Clinical Module · Vascular Emergency

Acute Mesenteric Ischaemia
Recognition, Diagnosis and Emergency Management

A time-critical vascular emergency caused by interruption of intestinal blood flow. Delay leads to bowel infarction, sepsis, multi-organ failure, and high mortality.

ESVS 2017 NICE RCEM Vascular Emergency
Section 1

Overview

Acute mesenteric ischaemia (AMI) is a time-critical vascular emergency and a surgical emergency. It occurs when blood flow to the intestine is acutely reduced or interrupted, leading to bowel ischaemia and, if untreated, infarction. It is uncommon but rapidly lethal: mortality reaches 60–80% once diagnosis is delayed beyond the first hours, because the window for salvaging viable bowel is short.

There are four principal mechanisms, each with a distinct cause, tempo and treatment: arterial embolism, arterial thrombosis, mesenteric venous thrombosis, and non-occlusive mesenteric ischaemia. One lesson runs through this module: think bowel ischaemia early, image with CT angiography, and escalate to vascular and general surgery without delay.

Central Teaching Point Think bowel ischaemia in patients with severe abdominal pain out of proportion to examination findings, especially in the presence of vascular risk factors, atrial fibrillation, shock states, or elevated lactate.
Section 2

Pathophysiology

The intestine is supplied by three vessels: the coeliac axis, the superior mesenteric artery (SMA) and the inferior mesenteric artery (IMA). The SMA supplies the small bowel and proximal colon and is the vessel most often involved in acute mesenteric ischaemia. Venous drainage is via the superior mesenteric and portal veins.

When perfusion falls below the metabolic demand of the bowel, the mucosa is injured first, because it is the most metabolically active and most vulnerable layer. Ongoing hypoperfusion drives a progression from reversible mucosal ischaemia, to transmural infarction, to perforation, peritonitis and septic shock. Reperfusion of ischaemic bowel can itself trigger systemic inflammatory injury. The practical consequence is that time is bowel: the longer flow is interrupted, the smaller the chance of salvage.

Mechanisms of Reduced Intestinal Blood Flow

Four Patterns
  • Arterial embolism — an embolus lodges in the SMA, abruptly cutting off flow
  • Arterial thrombosis — in-situ thrombosis of a pre-existing atherosclerotic stenosis
  • Mesenteric venous thrombosis — venous outflow obstruction causing bowel wall congestion and oedema
  • Non-occlusive ischaemia — splanchnic vasoconstriction and low flow without a vessel blockage
Section 3

Arterial Embolic Mesenteric Ischaemia

SMA Embolism

~50% of Cases

Key Features

  • The most common cause — an embolus lodges in the SMA, often just distal to its origin
  • Sudden onset of severe periumbilical or epigastric pain
  • Frequently accompanied by vomiting and diarrhoea (may be bloody)
  • Rapid clinical decompensation over 6–12 hours
  • Pain is classically disproportionate to abdominal examination findings

Embolic Sources

  • Atrial fibrillation with left atrial thrombus (the commonest source)
  • Left ventricular mural thrombus following myocardial infarction
  • Valvular heart disease or prosthetic valves
  • Infective endocarditis
  • Aortic atheroma or aneurysmal thrombus
TIME-CRITICAL: Urgent CT angiography (arterial phase) and immediate vascular surgery referral. Do not wait for lactate to rise — by that point bowel infarction has often begun.
Section 4

Arterial Thrombotic Mesenteric Ischaemia

SMA Thrombosis

~25% of Cases

Key Features

  • In-situ thrombosis of a pre-existing atherosclerotic SMA stenosis
  • Often preceded by weeks or months of postprandial pain and weight loss (“mesenteric angina”)
  • More insidious onset than embolism, but still a surgical emergency
  • Collateral circulation may have developed, so presentation varies

Distinguishing Clues

  • History of chronic mesenteric ischaemia: food fear (sitophobia) and significant weight loss
  • Heavy vascular risk-factor burden — smoking, diabetes, peripheral vascular disease
CT angiography urgently and vascular surgery review. May require surgical bypass, endarterectomy, or endovascular intervention. High mortality if bowel is already infarcted.
Section 5

Mesenteric Venous Thrombosis

Mesenteric Venous Thrombosis (MVT)

~10% of Cases

Key Features

  • Slower onset — symptoms may develop over days to weeks
  • Colicky, often poorly localised abdominal pain with nausea and diarrhoea
  • Venous outflow obstruction causes bowel wall congestion and oedema
  • Can progress to bowel infarction if the thrombus extends

Risk Factors

  • Inherited thrombophilia (Factor V Leiden, Protein C/S deficiency)
  • Malignancy, especially pancreatic and hepatic
  • Portal hypertension and cirrhosis
  • Recent abdominal surgery or intra-abdominal sepsis
  • Oestrogen-containing contraception or HRT
CT angiography with a portal venous phase. Anticoagulation is first-line treatment; surgery is reserved for peritonitis or perforation. Arrange a thrombophilia screen once stable.
Section 6

Non-Occlusive Mesenteric Ischaemia (NOMI)

Non-Occlusive Mesenteric Ischaemia (NOMI)

~15% of Cases

Key Features

  • No vessel occlusion — caused by splanchnic hypoperfusion and vasoconstriction in low-flow states
  • Typically affects critically ill, elderly, or post-operative patients
  • Often insidious — abdominal distension, ileus and unexplained metabolic acidosis
  • CT angiography may show diffuse mesenteric vasoconstriction without an occluded vessel

Common Precipitants

  • Cardiogenic shock or severe heart failure
  • Septic shock with splanchnic steal
  • Major surgery, cardiopulmonary bypass or ECMO
  • High-dose vasopressors (especially noradrenaline)
  • Haemodialysis-related hypotension
Treat the underlying cause. Restore cardiac output and volume status, reduce vasopressors where possible, and involve critical care early. Surgical review if peritonitis develops. Mortality exceeds 50%.
Section 7

Clinical Features

Presentation evolves with the duration of ischaemia. Early disease is deceptively benign, which is precisely why it is missed.

How It Presents Over Time

Evolving Picture

Early (Ischaemic) Phase

  • Severe, poorly localised abdominal pain
  • Pain out of proportion to a soft, minimally tender abdomen
  • Nausea, vomiting and an urgent desire to defaecate; diarrhoea may be bloody
  • Observations may initially be normal

Progressive Phase

  • Tachycardia and hypotension
  • Developing metabolic acidosis and rising lactate
  • Worsening distension and reducing bowel sounds (ileus)

Late (Infarction) Phase

  • Peritonism — guarding, rigidity, rebound tenderness
  • Septic shock and multi-organ dysfunction
  • By this stage transmural infarction has usually occurred
Section 8

Pain Out Of Proportion To Examination

The hallmark of early acute mesenteric ischaemia is severe pain with strikingly few examination findings. The visceral peritoneum localises poorly, so before the bowel becomes transmurally infarcted the abdomen can stay soft and only mildly tender even though the patient reports agonising pain.

Clinical Rule: Pain Out Of Proportion A patient with severe abdominal pain but an unremarkable abdomen should raise immediate suspicion of mesenteric ischaemia, particularly with vascular risk factors, atrial fibrillation, a shock state, or a rising lactate. The sign is not present in every case, and its absence does not exclude the diagnosis. When present, it demands urgent CT angiography rather than reassurance.
Section 9

Risk Factors

Arterial (Embolic & Thrombotic)

  • Atrial fibrillation
  • Recent myocardial infarction with mural thrombus
  • Valvular or prosthetic-valve disease, endocarditis
  • Established atherosclerosis and peripheral vascular disease
  • Smoking, diabetes, hypertension, hyperlipidaemia
  • Prior chronic mesenteric ischaemia (postprandial pain, weight loss)

Venous & Non-Occlusive

  • Inherited or acquired thrombophilia
  • Malignancy and recent abdominal surgery
  • Portal hypertension and cirrhosis
  • Oestrogen-containing contraception or HRT
  • Critical illness, shock and high-dose vasopressors
  • Cardiac surgery, cardiopulmonary bypass, ECMO, dialysis hypotension
Section 10

Laboratory Findings

Bloods & Their Limitations

Supportive, Not Diagnostic

What You May See

  • Raised lactate and a high-anion-gap metabolic acidosis on the venous blood gas
  • Leucocytosis, often marked
  • Haemoconcentration and acute kidney injury
  • Mildly raised amylase (non-specific)

The Lactate Pitfall

  • Lactate is a late marker — a normal lactate does not exclude AMI
  • Sensitivity for mesenteric ischaemia is only around 70–80%
  • By the time lactate is markedly elevated (>4 mmol/L) bowel infarction has often begun
  • A rising trend is more informative than a single value
No blood test confirms or excludes mesenteric ischaemia. Order CT angiography on clinical suspicion — not on lactate thresholds. A normal lactate in a patient with acute abdominal pain and atrial fibrillation is not reassuring. Also send FBC, U&E, LFTs, amylase, coagulation and a group & save.
Section 11

CT Angiography Findings

CT angiography (CTA) of the abdomen is the diagnostic investigation of choice. Request it with an arterial phase. A routine portal-venous-phase CT abdomen can miss an SMA embolus. Tell the radiologist the clinical question: “?mesenteric ischaemia — arterial phase required.”

Phase What It Shows When to Request
Non-contrast Bowel wall thickening, pneumatosis intestinalis, portal venous gas Included in most protocols as a baseline
Arterial phase SMA embolus or thrombus, aortic pathology, vessel cut-off Essential for suspected mesenteric ischaemia
Portal venous phase Mesenteric venous thrombosis, bowel wall enhancement, liver/spleen Add if MVT suspected or in a young patient
Delayed phase Bowel wall enhancement pattern, viability assessment Radiologist discretion for viability assessment

Radiological Signs of Established Ischaemia

Late & Ominous
  • Vessel filling defect or abrupt cut-off in the SMA
  • Reduced or absent bowel wall enhancement
  • Bowel wall thickening or, conversely, paper-thin dilated loops
  • Pneumatosis intestinalis (gas within the bowel wall)
  • Portal venous gas — a sign of advanced infarction
  • Free fluid, mesenteric stranding, or free air if perforated
A “normal” portal-venous-phase CT abdomen does not exclude AMI. If suspicion remains high, ensure a dedicated arterial-phase CTA is performed and discussed with the radiologist.

Associated ECG Findings

Adjunct Only
  • The ECG is not diagnostic of mesenteric ischaemia
  • It may identify atrial fibrillation as a potential embolic source
  • It may identify myocardial ischaemia
  • It may identify an alternative diagnosis
  • ECG findings should not delay CT angiography
An ECG is a reasonable adjunct in a patient with abdominal pain, but it neither confirms nor excludes mesenteric ischaemia. The diagnosis rests on clinical suspicion and CT angiography — do not let an ECG delay imaging or surgical referral.
Section 12

Emergency Department Management

Resuscitate, Investigate, Escalate

In Parallel

Immediate Resuscitation

  • A–E assessment; high-flow oxygen if hypoxic
  • Large-bore IV access and fluid resuscitation
  • Strong analgesia — do not under-treat because the abdomen looks soft
  • Keep nil by mouth (NBM); consider a nasogastric tube if distended or vomiting
  • Catheterise and monitor urine output; correct electrolytes

Investigations

  • Venous blood gas with lactate; FBC, U&E, LFTs, amylase, coagulation, group & save
  • Urgent CT angiography of the abdomen (arterial phase) — the priority investigation

Early Treatment

  • Broad-spectrum IV antibiotics once ischaemic bowel is suspected
  • Anticoagulation (e.g. IV heparin) after discussion with the surgical/vascular team
  • For NOMI, treat the underlying cause and minimise vasopressors where safe
Resuscitation, imaging and specialist referral should happen in parallel, not in sequence. Do not delay the vascular/surgical conversation while awaiting blood results.
Section 13

Immediate Surgical/Vascular Referral

Who to Call — and When

Do Not Delay

Refer Immediately If

  • Acute abdominal pain with atrial fibrillation (any age)
  • Pain out of proportion to examination findings
  • Unexplained metabolic acidosis or a rising lactate
  • Bloody diarrhoea with haemodynamic instability
  • Known vascular disease or recent MI with new abdominal symptoms
  • Critically ill or post-operative patient with new distension or acidosis

Specialist Roles

  • Vascular surgery — arterial embolism/thrombosis: embolectomy, bypass, endovascular revascularisation
  • General surgery — peritonitis, perforation, resection of non-viable bowel
  • Interventional radiology — catheter-directed thrombolysis, aspiration, stenting
  • Critical care — shock, multi-organ support, and NOMI in critical illness
A confirmed or strongly suspected occlusive AMI is a surgical emergency. Definitive management is revascularisation and resection of non-viable bowel — the patient belongs in theatre or the angiography suite, not in a holding area.
Section 14

Complications

Consequences of Delayed Diagnosis

High Mortality
  • Transmural bowel infarction
  • Bowel perforation and peritonitis
  • Sepsis and septic shock
  • Multi-organ failure
  • Short bowel syndrome after extensive resection
  • Reperfusion injury following revascularisation
  • Death — mortality of 60–80% when treatment is delayed
The single most important determinant of outcome is time to diagnosis and revascularisation. Every hour of delay increases the extent of irreversible bowel loss.
Section 15

Key Learning Points

Remember This Think bowel ischaemia in patients with severe abdominal pain out of proportion to examination findings, especially in the presence of vascular risk factors, atrial fibrillation, shock states, or elevated lactate.

Always

  • Suspect AMI early in at-risk patients with abdominal pain
  • Request CT angiography with an arterial phase
  • Resuscitate, image and refer in parallel
  • Involve vascular and general surgery without delay
  • Start antibiotics and discuss anticoagulation early

Never

  • Wait for lactate to rise before imaging
  • Be reassured by a soft abdomen or a normal lactate
  • Accept a portal-venous-phase CT as having excluded AMI
  • Let an ECG delay CT angiography or surgical referral
  • Discharge unexplained abdominal pain in a patient with AF or vascular disease
Sources & References
ESVS 2017 Clinical Practice Guidelines on the Management of Acute Mesenteric Ischaemia | NICE NG45 — Suspected Cancer: Recognition and Referral | RCEM Learning — Mesenteric Ischaemia | Resus Council UK | LITFL — Mesenteric Ischaemia
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