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MBBS Final Year II - General Surgery Sessional Exam Notes

SAMC & PGI, Indore

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TOPIC 1: BREAST

Applied Anatomy of the Breast

• Cooper's Ligaments (Suspensory ligaments): Fibrous bands running between the chest wall and dermis. They anchor the skin, so infiltration by cancer or edema causes dimpling and peau d'orange (orange skin appearance).
• Three tissue types: (1) Glandular epithelium, (2) Fibrous stroma, (3) Adipose tissue
• Ductal system: 15-20 lobes, each ending in a lactiferous duct opening at the nipple. Each major duct has a dilated lactiferous sinus below the nipple-areolar complex (NAC).
• Terminal duct lobular units (TDLUs): The milk-forming unit; site of origin of most breast carcinomas. Acini + efferent ductules = TDLU (lobule). Invested in specialized loose connective tissue with capillaries and lymphocytes.
• Intralobular stroma: Loose, cellular (contains migratory mononuclear cells) - distinct from denser interlobular stroma.
• Deep to pectoralis major: Pectoralis minor enclosed in clavipectoral fascia, which extends laterally to fuse with axillary fascia.
• Retromammary space: Loose areolar tissue between breast and pectoral fascia - allows breast movement; important for surgical access.

• Axillary nodes (75%): Most common pathway; drains the outer breast
  • Level I: lateral to pectoralis minor
  • Level II: behind pectoralis minor
  • Level III (apical): medial to pectoralis minor
• Internal mammary nodes (25%): Drains medial and central breast
• Supraclavicular nodes: Higher-level drainage
• Rotter's nodes (interpectoral): Between pectoralis major and minor

• Lateral thoracic artery and thoracodorsal artery (from axillary artery)
• Perforating branches of internal thoracic (mammary) artery
• Intercostal perforators

• Lateral and medial pectoral nerves (to pectoralis muscles)
• Long thoracic nerve (to serratus anterior) - damage → winged scapula
• Thoracodorsal nerve (to latissimus dorsi)
• Intercostobrachial nerve - damage → sensory loss in medial upper arm

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Investigations for Breast Diseases

Triple Assessment (Gold Standard)

1. Clinical examination
2. Imaging (mammography ± ultrasound)
3. Pathology (cytology/biopsy)

Imaging

• BIRADS 1-2: Negative/Benign - routine screening
• BIRADS 3: Probably benign - short-interval follow-up
• BIRADS 4: Suspicious - tissue sampling
• BIRADS 5: Highly suggestive of malignancy - biopsy mandatory
• BIRADS 6: Known biopsy-proven malignancy

Pathological Investigations

• FNAC (Fine Needle Aspiration Cytology): Quick, low cost; C1-C5 scoring (C5 = malignant)
• Core needle biopsy (Tru-cut/14G): Histological diagnosis; preserves architecture; preferred
• Vacuum-assisted biopsy: For small/deep lesions; image-guided
• Open excision biopsy: Diagnostic and therapeutic for benign lumps
• Sentinel Lymph Node Biopsy (SLNB): Technetium-99m + patent blue dye; first lymph node = sentinel node

Biochemical

• Serum CA 15-3, CEA (tumor markers for monitoring, not diagnosis)
• Hormone receptor status (ER, PR, HER-2) on biopsy specimens

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Benign Breast Diseases (ANDI Concept)

• Most benign disorders = minor aberrations of normal cyclical change and involution
• Replaces old confusing terms: fibrosis, adenosis, epitheliosis, fibrocystic disease

Three Phases:

1. Lobule development (15-25 yrs): Aberration → Fibroadenoma
2. Cyclical changes (15-50 yrs): Aberration → Cyclical mastalgia, cyclical nodularity
3. Involution (35-55 yrs): Aberration → Cyst, sclerosing adenosis, duct ectasia

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1. Fibroadenoma

• Most common benign breast tumor in young women (15-35 yrs)
• Derived from aberrant lobular development
• Clinical features: Smooth, firm, well-circumscribed, mobile ("breast mouse"), non-tender; usually solitary, <3 cm
• Investigations: USG (hypoechoic, well-defined oval lesion), FNAC or core biopsy
• Management: Reassurance if <3 cm and benign triple assessment; excision for >3 cm, growing, patient anxiety, or diagnostic uncertainty

2. Breast Cysts

• Derived from involuted lobules; common 35-55 yrs (perimenopausal)
• Clinical: Smooth, well-defined, may be tender; can be single or multiple
• USG: Anechoic with posterior acoustic enhancement (diagnostic)
• Management: Fine needle aspiration; no need to send clear fluid for cytology; recurrent/blood-stained cysts: send for cytology + biopsy

3. Cyclical Mastalgia

• Pain starts ~day 14 of cycle, peaks day 27-28, relieved by menstruation
• Usually bilateral; may radiate to upper arm (mimic angina)
• Cause unclear: excessive responsiveness of breast tissue to circulating oestrogen
• Treatment:
  • Reassurance (most important - >80% improve after normal examination)
  • Pain chart for 1 month (to document cyclical vs non-cyclical)
  • Drug treatment: Tamoxifen, Danazol, Bromocriptine, evening primrose oil (gamolenic acid)

4. Non-cyclical Mastalgia

• Pain at any time, any location; often well-localised
• Trigger spot: Very tender specific point
• Causes: duct ectasia, periductal mastitis, Tietze's syndrome (painful costochondral junction), trauma, cancer
• Distinguish from: angina, biliary colic, reflux oesophagitis, cervical spondylosis

5. Duct Ectasia / Periductal Mastitis

• Duct ectasia = dilatation of subareolar ducts with periductal inflammation
• Usually presents at/after menopause
• Clinical: Nipple discharge (thick, creamy, green, or blood-stained), nipple retraction (slit-like, in centre), periareolar mass, periareolar abscess/fistula
• Management: Microdochectomy (single duct) or Hadfield's operation (total duct excision) for persistent discharge

6. Sclerosing Adenosis

• Aberration of involution; proliferation of lobular acini with stromal fibrosis
• Can mimic carcinoma clinically and radiologically
• Diagnosis by biopsy; no malignant potential
• Management: Wide local excision if atypical hyperplasia present

7. Hyperplasia (Epithelial Hyperplasia)

• 2 layers of cells in duct/acini lining

• Without atypia: No increased cancer risk
• Atypical Ductal Hyperplasia (ADH): ×4 relative risk of cancer
• Atypical Lobular Hyperplasia (ALH): ×4 relative risk
• If ADH involves >2 ducts or >2 mm: classified as DCIS

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Infections of the Breast (Mastitis/Breast Abscess)

Lactational (Puerperal) Mastitis and Abscess

• Most common; occurs in 1st-6 weeks postpartum
• Organism: Staphylococcus aureus (MRSA increasingly common)
• Pathogenesis: Milk stasis → cracked nipple → bacterial entry → cellulitis → abscess
• Clinical: Tender, erythematous, swollen breast; fever, rigors; fluctuant mass if abscess
• Management:
  • Mastitis (no fluctuation): Antibiotics (flucloxacillin/co-amoxiclav) + continue breastfeeding/regular expression
  • Abscess: Ultrasound-guided needle aspiration (preferred - repeated if needed) OR incision and drainage (radial incision to avoid dividing ducts); antibiotics; stop breastfeeding from affected breast

Non-Lactational Periductal Mastitis

• Occurs in non-pregnant women; associated with smoking (nicotine damages subareolar ducts)
• Organisms: mixed (aerobes + anaerobes), Bacteroides, Staphylococcus
• Recurrent periareolar abscesses with mammary duct fistula (fistula between subareolar duct and periareolar skin)
• Management: Drainage + antibiotic (metronidazole + amoxicillin); total duct excision for recurrence; Hadfield's operation for fistula

Mondor's Disease

• Thrombophlebitis of superficial veins of the breast and chest wall
• Presents as tender cord in subcutaneous tissue; benign, self-limiting
• Treatment: NSAIDs; rarely surgical

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TOPIC 2: CARDIO-THORACIC SURGERY (Chest, Heart and Lungs)

• Stages: Exudative → Fibrinopurulent → Organized (pleural peel)
• Management: Antibiotics + drainage (VATS preferred in fibrinopurulent stage); decortication in organized stage

• Causes: Aspiration (most common), necrotizing pneumonia, foreign body, septic emboli
• Organism: Mixed anaerobes, Klebsiella, S. aureus
• CXR/CT: Thick-walled cavity with fluid level
• Management: Prolonged antibiotics (metronidazole + amoxicillin, 4-6 weeks); postural drainage; surgical resection for failure of medical treatment

• Symptoms: copious purulent sputum ("three layer" appearance), haemoptysis, clubbing
• Investigation: HRCT chest (gold standard); bronchoscopy
• Management: Physiotherapy, antibiotics for exacerbations; surgical resection for localised disease

• Types: Squamous cell (central, Pancoast, SVC obstruction), Adenocarcinoma (peripheral, most common overall), Small cell (SIADH, Cushing's - most aggressive), Large cell
• Spread: Direct, lymphatic (mediastinal/supraclavicular nodes), haematogenous (brain, bone, liver, adrenal)
• Staging: TNM; resectable = Stage I-IIIA; pancoast = superior sulcus tumor
• Management: Surgery (lobectomy/pneumonectomy) for operable NSCLC; chemotherapy (platinum-based) for SCLC; radiotherapy; immunotherapy (checkpoint inhibitors)

• Cardiopulmonary bypass; heart-lung machine; myocardial protection (cardioplegia)
• CABG (Coronary Artery Bypass Grafting): for multi-vessel disease; conduits = LIMA (best, 95% 10-yr patency), saphenous vein, radial artery
• Valvular surgery: Mitral valve repair/replacement; aortic valve replacement

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TOPIC 3: PERITONITIS

Definition

Causes (Summary Box from Bailey & Love)

• Chemical: bile, barium, urine, gastric juice
• Allergic: starch peritonitis
• Traumatic: operative handling
• Ischaemia: strangulated bowel, vascular occlusion

1. GI perforation: Perforated ulcer, appendix, diverticulum (most common)
2. Transmural translocation (no perforation): Pancreatitis, ischaemic bowel, primary bacterial peritonitis
3. Exogenous contamination: Drains, open surgery, trauma, peritoneal dialysis
4. Female genital tract: Pelvic inflammatory disease, salpingitis
5. Haematogenous spread (rare): Septicaemia

Classification

Clinical Features (Bailey & Love Summary Box 65.4)

• Abdominal pain, worse on movement, coughing, deep respiration
• Constitutional upset: anorexia, malaise, fever, lassitude
• GI upset: nausea ± vomiting
• Patient lies still to minimise fluid movement

• Pyrexia (may be absent in elderly/immunosuppressed)
• Tachycardia, hypotension (in advanced cases)
• Tenderness + guarding + rigidity + rebound of abdominal wall
• Board-like rigidity (diffuse peritonitis): reflex contraction of entire abdominal musculature
• Hippocratic facies: Gravely ill appearance
• Generalised ileus → abdominal distension
• Absent bowel sounds
• Digital rectal/vaginal examination: deep-seated tenderness (pelvic peritonitis)
• Phrenic pain (shoulder tip pain): Subdiaphragmatic inflammation → referred pain to C5 dermatome

Investigations

• FBC: Leucocytosis (elevated WBC); raised CRP
• LFTs, RFTs, Amylase
• Blood cultures (before antibiotics)
• Erect CXR: Free gas under diaphragm (subdiaphragmatic gas) = pneumoperitoneum (perforated viscus)
• Lateral decubitus X-ray: If patient too unwell for erect CXR
• Abdominal USS: Free fluid, collections, thickened bowel
• CT abdomen (gold standard): Identifies cause, location of perforation, free gas/fluid, collections, assess for peritoneal thickening

Complications

1. Septicaemia and septic shock
2. Multi-organ failure (MOF) - renal failure, ARDS, hepatic failure
3. Ileus - paralytic ileus progressing to intestinal obstruction
4. Adhesions - leading to future bowel obstruction
5. Intraabdominal abscess - subphrenic, pelvic, paracolic
6. Wound infection / dehiscence
7. Fistula formation
8. Death (mortality 30-50% in faecal peritonitis)

Principles of Management

Initial Resuscitation (ICU if necessary):

• IV access + aggressive IV fluid resuscitation (Hartmann's/0.9% saline)
• Nasogastric tube (decompression)
• Urinary catheter (monitor UO ≥0.5 mL/kg/hr)
• O2 therapy; analgesia (IV opioids)
• Blood cultures, then broad-spectrum IV antibiotics (e.g. Pip-Tazo; Metronidazole + Cephalosporin)

Surgery (definitive):

• Goal: Remove source of contamination, drain collections, restore GI continuity if possible
• Approach: Laparotomy (or laparoscopy in selected cases)
• Steps:
  1. Identify and control source (close perforation, resect gangrenous bowel)
  2. Peritoneal lavage (copious warm saline)
  3. Drain placement in collections
  4. Decision: primary anastomosis vs stoma (Hartmann's procedure if faecal contamination/unstable patient)
• Damage control surgery in septic shock: quick procedure to control contamination; re-look laparotomy in 48 hours

Specific:

• Tuberculous peritonitis: ATT (4-drug: HRZE for 2 months, then HR for 4 months)
• Spontaneous bacterial peritonitis (SBP): IV cefotaxime; no surgery
• Primary peritonitis in children: IV penicillin

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TOPIC 4: APPLIED ANATOMY AND PHYSIOLOGY OF THE STOMACH

Applied Anatomy

• Cardia, Fundus, Body (corpus), Antrum, Pylorus
• Lesser curvature: Short; between cardia and pylorus; right gastric and right gastro-omental vessels
• Greater curvature: Long; left and right gastro-omental vessels
• Pylorus: 2-3 cm thick muscular sphincter; prevents duodenogastric reflux

• Anteriorly: Left lobe of liver, anterior abdominal wall, left costal margin
• Posteriorly: Lesser sac, pancreas, splenic artery, left adrenal gland, left kidney
• Lesser omentum: Connects lesser curvature to liver; contains hepatic artery, portal vein, bile duct (portal triad) in its free edge
• Greater omentum: Hangs from greater curvature; "policeman of the abdomen" (walls off infections)

• Left gastric artery (from coeliac axis) - main supply
• Right gastric artery (from hepatic artery)
• Left gastro-omental artery (from splenic artery)
• Right gastro-omental artery (from gastroduodenal artery)
• Short gastric arteries (from splenic artery - to fundus)

• Vagus (X) nerve: Parasympathetic; stimulates acid secretion and motility; anterior vagus (left) and posterior vagus (right) travel along oesophagus
• Sympathetic: Via coeliac plexus (T5-T9); reduces motility, causes vasoconstriction

• Follows arterial supply → regional nodes → coeliac nodes → para-aortic nodes
• Important: Japanese classification of gastric lymph nodes (N1, N2, N3) determines extent of gastrectomy

Physiology

Key Points (Bailey & Love):

• Stomach is a reservoir for food and commences digestion
• Gastric acid produced by proton pump in parietal cells, controlled by histamine via H2-receptors
• Histamine produced by ECL cells in response to gastrin and vagal stimulation
• PPIs abolish gastric acid production (act on final common pathway - H+/K+ ATPase proton pump)
• H2-receptor antagonists markedly reduce (but do not abolish) acid secretion
• Gastric mucous layer is essential to mucosal integrity (prostaglandins maintain mucous)

Phases of Gastric Secretion:

1. Cephalic phase: Mediated by vagal activity (sensory arousal: sight, smell, taste of food - "Pavlov's experiment")
2. Gastric phase: Food in stomach → gastrin release from G cells → ECL → histamine → parietal cell → HCl; negative feedback loop: acid inhibits gastrin
3. Intestinal phase: Chyme in duodenum → secretin, GIP, CCK → inhibit gastric acid and emptying

Gastric Contents:

• Parietal cells (oxyntic cells): Produce HCl and intrinsic factor (for B12 absorption)
• Chief cells (peptic cells): Produce pepsinogen (converted to pepsin at pH <2)
• G cells (antrum): Produce gastrin
• ECL cells: Produce histamine
• D cells: Produce somatostatin (inhibitory)
• Mucous neck cells: Secrete mucus and HCO3-

Gastric Emptying:

• Liquids empty faster than solids
• Controlled by pylorus, duodenal feedback (CCK, secretin, GIP)
• Delayed by: fat, hyperosmolar solutions, acid, lying supine
• Accelerated by: metoclopramide, erythromycin (motilin agonist)

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TOPIC 5: DISEASES OF THE STOMACH

A. Congenital Hypertrophic Pyloric Stenosis (CHPS)

Definition

Epidemiology

• Incidence: 1 in 500 live births
• Male:Female = 4:1 (males predominantly)
• Firstborn males most commonly affected
• Presents at 3-6 weeks of age (rarely at birth or after 12 weeks)
• Familial; multifactorial inheritance (incidence 1 in 20 if mother affected)

Etiopathogenesis

• Hypertrophy and hyperplasia of the circular pyloric muscle
• Pylorus elongates to 2-4 cm (normal 1-1.5 cm) and thickens
• Deficiency of nitric oxide synthase (nNOS) in the pyloric muscle (impairs relaxation)
• Results in progressive gastric outlet obstruction
• Leads to: projectile vomiting → loss of HCl → hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria

Clinical Features

• Projectile vomiting: Non-bilious (no bile - obstruction is above ampulla), forceful, immediately after feeding
• Onset: 2-4 weeks of age, progressively worsening
• Baby hungry after vomiting ("hungry vomiter")
• Weight loss, dehydration, constipation
• Visible gastric peristalsis: Olive-shaped mass in right upper abdomen, left-to-right wave
• Palpable pyloric mass ("olive"): Felt in right hypochondrium/epigastrium after feed; firm, mobile, ~1.5-2 cm

Investigations

• Serum electrolytes: Hypochloraemia, hypokalaemia, metabolic alkalosis
• Serum Na: Usually normal or low
• Ultrasound (gold standard): Pyloric wall thickness >4 mm, pyloric channel length >16 mm, pyloric diameter >14 mm
• Upper GI contrast study (if USS inconclusive): "String sign" or "rail-road track sign" of thin trickle of barium through pylorus; "shoulder sign" of hypertrophied muscle indenting stomach

Principles of Management

• Correct dehydration with IV saline
• Correct metabolic alkalosis: IV 0.45% NaCl + KCl (do not give potassium until urinating)
• Aim: serum chloride >100 mEq/L, pH <7.45 before surgery
• NGT for gastric decompression

• Ramstedt's operation: Longitudinal incision through serosa and circular muscle of pylorus down to mucosa (without opening mucosa); splits hypertrophied muscle
• Approaches: Open (right upper quadrant or periumbilical incision) or laparoscopic (preferred in modern practice)
• Mucosa is NOT cut; submucosa should bulge freely
• Post-op: Resume feeding 4-6 hours after surgery

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B. Peptic Ulcer Disease (PUD)

Definition

Types:

• Duodenal ulcer (DU): More common; usually on anterior wall of 1st part of duodenum
• Gastric ulcer (GU): Less common; usually on lesser curvature at junction of body and antrum

Aetiology

1. H. pylori infection (most important): ~95% DU, ~70-80% GU; a gram-negative spiral bacterium that colonises antrum; produces urease, damages mucosa
2. NSAIDs: Inhibit COX-1 → decreased prostaglandins → reduced mucous and bicarbonate secretion → mucosal injury (often cause silent GU)
3. Acid hypersecretion: Zollinger-Ellison syndrome (gastrinoma)
4. Stress ulcers: Critically ill patients (Curling ulcer - burns; Cushing ulcer - head injury)
5. Smoking, alcohol, steroids (contributory)
6. Blood group O: DU more common

Pathogenesis (Imbalance of Aggression vs Defence):

• Aggressive factors: HCl, pepsin, H. pylori, NSAIDs, bile
• Defensive factors: Mucous layer, bicarbonate, mucosal blood flow, prostaglandins, cell turnover

Clinical Features

• DU: Epigastric pain, relieved by food and antacids ("hunger pain"), wakes patient at night; radiation to back; periodic (weeks of pain, weeks of remission)
• GU: Epigastric pain, worsened by food (fear of eating → weight loss), nausea
• Tenderness in epigastrium
• In perforation: Sudden onset severe abdominal pain → board-like rigidity

Investigations

• OGD (upper GI endoscopy): Gold standard; direct visualisation, biopsy to exclude malignancy in GU (mandatory), test for H. pylori (rapid urease test/CLO test)
• H. pylori testing:
  • Non-invasive: Urea breath test (gold standard non-invasive), stool antigen test, serology (IgG)
  • Invasive (endoscopic): Rapid urease test (CLO test), histology, culture
• Barium meal: "Niche sign" (filling defect) for GU; "incisura" deformity in healing
• Serum gastrin: If ZE syndrome suspected (fasting gastrin >1000 pg/mL)

Complications (mnemonic: P-H-O-S)

1. Perforation (DU anterior wall > GU): Sudden abdominal pain → peritonitis; Erect CXR: free gas
2. Haemorrhage (DU posterior wall - GDA erosion > GU): Haematemesis, melaena; Rockall score
3. Obstruction (Pyloric stenosis from cicatrisation): Succussion splash, vomiting of old food
4. Stress/Subacute: Penetration into pancreas (DU posterior) → pain radiating to back

Principles of Management

• H. pylori eradication: Triple therapy 14 days: PPI (omeprazole) + Clarithromycin + Amoxicillin; quadruple therapy if resistant
• Acid suppression: PPI (omeprazole 40mg OD for 4-8 weeks) or H2-blockers
• Stop NSAIDs; stop smoking; antacids
• Confirm eradication: Urea breath test 4 weeks after stopping antibiotics and PPI

• Perforated DU: Graham patch (omental patch closure) ± H. pylori eradication; laparoscopic preferred
• Perforated GU: Excision of ulcer with repair; always send biopsy
• Haemorrhage: Endoscopic (injection sclerotherapy, heat probe, clips) first; if fails → surgery (underrunning the vessel)
• Obstruction (pyloric stenosis): Balloon dilatation endoscopically; surgery: gastrojejunostomy or pyloroplasty
• Elective surgery (now rare): Highly selective vagotomy (HSV/parietal cell vagotomy)

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C. Carcinoma Stomach

Epidemiology

• 5th most common cancer worldwide; high incidence in Japan, Korea, Chile, Eastern Europe
• M>F (2:1); peak age 60-70 years
• Decreasing incidence in West (due to H. pylori treatment, refrigeration)

Aetiology

1. H. pylori infection (most important precancerous condition)
2. Diet: Smoked, salted, pickled food; nitrosamines; low fruit/vegetable intake
3. Precancerous conditions: Chronic atrophic gastritis, gastric polyps, pernicious anaemia, previous partial gastrectomy (10-20 yr later), Ménétrier's disease
4. Genetic: CDH1 mutation (hereditary diffuse gastric cancer), blood group A
5. Intestinal metaplasia → dysplasia → carcinoma (Correa cascade)
6. Smoking, alcohol
7. H. pylori → gastric lymphoma (MALT lymphoma)

Histopathology (Lauren Classification)

• Intestinal type: Well-differentiated; forms glands; related to H. pylori, intestinal metaplasia; better prognosis
• Diffuse type: Poorly differentiated; signet ring cells; infiltrates wall → linitis plastica ("leather bottle stomach"); worse prognosis; more in young women

Site: 50% in antrum (pyloric region), 25% lesser curvature, 10% fundus

Clinical Features

• Dyspepsia, epigastric pain/discomfort
• Anorexia, nausea, weight loss (most common presenting feature)
• Early satiety (especially diffuse type)
• Dysphagia (cardia/fundus involvement)
• Vomiting (pyloric involvement)
• Haematemesis or melaena (ulcerating lesions)

• Epigastric mass
• Virchow's node (Troisier's sign): Left supraclavicular lymph node enlargement (via thoracic duct)
• Sister Mary Joseph's nodule: Umbilical metastasis
• Krukenberg tumour: Ovarian metastasis (signet ring cells)
• Blumer's shelf: Peritoneal deposits in pouch of Douglas (felt on PR)
• Jaundice (liver metastasis), ascites, hepatomegaly

Investigations

• OGD (Upper GI endoscopy) + biopsy: Diagnostic gold standard; multiple biopsies from different sites
• CT chest/abdomen/pelvis: Staging (T, N, M); assess resectability
• Endoscopic USS (EUS): Best for T and N staging (depth of invasion)
• PET-CT: Distant metastasis detection
• Staging laparoscopy: Detects peritoneal metastasis not seen on CT
• Tumour markers: CEA, CA 19-9, CA 72-4 (limited diagnostic use; useful for monitoring)
• Bloods: FBC (anaemia), LFTs, albumin (nutritional status)

Staging: TNM + Japanese system

• T1: Mucosa/submucosa (early gastric cancer - EGC)
• T2: Muscularis propria
• T3: Subserosa
• T4: Through serosa (T4a) or adjacent organs (T4b)

Principles of Management

• Distal gastrectomy (subtotal): For antral/body tumours
• Total gastrectomy + oesophago-jejunal anastomosis (Roux-en-Y): For proximal lesions or linitis plastica
• D1 lymphadenectomy: Perigastric nodes
• D2 lymphadenectomy: Includes nodes along coeliac axis branches; standard in Asia; better survival
• Reconstruction: Billroth I (gastroduodenostomy) or Billroth II (gastrojejunostomy) after subtotal; Roux-en-Y after total

• Palliative chemotherapy: FOLFOX, XELOX, HER2-targeted (Trastuzumab if HER2+)
• Palliative surgery: Gastrojejunostomy (bypass) for obstructing antral tumour
• Endoscopic stenting; nutritional support (PEG, jejunostomy)

• 5-year survival: ~30% overall; Stage I: 80-90%; Stage IV: <5%
• Early gastric cancer (confined to mucosa/submucosa): 90%+ 5-year survival

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TOPIC 6: VASCULAR DISEASES

A. Occlusive Arterial Disease (Peripheral Arterial Disease - PAD)

Etiopathogenesis

• Primary cause: Atherosclerosis (>90% of cases)
• Risk factors: Smoking (most important, ×9 risk), diabetes mellitus, hypertension, hypercholesterolaemia, family history, male sex, advancing age
• Pathology: Lipid-laden macrophages (foam cells) → fatty streaks → fibrous plaque → calcification → stenosis/occlusion; platelet aggregation on irregular intima → thrombosis → acute on chronic ischaemia
• Multisystem disease: 50% have coronary artery disease; 25-50% have cerebrovascular disease
• Less common causes: Thromboangiitis obliterans (Buerger's disease), popliteal entrapment, cystic adventitial disease, fibromuscular dysplasia

Fontaine Classification (Clinical Staging):

Clinical Features

• Cramping pain in muscles, comes on with walking, relieved by rest (within 5 min) - NOT relieved by dependency
• Site depends on level of disease:
  • Aortoiliac: Buttock, thigh and calf claudication; absent femoral pulse bilaterally; Leriche syndrome (claudication + impotence + absent femoral pulses)
  • Iliac: Unilateral thigh and calf; unilateral absent femoral pulse
  • Femoropopliteal: Calf claudication; femoral pulse present, distal absent
  • Distal (tibial): Foot and calf claudication; femoral + popliteal pulses present, ankle absent

• Rest pain: Burning pain in forefoot; worse at night, relieved by dependency (hanging leg over bed)
• Tissue loss: Ischaemic ulcers (deep, punched-out, painful, dry, on pressure points/toes/heel), gangrene (dry initially → wet if infected)
• 6 Ps of Acute Ischaemia: Pain, Pallor, Pulselessness, Paraesthesia, Paralysis, Perishing cold (Poikilothermia)

• Pallor on elevation, rubor on dependency (Buerger's test)
• Trophic changes: thin skin, hair loss, nail changes, muscle wasting
• Absent pulses
• Bruits over stenosed vessels
• Low ABPI (<0.9 normal; <0.5 critical ischaemia)

Investigations (Bailey & Love):

• FBC (anaemia, polycythaemia), blood glucose, HbA1c, lipid profile, urea + electrolytes, creatinine
• ECG, echocardiogram (assess for coronary disease)
• CXR

• ABPI (Ankle-Brachial Pressure Index): Non-invasive screening; <0.9 = PAD; <0.5 = critical ischaemia; >1.3 = calcified (diabetics)
• Hand-held Doppler ultrasound: Assess flow; triphasic (normal) → biphasic → monophasic waveform
• Duplex USS (Doppler + B-mode): Maps anatomy, identifies stenosis/occlusion; first-line imaging
• CT Angiography (CTA): Excellent anatomical detail; rapid; pre-operative planning
• MR Angiography (MRA): No radiation; good for run-off vessels; useful in renal impairment
• Digital Subtraction Angiography (DSA): Gold standard for anatomy; also therapeutic (angioplasty at same sitting)
• Transcutaneous PO2 (TcPO2): Assess tissue perfusion; <30 mmHg = critical ischaemia

Principles of Treatment

• Risk factor modification: Stop smoking (MOST important), control diabetes, hypertension, hypercholesterolaemia
• Antiplatelet therapy: Aspirin 75 mg or Clopidogrel (reduces MI/stroke risk, not direct limb benefit)
• Statins: Atorvastatin (pleiotropic effects + lipid lowering)
• Supervised exercise programme: 30 min 3x/week; best evidence for claudication (improves walking distance by 100-150%)
• Cilostazol (phosphodiesterase inhibitor): Drug for claudication; improves walking distance
• Limb protection: Careful foot care, appropriate footwear (especially in diabetics)

• Percutaneous Transluminal Angioplasty (PTA) ± stenting: For iliac and femoropopliteal disease; preferred for short segment stenosis/occlusion
• Drug-eluting stents/balloons: Better patency in femoropopliteal segment

• Endarterectomy: Removal of plaque from vessel (common/external iliac, common femoral artery)
• Bypass grafting: For long segment occlusion; conduit choices:
  • Aortobifemoral bypass: For aortoiliac disease (Dacron or ePTFE graft)
  • Femoro-popliteal bypass: For femoropopliteal disease; autologous long saphenous vein (reversed or in-situ) preferred over synthetic
  • Femoro-distal bypass: For tibial vessel occlusion; requires vein graft
• Amputation: For non-viable limb, failed revascularisation, intractable infection
  • Level determined by viable skin (Burgess flap for below-knee, Gritti-Stokes for knee)

• Thrombosis (on pre-existing atherosclerosis - gradual): collateral circulation present, less acute
• Embolism (cardiac source - AF, MI - sudden): no collateral, more acute; pale, cold, pulseless limb
• Management: IV heparin → embolectomy (Fogarty catheter) within 6 hours for embolism; thrombolysis (tPA) as alternative for thrombosis

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B. Vasospastic Disorders

1. Raynaud's Phenomenon / Disease

• Connective tissue disease: Scleroderma (most common), SLE, RA, dermatomyositis
• Occupational: Vibrating tools (vibration white finger)
• Drugs: Beta-blockers, ergotamine, bleomycin, cisplatin
• Haematological: Polycythaemia, cryoglobulinaemia
• Thoracic outlet syndrome, atherosclerosis

1. White (Pallor): Vasospasm → ischaemia
2. Blue (Cyanosis): Capillary stasis → deoxygenation
3. Red (Erythema/Rubor): Reactive hyperaemia on rewarming

• Episodes triggered by cold, emotion
• Fingers (especially 2nd-4th); toes, ears, nose less commonly
• Pain and tingling during attacks
• In severe/secondary: digital ulcers, gangrene of fingertips, calcinosis

• Nailfold capillaroscopy: Abnormal capillary loops in secondary Raynaud's (enlarged, distorted)
• Full blood count, ESR, CRP
• Autoantibodies: ANA, anti-dsDNA, anti-Scl-70 (scleroderma), anti-centromere antibody
• Serum complement
• Chest X-ray: Cervical rib (thoracic outlet syndrome)
• Arterial Doppler: Assess baseline vasospasm
• Cold challenge test: Provocative test (standardised cooling)

• Non-pharmacological: Avoid cold; gloves, warm clothing; stop smoking; avoid precipitating drugs
• Pharmacological:
  • Calcium channel blockers (Nifedipine): First line; 10-20 mg TDS; reduces frequency and severity
  • Phosphodiesterase-5 inhibitors (Sildenafil): Vasodilation; good evidence in secondary Raynaud's
  • Prostanoids (Iloprost IV): For severe ischaemia/digital ulcers; vasodilatory + antiplatelet
  • ARBs (Losartan): Second line
  • SSRIs (Fluoxetine): Reduces frequency in mild cases
• Surgical (severe/failed medical):
  • Digital sympathectomy: Strips adventitia of digital arteries; good for digital ulcers
  • Cervical sympathectomy: Now rarely used (temporary effect); for upper limb
  • Lumbar sympathectomy: For lower limb vasospasm
  • Botulinum toxin injection: Into digital vessels; promising evidence

2. Buerger's Disease (Thromboangiitis Obliterans)

• Young male smokers (<45 years)
• Bilateral, distal extremity involvement
• Claudication of feet, calves, hands (arch claudication = pathognomonic)
• Superficial thrombophlebitis (migrating/recurrent)
• Rest pain, digital ulcers, gangrene of toes and fingers
• Raynaud's phenomenon (20-30%)

• No specific test; diagnosis of exclusion
• Normal lipid profile, glucose
• Allen test (hand): Abnormal (occlusion of radial/ulnar artery)
• Angiography: "Corkscrew" collateral vessels (pathognomonic)

• Stop smoking completely (most important): Only intervention that halts progression
• Wound care, antibiotics for infection
• Prostanoids (Iloprost) for ischaemia
• Sympathectomy: Lumbar (lower limb), cervical (upper limb)
• Amputation: For non-viable tissue

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TOPIC 7: VENOUS DISEASES - Applied Anatomy of the Venous System of the Lower Limb

Overview

1. Superficial venous system: Located in superficial tissues, above deep fascia
2. Deep venous system: Beneath deep fascia, accompanying arterial tree

• Superficial veins drain into deep system via junctions or fascial perforating (communicating) veins
• Blood flows: Superficial → Perforators → Deep → Right atrium

Deep Venous System

• Three pairs of venae comitantes accompany the three crural arteries (anterior tibial, posterior tibial, peroneal arteries) = 6 veins in the leg
• These 6 veins intercommunicate and converge in the popliteal fossa → popliteal vein
• Popliteal vein also receives soleal and gastrocnemius veins (the "venous muscle pump")
• Passes through adductor hiatus → becomes femoral vein in subsartorial canal (Hunter's canal)
• Receives deep femoral (profunda femoris) vein in the femoral triangle
• Passes behind inguinal ligament → external iliac vein
• External iliac + internal iliac = common iliac vein
• Left common iliac vein passes behind right common iliac artery (site of May-Thurner/Cockett syndrome - compression causing left-sided DVT)
• Right + left common iliac veins → Inferior vena cava (IVC) → right atrium

Superficial Venous System

Great Saphenous Vein (GSV) - Longest vein in body

• Origin: Medial end of dorsal venous arch of foot
• Course: Anterior to medial malleolus → medial surface of leg → loops posteriorly at medial knee condyle → medial thigh → groin
• Termination: Pierces cribriform fascia at saphenous opening → drains into common femoral vein (CFV) at saphenofemoral junction (SFJ) (~2.5 cm below and lateral to pubic tubercle)
• Nerve: Accompanied by the saphenous nerve (branch of femoral nerve) throughout its leg course
• Tributaries at SFJ (5 tributaries): Superficial epigastric, superficial iliac circumflex, superficial external pudendal, deep external pudendal, anterior accessory GSV (AAGSV)

Small Saphenous Vein (SSV)

• Origin: Lateral end of dorsal venous arch
• Course: Posterior to lateral malleolus → midline of posterior calf → popliteal fossa
• Termination: Drains into popliteal vein at saphenopopliteal junction (SPJ) in popliteal fossa (variable level)
• Nerve: Accompanied by sural nerve

Perforating (Communicating) Veins

• Connect superficial → deep system through holes in deep fascia
• Normal flow direction: Superficial → Deep (maintained by valves)
• In venous insufficiency: Valves become incompetent → reflux from deep to superficial = "venous hypertension"
• Named perforators:
  • Dodd's perforators: Mid-thigh
  • Boyd's perforator: Below knee (medial)
  • Cockett's perforators (Posterior tibial group): 7, 12, 18 cm above medial malleolus; most important clinically (incompetence → medial gaiter ulcers)

Venous Valves

• Bicuspid valves present throughout; more numerous in distal veins
• Prevent reflux; allow only centripetal flow
• The femoral vein valve just below SFJ is most important (loss → primary varicose veins)

Venous Return Mechanisms

1. Calf muscle pump (most important): Gastrocnemius and soleus contraction during walking compresses deep veins → propels blood proximally
2. Venous valves: Prevent retrograde flow
3. Thoracic negative pressure: Aspirates blood during inspiration
4. Arterial pulsation: Transmitted to adjacent veins
5. Vis-a-tergo: Residual arterial pressure

Clinical Relevance

• Varicose veins: Incompetent valves → superficial venous reflux; most commonly SFJ incompetence → GSV varicosity
• Deep Vein Thrombosis (DVT): Virchow's triad (stasis, hypercoagulability, endothelial damage); most commonly in calf veins; risk of PE
• Chronic Venous Insufficiency: Persistent venous hypertension → skin changes (lipodermatosclerosis, haemosiderin staining, atrophie blanche) → venous ulcers (painless/minimally painful, medial gaiter area, above medial malleolus, shallow with irregular edges, granulating base)
• GSV harvest: Used as conduit in CABG, peripheral vascular bypass
• Long saphenous vein stripping: Used in varicose vein surgery

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QUICK REVISION SUMMARY TABLE

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• Bailey and Love's Short Practice of Surgery, 28th Edition (primary reference for all surgical topics)
• Sabiston Textbook of Surgery: The Biological Basis of Modern Surgical Practice (breast anatomy, investigations)

1. Peritonitis management principles (common long question)
2. Carcinoma stomach - complete answer
3. PUD complications and management
4. Breast anatomy + ANDI framework
5. ABPI and PAD staging (Fontaine)