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Intestinal ischaemia
Intestinal ischaemia

Intestinal ischaemia

We will be discussing both acute and chronic mesenteric ischaemia:

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ACUTE MESENTERIC ISCHAEMIA

A sudden decrease in blood supply to the bowel results in acute mesenteric ischaemia (AMI). It requires prompt medical intervention and is a medical emergency.

Pathophysiology

AMI may be broken down into 4 common classifications of aetiology:

  1. Acute Mesenteric Arterial Thrombosis (AMAT) - due to a thrombus in-situ
  2. Acute Mesenteric Arterial Embolism (AMAE) - due to embolism
  3. Non-occlusive Mesenteric Ischaemia (NOMI) - due to aetiologies other than occlusion
  4. Mesenteric Venous Thrombosis (MVT) - due to venous occlusion and congestion

There are other rarer causes such as:

  • Takayasu’s arteritis
  • Fibromuscular dysplasia
TYPE
PROPORTION
UNDERLYING CAUSE
AMAT
25%
Atherosclerosis
AMAE
50%
AF (embolus from LA travels through aorta to SMA), post-MI thrombus, prosthetic heart valve, thoracic-abdominal aneurysm
NOMI
20%
Hypovolemic shock, cardiogenic shock. Inotropic medications may also cause this post-MI.
MVT
<10%
Coagulopathy, malignancy, autoimmune
  • Polyarteritis nodosa
  • Thoracic aorta dissection

⚠️ Risk factors

The risk factors are dependant on the underlying cause. For AMAE the risk factor are: smoking, hyperlipidaemia, hypertension (similar to chronic mesenteric ischaemia and similar to what you would expect for an MI which is essentially acute myocardial ischaemia).

😷 Presentation

The presentation of mesenteric ischaemia is normally:

⭐️ Generalised abdominal pain disproportionate to clinical findings. There will be non-specific tenderness and pain may be constant and diffuse.

⭐️ Nausea and vomiting is very common.

Later on we can have feautures of peritonism.

💭 Differentials

When there is an acute abdomen without an obvious cause, mesenteric ischaemia should always be included. Similar presentations include PUD, perforation, symptomatic AAA.

🔍 Investigations

📷
Imaging 🏆 CT angiography is required for definitive diagnosis: It will appear initially as an oedematous bowel 2º to the ischaemia and vasodilatory response. It will then appear with a loss of bowel wall enhancement. Finally we may see pneumatosis (gas within the small/large bowel).
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Laboratory tests ABG is needed urgently to assess acidotic state and lactate levels Amylase ⬆️ is raised but this is not a great indicator. We typically use amylase to exclude pancreatitis actually. LFTs ⬆️ if the coeliac trunk is affected particularly as this can cause ischaemia to the liver.

🧰 Management

It is a surgical emergency and so the only definitive management is surgical excision or revascularisation. However, before that we need to ensure the patient is catheterised, receiving IV fluids, receiving broad-spectrum antibiotics (due to risk of perforation), blood thinners.

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Surgical management:
  • Excision of necrotic bowel - if unsuitable for revascularisation. Patients often end up with a stoma and unfortunately short gut syndrome.
  • Revascularisation of bowel - here we use radiologically guided intervention to remove any thrombus/embolus. It is done with angioplasty, but an open embolectomy is possible in larger vessels such as the coeliac trunk, superior mesenteric artery, inferior mesenteric artery or aorta.

⛔️ Complications

  • Bowel necrosis
  • Perforation
  • Death (50-80%)
  • Short gut syndrome
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CHRONIC MESENTERIC ISCHAEMIA

Pathophysiology

It is essentially intestinal angina. It is relatively rare, however.

Atheroslcerotic plaques that block the coeliac trunk, superior mesenteric artery, inferior mesenteric artery are the causes of CMI. Due to collateral flow, usually 2 of the 3 vessels need to be occluded to feel any symptoms.

😷 Presentation

Patients are generally asymptomatic, but in any situation of increased blood demand (post-prandially or after haemorrhage) they may feel exacerbations.

Clinical examinations are generally insignificant.

⭐️ Postprandial pain - 10 mins → 4 hours after eating

⭐️ Weight loss - decreased caloric intake due to pain as well as malabsorption of nutrients

⭐️ Other vascular insufficiencies - MI history, stroke, PVD.

💭 Differentials

Chronic, non-specific abdominal pain may be due to:

  • Chronic pancreatitis
  • PUD
  • Upper GI cancer

🔍 Investigations

📷
Imaging 🏆 CT angiography is the gold standard to identify vascular issues, and allowing to assess for any interventions that may be required.

🧰 Management

The main thing is to reduce modifiable risk factors (smoking, diet, alcohol etc.).

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Medical management
  • Anti-platelet therapy
  • Statins
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⛔️ Complications

  • Bowel infarction
  • Malabsorption
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Surgical management
  • Endartectomy/bypass
  • 🏆+ stenting

Mesenteric angioplasty is done percutaneously via the femoral/brachial/axillary arteries with catheter guidance. Prognosis tends to be quite good.

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ISCHAEMIC COLITIS

Pathophysiology

Ischaemic colitis is when we have an acute, transient decrease in the blood flow to the large intestine. It can lead to inflammation, ulceration and haemorrhage of the bowel. It is more prevalent in watershed regions of the abdomen such as the splenic flexure.

⚠️ Risk factors

  • Atrial fibrillation

😷 Presentation

  • Acute bloody diarrhoea is a hallmark symptom.
  • Abdominal pain

🔍 Investigations

📷
Imaging
  • 🏆 CT angiography is the gold standard to identify the area of ischaemia.
  • Abdominal X-ray may show thumbprinting as a result of mucosal oedema/haemorrhage causing mucosal thickening.
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🧰 Management

Supportive measurements are required. However surgery may be indicated in cases of peritonitis, perforation, ongoing haemorrhage.

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