Intestinal Ischemia

Intestinal ischemia occurs when perfusion fails to meet the demands of the intestines, resulting in ischemic tissue injury that can be life-threatening if bowel necrosis and/or perforation occurs. Symptoms can range from mild indigestion or diarrhea to severe abdominal pain. Imaging techniques including CT and angiography are used to detect stenosis or occlusion. The chronic form of intestinal ischemia benefits from medical therapies and revascularization procedures (stents, bypass surgery) while acute forms require urgent interventions to restore blood flow and remove any dead bowel tissue. Delay in the diagnosis and management of acute intestinal ischemia results in high mortality and severe complications, including intestinal perforation and sepsis.

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Overview

Definition

Intestinal ischemia is a decrease in blood flow to the intestines resulting in hypoperfusion that may lead to bowel infarction. Mucosal sloughing occurs after approximately 3 hours of ischemia, and necrosis occurs after approximately 6–12 hours of ischemia.

Types of intestinal ischemia

  • Ischemic colitis (ischemia of colon): hypoperfusion of the large bowel
  • Acute mesenteric ischemia: acute loss of blood flow to the small intestine
  • Chronic mesenteric ischemia: constant or episodic hypoperfusion of the small intestine

Epidemiology

For all types, intestinal ischemia primarily affects adults > 60 years of age.

  • Ischemic colitis: most common type of intestinal ischemia (approximately 60%–70%) 
  • Acute mesenteric ischemia (AMI):
    • In addition to older adults, may also occur in younger people with:
      • Atrial fibrillation (Afib) 
      • Hypercoagulable states
    • Mortality rates:
      • Occlusive mesenteric infarction has a ↑↑ mortality rate (approximately 60%)
      • Nonocclusive disease has a lower mortality rate
  • Chronic mesenteric ischemia: ↓ incidence 

Acute Mesenteric Ischemia and Ischemic Colitis

Etiology

Whether in the colon or small intestines, acute bowel ischemia is the result of reduced blood flow. Causes include:

Vessel obstruction due to:

  • Acute arterial embolism (approximately 50%):
    • Atrial fibrillation
    • Valvular heart disease (i.e., infective endocarditis)
    • Cholesterol embolism from ruptured arterial plaques
    • Air embolism (can occur in neurosurgeries)
  • Arterial thrombosis (15%–25%) :
    • Atherosclerosis
    • Arteritis
    • Aortic aneurysm or dissection
  • Venous thrombosis in mesenteric vessels (approximately 5%, rarely involves the colon); risk factors include:
    • Malignancy
    • Hypercoagulable states/thrombophilias
    • Infections/inflammation
    • Estrogen therapy (e.g., oral contraceptive pills)
  • Vessel compression due to tumors or adhesions

Nonocclusive mesenteric ischemia (20%–30%) may be due to: 

  • Hypotension/shock
  • Hypovolemia from acute blood loss
  • Vessel laceration with abdominal trauma
  • Sepsis
  • Excessive vasoconstriction, which may be due to:
    • Congestive heart failure
    • Vasculitis
    • Vasopressor drugs
    • Cocaine abuse

Pathophysiology

  • Mechanisms:
    • Hypoperfusion → intestinal hypoxia → bowel wall damage/inflammation 
    • May progress to infarction and necrosis within 6–12 hours
    • Venous obstruction may lead to volvulus (twisting of bowel) or incarceration, leading to hypoperfusion.
  • Commonly involved sites in AMI:
    • Superior mesenteric artery (SMA)
      • 90% of cases
      • Supplies: the distal duodenum, jejunum, ileum, and colon to the splenic flexure
    • Superior mesenteric vein: drains blood from the small intestine
    • Inferior mesenteric artery (IMA) (uncommon)
    • Celiac artery (uncommon)
  • Involved sites in ischemic colitis: tends to occur in watershed areas of the colon with limited collateral circulation
    • Splenic flexure is between the areas supplied by:
      • SMA
      • IMA
    • Rectosigmoid junction is between the areas supplied by: 
      • IMA
      • Superior rectal artery
Watershed areas of the colon

Watershed areas of the colon

Image by Lecturio.

Clinical presentation

  • Abdominal pain:
    • AMI:
      • Classic finding: sudden onset of abdominal pain out of proportion to physical findings (i.e., intense pain without peritoneal signs early in presentation).
      • Diffuse abdominal pain
      • If no treatment is initiated, more focal abdominal tenderness occurs (due to local inflammation/infarction).
    • Ischemic colitis:
      • Rapid onset of mild abdominal pain over the affected bowel
      • Most common on the left
  • Other common findings:
    • Nausea or vomiting
    • Diarrhea, which may be bloody in later stages, indicating infarction
    • Abdominal distention
    • Hypoactive or absent bowel sounds
  • If necrosis and/or perforation present:
    • Peritoneal signs: acute rigid abdomen with guarding and rebound tenderness 
    • Septic shock: fever, hypotension, signs of end-organ damage
  • Venous thrombosis: more gradual onset of symptoms

Diagnosis

Patients with evidence of bowel infarction on exam should have an emergent surgical consultation. If the patient is stable enough, imaging should be performed.

  • CT angiography (1st line): detects disruption of blood flow and vascular stenosis; findings may include:
    • Lack of bowel-wall enhancement
    • Pneumatosis intestinalis: air in the bowel wall 
    • Portal vein gas
    • Distended intestinal loops
    • Bowel wall thickening
    • Air-fluid levels
    • Double halo sign (also known as the target sign): abnormal bowel wall enhancement in ischemic colitis
  • MR angiography: 
    • Findings similar to those seen on CT angiography
    • Pros: Higher sensitivity and specificity than CT
    • Cons: Less practical, owing to cost and time
  • Conventional mesenteric angiography may be performed if the diagnosis is unclear:
    • Pros: can treat and diagnose concomitantly; the traditional “gold standard”
    • Cons: invasive, requires IV dye, not always available
  • Laboratory findings may include:
    • ↑ Lactate
    • Metabolic acidosis 
    • ↑ Amylase and phosphate levels
    • CBC: leukocytosis, possible anemia (especially in ischemic colitis)
  • ECG: to look for dysrhythmias (e.g., atrial fibrillation), which may have led to an embolic event
  • Colonoscopy:
    • May be helpful in diagnosing ischemic colitis
    • Findings may include:
      • Mucosal pallor or cyanosis
      • Petechiae, hemorrhage

Management

  • Goals: 
    • Restore blood flow
    • Decrease vasospasm
    • Decrease clot propagation
  • Resuscitation and stabilization:
    • Oxygen therapy: intubate if necessary
    • IV fluids
    • Transfuse blood products as needed
    • Avoid vasoconstricting agents, if possible.
    • Nasogastric tube and bowel rest
    • Pain control
  • Broad-spectrum IV antibiotics: 
    • Ceftriaxone
    • Ciprofloxacin plus metronidazole
  • Anticoagulation:
    • May be used if a clot is present and in the absence of active bleeding
    • Typically a heparin infusion
  • Surgery/procedures:
    • Surgical revascularization: embolectomy, vascular bypass, angioplasty, and/or stenting 
    • Resection of necrotic and/or perforated bowel
    • Mesenteric angiography, which may include infusions of:
      • Vasodilators (e.g., papaverine) to relieve occlusion and vasospasm
      • Thrombolytics to dissolve clots
  • Long-term preventive measures to reduce future clot formation: 
    • Anticoagulation therapy in patients with atrial fibrillation
    • Smoking cessation
    • Optimize management of conditions that increase cardiovascular risk (e.g., hypertension, hyperlipidemia, diabetes mellitus).
    • Thrombophilia workup in patients with thrombosis, with appropriate treatment based on findings (typically long-term anticoagulation)

Complications

  • Reperfusion injury: 
    • Can occur following restoration of blood flow after a period of ischemia
    • Complex mechanism involving the release of toxic by-products of ischemic injury and neutrophil activation
    • May lead to multisystem organ failure
  • Perforation:
    • Necrotic areas of bowel may perforate, spilling contents into the abdominal cavity.
    • High mortality rate

Chronic Mesenteric Ischemia

Etiology

Chronic mesenteric ischemia results from chronic vascular disease, which can be caused by:

  • Atherosclerosis
  • Hypertension
  • Smoking
  • ↑ LDL
  • Diabetes mellitus

Pathophysiology

  • Progressive atherosclerosis of ≥ 2 main arteries → mismatch between the blood flow and intestinal metabolic demand (especially after a meal)
    • Leads to postprandial pain
    • Main arteries include SMA, IMA, and celiac artery
    • When only 1 main artery is affected, collateral connections between the arteries can form and compensate for the ↓ flow.
  • Sudden thrombus formation in addition to stenosis can lead to acute-on-chronic mesenteric ischemia.

Clinical presentation

  • Crampy, postprandial, epigastric pain: starts within the 1st hour after eating and resolves within the next 2 hours
  • Food aversion and weight loss
  • Other symptoms can include nausea, early satiety, and diarrhea.
  • Physical exam may reveal abdominal bruit.
  • May be asymptomatic, owing to the collateral blood supply

Diagnosis

  • Clinical suspicion based on history and physical exam
  • CT angiography (gold standard) or Doppler ultrasonography is used to identify atherosclerotic vascular disease and rule out other abdominal disorders.
CT angiogram showing stenosis of the superior mesenteric artery

Chronic mesenteric ischemia: CT angiogram showing stenosis of the superior mesenteric artery

Image: “Figure 1” by Spangler et al. License: CC BY 4.0

Management

  • Risk reduction:
    • Quit smoking
    • Healthy lifestyle habits
    • Manage chronic conditions (e.g., hypertension, hyperlipidemia, diabetes)
  • Nutritional support
  • Surgical revascularization:
    • Endovascular techniques (e.g., angioplasty or stenting): 1st line for symptomatic patients
    • Open surgery (e.g., vascular bypass or endarterectomy)
  • Consider anticoagulation therapy.

Differential Diagnosis

Since intestinal ischemia typically presents with abdominal pain, the differential diagnosis includes:

  • Appendicitis: acute inflammation of the appendix. Symptoms are periumbilical pain that migrates to the RLQ, fever, anorexia, nausea, and vomiting, but appendicitis can often cause constipation, as well. The diagnosis is clinical, but CT imaging is used in cases of uncertainty. The standard management is appendectomy, though there can be a role for antibiotics in some cases.
  • Bowel obstruction: interruption of the flow of the intraluminal contents through the small intestine. Typically, bowel obstruction presents with nausea, vomiting, abdominal pain, distention, constipation, and/or obstipation. The diagnosis is established via imaging. Most cases will resolve with supportive management (bowel rest, IV hydration, and nasogastric decompression). However, surgery is required for persistent or complicated cases.
  • Diverticulitis: inflammation of diverticula (protrusions of the bowel wall, often in the colon). Diverticulitis often presents with lower abdominal pain and changes in bowel habits. The condition may be further complicated by abscess, perforation, fistula, and bowel obstruction. Management consists of antibiotics, fluid resuscitation, and bowel rest. Surgery is required for complications.
  • Acute pancreatitis: inflammatory disease of the pancreas usually due to gallstones and/or excessive alcohol use. Patients typically present with epigastric pain radiating to the back. Diagnosis includes serum lipase 3 times the upper limit of normal or characteristic radiographic findings. Management includes aggressive IV hydration, analgesia, nutritional support, and treatment of the underlying cause.
  • Chronic pancreatitis: persistent inflammation, fibrosis, and irreversible cell damage to the pancreas. The most common etiologies of chronic pancreatitis are alcohol abuse and pancreatic duct obstruction. Patients present with recurrent epigastric abdominal pain, nausea, and features of malabsorption syndrome. CT findings include pancreatic atrophy, dilated pancreatic ducts, and pancreatic calcifications. Therapy focuses on alcohol cessation, diet changes, pain management, and treatment of pancreatic insufficiency.
  • Cholecystitis: inflammation of the gallbladder usually caused by the obstruction of the cystic duct (acute cholecystitis). The acute type of cholecystitis usually presents with RUQ pain, fever, and leukocytosis. The diagnosis is made clinically and confirmed with ultrasonography. The definitive management is cholecystectomy.
  • Acute coronary syndrome (ACS): clot formation obstructing blood flow to the coronary arteries. Symptoms include chest pressure and shortness of breath. Management includes medications, such as blood thinners, thrombolytics, and/or beta blockers. Depending on the severity, heart catheterization and balloon angioplasty may be required. 
  • Aortic dissection: may also present with sudden onset of severe epigastric pain. The pain associated with aortic dissection is typically sharp tearing chest pain that radiates to the back. Other features, such as asymmetrical blood pressure, and pulse deficit in 1 arm can help differentiate aortic dissection from acute mesenteric ischemia, though it is also possible for an aortic dissection to cause a nonocclusive mesenteric ischemia.
  • Ectopic pregnancy: implantation of a fertilized egg outside the uterine cavity, often in the fallopian tubes. Growth of the fetus may lead to abdominal pain and/or vaginal bleeding. Ectopic pregnancy can be diagnosed by ultrasonography and laboratory analysis of quantitative hCG levels over time. Management of nonruptured EPs can be expectant, medical, or surgical. Ruptured ectopic pregnancies are surgical emergencies.

References

  1. Tendler, D., Lamont, T. (2020). Overview of intestinal ischemia in adults. UpToDate. Retrieved April 26, 2021, from https://www.uptodate.com/contents/overview-of-intestinal-ischemia-in-adults
  2. Khan, A. (2016). Ischemic colitis imaging. Emedicine. Retrieved April 27, 2021, from https://emedicine.medscape.com/article/366808-overview
  3. Dang, C. (2020). Acute mesenteric ischemia. Emedicine. Retrieved April 27, 2021, from https://emedicine.medscape.com/article/189146-overview
  4. Alrayes, A. (2019). Chronic mesenteric ischemia. UpToDate. Retrieved April 26, 2021, from https://www.uptodate.com/contents/overview-of-intestinal-ischemia-in-adults
  5. Hundscheid, I.H., Grootjans, J., Lenaerts, K., et al. (2015). The human colon is more resistant to ischemia-reperfusion-induced tissue damage than the small intestine: an observational study. Ann Surg 262:304–311. https://pubmed.ncbi.nlm.nih.gov/25915914/
  6. Greenwald, D.A., Brandt, L.J. (1998). Colonic ischemia. J Clin Gastroenterol 27:122–128. https://pubmed.ncbi.nlm.nih.gov/9754772/
  7. Cappell, M.S. (1998). Intestinal (mesenteric) vasculopathy. I. Acute superior mesenteric arteriopathy and venopathy. Gastroenterol Clin North Am 27:783–825. https://pubmed.ncbi.nlm.nih.gov/9890114/

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