet (pedal spasm)
and is associated with tingling around the mouth and distally in the limbs.

Q. How to treat hypocalcemia? . ABC , Cardiac monitoring , IV calcium

gluconate. He asked for specific dose. I said IV infusion over 10 mins 10 mls of
10% calcium gluconate. He said he will accept that)

Q.Which hormones are involved in Ca regulation (name 3) ?

Q. What are their actions?

PTH : Overall ↑ Ca2+ and ↓PO43-
Bone: increases bone resorption by stimulating osteoclast
Kidney: Increases reabsorption of Ca2+ and Mg2+, increases excretion of PO43-
in the PCT. Increase production of activated vitamin D in the kidneys, PTH
upregulates the enzyme 1-α-hydroxylase
Stimulus : Decreased Ca2+ Increased PO4
Vitamin D
Overall ↑Ca2+ and ↑PO43—
Bone: increases bone resorption by stimulating osteoclast

Gut: increases absorption of Ca2+ and PO43-

Kidney: increase reabsorption of Ca2+ and PO43-
N.B. Vit D inhibits PTH production via negative feedback
Stimulus : PTH, Decreased PO43-
Calcitonin
Not physiologically significant except in hypercalcaemia
Bone: decreases bone resorption by inhibiting osteoclastic activity
Stimulus: Increased Ca2+
Q. Exact mechanism PTH causes phosphate excretion in the kidneys?.
PTH reduces the reabsorption of phosphate from the proximal tubule of the kidney,
which means more phosphate is excreted through the urine.

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Q.What are the physiological roles of Ca in the body? Name 4.

(Cardiac, nervous, haemostasis and bone) muscle contraction, Nerotransmitter

and nueromodulator, Activation of some enzymes, Glycogen metabolism,Cell
division,Mineralization of bone,Blood coagulation

Q.What is a more common cause? Ischemia to parathyroid glands.

Q. What would you be worried about in this lady? Tetany

Q .And so? Respiratory embarassment

Q.How does hypoCa cause SOB? laryngospassm , causing upper airway

obstruction

Q.What other signs of HypoCa do you know of ? Trousseau sign –

carpopedal spasm after inflating BP cuff above systolic BP x 3mins , Chvostek
sign – contraction of facial muscles while tapping on facial nerve anterior to ear

Q. What is the exact dose that you would give? and the concentration?
What would you ink up in the IMR? ( The first 100 to 200 mg of
elemental calcium (1 to 2 g calcium gluconate) should be given over 10 to 20
minutes) , 10 ml of 10% calcium gluconate, followed by 10-40 ml in saline
infusion over 4-8 hrs.

“Mild” hypocalcaemia (Asymptomatic, >1.9 mmol/L)

• Commence oral calcium supplements such as SandocalTM 1000, 2 tablets BD
• If post-thyroidectomy and patient asymptomatic, repeat calcium 24 hours later:
- When adjusted calcium is > 2.1 mmol/L, patient may be discharged and
recheck calcium within one week
- If serum calcium remains between 1.9 and 2.1 mmol/L increase SandocalTM
1000 to three BD
- If patient remains in mild hypocalcaemic range beyond 72 hours post

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operatively despite calcium supplementation, start 1-alfacalcidol 0.25 mcg/day

(calcitriol) with close monitoring.

Q. What other management? (Said A, B, C.. examiner not interested)

Monitoring -- ECG, SaO2 monitoring. Treat the cause, cardiac monitor,fluid
resuscitation, start Vitamin D and oral calcium early, recheck calcium level.
Coexisting hypomagnesemia should be corrected in every patient. Care should
be taken in patients with renal insufficiency because they cannot excrete excess
magnesium. Magnesium is given via infusion and initiated with 2 g magnesium
sulfate over 10 to 15 minutes, Hemodialysis may be necessary for patients with
symptomatic hypocalcemia and hyperphosphatemia, especially if renal function
is impaired.

Q.What else? Regular Ca monitoring? Digoxin? HD?

Q. Abdominal pain in hyper ca: d/d? peptic ulcer, acute pancreatitis,renal

colic, constipation due to low intestine.

Q. C/f Hyper ca? Bones, stones, groans, moans.

Q. Manage hypercalcemia? treat cause, cardiac monitor, rehydration with

crystalloid- add frusemide, Biphosphonate(palmidronate), high dose steroids(
prednisone), urgent surgery If hyperPTH.

Q. Hormones involved in calcium homeostasis ? PTH : increases plasma

Ca by breakdown the matrix and increased bone resorption(osteolytic and
osteoclastic), In kidneys, it increses alpha 1 hydroxylation of calcidiol to calcitriol

Vitamin D3:(kidney,bone,gut) 1. increase calcium calcification of bone matrix

and increases osteoblasts count activity n protien synthesis 2. Increased renal
Ca and PO4 reabsorption. 3. Increased Ca , PO4 absorption.

Calcitonin :(bone and kidney) : osteoclastic and excretion of ca, po4, Na, cl.

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Q . How is Vitamin D formed / Metabolism? skin, dietary – fatty fish &eggs –

need 600 IU /day

1. skin : 7-dehydrocholesterol -->cholecalciferol(sunlight) , bound to vit D

binding proteins - liver

2. diet (cholecalciferol D3 or ergocalciferol D2) – SB – chylomicrons –&; liver

3. liver : 25hydroxylase 25 hydroxy vit D or calcidiol

4. kidney (mitochondria PCT) – calcidiol - alpha 1 hydroxylase – 1,25 dihydroxy

vit D or calcitriol (physiologically active)

5. calcitriol – increased gut absorption of Ca, decreased renal excretion of Ca

PO4, bone resorption (thru PTH). Can also inhibit PTh in case of hypoPO4

(increase Ca n ; PO4 intestinal absorption with dec PO4 renal excretion

Q. Structural Names at each stage of Vitamin D Metabolism?

Q.How it is Metabolised? Vitamin D3 is made in the skin from 7-

dehydrocholesterol under the influence of UV light. Vitamin D2 (ergocalciferol) is
derived from the plant sterol ergosterol. Vitamin D is metabolized first to 25
hydroxyvitamin D (25OHD) in liver then to the hormonal form 1,25-
dihydroxyvitamin D (1,25(OH)2D) in kidney.

Q. Hormones involved in Ca+2 homeostasis ? PTH: ( Ca +): Increase bone

resorption, kidney reabsorption, 1alpha hydroxylase activity, Calcitonin: ( Ca -) :
Decrease bone resorption, Increase kidney excretion, 1,25
dihydroxycholecalciferol:( Ca +) : Increase kidney and gut reabsorption.

Q. How it is formed ? UV / Skin : Cholesterol à Cholecalciferol --> (in liver)

25,hydroxycholecalciferol à (In kidney ) 1,25 dihydroxycholecalciferol.

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Q. Signs of hypocalcemia ? Trousseau sign, Chovstek sign, Convulsions,

Anxiety,depression- Arrythmia, Circumoral parathesia- ECG: prolonged QT
interval, hyperactive tendon reflexes Numbness and tingling sensations in the
perioral area or in the fingers and toes, Muscle cramps, particularly in the back and
lower extremities; may progress to carpopedal spasm (ie, tetany), Wheezing; may
develop from bronchospasm, Dysphagia, Voice changes (due to laryngospasm)
Q. Muscle worried in tetany? Laryngeal muscle for the fear of laryngospasm

Q. How to treat hypocalcemic tetany? 10 ml ampoule of 10% calcium

gluconate ,diluted in 50-100 ml of 5% dextrose and infused slowly over 10
minutes with ECG.

Q. Management of hypocalcaemia? ( severe <1.9 mmol/L)

- IV calcium replacement: 10m 10% calcium gluconate in 50ml of D5 given over
10min (90 mg of elemental calcium per 10 mL) with ECG monitoring, repeat till
patient is asymptomatic. Followed by calcium gluconate infusion – dilute 100ml of
10% calcium gulconate in 1L of NaCl and infuse at 50-100ml/h, titrate to achieve
normocalcaemia.
- Concurrent hypomagnesemia: 2g of 10% magnesium sulphate over 10-20min
- Oral calcium replacement
- Vitamin D analogues: calcitriol 0.25mcg/day (Vit D metabolite of choice as it
does not need renal activation), ergocalciferol/cholecalciferol
- Check 2 hours post-replacement

Eneterocutaneous Fistula
Q . What is a fistula/ Definition ? abnormal communication lined by
granulation tissue between 2 epithelial or endothelial surfaces.

Q. Classify? Congenital/acquired, Etiology (infection,inflammation,malignancy,

RT), internal/External, simple/complex, Anatomy ( EE,EC,Colovaginal,
Vesicocolic) , Physiology (high/low output)

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Q. Cnservative management for ECF ? Principles of Management ?

SNAP: Sepsis and Skin care , ,Nutrition support, Anatomical assess/ Adequate
fluid, electrolyte replacement and Plan + Protect the skin .( 60%close
spontaneously in 1 month when sepsis controlled and distal obstruction relieved)
MDT following initial resuscitation and stabilisation with ABCDE approach ,
Dietician for nutrition, BLOODS ( WBC, CRP, U/ E),

Q. Imaging ? To see underlying Abscess , collection US, CT abdomen and

pelvis with contrast and Fistulogram to delineate the track length,Locating the
fistula, Locating any distal obstruction,

Q. Surgical management ? normally delayed until after a trial of conservative

measures has been undertaken; however, peritonitis with ongoing sepsis require
urgent surgical intervention. Aim of surgery is to excise the fistula tract with
resection of the bowel involved and anastomosis or exteriorisation of the
remaining bowel, followed by delayed anastomosis.

Q. Nutrition? TPN : Nutritional assessment by a dietician. It is based on a

patient’s body weight and how unwell they are. The energy requirement is 25-30
kcal/kg/day for a normal person and 45-55 kcal/kg/day for extensive trauma. In
addition the protein, fats, glucose, electrolytes and fluids are calculated and
adjusted based on regular blood tests
Q. Complications of ECF ? Triad of complications. SMF : 1. Sepsis, 2.
Malnutrition, 3. Fluid/ Electrolyte abnormalities. Loss of absorptive surfaces
loss of nutrients,los of water , electrolytes, loss of Alkline pancreatic juice may
cause metabolic acidosis, excoriation skin due to pancreatic trypsin enzyme.

Q.What brings the patient to OT within first 24 hrs? Distal obstruction,

Intraabdominal sepsis.

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Q. Signs of Intraabdominal sepsis? nausea, vomiting, swinging Pyrexia,

abdominal tenderness, rigidity, tachycardia, hypotension.

Q.Given Blood results: Low Na, K,HCO3 ,Why low bicarb ?sepsis cause
lactic acidosis ,which leads to low hco3….The Henderson-Hasselbalch
equation mathematically describes the relationship between blood pH and the
components of the bicarbonate buffering system

Q. Risk factors/ Predisposing for ECF ? Crohn's disease, Cancer, Infection,

Irradiation, Ischemia, Intestinal Anastomosis. (4 I, 2 C)

Q. Factors preventing spontaneous healing/closure ? Distal

obstruction,Foreign body, Malignancy ,Radiation, Crohn's , Malnutrition, High
output, mucocutaneous continuity, Associated untrained infection.

Q. Other complications besides metabolic disturbances? Dehydration,

wound infection , skin excoriation,

Q.Why would the patient be acidotic?loss of alkaline pancreatic juice leaders

to metabolic acidosis.

Q. Where is Bicarb mainly produced from? pancreas

Preoperative AS
Stem : elective TURBT

Q. Pathophysiology AS ? Fixed CO -----> limited coronary blood supply----->

can not respond to decreased afterload which may occur with anaesthesia or
blood loss.

Valve obstructionàintraventricular pressure increased to maintain CO à LVH

àincreased LVEDP àdecreased CPPà subendocardial ishcemia à
angina/syncope/dyspnea

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CPP = Systemic diastolic art. Pressure - LVED pressure

Q. Clilnical picture AS ? Symptoms: syncope , angina, dyspnea, Orthopnea,
PND , Signs: Pulsus alternans, Narrow PP, Paradoxical splitting S2, Ejection
Systolic murmur ( right 2nd IC space,right sternal border)

Q. ID : Read (ECG). ? +ve lead 1 , + ve lead avL, -ve lead 2 , -ve lead avL , Left
axis deviation = LVH

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Q. Calculate HR based on this ECG? 300/ No. of large squares between two
R-R intervals

Q. Complications AS ? LVH, HTN, CHF, VT, VF, Angina, Sudden Cardiac

Death(SCD)

Q. Investigations ? 2D echo, TEE

Q. What to do ? inform the consultant , anathesist, Cancel the operation, Call

the operating theatre to cancel listing, Explain to the patient, Discuss in MDT

Q. If this patient had a bladder cancer , will you proceed to bladder surgery
or valve surgery first? This will depend on the severity of AS: Normal aortic
valve surface area is 2.5-3.5 cm2, < 1cm2 = severe stenosis = transvalvular
gradient > 40mm.h

Q. If operation cancelled , what are you worried about? Spread of cancer

Q. if you will proceed to surgery ? preoperative antibiotics for prophylaxis

against infective endocarditis ( according to NICE guidlines)

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COMPARTMENT SYNDROME/ CRUSH/Rhabdo.

Stem : Leg crushed for few hours in 28 yr male. Left unobserved on ortho ward,
bloods consistent with AKI. Urine dipstick has blood.

Q. Clinical features of compartement syndrome ? 1. Worsening pain out of

proportion to injury on Passive stretching on the affected compartement, Not
responding to analgesia. (Normal compartement pressures = 0-15 mm.Hg) , >20
= indication of fasciotomy) 2. Paraesthesia, pecially loss of 2 point tactile
discrimination,Tense and swollen compartments,Sensory loss, Pain on passive
stretching, Loss of regional pulses: a late sign

Q. Labs /Diagnosis? Blood : Elevated CK-MM, Lactate ,LDH, Creatinine, dark

Urine due to Myoglobin , Hyperkalaemia with metabolic acidosis… and
Hypocalcaemia, Hyperphosphataemia, Hyperuricaemia

Q. How to do Fasciotomy ? 4 compartement fasciotomies through 2

incisions as an emergency procedure
Q. ARF, why ? The exact mechanism is not fully understood but may involve
Acute Tubular Necrosis: ischaemic tubular injury(nephrotoxic effect) caused by
myoglobin and its breakdown products accumulating in the renal tubules.

Q. Myoglobin ? respiratory pigment found in cardiac and skeletal muscle, is

composed of a single globin chain of 8 helical regions with a single haem
component, source of oxygen for muscle during times of increased activity.
Q. Rhabdomyolysis ? Release of potentially toxic muscle cell components into
the systemic circulation
Q. Causes? Trauma: fracture or lengthy compression of muscle, Massive burns,
Hypo or hyperthermia, Acute ischemia with reperfusion injury

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Q. Manage rhabdo and AKI due to this? Supportive – managing complications

and ensuring adequate renal function. Ensure good hydration( vigorous fluid
resuscitation) to support urine output with the use of i.v. crystalloids, Forced
Diuresis ( mannitol ), Alkalinising of Urine: sodium bicarbonate , Management of
associated electrolyte disturbances: hyperkalaemia (dialysis or haemofiltration)

Pregnancy : Open / LAP CHOLECYSTECTOMY

34 weeks pregnant undergoing laparoscopic cholecystectomy for necrotic ,
gangrenous cholecystitis. She is in reverse trendelenburg position. BP drops
from 107/60 to 85/56, HR 110. ( scenario changed to Open Chole . At
Hyderabad)

Q. Benefits/risks of LC ? Benefits : control of infection( which may lead to

sepsis) and induction of pre- term labor, low fetal depression due to low narcotic
requirements, decreased manipulation of uterus, faster recovery, low
postoperative complications like infections n hernias , low chances of Ileus, low
postoperative maternal hypo ventilation. Risks : IUFD , DVT ( long duration) ,
pre term labor, trocar injury to uterus, decreased uterine blood flow, fetal
acidosis , decreased visualisation due to grave uterus.

Q. Who should be involved in her care? Anaesthetist, Obstetrician

Neonatologist ,if preterm , ITU registrar (He wasn’t satisfied with 1 st 2, wanted
more) …General Surgeon !

Q. Where would she be monitored post- operatively? Obstetric HDU

Q. Why BP is decreasing? Compression of IVC by the uterus which will

decrease the VR , which will decrease Preload thus decreasing CO and
Reversed telendenberg position

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Q. Frank–Starling’s law ? greater EDV (volume of blood entering the heart

during diastole), the greater SV (volume of blood ejected during systole) and
vice versa

Q. How would mechanical DVT prophylaxis affect this?

Q. MOA of DVT Stockings ? Improves Venous Return , Reduces cross section

of legs, decreases amount of blood stasis. Milking effect to evacuate leg veins.

Q. In this lady, how would you manage this drop in BP? Pneumoperitoneum
minimised to 8-12 Hg, Tilt head down 30 degree, Lift uterus Up during surgery.

Q. What is preload? End diastolic volume EDV that stretches the right or left
ventricles of the heart to its greates dimension, The amount of myocardium that
has been stretched at the end of diastole. Preload is affected by venous BP and the
rate of VR . These are affected by venous tone and volume of circulating blood.

Volume of blood returning to heart,I.e. VENOUS RETURN( equal to CO) , It is

difference between Systemic filling pressure and CVP.

Q. What is afterLoad ?.Ventricular wall tension generated in order to eject blood

out of the ventricle. i.e. ARTERIAL PRESSURE. Afterload = CO * SVR

Q.What affects preload / Venous Return? Mechanisms?

1. Muscle contraction : Rhythmical contraction of limb muscles as occurs during

normal locomotory activity (walking, running, swimming) promotes VR by the
muscle pump mechanism.
2. Decreased venous compliance : Sympathetic activation of veins decreases
venous compliance, increases CVP and promotes VR indirectly by augmenting
CO through the Frank-Starling mechanism, which increases the total blood flow
through the circulatory system.

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3. Respiratory activity : During respiratory inspiration, the VR increases because

of decrease in right atrial pressure

4. 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 VR

5. Gravity.: decreases VR

Low Heart Rate and. High Atrial contractility, Aortic pressure, Ventricle
Compliance , CVP ( High Thoracic venous blood volume due to High Total blood
volume and High VR : Respiration: inspiration , Gravity, Muscle contraction/ Low
Venous Compliance due to Sympathetic activation of veins)

Q. How does preload affect you systemic circulation? Frank Sterling : greater
preload ..more stroke volume

Q. In this patient most likely cause? Surgical blood loss, Venous pooling due
to patient position, Reduced VR due compression of IVC by the Gravid uterus ,
pneumoperitoneum causes lower limb Venous stasis, pregnancy causes hyper
coagulation state -à decreased Preload.

Q. How would you treat to improve patients condition? fluid

resuscitation(adequate hydration), intraoperative co2 monitoring, Subcostal /
Open trocar, VTE prophylaxis, Fetal heart monitoring, left lateral position ,use of
Tocolytics.

Q. Do u think surgery is necessary? Factors for and against?

Q.What measures to prevent further hypotension? Lift the uterus up during

surgery and tilt the patient head down 30 degrees

Q. How VR differs in Standing versus Supine ?standing : venous pooling

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Q. How to prevent DVT ? Ambulation, intermittent pneumatic device, stockings,

Heparin.

Q. MOA of DVT Stockings ? Improves Venous Return , Reduces cross section

of legs, decreases amount of blood stasis.

Q. How improve preload of patient ? Fluids , inotropic, vasopressor agents

Q. Effects of Peumoperitoneum ? Low: VR, CO, FRC, Splanchnic blood flow.

Q. Actions of inotropes ? Receptors ? Adrenergic agonists : adrenaline,

noradrenaline, isoprenaline increase SVR through vasoconstriction,HR, SV and
resultant CO to increase the SBP, Dopaminergic agents : (with some
adrenergic activity) : dopamine, dobutamine, dopexamine increase the HR, SV
and resultant CO and contractility to increase the BP , but depending on dose,
decrease SVR to produce vasodilatation.

Q. Shock? Shock is circulatory failure resulting in inadequate organ perfusion,

e.g. cannot meet the metabolic demands.

Q. What will be the body response to decreased BP ? The autonomic

response is due to decreased VR (preload) which causes a drop in CO and
arterial pressure by the Frank–Starling mechanism.
Reflexes: Baroreceptor : stimulates sympathetic activity producing a
compensatory tachycardia, increased SV and peripheral vessel constriction ( ↑
SVR). This increases the CO and maintains BP. Hormones : Catecholamines :
the adrenal medulla is stimulated by pain and injury and releases hormones to
cause peripheral vessel constriction, e.g. noradrenaline ( ↑ SVR),
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.
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renin–angiotensin–aldosterone (RAA) cascade. A resultant increase in salt and

water retention helps to restore circulating volume over several hours .

Renal and hormonal –– A fall in blood pressure is also sensed by the volume
sensors in the right atrium (RA), leading to (ANP) production and reduction of
ADH from the posterior lobe of the pituitary. This in turn increases the production
of aquaporin 2 at the renal collecting duct and increases the reabsorption of
water, increasing the blood volume and increasing the intravascular pressure.
The reduction in renal arterial pressure (acutely below ~90 mmHg) stimulates the
(R-A-A) system, which in turn leads to a cascade of effects to further increase in
blood pressure.
Impulses sent from the mechanoreceptors are relayed to NTS and ultimately to the VMC the
brain. A sudden increase in blood pressure stretches the baroreceptors and the increased firing
results in the vasomotor center inhibiting sympathetic drive and increasing vagal tone on the SA
node of the heart. Signals from the carotid baroreceptors are sent via CN 9 , from the
aortic baroreceptors travel through the CN 10. Arterial baroreceptors inform reflexes about
arterial blood pressure but other stretch receptors in the large veins and right atrium convey
information about the low pressure parts of the circulatory system.

Q. 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.

Q. Talk about the sympathetic and parasympathetic control of the heart.

How does the body detect low BP? Where are these central and peripheral
receptors located? Baroreceptors? mechanoreceptors located in the carotid
sinus and in the aortic arch , function is to sense pressure changes by

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responding to change in the tension of the arterial wall.Supplied by sinus nerve of

Hering, a branch of CN 9

Q . Can you name some medical devices used in thromboembolic events

that can help improve the circulatory parameters of this patient? Intermittent
pneumatic compression devices(IPCD), venous foot pump(VFP) , graduated
compression stockings ( GCS)/ TEDS: Thromboembolism Deterrent Stockings.

Q. How to improve the preload of patient ? Fluids , inotropic and vasopressor

OBSTRUCTIVE JAUNDICE
Stem : Epigastric pain, N/V ,diarrhea, increased ALT, AST, ALP, GGT,
urobilinogen undetectable in urine( patient chart shown)

Q. What type of Jaundice? Obstructive

Q. Normal bilirubin level ? 3-30 umol/L (<26 micromol/ ltr), Direct (<7 micromol/
let) . Apparent jaundice > 35 umol/L
Direct (conjugated) bilirubin: 0 to 0.3 mg/dL, Total bilirubin: 0.3 to 1.9 mg/d

Q. Forms of Bilirubin in blood? Unconjugated/ Conjugated

Q. Why urobilinogen not detectable in urine in this patient ? Due to

obstruction, Bilirubin can't reach gut to form Urobilinogen.

Q. Bilirubin processing in gut ?

Q. How urobilinogen absorbed and excreted ?

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Q. Why clotting derranged? liver synthesize most clotting factors, vit. K

activate factors 2,7,9,10, severe liver damage and biliary obstruction there will be
decreased absorption of vit. k, this will lead to increased prothrombin time(PT)

Q. ALP ? increases in cholestasis to a far greater extent than ALT,AST, located

in the epithelium of bile canaliculi, bone and placental tissue, ALT,AST present
in hepatocytes and their increase is suggestive for liver damage rather than
obstructive jaundice. ALT>AST (Liver pathology)

Q. How and where bilirubin conjugate ? liver, Conjugates with glucouronic

acid by the enzyme glucuronyltransferase

Q. Bilirubin metabolism ? congugated bilirubin goes into the bile and thus out
into the small intestine. Though most bile acid(95%): Unconjugated 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 deconjugate and metabolize the bilirubin into colorless urobilinogen,
which can be oxidized to form stercobilin: these give stool its characteristic
brown color. 10% of urobilinogen is reabsorbed into the enterohepatic circulation

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to be re-excreted in the Bile: some of this is instead processed by the kidneys,

coloring the urine yellow.

Q. Enterohepatic circulation ? Reabsorption of bile salts(95%) from terminal

ileum and return them back to the liver

Q. How to correct clotting abnormality ? IV Vit.K, FFP, Prothrombin complex

concentrates , Consult hematologist

Q. Causes of jaundice? : Pre-hepatic : Hemolytic anemias: -hereditary

spherocytosis - G6PD- Sickle cell disease, Congenital defects:gilbert, Crigler-
Najjar, Hepatic : Viral hepatitis ,Drug induced, Chronic autoimmune hepatitis,

Wilson's disease, Post-hepatic( obstructive) : Gall stones, Sclerosing

cholangitis ,Cholangiocarcinoma Cancer head pancreas, Absorption Excreted in
urine as Urobilinogen Of the stool Gives the colour of urine urobilin] Oxidation.

Q. What is urobilinogen? It is a byproduct of bilirubin metabolism formed in the

intestine by gut flora.

Q. Function of Bile salts in digestion of fat? And what they need to achieve
this function? Emulsification of fat into fatty acids( detergent ) increasing
surface area , which can be absorped from the small intestine, aid digestive
enzymes( lipases) , Reduce surface tension and break fat globules into droplets(
emulsification by detergent action ) ,Enhance absorption of fatty acids and
Cholesterol, Help absorption / absorption of fat soluble vitamins. To do these
functions, they have to be negatively charged through conjugation with Glycine
and Taurine. Solubilization and transport of lipids in an aqueous environment: Bile acids
are lipid carriers and are able to solubilize many lipids by forming micelles - aggregates of lipids
such as fatty acids, cholesterol and monoglycerides - that remain suspended in water.

Q. Investigations ? Bloods, US HBS

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Q. USG findings of biliary obstruction?

Q. If US shows stones/ dilated biliary radicles , next step? Confirm with

MRCP ,followed by ERCP

Q. Why ERCP ? Papillotomy and Dormia basket stone extraction.

Q. Before that ? Stenting to relieve obstruction

Q . If this patient has fever and pain, U worried about? Ascending cholangitis

Q. What Antibiotics In Cholangitis ?

Q. Which ALP/ GGT more important? The gamma-glutamyl transferase (GGT) test may be used
to determine the cause of elevated alkaline phosphatase (ALP). Both ALP and GGT are elevated in disease of the
bile ducts and in some liver diseases, but only ALP will be elevated in bone disease. Therefore, if the GGT level is
normal in a person with a high ALP, the cause of the elevated ALP is most likely bone disease.
The GGT test is sometimes used to help detect liver disease and bile duct obstructions. It is usually ordered in
conjunction with or as follow up to other liver tests such as ALT, AST, ALP, and bilirubin. (Read also about the Liver
Panel.) In general, an increased GGT level indicates that a person's liver is being damaged but does not specifically
point to a condition that may be causing the injury.
GGT can be used to screen for chronic alcohol abuse (it will be elevated in about 75% of chronic drinkers) and to
monitor for alcohol use and/or abuse in people who are receiving treatment for alcoholism or alcoholic hepatitis.

Q. What are the Bile Salts? Bile acids are conjugated with taurine or glycine in the
liver, and the sodium and potassium salts of these conjugated bile acids are called bile
salts. Primary bile acids are those synthesized by the liver. Secondary bile acids result from
bacterial actions in the colon. In humans, taurocholic acid and glycocholic acid (derivatives
of cholic acid) and taurochenodeoxycholic acid and glycochenodeoxycholic acid(derivatives
of chenodeoxycholic acid) are the major bile salts in bile and are roughly equal in
concentration.[5] The conjugated salts of their 7-alpha-dehydroxylated derivatives, deoxycholic
acid and lithocholic acid, are also found, with derivatives of cholic, chenodeoxycholic and
deoxycholic acids accounting for over 90% of human biliary bile acids

Gastric outlet obstruction

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Lady vomiting, epigastric fullness. Labs show Na 125, K 1.9, Cl 59, pH 7.2 etc.

Q . What does she have? Hypocholeremic,hypokalemic, metabolic alkalosis

Q. Standard pathophysiology? In a peptic ulcer as a result of edema and

scarring of the ulcer, followed by healing and fibrosis, which leads to obstruction
of the gastroduodenal junction (usually an ulcer in the first part of the duodenum).
recurrent vomiting of food that has accumulated in the stomach, but which cannot
pass into the small intestine due to the obstruction. The stomach often dilates to
accommodate food intake and secretions, risk of aspiration pneumonia. Causes
of gastric outlet obstruction include both benign causes (such as peptic ulcer
disease af pylorus, tuberculosis, pseudocyst pancreas), as well as malignant
causes, such as gastric cancer.

Q. Symptoms to watch out for ? no bilious vomit after the meal, advanced
case : wasting and dehydration. Visible Peristalsis (VGP) , Succussion splash is
a splash-like sound heard over the stomach in the left upper quadrant of the
abdomen on shaking the patient, with or without the stethoscope. Bowel sound
may be increased due to excessive peristaltic action of stomach. Fullness in left
hypochondrium may also be present.

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Q. Causes ? Benign: pyloric stenosis secondry to cronic peptic ulceration,

Malignant ( gastric or pancreatic ) carcinoma

Q. Why got hypochloremic alkalosis? Loss of Cl- in vomit.

Q. Why got hyponatremia? In metabolic alkalosis , kidneys excrete more

NaHCO3 to reduce blood alkalinity-----> hyponatremia

Q. Classify hyponatremia with examples? Depletional : diarrhea, direutics,

burns,Dilutional : heart failure, post- operative over adminstration of 5%
glucose,Endocrine: Addison's ds., Hypothyroidism,Pseudohyponatrmia:multiple
myeloma, SIADH

Q. Complications of hyponatremia? Confusion, lethargy, muscle weakness,

cramps, seizures, cerebral edema, brain disease, herniation of the brain,
cardiopulmonary arrest, coma and even death.

Q.Why hypokalemia ?Increased Aldosterone in response to Hypovolemia

Q. Why Creatinine and Urea high ? Hypovolemia

Q. Why bicarbonate is increased ? 1. Increased uptake of bicarbonates in

renal tubules in response to loss of chloride in order to maintain electrochemical

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neutrality. 2. Reduction of pancreatic juice secretion due to loss of acid load in

the duodenum , pancreatic Juice is rich in bicarbonates which will be retained.

Q.Why got paradoxically aciduria? What is the key element in these

exchanges? (Sodium.) Hyponatremia------> stimulation of RAS system---->
more Na+ and h2o reabsorption in exchange of H+ and K+ -----> hypokalemia
and the urine becomes acidic due to prescence of H+

Q.How would you treat? Who else should be involved in management?

Correct fluid deficit with IV hydration, add K+ supplementation in the fluid
regimen, keep NBM, strict I/O charting, IDC insertion, endoscopy/ dilation
most common surgical procedures performed for GOO related to PUD are
vagotomy and antrectomy, vagotomy and pyloroplasty, truncal vagotomy and
gastrojejunostomy,
Q .When would this lady be fit for surgery?

Perforated viscous / AF

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Elderly gentleman has abdominal pain, looks confused. CXR : Free air under
diaphragm, ECG : AF.

Q .What must you confirm on CXR and ECG? CXR – gas under diaphragm /
ECG- absent P wave

Q.What is the problem with taking Consent from this dude? Patient is
confused , i will proceed for the operation for the patient best interest with 2
consultant signature on the consent.

Q. What do you call all this stuff about how patient must understand
information be able to repeat?

Q. Who should make decision?consultant

Q .What is differential diagnosis of perforated viscus? Ruptured diverticulum,

Perforated DU,Ischemic bowel,Necrotising enterocolitis

Q.What pathologies in the Large bowel could cause ? diverticulitis, ca colon ,

pseudo obstruction , caecum ca

Q .Tell me about this ECG. (Irregularly irregular.) How to read ECG ? What
is the rate? Q. What do I look out for in the ECG. How to calculate HR from
ECG? No. of QRS IN 30 Blocks ,multiplied by 10

Q.How different from my automatic reading? Can't measure irregularities,

because AF causes inadequate heart contraction resulting in a small volume puls

Q. What are the causes of AF in a SURGICAL population?

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Q.If stable how to manage?

Q.What 1st line drug? What dose?

Q.What are causes of his peritonitis?

Q .How to tell AF on ECG ? Absent P

Q. Why is this different from the one calculated during physical

examination? (130 on ECG vs 100 noted in the stem given).

Q. What does the ECG show. why is the HR on the ECG and the HR on the
BP cuff different - said something about the AF causing a smaller volume pulse,
BP puff cannot read.

Q.Causes of AF ? Cardiac -HT,MI,MVP,Cardiomyopathy,Endocarditis/.

Pulmonary-pneumonia, CA. Lung, sarcoidosis, septic, Others -
alcoholic,DM,AGE, hypovolemia, hypoxia, electrolyte,hyperthyroidism,fever

Q. Most likely cause of AF in this patient ? Sepsis and Hypokalemia

Q.Management/ Broad principles : AF ? Treat underlying cause( in less than

24 hrs) , Rate/rhythm control , Anticoagulants ,if Ventricular Rate more than 100,
use beta – blocker ( metoprolol IV 5mg or CCB( left ventricle impaired, BB
contraindicated) 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 (
UFH ) 70 units /kg as a bolus then 15 units / kg/ h till adjusting APTT to 40-60
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seconds . Non pharmacological options : Catheter ablation, Electrical devices (

AV node ablation, Pacemakers) , Surgery ( maze, mini-maze)

Q. SIDE EFFECTS of beta blockers : Fatigue, Cold hands and feet,weight

gain , depression,bronchospasm,sleep disorder,bradycardia,heart failure, sexual
disorder ..and CCBS : constipation, leg edema, dizziness,headache,
palpitations.

Q. Surgical problems with AF?anaesthesia risk (stroke), need to discontinue

warfarin,stress of surgery cause hypotension,underlying cause like IHD cause
more anaesthetic risk , stroke, heart failure.

Q. Beta blockers- MOA ? . Beta blockers inhibit normal epinephrine- and

norepinephrine-mediated sympatheticactions.

Steroids
Stem:RA patient on steroids / immunomodulators
Q. What is a steroid? organic compound that contains a characteristic
arrangement of 4 cycloalkane rings that are joined together.
Q. Layers of adrenal cortex ? GFR, zona glomerulosa: aldosterone, Zona
fasiculata: cortisol, Zona reticularis: sex hormones
Q. 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)

Q. 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,
Immunosupressive effect, Control body stress response.

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Q. Advice to patients starting steroids ? They should not stop the drug
suddenly , the drug shoud be tappered off slowly, Make doctors aware that they
are on steroids if they are admitted to hospital or prior to surgery( carry steroid
card, wear medicalert bracelet). There is increased possibility for infection,
delayed wound healing.Steroids may lead to osteoprosis with incraesd risk of
fracture, wight gain, increase blood sugar , if diabetic you will encounter poor

glycemic control, if not you can develop diabetes, muscle weakness, mood or
behviour change, incrase the risk of peptic ulcers, don not take NSAID's
Q. Addisonian crisis ? acute reduction of the circulating steroids due to:
Primary: Addisons disease: adrenal supply of cortisol can not meet the body
requirements, Secondary: to trauma, surgery, infection: exogenous steroids are
suddenly stopped rather than being tappered off. Cardinal features: abdominal
pain, Nausea,vomiting,Unexplained shock, Hyponatremia, hyperkalemia,
Management: CCRISP protocol,ABC protocol, I.v steroids,Adjust metabolic
disturbances. Prevention: increase the patient steroid dose prior to surgery,
Convert to i.v steroids.

Q. Adrenal gland . Cushing’s syndrome :complications during operation ?

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Q. What happens on long term steroids going for surgery ? Stop. Bridge
with IV hydrocort. .Hypotension Nausea ,Vomiting

Q.Wants to know where cortisol is produced. Wants to know what controls

cortisol production ?

Q.What are glucocorticoids? Glucocorticoids (GCs) are a class of

corticosteroids, which are a class of steroid hormones.

Q. What are their action?

Q. What is made in the adrenal medulla? Catecholamines

Q. What are the surgical problems associated with elevated cortisol? wound
infection, delayed healing

Q . What problems with wounds? infection,delayed healing

Q. What are the anaesthetic considerations of an elevated cortisol?Surgery

in CS presents a challenge to the anesthesiologist. The control of perioperative

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hypertension, hyperglycemia, hypokalemia, and cortisol blood level are hallmarks

of the anesthesiologist's role treating the patients with Cushing's syndrome.

PERFORATED GASTRIC ULCER/ Pneumoperitoneum

Stem: middle aged man, OA, NSAID's, peritonism, pneumoperitoneum( CXR)

Q. Comment on CXR ? Air under diaphragm

Q. Most likely diagnosis ? Perforated gastric ulcer or duodenal ulcer

Q.Risk factors of perforation ? NSAID's, H-pylori,Steroids,Previous peptic

ulcers, Malignancy

Q. How can NSAID's causes peptic ulceration? Pathophysiolgy ?

- topical irritant effect of these drugs on the epithelium,
- impairment of the barrier properties of the mucosa,
- suppression of gastric PG synthesis, ( inhibition of Cyclooxygenase)
- reduction of gastric mucosal blood flow
- interference with the repair of superficial injury.
Q. Management options ? Omental patch repair , good peritoneal toilet,
intraabdominal drain, perforated gastric ulcers : take a biopsy to rule out
malignancy
Q. Post- operative medications ? Long term PPI, Antibiotics( H. Pylori)

Q. 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

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Q. Actions of HCL? activated pepsinogen to pepsin which help in proteolysis

and antimicrobial

Q. Phases of Gastric secretions ?

Q. Likely diagnosis ? Perforated gastric/duodenal ulcer

Q. Management options for perforated ulcers? Omental patch repair , good

peritoneal toilet, intraabdominal drain ,In perforated gastric ulcers , we will take a
biopsy to rule out malignancy.
Q. Difference in management between PDU and PGU ? H. Pylori, life style
Take biopsies from PGU due to risk of malignancy causing perforation, PDU are
rarely due to malignancy .

Q. What medication will this patient require post-op ? PPIs

Q. 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

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Q. NCEPOD priority OT listing ? ...Said from 0-4, 0 is immediate, 1 is within 1

hour, 2 is within 4 hours, 3 is within 12 h and 4 is elective

Esophageal varieces and hematemesis:

Stem : 45 yrs old , chronic alcoholic, 3 times of hematemesis, low BP, high HR,
esophageal varices , Altered mental state.

Q. Differentials ? Bleeding esophageal varieces due to portal HTN ( cirrhotic

liver ), Mallory-weiss tear, Boerhave's syndrome, Bleeding peptic ulcer.

Q. Pathogenesis of portal HTN in chronic alcoholism ? Cirrhosis resulting

from Chronic liver disease( CLD) , characterized by Liver cell damage, Fibrosis
and Nodular Regeneration. The fibrosis obstructs portal venous return and portal
HT develops. AV shunts within the liver also contribute to the hypertension.
Q. Sites of portosystemic anastmosis?

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Q. Which varieces are usually bleeding? lower oesophagus

Q. How will you manage this patient ? ABC / Active resuscitation: Group
and cross-match blood • Establish i.v. infusion line( s) , Monitor (Pulse BP, Hourly
U/O, CVP), Fresh blood transfusion , FFP, Platlets, Assess coagulation
status: • PT/ Platelet count , Adjuncts – NBM, IDC insertion with strict I/O
charting, KIV intubation, Medications – IV omeprazole 80mg bolus + 8mg/hr
infusion for 3 days, IV somatostatin, IV antibiotics, Vasopressin/ Octetotide ,
stops NSAIDs/anti-coagulation, Close monitoring, Emergency OGD,Control of
bleeding : Endoscopic banding or injection sclerotherapy, Tamponade
(Minnesota tube) if bleeding uncontrolled, Surgical – TIPPS (Transjugular
intrahepatic porto-systemic shunt), shunt surgery e.g. portocaval (portal vein to

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IVC)
Q. Cause of thrombocytopenia here ? Liver dysfunction, Hypersplenism, DIC

Q. If you call haematologist, will you ask for platelets? Yes

Q. Indications for platelet transfusion?

- Actively bleeding – threshold is <50,000/microL & <100,000/microL in DIVC.
- Prevention of spontaneous bleeding – threshold is <10,000/microL in general,
<30,000/microL in septic / febrile patients.
Q. Macrocytic anemia, cause? Nutrition deficiency with chronic alcoholism.
Q. Surgical treatment options? 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 oesophageal transection : Modified Suguira technique (
abdominal ) , splenectomy is initially performed and is followed by devascularization
of the distal esophagus through the diaphragm hiatus , distal oesophagus is

transected and reanastomosed just above the cardia using a stapling gun ,
Orthotopic liver transplantation (OLT) : advanced liver disease

Q. 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, Immunosupression

Q. Sangstaken Blackemore tube ? Double ballon tamponade, Ports: port for

gastric ballon,oesphageal ballon, gastric suction, Modifiaction: Oesphageal
suction ( Minnesota tube)

Q. Describe usage ? Indication ? Used in oesophageal varicies that does not

respond to medical therapy (which includes endoscopic hemostasis and
vasoconstrictor therapy) OR when endoscopic intervention is unavailable.

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Q. How it works ( in broad principles)?

Q. How to use ? Position ( head end 45) , posterior pharynx / nostrils( topical
LA) , Coat ballons with lubricating jelly, Pass tube from the nostrils to at least 50
cm mark , Suction from gastric and oesphageal ports, When gastric ballon
positioned in stomach infalte the ballon 500 ml air and clamp,the port, pull the
tube back until resistence is felt against diaphragm, Inflate oesphageal ballon
to 30-45 mm.Hg , clamp port, When bleeding is controlled , reduce the
oesphageal ballon by 5 mm.Hg every 3 hours until 25 mm.Hg is reached without
bleeding then keep the tube form 12-24 hours. Deflate oesphageal ballon for 5
min. /6 hours to prevent oesphageal necrosis.

Q.Which varices are usually bleeding ? GE Jn.

Q. Risks and complications of using Sengstaken Blakemore tube?

Q. SB TUBE 3 ports : What are they for and Where do the balloon work ?

Q. If there is no modification, what do you do? Insert NGT

Q. Problems associated? aspiration pneumonia, airway obstruction (proximal

migration of the SB tube compressing upper airway), oesophageal
perforation/ulceration,

Q. Contraindications ? recent oesophagogastric surgery, oesophageal

stricture, oesophageal tear

TURP syndrome
Stem : post -TURP : confused, hypoxic, BP low, sats low.

Q. D/D ? TURP syndrome, Effects of analgesia and sedation,Hyponatremia,

Blood loss , Cerebrovascular disease.

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Q. C/F/ Definition ? dilutional hypotonic hypervolemia, due to glycine rich

irrigation solution,causing dilutional hyponatremia. Restlessness, confusion,
coma, blurred vision, hypertension followed by hypotension,pulmonary n cerebral
edema, tachypnea, heart failure.

Q. Diagnosis? There are no definite criteria to diagnose TURP syndrome. The

clinician must have a high index of suspicion for diagnosing TURP syndrome in a
patient who becomes unwell following a TURP procedure, findings soon after a TURP
procedure would be strongly suggestive of a TURP syndrome diagnosis:

§ acutely unwell, confused patient with a reduced Glasgow Coma Scale score
§ hyponatraemia: Na < 120 mmol/L
§ hyperkalemia: K > 6.0mml/L
§ hyperglycinemia
§ intra-vascular haemolysis, DIC (reduced platelet count, increased FDP)

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Q. Complications?

Q. What is glycine? Glycine(1.5%) is simplest amino acid , single hydrogen

atom at side chain., colourless. Complications: hyper ammonia, hyperoxaleuria,
visual disturbances , CNS toxicity, Myocardaial depression

Q. How manage? CCRISP , stop surgery , ABCD,Resuscitate ,BZD(

nausea,vomiting). Transfer HDU/ITU ,monitor invasive , CVP line fluid therapy in
view of hypoxia/low saturations, intra-arterial line to monitor BP,Pulse, intubation
and ventilation , Frusemide(diuretics) for pulmonary oedema, Respiratory
support( 100% oxygen by non breathable mask ) , CVS support( central line, add
initropes) , treat Hyponatremia ( slow : 1 mmol/ day) , correct coagulopathy (
PRBC, FFP, platelets ), Ix: Bloods: FBC, electrolytes, clotting panel, ABG,
glucose and ammonia levels. Fluid restriction to treat hypervolemic
hyponatremia, correct electrolyte imbalances(Replace sodium not more than 1 m
mol/Hr) and coagulopathy ( FFP, PLATLETS,Fibrinogen), correct hypothermia (
warm fluids, bairhugger), frusemide for fluid overload .

Q. Which diuretic to use? loop ( frusemide)

Q. Why do they use glycine? Being transparent, nontoxic, easy to sterilise ,

electro neutral , isotonic solution it is safe using an electrocautery loop to perform
TURP. NS cannot be used as irrigation solution because dissemination of the
electric current would be dangerous to both, surgeon and patient.

Q. How this SYNDROME occur ? Open prostatic venous plexus absorb glycine
causing fluid overload and pulmonary n cerebral edema, hypervolemia leads to
hypertension initially and bradycardia.

Q. Causes of confusion? glycine breakdown in liver cause increased

ammonia and low sodium ( cerebral edema)

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Q. Low Oxygen , why ? Tachypnea / pulmonary edema.

Q. How low Na. Cause confusion? Cerebral edema ( low sodium outside brain
cells withdraw water inside)

Q. Where will you manage this patient? HDU/ITU

Q. Will u give hypertonic NaCl? Yes, if Na< 110 mol/ L. I will only give 250-
500ml of 3% NaCl through the CVP line if the patient has seizures but not more
than 10 mol/L/Hr to avoid central pontine myelinosis( continued monitoring)

Q. Medical mx - diuretics, tell me how they work and where they act?
Diuretics can be divided into: Osmotic e.g. mannitol, work by
osmosis(PCT,LOOP,CD): inhibit Na, H2O absorption

Thiazide : DCT block Na/Cl resorption / Loop diuretics : Na/K pump /

ascending loop of Henle to inhibit Na Cl absorption, then DCT tries to preserve
Na and loses K / Spironolactone works by being an aldosterone antagonist
blocking aldosterone binding at DCT / Amiloride binds to Na channel at DCT

Q. Prevention ? Early intervention, Regional/ spinal anaesthesia, minimise .OT

time, avoid glycine,OT TABLE horizontal, Ht of irrigation fluid bag 60 cm
(optimum)

Q. Other system affected by TURP ? Cardiac

RENAL FAILURE / HYPERKALEMIA

Stem: 78/ dementia, renal impairment, h/o recurrent UTI , baseline creat. 250, developed UTI,
nausea, vomiting , Bloods : K+= 8 mmol( high) Na+ = 121( low) Creat. = 700( high)

Q. Interpret/ Diagnosis ? AKI, Obstructive uropathy(BPH: Post Renal ) , Pre-renal(decreased

oral fluid intake due to dementia)

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Q. Why are uraemic patients anaemic? Normocytic, normochromic anaemia due to Deficiency of
EPO,Presence of circulating Bone marrow toxins , Bone marrow fibrosis during osteitis fibrosa
cystica ,Increased RBC fragility caused by Uraemic toxins.

Q .Then pt had catheter inserted and subsequently had increased urine output (4L/day)
examiner wants to know why? Obstruction relieved and cause of AKI ccorrected(Diuretic phase
AKI), GFR is high.

Q. Indications : dialysis. ? Fluid overload ,Hyperkalemia (>6) , Acidosis with pH < 7.2 , Urea >30
, CRF with creatinine clearance < 10 ml/ minute , Encephalopathy.

Q. Ethical considerations of deciding dialysis ? patient 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. 4 Topic method : 1.
Medical indication(beneficiance n nonmaleficiance) 2. Patient preference 3. Quality of life (QOL) 4.
Cotextural features( health resources, family support)

Q. Causes of ARF ? DM, ATN, GN,IN,HRS,RAS

Q. Causes of ARF in this pt? postrenal failure( obstruction)

Q. Electrolytes: single most important finding? High K

Q. Function of Aldosterone ? Reabsorption of Na , Excretion of K, acid-base
balance, BP maintenance.
Q. What u worry in hyperkalemia ? Cardiac Arrest
Q. What you worry about in hypokalemia ? Irregular heart beat,paralytic ileus,
muscle weakness, confusion.
Q .Management of hyperkalemia ?
1. ABCDE , Shift in HDU , Continuous cardiac monitoring
2. Stop all K+ containing intravenous fluids, including Hartmann's
3. Ca. gluconate (10 ml of 10%) is given IV over 10 min( cardio protective )
4. Insulin(5-10 U) in 50 ml of 50% dextrose IV over 30 min( increases cell Uptake of K+)
5. Ca Resonium (15 g PO / 30 g PR) : Ion exchange resin therapy
6. Hemodialysis ( K + persistently high / severe acidosis pH <7.20)… also Bicarbonate
to correct acidosis.
Q. Functions of K in body ? Regulation of water,electrolytes in cell, nerve
conduction,muscle function, cell enzymatic activities, acid- base balance, heart
functions

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Q. High K : Drugs: ACEi, NSAIDS, excess IV FLUID, Renal failure,

Rhabomyolysis, Hypoaldosternoism , burn, crush injury, Addison disease, hypo
aldosteronism,hemolysis. ECG : Tall T, Wide QRS(sinusoidal) , Prolonged PR.
Symptoms : palpitations , muscle weakness
Q. Low K: Darrhoea, vomiting, fistula, conn/ Cushing , laxative, renal tubular
acidosis, Alkalosis, Insulin excess, diuretics, hypothermia ECG : U wave,inverted T ,
increased PR . Symptoms: weakness, abnormal heart rhythm( cardiac arrest) , leg
cramps, constipation
Q. Complication of AKI ? High K, acute pulmonary Edema
Q. Homeostasis of k+ ? Diet : the Western diet may contain 20–100 mmol of
potassium daily
Endocrine: 1. Aldosterone : stimulates Na. reabsorption in DCT and CD through an
active exchange with K , It promotes its excretion
2. Insulin : stimulates potassium uptake into cells, reducing the serum level
Renal: 1. Acid–base balance : potassium and H + are exchanged at the cell
membrane, producing reciprocal changes in concentration, e.g. acidosis leads to
hyperkalaemia, alkalosis lead to hypokalaemia. Also, renal reabsorption of one causes
excretion of the other .
2. Tubular fluid flow rate : increased flow promotes K secretion, one method by which
diuretics may cause hypokalaemia.
Q. What use does knowledge of the cardiac effects of potassium have for surgical
practice? K Rich cardioplegic solutions are used to arrest the heart in diastole to permit
cardiac surgery after established cardiopulmonary bypass.

Bloody diarrhea/Ishcemic Bowel

Stem : 55 yr / abdominal pain, bloody diarrhea(10 episodes) …stopped after 6 hrs.,
hypotensive,tachycardiac, feverish, adimitted , fluid resuscitation done? Labs: FBC :
Hb: 8.7 g( Low), platlets: 666000( High ) ,TLC :12000(High) , Na, K ( Both Low) , CRP
(High), Creat : 109 , Urea: 9
Q. Type of anemia ? Microcytic hypochromic anemia
Q. Do you think he has chronic or acute anaemia? Chronic? Why? MCHC
anaemia. NCNC in acute bleed
Q. Why platlets are elevated? Secondary to acute inflammation(Acute Phase
Reactants ) , Dehydration, Acute Bleeding .

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AXR : Dilatation of the ascending and transverse colon , with narrowing of the

descending colon : Thumbprinting sign ( radiographic sign of large bowel wall

thickening, usually caused by oedema, due to infective or inflammatory process, i.e.
colitis. The normal haustra become thickened at regular intervals appearing like
thumbprints projecting into the aerated lumen.)
Q. DD of bloody diarrhea ? UC/CD ( IBD) ,Ischaemic colitis ,Amoebic colitis, Bacillary
dysentery, Carcinoma colon, Infectious colitis (Clostridium difficile, Campylobacter
jejuni), Angiodysplasia, Diverticular disease.
Q. Why not to transfuse blood? State of sepsis ,Hb not below 7g ( no indication)
Q. Why low Na+ / K + ? Due to losses from diarrhea
Q. What Other Ix . ? ESR , CRP, CEA, Stool (analysis and culture) , Antiobodies for
( UC, Crhon's) ,Colonoscopy ( later stage) , Radionuclide scan
Q. How will U monitor the patient response? Clinically : fever and diarrhea settles
/Lab. : decrease ( CRP, TLC )
Q. Indications of urgent Sx ? Toxic megacolon/Fulminant attack refractory to medical
management, Bleeding ( Uncontrolled colonic ), Perforation (free or walled off) ,
Obstruction and stricture ( suspicion for cancer)
Q. What kind of Sx ? Pan-proctocolectomy with ileostomy.

Diverticular abscess + septic shock

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Stem: old lady ,critically ill, with LIF pain and tendeness
Q. What is D/D? diverticulitis, sigmoid volvulus , gastroentrits , acute constipation ,
pelvic tumour, uretric colic
Q. Interpret ABG: Metabolic acidosis with partial compensation , FBC : Increased TLC
Q. Define shock ? Shock is circulatory failure resulting in inadequate organ perfusion,
e.g. cannot meet the metabolic demands
Q. What kind of shock this patient having? Septic shock
Q. Define septic shock ? 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
Q. Basic principles of management of septic shock?
Circulatory support : to maintain the cardiac index and oxygen delivery to the
tissues(IV fluids, colloids and crystalloids 0.9% saline), Inotropes may be required to
increase SVR , Respiratory support (non-invasive or invasive ventilation -may be
required for ARDS and respiratory failure ), Renal support : to ensure that the urine
output is >0.5 ml/kg/h, Dopamine or a furosemide/ Replacement therapy , Cardiac
support helps maintain the renal perfusion pressure , Nutritional support : may be
enteral or parenteral. Enteral nutrition helps maintain mucosal integrity and reduce
bacterial translocation
Antimicrobials:empirical use of broad spectrum antibiotics and surveillance of
infection( early) , but in the latter stages, agents are targeted to grown microbiological
sensitivities from general, e.g. blood, and local sources
Q. CT confirmed presence of diverticular abscess, management options?
1.Open drainage: Advantages: proper drainage with peritoneal toilet - has the ability to
make a stoma if needed .
Disadvantages: liability of wound infection , high morbididty .
2.Image guided aspiration: Advantages:no wound infection - less hospital stay -
possbilty to leave peg-tail catheter for repeated drainage abd administration of
antibiotics , Disadvantages: less adequate drainage - does'' t have the ability to make a
stoma.

ABG / sepsis
Patient with abdominal pain post operative. Septic picture , Worried about
anastomotic leak .: Post-Anterior Resection POD4, Metabolic Acidosis, Fever,
Raised TLC, Renal Failure,Raised Respi Rate .

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Q. Describe UECR: Raised Urea, Creatinine, Hyperkalemia

Q.Causes of Acute Renal Failure in POD4 patient ? Abdominal Compartment

Syndrome

Q. Describe ABG: Compensated Metabolic Acidosis with Compensatory

Respiratory .

Q . Patient has oliguria post operativel . Reason for oliguria ?

pathophysiology, post IDC polyuria.

Q. HyperK+. Clinical relevance and management?

Q.. Patient with abdominal pain post operative Septic picture

Q.Interpret ABG results: metabolic acidosis with respiratory compensation.

Q. Explain every reading. including base excess and lactate. Reference

values provided. pH, buffer system?

Q. How would you manage patient ? .ABC, iv drip, iv abx, investigate for source
of infection (blood/urine cultures, CXR, review wound, abdo examination) shift to
HDU.

Intestinal Obstruction
Pt POD 5 post-ileostomy reversal with signs of sepsis: febrile, tachycardic. Also
noted to have a right UL patch on CXR. Dilated small bowel loops on AXR

Q.AXR shown: what is the diagnosis?

Q.What are the ddx for dilated SB loops on AXR? IO vs ileus

Q .How to differentiate them? Bowel sounds

Q. What are the possible causes for pt’s clinical presentation?

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Q. How to treat? What antibiotics to give?

Q. Why should not give cephalosporins? (apparently answer was because it

causes C. diff…)

Q.When would you opt for surgical management?

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