Mesenteric artery thrombosis has the highest mortality rate of all causes of mesenteric ischemia. First described in the late 15th century, little progress was made in its treatment before the 20th century.
In 1901, a patient with a long history of postprandial pain was found to have an atherosclerotic plaque with overlying thrombus of the superior mesenteric artery (SMA). The physician concluded that if a patient could develop pain of the lower extremities secondary to atherosclerosis, it would stand to reason that a patient could present with postprandial pain due to narrowing of the mesenteric vessels. An example of complete occlusion is illustrated in the image below. The pathophysiologic mechanism by which ischemia produces pain remains poorly understood.
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Complete aortic occlusion (Leriche syndrome) with acute embolism of the superior mesenteric artery.
By the middle of the 20th century, it was generally understood that mesenteric ischemia was a manifestation of visceral atherosclerosis. In 1958, Shaw and Maynard described the first thromboendarterectomy of the SMA for the treatment of acute and chronic mesenteric ischemia. Several other surgical solutions have since been tried, ranging from reimplantation of the visceral branch into the adjacent aorta to use of autogenous vein grafts.
In 1972, Stoney and Wylie introduced transaortic visceral thromboendarterectomy and aortovisceral bypass, both very effective surgical techniques.
A patient with acute mesenteric artery thrombosis presents with acute-onset abdominal pain. The patient may give a history of postprandial pain, typically occurring 10-20 minutes after eating and lasting up to an hour. The pain is diffuse, and the patient may complain of bloody stools. Typically, the patient has a history of other arterial involvement such as recent myocardial infarction (MI) or peripheral vascular disease.
Acute mesenteric ischemia comprises 0.1% of all hospital admissions. Risk factors for arterial thrombosis include atherosclerosis, hypovolemia, congestive heart failure, recent MI, advanced age, and intra-abdominal malignancy.[1, 3] Approximately two thirds of patients are women. In a population-based study by Hansen and colleagues, mesenteric artery stenosis occurred in up to 17.5% of patients.
Research indicates that inflammatory bowel disease (IBD) is another risk factor for mesenteric artery thrombosis.[4] Ha et al reviewed 17,487 patients with either Crohn disease or ulcerative colitis, comparing them with 69,948 controls.[5] The investigators detected a significantly higher risk of acute mesenteric ischemia in the patients with IBD (hazard ratio 11.2, P < 0.001).
Thrombosis of the superior mesenteric or celiac arteries is most often associated with a preexisting atherosclerotic lesion that already compromises flow. The most common preexisting pathology found in patients with acute mesenteric thrombosis is atherosclerosis.
Many patients present with histories consistent with chronic mesenteric ischemia. Wasting, postprandial pain, and phagophobia (fear of eating) are all common.
Typically, the atherosclerotic lesion gradually compromises flow to the gut, causing a progressive worsening of symptoms. During a period of low flow, the artery thromboses, and flow to the gut is compromised.
Unlike embolic events that occur in arterial branches and result in limited bowel ischemia, thrombosis occurs at the vessel origin, resulting in extensive bowel involvement.
The atherosclerotic plaque, usually at the origin of the SMA or celiac artery, grows over time. The SMA is the most common visceral branch to thrombose.
A thrombus forms during a state of low flow, resulting in acute cessation of flow to the gut. Bloody stools develop as the more sensitive mucosa dies first.
The bowel gradually becomes necrotic; subsequently, bacterial overgrowth develops, and the resulting bowel perforation causes sepsis and finally death. Gross specimens of dead bowels are shown in the images below.
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Gross specimen of dead bowel.
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Gross specimen of hemorrhagic dead bowel after resection from a patient with acute mesenteric ischemia.
Patients with acute mesenteric artery thrombosis present with a long history of weight loss, postprandial pain, and phagophobia. Symptoms worsen over time.
Patients complain of severe, acute, unrelenting abdominal pain. They may also complain of frank blood in their stools. Medical history may be significant for stroke, MI, or peripheral artery disease. Patients may have a long history of smoking or uncontrolled diabetes.
Due to the massive shifts in fluid volume and hypercoagulable state, patients in surgical intensive care are especially prone to developing arterial thrombosis.
Upon physical examination, patients experience pain disproportionate to that which might be expected. Abdominal examination findings may be benign. If signs of peritonitis are present, consider bowel perforation.
Patients with a history of chronic mesenteric ischemia may have physical findings consistent with a malnourished state.
Laboratory examinations should include (1) prothrombin time (PT); (2) activated partial thromboplastin time (aPTT); (3) complete blood count (CBC), which may reveal leukocytosis and/or hemoconcentration; (4) chemistries, which may show acidosis or increased amylase or lactate dehydrogenase (LDH) levels; (5) chest radiography; and (6) electrocardiography. A study of 9 patients with acute mesenteric thrombosis found that the D-dimer level was higher than that of patients with IBD or bowel obstruction.[6] The authors found a D-dimer level greater than 1.5 mg/L, atrial fibrillation, and female sex increased the likelihood ratio for acute SMA occlusion to 17.5.
Plain abdominal films provide a presumptive diagnosis in 20-30% of patients. Absence of intestinal gas, distended bowel, thickened bowel wall, and air fluid levels are all nonspecific findings. Computed tomography (CT) scan findings with a specificity greater than 95% include SMA or SM vein thrombosis, intestinal pneumatosis, portal venous gas, lack of bowel-wall enhancement, and ischemia of other organs.[7]
Late findings on plain films include intramural air and air in the portal venous system (see the image below). If bowel perforation occurs, free air in the abdomen may be observed.
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Gas in the colon wall, a late radiographic sign of bowel ischemia.
Biplane aortography is the criterion standard for the diagnosis of mesenteric ischemia, and it can confirm the presence and extent of occlusive disease. Anteroposterior views demonstrate collateral pathways, while lateral projections show the origins of visceral branches.
Unlike patients with embolic disease, those with acute thrombosis have well-developed collateral circulation due to long-standing, chronic ischemia. Also, thrombosis of the SMA generally occurs flush with the aortic origin of the vessel, resulting in an aortogram that fails to demonstrate any visualization of the SMA. Patients with embolization to the SMA have an aortogram that demonstrates filling of the proximal SMA vessels to a sharp cutoff with no visualization of the distal vessels.
Because arteriography can precipitate acute ischemia, it is important to make sure that the patient is well hydrated.
Once a diagnosis of acute mesenteric thrombosis is made, the patient should undergo surgery because of the risk of bowel infarction, perforation, sepsis, and death.
Mastery of the anatomy of the mesenteric vessels is key to understanding and treating patients with mesenteric ischemia. Vascular variations can make this difficult.
The celiac axis, the SMA, and the inferior mesenteric artery (IMA) supply the foregut, midgut, and hindgut, respectively.
The celiac axis arises from the ventral surface of the aorta at the T12, L1 vertebral body. It courses anteroinferiorly before branching into the common hepatic, splenic, and left gastric arteries. Variations are too numerous to describe here.
The hepatic artery gives off the gastroduodenal artery, which branches further to the right gastroepiploic artery and the anterosuperior and posterosuperior pancreaticoduodenal arteries. The right gastroepiploic artery communicates with the left gastroepiploic artery, which is an immediate branch of the splenic artery. The anterosuperior and posterosuperior pancreaticoduodenal arteries communicate with the corresponding inferior branches from the SMA.
As previously mentioned, the splenic artery gives off the left gastroepiploic artery as well as the dorsal pancreatic artery, which supplies the body and tail of the pancreas and communicates with the anterosuperior pancreaticoduodenal and gastroduodenal arteries and sometimes the middle colic or SMA.
The third important branch off of the celiac axis is the left gastric artery, which communicates with the right gastric artery along the posterior aspect of the lesser curvature of the stomach. The celiac artery supplies most of the blood to the lower esophagus, stomach, duodenum, liver, pancreas, and spleen.
The SMA comes off the ventral aorta and supplies the midgut by giving off the inferior pancreaticoduodenal artery, middle colic, right colic, and jejunal and ileal branches.
The inferior pancreaticoduodenal artery gives rise to the corresponding anteroinferior and posteroinferior branches that anastomose with the superior counterparts as described above. This communication is but one important connection that helps to maintain bowel perfusion in times of atherosclerosis of the mesenteric vessels. For an illustration of a meandering artery, see the image below.
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Meandering artery, a radiographic sign of preexisting bowel ischemia.
The ileocolic artery supplies the ileum, cecum, and ascending colon, whereas the middle colic gives its blood supply to the transverse colon and communicates with the IMA. The right colic typically branches at the same level as the middle colic. The right and middle colic arteries are an important supply of blood to the marginal artery of Drummond and give rise to the terminal vasa recta, which provide blood to the colon.
The IMA is the smallest mesenteric vessel and also comes off the anterior aorta. The IMA provides blood to the distal transverse, descending, and sigmoid colons as well as to the rectum. Many communications exist within the mesentery to the SMA, and rectal branches offer communication of the visceral blood supply with the common blood supply. The so-called watershed area near the splenic flexure was thought to be more susceptible to ischemia secondary to poor arterial flow; however, current thought holds that the poor development of this area results in an increased propensity for ischemia.
Acute mesenteric thrombosis is a surgical emergency because of the poor outcomes of untreated patients, and it should be surgically corrected without hesitation, as is indicated by a comparison of the 2 pathologic specimens below.
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Pathologic specimen of ischemic bowel after 2 hours.
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Pathologic specimen of ischemic bowel after 24 hours.
Acute mesenteric artery thrombosis cannot be cured medically. If vasospasm is observed on arteriogram, intra-arterial papaverine may be started to improve flow, but it is not curative. Commence anticoagulation therapy immediately upon diagnosis. Thrombolytics have shown no benefit.
Surgical treatment involves exploratory laparotomy, followed by identification of the involved artery and bowel. Because thrombosis occurs at the origin of the vessel, the entire small bowel and proximal large bowel appear ischemic. In contradistinction, embolization of the SMA results in the proximal jejunum being spared, reflecting the more distal occlusion. Remove dead bowel and attempt reanastomosis. Open the affected artery and perform an endarterectomy.
Bypass techniques may also be performed using prosthetic grafts. If a patient is found to have perforated bowel on laparotomy, use an autogenous saphenous vein graft because of the decreased risk of graft infection.
Endovascular therapies have been described for chronic mesenteric ischemia, and some authors have tried thromboaspiration.[9, 10] The criterion standard remains operative exploration to allow assessment of bowel viability.
Patients with acute ischemia should have immediate repletion of fluids and correction of any acid/base abnormalities; they should then undergo surgery without delay.
All patients should receive broad-spectrum antibiotic therapy prior to the start of the operation. Type and cross 4 units of packed red blood cells prior to surgery.
Assess the viability of the bowel during direct observation. Look for peristalsis and observe the color of the bowel (ie, pink and healthy vs red and edematous).
Intraoperative Doppler ultrasonography of the bowel can provide valuable information on the patency of the vessels. One gram of intravenous fluorescein followed by bowel examination under Wood lamp illumination can delineate poorly perfused bowel.
Treat mesenteric thrombosis by revascularization or endarterectomy.[11] If not already started, begin anticoagulation therapy with intravenous heparin. Following reconstitution of arterial flow, the viability of the bowel is reassessed. Reassessment is based on clinical findings, including the color of the bowel and the presence or absence of palpable pulses.
Postoperative care should include close monitoring of blood pressure and hemoglobin level to evaluate for sepsis or hemorrhage.
Patients should continue to have postoperative heparin anticoagulation therapy in order to reduce thrombotic events, and papaverine may be administered to reduce vasospasm. Perform a 12-lead electrocardiogram to evaluate for myocardial dysfunction.
Patients can be expected to have a postoperative ileus due to bowel reperfusion.
Because of the high incidence of atherosclerosis in patients with mesenteric ischemia, it is not surprising that one of the most common postoperative complications involves MI.
Prevention of postoperative MI involves preoperatively identifying correctable coronary artery disease. During the perioperative period, use a Swan-Ganz catheter to monitor fluid and cardiac function. Finally, when cross-clamping the supraceliac aorta, the anesthesiologist can ensure myocardial protection and afterload reduction to maximize cardiac output.
Acute renal failure in the immediate postoperative period can be prevented by keeping the patient well hydrated and administering mannitol before the aorta is cross-clamped.
Other possible complications include bleeding, infection, bowel infarction, prolonged ileus, and graft infection.
Unfortunately, the outcome of patients suffering from acute thrombosis is not as good as that of patients with chronic ischemia. The average mortality rate of patients with acute thrombosis is 75-80%.[12]
For those patients who do survive, the risk of rethrombosis is high, and lifestyle may be hindered by a lifetime of total parenteral nutrition.
The diagnosis and treatment of acute mesenteric thrombosis have improved little since the late 20th century.
A retrospective study by Mamode et al found that 32% of patients were properly diagnosed prior to surgery or death. In this same review, 46 of 57 patients died from mesenteric ischemia.
Progress in the diagnosis of mesenteric thrombosis includes some advances in CT scanning and magnetic resonance imaging (MRI). While these modalities show promise, they are not the diagnostic tests of choice in suspected mesenteric thrombosis. In his study, Alpern et al found that 26% of patients were appropriately diagnosed as having ischemia by CT scan; other studies have shown similar results.
Treatment options of acute thrombosis center on surgical methods, which have changed little since the late 20th century. Some patients may be good candidates for percutaneous transluminal angioplasty with stenting, as was the patient reported by Bertran and colleagues.
Deron J Tessier, MD, Staff Surgeon, Kaiser Permanente Medical Center, Fontana, CA
Disclosure: Nothing to disclose.
Specialty Editors
Burt Cagir, MD, FACS, Assistant Professor of Surgery, State University of New York Upstate Medical University; Consulting Staff, Director of Surgical Research, Robert Packer Hospital; Associate Program Director, Department of Surgery, Guthrie Clinic
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Michael A Grosso, MD, Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital
Disclosure: Nothing to disclose.
Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Disclosure: Nothing to disclose.
Chief Editor
John Geibel, MD, DSc, MA, Vice Chair and Professor, Department of Surgery, Section of Gastrointestinal Medicine, and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director, Surgical Research, Department of Surgery, Yale-New Haven Hospital
The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthors Yale D Podnos, MD, MPH, and Russell A Williams, MBBS, to the development and writing of this article.
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