Acute Mesenteric Ischemia

A 52-year-old man presented to theemergency department (ED) with a12-hour history of cramping abdominalpain, nausea, vomiting, andwatery, brown diarrhea. Mid upperquadrantpain had begun suddenlythe night before, 1 hour after the patienthad lifted heavy bags of rocks.The GI symptoms persisted with varyingintensity throughout the night.

The patient's white blood cell(WBC) count was 17,000/μL (no leftshift). Viral gastroenteritis was diagnosedby the ED physicians.

Very mild right-sided weakness andoccasional "pins and needles" sensationsin the right leg were residual effects of astroke the patient had suffered 9 yearsearlier. He also had hypercholesteremia,with a high low-density lipoprotein leveland a low high-density lipoprotein level(36 mg/dL). The patient was takinggemfibrozil, fexofenadine, and aspirin.

In the ED, intravenous narcoticswere needed to control the severe abdominalpain. Because of the extremepain and the history of cerebral infarction,bowel ischemia was considered inthe differential diagnosis. A contrastenhancedCT scan of the abdomenshowed a linear band with lack of contrastenhancement to the proximal portionof the superior mesenteric artery(Figure); this raised the suspicion of dissection.A CT angiogram confirmed thediagnosis of superior mesenteric arterydissection with concomitant celiacartery dissection.

The workup included assessmentof protein C and protein S activity andlupus anticoagulant, anticardiolipinantibody, and factor V Leiden levels.No abnormality was identified exceptfor an elevated C-reactive protein levelof 1.07 mg/dL (normal, 0.026 to 0.5mg/dL). The erythrocyte sedimentationrate was 10 mm/h (normal, 0 to 10mm/h); the glycated hemoglobin levelwas normal.

Intravenous heparin, pravastatin,and dextran were given; the pain resolvedin 48 hours. Warfarin was prescribed,a therapeutic internationalnormalized ratio was attained, and thepatient was discharged on the ninthhospital day. He was lost to follow-up.

CLINICAL FEATURES
Acute mesenteric ischemia-which is more common than chronicischemia-often remains undiagnoseduntil the bowel dies and mustbe resected. The arterial tree is involvedmore frequently than the venoussystem. Inadequate blood supplyfrom the superior mesentericartery causes ischemia in the smallintestine and the right half of the colon.Reduced blood flow from the inferiormesenteric artery leads to ischemiaof the distal transverse colonand proximal rectum. Possible sequelaerange from transient alterationsin bowel function to hemorrhageand death.

About 75% to 90% of affected patientspresent with acute abdominalpain that is usually out of proportionto the early physical findings (Table1). Typically, the pain is of suddenonset and followed by rapid and oftenforceful bowel evacuation. Occasionally, unexplained abdominal distentionor bleeding may be the only symptom.Distention, though uncommon,may signify the initial stage of intestinalinfarction.

When ischemia is associatedwith acute vessel wall dissection,nausea and vomiting often occur anda bruit may be heard. As many as75% of patients have occult blood inthe stool; maroon or bright redblood is likely from the right colonor small intestine and raises concernthat the superior mesenteric arteryis involved. Mental confusion can bean acute sign, especially in elderlypersons. Up to 75% of patients haveleukocytosis (WBC count greaterthan 15,000/μL).¹

CAUSES
The causes of acute ischemia aremany and varied (Table 2).^1,2 Spontaneousarterial dissection can occur incentral and peripheral vessels. Visceralarteries can be involved; the superiormesenteric artery is most frequentlyaffected. Many cases of carotid dissectionhave been reported.^3-5 Dissectionsoccur in the outer layer of the mediaand produce a characteristic doublelumen with separated smooth musclecells, decreased elastic tissue, anddegeneration of the internal elasticmembrane.

Silent and asymptomatic dissectionof the superior mesenteric arteryhas been reported. The thrombus inthe "false lumen" was absorbed withina month of detection; it did notrecur during 4 years of follow-up.⁶

DIAGNOSIS
Given the acute nature and gravityof the disease, intestinal ischemianeeds to be diagnosed promptly;however, early markers to aid diagnosishave been elusive. Both increasedplasma lactate concentration and elevatedD-dimer levels have been investigatedand show promise as markersof bowel ischemia.^7,8

TREATMENT
Therapeutic options are revascularization,resection, and anticoagulation.Nonoperative management ofsuperior mesenteric artery dissectionmay fail. According to one report, 12months after a 46-year-old man begantaking empiric heparin followed bywarfarin for dissection, an angiogramconfirmed disease progression. Operativerepair was curative.⁹

Successful reconstruction of visceralarteries affected by atheroscleroticaneurysms has been reported^10,11; however, most of the dissectionsor ruptures lead to resection,splenectomy, or death.³

Newer treatments have beenused with success. One investigationincluded 23 patients with chronicmesenteric ischemia who underwentpercutaneous transluminal angioplasty;the clinical success rate was 88%,and the incidence of complicationswas low.¹² Angioplasty with stentplacement has also been tried.^13,14 Inan animal model of mesenteric ischemia,verapamil enhanced cellularpreservation and cell recovery, presumablyby reducing the intracellularcalcium influx.¹⁵

In a 78-year-old man, spinal cordstimulation was used to alleviate unrelentingpain caused by mesentericischemia after oral narcotics and sympatheticceliac plexus block hadfailed.¹⁶ The stimulator continued toprovide complete analgesia 11 monthsafter implantation.

References:

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