Ischemic Colitis

Anatomy - The Foundation for Understanding IC

• Superior mesenteric artery (SMA): ileocolic, right colic, and middle colic branches - supplies ascending colon and proximal two-thirds of transverse colon
• Inferior mesenteric artery (IMA): left colic, sigmoid branches, and superior rectal artery - supplies the remainder

• Marginal artery of Drummond - runs parallel to the mesenteric margin from cecocolic to rectosigmoid junction; receives flow from both SMA and IMA terminal branches. Absent at the splenic flexure in up to 18% of people.
• Arc of Riolan (meandering mesenteric artery) - an inconstant vessel connecting the SMA/middle colic to the IMA/left colic near the mesenteric root. When present and prominent, it often signals occlusion of one of the major vessels.

Aetiology

Nonocclusive Causes (most common)

• Septic shock, hemorrhagic shock, cardiogenic shock
• Congestive heart failure
• Dehydration
• Post-major surgery (especially aortic surgery, AAA repair with IMA ligation)

• Cocaine and methamphetamine use (particularly in young patients without vascular risk factors)
• Vasopressor drugs (e.g., norepinephrine)
• Serotonergic drugs: sumatriptan, alosetron
• Decongestants: pseudoephedrine

• Diverticulitis, volvulus, tumor, adhesions, intestinal prolapse causing raised intraluminal pressure

Occlusive Causes (less common)

• Arterial embolism (e.g., from atrial fibrillation) - IMA rarely involved due to its small caliber compared with SMA
• Arterial thrombosis - on a background of atherosclerosis
• Venous thrombosis - in hypercoagulable states (nephrotic syndrome, antiphospholipid syndrome, OCP use, malignancy)
• Iatrogenic - aortoiliac instrumentation, endovascular AAA repair, post-colonoscopy

Drug-Related Causes

Infectious Causes

• E. coli O157:H7 (enterohemorrhagic, Shiga toxin-producing): the prototype - direct cytotoxic effect on endothelium causes mucosal ischemia ± hemolytic uremic syndrome; fibrin thrombi seen on biopsy
• Clostridioides difficile: can produce ischemic-pattern injury

Risk Factors

Pathogenesis

1. Mucosal ischaemia develops first (mucosa is the most metabolically active layer and farthest from the submucosal vessels)
2. Reperfusion injury from reactive oxygen species compounds the damage
3. Failure of the intestinal epithelial barrier allows bacterial translocation
4. Progression depends on severity and duration of ischaemia:
   • Reversible mucosal/submucosal ischaemia - most cases (~80%); resolves with supportive care
   • Irreversible transmural ischaemia - gangrene, perforation, peritonitis

• Marked surface injury with mucin loss
• "Atrophic microcrypts" and crypt dropout
• Hyalinisation of the lamina propria ("lamina propria collapse")
• In infectious (E. coli O157:H7) cases: prominent fibrin thrombi

Clinical Features

Symptoms

Location-Based Variants

• Left colon (including splenic flexure): most common location; typical presentation above
• Sigmoid colon: second most common
• Isolated right-sided IC: ~25% of cases; more likely to present with abdominal pain without bleeding; more often associated with atrial fibrillation, CAD, and chronic renal failure; higher rate of surgical intervention and poorer prognosis
• Pancolitis: rare; carries the worst prognosis

Physical Examination

• Mild-to-moderate tenderness over the affected colon segment
• Abdominal distension
• Signs of peritonitis (guarding, rigidity, rebound) when bowel perforation has occurred

Investigations

• Often non-specific in mild disease
• Severe disease: leukocytosis with neutrophilia, elevated BUN, elevated LDH, elevated lactate, decreased haemoglobin, decreased albumin, metabolic acidosis, low bicarbonate
• Send stool for C. difficile toxin, culture and sensitivity, ova and parasites (to exclude infectious aetiology)

• Most sensitive and specific modality when performed within 48 hours
• Visual inspection confirms mucosal ischaemia; biopsy differentiates IC from IBD or infectious colitis
• Must be performed with caution - risk of exacerbating ischaemia and perforation (low-pressure insufflation; avoid going beyond affected segment)
• Typical findings: pale/cyanotic mucosa, mucosal oedema, submucosal haemorrhage, ulceration, in severe cases necrosis

Complications

Management

Conservative (Non-operative) - ~80% of Cases

1. Bowel rest (nil by mouth)
2. IV fluid resuscitation - correct hypovolaemia and low-flow states
3. Broad-spectrum antibiotics - cover both aerobic and anaerobic gut flora to prevent/treat bacterial translocation (e.g., piperacillin-tazobactam or cephalosporin + metronidazole)
4. Nasogastric tube if ileus is present
5. Optimise cardiac output - treat heart failure, sepsis, arrhythmias
6. Discontinue offending medications - vasopressors where possible, constipation-inducing drugs, OCP, cocaine
7. Avoid cathartics (risk of perforation) and glucocorticoids (unless treating underlying SLE/RA)

• Phosphodiesterase type 5 inhibitors
• Pentoxifylline
• Prostaglandin E1

Elective Surgical Management

• Chronic ischaemic colitis with ongoing/recurrent bouts of abdominal pain, bloody diarrhoea, and sepsis (higher complication rate; requires segmental resection)
• Symptomatic colonic stricture after recovery from IC (or when malignancy cannot be excluded)

Emergency Surgical Management

• Peritonitis
• Haemodynamic instability
• Pneumoperitoneum (free air)
• Portal venous gas on CT
• Failure to improve or clinical deterioration on conservative management

• Examine entire small and large bowel for ischaemia
• Anatomic resection of the ischaemic segment with preservation of the marginal artery
• Anastomosis is generally avoided in the acute setting (risk of anastomotic leak due to evolving ischaemia, haemodynamic instability, sepsis)
• Staple ends in situ; temporary abdominal closure with planned second-look laparotomy at 24 hours to assess viability and extent of resection required
• Pancolitis: total colectomy with end ileostomy

Prognosis

• ~80% resolve with conservative management
• 30-day postoperative mortality after colectomy for IC: ~25-47%
• Independent predictors of perioperative mortality: elderly age, poor functional status, multiple comorbidities, preoperative septic shock, blood transfusions, acute renal failure, delay from admission to surgery
• Isolated right-sided IC carries a worse prognosis than left-sided disease

Mesenteric Ischemia

Anatomy

• Inferior anterior/posterior pancreaticoduodenal arteries
• Middle colic artery (transverse colon)
• Right colic artery
• Ileocolic artery
• Jejunal and ileal branches

Classification

ACUTE MESENTERIC ISCHEMIA (AMI)

Causes and Relative Frequencies

1. SMA Embolism (SMAE)

• Most common cause of AMI
• Embolic source is almost always cardiac: atrial fibrillation/flutter, left atrial/ventricular thrombus (after MI or in cardiomyopathy), valvular disease (mitral stenosis, endocarditis), aortic mural thrombus
• Up to 95% of SMAE patients have a documented cardiac disease history
• Up to 68% have simultaneous embolic events in other beds (cerebrovascular, peripheral)
• Emboli preferentially enter the SMA due to its oblique angle off the aorta
• ~50% lodge just distal to the middle colic artery origin - this is the classic site; spares proximal jejunum and the right colon (supplied by branches proximal to the embolus)
• ~15% lodge at the SMA origin itself
• Mortality without intervention: ~54%

2. SMA Thrombosis / Mesenteric Arterial Occlusive Disease (MAOD)

• Second most common arterial cause; accounts for 20-35%
• Occurs as acute-on-chronic event: in situ thrombosis superimposed on pre-existing severe atherosclerotic stenosis, most commonly within 2 cm of the SMA origin
• Because the occlusion is proximal (before the middle colic artery), it causes more extensive ischemia than embolism - involving both jejunum and ileum, and often right colon
• 20-50% of patients have a prodromal history of CMI (postprandial pain, weight loss) for weeks to months before the acute event
• Other thrombotic causes: hypercoagulable syndromes (Factor V Leiden, antiphospholipid syndrome, prothrombin gene mutations, antithrombin III deficiency, protein C/S deficiency), aortic dissection extending to SMA, in-stent or graft thrombosis
• Mortality without intervention: ~77% (higher than embolism due to larger bowel involvement)

3. Nonocclusive Mesenteric Ischemia (NOMI)

• Results from mesenteric vasospasm - no fixed mechanical obstruction
• Triggered by low cardiac output states that activate the sympathoadrenal axis causing intense splanchnic vasoconstriction
• Common trigger situations: septic shock, cardiogenic shock, post-cardiac surgery, haemodialysis, vasopressor use (norepinephrine, vasopressin)
• The vascular bed goes into persistent spasm even after the precipitating cause is corrected
• Angiographic hallmark: diffuse vasoconstriction of SMA and its branches without a discrete filling defect
• Predominantly affects critically ill patients in the ICU
• Incidence has declined in recent decades due to better ICU monitoring, prompt correction of hypotension, and systemic vasodilator use

4. Mesenteric Venous Thrombosis (MVT)

• Accounts for 5-15% of AMI; involves the superior mesenteric vein (SMV) in 95% of cases
• IMA is only rarely involved
• Leads to venous outflow obstruction → bowel wall oedema → arterial inflow impairment → mucosal ischaemia
• Primary MVT: no identifiable aetiology (~20%)
• Secondary MVT: identifiable aetiological factor (~80%):
  • Inherited thrombophilias: Factor V Leiden, prothrombin gene mutation, protein C/S deficiency, antithrombin III deficiency
  • Acquired: antiphospholipid syndrome, oral contraceptives, nephrotic syndrome, polycythaemia vera, paroxysmal nocturnal haemoglobinuria
  • Local intra-abdominal: cirrhosis/portal hypertension, pancreatitis, abdominal sepsis, inflammatory bowel disease, postoperative state
  • Malignancy
• More indolent course than arterial AMI; may present subacutely over days to weeks

Clinical Features of AMI

Symptoms

The hallmark of AMI is severe abdominal pain that is disproportionate to the degree of tenderness on examination - this "pain-sign discrepancy" is pathognomonic early on.

Physical Examination

• Early (mucosal/submucosal ischaemia): minimal or absent signs - abdomen soft, non-tender or mildly tender
• Late (transmural infarction): peritonitis - abdominal rigidity, guarding, rebound tenderness, abdominal distension, absent bowel sounds, fever, tachycardia, hypotension, passage of bloody stools

The transition from pain-sign discrepancy to peritonitis signals bowel infarction and constitutes a surgical emergency.

Temporal Pathology

• Mucosal sloughing begins within 3 hours of onset
• Full-thickness intestinal infarction by 6 hours

Investigations

Biochemistry

Imaging

• Often normal early
• Later: formless loops of small bowel, ileus, thumbprinting of small bowel or ascending colon
• Ominous late signs: pneumatosis linearis (air in bowel wall), portal/mesenteric vein gas - both presume intestinal gangrene
• Pneumoperitoneum = perforation - immediate laparotomy

• High sensitivity and specificity
• Identifies: arterial/venous occlusions, bowel wall thickening, pneumatosis, portal venous gas, free fluid/perforation
• SMAE: filling defect in SMA distal to middle colic artery
• MAOD: occlusion within 2 cm of SMA origin; surrounding calcification; prominent collaterals suggest chronic nature
• MVT: enlarged SMV with central lucency (thrombus), rim enhancement, bowel wall thickening, mesenteric oedema, collateral veins
• NOMI: diffuse SMA/branch narrowing without a discrete filling defect

• Now largely replaced by CTA for initial diagnosis
• Still used when: diagnosis uncertain, endovascular treatment planned, NOMI (for intra-arterial vasodilator infusion)
• Findings vary by aetiology (see management section)

• Can evaluate proximal SMA/SMV; limited by bowel gas, obesity
• Moderate sensitivity; cannot image smaller mesenteric vessels reliably
• Useful in chronic disease screening; less practical in acute setting

• MVT: sensitivity and specificity ~100% and 98% respectively
• Limited by availability, time, and cost

Management of AMI

General Principles (All Causes)

1. Immediate resuscitation: IV fluids, correct haemodynamic instability
2. Nil by mouth; nasogastric tube if distended
3. Broad-spectrum antibiotics - to cover gram-negative aerobes and anaerobes (bacterial translocation from ischaemic gut)
4. Anticoagulation with systemic heparin - prevents thrombus propagation; initiated once ischaemia is confirmed (unless contraindicated by bleeding)
5. Avoid vasopressors where possible (exacerbate splanchnic vasoconstriction); if unavoidable for haemodynamics, minimise and optimise
6. Urgent imaging (CTA) followed by intervention - "time is bowel"

SMA Embolism - Specific Management

• Catheter-directed thromboaspiration or thrombolysis via angiographic catheter placed in SMA
• Intra-arterial papaverine (vasodilator) infused at SMA catheter site even after embolectomy to prevent/treat associated vasospasm (30-60 mg/h)
• Balloon angioplasty ± stenting of associated stenosis

• Indicated when: peritonitis present, endovascular failure, or bowel infarction
• Transverse arteriotomy of SMA; Fogarty balloon catheter embolectomy
• Bowel assessment: resect clearly non-viable bowel; leave questionable bowel
• Planned second-look laparotomy at 24-48 hours - reassess bowel viability after revascularisation
• Papaverine infusion continued intra- and post-operatively via SMA catheter

MAOD/SMA Thrombosis - Specific Management

• Larger bowel involvement; higher mortality; typically requires revascularisation
• Endovascular: retrograde open mesenteric stenting (ROMS) - SMA catheterised retrogradely via infracolic segment, balloon-expandable covered stent deployed with flare into aortic ostium; or antegrade transfemoral approach with PTA ± stent
• Open surgical revascularisation:
  • Antegrade aortomesenteric bypass (from supracoeliac aorta - less often diseased) using Dacron or PTFE graft
  • Retrograde aortomesenteric bypass (from infra-renal aorta or iliac artery) - more accessible but higher risk of graft kinking
  • Transaortic endarterectomy - for proximal SMA and coeliac lesions
• Bowel resection and second-look laparotomy as needed
• Pre- and post-procedure: antiplatelet therapy + statin; dual antiplatelet therapy (DAPT) for 6-12 weeks post-stenting

NOMI - Specific Management

• Correct the underlying cause (treat shock, optimise cardiac output)
• Intra-arterial papaverine infusion via SMA catheter (30-60 mg/h) - the cornerstone of pharmacological treatment; dramatic reversal of vasospasm seen on repeat angiography after 24-48 hours
• Alternatively: prostaglandin E1 (PGE1) intra-arterially
• Infusion continued for 24 hours; repeat angiography to confirm resolution of vasospasm
• No operation unless peritoneal signs are present; if surgery needed, papaverine infusion is continued during and after exploration
• Leave bowel of questionable viability; second-look operation preferred over massive enterectomy

MVT - Specific Management

• Systemic anticoagulation with heparin (full-dose) is the mainstay - reduces thrombus propagation, allows collateral recanalization, reduces mortality from ~80% to ~20-30%
• Transition to long-term oral anticoagulation (warfarin or DOAC) for 3-6 months minimum; lifelong if underlying thrombophilia or idiopathic
• Thrombolysis/catheter-directed therapy: reserved for progressive disease despite anticoagulation (transhepatic or trans-splenic catheter-directed thrombolysis into SMV)
• Surgery: reserved for bowel infarction (peritonitis or CT evidence of transmural necrosis); resect non-viable bowel, second-look laparotomy
• Test for underlying thrombophilia; treat predisposing conditions

Second-Look Laparotomy

• Bowel viability was uncertain at the first operation
• Marginal bowel was left in situ
• General principle: better to perform a second look than to resect excessively - compromised but viable bowel often improves with revascularisation and supportive care

CHRONIC MESENTERIC ISCHEMIA (CMI)

Pathophysiology

• Results from atherosclerotic stenosis of two or more major splanchnic arteries (coeliac, SMA, IMA) - rarely symptomatic with single-vessel disease due to collateral compensation
• Post-prandial mesenteric blood flow demand (up to 25% of cardiac output) cannot be met by the stenotic vessels - "intestinal angina"
• The insidious development allows extensive collateral formation, so bowel infarction is rare; however, it is a precursor to acute thrombosis

Clinical Features

Investigations

• Duplex ultrasonography: first-line screening; elevated peak systolic velocities in SMA (>275 cm/s) and coeliac (>200 cm/s) indicate significant stenosis; limited by body habitus and bowel gas
• CT angiography (CTA): most commonly used confirmatory test; demonstrates stenosis, calcification, collaterals (prominent arc of Riolan or marginal artery = clue to significant occlusion)
• Catheter-based angiography: gold standard; required pre-operatively for surgical planning

Management

• Percutaneous transluminal angioplasty (PTA) + stent placement (balloon-expandable stents for ostial lesions; self-expanding for body lesions)
• Lower perioperative morbidity/mortality than open surgery
• Higher long-term restenosis rates (~30-40% at 3 years) vs. open surgery (~10-15%)
• Post-stenting: DAPT for 6-12 weeks, long-term single antiplatelet + statin
• Surveillance: CTA or duplex US at 1 month, then biannually for 2 years, then annually

• Better long-term durability
• Antegrade bypass from supracoeliac aorta (preferred; less atherosclerotic inflow)
• Retrograde bypass from infra-renal aorta/iliac
• Transaortic endarterectomy - suitable for proximal, discrete lesions
• Preferred in younger, fit patients, or after endovascular failure/recurrence

MESENTERIC VENOUS THROMBOSIS (MVT) - Chronic Form

• Chronic MVT involves the portal or splenic veins
• Often asymptomatic (extensive collateral venous drainage)
• May develop portal hypertension → oesophagogastric varices, splenomegaly, hypersplenism
• Some present with bleeding from oesophageal varices
• Management: anticoagulation; endoscopic variceal management; TIPS or surgical portosystemic shunting in refractory portal hypertension

Complications of AMI

Prognosis