The trusted source for
healthcare information and
Authors: James A. Castellone, MD, Senior Resident, University of Connecticut Integrated Residency in Emergency Medicine, Farmington, CT.
Robert D. Powers, MD, FACP, FACEP, Chief of Emergency Medicine, University of Connecticut School of Medicine, Farmington, CT.
Peer Reviewers: Eric R. Snoey, MD, Residency Director, Department of Emergency Medicine, Highland General Hospital, Oakland, CA; Assistant Professor, University of California, San Francisco Medical Center.
The presentation of ischemic bowel disease is frequently subtle, especially in the elderly, and can be confused with many other life-threatening conditions. The fact is, few diseases result in such a high mortality rate as acute mesenteric ischemia; mortality rates range from 50-100% in most series.1,2 The clinical course is frequently complicated by the fact that these patients have other comorbid conditions, including congestive heart failure (CHF), cardiac arrhythmias, or chronic dehydration.
The emergency physician’s primary role in evaluating patients with acute abdominal pain is to distinguish benign abdominal disorders from ischemia-related syndromes. Prompt recognition is essential. If patients with acute mesenteric ischemia are not detected rapidly, the risk of bowel infarction increases dramatically, and the probability of survival is low. A high index of suspicion is required, and, once the diagnosis is strongly supported, invasive evaluation and definitive surgical intervention are mandatory.2
With these issues in mind, the purpose of this article is to review the relevant anatomy, pathophysiology, and clinical presentations in the ED, in order to improve outcomes in this high-risk population.
Generally speaking, mesenteric ischemia can be separated into two distinct classes: acute mesenteric ischemia (AMI) and chronic mesenteric ischemia (CMI). Moreover, AMI can be further subdivided into occlusive (OMI) and nonocclusive (NOMI) mesenteric ischemia. Typically, OMI is the result of either thrombotic or embolicacute or subacutearterial or venous occlusion. Approximately 80% of cases of AMI are occlusive in etiology, with arterial emboli or thromboses predominating in 65% of cases and venous thrombosis in 15%.2-4 Arterial occlusions are the result of emboli in 75% of patients and are caused by in situ thrombosis in the remaining 25%. NOMI, which is associated with low perfusion states with or without microvascular pathology, is responsible for about 20% of patients who present with AMI.3-6
Arterial Anatomy. A fundamental understanding of the arterial anatomy of the gastrointestinal tract will aid the clinician in patient evaluation and management. Blood supply to the abdominal organs derives from three major vessels: the celiac trunk, the superior mesenteric artery (SMA), and the inferior mesenteric artery (IMA). Abdominal organs receive their blood supply based upon their embryological development. The pharynx, esophagus, stomach, proximal sections, parts of the duodenum, liver, gallbladder, pancreas and spleen are supplied by the celiac trunk. The distal duodenum, jejunum, ileum, cecum, ascending colon, and two-thirds of the transverse colon receive their blood supply from the SMA. The distal one-third transverse colon, descending and sigmoid colon, and rectum are supplied by the IMA. There is an abundant supply of collateral vessels and thus significant territorial overlap of blood flow that can be clinically significant.4
From a clinical perspective, the extensive collateral vasculature of the gastrointestinal tract protects the bowel from massive ischemia. As a rule, if there is occlusion of a mesenteric vessel, collateral vessels, if they are sufficiently patent, provide the needed blood supply. The main anastomotic regions include the pancreaticoduodenal arteries (celiac artery with the SMA), the marginal artery of Drummond (SMA and IMA), and the arc of Riolan (SMA and IMA). If the celiac artery is occluded, then the SMA can provide collateral flow via the pancreaticoduodenal arteries, and the same is true in reverse should the SMA occlude. Should the IMA occlude, then collateral flow via the arc of Riolan and marginal artery can provide anterograde flow. However, the acuity of the occlusionwhether the occlusion is secondary to an embolus or thrombusand its location will determine whether collateral flow is successful or intestinal necrosis develops.
Venous Vasculature. The general anatomy of the venous circulation parallels the arterial architecture. The inferior mesenteric vein (IMV) facilitates venous return from the IMA distribution to join the splenic vein. Likewise, the superior mesenteric vein (SMV) facilitates blood return from the SMA distribution to meet the splenic vein and form the portal vein that then drains into the liver. In cases of mesenteric venous thrombosis (MVT), portal vein thrombosis, or portal hypertension, the mesenteric venous collateral circulation and portacaval anastamoses become clinically significant.
The major portacaval anastomotic regions are the esophageal veins via the left gastric vein, paraumbilical veins, middle and inferior rectal veins with the IMV, and various retroperitoneal veins. As a result, patients can present clinically with either hematemesis secondary to portal hypertension or portal vein thrombosis or with hematochezia secondary to mesenteric vein thrombosis and venous engorgement.
Abdominal Pain Perception and Neural Innervation. A brief review of the innervation of abdominal viscera is helpful for understanding the progression and presentation of clinical disease in patients with mesenteric ischemia. As might be expected, abdominal pain is the most common presenting chief complaint of patients with AMI. Early in the presentation, pain is nonspecific and out of proportion to the physical findings, which can confound the correct diagnosis.
Visceral nerves that supply the intra-abdominal organs also supply the peritoneum, and are carried in the low thoracic and lumbar splanchnic nerves (T5-L2). Somatic nerves that supply the abdominal wall structures and skin also supply the parietal peritoneum.
One way to evaluate abdominal pain is by differentiating visceral from somatic pain. Visceral pain is derived from receptors located in the visceral peritoneum and is triggered by such stimuli as smooth-muscle contraction or spasm, distension or stretching, and ischemia, but not to physical palpation or temperature. Typically, there is no exacerbation or change in pain quality or quantity with movement. In contrast, somatic pain is derived from receptors located in the parietal peritoneum and is triggered by such stimuli as touch, cutting, ischemia, pressure, heat, or inflammation. Pain is exacerbated by movement because of the change in the relationship between the parietal peritoneum with the inflamed visceral peritoneum. This produces guarding, a phenomenon in which abdominal muscles contract in an attempt to prevent movement. Symptoms associated with visceral pain include salivation, nausea, vomiting, and sweating.
The processing of somatic pain occurs in the cortex and, as a result, has specific localization that is perceived at the respective dermatomal distribution. Somatic pain usually is described as sharp or knife-like and focal, but it can be diffuse as a result of widespread inflammation associated with a ruptured viscus. As is well-known, patients do present in atypical fashion, and significant overlap within the sympathetic nervous system can refer pain to an atypical location.7-10
Approximately 20-25% of cardiac output is delivered to the small and large intestine, with a 2:1 distribution of SMA to IMA. Eighty percent of this flow is for perfusion of the mucosa and 20% for the muscularis because of the high metabolic requirements of the mucosa. Accordingly, the visceral mucosa is very sensitive to the decreased perfusion and compromised oxygen delivery characterized by ischemic states.
Mesenteric Ischemia. Mesenteric ischemia can result from prolonged periods of vasoconstriction.11,12 Other precipitating factors include activation of the renin-angiotensin axis; angiotensin II is a potent mesenteric and peripheral vasoconstrictor. Vasopressin, which is released in significant quantities in low-flow states, affects splanchnic vascular resistance to a much greater degree than the systemic circulation and is useful for treating GI hemorrhage.11-13
Another significant factor in mesenteric ischemia is the countercurrent exchange mechanism that occurs in the small intestinal villi. In this regard, villi subjected to ischemia result in epithelial cell necrosis that stimulates release of endothelial factors, and leads to the attraction and activation of neutrophils and macrophages into the ischemic tissue. These cells release substances such as protease enzymes, TNF, platelet activating factor, arachadonic acid byproducts (prostaglandins and leukotrienes), and toxic oxygen radicals that produce further endothelial damage, increased vascular permeability, vasoconstriction, inflammation, and necrosis. Digestive enzymes in the intestinal lumen are then able to invade the injured cells, resulting in the leakage of fluid and net movement of fluid into the bowel lumen.11-13
From a metabolic perspective, cellular hypoxia results in decreased production of ATP and cellular acidosis. The clinical manifestations of metabolic acidosis are an increased respiratory rate and associated secondary respiratory alkalosis. Reperfusion injury can occur after reestablishment of blood flow. The anaerobic environment leads to the proliferation of anaerobic organisms in the intestinal lumen, absorption into the circulation, and translocation into the peritoneum, resulting in an increased risk for secondary sepsis.11-14
Animal models of mesenteric ischemia show that mild ischemia of short duration results in no permanent damage and intestinal mucosal repair. However, moderate to severe ischemia of longer duration does result in significant injury. The earliest injury is at the villus tips resulting in necrotic enterocytes being sloughed into the intestinal lumen. Edema develops within the bowel wall in the lamina propria and mucosal protection decreases. Cellular activation as described previously occurs and transmucosal necrosis ensues.11-13
Bowel Injury Patterns: Clinical Correlations. The severity of ischemic injury to the bowel depends upon the duration of ischemia, the etiology of the ischemia (embolus, thrombus, or low-flow state), and the integrity of the collateral circulation. As emphasized, collateral circulation protects the gut from developing ischemia. Moreover, it has been shown that, as a rule, at least two of the three major mesenteric vessels (celiac, SMA, and IMA) must be diseased in order to produce ischemia. However, acute occlusion of the SMA alone can result in acute mesenteric insufficiency. When a major mesenteric vessel is occluded, collateral vessels open immediately in response to the decreased arterial pressure distal to the occlusion. However, if the occlusion is prolonged, vasoconstriction develops regardless of whether the occlusion was secondary to an arterial embolus, thrombus, or low-flow state. It has been shown that even after an obstructed vessel is opened, vasoconstriction may persist.
Precise patterns and the extent of bowel injury secondary to ischemic insult depend upon etiologic factors, underlying anatomy, and compensatory mechanisms of the patient. Generally speaking, major emboli to the SMA do not lodge proximally, as is seen with thrombi, but they tend to occlude the vessel distally to branches of the middle colic and jejunal arteries. Consequently, the injury pattern usually involves the distal jejunum, the ileum, and the ascending colon, whereas the proximal jejunum, and transverse and distal colon are spared. Minor emboli to the SMA may involve distal branches, resulting in a focal segmental injury pattern. Arterial thromboses lodge at the origin of the vessel, and they occur much more commonly in the SMA due to the angle of take-off from the aorta45° vs. the celiac axis which is 90°. As a result, the entire small bowel from proximal jejunum to distal colon is affected by proximal thrombosis of the SMA.
Nonocclusive Mesenteric Ischemia. In NOMI, most of the small intestine and portions of the large intestine are affected in a patchy injury pattern. The splenic flexure is commonly affected because its perfusion is dependent on distal SMA and IMA branches. The descending and sigmoid colon are also commonly affected. In mesenteric venous thrombosis, the injury pattern usually involves short segments of the proximal and middle small intestine. Venous engorgement and extravasation of blood into the tissues is a common finding. (See Figure 1.)
Mechanical Causes of Ischemia. Mechanical causes that result in external compression of the bowel wall (incarcerated hernia, intussusception, volvulus, adhesions), and, therefore, the major vessels, are more common than primary vascular occlusions. The resulting injury pattern will be determined by the anatomic site of bowel compression. Ischemic injury also occurs proximally to obstructive lesions of the colon. Ischemic colitis is the most common form of intestinal ischemia secondary to obstructing or partially obstructing lesions of the colon (e.g., cancer), and ulcerative colitis. The spectrum of injury ranges from superficial ulcers to gangrenous necrosis and perforation. 11-13,15
Patients suffering from ischemic bowel disease can present with a wide range of signs and symptoms, ranging from vague abdominal discomfort to frank peritonitis and septic shock. Morbidity and mortality caused by mesenteric ischemia are linked to the time delay in making the diagnosis and underlying host factors.
Diagnostic Challenges. AMI remains a challenging diagnosis, primarily because of the lack of physical findings in these patients who complain of pain early in the ischemic process. At the other end of the spectrum are those patients with advanced ischemia who present with obvious surgical abdominal disease with significant physical findings. However, once peritonitis has occurred, the ischemic process is well-advanced and the mortality is greater than 70% in most published reports.
Overall, using an aggressive diagnostic approach has been shown to reduce mortality to approximately 45%. Lack of peritoneal signs is a positive predictive factor, with 90% of patients surviving who present without peritoneal signs and have AMI diagnosed at angiography.1 Accordingly, the challenge lies in making the diagnosis when a patient presents early in the course of their ischemia.
Mesenteric Arterial Embolism. The median age of patients presenting with mesenteric arterial embolism is 70 years, with approximately two-thirds of patients with arterial embolism being women.2 The overwhelming majority of emboli lodge in the SMA, although thrombotic emboli to the celiac trunk have been reported; emboli consisting of tumor and cholesterol have also been documented.2
SMA embolism has a more favorable prognosis than bowel ischemia secondary to thrombosis of the SMA. This is because emboli lodge distally to the middle colic and jejunal branches, sparing the proximal jejunum and distal colon. Emboli originating in the left atrium or ventricle are the most common cause of SMA embolism. Risk factors include advanced age, coronary artery disease, cardiac valvular disease, history of dysrrhythmias, atrial fibrillation, post-myocardial infarction mural thrombi, history of thromboembolic events, aortic surgery, aortography, coronary angiography, aortic dissection; one case has been reported following colonoscopy.3-6,16 (See Table 1.)
Approximately 20% of patients have a previous history of peripheral emboli. Patients recently converted to sinus rhythm from atrial fibrillation are particularly susceptible to thromboembolism. Reports have shown that there is a delay in normal mechanical contractility in the atrium after the conversion to normal sinus rhythm in atrial fibrillation, and, consequently, emboli have occurred days after conversion in patients without atrial thrombi at the time of conversion.5
Patients typically complain of the sudden onset of severe periumbilical pain, which is consistent with the innervation and vascular supply to the SMA distribution. Associated symptoms such as nausea, vomiting, and frequent bowel movements are more likely if the ischemia is secondary to an acute vascular occlusion.4,12,17 Pain may be the only presenting symptom, and it is typically intense but poorly localized. In a report of 82 patients with SMA embolus over 22 years, one study reported typical abdominal pain in only 74.5% of patients while finding it absent or atypical in 23%.18
Clearly, the most consistent finding is pain that is out of proportion to the physical findings. This is explained by the fact that only the visceral structures are ischemic early on, and the parietal peritoneum (which would affect physical findings) has not been irritated yet because transmural necrosis with its associated inflammatory process adjacent to the parietal peritoneum has not occurred. Accordingly, the abdomen may be soft with only mild tenderness. One review reported that more than than two-thirds of patients presented without typical signs, such as absent bowel sounds, abdominal distension or guarding, that are indicative of a significant abdominal process. Additionally, blood in the rectum was present in only 16% of patients.13 The presence of occult blood has also been reported as being present in 25% of patients.2,13
When the ischemic process becomes transmural, peritoneal signs become evident. Caution must be taken when a patient is on corticosteroids, since this may blunt an appropriate inflammatory response and, therefore, suppress pain and fever and mask typical findings in patients with significant abdominal disease.8
Mesenteric Arterial Thrombosis. The superior mesenteric artery originates at a 45° angle off the ventral aspect of the abdominal aorta, which explains why it is the most common location in the mesenteric circulation for thrombotic occlusion. Thrombotic occlusion portends a less favorable prognosis than occlusion secondary to embolization because a larger segment of intestine becomes ischemic.
Thrombosis usually occurs in the area of atherosclerotic narrowing in the proximal SMA. In most cases, the proximal jejunum through the distal transverse colon becomes ischemic. SMA thrombosis usually occurs in patients with chronic, severe, visceral atherosclerosis; a history of abdominal pain after meals is present in 20-50% of these patients.2,6,19 Patients are often elderly, have associated coronary artery disease, severe peripheral vascular disease, or hypertension.
One large trial reported on a series of autopsies, in which coronary, cerebral, and mesenteric arteries were examined to evaluate the frequency of atherosclerosis in the visceral arteries.19 They found that the percentage of cases with visceral atherosclerosis increased with increasing age. Five percent of patients younger than 40 years old had moderate mesenteric arterial stenosis, 14% in 40-59 year olds, 33% in the 60-79 age group, and 67% in those older than 80 years. Atherosclerotic changes were rare in distal mesenteric arteries with no luminal narrowing. Fifteen percent of autopsy cases had at least two significant mesenteric arterial stenoses; none of these patients had reported symptoms of chronic mesenteric ischemia. The celiac artery was the most common site of mesenteric arterial stenosis, followed in decreasing frequency by the SMA and IMA. They also found a strong association between mesenteric artery and coronary artery atherosclerosis.19
Patients with SMA thrombosis present with the gradual onset of abdominal pain and distension. A history of postprandial abdominal pain and weight loss in those with symptoms of chronic mesenteric ischemia can be elicited in fewer than half of cases. Finding subjective complaints that are well out of proportion to the physical findings is characteristic. Nausea and vomiting found in mesenteric arterial occlusion has been attributed to ischemic gastroparesis. As a result, patients with severe nausea and vomiting may have decreased-to-no bowel sounds secondary to this process, without peritoneal findings. These patients usually present later than patients with acute mesenteric insufficiency secondary to embolization, and they may well have had pain for 12-24 hours. Patients frequently will have physical findings consistent with peripheral vascular disease, such as carotid, femoral, or abdominal bruits, or decreased-to-absent peripheral pulses. Again, massive abdominal distension, absent bowel sounds, muscular guarding, rebound and localized tenderness, and rigidity indicate advanced necrosis of bowel.6,15,20
Mesenteric Venous Thrombosis. The mean age of presentation ranges from 48-60, but intestinal ischemia secondary to MVT can occur at any age.21-23 AMI itself is rare and ischemia secondary to MVT accounts for only 5-15% of cases. A few significant clinical factors should be emphasized. MVT occurs in a younger patient population, and the mortality rate is lower than the other causes of AMI, ranging from 20-50%.6,24 MVT has been traditionally classified as either primary (unknown etiology) or secondary to a predisposing condition. (See Table 2.) Primary MVT accounts for approximately 20% and secondary thrombosis for approximately 80% of cases. Hypercoagulable states associated with MVT include polycythemia vera, myeloproliferative disorders, antithrombin III deficiency, protein C and S deficiencies, DVT, malignancy, estrogen therapy, and pregnancy. One study of 30 patients with MVT secondary to hypercoagulable states noted polycythemia vera as the most common etiology, comprising 35% of the cases.21 Portomesenteric venous thrombosis occurs in patients with portal hypertension, cirrhosis, and following sclerotherapy for esophageal varices. Intra-abdominal inflammatory conditions such as pancreatitis, diverticulitis, appendicitis, peritonitis, abscesses and ileocolitis have all been shown to cause MVT. Additionally, up to 60% of patients with MVT have a history of peripheral deep venous thrombosis.6,21-29
Inadequate venous drainage results in massive vascular congestion and fluid sequestration, which can lead to hypovolemia, hemoconcentration, and, eventually, if untreated, cardiovascular collapse. Mesenteric arterial vasospasm uniformly coexists with venous occlusion and persists despite resolution of the occlusion. Portal vein thrombosis can produce esophageal varices and splenomegaly and can present as hematemesis or an upper gastrointestinal bleed. Splenic vein thrombosis, as seen after splenectomy or in pancreatic inflammatory conditions, may present as an upper GI bleed with varices within the stomach but without intestinal ischemia. Superior mesenteric vein thrombosis will result in small intestinal ischemia, and inferior mesenteric vein thrombosis is usually of no consequence.22,23,29
The clinical presentation of MVT depends upon the acuity of the venous occlusion and covers the spectrum from acute onset to insidious evolution of abdominal pain. In general, symptoms tend to develop less rapidly than with acute arterial insufficiency. It should be stressed that MVT may have an acute, subacute, or chronic onset.
A number of studies have helped characterize this ischemic syndrome.21,22 The symptoms of acute MVT include abdominal pain in 83-100% of patients, which, typically, is described as being out of proportion to the physical findings. The abdominal pain has a mean duration of 5-14 days, but 25% of patients present within 48 hours. Anorexia has been noted in 53-54%, vomiting in 41-77%, diarrhea in 36%, constipation in 13-34%, and hematemesis in 9-42% of patients. Physical findings include abdominal tenderness in 95-97%, distension in 51-84%, decreased bowel sounds in 42-77%, stool positive for occult blood in 26-54%, guarding in 42-53%, shock in 6-32%, and fever (> 38° C) in 24-47% of patients.21,22,25
The abdominal pain in MVT is described as being diffuse and nonspecific initially, but it later becomes constant in nature. Gastrointestinal bleeding, whether upper or lower, signifies bowel infarction and necrosis. The abdominal distension may not be accompanied with tympany to percussion due to massive venous congestion within the bowel wall, lumen, and peritoneal cavity. A significant number of patients present with fever and shock, indicative of cardiovascular collapse from hypovolemia, sepsis, and advanced disease.
Subacute MVT occurs in patients with venous thrombi and abdominal pain for several weeks to months but, even without evidence of intestinal infarction, some patients also complain of associated nausea or diarrhea. There are usually no physical findings. Chronic MVT is defined as patients without abdominal pain with thrombosis. These patients typically present with gastrointestinal bleeding from esophageal varices associated with thrombosis of the portal or splenic veins.22-24
Nonocclusive Mesenteric Ischemia. Acute mesenteric insufficiency due to NOMI occurs in approximately 20% of all cases with bowel ischemia.30 One study conducted over a 13-year period reported a mean age of 59. The study emphasized the presence of precipitating illnesses, which result in low-flow states and can occur in younger patients.30
The pathogenesis of NOMI appears to be multifactorial. Mesenteric vasoconstriction can result from the shunting of blood flow to the vital organs (heart and brain) during periods of hypotension or shock. Whether the hypotensive state is due to a primary cardiac event such as cardiogenic shock, an arrhythmia, or in a patient with sepsis, the end result is the shunting of blood away from the splanchnic circulation to the central circulation. The main mediators of this process appear to be angiotensin II and vasopressin.31
Ergot alkaloid poisoning, cocaine abuse, and calcium-channel blocking agent use and overdose have also been shown to result in nonocclusive ischemia secondary to severe mesenteric vasoconstriction.2,32,33 NOMI occurs in exacerbations of CHF, cardiogenic shock, and after cardiopulmonary bypass.15,36,38 In 3066 patients who underwent cardiopulmonary bypass over a five-year period, the incidence of postoperative NOMI was .36% (11 patients). A significant number of patients with NOMI have had long-term treatment with digitalis. Studies suggest that patients with CHF and increased portal venous pressure who are on digitalis may be susceptible to mesenteric vasoconstriction and NOMI.2,34
Clinically, patients who present with NOMI are often critically ill, usually as a result of the precipitating event that has led to the splanchnic vasoconstriction. Precipitating conditions include: cardiogenic shock with a myocardial infarction, congestive heart failure, or, in the intensive care unit, placement on vasopressors for the treatment of septic shock. Accordingly, abdominal pain in any patient with the risk factors described previously must raise the clinical suspicion of NOMI. (See Table 3.) If delays in diagnosis result, then the condition will progress and, if peritoneal findings appear, the patient may not be salvageable.
In general, the signs and symptoms of NOMI are similar to those of acute mesenteric ischemia. One retrospective review of NOMI over a 13-year period found abdominal pain to be present in 77% of patients, nausea and vomiting in 38%, diarrhea in 23%, and anorexia in 23%. In 54% of patients, abdominal tenderness and distension were present, and 46% had decreased bowel sounds. In 38% of patients, the presenting complaint of abdominal pain was diffuse and without signs of peritonitis, whereas the other 62% presented with peritonitis. Patients who presented early had a mortality of 40% and those who presented late had a mortality rate of 100%. The overall mortality rate in this study was 77%.30
Chronic Mesenteric Ischemia. CMI, also known as "intestinal angina," is a rare form of intestinal ischemia. Chronic mesenteric ischemia occurs in a 3:1 ratio of women to men and patients are generally older than 60 years of age. CMI is usually the result of severe stenosis of the proximal ostial portion of the main mesenteric arteries. (See Table 4.) Intestinal ischemia secondary to CMI is rare because of the rich collateral circulation previously described between the three main mesenteric arterial pathways. Those patients that do go on to develop CMI usually do not develop symptoms until at least two of the three major mesenteric arteries (CA, SMA, IMA) are occluded or significantly stenosed.
The severe pain that occurs in these patients appears to be the result of blood flow changes between the stomach and small intestine during a meal ingestion. After atherosclerosis, the second most likely cause of CMI is the celiac axis compression syndrome. In this syndrome, the median arcuate ligament of the diaphragm may compress the celiac axis during expiration and can result in CMI. However, only one-third of patients with celiac axis compression syndrome have postprandial abdominal pain, and weight loss is often absent. Celiac axis compression remains a diagnosis of exclusion.2,35
Several case reports have noted young patients with a history of cocaine abuse with postprandial abdominal pain, weight loss, and food aversion with diagnostic occlusion of the celiac and SMA. Cocaine is thought to cause intimal injury and platelet aggregation leading to thrombosis in addition to the vasospasm at the time of it’s use. The results of studies show that cocaine potentiates arterial thrombosis not only of the mesenteric vasculature but also of the coronary circulation, which results in mesenteric and coronary ischemia.36
Clinically, patients complain of epigastric or periumbilical pain which is dull, deep, crampy, or aching in character. The pain characteristically begins 15-30 minutes after eating, increases in severity, and then slowly diminishes over the subsequent 1-4 hours. The pain intensity depends upon the size of the meal, and, as the occlusive process progresses, patients develop symptoms with smaller and smaller meals, ultimately leading to the avoidance of food. As a result, patients develop significant weight loss. Physical examination usually reveals a patient who is cachectic (depending on the duration of the symptoms), has a soft and nontender abdomen with bowel sounds, and no signs of peritonitis.2,35,36
Laboratory Testing. Patients older than 50 years of age who present with abdominal pain need a thorough investigation to determine the etiology of their pain. Unfortunately, laboratory investigations in acute mesenteric ischemia are neither sensitive nor specific.
Putative markers for intestinal ischemia include: creatine phosphokinase (CPK), alkaline phosphatase, diamine oxidase, hexosaminidase, lactate dehydrogenase (LDH), aspartate transferase (AST/SGOT), leukocyte counts, electrolytes, hemoglobin/hematocrit, amylase, inorganic phosphate, serum lactate levels, and intestinal fatty acid binding protein. Unfortunately, none of these tests have been proven to be beneficial prior to the onset of intestinal necrosis.
One study has shown that the seromuscular enzyme CPK was elevated earlier and to a greater extent than the other seromuscular enzymes (LDH, AST) and mucosal enzymes (diamine oxidase and alkaline phosphatase). This investigation reported a sensitivity of 54% at two hours after experimentally induced ischemia secondary to SMA ligation and 75% at four hours with a specificity of 83% at both two and four hours. CPK levels were shown to rise in 3-4 hours and reach a peak at about eight hours.38
Studies examining the leukocyte count show it to be elevated in most cases of mesenteric ischemia. Leukocyte counts of 10-15,000/mm3 are present in approximately 25% of cases, 15-30,000 in 50%, and 25% of patients have values greater than 30,000.17 However, in early mesenteric ischemia, the leukocyte count may not be elevated, and the diagnosis of mesenteric ischemia can not be ruled out by a normal white blood cell count, but it probably makes the diagnosis less likely.38
Analysis of electrolytes also lacks sensitivity and specificity in early mesenteric ischemia. The finding of a metabolic acidosis would signify a significant pathologic process, but other abdominal surgical emergencies also have an associated metabolic acidosis. One study reported that in patients with SMA emboli, only 42% had a metabolic acidosis and it was shown not to be statistically significant.39 The serum amylase has been shown to be elevated in half of patients up to twice the normal values.17
Serum inorganic phosphate levels have been shown to be an indicator for intestinal ischemia in several retrospective studies. Up to 80% of patients with intestinal infarction have been shown to have increased levels, and, in cases where blood was obtained early (4-12 hours) after the onset of symptoms, 94% of patients had elevated levels vs. control patients with non-ischemic surgical abdominal emergencies.39 One group examined the lactate level in patients with acute abdominal disease. They reported a sensitivity of 100% and a specificity of 42% for mesenteric ischemia.40
Plain Radiography. The first radiological evaluation that should be performed on patients suspected of having acute mesenteric ischemia are abdominal and chest x-rays to exclude the presence of free air or bowel obstruction. In rare instances, plain films of the abdomen reveal findings consistent with ischemic bowel such as pneumatosis intestinalis, portal venous gas, or a thickened bowel wall with thumbprinting.13,41 However, in the majority of cases, plain films will be normal, and in early mesenteric ischemia, normal x-rays are the rule.42
Abnormal findings on plain films that are nonspecific for mesenteric ischemia include an ileus, gasless abdomen, small bowel pseudo-obstruction, splenic flexure cut-off sign, and free air. Findings highly suggestive of ischemia include a thickened bowel wall with thumbprinting, intramural air (pneumatosis intestinalis), and portal venous gas. Pneumatosis intestinalis results from mucosal ischemia and damage followed by dissection of intraluminal gas into the submucosa.42,43 In one study on diagnostic imaging in mesenteric infarction of patients with proven AMI, 67% had air fluid levels, 18% had dilated bowel loops, 10% had a gasless abdomen, 2% had pneumatosis, and portal venous gas was present in 2%.44
Computed Tomography. Due to the availability, improved quality, and speed of computed tomography (CT), it is commonly used for assessing undiagnosed abdominal pain in the ED. Findings in AMI include normal studies, nonspecific findings such as focal or diffuse bowel wall thickening, focal dilated fluid filled bowel loops, mesenteric edema, engorgement of mesenteric veins, peritoneal fluid, and intra-abdominal air. Specific findings include pneumatosis intestinalis, portal venous gas, mesenteric vessel occlusion, and enlargement of a thrombosed vein.
The sensitivity of CT in AMI has been reported to be from 64-82%.42,44,45 CT has been shown to be the most sensitive test for detecting thrombosis in the mesenteric venous bed and, therefore, is useful for confirming the diagnosis of MVT.21 One group relies upon contrast-enhanced CT as their first imaging study, especially when there is a strong suspicion for MVT.22 However, as will be discussed for patients with suspected AMI of unknown etiology, CT is not the first study of choice.
Ultrasonography. Ultrasound is used with increased frequency for the initial evaluation of patients with abdominal pain in the ED. Duplex ultrasound can identify major arterial or venous occlusions and additional findings suggestive of AMI. However, the usual shortcomings of abdominal ultrasound, such as respiratory motion, intra-abdominal gas, obesity, and the inability to satisfactorially visualize mesenteric vessels at all times prevent its use as an initial modality for diagnosing AMI.
Findings in patients with AMI include small intestinal bowel wall thickening (> 5mm), decreased or absent peristalsis, MVT, and intraperitoneal fluid.42 In a study on Doppler sonography for detection of AMI due to SMA occlusion, bowel wall abnormalities were detected in only 50% of patients (3 of 6), and the correct diagnosis of SMA occlusion was noted in five of six patients. Duplex ultrasound has been reported to be reliable for CMI and MVT, but very few studies have evaluated its use in AMI.42,46
Magnetic Resonance Imaging (MRI). MRI is useful for delineating the mesenteric vessels and bowel wall and has been shown to be better than nonenhanced CT but equal to contrast-enhanced CT for evaluating the mesenteric venous system. However, no studies have been reported for its use in AMI. An advantage of MRI is the avoidance of ionizing radiation, but the disadvantages, which include the duration of the exam and the lack of 24 hour availability, are significant.24,42
Laparoscopy. Laparoscopy demonstrates intra-abdominal fluid and transmural necrosis but does not evaluate the mucosa. Additionally, increased intraperitoneal pressures can decrease mesenteric arterial flow if greater than 20 mmHg. Therefore, a patient can experience an acute mesenteric ischemic event that may not be detected with laparoscopy.3
Endoscopy. Endoscopy can visualize mucosal injury at the site of injury but will give no information regarding the serosa, and a transmural infarct can go undetected. Additionally, there is a risk of perforation with a friable ischemic bowel wall.3
Angiography. Angiography is the gold standard for the diagnosis of AMI and is also used for therapeutic infusion of the vasodilator papaverine.2,15,47,48 However, the use of angiography to diagnose AMI remains controversial. Most clinical monographs on AMI recommend that after obtaining plain abdominal films to rule out the presence of free air or obstruction, angiography must be obtained early, especially in those patients in whom there is a strong clinical suspicion for AMI.
Many of the controversies and intervention bifurcation points surrounding timing and indications for angiography are highlighted in a landmark study by Moneta and Lee.2 In this study, the authors conclude that in patients without peritoneal signs, the use of angiography may avoid surgical intervention and may identify patients with NOMI who can be treated with an infusion of papaverine via a catheter secured in the superior mesenteric artery. In addition, these investigators recommend that patients suspected of having AMI secondary to emboli or thrombias opposed to NOMIshould undergo surgery, and patients with a delayed onset suspected of having NOMI should undergo angiography prior to laparotomy.2 However, other reports strongly suggest that patients diagnosed with either emboli or thrombi who do not have peritonitis can also be started on papaverine and have repeat angiography in 24 hours and avoid surgery.3-5
The majority of the clinical literature favors angiography if no peritoneal findings are present. (See Figure 2.) Should peritoneal findings be present then preoperative angiography may be performed. One problem with obtaining angiography is that it may delay surgical intervention, and that patients with peritoneal signs cannot afford such a delay in the face of ongoing ischemia. One group advocates that patients with physical findings that necessitate immediate surgical intervention should undergo angiography and that intra-arterial vasodilator therapy can be started intra- or postoperatively.32
Another group identifies mesenteric angiography as "the key to diagnosing mesenteric ischemia before bowel infarction and prior to laparotomy, as a definitive diagnosis cannot be made clinically." Furthermore, it is essential to obtain angiography and a diagnosis prior to infarction in order to decrease morbidity and mortality. An operative strategy regarding treatment can be made with information obtained from angiography. The following procedures may be considered: thrombectomy, embolectomy, endarterectomy, revascularization, and angioplasty, depending upon the etiology.48
Patients who are hypotensive, or on vasopressor support are not suitable for angiography because the severe mesenteric vasoconstriction may prevent differentiation of NOMI from OMI and intra-arterial vasodilators are also contraindicated.48
An Aggressive Diagnostic Approach. Because of the high mortality associated with AMI, especially when peritoneal findings are present and patients have an infarcted bowel, it is essential that those patients with possible mesenteric ischemia be detected early in the course of their illness to decrease the mortality. Studies have been done using an aggressive diagnostic approach in establishing the presence of mesenteric ischemia and providing treatment options. These studies suggest that mortality can be decreased from 70-90% to 45-50%; if the diagnosis is established prior to the development of peritonitis, it can be decreased to 10%.1,24,41
In order to identify all cases of AMI, the clinician must accept a significant percentage of patients with negative angiograms. As a general rule, therefore, patients who are older than 50 years of age, complaining of the sudden onset of abdominal pain for more than two hours’ duration, and have significant risk factors for AMI (thrombosis, embolus, NOMI, MVT), should be considered eligible for the management scheme outlined in the algorithm outlined in Figure 2.1
Stabilization and Initial Management. Initial treatment in the ED requires appropriate resuscitation, which includes intravenous fluid replacement, correction of predisposing or precipitating causes of ischemia, maintaining adequate oxygenation, and the institution of antibiotic coverage.1,13,17,49
After initial resuscitative efforts have been started, correction of any predisposing or precipitating causes of ischemia must be addressed. The main pathophysiological insult is a lack of mesenteric blood flow so cardiac output must be maintained. Patients presenting with CHF, dysrrhythmias, or in cardiogenic shock need immediate therapy. In patients with significant hypotension that is unresponsive to fluid resuscitation, vasopressors may be used, but the lowest possible dose should be infused, and alpha agonists should be avoided, with ionotropes being the preferred agents.1,13
In patients in shock, there is a lack of adequate end-organ perfusion; it is essential to maintain adequate oxygenation. If there is a lack of oxygen content due to decreased hemoglobin, then blood should be given. Endotracheal intubation and mechanical ventilation should be instituted when indicated. Patients suspected of having mesenteric ischemia who appear acutely ill should have parenteral antibiotic therapy started as soon as possible to cover for gram-negative enteric bacteria as well as anaerobes after blood cultures are drawn.13
An important factor in hypotensive patients is the increased renin-angiotensin-aldosterone axis and antidiuretic hormone (ADH) secretion. Since angiotensin is a potent mesenteric vasoconstrictor, it has been proposed that angiotensin converting enzyme (ACE) inhibitors may be beneficial in blunting the severe mesenteric vasoconstriction, but no studies have been done to examine this therapy in AMI.13
Papaverine. Since mesenteric vasoconstriction is present in patients with occlusive as well as nonocclusive etiologies, intra-arterial infusion into the superior mesenteric artery of papaverine is an important method for increasing mesenteric perfusion, and is considered definitive therapy in patients with NOMI. Papaverine is a potent inhibitor of phosphodiesterase, which degrades cyclic adenosine monophosphate (cAMP). Therefore increased cAMP results in vascular smooth-muscle relaxation. Infusion into the SMA is the most effective way of relieving mesenteric vasoconstriction.
Papaverine is started at angiography and continued postoperatively if laparotomy is performed. The dosing is 60 mg IV bolus followed by a 30-60 mg/h continuous infusion at a concentration of 1 mg/mL. Since 90% of papaverine is metabolized by the liver with each pass, there are no systemic effects noted as a result.5,14,58,60 It has been reported that papaverine improves survival 20-50%.12 Tolazoline is another vasodilator that has been used in patients with mesenteric vasoconstriction.1
Medical and Surgical Interventions: The Overview. Surgical consultation should be obtained early for all patients with suspected AMI. Immediate surgery is necessary for patients with peritonitis, for those requiring restoration of arterial or venous flow, and for the resection of necrotic bowel. In patients found to have massive small and large intestinal necrotic bowel who are not expected to survive, resection may not be indicated.
AMI With Embolism. There are many treatment options for AMI secondary to embolism. Once embolism is confirmed as the etiologic factor at angiography, and papaverine infusion is started, then laparotomy should be performed to evaluate bowel viability. Surgical intervention may involve arteriotomy with embolectomy and bowel resection if nonviable necrotic bowel is found. If bowel viability is equivocal, then the surgeon may perform a second look procedure 12-24 hours postoperatively to avoid extensive bowel resection at initial laparotomy.15
Patients without peritoneal signs with minor emboli, who achieve pain relief with vasodilator infusion, may be managed nonoperatively with repeated angiograms.1 (See Figure 2.) Intra-arterial infusion into the superior mesenteric artery (SMA) with thrombolytic agents has been used successfully in patients with confirmed embolism without evidence of peritonitis, normal abdominal films, and no evidence of an ileus.50 One report suggests that thrombolytics may take 36 hours to dissolve the embolus, thus exposing the bowel to a prolonged ischemia. Therefore, the authors do not recommend their use in AMI.1 In contrast, there have been several case reports supporting the use of urokinase and streptokinase in SMA emboli in patients without peritonitis with a duration of abdominal pain less than eight hours from the onset.51-53 Postoperative anticoagulation is recommended for all patients, but determining the proper time to start heparin remains controversial.18
AMI With Thrombosis. Acute mesenteric ischemia secondary to thrombosis also is treated initially with a papaverine infusion started at angiography. Several interventions are available to the surgeon. Patients without peritoneal signs with minor thrombi may be treated with papaverine only. Patients with major thrombi with good collateral vasculature, also without peritoneal signs, may be observed in the hospital without a papaverine infusion. (See Figure 2.) Patients with peritoneal signs and documented thrombosis require laparotomy as do patients with major thrombi and poor collateral flow even in the absence of peritoneal findings.
Preoperative angiography enhances the decision-making process regarding surgical revascularization. Endarterectomy, thrombectomy, and mesenteric revascularization with aortomesenteric bypass grafting have been the traditional methods of treatment with better long-term results using thrombectomy and bypass grafting.1,6,12,15
A retrospective review evaluated 16 patients who underwent percutaneous transluminal angioplasty (PTA) of the celiac, SMA, and IMA.54 The study included patients with chronic mesenteric ischemia and acute mesenteric ischemia secondary to thrombosis, which made interpretation difficult. Two of the 16 with an obvious acute presentation had unsuccessful primary PTA, with one resulting in death and the other requiring surgical revascularization. Recurrence rates after surgical revascularization have been reported at 7-50%, whereas recurrence rates for PTA have been from 17-63% requiring repeat PTA.54,55 Because of the danger of recurrence and extensive potential bowel loss, in addition to lack of methods to monitor bowel injury, PTA is not recommended for acute SMA thrombosis.1
AMI With MVT. AMI secondary to MVT mandates treatment with anticoagulation, as soon as the diagnosis is made. The aim is to limit the extent of thrombosis and to prevent recurrent thromboses.6,12 Numerous studies have shown that patients not treated with anticoagulation postoperatively had a significant increased incidence of recurrence with higher mortality rates.23 Therefore, heparin is the initial treatment of choice, followed by long term warfarin therapy.6 In patients without peritonitis, anticoagulation may be the only form of treatment instituted, but scattered studies on thrombolytic therapy have been performed.56 Necrotic nonviable bowel requires resection and revascularization should precede resection. Patients with equivocal bowel may require a second-look operation at 12-24 hours.6,57 There are also some reports of success with portomesenteric venous thrombectomy, but most patients with acute MVT have diffuse vein thrombosis not amenable to such therapy.21,23
NOMI. Patients diagnosed angiographically with NOMI are immediately started on intra-arterial papaverine for severe mesenteric vasoconstriction. (See Figure 2.) In patients without peritoneal signs, papaverine is the treatment of choice followed by repeat angiography at 12-24 hours. In patients with peritonitis, exploratory laparotomy is indicated immediately, with necrotic or nonviable bowel being resected and papaverine infusion continued postoperatively with repeat angiography in 24 hours. Therapy for NOMI remains nonsurgical unless there is evidence of peritonitis and necrotic bowel. Nonsurgical treatment includes correcting any underlying conditions that resulted in the diffuse mesenteric vasoconstriction, such as CHF, arrhythmias, or hypotension, in an effort to increase mesenteric blood flow. Additional therapy includes aggressive fluid resuscitation, antibiotics, and papaverine as has been previously addressed.1,6,12,15,30,32 Captopril has been recommended because of the significant increase in angiotensin and its potent mesenteric vasoconstrictive effects, but clinical reports in humans are lacking.32
CMI. CMI does not require emergent intervention unless there is AMI in a patient with underlying CMI. Patients with CMI can develop low-flow states, making them susceptible to NOMI in addition to OMI secondary to thromboembolism. Typically, patients with CMI are severely malnourished and require preoperative parenteral nutrition. Resolution of symptoms in patients with CMI requires mesenteric revascularization with the goal of therapy being the restoration of blood flow and alleviating abdominal pain. Successful interventions have included endarterectomy, PTA, and bypass grafting.6,35
Angioplasty is considered a reasonable alternative to surgery in patients who are high surgical risks, because the location of the lesion occurs at the origin of the artery making success with angioplasty less likely. Additionally, patients with initial successful PTA have a high recurrence rate requiring repeat PTA or surgical intervention.12,58 Vascular bypass grafting is the procedure of choice for patients with CMI. Studies have revealed that multiple vessel bypass decreases the recurrence rate from 50% to 11% vs. single vessel bypass.12 Thus, the vast majority of patients with CMI who present to the ED with abdominal pain will require vascular surgery consultation for definitive intervention.
AMI is a potentially lethal disease that requires early diagnosis. Due to the lack of physical findings in patients with early mesenteric insufficiency, an aggressive diagnostic approach is recommended in the appropriate clinical setting in order to avoid delays in diagnosis, which have been shown to have a significant impact on mortality. NOMI is a disease that continues to be unrecognized until the clinical picture is far advanced. Only clinicians with a high index of suspicion in those patients with the appropriate risk factors will suspect NOMI, which will facilitate an early diagnosis prior to the onset of intestinal necrosis, gangrene, peritonitis, and cardiovascular collapse.
Patients suspected of having AMI require early surgical consultation, and elderly patients with undiagnosed abdominal pain also need surgical consultation. A major pitfall is the failure of emergency physicians to obtain angiography in patients older than 50 with more than two hours of abdominal pain who have risk factors for AMI. Failing to obtain angiography results in failing to diagnose patients while they are still salvageable. Clinical judgement must prevail, and evaluation should be individualized.
1. Kaleya R, Sammartano R, Boley S. Aggressive approach to acute mesenteric ischemia. Surg Clin North Am 1992;72:157-184.
2. Moneta G, Lee R. Diagnosis of intestinal ischemia. In: Rutherford R. Vascular Surgery Vol. 2. Philadelphia: WB Saunders; 1995:1267-1278.
3. McGovern R, Franco R. Acute mesenteric ischemia after colonoscopy. Am J Gastroenterol 1995;90:170.
4. Taylor L, Porter J. Treatment of acute intestinal ischemia caused by arterial occlusions. In: Rutherford R. Vascular Surgery Vol 2. Philadelphia: WB Saunders; 1995:1278-1285.
5. Halkin A, Leibowitz, D. Management of acute mesenteric ischemia. New Engl J Med 1996;335:594.
6. Flinn W, Bergan J. Visceral ischemic syndromes: Obstruction of the superior mesenteric artery, celiac axis, and inferior mesenteric artery. In: Sabiston D, et al. eds. Textbook of Surgery: The Biological Basis of Modern Surgical Practice. Philadelphia: WB Saunders; 1997:1750-1759.
7. Stern J. Arteries to the gut and to its associated structures. In: Essentials of Gross Anatomy. Philadelphia: FA Davis Company; 1988:214-223.
8. Sterns E. Acute abdominal pain. In: Clinical Thinking in Surgery. Norwalk: Appleton and Lange; 1988:359-374.
9. Silen, W. The principles of diagnosis in acute abdominal disease. In: Cope’s Early Diagnosis of the Acute Abdomen. 18th ed. Oxford: Oxford University Press; 1991:3-19.
10. Sinanan M. Acute abdomen and appendix. In: Greenfield L, Mulholland M, Oldham K, et al. Surgery: Scientific Principles and Practice. Philadelphia: JB Lippincott; 1993:1120-1130.
11. Patel A, Kaleya R, Sammartano R. Pathophysiology of mesenteric ischemia. Surg Clin North Am 1992;72:31-41.
12. Levine J, Jacobson E. Intestinal ischemic disorders. Dig Dis 1995;13:3-24.
13. Unknown. Acute mesenteric ischemia: Pathophysiology, diagnosis, and treatment. Disease-a-Month 1993;39:131-210.
14. Zimmerman B, Granger D. Reperfusion injury. Surg Clin North Am 1992;72:65-83.
15. Schneider T, Longo W, Ure T, et al. Mesenteric ischemia: Acute arterial syndromes. Dis Colon Rectum 1994;37:1163-1174.
16. Scully R, Mark E, McKneely F, et al. Case records of the Massachusetts General Hospital: Weekly clinicopthological exercises.N Engl J Med 1995;332:804-810.
17. Walls R, Ho K. Mesenteric ischemia and infarction. In: Harwood-Nuss A, et al. eds. The Clinical Practice of Emergency Medicine. Philadelphia: Lippincott-Raven; 1996; 181-184.
18. Batellier J, Kieny R. Superior mesenteric artery embolism: Eighty-two cases. Ann Vasc Surg 1990;4:112-116.
19. Jarvinen O, Laurika J, Sisto T et al. Arteriosclerosis of the visceral arteries. VASA 1995;24:9-14.
20. Glover J, Blossom G. Mesenteric ischemia. In: Tintinalli J, Ruiz E, Krome R, et al. Emergency Medicine: A Comprehensive Study Guide. 4th ed. New York: McGraw-Hill; 1996;387-389.
21. Rhee R, Gloviczki P, Mendonca CT, et al. Mesenteric venous thrombosis: Still a lethal disease in the 1990s. J Vasc Surg 1994;20:688-697.
22. Boley S, Kaleya RN, Brandt LJ, et al. Mesenteric venous thrombosis. Surg Clin North Am 1992;72:183-202.
23. Kazmers A. Intestinal ischemia caused by venous thrombosis. In: Rutherford R. Vascular Surgery Vol 2. Philadelphia: WB Saunders; 1995:1288-1300.
24. Cecil B, Brandt L. Vascular disorders of the intestine. In: Bennett J, Plumb F. Cecil Text book of Medicine. 20th ed. Philadelphia: WB Saunders; 1997:20.
25. Hilaly M, Abu-Zidan F. Mesenteric vein thrombosis: Is it one disease? Eur J Vasc Endovasc Surg 1995;9:103-106.
26. Zigrossi P, Campanini M, Borden G, et al. Portal and mesenteric thrombosis in protein s deficiency. Am J Gastroenterol 1996;91:163-165.
27. Krummen D, Cannova J, Screiber H. Conservative management strategy for pancreatitis-associated mesenteric venous thrombosis. Am Surg 1996;62:432-434.
28. Coralnick J, Budin J, Sedarat A. Inferior mesenteric vein thrombosis in Crohn’s Disease: CT diagnosis. J Comput Assist Tomogr 1996;20:168-169.
29. Reinus J, Brandt L, Boley S. Ischemic diseases of the bowel. Gastroenterol Clin North Am 1990;19:319-343.
30. Howard T, Plaskon L, Wiebke EA, et al. Nonocclusive mesenteric ischemia remains a diagnostic dilemma. Am J Surg 1996;171:405-408.
31. Wilcox, M, Howard T, Plaskon L, et al. Current theories of pathogenesis and treatment of nonocclusive mesenteric ischemia. Dig Dis Sci 1995;40:709-716.
32. Rivers S, Veith F. Nonocclusive mesenteric ischemia. In: Rutherford R. Vascular Surgery Vol 2. Philadelphia: WB Saunders 1995;1284-1289.
33. Gennaro M, Ascer E, Matano R, et al. Acute mesenteric ischemia after cardiopulmonary bypass. Am J Surg 1993;166:231-235.
34. Kim E, Gewertz B. Chronic digitalis administration alters mesenteric vascular reactivity. J Vasc Surg 1987; 5:382.
35. Cunningham C, Reilly L, Stoney R. Chronic visceral ischemia. Surg Clin North Am 1992;72:231-245.
36. Myers S, et al. Chronic intestinal ischemia caused by intravenous cocaine use: Report of two cases and review of the literature. J Vasc Surg 1996;23:724-729.
37. Cipolla D, Boley S, Luchs S, et al. Chronic mesenteric ischemia presenting as chronic diarrhea and weight loss with pneumatosis intestinalis. Gastroenterologist 1996;4:134-141.
38. Thompson J, Bragg L, West W. Serum enzyme levels during intestinal ischemia. Ann Surg 1990;211:369-373.
39. Kurland B, Brandt L, Delany H. Diagnostic tests for intestinal ischemia. Surg Clin North Am 1992;72:85-104.
40. Lange H, Jackel R. Usefulness of plasma lactate concentration in the diagnosis of acute abdominal disease. Eur J Surg 1994;160:381-384.
41. Hockberger R, Henneman P, Boniface K. Mesenteric vascular occlusion. In: Rosen P, et al. Emergency Medicine: Concepts and Clinical Practice Vol 2. St. Louis: Mosby; 1992;1638-1642.
42. Wolf E, Sprayregen S, Bakal C. Radiology in intestinal ischemia. Surg Clin North Am 1992;72:107-124.
43. Scholz F. Ischemia bowel disease. Radio Clin North Am 1993;31:1197-1218.
44. Klein H, Lensing R, Kosterhalfen B, et al. Diagnostic imaging of mesenteric infarction. Radiology 1995;197:79-82.
45. Taourel P, Deneuville M, Praden J, et al. Acute mesenteric ischemia: Diagnosis with contrast-enhanced CT. Radiology 1996; 199:632-636.
46. Danse E, et al. Acute intestinal ischemia due to occlusion of the superior mesenteric artery: Detection with Doppler sonography. J Ultrasound Med 1996;15:323-326.
47. Walker J, Dire D. Vascular abdominal emergencies. Emerg Med Clin North Am 1996;14:571-592.
48. Bakal C, Sprayregen S, Wolf E. Radiology in intestinal ischemia: Angiographic diagnosis and management. Surg Clin North Am 1992;72:125-141.
49. Jamieson W, et al. Myocardial and circulatory performance during ischemic phase of superior mesenteric artery occlusion. Can J Surg 1993;36:435-439.
50. Turegano-Fuentes F, de Tomas-Palacios J, Perez-Diaz D, et al. Acute arterial syndromes in mesenteric ischemia. Dis Colon Rectum 1995;38:778-779.
51. Turegano-Fuentes F, Simo Muerza G, Echenaguisa Belda A, et al. Successful intra-arterial fragmentation and urokinase therapy in superior mesenteric artery embolisms. Surgery 1995;117:712-714.
52. Gallego A, Ramirez P, Rodriguez JM, et al. Role of urokinase in the superior mesenteric artery embolism. Surgery 1996;120:111-113.
53. McBride K, Gaines P. Thrombolysis of a partially occluding superior mesenteric artery thromboembolus by infusion of streptokinase. Cardiovasc Intervent Radiol 1994;17:164-166.
54. Hallisey M, et al. Angioplasty for the treatment of visceral ischemia. J Vasc Intervent Radiol 1995;6:785-791.
55. Bocchini T, Hoffman J, Zuckerman D. Mesenteric ischemia due to an occluded superior mesenteric artery treated by percutaneous transluminal angioplasty. J Clin Gastroenterol 1995;20:86-88.
56. Rivitz SM, Geller SC, Hahn C, et al. Treatment of acute mesenteric venous thrombosis with transjugular intramesenteric urokinase infusion. J Vasc Intervent Radiol 1995;6:219-228.
57. Babu S, Shah P. Celiac territory ischemic syndrome in visceral artery occlusion. Am J Surg 1993;166:227-230.
58. Taylor L, Porter J. Treatment of chronic visceral ischemia. In: Rutherford R, et al. Vascular Surgery Vol 2. Philadelphia: WB Saunders; 1995;1301-1311.
41. The most extensive bowel injury pattern seen intraoperatively is in patients with:
A. mesenteric venous thrombosis.
B. nonocclusive mesenteric ischemia.
C. mesenteric arterial thrombosis.
D. mesenteric arterial emboli.
42. All of the following physical exam findings are expected in a late presentation of AMI except:
A. abdominal percussion tenderness.
B. abdominal pain out of proportion to physical findings.
C. rigid abdomen.
D. involuntary guarding with shock.
43. The first radiological evaluation that should be done on a patient suspected of having AMI is:
A. abdominal ultrasound.
B. visceral angiography.
C. abdominal x-rays (flat and upright).
D. computed tomography.
E. magnetic resonance imaging.
44. The most common finding in early mesenteric ischemia or abdominal x-rays is:
A. air fluid levels.
B. free intra-abdominal air.
E. splenic flexure cut off sign.
45. Findings highly suggestive of AMI on plain radiography include all of the following except:
B. portal venous gas.
C. free intra-abdominal air.
D. thumbprinting of abdominal wall.
46. What is the appropriate initial management of patients diagnosed as angiography with nonocclusive mesenteric ischmeia without peritoneal findings?
A. Urokinase infusion
B. Exploratory laparotomy
C. Intra-arterial papaverine infusion
D. Systemic heparinization
47. Visceral pain:
A. is derived from receptors located in the parietal peritoneum.
B. is triggered by such stimuli as touch, cutting, ischemia, pressure, heat, or inflammation.
C. produces guarding.
D. is triggered by such stimuli as smooth-muscle contraction or spasm, distention or stretching, and ischemia, but not by physical palpation or temperature.
48. The majority of mesenteric arterial emboli lodge in the:
A. superior mesenteric artery (SMA).
B. the celiac trunk.
C. the inferior mesenteric artery (IMA).
D. none of the above