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Acute Mesenteric Ischemia: A Diagnostic Challenge in Clinical Practice
by Mamata Ravipati, Srikanth Katragadda, Betty Go, Edwin J. Zarling

Mesenteric ischemia remains a difficult condition to diagnose clinically. It can be classified as occlusive and non-occlusive, depending on the presence or absence of vascular occlusion. Occlusion due to embolic clot is the most common form, and accounts for nearly half the cases of acute mesenteric ischemia (AMI). Early diagnosis is essential as delay in diagnosis can result in bowel infarction and irreversible damage. The clinical presentation, serum markers and plain films may be non-specific in mesenteric ischemia. Angiography, ultrasonography and CT/MRI imaging are being increasingly used in its diagnosis. Although pharmacological therapy can be helpful, especially in the initial hours, surgery is usually advised. Despite new diagnostic and therapeutic modalities, the mortality and morbidity have remained high. This article reviews the anatomy, pathophysiology and clinical presentation of acute mesenteric ischemia, with a note on various diagnostic and therapeutic modalities.



esenteric ischemia is a morbid abdominal illness that poses a diagnostic challenge and a high rate of mortality. The term denotes a wide array of clinical symptoms ranging from mild abdominal pain to severe rigidity and guarding, depending on the visceral vascular compromise. In the past three decades, AMI has been diagnosed more frequently perhaps due to enhanced radiologic tools.

Mesenteric blood flow is derived from the celiac artery (which supplies the foregut, hepatobiliary system and

spleen); the superior mesenteric artery (which supplies the small intestine and proximal mid-colon) (Figure 1) and the inferior mesenteric artery (which supplies the distal colon and rectum) (Figure 2). Anatomically, there are rich collateral flow pathways between the superior and inferior mesenteric arteries. The gastroduodenal branch of the celiac artery and the pancreaticoduodenal artery of the superior mesenteric artery provide a potential source of collateral blood flow between mesenteric and non-mesenteric vessels. Due to this collateral blood flow in the intestine, at least two of the three major vessels have to be occluded to create mesenteric ischemia.

Mamata Ravipati, M.D.*, **; Srikanth Katragadda, M.D.***; Betty Go, M.D.*; Edwin J. Zarling, M.D.*, **. *Lovell Federal Health Care Center, 3001 Green Bay Road, North Chicago, IL (Drs. Ravipati and Go are staff physicians in Primary Care. Dr. Zarling is the Assistant Chief Medical Executive for Ambulatory Care. All can be reached at 224-610-3085). **Chicago Medical School, 3333 Green Bay Road, North Chicago, IL (Dr. Ravipati is Assistant Professor of Medicine, Dr. Zarling is Professor of Medicine). *** Mercy St Vincent Medical Center, 2213 Cherry St., Toledo, OH. (Dr. Srikanth Katragadda is a third year internal medicine resident).


These autonomic. The intestinal mucosa has a narrow range of oxygen tension and the low oxygen availability in the setting of intestinal ischemia may not be sufficient to meet needs of basal metabolism1. cardiogenic. prostaglandin E1 and glucagon can potentiate the vasodilating action of cAMP. Schematic diagram of inferior mesenteric artery and its branches. Intestinal ischemia can progress in a transmural fashion from mucosa to serosa. arachidonic acid metabolites and cAMP. Substances such as papaverine. generated by the renin-angiotensin system7. superior mesenteric embolism accounts for 40–50%. secretion and motility6. Schematic diagram of superior mesenteric artery and its branches. reperfusion injury resulting in free radicals which cause disruption of cell membranes and thus damage the mucosal barrier. and proliferation of intestinal bacteria4. or neurogenic shock). On analysis of various causes for AMI. (continued on page 38) . increased flux of fluid into the lumen3 due to increased mucosal permeability.Acute Mesenteric Ischemia A SPECIAL ARTICLE Figure 1. Factors that can affect splanchnic circulation include angiotensin II. non-occlusive mesenteric ischemia for 20% and mesenteric venous thrombosis accounts for 5% of all cases8. humoral and local factors can collectively affect the clinical outcome in a patient with 36 PRACTICAL GASTROENTEROLOGY • AUGUST 2011 mesenteric ischemia5: alpha adrenergic stimuli causing vasoconstriction. systemic hypotension from any cause stimulating the release of vasopressin which can further exacerbate the splanchnic vasoconstriction. PATHOPHYSIOLOGY General Factors Intestinal blood flow may be reduced as result of decreased circulating blood volume and poor systemic perfusion (hypovolemic. Figure 2. and beta adrenergic stimuli causing vasodilatation with altered bowel absorption. Specific Factors Acute mesenteric ischemia is more common than chronic ischemia. Several theories have been proposed to explain tissue injury in intestinal ischemia: neutrophil mediated injury to visceral organs2. superior mesenteric artery thrombosis for 18–25%.

antibiotics. Emboli most commonly originate from cardiac abnormalities such as atrial fibrillation. gastric decompression Presence of Bowel Infarct Gradual onset of postprandial pain. patients with acute mesenteric thrombosis often have delayed attention and diagnosis due to slow onset of symptoms. sepsis. absence of bowel sounds. sepsis Angiography Surgical revascularization Gradual onset of malaise and abdominal discomfort. In contrast to embolic mesenteric ischemia. absence of bowel sounds. cocaine and alpha adrenergic agents9. portal hypertension. ergotamine. superimposed on trauma. mental status changes. left ventricular aneurysm with mural thrombus and mitral stenosis. medications Mesenteric venous thrombosis Hypercoagulable states. Minimal physical findings Increasing pain. blunt trauma. absence of bowel sounds. myocardial infarction. MI. nausea. gross distention. left ventricular aneurysm Acute mesenteric arterial thrombosis Atherosclerotic disease. Untreated acute occlusion of the superior mesenteric artery carries a poor prognosis in patients with no pre-existing visceral artery occlusive disease. infection. valvular disease. Most of them have a history of symptoms suggestive of 38 PRACTICAL GASTROENTEROLOGY • AUGUST 2011 chronic mesenteric ischemia. sepsis Angiography Superior mesenteric embolectomy. or use of medications such as digitalis. bowel changes. . Chronic anticoagulation Late Diagnostic Study Treatment All types Hemodynamic support. infection Non-occlusive mesenteric ischemia Systemic hypoperfusion from cardiac failure. sepsis. The Four Causes of Abdominal Ischemia Types of Mesenteric Ischemia Pathology Acute mesenteric arterial embolism Atrial fibrillation. peritoneal signs. sepsis Angiography Vasodilator therapy (Papaverine) Surgery Surgery Surgery Surgery Acute mesenteric arterial embolism: Nearly half the cases of AMI are attributed to an embolism. mental status changes. gross distention. absence of bowel sounds. Acute mesenteric arterial thrombosis: Patients having acute thrombosis of the mesenteric vessels usually have an underlying atherosclerotic disease. pancreatitis. Non-occlusive mesenteric ischemia (NOMI): Non occlusive mesenteric injury usually occurs in systemic hypoperfusion resulting from cardiac failure. Minimal physical findings Increasing pain. The mortality is relatively high due to underlying systemic illness and delay in diagnosis. These patients may not have the classic symptom of severe abdominal pain. weight loss and early satiety. peritoneal signs. portal malignancy Subacute onset of abdominal pain. gross distention. peritoneal signs. Minimal physical findings Increasing pain. usually in the superior mesenteric artery. including pain after food intake. gross distention. peritoneal signs. correction of acidosis.Acute Mesenteric Ischemia A SPECIAL ARTICLE (continued from page 36) Table 1. sepsis Angiography Anticoagulant therapy (Heparin) Clinical Manifestation Early Abrupt onset of abdominal pain. mental status changes. Minimal physical findings Increasing pain. mental status changes.

malignancy involving the portal system and nephritic syndrome. Symptoms gradually progress over 12–24 hours of onset and as the bowel becomes more Table 2. intussusception. heart murmurs. portal hypertension. in the absence of peritonitis. volvulus. polycythemia vera and homocysteinemia increase the risk of venous thrombosis10. The pain is typically moderate to severe. Putrefaction of undigested alimentary material accumulated proximal to the pathologic site can cause foul breath. bowel sounds may be absent to hyperactive. atrial fibrillation. Risk factors for acute mesenteric ischemia may be noted. hypercoagulable states. Acute mesenteric arterial embolism: Acute mesenteric ischemia from an embolic cause usually occurs in patients over 50 years of age with a history of cardiac disease. Differential Diagnosis for Acute Mesenteric Ischemia Abdominal Abscess Abdominal Angina Abdominal Aortic Aneurysm Acute Abdomen Acute Pancreatitis Acute Pyelonephritis Aortic Dissection Appendicitis Bacterial Pneumonia Biliary Colic Biliary Obstruction Boerhaave Syndrome Cholangitis Cholecystitis Choledocholithiasis Cholelithiasis Colonic Obstruction Colonic Obstruction Diverticulitis Ectopic Pregnancy Esophageal Rupture Gastric Volvulus Helicobacter Pylori Infection Ileus Intestinal Perforation Myocardial Infarction Pneumothorax Pregnancy Sepsis Testicular Torsion Clinical Signs Physical findings in patients with acute mesenteric ischemia are similar among the different etiologies. diffuse. Early in the course of the disease. guarding and rigidity may point to underlying loss of intestinal viability and transmural infarction. anorexia and diarrhea progressing to obstipation. DVT or recent surgery. They have a history of postprandial pain. voluntary and involuntary guarding appear. There is minimal or no tenderness and stool may contain occult or gross blood. use of oral contraceptive pills. The most important finding is abdominal pain that is disproportionate to physical examination findings. Nausea and vomiting (75%). DIAGNOSIS OF MESENTRIC ISCHEMIA: Clinical Symptoms To some extent. non-localized. and constant and sometimes described as colicky. pancreatitis. a palpable mass may be present. Absence of peritoneal signs early on in mesenteric ischemia may mislead to an alternative diagnosis. Differences for each type are discussed below. The presence of sudden abdominal pain in patients with history of atrial fibrillation. The clinical distinction is made based on time of presentation. abdominal distention and GI bleeding (25%) are also commonly associated symptoms. tumor compression and aortic dissection). such as atrial fibrillation. lupus anticoagulant. hypotension. AMI should be highly suspected in any patient with abdominal pain disproportionate to physical findings. it may or may not respond to narcotics. atherosclerosis. when necrosis or perforation occurs. PRACTICAL GASTROENTEROLOGY • AUGUST 2011 39 . The differential diagnosis for AMI is listed in Table 2. evidence of tumor. physical signs are few and nonspecific. nausea and change in bowel frequency. recent MI. Factors that make AMI more likely include oral contraceptive use. tachycardia. Mesenteric artery thrombosis: Patients with thrombosis of mesenteric vessels usually present with less clinical intensity. Fever. or previous embolic disease should raise the suspicion of acute mesenteric ischemia.Acute Mesenteric Ischemia A SPECIAL ARTICLE Acute mesenteric venous thrombosis: Hypercoagulable states including anti-thrombin III. all types of acute mesenteric ischemia have similar clinical presentation. vomiting or diarrhea. Increasing abdominal pain. symptoms more suggestive of chronic mesenteric ischemia. abdominal bruits. Late in its course. protein C and S deficiency. tachypnea and altered mental status may be observed. and summarized in Table 1. decreased cardiac output from myocardial infarction or congestive heart failure. Other risk factors include visceral infections and perforations. peritoneal signs develop: tenderness becomes severe.

alpha adrenergic agents. congenital hypercoagulable states. 40 PRACTICAL GASTROENTEROLOGY • AUGUST 2011 Angiography Angiography has become a very important diagnostic and therapeutic intervention in intestinal ischemia.14. fever. tachypnea. Classic findings in barium studies of ischemic bowel include “thumbprinting” (due to mucosal edema) and delayed passage of contrast material through the paralytic segment. Ultrasonography Doppler ultrasonography has emerged as a useful alternative to angiography in screening and diagnosis of visceral ischemia. When these signs develop. Nearly a quarter of patients with NOMI do not have abdominal pain initially. and fixed dilated loops on repeated films. patients develop increased pain associated with vomiting. Barium studies should be avoided in patients having a clear diagnosis of intestinal perforation or ischemia and those in whom angiography is planned. and alkaline phosphatase may be helpful in diagnosis of transmural infarction. the role of laboratory markers in visceral ischemia is limited and the quest for a more definitive marker is still on. but if infarction occurs. hypotension. Elevated levels of amylase. Enzymes such as creatine kinase (CPK). Studies have shown that low lactate levels may help in ruling out the diagnosis of intestinal ischemia and avoid unnecessary laparotomies. Mesenteric venous thrombosis: Patients with mesenteric venous thrombosis usually have subacute onset of symptoms and nonspecific laboratory findings. ergot alkaloids or episodes of hypotension can help in making a provisional diagnosis of non-occlusive mesenteric ischemia. but are insensitive in early stages of ischemia. especially in the elderly12. hemoglobin or phosphate in the blood and also metabolic acidosis are some of the non-specific indicators of mesenteric ischemia. deep venous thrombosis. The chronic form may manifest as esophageal variceal bleeding. Many patients have risk factors for hypercoagulability i. The classic angiographic finding in superior mesenteric artery embolus is the mercury meniscus sign seen (continued on page 42) . Superior mesenteric artery occlusions usually take 12 hrs before the radiographic signs are elicited. tachycardia.Acute Mesenteric Ischemia ischemic. Non-occlusive mesenteric ischemia: Patients with NOMI usually have gradual onset of symptoms. Common radiographic findings include air-fluid levels. total leukocytic count. Plain films are usually normal in intestinal ischemia until the infarcted bowel undergoes irreversible ischemic changes. oral contraceptive use. Obesity.13. lactate dehydrogenase (LDH). distended adynamic ileus.e. Ultrasonography is a fine non-invasive imaging modality that can greatly help in reducing the latent period between the symptom onset and therapeutic intervention16. hypotension and tachycardia. Patients may complain of intermittent episodes of abdominal pain over a period of few days or prolonged period with gradual worsening. but only in late stages. whereas non-occlusive mesenteric ischemia may take several days for such radiographic changes15. Catastrophic outcome results if not properly and rapidly identified and treated.e. and altered mental status) develop. liver disease. Usage of drugs such as digitalis. Currently. Presence of gas in the portal vein and intestines (pneumatosis intestinalis) are poor prognostic signs in mesenteric ischemia. tumor or postcaval surgery. Normal blood flow observed in all visceral vessels may be sufficient to rule out mesenteric ischemia. This non-invasive diagnostic modality can detect arterial narrowing and blood flow velocity to identify stenotic lesions in the visceral vasculature. Radiography Plain radiographs of the abdomen are commonly ordered in patients presenting with acute abdominal pain to rule out visceral pathologies like perforation that may require emergent intervention. DIAGNOSTIC STUDIES Laboratory Laboratory indices may be helpful in ruling out or supporting the diagnosis of mesenteric ischemia. vessel wall calcifications and intestinal gas can sometimes hinder proper visualization of visceral vasculature. bowel injury may be severe and irreversible11. rectal bleeding and sepsis (i.

a vascular smooth muscle relaxant22. Angiography can be used preoperatively in embolic or thrombotic occlusions of the mesenteric artery17. and may supplant traditional angiography in the future. Thrombolytic therapy with streptokinase. sometimes referred to as the classic “sausage sign. Some studies have shown that management of acute mesenteric ischemia with revascularization and open surgical techniques may result in improved survival rates23. is usually not recommended due to high risk of thromboembolus. foley catheter and supplemental oxygen should also be considered. or presence of collateral vessels. embolectomy should follow papaverine to maintain the intestinal viability. CT and/or MRI imaging have the ability to rule out other causes of acute abdomen. best seen in anterio-posterior view. MRI angiography is rapid and noninvasive. There is no role for heparin in acute management of bowel ischemia. The role of angiography in mesenteric venous thrombosis is unclear and evidence from most recent studies emphasized the need of laparotomy in venous thrombosis18. In case of large embolus in the SMA. Intestines appearing marginally viable at initial operation should be allowed to remain.” Angiography can sometimes precipitate embolization and worsen ischemia. Angiographic findings in non-occlusive mesenteric ischemia include diffuse or focal narrowing of mesenteric vessels. nasogastric tube decompression. which classically show occlusion just distal to the origin of the superior mesenteric artery. Laparoscopy is a better option whenever angiography is precluded. the findings on MRI imaging could include edema and increased thickness of the bowel wall. Higher survival rates have been observed when vasodilators have been added to the treatment plan21. 42 PRACTICAL GASTROENTEROLOGY • AUGUST 2011 . MRI imaging is being increasingly used in the diagnosis of chronic mesenteric ischemia. Necrotic bowel is surgically removed and primary anastomosis is preferred in uncomplicated cases. through angiographic catheter at a rate of 30–60 mg/hour. Surgical intervention should be undertaken in patients who exhibit any signs of clinical deterioration. CT imaging with IV and oral contrast could be a valuable diagnostic modality and predictor of outcome in acute mesenteric ischemia19. Opting for angiography in case of severe acute occlusion can sometimes lead to delayed diagnosis and resulting in worsening of ischemia. Angiography has a definite diagnostic and therapeutic role (infusion of Papaverine and thrombolytics through the angiogram catheter) in nonocclusive mesenteric ischemia. Papaverine inhibits the phosphodiesterase enzyme and thus increases the tissue levels of C-AMP. showing alternating segments of narrowing and dilatation. Papaverine is the only treatment of non-occlusive mesenteric ischemia other than resection of gangrenous bowel. Clinically and angiographically guided papaverine therapy is generally given for a period of 24–48 hours. It is not compatible with papaver- CT/MRI In addition to helping establish the diagnosis of intestinal ischemia. The embolus appears as the shape of a crescent that is convex on the surface much like the meniscus formed by mercury. with the intent of undertaking a “second-look operation” 24–36 hours later.Acute Mesenteric Ischemia A SPECIAL ARTICLE (continued from page 40) approximately 3–8 cm distal to the origin of the superior mesenteric artery. However. urokinase or recombinant tissue plasminogen activator in acute arterial mesenteric ischemia is still in experimental phase25 and is limited to patients with contraindication to surgery and who present in the early phase of ischemia before infarction of bowel develops. lateral angiographic views are more helpful in superior mesenteric artery thrombosis. MANAGEMENT OF ACUTE MESENTERIC ISCHEMIA Acute arterial mesenteric ischemia: (thrombotic or embolic): In patients presenting with acute mesenteric ischemia. hypovolemia and hypotension need to be corrected first by appropriate administration of IV fluids and supportive care. Transcatheter administration of papaverine during angiography has been shown to be effective in both occlusive and non-occlusive mesenteric ischemia20. Similarly. Broad spectrum antibiotics. Although percutaneous angioplasty may be successfully tried in acute mesenteric ischemia24. A second-look operation is indicated whenever bowel of questionable viability is resected. free fluid in the abdomen. Repeat angiograms are advised every 24 hours until patient improves clinically.

Am J Surg 2001. Takagi K: Actions of papaverine on intestinal smooth muscle and its inhibition of cyclic AMP and cyclic GMP phosphodiesterases. Symptoms are often nonspecific. Simpson R. Brandt LJ: Mesenteric venous thrombosis. Miyamoto M. Kazmers A: Operative management of acute mesenteric ischemia. 64:611-616 13.355 17.Acute Mesenteric Ischemia A SPECIAL ARTICLE ine. 218(4):444–454 3. 1993. Phillips D: Treatment of acute mesenteric ischemia by percutaneous transluminal angioplasty. Siegelman SS et al: Initial results from an aggressive roentgenological and surgical approach to acute mesenteric PRACTICAL GASTROENTEROLOGY • AUGUST 2011 43 . Gewertz BL: Acute Mesenteric ischemia. 175:732-734 PRACTICAL GASTROENTEROLOGY REPRINTS Visit our website at www. Park IS. Boley.practicalgastro. Surgical Clinics of North America 1997. Heparin is to be followed by long term administration of warfarin for a period of 3 to 6 months. Gonze MD. McKinsey JF. so clinicians must maintain a high degree of suspicion in order to identify and treat this potentially fatal condition. Dig Disc Sci 1995. The Surgical Clinics of North America. 101:290-297 4. 84:129-132 26. Womack WA. Kieny R: Superior mesenteric artery embolism: Eighty two cases. Clark RA. Chui C. Radiology 1995. Alexander D. Am J Gastroenterol 1997. Lensing R Klosterhalfen B et al: Diagnostic imaging of mesenteric infarction. W. Hosp Pract 1981. Am J Med 1983. Valeri CR et al: Neutrophil and non neutrophil-mediated injury in intestinal ischemia-reperfusion Ann Surg. Crissnger KD. Boley SJ: Acute mesenteric ischemia: an aggressive diagnostic and therapeutic approach. In the presence of bowel infarction surgical resection is advised. Magnuson TH. Zawacki JK. Heparin is usually recommended 48 hrs after embolectomy or revascularization to prevent recurrent thrombosis and emboli26. MD. n References 1. Krausz MM. SJ: Early diagnosis of acute mesenteric ischemia. Deneuville M. Klempnauer J. Arch Surg 1970. through a transjugular27 or percutaneous approach. Newmann TS. 199:632-636 20. 74:1042-51 7. Kent Williamson. Manny J: Acute mesenteric ischemia: improved results—a retrospective analysis of ninety-two patients. Bulkley GB. Ahrendt SA et al: The changing face of mesenteric infarction. Mesenteric venous thrombosis: Patients with no clinical signs of bowel infarction can be effectively maintained with anticoagulant and thrombolytic therapy. Howard TJ. 4:112-116 27. Divino CM. Bektas H: Results of portal thrombectomy and splanchnic thrombolysis for the surgical management of acute mesentericoportal thrombosis. 181(1):20-23. Kobzik L. Nowak LR et al: Serum D(-) Lactate levels as an aid to diagnosing acute intestinal ischemia. 82:848-55 22. Plaskon LA et al: Current theories of pathogenesis and treatment of non-occlusive mesenteric ischemia. Angel LP et al: A retrospective study of diagnosis and management of mesenteric vein thrombosis. et al: Acute mesenteric ischemia: diagnosis with contrast enhanced CT. Alon R. Non-occlusive mesenteric ischemia: In non-occlusive mesenteric ischemia. Ohkubo H. MD et al: Dupplex ultrasonography in evaluation of splanchnic artery stenosis. Can J Surg 1992. Sprayregan S. Levy PJ. 100:57-165 8. 26:114–117 23. 19. 98:920-926 5. Mac Arthur JD et al: Mesenteric ischemia secondary to cocaine abuse: Case reports and literature review. Granger DN: Contributions of ischemia and reperfusion to mucosal lesion formation. Takayanagi I. Taourel PG. AJR 2000. Ellis DJ. Pradel JA. predisposing and precipitating factors should be corrected along with effective treatment of mesenteric vasoconstriction. 197:79-82 14. Farkas P et al: Beta adrenergic blockade and the gastrointestinal system. 107(4):372-80 24. Surgery 1977. O’Sullivan GJ. 77:307-318 9. Gallant TE: Acute mesenteric ischemia: angiographic spectrum. 92:1053-1054 10. Wilcox MG. Johnson DL: Mesenteric and Portal Venous Thrombosis Treated by Transjugular Mechanical Thrombolysis. 77(2): 339. Thrombolytics can be administered either intravenously or directly into the mesenteric venous circulation.1991 Roussel lecture. Brandt LJ. Kaleya RN. VanDeinse WH. 167:575-578 15. Granger DN: Mucosal injury induced by ischemia and reperfusion in the pelvic intestine: influence of the age and feeding. 40:709-716 2. Jpn J Pharmacol 1976. 35:613-623 12. Ann Vasc Surg 1990. Heparin anticoagulation is the main treatment of mesenteric venous thrombosis. Gastroenterology 1989. Surgery 1986. American Journal of Roentgenology 1984. Nicoloff. Boley SJ. Murray MJ. Gastroenterology 1986. Klein HM. Scott HJ et al: Ultrastructural changes in the canine ileal mucosal cell after mesenteric artery occlusion. Sai Sudhakar CB. 12:187-197 18. Surgery 1990. Jacob H. Ann Vasc Surg 1998. Brown RA. Radiology 1996. 16:63-70 16. 91(2):475-8 25. Bateller J. Am J Surg 1994. Anticoagulant therapy markedly reduces the risk of embolization in patients with atrial fibrillation. Am J Physiol 1979. British J Surgery 1997. Gastroenterologist 1994. Al Hakeem M. Sze DY. Am Surg 1998. 1997. 2:293-298 11. Thrombolysis should be followed by anticoagulants for 3–6 months. Downey JM et al: Collateral blood flow in segmental intestinal ischemia: effects of vasoactive agents. Parks DA. 247:G167 6. Grothues F. 142(3):555562 21. NOMI may be treated with papaverine alone and surgery is reserved for patients with suspected bowel infarction. SUMMARY Ischemic injury to the intestines can occur when blood flow is compromised by a variety of mechanisms.