Ischaemic gut
Ischaemic bowel can be classified anatomically into ischaemia of small bowel (mesenteric ischaemia) and large bowel (ischaemic colitis). Both conditions may be caused by arterial thromboembolism, non-occlusive ischaemia (due to hypoperfusion, vasospasm) and venous thrombosis, and may be acute or chronic. A rare entity is omental infarction, which is briefly discussed at the end of this pathway.
This pathway deals mainly with acute mesenteric ischaemia and ischaemic colitis. Diagnosis of both conditions is challenging and requires a high index of clinical suspicion.
Mesenteric ischemia is a medical emergency and will often lead to bowel necrosis. Early diagnosis and intervention is key. Mortality for patients undergoing revascularization ranges from 44% to 90%.
Mesenteric ischaemia may be acute or chronic. Chronic mesenteric ischemia (also called intestinal angina) refers to episodic or constant intestinal hypoperfusion, which usually develops in patients with mesenteric atherosclerotic disease.
Ischaemic colitis is usually not related to blood vessel occlusion but to a compressive lesion in the large bowel (e.g., colon carcinoma, stricture, diverticulosis, fecal impaction) . Ischaemic colitis is commonly transient, but may be chronic or recurrent. Although most cases will resolve on their own, 15% will develop gangrene and up to 20% will require surgical intervention.
Large versus small bowel ischemia
Table 1: Differentiating Acute Mesenteric Ischemia from Colonic Ischemia
Acute mesenteric ischaemia | Colonic ischaemia |
Most patients over 50 years | 90% of patients over 60 years |
Acute precipitating cause is usual (e.g.,myocardial infarction, congestive heart failure, cardiac arrhythmias, hypotensive episodes) | Acute precipitating cause is rare |
Predisposing lesion is uncommon (excluding atherosclerosis) | Associated predisposing lesion (e.g., colon carcinoma, stricture, diverticulosis, fecal impaction) |
Patients usually appear seriously ill | Patients do not appear ill |
Pain more severe; abdominal findings minimal early in course but become pronounced later | Mild abdominal pain with tenderness and guarding usual |
Rectal bleeding and diarrhea uncommon | Moderate rectal bleeding or bloody diarrhea |
Table adapted from Greenwald DA, Brandt LJ, Reinus JF. 'Ischemic bowel disease in the elderly', Gastroenterol Clin North Am. June 2001; 30(2): 445-73.
Acute Mesenteric Ischaemia
Pathophysiology
- Arterial embolism (50%)
- Arterial thrombosis (15-25%)
- Non-occlusive (due to hypoperfusion, vasospasm) (20-30%)
- Venous thrombosis (5%).
Step 1: Pathway Entry
Severity of abdominal pain out of proportion to physical findings.
May be associated with shock from dehydration and excessive fluid loss - mental confusion, tachycardia, tachypnoea and circulatory collapse.
In bowel infarction - peritoneal signs, haemodynamic instability, signs of sepsis with multiorgan failure.
Risk factors to consider for arterial thromboembolism:
- Age>60
- AF
- Recent AMI
- Valvular heart disease
- Aortic atlerosclerosis or aneurysm
- Aortoiliac instrumentation or surgery.
Venous thrombosis is uncommon, occurs in younger patients and risk factors include:
- hypercoagulable states
- dehydration
- portal hypertension
- abdominal infections
- blunt abdominal trauma
- pancreatitis
- splenectomy
- malignancy in the portal region.
Step 2: Is the Patient Stable?
Initiate resuscitation measures: IV fluid resuscitation with crystalloids and blood products should be started promptly to correct the volume deficit and metabolic derangement.
Consideration of other life threatening diagnoses: acute pancreatitis, ruptured AAA, perforated viscus, septic shock from intraabdominal source.
Step 3: Initial Assessment
History and examination concurrent with resuscitation.
Bedside tests: 12 lead ECG, VBG, FAST to rule out ruptured AAA if this is a differential. An elevated or rising lactate is suggestive of ischaemic bowel. However it is non-specific and a normal lactate does not exclude the diagnosis (sensitivity 77-100%, specificity 42%).
Blood tests should include FBC, EUC, LFT, lipase, Coagulation profile and Group and Hold.
Step 4: Imaging
X-rays not diagnostic of ischaemic bowel but may help in exclusion of differential diagnoses.
AXR if done, may show thumbprinting or thickening of bowel loops (40% of ischaemic gut), air in the portal vein is a late finding.
CT may show focal or segmental bowel wall thickening, intestinal pneumatosis with portal vein gas, bowel dilation, mesenteric stranding, portomesenteric thrombosis, or solid organ infarction, in addition to ruling out other causes of acute abdominal pain. The CT scan should be performed without oral contrast, which can obscure the diagnosis. Bowel wall changes are sensitive but not specific. CT angiography may show thromboembolic occlusion which increases the specificity for the diagnosis (64% sensitivity, 92% specificity). The absence of occlusions is not sufficiently sensitive to rule out ischaemic bowel.
If the diagnosis is still in question then options are:
- laparotomy (which may be diagnostic and therapeutic).
- arteriography (facilitates therapies such as vasodilators or thrombolytic agents, angioplasty, placement of a vascular stent, and embolectomy).
Step 5: Management
Early notification of surgeons and ICU (and interventional radiology if appropriate).
Early laparotomy or arteriography.
Broad spectrum IV antibiotics (ampicillin and gentamicin or 3rd generation cephalosporin and metronidazole).
IV heparin if no contraindications to anticoagulation.
Supportive measures: fluid resuscitation, oxygen to correct hypoxia, analgesia, NG tube for gastric decompression.
Ischaemic colitis
Pathophysiology
- Non-occlusive (95%)
- Arterial thromboembolism
- Mesenteric vein thrombosis.
Step 1: Pathway Entry
Mild-moderate abdominal pain, often left sided, diarrhoea, PR bleeding. Pain is not as severe as that of mesenteric ischaemia.
Risk factors are similar to those for mesenteric ischaemia.
Step 2: Is the Patient Stable?
Initiate resuscitation measures if unstable.
Consideration of other life threatening diagnoses aortoenteric fistula, ruptured AAA, perforated viscus, septic shock from intraabdominal source (e.g. diverticulitis).
Step 3: Initial Assessment
History and examination concurrent with resuscitation.
Bedside tests: 12 lead ECG, VBG, FAST to rule out ruptured AAA if this is a differential. An elevated or rising lactate is suggestive of ischaemic bowel but not specific.
Blood tests should include FBC, EUC, LFT, lipase, Coagulation profile and Group and Hold.
Step 4: Imaging
Abdominal X-rays non-specific, may show distension, pneumatosis, thumbprinting.
CT abdomen with IV contrast: non-specific and may be normal. May show segmental bowel wall thickening, pneumatosis, mesenteric vein and hepatic portal vein gas.
Arteriography rarely helpful (unless small bowel ischaemia needs to be excluded).
If diagnosis unclear then will require colonoscopy.
Step 5: Management
Supportive care - IV fluids, oxygen to correct hypoxia, analgesia, NG tube if ileus present.
Broad spectrum IV antibiotics (ampicillin and gentamicin or 3rd generation cephalosporin and metronidazole).
Anticoagulant therapy is not normally indicated except for patients who develop ischemia due to mesenteric venous thrombosis or due to cardiac embolization.
Patients with colonic infarction and necrosis require urgent surgical intervention, which can be life-saving.
Omental infarction
Omental infarction is a rare cause of abdominal pain, with about 400 cases reported in the literature (incidence not determined). About 85% of all reported cases of omental infarction have occurred in adults, most frequently in the age group of 40–50 years and twice more commonly in males than in female. Omental infarction appears to occur more commonly on the right, and may be primary, which is associated with obesity, local trauma, occupational vibration, heavy food intake, excessive exercise, coughing, excessive strain, sudden changes in position, and the use of laxatives. Secondary infarction can be induced by the following causes: torsion due to adhesion between the omentum and pathologic foci such as surgical scars, inflammation, cysts, tumours and hernias; thrombosis due to various causes such as hypercoagulopathy and vascular abnormalities; and congestion of the mesenteric vein due to systemic diseases such as right-sided heart failure.
Omental infarction may be diagnosed by:
- CT: triangular or oval-shaped fatty mass or an interspersed area with hyperattenuating streaky infiltration is pathognomonic for omental infarction.
- Ultrasound is less useful, it may misinterpret the infarcted fatty lesion as normal intra-abdominal fat.
- Omental infarction has previously been diagnosed on exploratory surgery, however this diagnostic modality is now infrequently used with the widespread availability of CT.
Evidence to guide management is limited. Omental infarction appears to be a self-limiting disease. Treatment is mainly conservative (analgesia with opiates / NSAIDs) with close observation for 24-48 hours. Surgery may be considered if there are deteriorating symptoms, signs or clinical markers. If surgery is performed, omental necrosectomy is done either via laparoscopy (preferred) or laparotomy. Surgery may hasten symptom resolution.
Further References and Resources
Online resources
- BMJ Best Practice - ischaemic bowel (subscription required)
- Uptodate (requires login) Acute mesenteric ischemia and Colonic ischemia,
Journal articles and textbooks
- Barai, K, Knight, B. 'Diagnosis and management of idiopathic omental infarction: A case report'. Int J Surg Case Rep. 2011; 2(6): 138–140.
- Greenwald DA, Brandt LJ, Reinus JF. 'Ischemic bowel disease in the elderly'. Gastroenterol Clin North Am. 2001 Jun;30(2):445-73.
- Anderson JL et al, 'ACC/AHA Practice Guidelines: Management of Patients with Peripheral Artery Disease (Compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations)', Circulation. 2013;127:1425-1443.
- Oldenburg WA, Lau LL, Rodenberg TJ, et al: 'Acute mesenteric ischemia'. Arch Intern Med 164: 1052, 2004