‫‪SURGERY‬‬

‫سبحان هللا‬

‫عن بريدة رضي هللا عنه قال‪ :‬قال النبي صلى هللا عليه وسلم‪َ (( :‬من ترك صالةَ العصر‪ ،‬فقد حبط عمله))؛ رواه البخاري والنسائي‪.‬‬

‫رواه البخاري ومسلم‬ ‫عن ابن عمر رضي هللا عنهما‪ ،‬عن النبي ِ صلى هللا عليه وسلم قال‪(( :‬الذي تَفوته صالة العَصر فكأنَّما وتر أهله وماله))؛‬

‫عن أنس بن مالك رضي هللا عنه قال‪ :‬قال رسول هللا صلى هللا عليه وسلم‪َ (( :‬من صلَّى هلل أربعين يوما في جماعة يدرك التكبيرةَ األولى‪ ،‬كتب‬
‫له براءتان‪ :‬براءة من النَّار‪ ،‬وبراءة من ال ِنفاق))؛ السلسلة الصحيحة‬

‫وقال محمد بن واسع‪" :‬ما أشتهي من الدنيا إال ثالثة‪ :‬أخا إن تعوجت قومني‪ ،‬وقوتا من الرزق عفوا من غير تَبِعة‪ ،‬وصالة في جماعة يرفع‬
‫عنِي سهوها ويكتب لي فضله"‬

‫صل على الحبيب‬

 Types of shock, hypovolemic shock, anaphylactic shock
Shock: is a pathophysiological condition that leads to inadequate tissue perfusion through the micro-
circulation with impaired cellular metabolism.
 Classification of shock
 Hypovolemic shock; diminished blood volume
 Cardiogenic shock; inefficient myocardial function
 Neurogenic shock; peripheral pooling of blood
 Anaphylactic shock; antigen antibody reaction
 Septic shock; severe infection
 Endocrine shock; acute deficiency of corticosteroid

Hypovolemic Shock
 Etiology:
• Blood loss as in internal or external hemorrhage
• Plasma loss as in burns and peritonitis
• Fluid loss as in severe vomiting, diarrhea or dehydration
 Compensatory mechanisms of hypovolemia
 The physiological response to hemorrhage has two aims:
1. Stopping the bleeding by immediate vasoconstriction & clot formation.
2. Maintaining effective circulatory volume and perfusion of critical tissues (brain & heart), this
achieved by neural & endocrine factors.
 factors (rapid): stimulation of sympathetic system
 Stimulus: drop blood pressure, decreased venous return
 Receptors: arterial baroreceptors, atrial stretch receptors
 Response: stimulation of sympathetic system
 Effects:
• constriction of veins, that displacing blood from the capacitance side of the circulation into the heart
• Constriction of arterioles raises the peripheral resistance
• Increased rate & strength of cardiac contraction
 Endocrine factors (delayed);
 Catecholamine; released from adrenal medulla & nerve endings, they increase the heart rate &
myocardial contraction, and cause vasoconstriction at skin, kidney, viscera
 Metabolic hormones; ACTH, cortisol, growth hormone, glucagon are increased; that leads to
hyperglycemia, increase extracellular fluid osmolality that lead to withdraws water from the
intracellular fluid
 Renin-angiotensin aldosterone system; renin secreted in response to renal hypo perfusion that
convert angiotensinogen into angiotensin I which converted into angiotensin II in lung;
 • Actions of angiotensin II: powerful vasoconstrictor, stimulates sodium & water retention by release
of aldosterone
 Vasopressin (ADH); stimulate water retention from kidney

 Clinical picture: the manifestations correlate with the amount of hemorrhage on one hand and the
cardiovascular reserve on the other hand
 Symptoms: weakness, fainting, the patient feels cold & thirsty
 Signs: the patient looks anxious to drowsy
 Pulse & blood pressure;
• Mild blood loss (less than 500ml); remain normal
• Loss (500 – 1500ml) rapid weak pulse but stable blood pressure
• Loss (more than 1500ml) tachycardia & hypotension
 Pulse pressure; decreases (thready pulse)
 Respiratory rate; tachypnea and air hunger
 Temperature; hypothermia
 Skin; pale, cold, clammy (sweat secretion) & vasoconstriction
 Oliguria; diminished renal perfusion, release of ADH
 Monitoring the severely shocked patient:
 Clinical parameters; pulse, Bl pressure, RR, temp, capillary refill
 A Foley’s catheter insertion; check urinary output (n; 1-2ml/kg/hr)
 Central venous pressure (CVP); roughly corresponds to blood volume (high indicates overtransfusion,
low indicate hypovolemia)
 Pulmonary artery wedge pressure (PAWP); measured by Swan-Ganz catheter inserted into a small
branch of pulmonary artery
 ECG
 Temperature; difference between the peripheral & core temperature may assess cardiac output &
peripheral perfusion
 Peripheral temp measured by sensor at big toe, while core temp by probe placed in rectum or
esophagus
 Blood gases; Po2 (n; 80-100mmHg), PCO2 (n; 35-45mmHg)
 Serial detection of hemotocrit in cases of bleeding
 Treatment of hypovolemic Shock
Anti-Shock measures & Treatment of the cause
Anti-Shock Measures
 Stop hemorrhage;
 Packing
 Pressure is applied manually
 Elevation of the leg above the level of the heart stop venous bleeding & decrease arterial bleeding
 Supporting devices; pneumatic anti-shock garment which can tamponade lower limb, pelvis,
abdominal bleeding. Balloon tamponade to compress bleeding esophagel V
 Maintain air way & oxygenation
 Analgesia; to relief pain & anxiety, to improve blood flow to brain
 Positioning of the patient; recumbent position with moderate elevation of lower limbs
 Temperature; keep the patient comfortably warm
 Start intra-venous fluid resuscitation;
 2 large bore cannulas or do venous cut-down
 A blood sample is withdrawn for cross-matching
 Regimen; rapid infusion of lactated Ringer’s solution started immediately. Then blood transfusion
may indicate Alternative to blood transfusion; human plasma, Dextran, artificial blood substitutes
 Pharmacological support;
 Inotropic drugs; Dopamine in myocardial insufficiency
 Vasodilator drugs; given when blood volume & CVP has been restored to normal; to reduce
afterload, increase cardiac output & decrease myocardial work
 Steroids
 Irreversible Shock
Def: hypovolemic shock becomes refractory to the ant-shock therapy with severe central nervous system &
cardiac dysfunction
Causes:
 Inadequate volume replacement
 Multisystem trauma with occult injuries as cardiac tamponade or hemopneumothorax
 Acute myocardial insufficiency either from direct cardiac injury or secondary to prolonged coronary
hypoperfusion

Anaphylactic Shock
Etiology: it follows administration of an antigens like; antibiotics, anesthetics, sera, dextran
 The antigen unites with antibodies leading to release of large amount of histamine resulting in
capillary paralysis with pooling of blood in the capillary bed
Clinical picture:
 Bronchospasm, laryngeal edema, respiratory distress
 Hypotension with massive vasodilatation
Treatment:
 Intravenous crystalloid infusion
 Antihistaminic
 Endotracheal intubation may be needed
Quiz

 Define shock
 Enumerate types of shock
 Recognize etiology of hypovolemic shock
 Outline compensatory mechanisms of hypovolemia
 Describe neural and endocrine factors compensate hypovolemia
 Describe changes in vital signs & skin in case of hypovolemic shock
 Why oliguria occur in hypovolemic shock?
 Describe changes in pulse & blood pressure in different stages of hemorrhagic shock
 How to monitor the patient with severe hypovolemic shock?
 First aid management of patient with hypovolemic shock
 Outline replacement therapy in patient with hypovolemic shock
 Drug therapy in case of hypovolemia
 Define irreversible shock
 Enumerate causes of irreversible shock
 Define anaphylactic shock
 Describe clinical presentation of anaphylactic shock & how to manage?
 Septic Shock
Etiology: due to serious infection by Gram-negative & anaerobic organisms and less common Gram-positive
organisms
Predisposing factors:
 Extreme of age
 Diabetes, malnutrition, malignancy, uremia
 Patient under corticosteroid or immunosuppressive
drugs
Common causes: the sources of Gram-negative bacteria
 Genitourinary system
 Respiratory system
 Alimentary & biliary tracts
Pathophysiology
The septic shock is the end result of interaction between endogenous & exogenous mediators and host
responses that leads to poor perfusion of vital organs combined with vasodilatation in other vascular beds
and low peripheral resistance
Endotoxin; is a cell wall extracts from killed bacteria, usually Gram-negative
 The effect of endotoxin on macrophages release cytokines that cause the following:
1- Adherence of platelets & leucocytes to the vascular endothelium which leads to:
 Microvascular occlusion; hypoxic tissue damage
 Local release of toxic concentrations of growth factors, cytokines, free oxygen radicals
2- Damage of the barrier function of the intestinal mucosa allowing the intestinal pathogens into the
circulation
3- Stimulation of excessive production of nitric oxide by the vascular endothelium leading to decreased
peripheral resistance
Cytokines
 They are a broad category of small proteins (polypeptides) important in cell signaling.
 They include chemokines,
interferons, interleukins,
lymphokines, and tumour necrosis
factors, but generally not hormones
or growth factors.
 Cytokines are produced by a broad
range of cells, including immune cells
like macrophages, B lymphocytes, T
lymphocytes and mast cells, as well
as endothelial cells, fibroblasts, and
various stromal cells.
 They are different from hormones,
which are also important cell
signaling molecules. Hormones circulate in higher concentrations, and tend to be made by specific kinds
of cells.
 Cytokines are important in health and disease, specifically in host immune responses to infection,
inflammation, trauma, sepsis, cancer, and reproduction.
Clinical picture; the patient presented with either:
Hyperdynamic early (warm) stage;
 Skin; warm, dry
 Vital signs; fever above 38 C, chills, hypotension, tachycardia
 Cardiac output is normal or increased
Prompt treatment at this stage can lead to survival
Hypodynamic late (cold) stage;
 Skin; cold, clammy Severe sepsis & gangrene
 Vital signs; hypothermia, hypotension, tachycardia, tachypnea
 Cardiac output is decreased
 Multiple organ failure; cardiac depression, pulmonary edema, renal failure
Efficient treatment can convert the patient to the hyperdynamic stage
Prognosis
Mortality rate of a septicemic patient is above 30%, the mortality arise above 80% with multiple organ
failure
Treatment
1- The most important line of treatment is source of sepsis e.g. amputation of a severely infected limb
2- Antibiotics:
 Start with multiple & broad spectrum antibiotic – especially against Gram-negative bacteria - without
waiting the result of culture and sensitivity
 May start with a combination of 3rd generation cephalosporin, aminoglycoside & metronidazole
3- Correction of pre-existing fluid deficits (3rd space fluid loss), Ringer’s lactate, saline, may packed RBCs
4- Respiratory distress (ARDS); oxygen mask, may endotracheal intubation & mechanical ventilation
5- Inotropic drugs as dopamine or dobutamine and vasopressors as norepinephrine can be used in the
patient with persistent hypotension inspite of active measures of treatment
not: Steroids are not indicated in treatment of septic shock

Neurogenic Shock
Definition: paralysis of vasomoter fibers result in peripheral pooling of blood and inadequate venous return
Etiology;
 Vasovagal attack; due to hearing bad news, seeing an unpleasant event, or follow severe painful stimuli
as a blow to the testis or larynx.
 Mechanism; excessive VD in the splanchnic area, a temporary loss of venous return and sudden fall
in blood pressure, & blood supply to vital organs. Excessive vagal stimulation of the heart which
cause bradycardia
 Spinal shock; sudden extreme VD in patient with a high transection of the spinal cord due to spine
fracture, or following spinal anethesia
Clinical picture;
 Hypotension, normal pulse or bradycardia, warm dry skin
Treatment;
 Position; lie flat, elevation of the legs helps to increase venous return
 Intravenous crystalloid infusion as saline & Ringer’s lactate
 Vasopressors & corticosteroids may indicated
Quiz

 Recognize etiology of septic shock

 Enumerate the predisposing factors of septic shock
 Outline pathophysiology of septic shock
 Describe clinical picture of septic shock
 Describe changes in vital signs & skin in case of septic shock
 Differentiate between early and late stages of septic shock
 How to monitor the patient with septic shock?
 Describe the treatment of patient presented with septic shock
 Define cytokines & their rule in pathogenesis of septic shock
 Define neurogenic shock
 Describe etiology of neurogenic shock
 Describe clinical presentation of neurogenic shock & how to manage?
 wound
Definition of wound: A breach in a body surface as the skin or mucous membrane, thus exposing deeper tissues
Types of wounds:

A) Closed wounds B) Open wounds

1- Abrasions 1- Incised wounds

2- Contusions 2- Lacerated wounds
3- Hematoma 3- Crushed wounds
4- Penetrating wounds
5- Missile injuries

Abrasions Contusions

Clean incised wound Lacerated wound

Crushed wound
 Mechanism of wound healing

There are 3 phases

1- Lag phase (2-3 days): initial vasoconstriction, then vasodilatation & increased capillary permeability, exudation of
red &white blood cells & plasma, clot is formed with fibrin network over the wound

2- Proliferative phase (3 weeks): fibroblast migration & capillary ingrowth, collagen synthesis, wound contraction

3- Maturation phase (up to 6 months): scar tissue formation, remolding, tensile strength

 Healing of epithelial surface: at 24 hours, basal cells of the epidermis start to undergo hypertrophy & mitosis to
close the epithelial defect

 Factors affecting wound healing

General Factors
1- Age; healing is slow in elderly due to a reduced protein turnover
2- Nutritional state:
• Protein deficiency; diminished collagen & ground substance synthesis
• Vit C deficiency; lack of maturation of protocollagen
• Vit A deficiency; deficient epithelialization
• Calcium, zinc, copper, manganese also affect healing
3- Pre-existing long illness; as uremia, cirrhosis, diabetes, malignancy; delay healing
4- Drug intake; steroid affect formation of fibroblast, long standing antibiotic impair healing
5- Irradiation; inhibit granulation tissue formation due to ischemia that result from end arteritis oblitrans

Local Factors
1- Vascularity; a good blood supply (e.g. face & scalp) leads to rapid healing
2- Immobilization; movement and shearing forces damage the blood supply of granulation tissue
3- Tension:
• Increased tension in the wound leads to ischemia & impaired healing
• Suture under tension, hematoma, infection increase the tension in the wound
4- Infection; impaired healing
• Fibroblast compete with bacteria for oxygen & nutrition
• Bacteria secrete collagenolytic enzymes
5- Foreign bodies; & necrotic tissue impair healing
6- Adhesion of wound to a bony surface prevent wound contraction e.g. wounds over shin of tibia
 Types of wound healing
1- Healing by primary intention; (healing of clean surgical wounds which are well coapted)
Little amount of granulation tissue, fibrosis is minimal. This result in a fine linear scar
2- Healing by secondary intention; (healing of a septic wounds or with tissue loss, preventing approximation of edges)
Excessive amount of granulation tissue & fibrosis. This result in a weak ugly scar & deformity
3- Healing by tertiary intention: wounds which are potentially contaminated are left open for about 5 days; then if
there is no signs of infection, delayed primary sutures can be performed to obtain a fine linear scar similar to that of
primary intention
Complications of wounds

General:
1- Shock; neurogenic, hypovolemic, septic

2- Crush syndrome;

Causes; major trauma causing crushing of muscles

Pathology;

• Myoglobulin enter the circulation & acute renal tubular necrosis results

• Hyperkalemia may result in heart failure

• The crush muscle swells within unyielding compartmental fascia, result in increased compartmental pressure
(compartmental syndrome), impending circulation & increasing extent of ischemic damage

• The limb feels tense & pain is severe

Treatment:

• Early cases; first aid treatment, alkalinize the urine by IV sodium bicarbonate, flush the kidney with manitol IV
drip, fasciotomy to relieve tension

• Late cases; amputation & renal dialysis

Local:
1- Infection
2- Gangrene; infective, vascular
3- Injury of important structure
4- Wound dehiscence
5- Complications of scars; keloid & hypertrophic scar, deformity, malignant changes
6- Hypothesia
7- hematoma & seroma
 Wound infection

 Hypertrophic scar

 Keloid

Quiz

Define wound

Enumerate phases of wound healing

Enumerate general factors affecting wound healing

How protein, Vit C, Vit A deficiency affect wound healing?

How corticosteroid affect wound healing?

How irradiation impair wound healing?

Enumerate local factors affecting wound healing

How infection affect wound healing?

How tension affect wound healing?

Describe types of wound healing

Define healing by tertiary intention

Compare between healing by primary & secondary intention as regard shape of scar

Define crush syndrome, its pathology & treatment

Enumerate local complications of wounds

 Salivary Gland Disorders; Anatomy, Inflammation, Tumors

Introduction
 The salivary glands are exocrine glands that
produce saliva through a system of ducts.
Humans have three paired major salivary
glands (parotid, submandibular, and
sublingual), as well as hundreds of minor
salivary glands in oral cavity. Salivary glands
can be classified as serous, mucous, or
seromucous (mixed).
 In serous secretions, the main type of
protein secreted is alpha-amylase, an
enzyme that breaks down starch into
maltose and glucose, whereas in mucous secretions, the main protein secreted is mucin, which acts as a
lubricant.
 In humans, 1200 to 1500 ml of saliva are produced every day. The secretion of saliva (salivation) is
mediated by parasympathetic stimulation

Parotid Gland
 The two parotid glands are major
salivary glands wrapped around the
mandibular ramus. These are largest of
the salivary glands, secreting saliva to
facilitate mastication and swallowing,
and amylase to begin the digestion of
starches. It is the serous type of gland
which secretes alpha-amylase. It enters
the oral cavity via the parotid duct.

Submandibular gland
 The submandibular glands are a pair of major salivary glands located beneath the lower jaws. The
secretion produced is a mixture of both serous fluid and mucus, and enters the oral cavity via the
submandibular duct or Wharton duct. Around 70% of saliva in the oral cavity is produced by the
submandibular glands, though they are much smaller than the parotid glands.
Sublingual gland
 The sublingual glands are a pair of major salivary glands located inferior to the tongue. The secretion
produced is mainly mucous in nature, but it is categorized as a mixed gland. Saliva exits directly from
8-20 excretory ducts. 5% of saliva entering the oral cavity comes from these glands.
Non-neoplastic salivary gland disorders
This term includes;
 Congenital disorders
 Infections
 Salivary stones
 Salivary fistula
 Degenerative diseases
 Autoimmune salivary disorders
 Drug-induced, endocrine, metabolic salivary gland enlargement
Infections
Acute bacterial sialadenitis:
Predisposing factors; poor oral hygiene, obstruction of the duct by a stone
Organism; commonest is staphylococcus aureus
Clinically; pain, swelling. Pain is severe because the glands are enclosed in tough fascia, and so the
formation of an abscess does not produce fluctuation
A stone sometimes be felt in the duct
Treatment; antibiotic as clindamycin, analgesics & antipyretics, hot packs
Indications of surgery; Failure of 48 hours conservative treatment & evidence of abscess formation
Recurrent subacute & chronic sialadenitis
Predisposing factors; an abnormality in the salivary gland as sialectasia, stones, autoimmune diseases
Clinically; common in submandibular gland; recurrent pain, swelling that increases in size during eating
Swelling is solitary and cannot be rolled over the edge of the mandible (D. D of submandibular lymph nodes)
Inspection of the floor of the mouth may reveal redness of the duct orifice
Treatment; Usually surgery (sialadenectomy)
Viral parotitis
Mumps, commonest cause of salivary gland swelling
Clinically; bilateral painful parotid swelling with fever in a child.
The disease is self-limiting
TB & sarcoidosis; are rare, they usually affect the parotid lymph nodes rather than the glandular stroma
Salivary stones
Predisposing factors; infection (chronic & recurrent), stasis as in cases of Sjogren’s syndrome
Incidence; submandibular-parotid = 50-1, due to viscous saliva of submandibular gland & its duct ascends
upward & opening lies in floor of mouth
Clinically; the stones either in the gland or the duct. Recurrent pain & swelling in submandibular triangle
which increase during eating. May cause acute or recurrent attaches of sialadenitis
Investigations; plain X-ray, sialography
Treatment; surgery;
 Ductal stone; meatotomy
 Within the gland (sialadenectomy)
Salivary fistula
Etiology; trauma to the gland or duct, less commonly it complicates surgery on the gland
Investigations; sialography to exclude distal duct obstruction by stones or stricture
Treatment;
 A fistula arising from gland substance usually heals spontaneously, but one arises from duct is
unlikely to heal because of the high rate of flow and need surgery either repair of duct or excision of
gland

Stones Fistula

Autoimmune salivary diseases

Mikulicz’s disease; consists of enlargement of salivary & lacrimal glands, and dryness of mouth
Sjogren’s disease; there are two types
• Primary; dryness of mouth, dryness of eye, & widespread exocrine glands dysfunction and no
connective tissue affection
• Secondary; dryness of mouth, dryness of eye, connective tissue affection as rheumatoid arthritis,
systemic lupus, …….
• Etiology; unknown, but may due to cytomegalovirus.
• Patients with Sjogren’s disease are 44 times prone to develop lymphoma
• Investigations; sialography, antinuclear antibodies, protein electrophoreseis
Benign lymphoepithelial lesion; uncommon disease characterized by progressive lymphocytic infiltration
and diffuse enlargement of salivary glands
Salivary tumors
 The majority of salivary gland tumors are benign (85%)
 5% of head & neck tumors
 Parotid 75%, submandibular 10%, sublingual o.3 %, minor salivary glands 15%
 Pleomorphic adenoma is the commonest
classification

Benign tumors
Pleomorphic adenoma
 The most common salivary tumors, 75% of parotid tumors, 50% of submad
 Main age 42 years
 Microscopically; epithelial sheets and duct like structures are interspersed by mucoid material. There
is incomplete capsule, so enuculation of the tumor carries a high rate of recurrence
Wartin’s tumor (adenolymphoma)
 Site; lower part of parotid gland, bilateral in 10% of cases
 Age; 60 years
 Microscopically; epithelial lined spaces filled with creamy materials, and surrounded by lymphoid
tissue
Malignant tumors
Mucoepidermoid carcinoma
 The most common malignant tumors, usually affect parotid
 Origin; duct epithelium
 Microscopically; is a variant of adenocarcinoma, there are three grades; low, intermediate & high
grades
Adenoid cystic carcinoma
 Site; the commonest malignant tumor affecting minor salivary glands
 Slow rate of growth
 Perineural spread; infiltrate for a long distance in the perineural tissues of adjacent nerves, so the
tumor is likely to be incompletely removed, and hence it has a high recurrence rate
Clinical picture
Benign tumors
 Symptoms; painless slowly growing mass at the side of face
 Signs; localized swelling usually in the parotid, non tender, firm, smooth or bosselated surface.
Adenolymphoma feel soft or cystic. No facial nerve infiltration
 Tumors arising from deep part of parotid may bulge in the oropharynx behind the tonsil
Malignant tumors
 Symptoms; rapidly enlarging swelling on the side of face, sometimes painful, the pain may radiate to
the ear and increased by mastication
 Signs; mass; usually worm, mildly tender, firm or hard, irregular surface, usually adherent to skin or
masseter or mandible, may infiltrate facial nerve (weakness or paralysis of facial muscles)
 Cervical lymph nodes; may enlarged, firm or hard
D. D
Extra-parotid swellings
 Lymph nodes, seb cyst, lipomas
 Mandibular, maxillary & inferatemporal tumors
 Hypertrophy of the masseter muscle; is usually bilateral
True parotid enlargement; caused by non neoplastic salivary gland diseases; the gland is diffusely enlarged
with no definite lump
Investigations
In general; a pathological diagnosis is not a necessity for tumors that behave in a benign way, but is
essential before operating on tumors that are clinically malignant
 Biopsy; FNAC (parotid or submand), punch biopsy (tumors of minor salivary gland in the oral cavity)
 CT scan or MRI
Treatment
 Surgery is the only reliable form of treatment
 The patient should be warned against the possibility of accidental facial nerve injury or concussion
(weakness & neuropraxia)
Benign Tumors
 The tumor is excised with safety margin, no place for enucleation guard against recurrence
 Superficial parotidectomy (tumor of superficial part), total conservative parotidectomy (tumor of
deep part)
 Submandibular sialadenectomy
 Simple excision with safety margin; for minor salivary gland tumors
 In the cases of accidental facial nerve injury; immediate repair by microsurgical techniques either by
direct suturing, or nerve graft taken from the great auricular nerve
Treatment
 Surgery is the only reliable form of treatment
 The patient should be warned against the possibility of accidental facial nerve injury or concussion
(weakness & neuropraxia)
Malignant Tumors
 If the pathological diagnosis has not been obtained prior to the operation, frozen section is helpful
 The standard treatment is radical excision; which entails wide surgical clearance with cervical lymph
nodes if they are enlarged
 Parotid; excise or scarify the facial nerve, and probably may excise a part of masseter or the
mandible
 Post-operative adjuvant radiotherapy for high grade tumors

Quiz

 Enumerate 4 types of salivary glands

 Enumerate structures passes through the parotid gland

 Describe acute bacterial sialadenitis

 Describe recurrent subacute or chronic sialadenitis

 Describe salivary gland stones

 Describe parotid gland fistula

 Identify Sjogren’s disease

 Classify salivary gland tumors

 Identify the incidence of salivary gland tumors

 Recognize pleomorphic adenoma, adenolymphoma, mucoepidermoid carcinoma, adenoid cystic carcinoma

 Describe the clinical presentation of salivary gland tumors

 Differentiate parotid and submandibular region swellings

 How to investigate a case of salivary gland diseases?

 Outline the treatment of salivary gland tumors

 How to manage an accidental injury of facial nerve during surgery on parotid gland?
 Tongue Ulcers, Tumors of the Tongue and Lip, Ranula

Tongue Ulcers
A localized defects or erosions in
the tongue mucosa, in which the
covering epithelium is destroyed
leaving an inflamed area of
exposed connective tissue.
Classifications;
1- Traumatic ulcers
Dental ulcers; due to repeated
trauma by a broken tooth or ill
fitted denture
 Site; side of the tongue near the affected tooth
 Clinically; acute cases (painful ulcer with painful enlarged drainage lymph nodes),
chronic cases (raised edge, indurated base, biopsy is needed to exclude malignancy)
 Treatment; removal of the offending cause, and the use of an antiseptic mouth wash
Post pertussis ulcer; due to repeated trauma of fully protruded tongue during bouts of
severe cough
Physical or chemical ulcers; due to exposure to hot or cold objects or chemicals
2- Inflammatory ulcers
Acute ulcers;
 Dyspeptic ulcer (aphthus); its etiology is not exactly known. There are multiple, small,
painful ulcers. Treated by antiseptic mouth wash and anesthetic jell
 Lichen planus; supposed to be due to autoimmune mechanisms, it affect the skin and
oral mucosa
 Herpetic ulcer; painless, multiple, small ulcers in children
Chronic ulcer;
 TB; multiple ulcers occur at the sides and tip of the tongue, they are small, shallow,
oval, very painful with undermined edge, enlarged submandibular lymph nodes.
Treated by anti TB therapy, oral hygiene, anesthetic jell
 Syphilis; snail track ulcer or gummatous ulcer
 Ulcers due to chronic superficial glossitis
3- Malignant ulcer
 Usually squamous cell carcinoma
Tumors of the Tongue
Benign tumors;
 Papilloma; sessile or pedunculated
 Fibro-epithelial polyps
 Hemangioma & lymphangioma
 Plexiform neuroma & neurofibroma
 Granular cell myoblastoma; firm mass with overlying hyperkeratosis
 Juvenile fibroma
Malignant tumors;
 Squamous cell carcinoma (commonest)
 Basal cell carcinoma (rare)
 Adenocarcinoma (from minor salivary glands)
 Carcinoma of the Tongue
Incidence & etiology;
 Anterior 2/3, affect more males
 Posterior 1/3 equal in both sexes.
 Age over 60 years.
 More in India; due to tobacco chewer & high consumption of spices
Predisposing factors;
 Smoking, sepsis, spices, spirits, sharp teeth, clay pipe, bad oral hygiene
 Precancerous lesions;
o Chronic mucosal atrophy
o Chronic superficial glossitis
o Chronic dental ulcers
o Syphilitic, leukoplakia and erythroplakia
o Papilloma
Pathology;
 Squamous cell carcinoma (90%) of malignant lesions
Site; lateral edge of tongue (47-55%), tip of tongue (2-4%), dorsum of tongue (6%), posterior
1/3 (20%)
Naked eye appearance;
 Malignant ulcer; deep irregular, raised nodular everted edge, hard indurated base
 Raised oval plaque
 Hard submucosal nodule
 Deep indurated fissure
 Diffuse infiltrating tumor (wooden base)
Microscopic appearance; usually squamous cell carcinoma with variable degree of
differentiation
Staging (TNM);
T
Tis carcinoma in situ
T1 < 2.0 cm
T2 2.1 – 4.0 cm
T3 4.1 – 6.0 cm
T4 > 6.1 cm or invading adjacent structures
N
N0 No regional adenopathy
N1 Ipsilateral adenopathy
N2 single Ipsilateral node node 3-6 cm or multiple Ipsilateral nodes < 6.0 cm
N3 Massive Ipsilateral or contralateral nodes
M
M0 No evidence of Metastases
M1 Metastases beyond the cervical lymph nodes
Mx Metastases not assessed
Spread;
 Direct spread; to nearby structures
 Lymphatic spread; it disseminated early to lymph nodes of the neck;
o Tip; to sudmental then to both submandibular and upper deep cervical nodes on both
sides
o Anterior two third; lateral third to ipsilateral submandibular and to upper deep
cervical nodes. Those near the midline disseminate bilaterally
o Posterior third; directly to the upper deep cervical nodes
 Blood spread; more likely for tumors of posterior third
Clinical presentation;
 Early; may be symptomless, patient may complain of a persistent ulcer
 Late;
o Pain; first due to infection, later due to infiltration of lingual nerve, referred to the ear
o Salivation; due to pain and restricted tongue movement
o Inability to articulate clearly
o Secondaries in the neck
Complications;
o Inhalation of necrotic tissues, leading to bronchopneumonia
o Cancer cachexia and starvation, due to pain and dysphagia
o Hemorrhage from erosion of lingual artery
Investigations;
o Biopsy from the edge of the ulcer
o FNAC from suspected cervical lymph nodes
o CT of the neck and mandible
Treatment;
 Surgery & Radiotherapy are the main lines of treatment
 Chemotherapy is used as an adjuvant therapy in some cases
Surgery
Indications; early (Tis, T1, T2), incomplete regression by radiotherapy, recurrence after
radiotherapy, cancer on top of precancerous lesions, cancer infiltrating the bone
Procedures;
 Carcinoma in situ; excision with 1cm safety margin
 Carcinoma of anterior two third; excision with 1.5 cm safety margin (partial, hemi, or
near total glossectomy), then reconstruction by flaps
 Carcinoma of the posterior third; either by total glossectomy or radiotherapy
 Lymph node affection; complete neck dissection
 If the mandible is affected; excised together with the tongue and the affected lymph
nodes (Com ando operation)
Radiotherapy
T1 and T2 (less than 4 cm) may equally benefit from surgery or radiotherapy
Advantage; avoid the disfiguring side effects of surgery
Disadvantage; mucositis, dysphagia, osteoradionecrosis
Methods;
 Caseum or iridium needles
 External beam radiotherapy
Prognosis (prognostic factors)
1- Lymph node involvement is the most important
2- TNM
3- The degree of tumor differentiation
4- Extension of the tumor posteriorly to the oropharynx
 Carcinoma of the Lip
Etiology;
• Chronic irritation; chronic ulcer, irradiation, leukoplakia, sepsis, spirits, smoking pipe,
spices
• Benign tumors; papilloma
Pathology;
Site; lower lip at the junction of the middle & outer third
Naked eye picture;
• Malignant ulcer (commonest)
• Malignant nodule
• Diffuse infiltrating type (woody lip)
• Malignant fissure
Microscopically; squamous cell carcinoma
Spread;
• Direct; in the substance of the lip, check, gum, mandible
• Lymphatic; is late and slow, to submental, submandibular, upper deep cervical
• Blood; extremely late & rare
Clinical picture;
• Age & sex; common in elderly male
• Rapidly growing ulcer having the characters of malignant ulcers
• Examine for fixity & local infiltration
• Examine for lymph node involvement
Complications;
• Hemorrhage
• Infection
• Dysarthria & dysphagia
• Upper respiratory tract infection
Investigations; biopsy
Treatment;
• Surgery; for (small lesion, bone infiltration, recurrent ulcer, or resistant to
radiotherapy), excision of the tumor with 1.5 cm safety margin & plastic
reconstruction
• Radiotherapy; radium needle
• Lymph nodes; no lymph nodes (no surgery), if palpable (suprahyoid block dissection is
sufficient). Total block neck dissection if upper deep cervical lymph nodes are affected
 Ranula
Definition; is a retention cyst arising from a sublingual salivary gland
Clinical picture;
• A translucent, bluish, cystic swellings on one side of
midline of the floor of the mouth
• It may extend behind the posterior margin of mylohyoid
muscle, hence it will appear in the neck (known as
Plunging or Thomson’s ranula)
Treatment;
• Partial excision of the roof, the edges of which are sutured to mucosal lining of the
floor of the m outh (marsupialization)

Quiz
 Enumerate anatomical parts of the tongue
 Classify types of tongue ulcers
 Describe dental ulcer of the tongue
 Define aphthus ulcer
 Enumerate benign tumors of the tongue
 Mention the commonest malignant tumor of the tongue
 Enumerate the predisposing factors of the carcinoma of the tongue
 Recognize the site incidence of the carcinoma of the tongue
 Describe naked eye picture of the carcinoma of the tongue
 Describe the spread of carcinoma of the tongue
 Describe the clinical presentation of carcinoma of the tongue
 Outline the treatment of carcinoma of the tongue
 Mention the commonest site of lip cancer
 Describe naked eye picture of lip cancer
 Enumerate complications of lip cancer
 Outline the treatment of lip cancer
 Define ranula, its presentation, & treatment
 Trauma; Basic and Advanced Life support

trauma
Incidence;
• Is the leading cause of mortality & disability during the first 4 decades of life
• Is the third most common cause of death overall
Types of injuries;
• Penetrating injuries; caused by knives, glass, …. The injury is usually focused over a
small area.
• High velocity injuries; shock waves spread out from the main missile tract and affect
areas far from the primary missile tract.
• Blunt injuries; as a result of direct blows, fall from a height, road traffic accidents
(RTA)
• A person inside a moving car
acquires the same velocity of the
car, if the car stops suddenly, the
person will continue moving
forwards and if he is wearing the
seat belt, the head will strike against
the car. Also the seat belt may cause
damage of small intestine,
mesentery, stomach, duodenum or major intra-abdominal vessels
Triage
Is the process of determining the priority of patients' treatments by the severity of their
condition or likelihood of recovery with and without treatment.
Simple triage is usually used in a scene of an accident or "mass-casualty incident" (MCI), in
order to sort patients into those who need critical attention and immediate transport to the
hospital and those with less serious injuries.
Advanced triage, specially trained doctors, nurses and paramedics may decide that some
seriously injured people should not receive advanced care because they are unlikely to
survive. It is used to divert resources away from patients with little chance of survival in
order to increase the chances for others with higher likelihoods.
Triage Scale

Trauma Courses
First Aid Course (FAC) ------(Pre-Hospital)
Basic Trauma Life Support (BTLS)-----------(Pre-Hospital)
Advanced Trauma Life Support (ATLS)-------------------(Hospital)
Basic Trauma Life Support
This course focuses on Pre Hospital Trauma care.
After your basic First Aid Course, BTLS Course will give you more skills and Knowledge
needed to save lives.
Pre-Hospital care;
Airway; check patent airway, support the mandible forwards & suck secretions in the
mouth. If necessary insert oropharyngeal airway.
Control of external bleeding
Precautions during transfer; care should be taken to avoid flexion of the spine, if the cervical
spine injury is suspected, a rigid cervical coller is applied
Advanced Trauma Life Support
(ATLS) is a training program for medical providers in the management of acute trauma cases.
1) Primary survey
• Airway maintenance with cervical spine protection
• Breathing and ventilation
• Circulation with bleeding control
• Disability/Neurologic assessment
• Exposure and environmental control
2) Secondary survey
3) Tertiary survey
Primary Survey (ABCDE) Secondary Survey
During this survey, life-threatening injuries are identified and simultaneously It begin when the
treated. primary survey is
Cervical spine stabilization is the first step, after that follow ABCD. The first completed,
stage of the primary survey is to assess the airway. resuscitation efforts
Airway maintenance with cervical spine protection are well established,
If the patient is able to talk, the airway is likely to be clear. If the patient is and the vital signs
unconscious, patient may not be able to maintain own airway; are normalizing.
• Place the patient on his side and lower the head slightly. The secondary
• Insert an oropharyngeal airway survey is a head-to-
• Suck any secretions or blood in the mouth toe evaluation of the
• Deeply comatosed patient, insert a cuffed endotracheal tube. trauma patient
• Tracheostomy or cricothyroidotomy; rarely needed including;
Breathing and ventilation • Complete
The chest must be examined by inspection, palpation, percussion and history and
auscultation. Subcutaneous emphysema and tracheal deviation must be physical
identified if present. The aim is to identify and manage six life-threatening examination,
thoracic conditions as Airway Obstruction, Tension Pneumothorax, Massive including the
Haemothorax, Open Pneumothorax, Flail chest segment with Pulmonary reassessment
Contusion and Cardiac Tamponade. of all vital
Open chest wound with open pneumothorax should be sealed with an adhesive signs. Each
bandage. region of the
Tension pneumothorax should be decompressed by inserting a needle in the body must be
second intercostal space anteriorly, an urgent chest tube insertion should follow fully
Circulation with bleeding control examined.
Control of hemorrhage & treatment of shock • Monitoring
Hge is the predominant cause of preventable post-injury deaths and is controlled by • Investigations
direct pressure (best) or tourniquet (not recommended except for limited period). according; as
Hypovolemic shock is caused by significant blood loss.
CBC, blood
• Insertion of two large-bore intravenous lines and start crystalloid solution
grouping, X-
infusion or colloids.
• If the person does not respond to this, type-specific blood, or O-negative if this rays, blood
is not available, should be given. urea &
• Occult blood loss may be into the chest, abdomen, pelvis or from the long creatinine,
bones. electrolytes.
Disability/Neurologic assessment • If at any time
• During the primary survey a basic neurological assessment is made, during the
(alertness, verbal stimuli response, painful stimuli response, or secondary
unresponsive). This establishes the patient's level of consciousness, pupil survey the
size and reaction, lateralizing signs, and spinal cord injury level. A more patient
detailed neurological evaluation is performed in the secondary survey. deteriorates,
• Sprint any fracture to relieve the pain and to avoid further trauma to soft another
tissues primary
• Any compound fracture should be covered by a sterile dressing survey is
Exposure and environmental control carried out as
• The patient should be completely undressed. It is imperative to cover the a potential
patient with warm blankets to prevent hypothermia in the emergency life threat
department. may be
• Intravenous fluids should be warmed and a warm environment present.
maintained.
• Patient privacy should be maintained.
Tertiary Survey
• A careful and complete examination followed by serial assessments help recognize
missed injuries and related problems, allowing a definitive care management.
• The rate of delayed diagnosis may be as high as 10%
Trauma severity scores
1) Glasgow Coma Scale
2) Revised trauma score: widely accepted & applied

Revised trauma score

The Revised Trauma Score (RTS) is a physiologic scoring system, based on the initial vital
signs of a patient. A lower score indicates a higher severity of injury.
It made up of a three categories: Glasgow Coma Scale, systolic blood pressure, and
respiratory rate. The score range is 0-12.
In START triage;
• Patients with RTS score of 12 is delay (not urgent)
• 11 is urgent,
• 3–10 is immediate
• Those who have an RTS below 3 are declared dead and should not receive certain care
because they are highly unlikely to surviv e without a significant amount of resources
Arrangement of injuries according to priorities
 Postoperative wound infection, cellulitis, abscess &
General principles of antibiotic therapy

Postoperative wound infection

Definition; a surgical wound contaminated by organisms derived from patient himself
(endogenous) or from his environment (surgical team, instruments, dressing, etc)
Predisposing factors;
General factors;
 Poor general condition as malnutrition
 Systemic disease that impair host defense as DM, uremia
 Drugs that cause immunosuppression as corticosteroid or chemotherapy
Local factors;
 Poor blood supply;
 Wounds of lower part of the legs
 Suture of tissues under tension
 Poor surgical technique;
 Rough handling of tissues
 Excessive use of diathermy
 Improper hemostasis leading to hematoma formation
 Presence of foreign bodies as prosthetic implants
 Nature of operation; as operations on peritonitis, colonic resection
 Defect in the sterilization technique
Types of wounds;
 Clean;
 No gross contamination; e.g. herniorrhaphy & thyroidectomy
 The risk of infection 1-2 %
 Clean contaminated;
 Wounds involves regions of the body that may contain low numbers of resistant
microflora; e.g. urogenital & oropharyngeal, or the original microflora has reduced inq
number by certain measures; e.g. surgery on prepared colon
 The risk of infection 2-5 %
 Contaminated;
 An unprepared region of the body with large number of microflora; e.g. surgery on
unprepared colon, or operation on grossly infected area; e.g. surgery for peritonitis
 The risk of infection 5-30 %
Clinical Picture
 Wound infection usually appears between the 5th & 10th days postoperative, but can
appear earlier or later
 Postoperative fever & pain in the wound is the earliest manifestations
 The wound is swollen, tender, red
 Fluctuant areas or crepitus can occasionally be felt
Differential Diagnosis
 Other causes of postoperative fever; e.g. chest infection, UTI, DVT
 Other causes of wound swellings; e.g. hematoma, incisional hernia
Prophylaxis
 Improvement of predisposing factors; e.g. DM, malnutrition, anemia
 Prophylactic antibiotics especially;
 In clean contaminated & contaminated wounds
 In wounds where foreign material is implanted
 Method; it given preoperatively, during operation & early postoperative
 Mechanical & chemical preparation of the colon before any elective operation on the
colon
 Gentle handling of the tissues, adequate hemostasis
 Heavily contaminated wounds should be left open (skin & SC) for delayed primary
closure on the 4th or 5th days, when there is no infection
Treatment
 The wound opened and stitches removed to allow pus drainage
 Antibiotic; in invasive infection guided by culture & sensitivity
 Possible sources of hospital acquired infection should be traced
 Acute Abscess
Definition; a localized suppurative inflammation
Organisms; the commonest is staph. aureus, that produce coagulase enzyme that help
localization.
Pathogenesis; the organisms reach the tissue by;
 Direct access through wounds, scratches or abrasions
 Local extension from adjacent focus; e.g. osteomyelitis
 Lymphatic spread; infection reaches the regional lymph nodes from septic focus
 Blood spread; organisms gaining access into the blood as in bacteremia or pyemia,
may lodge in distant tissues as pyemic liver & lung abscess
Pathology; the abscess consists of three zones;
 A central zone of coagulative necrosis; contain Pus which composed of inflammatory
exudate, dead leukocytes, necrotic tissue & organisms
 A intermediate zone of granulation tissue
 A peripheral zone of acute inflammation fades gradually into healthy surrounding
tissues
Fate; acute abscess may end in one of the followings;
 Resolution; if resistance is high & treatment is started ealy before pus formation
 Pointing & rupture
 Spread of infection either locally, by lymphatic or blood
 Chronicity; a dense fibrous tissue reaction forms around the incompletely resolved
abscess
Clinical picture; the abscess consists of three zones;
 Systemic; fever, malaise, headache, tachycardia, anorexia
 Local;
 Starts as a painful tender mass
 The covering skin is red, edematous
 The draining lymph nodes are usually enlarged & tender
 When pus forms, throbbing pain, hectic fever, pitting edema, more localization,
fluctuation, shooting leucocytosis with shift to the left
Do not wait for fluctuation; the sign is absent or difficult to elicit in;
 Deep abscess; e.g. gluteal, perianal
 Too tender abscess
 Abscess covered by strong fascia; e.g. parotid, hand abscess
 Breast abscess
Treatment;
 Before suppuration; proper antibiotic therapy, rest, hot application.
 After suppuration;
 Once pus forms, the only treatment is incision & adequate free drainage
 A specimen of pus is sent for culture & sensitivity
 Helton’s method for drainage is used in dangerous areas
 All abscesses should be incised & drained except; amebic liver abscess, brain abscess,
cold abscess
 Cellulitis
Definition; an invasive non-suppurative infection of loose connective tissue
Organisms;
 Gram-positive bacteria mostly streptococci, occasionally
staphylococci
 Route of entry; may be trivial e.g. scratch or prick
Clinical Picture;
 The affected area is red or reddish brown, indurated, hot painful
 It spread rapidly, edge is ill defined
 Moderate or high fever
 Lymphangitis (red streaks), lymphadinitis (enlarged tender regional lymph nodes)
Differential Diagnosis; contact allergy, DVT, chemical inflammation at the site of drug
injection
Treatment;
 Rest & elevation of the affected part, hot packs, suitable antibiotics
 If no response within 24-48 hours, abscess should be suspected
Erysibelas
Definition; rapidly spread ing non-suppurative inflammation of the lymphatic of the skin
Organisms;
 Hemolytic streptococci, route of entry; scratch, abrasion or prick
Clinical Picture;
 Similar to cellulitis with the following differences; color of skin is
rose-pink, the edge is well defined, slightly elevated, minute vesicles, there are islets
of inflammation beyond the margin separated by normal skin
 Symptoms of toxemia may present
Complications; Facial erysibelas may lead to cavernous sinus thrombosis, recurrent
erysibelas may lead to chronic lymphatic obstruction (elephantiasis),
septicemia
Treatment;
 The patient need to be isolated
 Treatment is similar to cellulitis
 Carbuncle
Definition; infective gangrene of subcutaneous tissues, multiple areas of necrosis &
thrombosis occur
Organisms; staph. aureus, common in immunocompromised & diabetic patients
Clinical Picture;
 It occur mainly in face, nape of the neck & the back
 Symptoms of toxemia may present
 Start as a painful red induration, then central part becomes
soft, multiple areas of skin thin out forming multiple sinuses
Complications; local spread, facial carbuncle may lead to cavernous
sinus thrombosis, septicemia & pyemia
Treatment;
 Antibiotic against staph, culture & sensitivity if resist
 Excision of sloughs
 Proper control of diabetes
Boil
Definition; staphylococcal infection of hair follicle or seb gland,
common in diabetic patients
Clinical Picture; a small painful indurated swelling, hot, very tender,
red
Treatment; antibiotic (systemic & local), hot packs

Acute Lymphangitis & lymphadenitis

Definition; infection of lymph vessels / lymph nodes, usually by
streptococci through an abrasion or a wound in an area drained by
lymphatics
Clinical Picture;
The affected lymphatics; red streaks on the skin
The affected lymph nodes; enlarged, tender, painful
General; fever, malaise, primary focus in drainage areas
Treatment; antibiotic, hot packs, if suppuration occur; incision & drainage
Bacteremia & Septicemia
Bacteremia; presence of non-multiplying bacteria in the blood, usually due to dental work,
instrumentation of UT, septic focus anywhere
Hazards; patients with damaged heart valves or prosthetic valves (leads to more damage),
immunocompromised patients
Antibiotic prophylaxis is essential especially against Gram-negative (more dangerous)
Septicemia; presence of multiplying bacteria in blood plus lecocytosis, with production of
bacterial toxin & inflammatory mediators
 Antibiotics
ž An antibiotic is a type of antimicrobial substance active against bacteria
ž They may either kill or inhibit the growth of bacteria
ž Choice of suitable antibiotics;
 An initial diagnosis is essential before starting antibiotic therapy
 The initially chosen antibiotic should be effective against the most likely pathogens;
 Staphylococci; is the commonest seen clinically
 Skin & soft tissues; mostly Gram-positive bacteria
 GIT; mostly Gram-negative bacteria & anaerobes
 UT; mostly Gram-negative bacteria
 MRSA & Pseudomonas; should be suspected in resistant infections
 If there is unsatisfactory clinical response, we do culture & sensitivity
Types of antibiotics
B-Lactam antibiotics; inhibition of cell wall synthesis
 Penicillin; penicillin G, semi-synthetic penicillin as methicillin, ampicillin, combining
amoxicillin with B lactamase inhibitors (e.g. clavulanate) as some bacteria secrete B
lactamase enzyme. Penicillins active mainly against Gram-positive, some Gram-negative
bacteria
 Cephalosporins;
 1st generation; Gram-positive bacteria
 2nd generation; slightly Gram-positive but a much better Gram-negative
 3rd generation; excellent anti-Gram-negative, some anaerobes
 4th generation; excellent anti-Gram-negative, more against Gram-positive, some
anaerobes
 Monobactam; only Gram-negative bacteria
 Carbapenems; as imipenem, have a wide spectrum, Gram-positive, most Gram-negative,
pseudomonas & anaerobes
Aminogycosides; interfering with bacterial protein synthesis
 Gentamycin, tobramycin, amikin
 Mainly against Gram-negative
 Complications; nephrotoxicity, ototoxicity, so its use is guided by renal function
Quinolone & Fluoroquinolones; as ciprofloxacin, nalidixic acid, norfloxacin, flurofloxacin
against mainly Gram-negative
Glycopeptide; as vancomycin, the most potent against Gram-positive bacteria & MRSA
Metronidazole; has excellent anaerobic activity
Erythromycin; a macrolide drug, Gram-positive
Clindamycin; good activity against anaerobes, some Gram-positive
Oxazolidinone; as linozolid, a new antibiotic actively against Gram-positive bacteria that are
resistant to other antibiotics, including streptococci, vancomycin-resistant enterococci , and
methicillin-resistant Staphylococcus aureus (MRSA)
 Quiz
What is meaning by postoperative wound infection?
Describe local predisposing factors of postoperative wound infection
Describe types of surgical wounds as regard susceptibility to infection
Infection of a surgical wound; how to diagnose?
How to prophylaxes against surgical wound infection?
How to treat a surgical wound infection?
Describe the pathology of acute abscess
Outline the fate of acute abscess
When you don’t wait for fluctuation in a case of acute abscess?
How to diagnose a case of subcutaneous acute abscess? & how to treat it?
What is Helton’s method for drainage of acute abscess?
Define cellulitis, most common organism, clinical presentation, treatment
Define erysibalas, causative organism, clinical presentation, complications, treatment
How can you clinically differentiate between cellulitis & erysibalas?
Define carbuncle, suspected patients, common sites, presentation, treatment
Define boil, presentation, treatment
Define bacteremia, its hazards
Define septicemia
How can you choice the type of antibiotic according to the site of surgical infection?
Enumerate types of B-lactam antibiotics
Enumerate antibiotics sensitive to Gram-positive bacteria
Enumerate antibiotics sensitive to Gram-negative bacteria
Enumerate antibiotics sensitive to anaerobic bacteria
Enumerate antibiotics sensitive to MRSA
Aminoglycosides not used for long periods, why?
A surgical wound resistant to the antibiotic therapy, how to explain & manage?
1. Healthy patients undergoing uncomplicated surgery can remain N.P.O. (with intravenous fluid
support) for how many days before significant protein catabolism occurs?
a) 2 days.
b) 4 days.
c) 7 days.
d) 10 days.
The answer: is (d).
2. Signs and symptoms of hemolytic transfusion reactions include:
a) Hypothermia.
b) Hypertension.
c) Polyuria.
d) Abnormal bleeding.
e) Hypothesis at the transfusion site.
The answer: is (d).
3. Which of the following are the most potent mediators of the inflammatory response?
a) Corticosteroids.
b) Heat shock proteins.
c) Cytokines.
d) Eicosanoids.
Answer: is (c).
4. A patient suspected of having a hemolytic transfusion reaction should be managed with:
a) Removal of non-essential foreign body irritants
e.g. Foley catheter.
b) Fluid restriction.
c) 0.1ml HCL infusion.
d) Steroids.
e) Fluids and Mannitol.
The answer: is (e).
5. Shock can best be defined as:
a) Hypotension.
b) Hypo perfusion.
c) Hypoxemia.
d) All of the above.
The answer: is (b).
6. All of the following are true about neurogenic shock except:
a) There is a decrease in systemic vascular resistance and an increase in venous capacitance.
b) Tachycardia or Bradycardia may be observed, along with hypotension.
c) The use of an alpha agonist such as phenylephrine is the mainstay of treatment.
d) Severe head injury, spinal cord injury, and high spinal anesthesia may all cause neurogenic shock.
The answer: is (c).
7. Which of the following is not associated with increased likelihood of infection after major elective
surgery?
a) Chronic malnutrition.
b) Infection at a remote body site.
c) Controlled diabetes mellitus.
d) Long-term steroid use.
The answer: is (c).
8. The most common cause of fatal transfusion reactions is:
a) An allergic reaction.
b) An anaphylactic reaction.
c) A Technical error.
d) An acute bacterial infection transmitted in blood.
The answer: is (c).
9. Which of the following in NOT one of the four major physiologic events of hemostasis?
a) Fibrinolysis.
b) Vasodilatation.
c) Platelet plug formation.
d) Fibrin production.
The answer: is (b).
10. The half-life of platelets is:
a) 2 – 3 days.
b) 7 – 10 days.
c) 14 – 21 days.
d) 30 – 40 days.
The answer: is (b).
11. Which congenital factor deficiency is associated with delayed bleeding after initial hemostasis?
a) Factor VII.
b) Factor IX.
c) Factor XI.
d) Factor XIII.
The answer: is (d).
12. Each of the following is a symptom of a hemolytic transfusion reaction Except:
a) Constricting chest pain.
b) Flushing of the face.
c) Lumbar pain.
d) Syncope.
The answer: is (d).
13. The most common clinical manifestation of a hemolytic transfusion reaction is:
a) Flank pain.
b) Jaundice.
c) Oliguria.
d) A shaking chill.
The answer: is (c).
14. The most common fatal infection complication of a blood transfusion is:
a) Acquired immune-deficiency syndrome.
b) Cyto-megalo-virus.
c) Malaria
d) Viral hepatitis.
The answer: is (d).
15. In the presence of acute blood loss, adequate preload to the heart is maintained initially by the:
a) Development of tachycardia.
b) Hormonal effects of angiotensin.
c) Hormonal effects of renin.
d) Increase in systemic vascular resistance.
The answer: is (d).
16. Neurogenic shock is characterized by the presence of:
a) Cool moist skin.
b) Increased cardiac output.
c) Decreased blood volume.
d) Decreased peripheral vascular resistance.
The Answer: is (d).
17. Which of the following (if present) is a distinguishing feature of neurogenic shock?
a) Hypotension.
b) Bradycardia.
c) Vaso-dilation.
d) Vaso-constriction.
The Answer: is (b).
18. Scar formation is part of the normal healing process following injury, which of the following
tissues has the ability to heal without scar formation?
a) Liver. b) Skin. c) Bone. d) Muscle.
The answer: is (c).
19. Infections that require operative treatment include all of the following Except:
a) Empyema.
b) Infected ascites.
c) Necrotizing fasciitis of the thigh.
d) Vascular graft infection.
The answer: is (b).
20. Which of the following is the most commonly acquired infection in hospitalized surgical patients?
a) Lower gastro-intestinal tract.
b) Lower respiratory tract.
c) Naso-pharynx.
d) Surgical wound.
The answer: is (d).
21. An exotoxin plays in important part in the pathogenicity of infection with each of the following
Except:
a) Clostridium botulinum.
b) Clostridium tetani.
c) Escherichia coli.
d) Staphylococcus aureus.
The answer: is (c).
22. The drug of choice for clostridial myonecrosis is:
a) Penicillin G. b) Ampicillin. c) Amikacin. d) Cephalosporin. The answer: is (a).
23. An infection with Staphylococcus aureus acquired in an intensive care unit should be treated initially
with:
a) Aztreonam. b) Erythromycin. c) Methicillin. d) Vancomycin. The answer: is (d).
24. What percentage of blood volume must be lost in healthy patients before hypotension occurs?
a) 10 – 30%. b) 20 – 30%. c) 30 – 40%. d) 40 – 50%. The answer: is (c).
25. The best cosmetic results for large capillary (port-wine) hemangiomas are achieved by:
a) Excision and split-thickness graft.
b) Tattooing.
c) Cryo-surgery.
d) Laser destruction.
The answer: is (d).
26. The proliferative phase of wound healing occurs how long after the injury?
a) 1 day. b) 2 days. c) 7 days. d) 14 days. The answer: is (c).
27. Steroids impair wound healing by:
a) Decreasing angio-genesis and macrophage migration.
b) Increasing release of lysosomal enzymes.
c) Decreasing platelet plug integrity.
d) Increasing fibrinolysis.
The answer: is (a).
28. Bradykinin, serotonin and histamine in wounds are released from:
a) Lymphocytes.
b) Mast cells.
c) Polymorpho-nuclear leukocytes.
d) Platelets.
The answer: is (b).
29. Platelets in the wound form a hemostatic clot and release clotting factors to produce:
a) Fibrin. b) Fibrinogen. c) Thrombin. d) Thromboplastin. The answer: is
(a).
30. Lympho-granuloma venereum is caused by:
a) Treponema pallidum.
b) Chlamydia trachomatis.
c) Neisseria gonorrhea.
d) Mycobacterium fortuitum.
The answer: is (b).
31. Appropriate treatment for an acute stable hematoma of the pinna of the ear includes which of the
following measures?
a) Ice packs and prophylactic antibiotics.
b) Excision of the hematoma.
c) Needle aspiration.
d) Incision, drainage, and pressure bandage.
e) Observation alone.
The answer: is (d).
32. Water constitutes what percentage of total body weight?
a) 30-40%.
b) 40-50%.
c) 50-60%.
d) 60-70%.
The answer: is (c).
33. A patient who has spasms in the hand when a blood pressure cuff is blown up most likely has :
a) Hypercalcemia.
b) Hypocalcemia.
c) Hypermagnesemia.
d) Hypomagnesemia.
The answer: is (b).
34. Which congenital factor deficiency is associated with delayed bleeding after initial hemostasis?
a) Factor VII.
b) Factor IX.
c) Factor XI.
d) Factor XIII.
The answer: is (d).
35. Which of the following (if present) is a feature of neurogenic shock?
a) Hypotension.
b) Bradycardia.
c) Vaso-dilatation.
d) Vaso-constriction.
The answer: is (b).
36. Dobutamine:
a) Increases cardiac output and causes peripheral vaso-dilatation.
b) Decreases cardiac output and causes peripheral vaso-dilatation.
c) Increases cardiac output and causes peripheral vaso-constriction.
d) Decreases cardiac output and causes peripheral vaso-constriction.
The answer: is (a).
37. The proliferative phase of wound healing occurs how long after the injury?
a) 1 day.
b) 2 days.
c) 7 days.
d) 14 days.
The answer: is (c).
38. Steroids impair wound healing by:
a) Decreasing angiogenesis and macrophage
migration.
b) Increasing release of lysosomal enzymes.
c) Decreasing platelet plug integrity.
d) Increasing fibrinolysis.
The answer: is (a).
39. Signs of malignant transformation in a chronic wound include:
a) Persistent granulation tissue with
bleeding.
b) Non-healing after 2 weeks of therapy.
c) Over-turned wound edges.
d) Distal oedema.
The answer: is (c).
40. The major cause of impaired wound healing is:
a) Anaemia.
b) Diabetes mellitus.
c) Local tissue infection.
d) Mal-nutrition.
The answer: is (c).
41. Among the physiologic responses to acute injury is:
a) Increased secretion of insulin.
b) Increased secretion of thyroxine.
c) Decreased secretion of vasopressin.
d) Decreased secretion of aldosterone.
The answer: is (a).
42. The response to shock includes which of the following metabolic effects?
a) Increase in renal perfusion.
b) Decrease in cortisol level.
c) Hyperkalemia.
d) Hypoglycemia.
The answer: is (c).
43. Appropriate treatment for an acute stable hematoma of ear pinna includes which of the following
measures?
a) Ice packs and prophylactic antibiotics.
b) Incision, drainage, and pressure bandage.
c) Needle aspiration.
d) Observation alone.
The answer: is (b).
44. Naso-tracheal intubation is:
a) Preferred for the unconscious patient without cervical spine injury.
b) Preferred for patients with suspected cervical spine injury.
c) Maximizes neck manipulation.
d) Contraindicated in the patients who is breathing spontaneously.
The answer: is (b).
45. Which of the following statements about maxilla-facial trauma is/are false?
a) The major cause of death from facial injuries is asphyxia from upper airway obstruction.
b) The mandible is the most common site of facial fracture.
c) The Le-Fort II fracture includes a horizontal fracture of the maxilla along with nasal bone fracture.
d) Loss of upward gaze may indicate either an orbital floor or orbital roof fracture.
The answer: is (b,d).
46. Normal saline is:
a) 135 mEq NaCl/L.
b) 145 mEq NaCl/L.
c) 148 mEq NaCl/L.
d) 154 mEq NaCl/L.
The answer: is (d).
47. The classic chest X-Ray finding in Anthrax is:
a) Bilateral apical pneumo-thorax.
b) Basilar pneumonia.
c) Widened mediastinum and effusions.
d) Pulmonary oedema.
The answer: is (c).
48. Which of the following is the most common type of melanoma?
a) Acral lentiginous.
b) Superficial spreading melanoma.
c) Nodular.
d) Lentigo maligna.
The answer: is (b).
49. What is the most common melanoma in dark-skinned people?
a) Acral lentiginous.
b) Superficial spreading.
c) Nodular.
d) Lentigo maligna.
The answer: is (a).
50. The tumor, node, metastases classification for melanoma uses the following in its classification
Except:
a) Regional lymph nodes.
b) Serum protein level.
c) Depth of invasion of the primary tumor.
d) Metastases.
The answer: is (b).
51. True statements regarding squamous cell carcinoma of the lip include:
a) The lesion arises in areas of persistent hyperkeratosis.
b) > 90 % of cases occur on the upper lip.
c) Radiography is considered inappropriate treatment for these lesions.
d) Initially metastases are to the ipsilateral posterior cervical lymph nodes.
The answer: is (a).
52. Management of leukoplakia of the oral cavity includes:
a) Excisional biopsy of all lesions.
b) Application of topical antibiotics.
c) Ascertaining that dentures fit properly.
d) Application of topical chemo-therapeutic
agents.
The answer: is (c).
53. The best antibiotic for post-exposure prophylaxis to Bacillus anthracis (anthrax) is:
a) Rifampin.
b) Clindamycin.
c) Doxycycline.
d) Amoxicillin.
The answer: is (b).
54. A 30-years-old, otherwise healthy woman undergoes an open appendectomy with primary closure of
the wound for a perforated appendix. No antibiotics are administered. Should this patient develop an
intra-abdominal abscess, which of the following organisms would most likely the responsible?
a) Escherichia coli.
b) Bacteroides.
c) Streptococcus faecalis.
d) Serratia.
The answer: is (b).
55. The drug of choice for clostridial myonecrosis is:
a) Penicillin G.
b) Ampicillin.
c) Amikacin.
d) Cephalosporin.
The answer: is (a).
56. An infection with Staphylococcus aureus acquired in an intensive care unit should be treated initially
with:
a) Aztreonam.
b) Erythromycin.
c) Methicillin.
d) Vancomycin.
The answer: is (d).
57. Haemangioma of the face in children:
a) Should be resected in the newborn period.
b) Should be resected only if it persists 10 years of age.
c) Will involute by 3 years of age in most children.
d) Can be treated by laser ablation.
The answer: is (d).
58. Le Fort II fracture entails injuries to all of the following Except:
a) Medial wall of the orbit.
b) Zygomatico-maxillary articulation.
c) Naso-frontal buttress.
d) Mandible.
The answer: is (d).
59. The most common site of Kaposi's sarcoma in the head and neck is:
a) Buccal mucosa.
b) Palate.
c) Tongue.
d) Floor of mouth.
The answer: is (b).
60. Scar formation is part of the normal healing process following injury Which of the following tissues
has the ability to heal without scar formation?
a) liver. b) Skin. c) Bone. d) Muscle. The answer: is (c).
61. Narcotics are commonly used in administration of general anesthesia. Which of the following
statement (s) is/are true concerning this class of agents?
a) Narcotics have both profound analgesic and amnestic properties.
b) Narcotics can cause hypotension by direct myocardial depressive effects.
c) Naloxone should be used routinely for the reversal of narcotic analgesia.
d) Acutely injured hypovolemic patients are significant risk for decreased blood pressure
with the use of narcotic analgesia.
e) propofol is a new intra-venous short-acting narcotic used frequently in the outpatient
setting.
The answer: is (d).
62. A patient who has spasms in the hand when a blood pressure cuff is blown up most likely has:
A. Hypercalcemia.
B. Hypocalcemia.
C. Hypermagnesemia.
D. Hypomagnesemia.
The answer: is (b).
 OPHTHALMOLGY
Anatomy of eye:
1.anterior segment (translucent): cornea
2.posterior segment (opaque): 3 layers
a) outer fibrinous layer : sclera
b) inner nervous coat : retina
c) middle vascular coat : uveal tract ‫ حاجات‬3 ‫بتتكون من‬

o Iris
o cilliar body
o choroid
limbus: junction between ant and post segment ant and post chamber
have aqueous humor ‫سائل شفاف‬

Aqueous humor‫ وظيفته‬:

→ Refractive rays – nutrition of cornea and lens – form contour of the eye

‫مهم الرسم ة دي في االمتحان‬

Why cornea is transparent?
- Regular arrangement of fibers
- absence of blood vessels
- absence of keratinization
- absence of myelinated nerve fibers
- gradiant of refractive index between fibrous and matrix
- contain limited water.
Circulation of aqueous humor:
Secreted by cilliar body and passes to posterior chamber then to the pupils, and passes to
anterior chamber then to the angle of the eye, then drainage .
Normal intra ocular pressure: (10:22)mm Hg
‫ وهو ارتفاع الضغط المائي‬glucoma‫ لو زاد الضغط ده عن الطبيعى هيدينا مرض المياه الزرقاء‬-
cataract ‫ لو اصبحت معتمه هيدينا مرض المياه البيضاء‬, ‫ اللينس او العدسه المفروض انها شفافه‬-

Refractive media of the eye : Cornea – aqueous humor – lens – vitreous

ANATOMY OF LID ‫الدكتور قال ممكن اجبلك ترسمها برضه‬

Lid have 5 layer
1- cutaneous layer :
skin – zeis gland –eyelashes
2-muscular layer :
- Orbicularis occuli – levator palpebrae
- muller muscle
3- connective tissue layer :
Nerves – veins – arteries – lymphatic
4- fibrous layer :
Tarsus layer – Meibomian gland
5- palpebral conjuntive :
Goblet cells – accessory lacremal glands – bloos vessles
- Lymphatic tissue

Lens ‫ وظيفه‬: Allow rays to enter eye – Accommodation –refractive media

 STYE Chalazion

defination • it is acute suppurative inflammation  It is chronic granulomatous

of cilia follicle or its associated inflammation of one of oily tarsal
glands. glands.

cause Due to staph or strept infection Due to duct infection or vit A deficiency
predisposed by decrease resistance .
 May be small or large , single or
multiple , hard or soft , infected or
non infected , external or internal .

Signs and edema, redness, pain, swelling, pus, Painless - non-tender swelling
symptoms: tender

Complications: Rubbing lashes -Orbital cellulitis Painless - non-tender swelling

treatment • Medical treatment early local &  Management depend on its type,
systemic antibiotics. antibiotic.but commonly needs
vertical incision and curette of its
• Surgical treatment when pus is
contents.
formed, epilation or horizontal
incision.

Different between stye and chalazion ‫سؤال شائع ف االمتحانات‬

 Mal-directed lashes Symblepheron
 It is backward direction of lashes  It is adhesion between bulbar and palpebral
‫المكان بتاعها مش صح وبتحك ف العين‬ conjunctiva. Diphtheria ‫قال‬
‫ف الشرح انتريور‬
 May be aquaired due to fibrosis Cause: It is due to fibrosis.
o rubbing lashes ‫بعض الرموش‬ Site: It may be anterior due to chemicals, posterior due to
‫مش كلها داخله لجوا وبتحك ف العين‬ trachoma, total due to diphtheria.
o trichiasis ‫الرموش كلها بقا طالعه‬
‫لجوا وبتحك ف العين‬  May interfere with ocular movement, deplobia .
 or congenital
Treatment: Surgical interference is required
o dis –trichiasis ‫رموش ابنورمال‬
‫طالعه ف مكان ابنورمال وبتحك ف‬
‫العين‬
 Leads to ocular irritation , corneal
abrasion;pain, photophobia , Madarosis
lacremation
 IT is absence of lid lashes .
 Managed by different methods  It may be local or total ,also uni lateral or bilateral
epilation ‫ بنشيل الرموش‬, electrolysis , .
diathermy , laser ,Cryo, Snellen ,s  Either due to local causes as trauma , styes ,
operation , Van - Mellenge operation , blepharitis or due to systemic causes as leprosy
Webester, s operation  Treatment hair implantation or artificial lid lashes

Entropion Ectropion
 it is inward rolling of the lid  It is outward rolling of the lid margin .
margin
 Different types:
 Types :
1. Spastic .
1. Spastic .
2. Cicatricial ‘
2. Cicatricial
3. Senile .
3. Congenital
4. Paralytic .
4. Mechanical
5. Congenital .
 treatment directed to the cause
6. Mechanical
, then surgical line.
 Treatment: varies according to the types .
 CATARACT‫مهمه‬
 It is opacity of the lens . ‫بتيجى غالبا للناس الكبيره‬
According to the etiology may be:
1.congenital .‫مولود بيها‬
2.senile .‫مع تقدم العمر‬
3.complicated .‫نتيجة لحاجة‬
4. Traumatic .
(Congenital cataract)
Senile cataract
since birth ,due to: May be
1.gene defect 1.nuclear‫ منتصف‬or
2.placental haemorrhge‫نزيف ف المشيمة‬ 2. cortical
3.germinal measles‫ الحصبه‬, 4 stages
4.birth trauma , (incipient , immature , mature ,hypermature ‫ ) ناشفه حجر‬.
5.metabolic defect ,
 immature stage & hypermature stage
6. drugs ‫بعض االدويه‬.
May be
- Iris shadow to be seen needs light, lens opacity
1.Ant polar,
,space between iris and opacity so it is present
2. post polar ( affect vision ) ,
both this stages(immature – hypermature)
3.coronary ‫ (ع االطراف‬with club ends or
‫بروزات‬
4.lamellar  absent in mature stage‫مفيش شادو وال اسبيس‬
5.zonular (wheel shaped opacity  Complications of hypermature stage are
common type ), - phacolytic glaucoma‫ ماده بتطلع من العدسه ف بتسد الفتحة‬,
6. blue dots‫نقط كده ومبتاثرش ع الرؤيه‬ - glaucoma capsularis ,
( faint opacity not affect vision ) , - glaucoma inversus‫عدسه بتطلع لقدام ف بتسد الفتحة‬
7.total ,disc shaped . - phaco-anaphylactic endophthalmitis ‫ حساسية‬,
- Treated by: - lens dislocation‫ العدسه بتسيب كليا‬and
- sublaxation ‫ بتسيب جزئيا‬.
1. needling‫ ادحل حقنه واكسر االوبيك ده‬,
2.pars plana lensectomy ‫ نشيل العدسه اصال‬,  Also cataract can produce uni- ocular‫عين واحده‬
diplopia and astigmatism‫ ملغوشه‬and morphologic
3.ECCE . glaucoma .
4.also LAL lenses may be used ‫عدسات مكان‬  Cataract leads to gradual painless diminution of
‫ اللي شيلتها‬. vision ,MV , black spots , change in color of
objects .
Senile cataract treated by‫ عمليات‬ICCE , ECCE , PHACO &
IOLI .
COMPLICATED CATARACT . TRAUMATIC CATARACT
 may be due  may be
local causes
rosette shaped ‫الفراوله او النجمه وطبعت عليها‬ due to imprint of iris
e g iridocyclitis‫التهابات‬
on the lens.
systemic causes
e g DM .‫مثل السكر‬

Ttt : glasses or contact lens – surgical as intra or extracapsular extraction

 Glaucoma‫مهمه‬
 It is rise of intra ocular pressure , leads to ocular damage .
 IOP is formed by aqueous humor. ‫ده السائل اللي بيعمل ضغط‬
 Aqueous is formed by ciliary body .
 Aqueous is drained via trabecular meshwork & uveo- scleral pathway .
 IOP is measured by digital‫ جهاز‬,indentation‫ بنضغط عليها نالقيها ناشفه‬,
 Applanation & air puff tonometer ‫اجهزة معينه‬.
 Normal IOP is 10 – 22 mmgh .
Types of glaucoma are:
1. Congenital glaucoma.‫ قزواج االقارب وكده والزم نعالجه ونعمل درينيج للسائل ده‬.. ‫والعين لونها ازق‬
2. Primary open angle glaucoma. ‫ الزاويه اللي بين االيرز والكورنيا مفتوحة بس الفتحات اللي فيها مسدوده‬.. ‫اكوايرد وكرونيك‬
3. Primary closed angle glaucoma. ‫ هنا الزاويه قالفه الفتحات‬.. ‫اكوايرد واكيوت‬
4. Secondary glaucoma.‫نتيجة لمرض ما‬
Common signs are
- decrease vision,
- rise of IOP, hallos,
- field defect,
- optic cupping,
- headache,
- nausea
- vomiting,
- seeing colored rings around lights,
- sudden blurred vision
Complications 3rd cause of blindness.
Treatment ‫ات قطر‬may be
 medical pilocarpine
 Beta blockers timolol
 dorzolamide
 xalatane
 brimodine
 surgical
 laser therapy