Intestinal Ischemia

I. Definition

Intestinal ischemia refers to any process that reduces intestinal blood flow below the threshold required to maintain cellular viability, leading to tissue hypoxia and, if uncorrected, transmural necrosis of the bowel wall ^[1][2]. The name itself is instructive:

• "Intestinal" = relating to the intestine (Latin intestinum)
• "Ischemia" = from Greek ischein (to hold back) + haima (blood) — literally "holding back blood"

So intestinal ischemia is the bowel being starved of its blood supply.

Intestinal ischemia can progress to sepsis, peritonitis, free intraabdominal air, bowel infarction, gangrene, and death ^[1].

Classification

Intestinal ischemia is classified along two axes ^[1][2]:

By anatomical segment affected:

• Small bowel ischemia = Mesenteric ischemia (SMA territory predominantly)
• Large bowel ischemia = Colonic ischemia / Ischaemic colitis (IMA territory predominantly)

By time course:

• Acute mesenteric ischemia — sudden onset of intestinal hypoperfusion due to occlusive or non-occlusive obstruction of arterial supply or venous outflow
• Chronic mesenteric ischemia — develops in patients with mesenteric atherosclerosis, causing episodic intestinal hypoperfusion related to eating ("mesenteric angina")

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II. Epidemiology

• Accounts for approximately 0.1% of all hospital admissions, but carries a disproportionately high mortality (50–80% for acute mesenteric ischemia if not treated promptly) ^[1][2]
• Ischaemic colitis is the most common form of intestinal ischemia overall, and the most common cause of colonic ischemia
• Acute mesenteric ischemia (AMI) is less common but far more lethal

Demographics

• Majority of patients are > 60 years old — reflecting the high prevalence of atherosclerosis, AF, and cardiac disease in this age group ^[2][3]
• Female predominance for ischaemic colitis; roughly equal gender distribution for acute mesenteric ischemia
• In Hong Kong, the ageing population and high prevalence of cardiovascular risk factors (hypertension, diabetes, smoking) make intestinal ischemia an increasingly important diagnosis

Risk Factors [1][2][3]

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III. Anatomy and Function of Intestinal Blood Supply

Understanding the vascular anatomy is absolutely essential because it explains where ischemia hits, why certain watershed zones are vulnerable, and how collaterals protect (or fail to protect) the bowel.

A. Arterial Supply

The gut receives its blood from three major aortic branches ^[1]:

The SMA supplies the entire small intestine EXCEPT the proximal duodenum ^[1]. This is why SMA occlusion is devastating — it takes out most of the absorptive surface.

B. Collateral Circulation

The intestine has a rich network of collaterals, which is both a strength (protective) and a weakness (watershed zones):

• Pancreaticoduodenal arcades — connect celiac trunk ↔ SMA
• Marginal artery of Drummond — runs along the mesenteric border of the colon, connecting SMA ↔ IMA branches
• Arc of Riolan (meandering mesenteric artery) — a more central connection between SMA and IMA (present in some but not all individuals)

C. Watershed Zones (Critical Vulnerability Points)

These are areas where two end-arterial territories meet with tenuous anastomoses. They are the first to become ischemic during systemic hypoperfusion:

1. Griffith's point — at the splenic flexure ^[1][2]

   • This is the point where the terminal branches of the SMA (via middle colic artery) and IMA (via ascending branch of left colic artery) meet
   • The anastomotic bridging here is often weak or absent in some individuals
   • Why it matters: The splenic flexure is the most common site of ischaemic colitis

2. Sudeck's point — at the rectosigmoid junction ^[1][2]

   • Where the descending branch of the left colic artery (IMA territory) forms an anastomosis with the superior rectal artery
   • Terminal narrow branches make this area vulnerable
   • Why it matters: Relevant during anterior resection — the surgeon must ensure adequate blood supply to the rectal stump

D. Venous Drainage

• Venous drainage parallels arterial circulation ^[1]
• Drains into the portal venous system: SMV + splenic vein → portal vein → liver
• IMV drains into splenic vein (or SMV directly)
• Venous thrombosis causes outflow obstruction → increased intramural pressure → bowel wall edema → hemorrhagic infarction

E. Normal Physiology of Splanchnic Circulation [1]

• Splanchnic circulation receives 10–35% of cardiac output — 10% fasting, up to 35% postprandially
• After eating, blood flow increases to meet the metabolic demands of digestion and absorption
• Intrinsic autoregulation redirects blood from the gut to brain/heart during systemic hypotension — this is a survival mechanism but makes the gut a sacrificial organ in shock states
• Capillary density in the intestinal vasculature is high, but intestinal oxygen extraction is relatively low under normal conditions
  • Why? Because the gut must let oxygen-rich blood pass through to the liver via the portal vein — the liver has its own high metabolic demand
  • This means the intestine has a reserve of oxygen extraction it can tap into during mild ischemia

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IV. Pathophysiology

A. Thresholds of Ischemia [1]

• Intestinal blood flow must be reduced by > 50% from the normal fasting level before oxygen delivery becomes compromised
• The intestine can compensate for up to ~75% reduction in mesenteric blood flow for up to 12 hours without substantial injury, through:
  • Vasodilation of collateral vessels
  • Increased oxygen extraction from remaining blood flow
• Beyond this compensation threshold → tissue hypoxia → injury

B. Two-Phase Injury Model [1][2]

Intestinal injury results from both ischemia AND reperfusion — in fact, reperfusion injury may cause more damage than the initial ischemic insult.

Phase 1: Ischemic (Hypoxic) Injury

• Insufficient oxygen and nutrients for cellular metabolism
• Mucosal cells (which have the highest metabolic rate and sit at the tips of villi) are affected first
• ATP depletion → failure of Na⁺/K⁺-ATPase → cellular swelling → loss of mucosal barrier integrity
• Bacterial translocation across compromised mucosa → systemic inflammatory response
• Mucosa sloughs → bloody diarrhea/PR bleeding

Phase 2: Reperfusion Injury ^[2]

• Occurs when blood flow is restored after a period of ischemia
• ↑ ROS (reactive oxygen species) from the sudden increase in O₂ supply to cells that have accumulated hypoxanthine during ischemia
• ↑ Inflammation from the influx of leukocytes and complement activation
• Paradoxically, restoring blood flow can worsen tissue damage
• This is why there is a "window" for revascularization — too late, and reperfusion may cause more harm than good

Phase 3: Prolonged Ischemia ^[1]

• Progressive vasoconstriction develops in the obstructed vascular bed, increasing pressure and reducing collateral flow
• Vasoconstriction persists even after blood flow is restored — a vicious cycle
• Persistent ischemia → full-thickness (transmural) necrosis → perforation → peritonitis → sepsis → death

C. Clinical Phases of Ischemic Bowel [2]

This maps to what you see at the bedside:

1. Hyperactive phase — Bowel initially responds to ischemia with hyperperistalsis → severe crampy pain, vomiting, diarrhea (may be bloody). Pain is out of proportion to physical findings because the bowel wall is not yet necrotic/perforated.
2. Paralytic phase — Peristalsis ceases as the bowel wall musculature becomes injured → absent bowel sounds, increasing distension
3. Shock phase — Fluid leaks through the damaged bowel wall → third-spacing → hypovolemia → sepsis → multi-organ failure

D. Pathophysiology by Mechanism of Ischemia

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V. Etiology

A. Causes of Intestinal Ischemia — Comprehensive Summary [1][2][3]

1. Acute Mesenteric Ischemia

2. Chronic Mesenteric Ischemia

• Almost exclusively due to atherosclerosis of the celiac trunk, SMA, and/or IMA ^[2]
• Usually requires ≥2 of the 3 major mesenteric vessels to be significantly stenosed (due to robust collateral network)
• Less common causes: median arcuate ligament syndrome (celiac artery compression), vasculitis (Takayasu, PAN), fibromuscular dysplasia

3. Ischaemic Colitis

• Most commonly non-occlusive (related to systemic hypoperfusion affecting watershed zones)
• Can be caused by any of the above mechanisms when the colon is the target
• Extrinsic causes: strangulating hernia, volvulus ^[2]

B. Hong Kong-Relevant Considerations

• High prevalence of hypertension, diabetes, and smoking in the elderly Hong Kong population → significant burden of atherosclerotic mesenteric disease
• AF prevalence is rising with the ageing population → increasing embolic risk
• Post-cardiac surgery patients in ICU settings → NOMI risk
• Renal failure patients on haemodialysis → intradialytic hypotension → NOMI

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VI. Classification

A. By Anatomical Territory

B. By Time Course

C. By Mechanism (Most Clinically Useful)

1. Occlusive mesenteric ischemia
   • Arterial embolism
   • Arterial thrombosis
   • Venous thrombosis
2. Non-occlusive mesenteric ischemia (NOMI)
3. Chronic mesenteric ischemia
4. Mechanical (volvulus, hernia) ^[3]

D. Colon Ischemia Severity Classification (Brandt and Boley / AGA)

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VII. Clinical Features

A. Symptoms

The clinical presentation varies by the mechanism, acuity, and segment of bowel involved. The unifying theme is that early ischemia causes severe pain with deceptively few findings — then things deteriorate rapidly.

1. Abdominal Pain — THE cardinal symptom [1][2][3]

• MOST common presenting symptom in intestinal ischemia ^[1]
• Classical description: "Abdominal pain out of proportion to physical examination" ^[1][2]
  • Why? In early ischemia, the bowel is in agony (visceral pain from ischemic smooth muscle spasm and mucosal injury) but the peritoneum is not yet involved (no peritonitis, so minimal tenderness on palpation). The disconnect between the patient screaming in pain and a relatively soft, non-tender abdomen is the hallmark.
  • Once transmural necrosis and perforation develop → peritonitis → now the signs "catch up" with the symptoms, but by then it's often too late.

Pattern by etiology:

2. PR Bleeding / Bloody Diarrhea [1][2]

• Typically develops within 24 hours of onset of abdominal pain ^[1]
• More common and earlier in colonic ischemia than mesenteric ischemia ^[1]
• Mechanism: Mucosal ischemia → mucosal sloughing and ulceration → bleeding into the lumen. The mucosa is the first layer to die (highest metabolic rate, furthest from serosal blood supply — the "countercurrent" oxygen exchange in villi makes villous tips particularly vulnerable)
• In mesenteric ischemia, bleeding is uncommon in early stages ^[1] — it appears later as transmural necrosis progresses

3. Nausea and Vomiting [1]

• Common early symptom, especially with arterial embolism
• Mechanism: Visceral afferent stimulation from ischemic bowel → vagal activation → nausea/vomiting center in medulla. Also reflects the acute periumbilical pain → reflex vomiting.

4. Diarrhea (Non-Bloody Initially)

• Early ischemia causes hyperperistalsis (hyperactive phase) → diarrhea
• Mechanism: The ischemic bowel initially "spasms" — smooth muscle irritability from hypoxia and local inflammatory mediators → increased motility → diarrhea

5. Chronic Symptoms (Chronic Mesenteric Ischemia)

• Postprandial abdominal pain ("mesenteric angina") — typically 15–30 min after eating, lasting 1–3 hours ^[2]
• Sitophobia (fear of eating) — patients learn to avoid food because eating causes pain → significant weight loss ^[2]
• Weight loss — from both reduced intake (sitophobia) and malabsorption (chronically ischemic mucosa cannot absorb nutrients efficiently)

B. Signs

1. Early Signs (Hyperactive Phase)

2. Late Signs (Paralytic and Shock Phases)

C. Comparison: Acute Mesenteric vs. Acute Colonic Ischemia [1]

D. Special Clinical Scenarios

Embolism vs. Thrombosis — Clinical Differentiation

Assessment of Bowel Viability (Intraoperative) [2]

At laparotomy, the surgeon must determine which bowel is viable and which must be resected. Criteria for viability:

• Pink serosa (not dusky/black)
• Visible peristalsis
• Mesenteric pulsation palpable
• Bleeding from marginal arteries when cut
• Intraoperative Doppler USG
• Fluorescein injection → Wood's lamp examination (viable bowel fluoresces)

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VIII. Summary of Clinical Approach

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Active Recall - Intestinal Ischemia (Definition, Epidemiology, Anatomy, Etiology, Pathophysiology, Clinical Features)

1. What is the classical clinical description of acute mesenteric ischemia and why does it occur?

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Pain out of proportion to physical examination. Occurs because early ischemia causes severe visceral pain (ischemic smooth muscle spasm) but peritoneum is not yet involved (no peritoneal signs). By the time peritoneal signs develop, transmural necrosis/perforation has occurred.

2. Name the two watershed zones of the colon, their anatomical locations, and the arterial territories that meet at each.

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1. Griffith's point at the splenic flexure (SMA via middle colic artery meets IMA via left colic artery). 2. Sudeck's point at the rectosigmoid junction (sigmoid artery meets superior rectal artery from IMA). Both are vulnerable in NOMI and systemic hypoperfusion.

3. List the four major causes of acute mesenteric ischemia with their approximate proportions.

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1. Arterial embolism (50%) - cardiac source, especially AF. 2. Arterial thrombosis (15-25%) - superimposed on atherosclerosis. 3. Venous thrombosis (5%) - hypercoagulable states. 4. Non-occlusive mesenteric ischemia / NOMI (20-30%) - low-flow states, vasoconstrictors.

4. Explain the two-phase injury model in intestinal ischemia. Why can reperfusion be paradoxically harmful?

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Phase 1: Ischemic injury - ATP depletion, loss of mucosal barrier, bacterial translocation. Phase 2: Reperfusion injury - sudden oxygen supply generates reactive oxygen species (ROS) via accumulated hypoxanthine; influx of leukocytes and complement activation cause further tissue damage. Reperfusion can cause more harm than the initial ischemia.

5. How do you clinically differentiate an arterial embolism from an arterial thrombosis as the cause of acute mesenteric ischemia?

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Embolism: hyperacute onset (seconds-minutes), AF or cardiac source identifiable, proximal SMA pulse present at surgery (embolus lodges distally), no prior chronic symptoms. Thrombosis: acute onset (hours-days), history of chronic postprandial pain and PVD/cardiovascular risk factors, absent proximal SMA pulse (thrombosis at ostium), more extensive ischemia.

6. What bedside clinical triad should immediately raise suspicion for ischaemic bowel?

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Acute abdomen plus metabolic acidosis (raised lactate, high anion gap metabolic acidosis on ABG) equals ischaemic bowel until proven otherwise. Especially in elderly with AF or cardiovascular disease.

References

^[1] Senior notes: felixlai.md (Intestinal Bowel Ischemia section) ^[2] Senior notes: maxim.md (Ischemic bowel disease section) ^[3] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p31-32)

Differential Diagnosis of Intestinal Ischemia

The differential diagnosis of intestinal ischemia is essentially the differential of acute abdomen — particularly in an elderly patient presenting with severe abdominal pain, and often with metabolic acidosis. The challenge is that intestinal ischemia has notoriously non-specific early features: the pain is diffuse, the abdomen can be soft, and lab markers lag behind the pathology. You need to actively think about what else could look like this, and equally, what conditions might coexist with or be mistaken for ischemic bowel.

Approach to the Differential

The key clinical anchor is: elderly patient, history of AF or IHD, constant severe non-specific abdominal pain, rectal bleeding or bloody diarrhoea, lack of peritoneal sign, leukocytosis, metabolic acidosis ^[3]. When you see this picture, ischemic bowel is high on the list — but you must exclude mimics and identify coexisting pathology.

Think about the differential systematically by asking: what else causes acute abdominal pain + metabolic acidosis + PR bleeding in an elderly patient?

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A. Conditions That Mimic Acute Mesenteric Ischemia

These conditions share the pattern of severe abdominal pain, systemically unwell, ± metabolic acidosis:

B. Conditions That Mimic Ischaemic Colitis

When the dominant presentation is abdominal pain + PR bleeding/bloody diarrhea (i.e., colonic ischemia pattern), consider:

C. Other Important Differentials of the Acute Abdomen That Must Be Excluded [4]

These are the life-threatening differentials of acute abdomen that overlap with the presentation of mesenteric ischemia:

• Perforated viscus (PPU, perforated diverticulitis, perforated CRC) — free air on erect CXR/CT
• Ruptured AAA — pulsatile mass, hemodynamic instability, CT shows aneurysm/haematoma ^[4]
• Acute mesenteric ischemia (itself is one of the life-threatening differentials of any acute abdomen) ^[4]
• Acute intestinal obstruction — cardinal tetrad of pain, vomiting, distension, constipation ^[6]
• Severe pancreatitis — amylase/lipase ≥ 3× ULN, CT shows pancreatic necrosis ^[1]
• Ruptured HCC — in Hong Kong, always consider in a patient with known hepatitis B/cirrhosis presenting with acute abdominal pain and hemodynamic instability ^[4]
• Medical causes: DKA (ketoacidosis causes abdominal pain and metabolic acidosis — can closely mimic ischaemic bowel), Addisonian crisis, acute MI ^[4]
• Obstetric: ruptured ectopic pregnancy, placental abruption ^[4]

D. Differentials Specific to the Subtype of Ischemia

For Mesenteric Venous Thrombosis (insidious pain, waxing and waning)

• Portal vein thrombosis (from cirrhosis, malignancy)
• Budd-Chiari syndrome (hepatic vein thrombosis)
• Other hypercoagulable complications (DVT/PE) — ask about leg swelling, dyspnea

For Chronic Mesenteric Ischemia (postprandial pain, weight loss, sitophobia)

• Pancreatic cancer — also causes postprandial pain, weight loss, back pain; CT/MRCP differentiates
• Peptic ulcer disease — postprandial pain (GU) or relief (DU); OGD differentiates
• Chronic pancreatitis — epigastric pain radiating to back, steatorrhea, calcifications on imaging
• Gastric malignancy — early satiety, weight loss; OGD with biopsy

E. Differentials of Mechanical Causes of Intestinal Ischemia

Mechanical (volvulus, hernia) ^[3] — these are both differentials of and causes of intestinal ischemia:

F. Summary: Differentiating by Key Clinical Features

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Active Recall - Differential Diagnosis of Intestinal Ischemia

1. Name 5 life-threatening differentials of an acute abdomen that must be excluded when considering mesenteric ischemia.

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Any 5 of: perforated viscus (PPU), ruptured AAA, acute mesenteric ischemia itself, acute intestinal obstruction, severe pancreatitis, ruptured HCC, DKA, acute MI, Addisonian crisis, ruptured ectopic pregnancy.

2. Why can acute pancreatitis be confused with mesenteric ischemia, and how do you differentiate them?

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Both cause severe abdominal pain, metabolic acidosis, ileus, and haemodynamic instability. Mesenteric ischemia can elevate amylase in ~50% of cases. Differentiate by: pancreatitis has lipase at least 3x ULN, pain radiates to back and is relieved by leaning forward, CT shows pancreatic inflammation not vascular occlusion. CT angiography shows mesenteric vascular occlusion in ischaemic bowel.

3. How does ischaemic colitis differ from IBD on clinical presentation?

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In IBD, diarrhoea is the predominant symptom rather than abdominal pain. IBD affects younger patients with chronic relapsing course. Ischaemic colitis affects elderly with cardiovascular risk factors, has acute onset, and follows watershed distribution (splenic flexure, rectosigmoid junction). IBD has characteristic colonoscopic patterns (continuous from rectum in UC, skip lesions in Crohns). Treatment is fundamentally different.

4. Explain why MI and aortic dissection are not just differentials but also potential causes of mesenteric ischemia.

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MI can cause mesenteric ischemia via: (1) cardiogenic shock leading to NOMI from splanchnic hypoperfusion, (2) new-onset AF leading to thrombus formation and embolism, (3) LV mural thrombus embolising to SMA. Aortic dissection can cause mesenteric ischemia when the dissection flap extends to occlude the SMA ostium (malperfusion syndrome). Both can coexist with mesenteric ischemia.

5. A patient presents with colicky abdominal pain that has become constant, with rising lactate. What does this transition from colicky to constant pain signify, and what is the diagnosis?

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Transition from colicky to constant pain signifies development of bowel ischaemia in the setting of intestinal obstruction (strangulation). Colicky pain reflects peristalsis against obstruction; constant pain reflects ischaemic necrosis of the bowel wall. This is strangulated obstruction, which is a mechanical cause of intestinal ischemia. Urgent surgical intervention is required.

References

^[1] Senior notes: felixlai.md (Intestinal Bowel Ischemia section; Lower GI Bleeding section; Acute Diverticulitis section; Acute Pancreatitis section) ^[2] Senior notes: maxim.md (Ischemic bowel disease section) ^[3] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p31-32) ^[4] Senior notes: felixlai.md (Ruptured AAA section); Senior notes: maxim.md (Acute abdomen DDx section) ^[5] Senior notes: maxim.md (Volvulus section); Senior notes: felixlai.md (Volvulus section) ^[6] Senior notes: maxim.md (Intestinal obstruction section); Senior notes: felixlai.md (Intestinal obstruction section)

Diagnostic Criteria, Diagnostic Algorithm, and Investigation Modalities for Intestinal Ischemia

I. Diagnostic Criteria — A Clinical Diagnosis

Unlike conditions such as acute pancreatitis (which has a neat 2-of-3 criteria), intestinal ischemia does not have formal universally accepted diagnostic criteria. Instead, the diagnosis rests on a synthesis of clinical suspicion, laboratory markers, and imaging findings. This is important to understand: by the time you have "definitive proof," the bowel may already be dead. The diagnosis is therefore driven by a high index of suspicion in the right clinical context.

The diagnostic reasoning can be distilled into three pillars:

Specific Diagnostic Patterns by Subtype

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II. Diagnostic Algorithm

The algorithm branches based on hemodynamic stability and presence of peritoneal signs, because this determines whether you have time for imaging or must go straight to theatre.

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III. Investigation Modalities — Detailed Breakdown

A. History Taking [1]

Before any test, a focused history provides critical diagnostic clues:

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B. Physical Examination [1][3]

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C. Biochemical Investigations

These are ordered urgently and simultaneously with imaging. No single blood test is diagnostic, but the constellation of findings supports the diagnosis and indicates severity.

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D. Radiological Investigations

1. Plain Abdominal X-ray (AXR) [1][2][7][8]

AXR is the first-line imaging in any acute abdomen. It is quick, available, and cheap — but for intestinal ischemia it is relatively non-specific and can be completely normal ^[1]. Its main role is to exclude other diagnoses (e.g., perforation, obstruction) and look for late signs of ischemia.

Questions to ask on AXR (from lecture slides) ^[7]:

• Are there dilated bowel loops?
• Are air fluid levels present in erect film?
• Any gas in the colon and the level of cut off?
• Any evidence of strangulation: thumbprinting, pneumatosis cystoides intestinalis, free peritoneal gas?
• Any massive dilatation of colon?
• Any air in the biliary tree?

2. CT Angiography (CTA) — The Gold Standard [1][2][8][9]

CTA is the single most important investigation for suspected mesenteric ischemia. It simultaneously:

1. Identifies the cause (arterial occlusion, venous thrombosis, or NOMI pattern)
2. Demonstrates the consequences (bowel wall changes, perforation)
3. Excludes other causes of acute abdomen ^[1]
4. Allows planning for endovascular intervention if appropriate

CT scan: more sensitive than plain abdominal X-rays ^[8]. It identifies level of obstruction (transition between dilated and collapsed loop), lesions (tumor, foreign bodies), viability of bowel (intravenous contrast) ^[8].

Protocol: Triphasic CT — non-contrast, arterial phase, and portal venous (delayed) phase ^[1][2]

CT findings of acute ischemia ^[1][2]:

CT abdomen with contrast is sensitive for ischemic bowel and SMA occlusion, and can exclude other DDx ^[2].

Investigations for acute mesenteric ischemia: MRA or MDCT angiography (CTA) ^[1]. Investigations for acute colonic ischemia: Colonoscopy ^[1].

3. MR Angiography (MRA) [1]

4. Duplex Ultrasound [9]

• Duplex USG = B-mode (2D) USG + Doppler ^[9]
• Can locate the level of obstruction and assess flow in mesenteric vessels
• Normal arterial flow waveform should be triphasic ^[9]; monophasic or biphasic waveforms are abnormal
• Advantages: Non-invasive, no radiation, bedside availability (useful in ICU for NOMI patients)
• Disadvantages: Highly operator-dependent; bowel gas obscures views; poor sensitivity for distal SMA and branch vessels; not reliable in acute emergencies
• Main role in intestinal ischemia: Screening tool for chronic mesenteric ischemia (elevated peak systolic velocity in SMA/celiac indicating stenosis); limited role in acute setting

5. Catheter-Based Digital Subtraction Angiography (DSA) [9]

• Gold standard for evaluation of arterial tree before planning revascularization ^[9]
• Indicated only in patients with planned intervention (angioplasty/stenting) ^[9]
• Allows simultaneous diagnostic and therapeutic intervention (catheter-directed thrombolysis, vasodilator infusion for NOMI)
• Digital subtraction removes underlying bone from images to better visualize arteries
• Risks: Invasive; contrast allergy; contrast nephropathy; arterial puncture site bleeding; arterial dissection; embolization; hematoma; local infection ^[9]
• Largely superseded by CTA for diagnostic purposes, but remains essential when endovascular intervention is planned

6. Colonoscopy [1]

• Investigation of choice for acute colonic ischemia (ischaemic colitis) ^[1]
• Performed after initial stabilization, not in the acute resuscitation phase
• Findings:
  • Segmental mucosal edema, hemorrhage, and ulceration — typically at watershed zones (splenic flexure, rectosigmoid)
  • "Single-stripe sign" (linear ulceration along the anti-mesenteric border) — good prognosis
  • "Circumferential cyanosis" — poor prognosis (indicates transmural involvement)
  • Mucosal biopsy shows ischemic changes (mucosal necrosis, ghost cells, hemosiderin-laden macrophages)
• Contraindicated if peritonitis suspected (risk of perforation with insufflation) ^[6]

7. Adjunct Investigations [1][9]

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IV. Summary of Investigation Approach by Subtype

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V. Intraoperative Assessment of Bowel Viability [2]

When the patient reaches the operating table, the surgeon must determine which bowel to resect and which to save. This is not an "investigation" in the traditional sense, but it is a critical diagnostic step.

Criteria for viable bowel ^[2]:

• Pink serosa — healthy bowel has good colour; dusky/black = necrotic
• Visible peristalsis — actively contracting bowel is alive
• Mesenteric pulsation — palpable arterial pulsation in the mesentery indicates blood flow
• Bleeding from marginal arteries — if you cut the mesenteric edge and it bleeds, the bowel has blood supply

Additional intraoperative techniques ^[2]:

• Intra-operative Doppler USG — quantitative assessment of bowel wall blood flow
• Fluorescein injection → Wood's lamp — IV fluorescein distributes to perfused tissue; under Wood's lamp (UV), viable bowel fluoresces green. Non-viable bowel stays dark.

Intraoperative differentiation of embolism vs thrombosis ^[2]:

• Palpate SMA to differentiate:
  • Present proximal SMA pulse = embolism (embolus lodged distally)
  • Absent SMA pulse = thrombosis (thrombosis at proximal vessel/ostium)

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Active Recall - Diagnosis of Intestinal Ischemia

1. What is the gold standard investigation for suspected acute mesenteric ischemia, and what are its key findings for arterial occlusion versus venous thrombosis?

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CT angiography (CTA) is the gold standard. Arterial occlusion: lack of enhancement of arterial vasculature with timed IV contrast (filling defect in SMA). Venous thrombosis: filling defects or absent flow during venous/delayed phase in SMV or portal vein. CTA also shows bowel wall changes (thickening, reduced enhancement, pneumatosis, portal gas) and excludes other DDx.

2. List 4 AXR findings suggestive of bowel ischemia and explain what each represents pathologically.

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1. Thumbprinting sign - submucosal oedema causing regular indentations along bowel wall. 2. Pneumatosis intestinalis - gas within bowel wall from transmural necrosis allowing bacterial gas dissection. 3. Portal venous gas - gas from necrotic bowel entering mesenteric/portal veins (late, ominous). 4. Bowel wall thickening - mucosal and submucosal edema from ischemia. Also accept: dilated bowel loops (paralytic ileus), pneumoperitoneum (perforation), Riglers double wall sign (perforation).

3. An elderly patient with AF presents with acute abdominal pain. Bloods show WCC 18, lactate 6.2, pH 7.22, HCO3 14. He has peritoneal signs. What is the next step and why?

Your answer

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Urgent midline laparotomy within 6 hours (not CT scan). Patient has peritoneal signs indicating transmural necrosis or perforation. Imaging would delay definitive treatment. At surgery: palpate SMA to differentiate embolism (pulse present) from thrombosis (pulse absent), perform revascularization and resect non-viable bowel. Anticoagulation and antibiotics should be started immediately.

4. Why can serum amylase be misleadingly elevated in mesenteric ischemia, and how do you distinguish this from acute pancreatitis?

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Amylase is elevated in approximately half of intestinal ischemia patients because ischemic small bowel mucosa releases intracellular amylase. Distinguished from pancreatitis by: (1) amylase rise is typically modest (less than 3x ULN) whereas pancreatitis requires lipase at least 3x ULN; (2) pancreatitis pain radiates to back, relieved by leaning forward; (3) CT shows pancreatic inflammation in pancreatitis vs vascular occlusion and bowel wall changes in ischemia.

5. Name 4 criteria used intraoperatively to assess bowel viability at laparotomy for mesenteric ischemia.

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Pink serosa (not dusky or black), visible peristalsis, mesenteric pulsation (palpable arterial pulse in mesentery), bleeding from marginal arteries when cut. Additional techniques: intra-operative Doppler USG for blood flow assessment, fluorescein injection with Wood lamp examination (viable bowel fluoresces, non-viable stays dark).

6. In what clinical scenario is colonoscopy the investigation of choice for intestinal ischemia, and when is it absolutely contraindicated?

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Colonoscopy is the investigation of choice for acute colonic ischemia (ischaemic colitis) in a stable patient after initial resuscitation. It shows segmental mucosal oedema, haemorrhage and ulceration at watershed zones. It is absolutely contraindicated when peritoneal signs are present or perforation is suspected, because gas insufflation during endoscopy can open a sealed-off perforation causing faecal peritonitis.

References

^[1] Senior notes: felixlai.md (Intestinal Bowel Ischemia — Diagnosis section) ^[2] Senior notes: maxim.md (Ischemic bowel disease — Investigations section) ^[3] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p31-32) ^[6] Senior notes: maxim.md (Intestinal obstruction section — "Do NOT order colonoscopy/barium enema in acute settings") ^[7] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (p15) ^[8] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (p18, p46) ^[9] Senior notes: felixlai.md (Acute arterial insufficiency — Radiological tests section); Senior notes: maxim.md (PVD investigations section)

Management of Intestinal Ischemia

The management of intestinal ischemia is fundamentally a race against time. Every hour of delay increases the amount of bowel that dies, and once bowel is dead, the only option is resection. The overarching principle is:

Treatment is resuscitation, resect non-viable bowel ^[3]

This is deceptively simple but captures the essence: stabilize the patient, restore blood flow if possible, and remove what cannot be saved. Let's break this down systematically.

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I. Master Management Algorithm

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II. Initial Resuscitation — ALL Patients

Regardless of the subtype or severity, every patient with suspected intestinal ischemia receives the same initial stabilization. The rationale for each step flows directly from the pathophysiology:

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III. Management by Clinical Stability — The Critical Branch Point

A. UNSTABLE Patient (Peritoneal Signs Present)

This patient has transmural necrosis, likely perforation, and is systemically septic. There is no time for CT.

Unstable (with peritoneal signs): urgent midline laparotomy (within 6h) ^[2]

Why midline laparotomy?

• Provides the widest possible exposure of the entire abdomen
• Allows assessment of the full length of small and large bowel
• Permits revascularization, resection, and stoma creation in a single operation
• Decision on surgery and timing of surgery is important ^[7]; high mortality if complications occur ^[7]

Intraoperative Steps:

Step 1: Mesenteric Revascularization ^[2]

Palpate the SMA to differentiate embolism from thrombosis — this determines the surgical approach ^[2]:

Step 2: Assessment of Bowel Viability ^[2]

After restoring blood flow, the surgeon must determine which bowel is salvageable:

Step 3: Resection and Stoma ^[2]

• Resect non-viable bowels + stoma ^[2]
• Do NOT attempt primary anastomosis ^[2]
  • Why? Ischemic tissue has poor healing capacity. Anastomotic leak risk is extremely high in the setting of contamination, sepsis, hemodynamic instability, and uncertain viability of remaining bowel edges. An anastomotic leak in this context is frequently fatal.
  • Risk factors for anastomotic leak: ischaemia, tension, active infection ^[12]
• Stoma creation (ileostomy or jejunostomy) allows bowel to decompress and heal; can be reversed electively when the patient is stable

Step 4: Second-Look Laparotomy ^[2]

• Second-look laparotomy 24–48h after initial operation ^[2]
• Indication: If the extent of bowel viability is uncertain at the first operation
• Rationale: After revascularization, it takes 24–48h for the full effects of reperfusion to declare themselves. Some borderline bowel may recover (save it); some may declare as necrotic (resect it). This staged approach minimizes both unnecessary resection (short bowel syndrome) and retained dead bowel (ongoing sepsis)
• The decision to perform second-look should be made at the first operation, not based on post-op clinical deterioration

High risk of short gut syndrome: diarrhoea, steatorrhea → dehydration, malabsorption, weight loss ^[2]. This is why you conserve every centimetre of viable bowel you can.

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B. STABLE Patient (No Peritoneal Signs)

This patient has ischemia but the bowel is likely not yet transmurally necrotic. There is time for imaging to guide targeted therapy.

Stable (no peritoneal signs): CT scan / angiography → thrombolysis (if no C/I) ^[2]

The management is then determined by the CTA findings:

Thrombolysis — Details [1][2]

• Local infusion of thrombolytic agent ^[1] (e.g., tPA — tissue plasminogen activator, or urokinase) via catheter placed directly into the SMA during angiography
• Converts plasminogen → plasmin → dissolves fibrin clot
• Advantage: Can dissolve clot without surgery; less invasive
• Risks: Possible catheter-related embolism to more distal arterial mesenteric branches ^[1]; systemic bleeding; hemorrhagic transformation of ischemic tissue
• Contraindications to thrombolysis:
  • Peritoneal signs (need surgery, not thrombolysis)
  • Active bleeding
  • Recent surgery ( < 10 days)
  • Stroke within 2 months
  • Uncontrolled hypertension

Endovascular Approaches

Surgical Revascularization Options

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IV. Post-Operative Management [2]

Post-operative care is as critical as the surgery itself:

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V. Management of Chronic Mesenteric Ischemia [2]

Chronic mesenteric ischemia is a very different beast — these patients are not acutely dying but have progressive weight loss and disability from postprandial pain.

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VI. Management of Ischaemic Colitis

Most ischaemic colitis is self-limiting and does not require surgery. Management is largely conservative.

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VII. Management of Mechanical Causes (Volvulus/Hernia)

These are specific causes of intestinal ischemia with tailored management:

Sigmoid Volvulus [2][5]

• Initial: NPO, drip and suck, IV antibiotics
• Endoscopic decompression (first line) ^[5]: flexible sigmoidoscopy de-rotation with cautious insufflation
  • Success: sudden expulsion of gas and stool → leave rectal tube in-situ for 24h → serial AXR monitoring
• Urgent laparotomy if: failed endoscopic treatment, signs of ischaemic bowel (e.g., acidosis, tenderness/guarding/rigidity/rebound), necrotic bowel at endoscopy
  • Sigmoidectomy → primary anastomosis + on-table lavage (if bowel viable and patient stable)
  • Emergency Hartmann's operation ^[5]: resection with end colostomy + rectal stump closure (if bowel compromised or patient unstable)
• Elective sigmoidectomy for young patients or elderly with recurrent volvulus ^[5]

Caecal Volvulus [5]

• Surgery is indicated — caecal volvulus is usually ischemic ^[5]
• Right hemicolectomy ^[5] — definitive treatment
• Colonoscopic derotation ± caecopexy — high recurrence rate

Strangulated Hernia [6]

• Urgent exploration: assess viability (cold, pulsation, pallor, peristalsis)
• Viable bowel → hernia repair
• Non-viable bowel → resection + stoma ^[6]
• Manual reduction should not be performed ^[6]: risk of peritonitis from reducing ischaemic bowel into abdomen, risk of reduction "en masse"

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VIII. Summary of Indications for Urgent Surgery

Indications for urgent surgery ^[7]:

• Incarcerated, strangulated hernia
• Suspected or proven strangulation
• Peritonitis
• Pneumoperitoneum
• Pneumatosis cystoides intestinalis
• Closed-loop obstruction
• Volvulus with peritoneal signs

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IX. Special Considerations

Short Bowel Syndrome [2]

• A devastating complication of extensive bowel resection
• Diarrhoea, steatorrhea → dehydration, malabsorption, weight loss ^[2]
• Occurs when remaining small bowel is insufficient for adequate absorption (typically < 200 cm of jejunum without colon, or < 100 cm with intact colon)
• Management: TPN initially → gradual enteral feeding as bowel adapts; oral rehydration solutions; anti-diarrhoeals; possible intestinal transplant in severe cases

Long-Term Anticoagulation

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Active Recall - Management of Intestinal Ischemia

1. Describe the initial resuscitation steps for a patient with suspected acute mesenteric ischemia, and explain the rationale for systemic anticoagulation.

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NPO (reduce mesenteric demand and aspiration risk), IV fluids (replace third-space losses), NG decompression (reduce intraluminal pressure and aspiration risk), IV broad-spectrum antibiotics (bacterial translocation through ischaemic mucosa), parenteral opioids for pain, hemodynamic monitoring. Systemic anticoagulation with IV heparin prevents further thrombus propagation into unaffected vascular bed and inhibits secondary thrombosis distally due to low-flow stasis. Target APTT 2-2.5x normal. Contraindicated if active bleeding.

2. At laparotomy for acute mesenteric ischemia, how do you differentiate embolism from thrombosis, and how does this change the surgical approach?

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Palpate the SMA. Present proximal SMA pulse = embolism (lodged distally) → perform open surgical embolectomy using Fogarty catheter. Absent proximal SMA pulse = thrombosis (at ostium) → need surgical revascularization (thromboendarterectomy, mesenteric bypass, or retrograde stenting) because the underlying vessel is diseased and simple clot extraction will not address the stenosis.

3. Why should you NOT attempt primary anastomosis after resecting non-viable bowel in acute mesenteric ischemia? What do you do instead?

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Ischaemia is the number one risk factor for anastomotic leak. In a septic, haemodynamically unstable patient with contaminated peritoneal cavity and uncertain viability at resection margins, anastomotic leak risk is extremely high and frequently fatal. Instead: create a stoma (ileostomy or jejunostomy). Reverse the stoma electively 3-6 months later when patient has recovered. Plan second-look laparotomy at 24-48h if viability of remaining bowel is uncertain.

4. A stable patient with no peritoneal signs has CT angiography showing patent mesenteric arteries and veins but diffuse bowel wall changes at the splenic flexure. What is the likely diagnosis and how do you manage it?

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Likely NOMI (non-occlusive mesenteric ischemia) affecting the watershed zone at the splenic flexure (Griffiths point). Patent vessels with bowel wall changes = vasoconstriction, not occlusion. Management: treat underlying cause (optimize cardiac output, wean vasopressors, correct hypovolemia), consider transarterial vasodilator infusion (papaverine via SMA catheter during angiography), supportive care with antibiotics and anticoagulation. Surgery only if peritoneal signs develop.

5. List the indications for urgent surgery in the setting of intestinal ischemia or obstruction.

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Incarcerated or strangulated hernia, suspected or proven strangulation, peritonitis, pneumoperitoneum, pneumatosis cystoides intestinalis, closed-loop obstruction, volvulus with peritoneal signs. Also: failed conservative treatment after 48-72 hours, and haemodynamic instability not responding to resuscitation.

6. How does the management of chronic mesenteric ischemia differ from acute mesenteric ischemia?

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Chronic mesenteric ischemia is managed electively, not emergently. Treatment: (1) Risk factor modification - smoking cessation, antihypertensives, statin therapy. (2) First-line revascularization: endovascular mesenteric angioplasty with stenting. (3) Surgical bypass or endarterectomy reserved for failed endovascular therapy or unfavorable anatomy. No emergency laparotomy needed. The underlying cause is atherosclerosis affecting at least 2 of 3 mesenteric vessels.

References

^[1] Senior notes: felixlai.md (Intestinal Bowel Ischemia — Treatment section) ^[2] Senior notes: maxim.md (Ischemic bowel disease — Management section) ^[3] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p32) ^[5] Senior notes: maxim.md (Volvulus — Management section) ^[6] Senior notes: maxim.md (Intestinal obstruction — Strangulated hernia management) ^[7] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (p25, p29, p67) ^[10] Senior notes: felixlai.md (Intestinal obstruction — Supportive management section) ^[11] Senior notes: felixlai.md (Acute arterial insufficiency — Medical treatment section) ^[12] Senior notes: maxim.md (Anastomotic leak — Risk factors)

Complications of Intestinal Ischemia

Complications of intestinal ischemia can be understood as a cascading sequence: ischemia → necrosis → perforation → peritonitis → sepsis → multi-organ failure → death. But the picture is richer than that. Complications arise from the disease itself, from the treatment (surgery and revascularization), and from the long-term consequences of having lost bowel. Let's work through each systematically, always asking "why does this happen?"

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I. Complications of the Disease Process (Ischemia → Necrosis → Death)

These complications follow directly from the pathophysiology of ischemia described in earlier sections. Think of them as a timeline of progressive bowel destruction:

A. Transmural Bowel Necrosis

• Mechanism: Prolonged ischemia ( > 6–12 hours depending on collateral flow) → mucosal injury progresses through submucosa → muscularis → serosa → full-thickness (transmural) necrosis ^[1]
• Persistent ischemia can lead to full-thickness necrosis of bowel wall and subsequent perforation ^[1]
• Why does it progress transmurally? The mucosa dies first (highest metabolic rate, furthest from serosal blood supply via countercurrent oxygen exchange in villi). Progressive vasoconstriction in the obstructed vascular bed increases pressure and reduces collateral flow ^[1], and this vasoconstriction persists even after blood flow has been restored ^[1] — a vicious cycle that drives necrosis deeper through the wall
• Clinical significance: Necrotic bowel is a source of bacterial translocation, endotoxemia, and the nidus for perforation. Morbidity and mortality are dependent on duration of ischemia and its extent ^[10]

B. Bowel Perforation

• Mechanism: Full-thickness necrosis destroys the structural integrity of the bowel wall → intraluminal contents (bacteria, faeces, digestive enzymes) leak into the peritoneal cavity
• Clinical features: Sudden worsening of pain → generalized peritonitis (guarding, rigidity, rebound tenderness); pneumoperitoneum on imaging ^[2]; haemodynamic deterioration
• Radiological signs of perforation ^[2]:
  • Pneumoperitoneum — free gas under diaphragm on erect CXR
  • Rigler's double wall sign — both sides of the bowel wall visible because free gas outlines the serosal surface ^[2]
• Any length of ischemic bowel can cause significant systemic effects secondary to sepsis and dehydration ^[10]

C. Peritonitis

• Mechanism: Perforation → contamination of the peritoneal cavity with bowel contents → chemical and bacterial peritonitis
• Alternatively, bacterial translocation through intact-but-ischemic mucosa can cause peritonitis even before frank perforation
• Types:
  • Chemical peritonitis — digestive enzymes and bile irritate the peritoneum
  • Bacterial (faecal) peritonitis — gut flora (E. coli, Bacteroides, Enterococcus) infect the peritoneal cavity
• Clinical features: Board-like abdominal rigidity, absent bowel sounds, guarding, fever, tachycardia

D. Sepsis and Systemic Inflammatory Response Syndrome (SIRS)

• Mechanism: Necrotic bowel + bacterial translocation → endotoxins and bacteria enter the systemic circulation → overwhelming inflammatory response
• Intestinal ischemia can progress to sepsis, peritonitis, free intraabdominal air, bowel infarction, gangrene or even death ^[1]
• The ischemic gut becomes a "motor" driving systemic inflammation: damaged mucosal barrier loses its ability to contain ~10¹⁴ bacteria normally resident in the gut lumen
• Clinical progression: SIRS → sepsis → severe sepsis → septic shock → multi-organ dysfunction syndrome (MODS)

E. Multi-Organ Failure

• Mechanism: Sepsis + hypovolemia (third-spacing through damaged bowel wall) + reperfusion injury → haemodynamic collapse → end-organ hypoperfusion
• Specific organ systems affected:

F. Metabolic Complications During the Acute Phase

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II. Complications of Treatment (Surgical and Revascularization)

A. Reperfusion Injury [1][13]

This is one of the most important and counter-intuitive complications: restoring blood flow can paradoxically make things worse.

• Mechanism: During ischemia, cells accumulate hypoxanthine (a purine metabolite). When oxygen is suddenly restored, xanthine oxidase converts hypoxanthine to xanthine, generating massive amounts of reactive oxygen species (ROS) ^[2]. Simultaneously, the influx of leukocytes and complement ^[2] into the reperfused tissue amplifies the inflammatory damage.
• Reperfusion injury results from formation of oxygen-free radicals that directly damage the tissue and cause WBC accumulation and sequestration in microcirculation ^[13]
• Prolongs ischemic interval since it impairs adequate nutrient flow to the tissue despite restoration of axial blood flow ^[13]
• Clinical consequence: Tissue that appeared borderline viable at surgery may deteriorate after revascularization — this is precisely why second-look laparotomy at 24–48 hours ^[2] is so important

B. Compartment Syndrome (Abdominal)

• Mechanism: Massive fluid resuscitation + reperfusion edema + bowel oedema → increased intra-abdominal pressure → abdominal compartment syndrome
• When intra-abdominal pressure exceeds ~20 mmHg → compression of IVC (reduced venous return), compression of renal veins (oliguria/AKI), splinting of diaphragm (respiratory failure)
• Management: Decompressive laparotomy with temporary abdominal closure

C. Compartment Syndrome (Limb — Parallel Concept) [13]

Although this is classically taught with limb ischaemia, the same principles apply when mesenteric ischaemia is part of a systemic embolic event (e.g., saddle embolus):

• Prolonged ischemia → cell membrane damage → fluid leaks into interstitial space within non-distensible fascial compartments ^[13]
• Intracompartmental pressure > 30 mmHg ^[13]
• Signs: pain out of proportion worsening despite analgesia, numbness, tense compartment, pain on passive stretching ^[13]
• Management: urgent fasciotomy ^[13]

D. Anastomotic Leak (If Anastomosis Performed)

• Mechanism: Ischaemia, tension, and active infection are the top three risk factors for anastomotic leak ^[12]
• This is why primary anastomosis is generally avoided in the acute setting (stoma is preferred) ^[2]
• If anastomosis was performed (e.g., during second-look when bowel looked viable), monitor for:
  • Deviation from normal post-op course (prolonged ileus, fever, unexplained tachycardia)
  • 50% present with abdominal signs (pain, distension); 50% with systemic signs (fever, oliguria, altered mental state) ^[12]
  • Diagnose with contrast CT abdomen ^[12]
• Management: minor contained leaks → NPO, antibiotics, percutaneous drainage; major leaks → re-laparotomy, take down anastomosis, create stoma ^[12]

E. Complications of Thrombolysis [13]

• Stroke and haemorrhage — patients treated with endovascular thrombolysis have higher risk of:
  • Cerebrovascular events (thrombolytic agent can lyse protective clots elsewhere)
  • Major haemorrhage including GI bleeding and haematoma at vascular puncture site ^[13]
  • Catheter-related embolism to more distal arterial mesenteric branches ^[1] — fragments of clot break off during catheter manipulation and occlude smaller downstream vessels

F. Stoma-Related Complications

After emergency bowel resection with stoma formation, patients face:

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III. Long-Term Complications

A. Short Bowel Syndrome (SBS) [2][14]

This is the most devastating long-term complication of extensive bowel resection for mesenteric ischaemia.

High risk of short gut syndrome: diarrhoea, steatorrhea → dehydration, malabsorption, weight loss ^[2]

Definition: SBS occurs when the remaining functional small bowel is insufficient for adequate nutrient and fluid absorption. In adults, this typically means < 200 cm of jejunum without colon, or < 100 cm with intact colon ^[14].

Why does it happen? When large segments of necrotic bowel are resected, the remaining intestine cannot compensate for the lost absorptive surface area. The consequences depend on which segment was resected:

Complications of SBS ^[14]:

Malabsorption ^[14] — the core problem, with downstream consequences:

• Watery diarrhoea ^[14] — from unabsorbed solutes creating an osmotic gradient
• Fat-soluble vitamin deficiency (A, D, E, K)
  • Metabolic bone disease (osteomalacia, osteoporosis) from malabsorption of calcium and vitamin D ^[14]
• Hypomagnesaemia → neuromuscular excitability (magnesium binds to unabsorbed fatty acids) ^[14]
• Hypocalcaemia → tetany, Trousseau's/Chvostek's sign (secondary to hypomagnesaemia) ^[14]
• Iron deficiency anaemia ^[14]
• Trace element deficiency (zinc → poor wound healing; copper → bone disease; selenium → cardiomyopathy) ^[14]

Gallstones (cholelithiasis) ^[14]

• Why? Disrupted enterohepatic circulation → altered bile composition (supersaturated with cholesterol); absence of oral intake → reduced CCK-mediated gallbladder contraction → bile stasis → gallstone formation

Kidney stones (nephrolithiasis) ^[14]

• Why? Calcium binds to unabsorbed fatty acids in the gut lumen → free oxalate is absorbed by the colon → hyperoxaluria → calcium oxalate stones in the kidneys
• Prevention: increased fluid intake, low oxalate diet, potassium citrate ^[14]

TPN-associated complications ^[14]:

• Catheter-associated infection (line sepsis) — central lines are colonized by bacteria
• TPN-related cholestasis and liver failure ^[14] — lack of enteral feeding → reduced CCK → biliary stasis; TPN lipid infusions are hepatotoxic over time
• Central line sepsis ^[14]

Complications of extensive small bowel resection — short bowel syndrome: Malabsorption, TPN related cholestasis, liver failure, Central line sepsis, Long term quality of life ^[14]

B. Ischaemic Stricture

• Mechanism: Sublethal ischemic injury heals with fibrosis → circumferential narrowing of the bowel lumen → stricture formation
• Most common in ischaemic colitis that resolves without surgery
• Can present weeks to months later with symptoms of partial bowel obstruction (colicky pain, distension, constipation)
• Management: Endoscopic balloon dilatation if short and accessible; surgical resection if long or symptomatic

C. Recurrent Ischaemia

• Patients who have survived one episode are at high risk of recurrence, because the underlying risk factors (AF, atherosclerosis, hypercoagulable state) persist
• Prevention: Long-term anticoagulation (for embolic/venous causes); antiplatelet therapy + statins + risk factor modification (for atherosclerotic causes); optimization of cardiac function

D. Chronic Malnutrition and Functional Impairment

• Even patients who avoid SBS may have chronically impaired absorption from residual bowel injury
• Sitophobia (fear of eating) may persist even after revascularization for chronic mesenteric ischemia
• Weight loss, sarcopenia, and deconditioning compound the problem

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IV. Mortality Overview

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V. Summary Diagram — Complications Cascade

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Active Recall - Complications of Intestinal Ischemia

1. Describe the pathophysiological cascade from intestinal ischemia to multi-organ failure, naming at least 4 specific organ complications.

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Ischemia causes transmural necrosis then perforation then peritonitis (chemical and bacterial) then sepsis/SIRS then multi-organ failure. Specific organs: (1) Kidneys - AKI from hypovolaemia, sepsis, ATN; (2) Lungs - ARDS from systemic inflammatory mediators damaging pulmonary capillaries; (3) Heart - arrhythmias from hyperkalaemia and acidosis, myocardial depression from sepsis; (4) Coagulation - DIC from massive tissue factor release; (5) Liver - ischaemic hepatitis, portal venous gas injury.

2. Explain the mechanism of reperfusion injury after mesenteric revascularization. Why is second-look laparotomy planned?

Your answer

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During ischemia, hypoxanthine accumulates. On reperfusion, sudden oxygen supply allows xanthine oxidase to generate massive reactive oxygen species (ROS). Simultaneously, leukocytes and complement flood the reperfused tissue, amplifying inflammatory damage. This can worsen borderline-viable bowel. Second-look laparotomy at 24-48h is planned because it takes this long for reperfusion effects to declare - bowel that looked viable at first operation may prove necrotic, and bowel that looked borderline may recover.

3. A patient undergoes extensive small bowel resection including the terminal ileum for mesenteric infarction. What specific long-term complications would you anticipate and why?

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Short bowel syndrome with: (1) Vitamin B12 deficiency - terminal ileum is the only absorption site for B12-IF complex; (2) Bile acid malabsorption causing fat malabsorption and steatorrhoea - terminal ileum is selective bile acid reabsorption site, loss disrupts enterohepatic circulation; (3) Gallstones - altered bile composition plus bile stasis; (4) Calcium oxalate kidney stones - calcium binds unabsorbed fatty acids leaving free oxalate to be absorbed; (5) Fat-soluble vitamin deficiency (A, D, E, K) causing metabolic bone disease; (6) TPN dependence with risks of catheter sepsis and liver failure.

4. What is the mortality difference between non-strangulating and strangulating intestinal obstruction, and why?

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Non-strangulating obstruction mortality approximately 2%. Strangulating obstruction mortality 10-30%. The difference is because strangulation involves bowel ischaemia leading to necrosis, perforation, peritonitis and sepsis. Any length of ischaemic bowel can cause significant systemic effects from sepsis and dehydration. Timely surgery is the key prognostic factor.

5. Why is primary anastomosis avoided after resection of necrotic bowel in acute mesenteric ischemia?

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Ischaemia is the number one risk factor for anastomotic leak. In the acute setting there is contaminated peritoneal cavity, haemodynamic instability, uncertain viability at resection margins, and active infection - all further increase leak risk. Anastomotic leak in this context is frequently fatal. A stoma is created instead, and reversed electively 3-6 months later when the patient has recovered.

References

^[1] Senior notes: felixlai.md (Intestinal Bowel Ischemia — Overview and Pathogenesis sections) ^[2] Senior notes: maxim.md (Ischemic bowel disease — Investigations and Management sections) ^[3] Lecture slides: GC 195. Lower and diffuse abdominal pain RLQ problems; pelvic inflammatory disease; peritonitis and abdominal emergencies.pdf (p32) ^[6] Senior notes: maxim.md (Intestinal obstruction — Complications section) ^[7] Lecture slides: GC 194. Intestinal obstruction colorectal cancer.pdf (p38, p67) ^[10] Senior notes: felixlai.md (Intestinal obstruction — Strangulation complications section) ^[12] Senior notes: maxim.md (Anastomotic leak section) ^[13] Senior notes: felixlai.md (Acute arterial insufficiency — Complications section); Senior notes: maxim.md (Acute limb ischaemia — Complications section) ^[14] Senior notes: felixlai.md (Short bowel syndrome section); Lecture slides: Case Study – Paediatric Surgery Bilious vomiting of new-born _ACH Fung.pdf (p22)