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A Rare Cause of Small-Bowel Ischemia

Educational Objective
Based on this clinical scenario and the accompanying image, understand how to arrive at a correct diagnosis.
1 Credit CME

A 68-year-old African American man presented to the emergency department with 72 hours of progressively worsening diffuse abdominal pain, distension, nausea, and nonbilious emesis. He was previously healthy and had no prior abdominal operations. The patient noted pencil-thin stools that occurred during the past several months but had not had a colonoscopy in more than a decade. The rest of his history was noncontributory. He was mildly tachycardic but normotensive and afebrile. Physical examination revealed a lethargic patient with a distended abdomen, diffuse rebound tenderness, and involuntary guarding. No surgical scars or inguinal hernias were apparent on examination. The only abnormal laboratory values were as follows: sodium concentration, 126 mEq/L (reference range, 135-145 mEq/L) (to convert to millimoles per liter, multiply by 1); lactate concentration, 58.6 mg/dL (reference range, 0-18.0 mg/dL) (to convert to millimoles per liter, multiply by 0.111); and white blood cell count, 18 500/μL (reference range, 3400-10 000/μL) (to convert to ×109/L, multiply by 0.001). He was resuscitated with 2 L of lactated Ringer solution and underwent computed tomography of the abdomen and pelvis with intravenous contrast. Computed tomography revealed diffuse free fluid but without free air and several loops of dilated small bowel with thickened, hypoenhancing bowel walls. The mesentery was markedly edematous (Figure). The rest of the small bowel were dilated and air and fluid filled but had normal bowel wall enhancement. The colon was normal.

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C. Mesenteric venous thrombosis

Acute mesenteric venous thrombosis has an estimated incidence of 2.7 per 100 000 population.1 Its origin is multifactorial and can be divided into acquired vs inherited conditions. Localized inflammatory processes, such as infection, trauma, pancreatitis, or tumor leading to compression or invasion into surrounding structures, may increase the risk of mesenteric venous thrombosis that affects predominantly the larger veins. If cirrhosis and solid organ neoplasms, the most common underlying causes, have been ruled out, diagnostic studies for thrombophilia and myeloproliferative disorders should performed.2 Nonoperative treatment for mesenteric venous thrombosis centers around anticoagulation along with treatment of the underlying process.3

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Article Information

Corresponding Author: Matthew Y. C. Lin, MD, Division of General Surgery, University of California, San Francisco, 513 Parnassus Ave, Health Sciences West 1601, San Francisco, CA 94143-1932 (matthew.lin@ucsf.edu).

Published Online: November 29, 2017. doi:10.1001/jamasurg.2017.4595

Conflict of Interest Disclosures: None reported.

Additional Contributions: We thank the patient for granting permission to publish this information.

References
1.
Hmoud  B, Singal  AK, Kamath  PS.  Mesenteric venous thrombosis.  J Clin Exp Hepatol. 2014;4(3):257-263.PubMedGoogle ScholarCrossref
2.
De Stefano  V, Qi  X, Betti  S, Rossi  E.  Splanchnic vein thrombosis and myeloproliferative neoplasms: molecular-driven diagnosis and long-term treatment.  Thromb Haemost. 2016;115(2):240-249.PubMedGoogle ScholarCrossref
3.
Clair  DG, Beach  JM.  Mesenteric ischemia.  N Engl J Med. 2016;374(10):959-968.PubMedGoogle ScholarCrossref
4.
Selinger  HA, Ma  X.  Jakking up tumor registry reporting of the myeloproliferative neoplasms.  Am J Hematol. 2009;84(2):124-126.PubMedGoogle ScholarCrossref
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Vardiman  JW, Thiele  J, Arber  DA,  et al.  The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes.  Blood. 2009;114(5):937-951.PubMedGoogle ScholarCrossref
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Baxter  EJ, Scott  LM, Campbell  PJ,  et al; Cancer Genome Project.  Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders.  Lancet. 2005;365(9464):1054-1061.PubMedGoogle ScholarCrossref
7.
Tefferi  A, Elliott  M.  Thrombosis in myeloproliferative disorders: prevalence, prognostic factors, and the role of leukocytes and JAK2V617F.  Semin Thromb Hemost. 2007;33(4):313-320.PubMedGoogle ScholarCrossref
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