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Mesenteric ischemia: Rapid diagnosis and prompt treatment are essential

Anzalone, Justin PA; Acevedo, Frank A. PA-C, MS, DFAAPA

Journal of the American Academy of PAs: July 2011 - Volume 24 - Issue 7 - p 44–48
CME Mesenteric ischemia
  • Discuss the etiology, epidemiology, and pathophysiology of mesenteric ischemia
  • Describe the clinical presentation and diagnostic workup of mesenteric ischemia
  • List the differential diagnosis for mesenteric ischemia
  • Outline the nonsurgical and surgical management of mesenteric ischemia

Discuss the etiology, epidemiology, and pathophysiology of mesenteric ischemiaDescribe the clinical presentation and diagnostic workup of mesenteric ischemiaList the differential diagnosis for mesenteric ischemiaOutline the nonsurgical and surgical management of mesenteric ischemia Immediate attention is required if the patient is to have a chance of survival. Critical care, surgical, and vascular consultations should be obtained early in the disease process.

The authors are from the PA program at the New York Institute of Technology in Old Westbury, New York. Justin Anzalone was a student in the program when this article was written and will start at Duke University Medical Center as a PA surgery resident this fall. Frank Acevedo is academic coordinator/associate director of the program and practices in surgical critical care at Winthrop University Hospital, Mineola, New York. The authors have indicated no relationships to disclose relating to the content of this article.

Almost all PAs will encounter cases of mesenteric ischemia at some point during their career. Although relatively rare, accounting for 1 in every 1,000 hospital admissions, mesenteric ischemia carries a high mortality rate, which ranges from 60% to 100% depending on the cause of the ischemia.1,2 Recent data show that the true mortality rate of mesenteric ischemia may exceed 90%, and in only 33% of cases was the diagnosis considered prior to death.2 A high clinical suspicion is thus essential to reduce morbidity and mortality.

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Mesenteric ischemia can be categorized as either acute or chronic (Table 1). Acute mesenteric ischemia (AMI) results from a diminution in the blood supply to the intestinal circulation that compromises the viability of the affected organs.3 An estimated one-third of AMI cases occur from arterial embolism, one-third from acute arterial thrombosis, and the remaining from nonocclusive and venous occlusive events.1 A recent review found that thrombosis of the arterial mesenteric blood supply accounts for only 15% to 30% of cases; when it does occur, however, the mortality rate is 90%.2



Because of its large intraluminal diameter and narrow take-off angle from the aorta, the superior mesenteric artery (SMA) is the intra-abdominal artery most susceptible to an occlusive event. Proximal SMA stenosis secondary to atherosclerosis increases this susceptibility.4 In an SMA occlusion, the mid-jejunum is at the highest risk of ischemic damage, primarily because of its distance from the collateral circulation of the celiac and inferior mesenteric arteries.4 In acute occlusion, collateral circulation is very limited, resulting in severe symptoms and rapid decompensation. Common risk factors for AMI are listed in Table 2.2 One study showed that patients with an in-hospital diagnosis of atrial fibrillation had an increased risk for thromboembolic events in the mesenteric arteries (a relative risk of 4.0 and 5.7 for men and women, respectively).5 In a review, 30% to 50% of AMI cases were attributed to emboli of the visceral vasculature of the intestines.4



Figure. C

Figure. C

Nonocclusive mesenteric ischemia (NOMI) usually occurs during periods of relative hypotension (or reduced flow), resulting in diminished blood supply to visceral vessels; hypovolemia with resultant hypoperfusion is typically a causative factor.3 Mesenteric venous thrombosis is more commonly associated with hypercoagulable states resulting from recent injury or surgery, prolonged bed rest, pregnancy, cancer, or inherited coagulopathies (Table 3). Chronic mesenteric ischemia (CMI) is defined as a continuous reduction in intestinal blood flow, more commonly due to severe stenosis or atherosclerotic plaque buildup in two or more mesenteric vessels. The occurrence of CMI is rarely associated with emboli.1 Chronic mesenteric ischemia is often asymptomatic; when signs and symptoms are present, they include abdominal pain after eating, avoidance of food to prevent pain, and weight loss.



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At the cellular level, two important features must be considered: systemic inflammatory response syndrome (SIRS) and ischemic/reperfusion (double-hit) injury.

With SIRS, ischemia causes mitochondrial malfunction, which results in loss of ion transfer regulation and intracellular acidosis. Membrane permeability becomes distorted; cell death and necrosis are preceded by the release of free radicals and degradative enzymes. The resultant ischemic tissue activates neutrophils, endothelium, monocytes, and platelets, which in turn produce proinflammatory cytokines such as tumor necrosis factor (TNF), interleukins, plateletactivating factor, and leukotrienes. New evidence suggests that proinflammatory cytokines are significant inflammatory mediators that regulate the process of microvascular thrombi.6 Subsequent injury to the tissue is due to leukocyte adhesion, platelet aggregation, and impairment of nitric oxide production. Superoxide substances such as superoxide (O2), peroxide (H2O2), and hydroxyl radicals (OH) are produced by neutrophils, causing more damage to adjacent tissue.7

Ischemic/reperfusion injury consists of the initial hypoxic insult followed by subsequent reperfusion insult due to reestablishment of flow. The activated neutrophils, superoxide molecules, and proinflammatory substances produced during the ischemic phase are released into the blood stream, resulting in distant organ damage. Because capillary perfusion is significantly increased during ischemic events, reperfusion causes swelling of parallel organs. Ultimately, damage to the intestinal microvessels and mucosal barrier causes leakage of bacteria and water content, resulting in an increased risk of bacteremia and endotoxemia. Multisystem organ dysfunction syndrome (MODS) may then develop and potentially involve the liver, heart, lungs, and kidneys. The increased microvascular permeability will continue to the pulmonary system, resulting in an influx of fluids and proteins causing pulmonary edema. As few as 6 hours of ischemic insult can produce significant damage to bowel, resulting in necrosis.7

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  • Although relatively rare, mesenteric ischemia carries a high mortality rate, which ranges from 60% to 100% depending on the cause of the ischemia.
  • Mesenteric ischemia can be categorized as either acute or chronic.
  • Despite recent advancements in diagnostic technology, only one-third of patients with mesenteric ischemia present with the classic triad of abdominal pain, fever, and heme-positive stool. A positive outcome continues to depend on the clinician having a high index of suspicion and intervening promptly.
  • Angiography is the gold standard for diagnosing acute mesenteric ischemia because it is both diagnostic and potentially therapeutic when combined with emergent fibrinolytic intervention.
  • Supportive medical treatment is essential, and surgery is usually required as well.
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Despite recent advancements in diagnostic technology, only one-third of patients with mesenteric ischemia present with the classic triad of abdominal pain, fever, and heme-positive stool;1,2,8,9 a positive outcome continues to depend on the clinician having a high index of suspicion and intervening promptly.1 When physical findings plus a history of rapid, forceful, heme-positive bowel evacuation are present, the practitioner should immediately consider a diagnosis of AMI (Table 4).9 Clinicians should note also that the physical examination may be unremarkable unless peritonitis has developed. Any sign of developing peritonitis requires exploratory laparotomy without delay.7 Patients with CMI most often present with postprandial pain coupled with weight loss. These findings are attributed to the increased splanchnic blood flow demand after a large meal, from 10% up to 35% of cardiac output at rest.2



Ideally, laboratory testing would be able to detect ischemia before gangrene develops, if the time between presentation and diagnosis permits.10 Although several laboratory tests can be helpful, a gold standard for laboratory diagnosis of mesenteric ischemia is not yet available.

Several studies have evaluated the D-dimer test, most commonly used to rule out hypercoaguable states. In a study of 92 patients with acute SMA occlusions, d-dimer was the only marker of coagulation or fibrinolysis that was significantly raised. The median d-dimer concentration in these patients was 1.6 mg/L (range, 0.4-5.6 mg/L; P = .009; sensitivity, 100%; specificity, 36%; negative and positive predictive values, 100% and 13%, respectively).8

C-reactive protein levels are somewhat insensitive in the early stages of the ischemic event and nonspecific at later stages.8 Common laboratory findings include an elevated anion gap, elevated serum lactate level, and leukocytosis; however, these findings again are nonspecific.2 Additional studies may help to identify the effectiveness of measuring intestinal mucosal oxygen tension (the mucosal intestinal layer is most vulnerable to ischemia), which may allow an earlier, more accurate diagnosis.2 The total laboratory picture should be considered when pursuing the diagnosis. Unexplained leukocytosis with an associated lactic acidosis should always raise suspicions. In postoperative patients who have undergone abdominal aortic aneurysm repair, mesenteric ischemia should be suspected in every patient who has an early bowel movement (24-48 hours after surgery). An early bowel movement in these patients may represent segmental colonic contraction in response to ischemia. Sigmoidoscopy is essential in making the diagnosis of postoperative colonic ischemia.

Plain radiographs of the abdomen may reveal thumbprinting, colonic wall thickening, pneumatosis intestinalis, or free intraperitoneal air. Though all of these findings may be associated with mesenteric vascular events, they are nonspecific and can be found in association with many other intra-abdominal events.

In a study of 60 patients with acute thromboembolic occlusion of the SMA, 5 were examined with duplex ultrasonography; one examination was considered nondiagnostic because of disproportionate bowel gas, arterial flow was confirmed in the proximal portion of the SMA in three patients, and no flow was detected in one patient.10 Although duplex ultrasonography has its limitations, when used concurrently with a reference test like the angiography, it is very helpful in the diagnosis of mesenteric ischemia.1

Intraoperative thermal imaging has been implemented to detect bowel viability and the extent of bowel necrosis. This imaging modality has demonstrated a sensitivity and positive predictive value of 100% and 69.5%, respectively.11 Intravenous fluorescein with a Wood lamp has also been utilized to determine bowel viability and subsequent bowel necrosis and had a positive predictive value of 91.8%.11 MRI has shown promising results but is too slow for emergent situations.7 CT, which is fast, widely available, and noninvasive, is considered a first-line imaging test when suspicions of mesenteric ischemia are high.7

Angiography is the gold standard for diagnosing acute mesenteric ischemia because it is both diagnostic and potentially therapeutic when combined with emergent fibrinolytic intervention. Multidetector row CT has allowed for a more detailed analysis of the mesenteric vasculature flow while relegating angiography to a more confirmatory role.2 This modality is being used more frequently because of its noninvasive nature, better delineation of blood vessels, clarity in demonstrating an anatomical three-dimensional relationship with the surrounding tissues, and ability to delineate surrounding tissues.7 Multidetector row CT has shown notable results with a sensitivity of 92% to 96% and a specificity of 94% to 100%, with positive and negative predictive values of 90% and 98%, correspondingly.7 When all diagnostic modalities are considered, however, angiography is still the gold standard in AMI, offering both anatomic visualization of the vasculature and therapeutic options with a sensitivity and specificity of 74% to 100% and 100%, respectively.7

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Because mesenteric ischemia (acute or chronic) often manifests with nonspecific abdominal pain, the differential diagnosis is broad and includes conditions such as pancreatitis, appendicitis, diverticulitis, and gastritis. In women, ovarian cysts, endometriosis, and ectopic pregnancy must also be considered and appropriate diagnostic tests utilized to rule them in or out.

Appendicitis commonly starts as vague periumbilical pain that eventually localizes to the right lower quadrant (McBurney point). It is accompanied by positive involuntary and voluntary guarding, cutaneous hyperthesia, and usually a positive Rovsing sign, psoas sign, and obturator sign.

Acute pancreatitis and mesenteric ischemia can both manifest with an acute abdomen. A hallmark of acute pancreatitis is pain radiating to the back. The history can help to rule out pancreatitis if the patient is asked about alcohol use, a personal or family history of gallstones, and abdominal trauma. A thorough medication history should also be obtained as numerous medications are implicated in acute pancreatitis. Along with the history, laboratory investigation of serum amylase and lipase can be performed. These tests are nonspecific but help to determine whether abdominal pain is pancreatic.

Diverticulitis is ruled out, in part, by localizing the patient's pain. The pain of mesenteric ischemia is historically nonspecific, whereas the pain of diverticulitis is most often specific to the left lower quadrant. Common to both conditions are heme-positive stool, leukocytosis, and metabolic acidosis. Diverticulitis should be ruled out early simply because time is valuable when dealing with mesenteric ischemia; delay in diagnosing diverticulitis can also lead to severe complications.12

Gastritis usually manifests with mild epigastric pain, whereas mesenteric ischemia typically causes abdominal pain out of proportion to the physical examination findings. Gastritis also typically causes nausea (with or without vomiting), whereas nausea is usually absent in mesenteric ischemia.

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Mesenteric ischemia can increase capillary leakage with considerable fluid shifts; thus aggressive fluid resuscitation must be initiated as soon as possible. Use of a central line is beneficial because of the volume of fluid resuscitation that is required.13 To avert visceral ischemia, the patient should receive a beta-adrenergic agonist such as norepinephrine (Levophed, generics) when vasopressors are essential. Norepinephrine is the drug of choice for mesenteric ischemia because of its ability to reverse hypotension, stabilize hemodynamics, rapidly reduce lactate levels in septic shock, and increase arterial pressure when hypotension persists after fluid resuscitation.14 The use of vasopressin to support BP should be avoided as it decreases mesenteric blood flow and increases ischemia. Because ischemia increases the frequency of bacterial translocation via the intestinal walls, a broad-spectrum antibiotic that is active against aerobic and anaerobic coliform bacteria should be started. To prevent further propagation of the occlusion, anticoagulation measures should be started in the form of an unfractionated heparin drip to allow for rapid titration, especially if surgery will be necessary.2 Other treatment modalities, such as immune-enhancing enteral diets, have been shown to improve outcomes, particularly after reperfusion; perhaps this is due to the preservation of the gut barrier function.15 Thrombolytic therapy, when indicated and thromboembolism is confirmed by angiography, has been successful when given within 12 hours of the onset of mesenteric ischemia symptoms.7 Vasodilators have been used in some studies, but none has proven to be very effective in the setting of mesenteric ischemia. In particular, papaverine has been shown to significantly increase mesenteric blood flow in normally vascularized rats but significantly reduced the length of the devascularized segment maintained viable by the collateral blood flow after 48 hours.16

Hemodynamic monitoring is valuable in mesenteric ischemia, particularly monitoring of mean arterial pressure (MAP); an MAP of 70 mm Hg or greater has been considered a valuable target for critically ill patients.13 When NOMI is suspected and hemodynamic monitoring confirms a low flow cardiac state, judicial use of inotropic agents such as dobutamine may help to increase splanchnic perfusion. Systemic anticoagulation has remained the backbone for nonoperative therapy in mesenteric ischemia. As mentioned, heparin therapy started in the early stages of disease can significantly improve survival.2 Heparin has also been utilized postoperatively in an attempt to decrease propagation of ischemia due to thrombosis prior to a second-look surgical procedure.

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Determining bowel viability is critical in mesenteric ischemia. Because it is impossible to predict if the bowel will remain viable, a second-look laparotomy scheduled 12 to 24 hours after the first procedure has been recommended.17 Failure to clear lactate levels after initial resection is an important clue to ongoing ischemia and problems with viability. A study of 43 patients who underwent open mesenteric revascularization found that 11 of 23 patients having second-look surgery required bowel resection.2 An alternative to the more invasive second-look laparotomy is a second-look laparoscopy, which is performed using a laparoscopic trocar that is inserted in the left or right lower quadrant during the first surgery, prior to closing the abdominal wall.17

“Crucial medical treatment should include anticoagulation, fluid resuscitation, and broad-spectrum antimicrobial therapy.”

Mesenteric bypass is an effective surgical therapy and may be performed in an anterograde fashion via the supraceliac aorta or in a retrograde manner by using the iliac vessels. One researcher implied that the anterograde technique is favored simply because the retrograde technique is more liable to kink.2 This study determined that at the time of exploration, unless the bowel is frankly necrotic, revascularization should be attempted before bowel resection.2 When resection of frankly necrotic bowel is being considered, short bowel syndrome-defined as the presence of less than 200 cm of remaining small bowel in adult patients—must be avoided. In adult patients, resection of less than 50% of the small intestine is usually well-tolerated, whereas larger resections can cause clinically significant malabsorption.18

For every surgical technique that provides positive results, other techniques are not advised for mesenteric ischemia because of associated poor outcomes. Historically, patients who underwent exploratory laparotomy (open-and-closed procedure) died in almost all cases from massive bowel infarction.19 Ultimately, the goal of treatment is to restore mesenteric blood flow and resect nonviable bowel as needed.20

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Whether the condition is AMI, CMI, or NOMI, immediate attention is required in a situation where time is not on the clinician's—or the patient's—side. Crucial medical treatment includes fluid resuscitation, anticoagulation, and broad-spectrum antimicrobial therapy; surgery will almost always be needed as well for the best long-term outcome. To increase chances of success, surgical, vascular, and critical care consultations should be obtained early in the disease process. Survival can be enhanced only with the application of best practice interventions, including early diagnosis and therapy along with supportive critical care.

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        Section Description

        EARN CATEGORY I CME CREDIT by reading this article and the article beginning on page 20 and successfully completing the posttest on page 49. Successful completion is defined as a cumulative score of at least 70% correct. This material has been reviewed and is approved for 1 hour of clinical Category I (Preapproved) CME credit by the AAPA. The term of approval is for 1 year from the publication date of July 2011.

        © 2011 American Academy of Physician Assistants.