Acute Mesenteric Ischemia Clinical Presentation
- Author: Chat V Dang, MD; Chief Editor: John Geibel, MD, DSc, MA more...
History
To some extent, all types of acute mesenteric ischemia (AMI) present similarly. Differences in clinical appearance for each type are discussed below. The most important finding is pain that is disproportionate to physical examination findings. Typically, pain is moderate to severe, diffuse, nonlocalized, constant, and sometimes colicky.
Onset varies from type to type. Nausea and vomiting are found in 75% of affected patients. Anorexia and diarrhea progressing to obstipation are also common. Abdominal distention and gastrointestinal (GI) bleeding are the primary symptoms in as many as 25% of patients. Pain may be unresponsive to narcotics. As the bowel becomes gangrenous, rectal bleeding and signs of sepsis (eg, tachycardia, tachypnea, hypotension, fever, altered mental status) develop. A review of systems, looking for risk factors of AMI, should be performed.
This syndrome has a catastrophic outcome if not properly and rapidly treated. It should be considered in any patient with abdominal pain disproportionate to physical findings, gut emptying in the form of vomiting or diarrhea, and the presence of risk factors, especially age older than 50 years.
Embolic acute mesenteric ischemia
AMI from embolic causes typically has the most abrupt and painful presentation of all types, as a consequence of the rapid onset of occlusion and the inability to form additional collateral circulation. It has been described as abdominal apoplexy and can be labeled as a “bowel attack."
Often, vomiting and diarrhea (gut emptying) are observed. Patients are usually found to have a source of embolization. Because most emboli are of cardiac origin, patients often have atrial fibrillation or a recent myocardial infarction (with mural thrombus). Infrequently, patients may report a history of valvular heart disease or previous embolic episode.
Thrombotic acute mesenteric ischemia
AMI caused by a thrombus typically happens when an artery already partially blocked by atherosclerosis becomes completely occluded.
As with myocardial infarction preceded by angina pectoris, 20-50% of patients with thrombotic AMI have a history of abdominal angina. Abdominal angina is a syndrome of postprandial abdominal pain that starts soon after eating and lasts for up to 3 hours. The digestion of food requires increased perfusion of the intestine, so the mechanism is similar to that of exercise-induced angina pectoris. Weight loss, “food fear,” early satiety, and altered bowel habits may be present.
The precipitating event that initiates thrombotic AMI may be a sudden drop in cardiac output from myocardial infarction or congestive heart failure (CHF) or a ruptured plaque. Dehydration from vomiting or diarrhea due to an unrelated illness may also precipitate thrombotic AMI.
These patients have undergone a gradual progression of arterial occlusion and frequently have a better collateral supply. Bowel viability is better preserved, often leading to a less severe presentation than with embolic AMI. Symptoms tend to be less intense and of more gradual onset. As might be expected, these patients typically have a history of atherosclerotic disease at other sites, such as coronary artery disease, cerebral arterial disease, peripheral artery disease (especially aortoiliac occlusive disease), or a history of aortic reconstruction.
Nonocclusive mesenteric ischemia
Nonocclusive mesenteric ischemia (NOMI) occurs more frequently in older patients than other forms of AMI do. Often, these elderly patients are already in an intensive care unit (ICU) with acute respiratory failure or severe hypotension from cardiogenic or septic shock, or they are taking vasopressive drugs. Most of them are taking digitalis.
Symptoms typically develop over several days, and patients may have had a prodrome of malaise and vague abdominal discomfort. When infarction occurs, the clinical condition of the ICU patient deteriorates with no apparent reason. Patients may report increased pain associated with vomiting. They may become hypotensive and tachycardic, with loose bloody stool.
Mesenteric venous thrombosis
Mesenteric venous thrombosis (MVT) is often observed in a much younger patient population than other types of AMI are. MVT patients can present with an acute or subacute abdominal pain syndrome related to involvement of the small intestine rather than the colon.
The symptoms are frequently less dramatic. Diagnosis can be even more difficult, because symptoms may have been present for weeks (ie, 27% have symptoms for >30 d). Typical symptoms of MVT may have been experienced for a prolonged period with gradual worsening. The chronic form may manifest as esophageal variceal bleeding.
Many patients have a history of 1 or more of risk factors for hypercoagulability. These include oral contraceptive use, congenital hypercoagulable states, deep vein thrombosis (DVT), liver disease, tumor, and portocaval surgery.
Physical Examination
The different etiologies notwithstanding, physical examination findings are generally similar in patients with AMI. The main distinction is between early and late presentation. Early in the course of the disease, in the absence of peritonitis, physical signs are few and nonspecific. Tenderness is minimal to nonexistent. Stool may be guaiac positive.
Peritoneal signs develop late, when infarction with necrosis or perforation occurs. Tenderness becomes severe and may indicate the location of the infarcted bowel segment. A palpable tender mass may be present. Bowel sounds range from hyperactive to absent. Voluntary and involuntary guarding appears. Fever, hypotension, tachycardia, tachypnea, and altered mental status are observed. Foul breath may be noted with bowel infarction, from the putrefaction of undigested alimentary material accumulated proximal to the pathologic site.
Signs reflecting risk factors for AMI may be noted. Patients with embolic AMI may have atrial fibrillation or heart murmurs. Those with thrombotic AMI or NOMI may have an abdominal murmur or the scar from an abdominal aortic repair with or without reimplantation of the superior mesenteric artery (SMA). Those with MVT may have evidence of tumor, cirrhosis, DVT, or recent abdominal surgery.
Complications
The following are potential complications of AMI:
- Bowel necrosis necessitating bowel resection
- Septic shock
- Death
Cokkinis AJ. Observations on the mesenteric circulation. J Anat. Jan 1930;64:200-205. [Medline].
Kozuch PL, Brandt LJ. Review article: diagnosis and management of mesenteric ischaemia with an emphasis on pharmacotherapy. Aliment Pharmacol Ther. Feb 1 2005;21(3):201-15. [Medline].
Rosenblum JD, Boyle CM, Schwartz LB. The mesenteric circulation. Anatomy and physiology. Surg Clin North Am. Apr 1997;77(2):289-306. [Medline].
Leung DA, Schneider E, Kubik-Huch R, Marincek B, Pfammatter T. Acute mesenteric ischemia caused by spontaneous isolated dissection of the superior mesenteric artery: treatment by percutaneous stent placement. Eur Radiol. 2000;10(12):1916-9. [Medline].
Miyamoto N, Sakurai Y, Hirokami M, Takahashi K, Nishimori H, Tsuji K, et al. Endovascular stent placement for isolated spontaneous dissection of the superior mesenteric artery: report of a case. Radiat Med. Nov 2005;23(7):520-4. [Medline].
Ko GJ, Han KJ, Han SG, Hwang SY, Choi CH, Gham CW, et al. [A case of spontaneous dissection of the superior mesenteric artery treated by percutaneous stent placement]. Korean J Gastroenterol. Feb 2006;47(2):168-72. [Medline].
Casella IB, Bosch MA, Sousa WO Jr. Isolated spontaneous dissection of the superior mesenteric artery treated by percutaneous stent placement: case report. J Vasc Surg. Jan 2008;47(1):197-200. [Medline].
James AW, Rabl C, Westphalen AC, Fogarty PF, Posselt AM, Campos GM. Portomesenteric venous thrombosis after laparoscopic surgery: a systematic literature review. Arch Surg. Jun 2009;144(6):520-6. [Medline].
Acosta S, Nilsson TK, Bjorck M. Preliminary study of D-dimer as a possible marker of acute bowel ischaemia. Br J Surg. Mar 2001;88(3):385-8. [Medline].
Altinyollar H, Boyabatli M, Berberoglu U. D-dimer as a marker for early diagnosis of acute mesenteric ischemia. Thromb Res. 2006;117(4):463-7. [Medline].
Herbert GS, Steele SR. Acute and chronic mesenteric ischemia. Surg Clin North Am. Oct 2007;87(5):1115-34, ix. [Medline].
Hladík P, Raupach J, Lojík M, Krajina A, Voboril Z, Jon B, et al. Treatment of acute mesenteric thrombosis/ischemia by transcatheter thromboaspiration. Surgery. Jan 2005;137(1):122-3. [Medline].
Hansen KJ, Deitch JS. Transaortic mesenteric endarterectomy. Surg Clin North Am. Apr 1997;77(2):397-407. [Medline].

