• Clinical science

Intestinal ischemia

Abstract

Intestinal ischemia occurs when blood flow to the bowels is reduced. The condition can be acute or chronic and may affect the large and/or the small intestine. Possible causes for decreased blood flow include thromboembolism, atherosclerosis, and severe hypotension. Mild forms of intestinal ischemia lead to abdominal discomfort (e.g., postprandial pain) and a change in bowel habits (e.g., bloody diarrhea). In severe cases, infarction of intestinal tissue leads to perforation of the bowel, sepsis, and death. Early diagnosis and therapy are, therefore, essential and sometimes emergency surgery is vital. Imaging techniques (e.g., CT angiography, ultrasound, colonoscopy) are used to detect stenoses, occlusions, and/or mucosal changes. Chronic and mild acute forms are associated with a better prognosis and patients benefit from revascularization procedures (e.g., stents, bypass surgery) and symptomatic therapy. Complications such as peritonitis and sepsis result in a poor prognosis.

Definition

Intestinal ischemia is classified into three main types:

References:[1][2][3][4]

Ischemic colitis

Epidemiology

  • Most common form of intestinal ischemia
  • Mainly occurs in adults > 60 years
  • In ∼ 80–85% mild, non-gangrenous form

Etiology

Usually caused by transient hypoperfusion

  • Thromboembolism
  • Hypotension, hypovolemia (e.g., sepsis, dehydration, hemorrhage)
  • Cardiovascular surgery (especially aortic repairs or cardiac bypass)
  • Vasoconstrictive drugs
  • Thrombophilias (e.g., anticardiolipin syndrome)
  • Colonic obstruction from tumors, adhesions, etc.

Pathophysiology

  • Intestinal blood flow of the superior mesenteric artery (SMA) and/or inferior mesenteric artery (IMA) is suddenly compromised (see “Etiology” for causes) → intestinal hypoxia → intestinal wall damage → mucosal inflammation + possibly bleeding → may progress to infarction and necrosis (gangrenous type) → disruption of mucosal barrier and perforation → release of bacteria, toxins, vasoactive substances → life-threatening sepsis
  • Depending on the degree of ischemia, there may be two types:
    • Non-gangrenous (80–85%)
      • Reversible
      • Non-reversible (chronic colitis, strictures)
    • Gangrenous (15–20%)
  • Sites of compromise

The intestines can tolerate a state of ischemia for approx. 6 hours!

Clinical features

Typically presents with 3 clinical stages:

  • Hyperactive phase
    • Sudden onset of crampy abdominal pain (usually left lower quadrant)
    • Bloody, loose stools
    • > 80% of patients recover and do not progress beyond this phase
  • Paralytic phase
    • Pain more diffuse
    • Bowel sounds become absent.
    • Bloating
    • Bloody stools cease
  • Shock phase

A classic case of ischemic colitis is a patient who presents with bloody diarrhea and severe abdominal pain after an abdominal aortic aneurysm repair!

Diagnostics

Differential diagnoses

See also acute abdomen

Therapy

Complications

Prognosis

References:[1][5][6][4]

Acute mesenteric ischemia

Epidemiology

Etiology

  • Acute arterial embolism; (∼ 50% of cases): generally resulting from atrial fibrillation, myocardial infarction, valvular heart disease, or endocarditis
  • Arterial thrombosis; (∼ 25% of cases): due to preexisting visceral atherosclerosis, arteritis, aortic aneurysm, or dissection
  • Nonocclusive mesenteric ischemia (NOMI; ∼ 20% of cases)
  • Venous thrombosis; (< 10% of cases): Predisposing factors include infection, malignancies, estrogen therapy, and hypercoagulability disorders.

Pathophysiology

  • Sudden interruption of blood flow to small bowel (see “Etiology” above for cause) → intestinal hypoxia → hemorrhagic infarction and necrosis → disruption of mucosal barrier and perforation → release of bacteria, toxins, vasoactive substances → life-threatening sepsis
  • Sites of interruption
    • SMA (∼ 90% of cases): supplies the distal duodenum, jejunum, ileum, and colon to the splenic flexure
    • Superior mesenteric vein (∼ 10% of cases): drains blood from the small intestine
    • IMA and the celiac artery are less commonly affected.

Clinical features

  • Periumbilical pain that is disproportionate to physical findings
  • Nausea and vomiting
  • Diarrhea (bloody in later stages)
  • Gangrenous bowel: rectal bleeding and signs of sepsis (e.g., tachycardia, hypotension)
  • Clinical courses
    • Acute arterial embolism: most abrupt and painful onset of all types (“abdominal apoplexy”)
    • Acute arterial thrombosis: presentation less severe because patients have better collateral supply
    • Nonocclusive ischemia: symptoms develop over several days
    • Venous thrombosis: symptoms less dramatic, worsen gradually (e.g., abdominal discomfort evolves over a week)

A patient with acute arterial embolism typically presents with severe abdominal pain, fever, bloody diarrhea, leukocytosis and atrial fibrillation!
A patient with acute arterial thrombosis typically has a known cardiovascular or peripheral vascular disease and/or symptoms of chronic mesenteric ischemia in addition to acute symptoms!

Diagnostics

  • Laboratory findings
  • CT angiography (confirmatory test)
    • Detects disrupted flow and vascular stenosis
    • Distended intestinal loops and air-fluid levels, wall thickening, pneumatosis intestinalis (suggests transmural ischemia or infarction)
    • Alternative: MR angiography
      • Advantage: no radiation
      • Disadvantage: less accurate evaluation of the IMA
  • Ultrasound
    • Detection of distended intestinal loops and free fluid in the abdominal cavity in case of perforation
    • Color Doppler ultrasound to detect stenosis in arterial branches
  • Evaluation of underlying disease (e.g., ECG for atrial fibrillation or myocardial infarction)

If an acute mesenteric ischemia is suspected, quickly initiating imaging studies (CT angiography, color Doppler sonography) is essential. In cases with peritonitis or risk of shock, however, emergency surgery without prior imaging is indicated!

Differential diagnoses

Therapy

  • If signs of advanced ischemia (e.g., peritonitis, sepsis) or hemodynamically unstable patient emergency laparotomy ;
    • Open surgical embolectomy or mesenteric artery bypass depending on the cause of occlusion
    • Resection of necrotic bowel segments
  • Hemodynamically stable patients without signs of advanced ischemiaendovascular approach
    • Balloon angioplasty and stenting
    • Catheter-based pharmacologic (thrombolytics) and/or mechanical thrombectomy
  • Supportive: IV fluids, nasogastric tube; , analgesics and broad-spectrum antibiotics
  • Infusion of a vasodilator (e.g., papaverine) during arteriography to relieve occlusion and vasospasm
  • Heparin anticoagulation in cases of venous thrombosis
  • Long-term measures
    • Reduce risk of further atherosclerosis (antiplatelet and statin therapy)
    • Treat underlying cardiac disease (e.g., anticoagulation therapy in patients with A-fib)

Complications

Peritonitissepsismulti-organ failure

Prognosis

References:[2][7][8]

Chronic mesenteric ischemia

Epidemiology

Etiology

Pathophysiology

  • Slowly progressing stenosis of two or more main arteries (SMA, IMA; , or celiac artery) → postprandial mismatch between splanchnic blood flow and intestinal metabolic demand → postprandial pain
  • If only one main artery is affected, collateral connections between the arteries can form and compensate for the reduced flow → patient may be asymptomatic
  • Thrombus formation in addition to progressive stenosis can lead to acute-on-chronic mesenteric ischemiaacute mesenteric ischemia

Clinical features

  • Some patients may be asymptomatic (see “Pathophysiology”)
  • So-called 'abdominal/intestinal angina'
    • Recurrent, dull, postprandial epigastric pain usually within the first hour after eating
    • Can lead to a fear of eating → weight loss and malabsorption
  • Bloating, nausea, occasional diarrhea
  • Abdominal bruit caused by stenosis of mesenteric vessels

A patient typically presents with postprandial abdominal pain (abdominal angina), food aversion, and weight loss!

Diagnostics

  • No specific laboratory findings in chronic mesenteric ischemia
  • Clinical suspicion → CT scan of the abdomen (identifies atherosclerotic vascular disease and rules out other abdominal disorders)
  • CT angiography or MR angiography: High-grade stenoses of at least two major vessels must be established for diagnosis
  • Duplex sonography of the mesenteric vessels: best screening modality in an office setting

Differential diagnoses

Therapy

  • Nutritional support (frequent, small meals; low-fiber diet)
  • Long-term anticoagulation for patients not healthy enough for vascular repair
  • Revascularization procedures to prevent bowel infarction in patients with abdominal pain and weight loss:
    • Angioplasty and stenting
    • Mesenteric artery bypass surgery

Prognosis

References:[3][9]