31st July 2023

Vascular Disorders of the GI Tract

Acute Mesenteric Ischaemia

Describes sudden-onset ischaemia of the small bowel secondary to hypoperfusion of the superior mesenteric artery (SMA) or its branches. The hypoperfusion can be secondary to arterial thrombosis, arterial embolism or non-occlusive ischaemia due to poor cardiac output.

The predisposing factors, and signs and symptoms, of all syndromes of ischaemia to the lower gastrointestinal tract are similar and are summarised in Table 1. However, the management and prognosis vary greatly; therefore, it is important to differentiate the various types.

Table 2: Common risk factors and clinical features to both mesenteric ischaemia and ischaemic colitis

The sudden-onset, severe pain is usually constant, central within the abdomen and responds poorly to analgesia. Typically, there are no other abdominal signs. Along with a raised serum lactate, there may be an increased serum amylase and leucocytosis.

The diagnosis is usually made on CT abdomen and pelvis with contrast, though this should not delay laparotomy if there is high suspicion for the condition. The CT may reveal gas in the intestinal wall or portal vein.

The general surgery team will typically organise an emergency laparotomy, and the prognosis is especially poor if the operation is delayed. The bowel is assessed for viability and the necrotic bowel is removed. Endovascular thrombolysis or thrombectomy may be an option in a minority of patients. Patients will usually remain on long-term anticoagulation.

Complications include peritonitis, with or without sepsis, due to bacterial translocation across the necrotic bowel. Therefore, broad-spectrum antibiotics are usually commenced, with a regimen that will also target anaerobic bacteria (e.g., ceftriaxone + metronidazole). Mortality rate is high, estimated at around 50%.

Acute bowel ischaemia leading to necrosis

Image Source: Wikimedia Commons (2008). Intestinal Obstruction, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Intestinal_Obstruction.JPG (Accessed: 28 June 2023).

Chronic Mesenteric Ischaemia

Also known as intestinal angina. Usually a consequence of atherosclerotic plaques in the large mesenteric vessels, leading to colicky, post-prandial abdominal pain. Typically, the pain commences around thirty minutes after eating and lasts approximately one hour. Other symptoms include weight loss (due to ‘fear’ of eating and/or malabsorption), nausea & vomiting and PR bleeding. Examination may reveal bruits of the mesenteric vasculature.

Patients will almost always have atheromatous disease elsewhere, thus enquire about features of cardiovascular disease, cerebrovascular disease, peripheral arterial occlusive disease and renovascular disease.

Diagnosis is usually made with CT or MR angiography, which will reveal atherosclerosis. Duplex ultrasound of the mesenteric arteries may aid in analysis of blood flow through a blockage in real time.

Conservative approaches target the underlying causes of atherosclerosis. Surgical options include angioplasty + stenting, or bypassing the blocked vessel with an open procedure.

Ischaemic Colitis

Describes compromised blood flow to the large bowel. Severity can range from mild ischaemia to severe gangrenous colitis. Most commonly occurs at ‘watershed’ areas, such as the splenic flexure (Griffiths point), which is located at the border of the territory supplied by the superior and inferior mesenteric arteries.

The most common symptoms are left iliac fossa pain and haematochezia.

Abdominal XR may reveal ‘thumbprinting’ due to submucosal oedema. CT is usually diagnostic, with bowel walls thickening a common feature.

Management is conservative in the first instance and involves fluids and antibiotics. A small proportion of patients will require bowel resection with stoma formation.

Complications in severe ischaemic colitis include ongoing haemorrhage, bacterial contamination causing peritonitis and perforation.

Watershed areas of the colon. 

Image Source: Wikimedia Commons (2008). Colonic blood supply, Licensed under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:Colonic_blood_supply.svg (Accessed: 28 June 2023).

Ischaemic Hepatitis

A cause of acute liver failure secondary to insufficient perfusion to the liver. This is frequently due to systemic hypotension, though it can rarely be caused by a clot in the hepatic artery or significant activation of the renin-angiotensin system, which results in splanchnic vasoconstriction. The condition is often termed ‘shock liver’ and is commonly a result of septic, hypovolaemic, cardiogenic or other types of shock. Therefore, it is very likely that there will be concurrent damage to other end organs that are sensitive to ischaemia, such as the kidneys and brain.

The patient may present with jaundice and features of hepatic encephalopathy, such as confusion and asterixis. However, the diagnosis is usually made on the basis of a marked increase in aminotransferase levels after an inciting event. The differential for a very high ALT level (>1000 IU/L) includes paracetamol overdose and acute viral hepatitis, and these should be excluded.

Treating the underlying cause of the ischaemia is the mainstay of management, and critical care support may be required to restore and maintain adequate blood pressure.

The typical histopathological findings of the liver at post-mortem are centrilobular necrosis with normal periportal hepatocytes.

Budd-Chiari Syndrome 

The eponymous name for hepatic vein occlusion. Typically caused by a thrombus but can also be secondary to infiltration by a tumour.

The classic triad includes right upper quadrant pain, ascites and hepatomegaly. The clinical features are summarised in Table 3.

Table 3: Features of Budd-Chiari syndrome

Budd-Chiari syndrome is exceptionally rare in the absence of a procoagulant condition, and its presence should trigger investigation for the cause of hypercoagulability. A rarer alternative is the direct extension of a tumour mass into the hepatic vein. The causes are shown in Table 2.

Table 4: Causes of Budd-Chiari syndrome

If Budd-Chiari syndrome is suspected, the initial radiological investigation is typically ultrasound with doppler flow studies, which is highly sensitive for hepatic vein occlusion. An alternative is a CT with contrast, for which hypertrophy of the caudate lobe is a characteristic sign (highly specific but only seen in ~50% of cases).

The management is variable and will typically be made by the hepatology team. Lifelong anticoagulation is often required, though this may be contraindicated with concurrent oesophageal varices. The occlusion may need to be bypassed with a surgical shunt or a transjugular intrahepatic portosystemic shunt (TIPSS). If fulminant liver failure is present, the patient may be eligible for a liver transplant.