Acute Mesenteric Ischaemia | AMI

Introduction

Acute mesenteric ischaemia (AMI) is a life-threatening condition caused by a sudden reduction in blood flow to the bowel, leading to ischaemia, necrosis, and, if untreated, death.¹

It most commonly results from an embolism obstructing a major artery, such as the superior mesenteric artery, often in individuals with atrial fibrillation, which increases the risk of clot formation.²

The condition has a high mortality rate of 60-80% and an incidence of 25 cases per 100,000 person-years, primarily affecting those over 70 years.³

Aetiology

 The aetiology of AMI is broadly classified into four main causes.

Arterial embolism (40-50%)

The most common cause of AMI is arterial embolism, typically affecting the superior mesenteric artery (SMA).

Most often, the emboli originate from cardiac sources such as atrial fibrillation, myocardial infarction, or valvular disease.^3-4

Arterial thrombosis (25-30%)

Arterial thrombosis occurs due to acute occlusion of a previously atherosclerotic mesenteric artery.

Many affected patients have a history of chronic mesenteric ischaemia, presenting with post-prandial abdominal pain and weight loss.^3-4

Non-occlusive (20%)

Non-occlusive mesenteric ischaemia is caused by vasoconstriction.

It is commonly seen in patients with prolonged hypotension or secondary to shock.^3-4

Venous thrombosis (5-10%)

Mesenteric venous thrombosis is caused by thrombosis of mesenteric veins, leading to impaired venous drainage.

It is commonly seen in patients with intra-abdominal infections, inflammatory conditions, and hypercoagulable states, such as Factor V Leiden mutation or malignancy.^3-4

Risk factors

Risk factors for the development of AMI include:

Clinical features

History

Typical symptoms of AMI include:

• Abdominal pain: severe, sudden onset, sharp (stabbing), diffuse and constant
• Nausea and vomiting
• Diarrhoea or constipation
• Fever
• Rectal bleeding and haematochezia
• Septic shock (if delayed diagnosis)^{3, 5}

Other important areas to cover in the history include:

Clinical examination

In the context of suspected AMI, a thorough abdominal examination is necessary. 

Typical clinical findings in AMI include:

• Generalised abdominal tenderness
• Generalised peritonism (guarding and rebound tenderness) in later stages
• Systemic inflammatory response syndrome (SIRS): tachycardia, hypotension and pyrexia^{3, 5}

Differential diagnoses

Differential diagnoses of suspected AMI include:

Investigations

Bedside investigations

Relevant bedside investigations may include:

• Basic observations: to monitor for systemic inflammatory response syndrome
• ECG: as arrhythmias are a risk factor

Laboratory investigations

Relevant laboratory investigations may include:

• Full blood count: microcytic anaemia secondary to iron deficiency with significantly elevated white blood count, suggesting bowel ischaemia (non-specific)
• C-reactive protein: raised in inflammation (non-specific)
• Urea and electrolytes: baseline before investigations or treatment
• Liver function tests: deranged liver function due to coeliac trunk involvement resulting in hepatic ischaemia
• D-dimer: highly sensitive but low specificity; normal value excludes AMI
• Coagulation profile: coagulopathy as a cause of AMI or secondary to disseminated intravascular coagulation
• Venous blood gas: lactic acidosis secondary to severe intestinal ischaemia. Normal blood gas does not exclude AMI, especially in the early stages^3-4

Imaging

Relevant imaging includes:

• High-resolution CT abdomen and pelvis: may show oedematous bowel loops, suggesting bowel ischaemia
• CT angiography: may show intestinal dilation, reduction of visceral enhancement, portal venous gas and free intraperitoneal air (if perforation). This is the gold standard and performed immediately in suspicion of AMI.^{3, 5}

Management

AMI is a life-threatening surgical emergency.^2-5

Initial medical management

The primary approach involves ABCDE assessment and resuscitation, including intravenous fluids and correcting electrolyte disturbances.

Prompt initiation of broad-spectrum antibiotics is required due to the risk of faecal peritonitis from ischaemic bowel perforation (bacterial translocation).

A multidisciplinary team approach is crucial, incorporating input from general surgery, vascular surgery, and interventional radiology.

Mesenteric venous thrombosis is primarily treated with anticoagulation, while non-occlusive mesenteric ischaemia requires haemodynamic support and intra-arterial vasodilators; surgery is reserved for bowel infarction.^{1, 4-5}

Definitive surgical management

Surgical management is the definitive management of AMI and involves revascularisation ± bowel resection.

A laparotomy is first conducted to:

• Establish the viability of the bowel and the extent of any necrotic bowel
• Attempt revascularisation of the bowel if possible. When treating occlusive mesenteric artery ischaemia, either open or endovascular thrombo-embolectomy (or thrombolysis) is the mainstay of treatment, depending on the nature and location of the vessel occlusion.

After revascularisation, the bowel’s viability should be evaluated by:

• Assessing the presence of pulses using a continuous wave Doppler
• Observing peristalsis
• Ensuring a normal colour

If the bowel is non-viable or necrotic, revascularisation is not an option; surgical resection is required. Often, some bowel is non-viable, and the rest may be salvageable.

Complications

If AMI is not diagnosed and treated promptly, complications can include:

• Bowel necrosis: prolonged ischaemia leads to tissue death, resulting in necrosis
• Peritonitis
• Sepsis: bacterial translocation from necrotic bowel into the bloodstream
• Multiple organ dysfunction syndrome: severe sepsis can lead to multiple organ failure
• Death: mortality rate is high (70%-90%)^2-4

Complications of surgical management can include:

• Short gut syndrome: extensive resection of bowel can lead to malabsorption
• Anastomotic leak
• Wound infection
• Adhesions: intrabdominal adhesions leading to bowel obstruction
• Death: risk remains significant due to extensive bowel necrosis and co-morbid conditions

Reviewer

Professor Vassilis Hadjianastassiou DM(Oxon) BMBCh(Oxon) F.E.B.S.(Transplant) F.E.B.S.(Vascular) FRCS(Gen)

Consultant Vascular, General and Transplant Surgeon

Bart’s Health NHS Trust, Royal London Hospital and London Bridge Hospital

Editor

Dr Jamie Scriven

References

1. Clair DG, Beach JM. Mesenteric Ischemia. 2016. New England Journal of Medicine. Available from: [LINK].
2. Becquemin JP. Management of the Diseases of Mesenteric Arteries and Veins: Clinical Practice Guidelines of the European Society for Vascular Surgery (ESVS). 2017. European Journal of Vascular and Endovascular Surgery. Available from: [LINK].
3. Weisters M, Baker T. Mesenteric and other visceral disease: All you need to know about Vascular Surgery. Vascular Society of Great Britain & Ireland. 2023. Available from: [LINK].
4. Monita MM, Gonzalez L. Acute Mesenteric Ischemia. 2023. StatPearls. Available from: [LINK].
5. Bala M, Catena F, Kashuk J, et al. Acute mesenteric ischemia: updated guidelines of the World Society of Emergency Surgery. World Journal of Emergency Surgery. 2022. Available from: [LINK].