Intestinal Ischaemia
Intestinal ischaemia (ischaemic bowel disease) can be classified into 3 subtypes:
- Acute mesenteric ischaemia
- Chronic mesenteric ischaemia
- Colonic ischaemia (ischaemic colitis)
Acute Mesenteric Ischaemia (AMI)
Definition
AMI is defined as a sudden reduction in blood flow to the small intestine (and less commonly the large intestine)
Aetiology
~90% cases are caused by superior mesenteric artery occlusion
There are 4 main causes: [Ref]
| Arterial embolism – most common cause of AM | Most commonly cardiac embolism (e.g. atrial fibrillation or recent MI) causes sudden occlusion of the superior mesenteric artery |
| Arterial thrombosis | Typically superimposed on chronic atherosclerotic disease |
| Mesenteric venous thrombosis | Usually associated with hypercoagulable states, local inflammation (e.g. pancreatitis, diverticulitis) |
| Non-occlusive mesenteric ischaemia | Caused by global hypoperfusion and mesenteric vasoconstriction |
Clinical Features
Typical clinical features: [Ref]
| Early features |
|
| Late features |
|
Triad of acute mesenteric artery embolism:
- AF (history / ongoing)
- Severe abdominal pain
- Bloody diarrhoea
In acute mesenteric arterial thrombosis, there is often a preceding history of abdominal angina (crampy post-prandial abdominal pain – see CMI section below for more details), followed by abdominal pain. However, the presentation is typically subacute, and the pain is usually less severe compared to embolic causes.
Complications
Prolonged ischaemia can cause bowel infarction (necrosis), which can lead to the subsequent events:
- Bowel perforation
- Peritonitis
- Sepsis
Investigation and Diagnosis
1st line (and gold standard)L: CT angiography of the abdomen and pelvis
- Filling defect suggests occlusion / narrowing of the mesenteric arteries
- Bowel wall oedema and hypoenhancing
- Pneumatosis intestinalis, portal venous gas, and free peritoneal air suggest complicated AMI (advanced ischaemia with necrosis)
Biochemical changes seen in AMI:
- ↑ Lactate (with potential lactic acidosis) – marker of anaerobic metabolism due to impaired intestinal perfusion
- Leukocytosis (↑ neutrophils)
- ↑ CRP
Management
Initial Management
Immediate supportive measures:
- Fluid resuscitation
- IV broad-spectrum antibiotics
- Correct any electrolyte abnormalities
- NG tube decompression
Definitive Management
If acute mesenteric ischaemia progresses to bowel perforation with diffuse peritonitis, sepsis, or haemodynamic instability, an urgent exploratory laparotomy via a midline incision is required.
See the Gastrointestinal (GI) Perforation article for more details.
Definitive management depends on the underlying cause of AMI: [Ref1][Ref2]
| Arterial embolism (most common) | Endovascular revascularisation
|
| Arterial thrombosis | Endovascular revascularisation with angioplasty and stenting
Open surgical bypass is indicated for extensive atherosclerotic disease |
| Mesenteric venous thrombosis | Full-dose UFH |
| Non-occlusive mesenteric ischaemia | Treat the underlying cause (e.g. hypovolaemia, heart failure) |
Chronic Mesenteric Ischaemia (CMI)
Definition
CMI refers to the clinical manifestation of bowel ischaemia due to mesenteric artery occlusive disease, for at least 3 months
Note that asymptomatic mesenteric artery occlusive disease is not CMI.
Aetiology
CMI is almost always caused by atherosclerotic occlusive disease affecting the origin of mesenteric arteries (primarily coeliac trunk, superior mesenteric artery and inferior mesenteric artery) [Ref]
Rarer non-atherosclerotic causes:
- Vasculitis
- Fibromuscualr dysplasia
Clinical Features
Symptoms typically develop only when there is significant stenosis or occlusion in at least two of the three major mesenteric vessels, due to the extensive collateral network in the mesenteric circulation.
Classic presentation: post-prandial abdominal pain that is crampy / dull in nature (which occurs because oxygen demand in the intestines significantly increases during digestion, and atherosclerotic stenosis causes a mismatch between oxygen supply and demand) [Ref]
- The pain causes food avoidance (fear of eating because of the post-prandial pain) → unintended weight loss
- Abdominal bruits on auscultation (turbulent blood flow due to atherosclerotic stenosis)
- Non-specific features: nausea, vomiting, early satiety, diarrhoea, constipation
Investigation and Diagnosis
Choice of test: [Ref]
- Initial screening test: duplex ultrasound
- Gold standard test: CT angiography
Diagnosis requires both the appropriate clinical scenario and radiologic evidence of significant stenosis (>70%) in the coeliac axis and/or superior mesenteric artery, with exclusion of other causes (exclusion of malignancy with upper GI endoscopy and colonoscopy is important) [Ref]
Management
Definitive management: endovascular revascularisation (usually angioplasty with stenting) (primary target: superior mesenteric artery)
- All symptomatic patients should receive revascularisation
- Total parenteral nutrition is NOT an acceptable alternative to revascularisation
Long-term management involves addressing cardiovascular risk factors: [Ref]
- Smoking cessation
- Blood pressure control
- Glycaemic control
- Lipid-lowering therapy and antiplatelet therapy (usually aspirin)
Colonic Ischaemia (Ischaemic Colitis)
Definition
Colonic ischaemia results from hypoperfusion of the colon
Colonic ischaemia most commonly affects the watershed areas (splenic flexure and rectosigmoid junction)
- Watershed areas are segments of the colon situated between the territories supplied by different mesenteric arteries; they receive relatively less blood flow and have limited collateral circulation, making them more vulnerable to ischemia during systemic or localised hypoperfusion
Colonic ischaemia and ischaemic colitis are often used interchangeably; however the term ‘colonic ischaemia’ is preferred as the term ‘colitis’ implies inflammation of the colon, and some patients do not have a documented inflammatory phase of disease. [Ref]
Aetiology
~95% cases are caused by transient hypoperfusion due to non-occlusive disease [Ref]
Key risk factors: [Ref]
- Advanced age
- Heart failure
- Diabetes
- CKD
- Peripheral vascular disease
Clinical Features
Colonic ischaemia usually occurs after a preceding event that leads to hypoperfusion of the colon
- States of hypovolaemia / hypotension (e.g. sepsis, dehydration, haemorrhage)
- Surgery (esp. aortic aneurysm repair and abdominal surgery affecting mesenteric arteries)
- Acute cardiac event (e.g. MI, arrhythmia)
- Use of diuretics / vasoconstrictive medications
Spontaneous onset is possible, especially in the elderly with multiple comorbidities.
Typical presentation
- Sudden-onset cramping abdominal pain (usually left upper or lower quadrant – due to splenic flexure and rectosigmoid junction involvement)
- Typical mild pain, not like the severe, out-of-proportion pain seen in AMI
- Urge to defecate
- Bloody diarrhoea / rectal bleeding within 24 hours of symptom onset
As opposed to AMI, colonic ischaemia presents with early-onset bloody diarrhoea (<24 hours of abdominal pain onset). While in AMI, bloody diarrhoea is a late presentation secondary to bowel infarction.
Investigation and Diagnosis
1st line test: CT abdomen and pelvis with IV contrast [Ref]
- Segmental bowel wall thickening
- Thumbprinting (focal indentations along the oclonic wall) – caused by submucosal oedema and haemorrhage
- Pericolonic fat stranding
Gold standard: colonoscopy with biopsy [Ref]
- Allows direct visualisation of the ischaemic mucosa (e.g. segmental erythema, ulceration, sharply demarcated lesions)
Management
The mainstay of treatment is supportive care [Ref]
- Fluid resuscitation
- Correction of predictive factor (e.g. hypovolaemia)
- NBM
- Avoidance of vasoconstrictive drugs
Antibiotics are reserved for moderate/severe disease, and surgery is indicated for complications or failure of conservative therapy.