Chronic Mesenteric Ischemia

Etiology

Atherosclerosis is the leading cause of chronic mesenteric ischemia, resulting in a narrowing of the mesenteric vessels and a reduction in blood flow to the gastrointestinal tract. This narrowing, often involving the ostia of the mesenteric vessels, particularly the SMA, creates an imbalance between the oxygen supply to and consumption by the intestine. When increased blood flow is required, eg, during digestion, the compromised vessels fail to meet the demand, leading to severe abdominal pain and, in some cases, mesenteric ischemia.[8][9]

Several factors predispose mesenteric vessels to atherosclerosis, including diabetes, hypertension, smoking, and hyperlipidemia.[8][9] Smoking and hyperlipidemia are particularly significant risk factors for the development of SMA atherosclerosis.[10][11] This condition underscores the critical importance of recognizing and addressing these risk factors to mitigate the progression of vascular compromise and its associated symptoms.

Epidemiology

Mesenteric artery stenosis is relatively common, occurring in up to 10% of the population older than 65. However, CMI has a very low incidence, accounting for less than 1 in 1000 hospital admissions for abdominal pain. Patients are typically between the ages of 50 and 70 years, with a strong female predominance (estimated to outnumber males 3:1), and have other coexisting manifestations of atherosclerotic disease. Because of its rarity, CMI has no large studies to determine which population is most at risk.[12]

Pathophysiology

Around 20% of cardiac output is directed to the mesenteric arteries during fasting, but this can rise to 35% after eating. Following a meal, blood flow to the gastrointestinal tract increases significantly, reaching approximately 100% to 150% above baseline (around 2000 mL/min) and remains elevated for 3 to 6 hours. The mesenteric circulation consists of 3 primary vessels that supply blood to the small and large bowel: the celiac artery, SMA, and inferior mesenteric artery. Blood flow through these arteries increases within an hour after eating due to an increase in metabolic demand of the intestinal mucosa. Diffuse atherosclerosis, usually occurring at the origin of these vessels, diminishes blood flow due to the narrowing of the mesenteric vessels, is the primary mechanism, and accounts for 95% of CMI. Patients with chronic mesenteric ischemia (CMI) develop symptoms when the primary and collateral blood flow is insufficient to meet the increased oxygen demand during the postprandial hyperemic response, which is necessary for secretion, absorption, and enhanced peristaltic activity.Chronic occlusion of a single vessel allows collateral blood flow to compensate, thus symptoms do not typically present until at least 2 primary vessels are occluded. Shortly after eating, patients with CMI are unable to increase flow in the mesenteric vessels, and they develop pain. Less common causes include vasculitis, fibromuscular dysplasia, and radiation.[13][14] 

Histopathology

The surgically excised bowel usually reveals diffuse atherosclerosis in the mesenteric vessels. Atrophy of the villi, which leads to a loss of absorptive surface, is also typically present.

History and Physical

The clinical presentation of chronic mesenteric ischemia (CMI) can be nonspecific in some patients. Symptoms like vague abdominal pain, nausea, vomiting, or changes in bowel habits, such as diarrhea or constipation, may occur without the typical postprandial pain. When paired with weight loss, these subtle complaints may point toward a CMI diagnosis. Endoscopic findings, if performed, often reveal diffuse small ulcerations in the stomach or proximal duodenum or patchy ischemic areas in the colon. Some patients may also present with abnormal liver function tests. Common risk factors include hypertension, hyperlipidemia, and a history of smoking.

Clinical History

CMI commonly presents with acute episodes of postprandial abdominal pain, often termed "abdominal angina" or "intestinal angina," which begins 15 to 30 minutes after eating and lasts up to 4 hours. This severe pain is often disproportionate to findings on physical examination and may gradually subside but can lead to a significant fear of eating, resulting in marked weight loss. However, long-standing narrowing of the mesenteric vessels frequently results in nonspecific symptoms, including nausea, vomiting, early satiety, diarrhea, or constipation, developing over time, which is characteristic of CMI. Many patients have a history of diffuse atherosclerotic disease, including angina, transient ischemic attacks, cerebrovascular accidents, or lower extremity claudication.

Physical Examination Findings

On physical examination, findings are often minimal, with the abdomen typically soft and without peritoneal signs, though mild diffuse tenderness may be present. An abdominal bruit is audible in up to 50% of patients but lacks sensitivity and specificity. Marked weight loss is frequently observed, and features of peripheral vascular disease, eg, diminished leg pulses, may also be noted. The digital rectal exam is usually guaiac negative, ruling out gastrointestinal bleeding. A thorough history, including risk factors such as smoking, hyperlipidemia, and claudication, is critical for diagnosis.

Evaluation

The diagnosis of CMI is often delayed, as most patients initially undergo extensive evaluation for more common causes of postprandial abdominal pain and weight loss, such as peptic ulcers, cholecystitis, or malignancy. Definitive diagnosis requires vascular imaging to demonstrate stenosis or occlusion of the primary mesenteric vessels. CTA is the preferred initial noninvasive modality, as it not only identifies or excludes atherosclerotic stenosis but also rules out other abdominal pathologies. In outpatient settings, duplex ultrasonography is a reasonable screening tool, with peak systolic velocities exceeding 275 cm/second and 200 cm/second, indicating >70% stenosis of the superior mesenteric and celiac arteries, respectively.

For cases with inconclusive noninvasive imaging results, arterial DSA remains the gold standard, offering definitive diagnosis and assisting in therapeutic planning. Laboratory tests are not diagnostic for CMI but are essential for ruling out malignancies of the stomach and colon. While ultrasound lacks sensitivity for diagnosing mesenteric ischemia, CTA has largely replaced mesenteric angiography as the diagnostic test of choice due to its comparable sensitivity and noninvasive nature. Given the frequent presence of atherosclerotic disease in CMI patients, a comprehensive evaluation for cardiac and peripheral vascular disease is essential. For heavy smokers or surgical candidates, arterial blood gas analysis and pulmonary function tests are also recommended to optimize preoperative care.[15]

Treatment / Management

The primary objectives of treating chronic mesenteric ischemia (CMI) are to alleviate abdominal symptoms, facilitate weight gain, and prevent progression to acute mesenteric ischemia (AMI). The timing and method of intervention should be guided by the severity of symptoms and the patient’s overall surgical risk. In select cases, short-term medical management with bowel rest and parenteral nutrition can be used as a bridge to revascularization. However, long-term reliance on parenteral nutrition or noninterventional therapy is not recommended, as delays in definitive revascularization have been linked to worsening clinical outcomes, including bowel infarction and sepsis from catheter-related complications.

Conservative Management

Management of CMI varies based on symptom severity and patient condition. Asymptomatic patients are managed conservatively with lifestyle modifications, including smoking cessation and antiplatelet therapy. Despite these measures, their 5-year mortality rate remains at 40%, with most deaths resulting from myocardial infarction or cardiovascular causes.[16][17][18]

Surgical Management

Symptomatic CMI necessitates prompt intervention, as untreated cases carry a 5-year mortality rate approaching 100%. Surgical or endovascular revascularization is indicated for symptomatic patients, with endovascular techniques now favored due to their minimally invasive nature and fewer perioperative complications.[19][20] Indications for surgery include:(A1)

• Signs of peritonitis on physical exam
• Massive lower gastrointestinal hemorrhage
• Ongoing signs of abdominal pain, fever, or sepsis
• Symptoms that have persisted for more than 14 to 21 days
• Chronic malabsorption leading to protein-losing colopathy
• Colonoscopic evidence of segmental colitis with frank ulceration
• Ischemic stricture and abdominal symptoms

Endovascular revascularization involves accessing the occluded mesenteric vessels via the femoral artery, followed by balloon angioplasty and stent placement to restore blood flow. For patients requiring open revascularization, options include antegrade inflow (eg, aortomesenteric or aortoceliac bypass) or retrograde inflow (eg, iliac artery bypass) using either a vein or prosthetic conduit. Preoperative nutritional optimization, often through total parenteral nutrition, is critical, as many patients are malnourished at the time of diagnosis. Total parenteral nutrition may be required both before and after surgery. The choice of revascularization approach depends heavily on the patient’s anatomy and preoperative status.

When endovascular techniques are not viable, surgical options include transverse or longitudinal arteriotomy and bypass procedures. Other surgical options include an antegrade or retrograde bypass. There continues to be debate over the choice of a conduit. While prosthetic grafts have been used, some experts recommend using the reversed saphenous vein. For the surgeon who has never done a superior mesenteric bypass, the vessel is usually <2 to 3 mm and can be easily narrowed with large bites of the vessel. Consequently, failures after surgery are not uncommon because of technical problems. Therefore, the surgeon must employ meticulous techniques and wear micro-loops when performing the anastomosis.[1][10][21](B3)

Postoperative Management

Postoperatively, patients require close cardiac monitoring within an intensive care unit, with some surgeons employing tabletop Doppler to verify the patency of the repair. Smoking cessation, management of hyperlipidemia, and referrals to cardiologists and vascular surgeons are vital components of long-term care. While the utility of preoperative total parenteral nutrition remains debated, it may benefit select malnourished patients. Once surgery is completed, dietary restrictions are typically unnecessary, and patients can gradually return to normal eating patterns. Comprehensive care involving lifestyle changes and close monitoring is essential to improving outcomes in patients with CMI.

Surgical Complications

Surgical complications are not uncommon due to the diffuse atherosclerosis associated with CMI. Patients are at increased risk for myocardial infarction during and after surgery, necessitating comprehensive preoperative assessment and hydration. Renal failure is another frequent complication, highlighting the need for preoperative nephrology consultation and vigilant perioperative hydration. Endovascular procedures carry risks such as groin hematoma, acute limb ischemia, mesenteric artery dissection, rupture, or embolization of atherosclerotic plaques.

Differential Diagnosis

Differential diagnoses that should be considered when evaluating a patient for CMI include:

• Acute Cholecystitis
• Acute Gastritis
• Acute mesenteric ischemia
• Biliary obstruction
• Cholangitis
• Cholecystitis
• Chronic gastritis
• Chronic pancreatitis
• Diverticulitis
• Gastric cancer
• Peptic ulcer disease

Prognosis

The prognosis for CMI varies based on the timing of diagnosis, the effectiveness of treatment, and the presence of complications. Surgical management remains the standard treatment and offers long-term relief for many patients. Following surgery, 86% to 96% of patients remain asymptomatic for 5 to 10 years, with similar graft patency rates. Endovascular treatment provides symptom relief in approximately 85% of patients and is considered a safe and effective alternative, though it carries a higher risk of restenosis and shorter long-term patency than open surgery. Despite advancements in treatment, the mortality rate for untreated or delayed CMI remains alarmingly high, ranging from 60% to 95%.[22][23]

Complications such as access site hematomas, pseudoaneurysms, thrombosis, and bowel infarction (reported in 4.6% of cases) may occur following an intervention, potentially necessitating additional procedures. Reocclusion rates are higher in males than females, and some patients may experience recurrent symptoms, leading to repeated hospital admissions.[22][23] The constant postprandial pain associated with CMI often results in significant weight loss, malnutrition, and a poor quality of life. Chronic malnutrition can further lead to metabolic imbalances, bone thinning, easy bruising, and endocrine disturbances, exacerbating the overall burden of the disease. Early diagnosis and comprehensive management are critical to improving outcomes and minimizing the adverse effects of this condition.

Complications

Complications associated with CMI include:

• Cardiovascular 
  • High mortality from adverse cardiac events, eg, myocardial infarction
  • Risk of cardiac complications exacerbated by comorbid conditions, including smoking, diabetes, hypertension, and hyperlipidemia
• Gastrointestinal 
  • Bowel ischemia due to inadequate mesenteric blood supply
  • Graft thrombosis or restenosis following revascularization procedures, leading to recurrent symptoms or ischemia
  • Severe cases may result in bowel infarction, necessitating emergent surgery
  • Massive bowel resection leading to short gut syndrome in cases of treatment failure
• Postsurgical or endovascular procedure
  • Access site hematoma, pseudoaneurysm, or thrombosis
  • Long-term patency issues with endovascular revascularization, resulting in symptom recurrence
• Delayed diagnosis 
  • High morbidity and mortality rates associated with delayed recognition and treatment of CMI
  • Progression to acute mesenteric ischemia if left untreated
• Systemic
  • Malnutrition and weight loss due to fear of eating and reduced caloric intake
  • Protein-losing colopathy secondary to chronic malabsorption
  • Risk of septic complications if bowel infarction occurs
• Mortality
  • Overall mortality rates for untreated symptomatic CMI ranging from 60% to 95%
  • Morbidity rate of approximately 30%, even with treatment