Small Bowel
Applied anatomy, physiology and high-yield surgical pathology for MRCS Part A & B.
Small Bowel Anatomy
The small intestine is the principal site for digestion and absorption, extending approximately 6–7 metres from the pylorus to the ileocaecal valve. It is divided into three segments: the duodenum, jejunum, and ileum.
The duodenum is the first, widest, and shortest segment (~25 cm — “twelve finger breadths”). C-shaped, curling around the head of the pancreas. Almost entirely retroperitoneal except for the first 2 cm (duodenal cap/bulb), which has a mesentery and is mobile.
- D1
Superior / First Part (Duodenal Cap / Bulb)
Begins at the pylorus, runs posterosuperiorly. The first 2 cm is mobile. Most common site for peptic ulceration. The gastroduodenal artery (GDA) lies immediately posterior — a posteriorly perforating D1 ulcer bleeds from the GDA.
- D2
Descending / Second Part
Descends on the right side of the spine. Contains the major duodenal papilla (Ampulla of Vater) on its posteromedial wall — the opening of the common bile duct and main pancreatic duct (Wirsung). Also contains the minor papilla (accessory duct of Santorini). Pancreatic head carcinoma compresses the CBD here → obstructive jaundice.
- D3
Horizontal / Third Part
Crosses the midline horizontally. Passes between the aorta posteriorly and the SMA anteriorly — basis of SMA syndrome. With extreme weight loss, the fat pad between SMA and aorta disappears, narrowing the aortomesenteric angle → compression of D3 → proximal obstruction.
- D4
Ascending / Fourth Part
Ascends to the left to reach the duodenojejunal (DJ) flexure, supported by the ligament of Treitz (fibromuscular band connecting DJ flexure to the right crus of the diaphragm). The DJ flexure marks the start of the midgut. Upper GI bleeds are proximal to the DJ flexure; lower GI bleeds are distal.
The Ligament of Treitz — The Key Landmark
Fixes the DJ flexure to the right crus of the diaphragm, tethering the duodenum. Critical landmark for:
🔵 Upper vs Lower GI bleed: proximal = upper (haematemesis ± malaena); distal = lower (PR blood)
🔵 Nasojejunal tube placement: tip must be beyond the DJ flexure for post-pyloric feeding
🔵 Ladd’s procedure (malrotation): the ligament of Treitz is released to straighten and fix the duodenum; Ladd’s bands obstructing the duodenum are divided
The Jejunum — Key Distinguishing Features
Thick, heavy wall · Deep red/rose colour (more vascular) · Large, closely packed plicae circulares (“stacked coins”) · Long vasa recta · Few, large arterial arcades (1–2 tiers) · Less mesenteric fat (vessels visible through mesentery) · No Peyer’s patches · Left and upper abdomen
The Ileum — Key Distinguishing Features
Thin, soft wall · Paler pink (less vascular) · Low/absent plicae circulares distally · Short vasa recta · Many, short arterial arcades (3–5 tiers) · More mesenteric fat (“creeping fat” in Crohn’s) · Peyer’s patches present (raised oval lymphoid plaques) · Right and lower abdomen, ends at ileocaecal valve
The jejunum (~2/5 of post-duodenal small bowel) and ileum (~3/5) are suspended from the posterior abdominal wall by the fan-shaped mesentery, which contains the SMA, SMV, lymphatics, and autonomic nerves. There is no fixed external landmark distinguishing them — identification relies on the features below.
| Segment | Arterial Supply | Venous Drainage | Notes |
|---|---|---|---|
| Proximal duodenum (D1–D2 above ampulla) | Gastroduodenal artery → superior pancreaticoduodenal artery (coeliac trunk territory) | Portal vein | Foregut–midgut watershed at the ampulla of Vater. Dual arterial supply protects against ischaemia. |
| Distal duodenum (D2 below ampulla, D3, D4) | SMA → inferior pancreaticoduodenal artery | SMV → portal vein | Midgut territory. Pancreaticoduodenal arcade connects coeliac + SMA — important collateral in aortic surgery. |
| Jejunum & ileum | SMA → 15–18 jejunal/ileal branches → arterial arcades → vasa recta (end-arteries) | SMV → portal vein | Vasa recta are end-arteries with no collateral — injury causes a localised ischaemic segment. |
| Terminal ileum | Ileocolic artery (terminal branch of SMA) | Ileocolic vein → SMV | Most consistent SMA branch — used as the vascular pedicle in right hemicolectomy. |
- Sympathetic (T8–T10): Inhibit peristalsis and secretion; vasoconstriction. Afferent pain fibres travel with the sympathetics → periumbilical referred pain for midgut pathology (appendicitis, SMA ischaemia).
- Parasympathetic (vagus, CN X): Stimulates peristalsis and secretion. Does NOT carry pain afferents.
- Enteric nervous system: Myenteric plexus (Auerbach’s) — controls motility. Submucosal plexus (Meissner’s) — controls secretion. Functions independently but is modulated by the ANS.
Physiology & Absorption
The gut processes approximately 7500 mL of fluid daily. The small bowel reabsorbs over 5000–6000 mL (>80%), leaving only ~1500 mL to enter the colon.
| Source | Volume/day | Notes |
|---|---|---|
| Oral intake | ~2000 mL | Variable |
| Saliva | ~1500 mL | Contains amylase, lysozyme |
| Gastric juice | ~2000 mL | HCl, pepsinogen, intrinsic factor |
| Bile | ~500 mL | Bile acids, bilirubin, cholesterol |
| Pancreatic juice | ~1500 mL | Bicarbonate, digestive enzymes |
| Total entering small bowel | ~7500 mL | — |
| Absorbed by small bowel | ~5000–6000 mL | Very efficient reabsorption |
| Delivered to colon | ~1500 mL | Colon absorbs ~1400 mL → 100–150 mL stool |
| Nutrient / Substance | Site of Absorption | Mechanism & Clinical Notes |
|---|---|---|
| Iron (Fe²⁺) | Duodenum and proximal jejunum | Ferric (Fe³⁺) → ferrous (Fe²⁺) by duodenal ferrireductase. Absorbed via DMT-1 transporter. Requires acidic pH — PPIs impair iron absorption. Iron deficiency anaemia in Crohn’s (proximal disease) or post-gastric surgery. |
| Calcium | Duodenum and jejunum | Vitamin D-dependent (active) + passive diffusion. Requires acid for ionisation. Bypassed in RYGB → calcium malabsorption → osteoporosis risk. |
| Folate | Duodenum and proximal jejunum | Absorbed via PCFT transporter. Folate deficiency causes megaloblastic anaemia. Impaired in coeliac disease, Crohn’s, methotrexate therapy. |
| Fat-soluble vitamins (A, D, E, K) | Jejunum (requires bile salts) | Absorbed as part of mixed micelles. In cholestatic liver disease or ileal disease (reduced bile salt pool) → deficiency. Vitamin K deficiency → coagulopathy (PT prolonged). |
| Carbohydrates | Duodenum and jejunum | Starch → maltose (pancreatic amylase) → glucose (brush border enzymes). Glucose/galactose absorbed by Na⁺-coupled SGLT1 (active). Fructose by GLUT5. Oral rehydration solution exploits the Na⁺-glucose co-transporter. |
| Proteins / amino acids | Duodenum and jejunum | Pancreatic proteases → oligopeptides → Na⁺-coupled transporters. Di/tripeptides absorbed more efficiently than single amino acids. |
| Fats | Proximal jejunum | Emulsified by bile salts → mixed micelles → pancreatic lipase → fatty acids + monoglycerides → enterocytes → triglycerides → chylomicrons → lacteals → lymphatics → thoracic duct. Bypasses portal circulation. |
| Bile acids / salts | Terminal ileum ONLY (active, specific — ASBT transporter) | 95% actively reabsorbed → enterohepatic circulation → portal vein → liver. Loss (Crohn’s, ileal resection) → depleted bile acid pool → fat malabsorption + steatorrhoea AND bile acid diarrhoea (bile acids in colon → secretory diarrhoea). Treatment: cholestyramine. |
| Vitamin B12 (cobalamin) | Terminal ileum ONLY (specific — IF-cubilin receptor) | B12 binds intrinsic factor (from gastric parietal cells) → IF-B12 complex binds cubilin receptor in terminal ileum. Loss of >60 cm → B12 malabsorption → megaloblastic anaemia + SACD. Requires lifelong IM hydroxocobalamin. Oral B12 is ineffective (absorptive mechanism destroyed). |
| Water and electrolytes | Throughout small bowel | Na absorbed by multiple mechanisms (Na-H exchanger, Na-glucose co-transporter, Na-amino acid). Water follows osmotically. Chloride absorbed in exchange for bicarbonate. |
The Critical 60 cm of Terminal Ileum
The terminal ileum has two irreplaceable functions — no other gut segment can compensate for their loss:
1. Active bile acid reabsorption (ASBT transporter) — 95% of bile acids recirculated
2. Vitamin B12 absorption (IF-cubilin receptor)
Resection of >60 cm of terminal ileum produces:
🔵 B12 deficiency → megaloblastic anaemia, SACD → lifelong IM hydroxocobalamin
🔵 Fat malabsorption and steatorrhoea (depleted bile acid pool)
🔵 Bile acid diarrhoea → cholestyramine
🔵 Gallstones (reduced bile acid pool → cholesterol stones)
🔵 Oxalate kidney stones — normally calcium binds oxalate in the gut → excreted. With fat malabsorption, calcium binds to fatty acids instead → free oxalate absorbed → hyperoxaluria → calcium oxalate stones
Conjugated bile salts are secreted by the liver in bile → pass through the GI tract → 95% actively reabsorbed by specific transporters in the terminal ileum → portal vein → liver for reconjugation and re-secretion. Only ~5% lost in stool (replaced by hepatic synthesis).
Primary Bile Salt Diarrhoea (BAM)
When bile acid reabsorption is impaired (terminal ileal disease or resection), excess bile acids reach the colon → stimulate colonic secretion → watery secretory diarrhoea. Responds to cholestyramine (bile acid sequestrant). Distinguish from fat malabsorption diarrhoea (steatorrhoea = pale, fatty, offensive, floats).
During fasting, the MMC (“housekeeper wave”) sweeps through the stomach and small bowel every 70–90 minutes, clearing residual food, bacteria, and debris distally. Initiated by motilin. Abolished by eating.
- Phase I: quiescence (40–60 min)
- Phase II: irregular contractions (20–30 min)
- Phase III: intense regular contractions — the actual sweeping wave (5–10 min)
Clinical significance: Loss of the MMC (post-vagotomy, diabetic autonomic neuropathy, opiates, scleroderma) → Small Intestinal Bacterial Overgrowth (SIBO). Erythromycin is a motilin receptor agonist — used as a prokinetic in gastroparesis.
Why Fluid Balance Matters in Small Bowel Disease
A high-output small bowel fistula or ileostomy produces 2000–4000+ mL/day, rapidly causing:
🔴 Dehydration — large volume losses
🔴 Hyponatraemia — sodium-rich intestinal fluid lost
🔴 Hypokalaemia — potassium-rich secretions lost
🔴 Hypomagnesaemia — magnesium absorbed predominantly in the jejunum
🔴 Metabolic acidosis — bicarbonate-rich fluid lost (opposite of pyloric obstruction → metabolic alkalosis)
Management: loperamide, codeine phosphate, oral rehydration solutions (NOT free water — worsens sodium loss), IV supplementation. PPIs reduce gastric secretion volume. IV magnesium replacement frequently needed.
Intraoperative Bowel Viability Assessment
Assessing bowel viability is a critical intraoperative decision — returning non-viable bowel to the abdomen leads to perforation, peritonitis, and death. Every surgeon must be able to confidently classify bowel as viable, ischaemic, or non-viable.
- Pink/red healthy colour
- Glistening serosa
- Peristalsis present
- Mesenteric arterial pulsation present
- Bowel wall tone normal
Action: Safe to return to abdomen or anastomose.
- Pale or grey colour
- Reduced peristalsis
- Arterial pulsation reduced
- Some wall tone maintained
Action: Wrap in warm moist gauze for 10 minutes then reassess. Use Doppler probe or fluorescein (IV fluorescein + Wood’s lamp — perfused bowel fluoresces). If still uncertain → leave in abdomen and plan a “second look” laparotomy at 24–48h.
- Dusky, blue-black, or black colour
- Absent peristalsis
- NO arterial pulsation
- Flaccid, no wall tone
- May be gangrenous or perforated
Action: MUST RESECT. Do NOT return to abdomen. Resect with a margin into healthy bleeding bowel on both sides. Primary anastomosis if patient is stable and bowel ends are healthy; otherwise defunctioning stoma.
| Method | How It Works | Notes |
|---|---|---|
| Warm ischaemia test | Wrap questionable bowel in warm moist gauze for 10 minutes, then reassess colour, peristalsis, and pulsations | Simple, no equipment needed. Most commonly used first-line adjunct. |
| Doppler probe | Handheld Doppler applied directly to the bowel wall or mesenteric vessels — detects arterial signal in the wall | Useful for assessing the adequacy of blood supply at an anastomotic margin before division. |
| Fluorescein + Wood’s lamp | IV sodium fluorescein injected → 5 minutes wait → inspect bowel under UV (Wood’s lamp). Perfused bowel fluoresces yellow-green; non-perfused appears dark. | Useful for subtle ischaemia not apparent visually. Can assess anastomotic perfusion. Repeated doses limited by accumulation. |
| Second-look laparotomy | Planned return to theatre at 24–48 hours after initial damage control surgery to reassess bowel viability once resuscitation is complete | Indicated when: viability uncertain, damage control approach taken, patient too unstable for definitive surgery at first look. Reduces unnecessary bowel resection at initial operation. |
The Warm Ischaemia Test — Practical Detail
Unwrap the bowel from any constriction (hernia ring, adhesion band). Apply warm moist gauze packs for 10 minutes. Re-examine:
🟢 Bowel becomes pink + peristalsis returns + pulsation returns → viable → return to abdomen
🟡 Improvement but still uncertain → fluorescein or Doppler → if still uncertain → plan second look
🔴 No change / worsening → non-viable → RESECT
Small Bowel Obstruction (SBO)
Small bowel obstruction accounts for approximately 80% of all bowel obstructions. Key distinction: simple obstruction (bowel occluded but viable) vs strangulated obstruction (compromised blood supply — surgical emergency).
🏆 Adhesions (~60%)
Most common in the Western world. Previous abdominal surgery, peritonitis, endometriosis. Nasogastric decompression ± adhesiolysis if not resolving. Gastrografin challenge at 24–48h predicts and speeds spontaneous resolution.
Hernias (~20%)
Inguinal (most common), femoral (highest strangulation risk), umbilical, incisional, obturator, internal hernias (post-RYGB — Peterson’s hernia). Always examine ALL hernia orifices in any bowel obstruction.
Neoplasms (~5%)
Primary small bowel tumours (rare) or external compression from peritoneal carcinomatosis. Lymphoma can cause intussusception in adults. Carcinoid causes mesenteric fibrosis → kinking.
Volvulus
Twisting around the mesenteric axis → closed-loop obstruction → rapid strangulation. Small bowel volvulus more common in developing countries (large bolus meals).
Intussusception
Children: Ileocolic, idiopathic (Peyer’s patch hypertrophy post-viral). Triad: colicky pain, redcurrant jelly stools, sausage-shaped RUQ mass. Air/hydrostatic enema reduction (~80% success). Adults: Always has a pathological lead point → resection required.
Crohn’s Stricture
Transmural fibrosis → progressive luminal narrowing → acute-on-chronic obstruction. Often managed with stricturoplasty to preserve bowel length.
Gallstone Ileus
Large gallstone erodes through cholecystoduodenal fistula → impacts at terminal ileum (narrowest segment). Rigler’s triad on AXR: SBO + pneumobilia + ectopic stone.
Radiation Enteritis
Late complication of pelvic radiotherapy. Progressive endarteritis → ischaemia → fibrosis → stricture. Presents years after treatment. Surgery in radiated tissue carries very high complication rates.
Closed Loop Obstruction
When both limbs of a bowel loop are occluded, the loop cannot decompress proximally or distally — pressure rapidly increases within the closed loop → ischaemia → perforation. High-risk scenarios: volvulus, internal hernia, single adhesion causing a U-shaped loop obstruction.
CT appearance: beak sign, whirl sign (twisted mesentery), U-shaped or C-shaped dilated loop with thickened walls and mesenteric oedema. Closed loop obstruction = emergency laparotomy regardless of clinical appearance — do NOT attempt Gastrografin trial.
| Feature | Simple SBO | Strangulated SBO |
|---|---|---|
| Pain | Colicky, central/periumbilical, intermittent | Constant, severe — peritonitic when transmural ischaemia develops |
| Vomiting | Early and bilious. High obstruction: early. Low obstruction: late and faeculent. | Prominent, may become faeculent |
| Distension | Present — more with distal obstruction | Present, may be asymmetric |
| Bowel sounds | Tinkling, high-pitched “rushes and gurgles” | Absent (ileus from peritonitis) |
| Absolute constipation | Complete — no flatus or faeces | Complete |
| Systemic signs | Tachycardia from dehydration; minimal pyrexia | High fever, tachycardia out of proportion, hypotension, peritonism, raised lactate, raised WBC |
| Peritonism | Absent | Present — rebound, guarding, rigidity |
Strangulation Red Flags — Any One = Emergency Laparotomy
🔴 Pain changing from colicky to constant
🔴 Localised peritonism or rebound tenderness
🔴 Pyrexia >38.5°C
🔴 Tachycardia disproportionate to dehydration
🔴 Raised lactate (tissue ischaemia)
🔴 Raised WBC >18 × 10⁹/L
Any suspicion of strangulation = emergency laparotomy. Do NOT delay for Gastrografin trial.
| Investigation | Findings |
|---|---|
| AXR (supine + erect) | Dilated small bowel loops (>3 cm) with valvulae conniventes / plicae circulares (run fully across bowel width — distinguish from haustra which are incomplete). Central loops. Erect: air-fluid levels. Absent colonic gas. Rigler’s triad if gallstone ileus. |
| CT abdomen/pelvis (gold standard) | Identifies level, cause, strangulation signs (thickened wall, mesenteric stranding, portal venous gas, free fluid, pneumatosis intestinalis, closed-loop). Sensitivity >90%. |
| Bloods | FBC (raised WBC), U&E (dehydration), VBG (lactate — ischaemia, metabolic acidosis), CRP, G&S |
| Gastrografin challenge | Water-soluble contrast given orally/NG. Contrast in colon within 24h predicts resolution of adhesional SBO (90% sensitivity). Also acts as osmotic agent pulling fluid into bowel lumen. |
Management — “Drip and Suck”
Non-operative (initial — for simple adhesional SBO):
🟢 NBM + IV fluid resuscitation + electrolyte correction
🟢 Nasogastric tube (NG) — decompresses stomach, reduces aspiration risk
🟢 Urinary catheter — monitor urine output (>0.5 mL/kg/hr)
🟢 Analgesia and anti-emetics
🟢 Gastrografin challenge at 24–48h if not resolving
🟢 Serial clinical reassessment — any deterioration → operative
Operative indications (emergency):
🔴 Any sign of strangulation
🔴 Closed-loop obstruction on CT
🔴 Complete obstruction not resolving (>48–72h)
🔴 Hernia causing obstruction (especially femoral)
Surgical approach: Laparoscopic preferred for adhesiolysis. Open for complex cases or strangulation. Assess bowel viability intraoperatively — warm saline + 5 minutes. If uncertain → second-look laparotomy at 36–48h.
Meckel’s Diverticulum
Meckel’s diverticulum is a true diverticulum (contains all three layers of the bowel wall) arising from the antimesenteric border of the distal ileum. It is the most common congenital anomaly of the GI tract, resulting from incomplete obliteration of the vitello-intestinal (omphalomesenteric) duct.
Prevalence — found in 2% of the population
Most common congenital GI anomaly. 95–98% remain asymptomatic lifelong. Risk of complications decreases with age.
Length — approximately 2 inches (5 cm) long
True diverticulum — contains all three bowel wall layers. Receives its own end-artery directly from the SMA (vitello-intestinal artery remnant).
Location — 2 feet (60 cm) proximal to the ileocaecal valve
Always on the antimesenteric border of the ileum. The position means no mesenteric vessels supply it directly.
Presents before age 2 (in children)
Painless massive PR bleeding (maroon stool) = ectopic gastric mucosa + ileal ulceration. Most common presentation in children under 2.
2 types of ectopic tissue — gastric (most common, ~50%) and pancreatic
Gastric mucosa → HCl → adjacent ileal ulceration → painless haemorrhage. Pancreatic tissue → diverticular pancreatitis.
| Presentation | Age Group | Mechanism | Notes |
|---|---|---|---|
| Painless lower GI haemorrhage | Children <2 years | Ectopic gastric mucosa → HCl ulcerates adjacent normal ileal mucosa → haemorrhage. Classic: maroon/brick-red stool. Profuse, can cause haemodynamic instability. | The “painless” nature distinguishes it. A child with unexplained painless rectal bleeding = Meckel’s until proven otherwise. |
| Meckel’s diverticulitis | Adults and children | Inflammation identical to appendicitis. Can perforate. Clinically indistinguishable from acute appendicitis. | At laparoscopy for suspected appendicitis with normal appendix → always examine the last 60–100 cm of terminal ileum. |
| Obstruction | Adults | (1) Fibrous band from diverticulum tip to umbilicus — acts as fixed point around which bowel wraps. (2) Intussusception — the diverticulum acts as a lead point. | Most common complication in adults. Intussusception with Meckel’s lead point in adults requires resection. |
| Volvulus | All ages | The fibrous band acts as a fixed pivot point — midgut twists around it → catastrophic midgut volvulus. | Can cause rapid irreversible midgut ischaemia. |
Meckel’s Scan (Tc-99m Pertechnetate)
Technetium-99m pertechnetate is taken up by mucus-secreting cells of gastric mucosa. IV injection → scintography → “hot spot” in the right iliac fossa = ectopic gastric mucosa = Meckel’s.
- Sensitivity: ~85% in children, ~60% in adults
- Specificity: ~95%
- H2 blockers improve sensitivity by preventing secretion of Tc-99m back into the lumen
Management — Symptomatic vs Incidental
Symptomatic: Always requires surgical excision.
🟢 Simple diverticulectomy — stapled transverse excision. For narrow base + healthy adjacent ileum.
🟢 Segmental ileal resection + anastomosis — required for wide base, ischaemic/perforated adjacent ileum, or intussusception with bowel wall compromise.
Incidental (asymptomatic): Current consensus is do NOT routinely excise in adults — operative risk exceeds lifetime complication risk. Exception: palpable ectopic tissue (suggests gastric mucosa), fibrous band present, long diverticulum (>2 cm), or narrow base.
Crohn’s Disease
Crohn’s disease is a chronic, relapsing transmural inflammatory bowel disease that can affect any part of the GI tract from mouth to anus. Characterised by transmural inflammation, non-caseating granulomas, skip lesions, cobblestone appearance, and “rose thorn” deep fissuring ulcers.
| Location | Frequency | Notes |
|---|---|---|
| Terminal ileum ± caecum (ileocaecal) | ~50% | Most common. RIF pain, diarrhoea, weight loss — frequently misdiagnosed as appendicitis. |
| Small bowel alone | ~30% | Multiple skip lesions. Highest nutritional deficiency risk. |
| Colon alone (Crohn’s colitis) | ~20% | Rectal sparing common (distinguishes from UC). |
| Perianal | ~20–30% | Fissures, fistulae, skin tags, abscesses. Complex perianal fistulas = hallmark of Crohn’s. |
| Upper GI | ~5% | Dyspepsia or pyloric obstruction. |
| Complication | Mechanism | Management |
|---|---|---|
| Stricture / Obstruction | Transmural inflammation → fibrosis → progressive luminal narrowing. Most common in terminal ileum. | Short fibrotic strictures (<10 cm): stricturoplasty (preserves bowel length). Multiple/longer: resection + anastomosis. Always biopsy — exclude malignancy in chronic strictures. |
| Abscess | Deep fissuring ulcers → microperforations → localised collection. RIF / pelvic / psoas. | Antibiotics + CT-guided percutaneous drainage. Definitive: resect the driving segment after sepsis control and nutritional optimisation. |
| Fistula | Transmural inflammation + microperforations + tissue planes → fistula to adjacent structures. Enteroenteric, enterovesical (pneumaturia, faecuria), enterocutaneous, rectovaginal. | SNAP protocol (see fistulas tab). Anti-TNF (infliximab) for perianal fistulas. Resect diseased loop. Seton for complex perianal fistulas. |
| Free perforation | Deep ulceration perforates → generalised peritonitis | Emergency laparotomy. Resect perforated segment. Defunctioning stoma if patient unstable. |
| Cancer | Chronic transmural inflammation → malignant transformation in long-standing strictures | Always biopsy at stricturoplasty. Suspect if stricture feels unusually hard or irregular. |
| Technique | Stricture Length | Method |
|---|---|---|
| Heineke-Mikulicz | <10 cm (short) | Open stricture longitudinally, close transversely — widens the lumen without resection. Simple, widely used. |
| Finney | 10–20 cm (medium) | Fold the stricture on itself and create a side-to-side anastomosis — relieves the obstruction. |
| Michelassi (isoperistaltic side-to-side) | >20 cm (long) | Side-to-side isoperistaltic stricturoplasty for very long strictures — preserves maximum bowel length. |
Surgical Principles — “Minimal Resection, Maximal Conservation”
Surgery cannot cure Crohn’s — it is pan-intestinal and recurs. The surgical mantra:
🔵 Operate for complications, not the disease itself
🔵 Preserve every centimetre of bowel — prevent short bowel syndrome
🔵 Minimal resection margins — macroscopic clearance only; no oncological margin needed
🔵 Stricturoplasty over resection when feasible for multiple short strictures
🔵 Always biopsy every stricturoplasty — exclude malignant transformation
🔵 Smoking cessation — single most important intervention to reduce post-operative recurrence
🔵 Post-op surveillance colonoscopy at 6–12 months (Rutgeerts score at anastomosis)
Short Bowel Syndrome & Ileostomy
Short bowel syndrome (SBS) occurs when less than ~200 cm of functional small bowel remains (normal = 6–7 m). Results in malabsorption, chronic diarrhoea, dehydration, and malnutrition.
Causes
- Crohn’s disease (repeated resections)
- Mesenteric ischaemia — SMA thrombosis or embolism (may lose the entire midgut)
- Volvulus (midgut)
- Trauma
- Radiation enteritis with extensive resection
| Remaining bowel | Prognosis | Notes |
|---|---|---|
| >200 cm | Likely independent of PN | Intestinal adaptation (villus hypertrophy) over months–years with appropriate nutritional support |
| 100–200 cm + intact colon | Possible independence from PN | The colon salvages fluid and ferments undigested carbohydrates → short-chain fatty acids → additional calories. The colon is invaluable in SBS. |
| <100 cm, no colon | Likely permanent PN dependence | May be a candidate for intestinal transplantation (complex, limited centres) |
Management of Short Bowel Syndrome
- Total parenteral nutrition (TPN) — often lifelong in severe SBS
- Oral rehydration solutions (ORS) — specifically isotonic solutions (NOT hypotonic free water which worsens sodium loss)
- Antimotility agents — loperamide, codeine phosphate
- Proton pump inhibitors — reduce gastric secretion volume in the early post-resection period
- IV magnesium supplementation — frequently required
- Teduglutide (GLP-2 analogue) — increases intestinal absorption; reduces PN requirements in SBS
- Intestinal transplantation — for PN-dependent patients with PN complications
High-Output Ileostomy — The Electrolyte Catastrophe
Output >1500 mL/24 hours causes rapid and potentially fatal electrolyte derangements:
🔴 Dehydration — large volume isotonic losses
🔴 Hyponatraemia — sodium-rich intestinal fluid lost. Key: do NOT give free water or hypotonic fluids — this worsens the sodium loss. Give isotonic oral rehydration solutions (ORS: 1L water + 6 tsp sugar + 1 tsp salt).
🔴 Hypomagnesaemia — magnesium absorbed in the jejunum; lost in high-output states. Magnesium deficiency causes muscle cramps, tetany, arrhythmias. Replace IV.
🔴 Hypokalaemia — potassium lost in effluent
🔴 Metabolic acidosis — bicarbonate-rich fluid lost
🔴 Pre-renal acute kidney injury from persistent dehydration
Management of High-Output Ileostomy
- Oral rehydration solution (ORS) — NOT free water or hypotonic fluids
- Loperamide — first-line antimotility agent; reduces output by slowing transit
- Codeine phosphate — second-line antimotility; can be added to loperamide
- Proton pump inhibitors — reduce gastric secretions contributing to output
- Octreotide (somatostatin analogue) — reduces GI secretions; for refractory high output. Reserved for cases not responding to above.
- IV fluids + electrolyte replacement (Na, K, Mg) if severe
- Consider underlying cause — obstruction distally? Crohn’s recurrence?
| Complication | Definition | Management |
|---|---|---|
| High output | >1500 mL/24h (ileostomy) | ORS, loperamide, codeine, PPI, octreotide (refractory), IV replacement |
| Prolapse | Bowel telescopes through the stoma opening >2–3 cm | Manual reduction if reducible. Surgical revision if irreducible, recurrent, or ischaemic. Loop ileostomies more prone to prolapse. |
| Retraction | Stoma recedes below skin level — contents pool under the flange → leakage + skin breakdown | Convex appliances to improve seal. Surgical revision if severe. |
| Parastomal hernia | Defect in the abdominal wall around the stoma → bowel herniates alongside it | Most common stoma complication long-term. Conservative (support belt) or surgical repair (mesh with stoma relocation). Prevention: placing stoma through the rectus abdominis muscle. |
| Stenosis | Narrowing of the stoma aperture → partial or complete obstruction | Gentle digital dilatation if mild. Surgical refashioning if severe. |
| Skin excoriation | Liquid ileostomy effluent contacts skin → enzymatic digestion → severe painful skin breakdown | Stoma nurse — correct appliance fit; barrier creams; stoma paste. Prevention: adequate spout length (2–3 cm). |
| Ischaemia / necrosis | Inadequate blood supply → stoma turns dark/black. Early complication. | Assessment: insert a lubricated glass test tube to assess mucosal colour. If ischaemia confined to above the fascia → revise the spout. If below the fascia → urgent reoperation. |
Mesenteric Ischaemia & Enterocutaneous Fistulas
| Cause | Frequency | Key Features |
|---|---|---|
| SMA embolism | ~50% | Most common cause. Source: cardiac (AF, post-MI thrombus, valvular disease). Sudden onset. Often lodges at the origin of the middle colic artery — sparing the proximal jejunum (coeliac territory). Emergency embolectomy or catheter-directed thrombolysis. |
| SMA thrombosis | ~25% | Thrombosis on pre-existing atherosclerotic plaque. History of chronic mesenteric ischaemia (post-prandial pain, weight loss, “food fear”). More gradual onset. Requires revascularisation. |
| Non-occlusive mesenteric ischaemia (NOMI) | ~20% | Mesenteric vasoconstriction without mechanical obstruction in critically ill patients (septic shock, cardiogenic shock, post-cardiac surgery). CT: “pruned tree” pattern. Treatment: vasodilators (papaverine), treat underlying cause. Mortality ~70%. |
| Mesenteric vein thrombosis (MVT) | ~5% | SMV thrombosis → venous outflow obstruction → oedema and ischaemia. Gradual onset. Causes: hypercoagulable states, portal hypertension, pancreatitis. Treatment: anticoagulation (heparin). Surgery if bowel non-viable. |
“Pain Out of Proportion to Examination” — The SMA Warning
Classic presentation: severe agonising periumbilical pain with an initially soft and non-tender abdomen.
In the early phase, visceral afferents fire intensely (severe central pain) but the parietal peritoneum is not yet inflamed (no tenderness). Once transmural ischaemia develops, the parietal peritoneum becomes involved → peritonism. By this point, significant bowel necrosis has occurred.
Any elderly patient with AF or known cardiac disease + severe central abdominal pain + soft abdomen = CT angiography of the mesenteric vessels immediately.
An enterocutaneous fistula (ECF) is an abnormal connection between the intestinal lumen and the skin. The vast majority (>80%) are postoperative complications — leaking anastomoses, inadvertent enterotomies during adhesiolysis, or surgery in a hostile abdomen. A minority arise spontaneously (Crohn’s, radiation, malignancy).
Immediate priority. Uncontrolled sepsis prevents fistula closure and will kill the patient.
- CT abdomen — identify undrained collections
- CT-guided or surgical drainage of abscesses
- Broad-spectrum IV antibiotics
- Source control — may include defunctioning stoma
Critical for healing and surgical fitness. Fistulas cannot close in a malnourished patient.
- TPN — especially for high-output proximal fistulas
- Target: albumin >30 g/L; positive nitrogen balance
- Octreotide — reduces GI secretions + fistula output
- Skin protection (stoma nurse, barrier creams, pouching)
Fully define the fistula before any surgery.
- Fistulogram — contrast into tract under fluoroscopy. Defines origin, tract, cavities.
- CT with oral + IV contrast — assess downstream anatomy, distal obstruction
- FRIEND factors predicting non-closure: Foreign body, Radiation, Inflammation/IBD, Epithelialisation, Neoplasm, Distal obstruction
Definitive surgery — only when fully optimised.
- Low output (<200 mL/day): often close spontaneously (6–8 weeks)
- High output (>500 mL/day): rarely close — need surgery
- Surgery delayed minimum 3–6 months — let adhesions soften (“abdomen unfreezes”)
- Resect fistula-bearing segment + primary anastomosis
- Mortality 5–20%
Tumours of the Small Bowel
Primary small bowel tumours are exceptionally rare — <5% of all GI tumours despite the small bowel comprising 75% of GI tract length and 90% of mucosal surface area. The relative rarity is attributed to: rapid transit, alkaline secretions, high IgA, and low bacterial counts.
The most important and most common primary small bowel tumours. Arise from enterochromaffin cells (Kulchitsky cells) in the crypts of Lieberkühn. Classified as well-differentiated neuroendocrine tumours (NETs).
- Most common site: terminal ileum (40%), appendix (30%), rectum
- Secrete: serotonin (5-HT), substance P, histamine, bradykinin, prostaglandins
- Tumour markers: Chromogranin A (CgA) + urinary 5-HIAA (serotonin metabolite)
Carcinoid Syndrome — Only With Liver Metastases
Carcinoid syndrome (flushing, diarrhoea, bronchospasm, right-sided valvular heart disease) occurs when vasoactive peptides reach the systemic circulation. A localised gut NET’s serotonin enters the portal vein → first-pass hepatic inactivation → no systemic syndrome.
With hepatic metastases, serotonin is secreted directly into the hepatic veins, bypassing first-pass metabolism → systemic carcinoid syndrome. This is why carcinoid syndrome is a marker of hepatic metastatic disease.
Carcinoid heart disease: serotonin causes endocardial fibrosis of the right side of the heart (tricuspid + pulmonary valves). Left side protected — serotonin inactivated in the pulmonary circulation.
Carcinoid crisis: triggered by surgery, anaesthesia, or tumour manipulation → extreme flushing, bronchospasm, haemodynamic instability. Prevent with IV octreotide pre-operatively.
Mesenteric fibrosis: NETs secrete TGF-β → intense desmoplastic reaction → bowel kinking and obstruction + vascular encasement → ischaemia. May be the presenting feature even with a tiny primary tumour.
Mesenchymal tumours arising from the interstitial cells of Cajal (gut pacemaker cells). Stomach (60%) and small bowel (30%) most common sites.
| Feature | Detail |
|---|---|
| Driver mutation | KIT gene (c-KIT, CD117) in ~85%. PDGFRA mutation ~10%. Both are tyrosine kinase receptors — basis for targeted therapy. |
| Histology | Spindle cells (most common). CD117 (c-KIT) positive on immunohistochemistry — pathognomonic. |
| Presentation | Often incidental. Symptomatic: abdominal pain, GI bleeding (submucosal → mucosal ulceration), palpable mass. Small bowel GISTs bleed more than gastric GISTs. |
| Malignant potential | Assessed by size and mitotic count (Fletcher/Miettinen criteria). All GISTs have some malignant potential. |
| Management | Surgical resection (wedge/segmental) with clear margins. Do NOT biopsy pre-operatively (haemorrhage, seeding risk). Adjuvant imatinib (tyrosine kinase inhibitor) for high-risk resected GISTs and metastatic disease. |
Extremely rare. Most common site: duodenum (periampullary region). Risk factors: coeliac disease, Crohn’s disease, FAP (periampullary adenomas), Lynch syndrome, Peutz-Jeghers syndrome.
Most common extranodal lymphoma site. Most are B-cell non-Hodgkin lymphomas. Enteropathy-associated T-cell lymphoma (EATL) — strongly associated with coeliac disease, very aggressive, poor prognosis. Lymphoma can present as intussusception — in adults, always resect (pathological lead point).
Mnemonics & Clinical Pearls
2% of the population
Most common congenital GI anomaly. 95–98% asymptomatic lifelong.
2 inches (5 cm) long
True diverticulum on antimesenteric border. Has its own end-artery.
2 feet (60 cm) from ileocaecal valve
Always antimesenteric. In RIF at laparoscopy — always check last 60–100 cm of terminal ileum if appendix is normal.
Presents before age 2 in children
Painless PR bleeding (maroon stool) = ectopic gastric mucosa. Use Tc-99m scan for diagnosis.
2 types of ectopic tissue: gastric (50%) and pancreatic
Gastric → HCl → ileal ulceration → bleeding. Pancreatic → diverticular pancreatitis.
Long vasa recta
Jejunum has long vasa recta; ileum has short ones.
Arcades — few, large (jejunum) vs many, small (ileum)
Mesentery of jejunum is almost transparent. Ileal mesentery is fatty and opaque.
Vascular — deeper red, more vascular
Internal folds (plicae circulares) — large and packed in jejunum
“Stacked coins” on small bowel imaging. Absent distally in ileum.
Size — thicker, heavier wall in jejunum
Palpably thicker. Ileum is thin-walled.
Higher up — left side / upper abdomen (jejunum)
Ileum occupies the right and lower abdomen, ending at the RIF.
B12 (cubilin receptor) — only in terminal ileum → lifelong IM hydroxocobalamin if >60 cm lost
Oral B12 is useless after terminal ileal resection — the absorptive mechanism itself has been removed.
Bile acid reabsorption (ASBT) — 95% recirculated; loss → steatorrhoea + bile acid diarrhoea + gallstones
Cholestyramine for bile acid diarrhoea. Fat malabsorption → fat-soluble vitamin deficiency.
Oxalate stones — fat malabsorption → Ca binds fatty acids → free oxalate absorbed → hyperoxaluria
Normally calcium binds oxalate in the gut → excreted. Fat malabsorption breaks this protective mechanism.
Sepsis — control it first. CT + percutaneous drainage + antibiotics.
No fistula will close until sepsis is controlled. Unrecognised abscess = surgical emergency.
Nutrition — TPN often required. Target albumin >30 g/L. Octreotide reduces output.
High-output proximal fistulas require TPN (enteral feeds drive more output).
Anatomy — fistulogram + CT. FRIEND factors predict non-closure.
Foreign body, Radiation, Inflammation/IBD, Epithelialised tract, Neoplasm, Distal obstruction → unlikely to close spontaneously.
Plan — wait 3–6 months minimum. Low output: may close. High output (>500 mL): needs surgery.
Let the abdomen “unfreeze”. Never rush to the operating room acutely.
Viable: Pink/red · Glistening serosa · Peristalsis · Arterial pulsation
All four features present → safe to return to abdomen.
Uncertain: Pale/grey · Reduced peristalsis · Reduced pulsation
Wrap in warm moist gauze 10 mins → reassess. Use Doppler/fluorescein. Plan second look if still uncertain.
Non-viable: Dusky/black · Absent peristalsis · NO pulsation → MUST RESECT
Do NOT return to abdomen. Resect to healthy bleeding bowel on both sides.
RIF · Spout (everted 2–3 cm) · Liquid output · Loop (defunctioning) or End (permanent)
High output >1500 mL/24h → hyponatraemia, hypomagnesaemia, dehydration. Treat with ORS (not free water), loperamide, codeine, PPI, octreotide.
LIF · Flush with skin · Formed output · Hartmann’s end colostomy or loop defunctioning
Sigmoid colostomy in LIF. Transverse loop colostomy in upper abdomen (when sigmoid used for other purpose).
Localised NET: serotonin → portal vein → liver first-pass → inactivated → no systemic syndrome
Local NET causes obstruction, bleeding, mesenteric fibrosis — but NOT flushing/diarrhoea.
Liver metastases: serotonin → hepatic veins → systemic → flushing, secretory diarrhoea, bronchospasm, right-sided valve disease
Left side protected — serotonin inactivated in the pulmonary circulation.
Octreotide — controls symptoms AND has anti-tumour effect. Give IV pre-op to prevent carcinoid crisis.
Depot formulation (lanreotide/octreotide LAR) for long-term maintenance.