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Portal Vein Thrombosis: an Unexpected Finding in a 28-Year-Old Male with Abdominal Pain

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Portal Vein Thrombosis: an Unexpected Finding in a 28-Year-Old Male with Abdominal Pain J Am Board Fam Med: first published as 10.3122/jabfm.2008.03.070157 on 8 May 2008. Downloaded from BRIEF REPORT Portal Vein Thrombosis: An Unexpected Finding in a 28-Year-Old Male With Abdominal Pain Jason L. Ferguson, DO, and Duane R. Hennion, MD Background: Abdominal pain is a common primary care complaint. Portal vein thrombosis (PVT) is a rare cause of abdominal pain, typically associated with cirrhosis or thrombophilia. The following de- scribes the presentation of PVT in a young male, the search for risk factors and underlying etiology, and the debate of anticoagulation therapy. Case: A 28-year-old male presented with periumbilical pain, post-prandial nausea, and sporadic he- matemesis for 3 weeks. The diagnosis was confirmed with a triphasic liver computerized tomography after obtaining an abnormal right upper quadrant ultrasound. This unexpected finding prompted inves- tigation for intrinsic hepatic disease and potential hypercoagulable disorders. Laboratory analysis re- vealed a heterozygous genotype for the prothrombin 20210G/A mutation, an identified risk factor for venous thrombosis. Discussion: Recommendations concerning anticoagulation for PVT in the absence of cirrhosis are not clearly defined. Current literature describes the following factors as indications for anticoagulation: acute thrombus, lack of cavernous transformation, absence of esophageal varices, and mesenteric ve- nous thrombosis. This patient had clinical indications both for and against anticoagulation. Weighing this individual’s clinical circumstances, we concluded the risk of thrombus in the setting of a hypercoag- ulable disorder outweighed the risk of variceal bleeding. A minimum of 6 months of anticoagulation was initiated. copyright. Conclusion: PVT is an uncommon cause of abdominal pain, and the absence of hepatic disease should raise the index of suspicion for an underlying thrombophilia. Specific recommendations for an- ticoagulation are not well defined, demonstrating the importance of weighing the individual risks and benefits in treatment with anticoagulation for young persons with thrombophilia. (J Am Board Fam Med 2008;21:237–243.) Abdominal pain has been shown in the general lable states. The prevalence of idiopathic PVT is http://www.jabfm.org/ population to make up between 4.4% and 7.5% of not well known but experts agree it is rare.12,16 The primary care and emergency department visits.1–3 following case report describes the clinical presen- Although the spectrum of disease processes pro- tation of a young adult male with abdominal pain ducing abdominal pain is vast, portal vein throm- and the subsequent discovery of PVT, the etiology bosis (PVT) is not commonly considered in the of which can probably be attributed to a heterozy- differential diagnosis among the average, otherwise gous prothrombin gene mutation. In addition to healthy, adult population. Although PVT has been the statistical contrast between this common pre- on 30 September 2021 by guest. Protected well documented since 1868, the entity is usually senting complaint and rare subsequent diagnoses, associated with cirrhosis, liver transplantation, ma- this case is distinct because recommendations for lignancies, inflammatory disorders, or hypercoagu- anticoagulation are vaguely defined for individuals with the heterozygous prothrombin gene and ve- nous thromboses. This article was externally peer reviewed. Submitted 26 June 2007; revised 25 December 2007; ac- cepted 7 January 2008. From the Department of Family Medicine, Tripler Army Case Report Medical Center, Honolulu, HI. Funding: none. A 28-year-old white male presented with a chief Conflict of interest: none declared. complaint of a 3-week history of mid-epigastric Corresponding author: Jason L. Ferguson, DO, Depart- ment of Family Medicine, Tripler Army Medical Center, pain described as a “tight band” surrounding his Honolulu, HI 96859 (E-mail: [email protected]). abdomen. This 3-inch horizontal, band-like distri- doi: 10.3122/jabfm.2008.03.070157 Abdominal Pain and Portal Vein Thrombosis 237 J Am Board Fam Med: first published as 10.3122/jabfm.2008.03.070157 on 8 May 2008. Downloaded from bution included the umbilicus and radiated to the Table 1. Initial Laboratory Results patient’s back bilaterally. The abdominal pain was Laboratory Exam Result Reference Range associated with meals, consisting of a significant increase in pain approximately 10 to 15 minutes White blood cell count 3,200 cells/mm3 3.9 to 10.6 after eating and intermittent post-prandial nausea Hemoglobin 14.5 g/dL 13.3 to 17.7 and occasional vomiting. The patient reported a Hematocrit 43.2% 40.0 to 53.1 3 single episode of hematemesis and 2 melena stools Platelets 99,000/mm 150 to 440 AST 35 IU/L 0 to 37 approximately 1 week before presentation to the ALT 51 IU/L 0 to 51 clinic. He denied hematochezia, changes in stool GGT 38 IU/L 11 to 51 consistency or frequency, weight loss, night sweats, Alkaline phosphatase 127 IU/L 38 to 126 or easy bruising or bleeding. There was no history Total bilirubin 0.8 mg/dL 0.2 to 1.0 of recent travel, unusual environmental exposures, Direct bilirubin 0.2 mg/dL 0 to 0.3 or any trauma to the abdomen. The patient noted Amylase 47 IU/L 30 to 110 1 month of increasing fatigue and a 10-pound Lipase 29 IU/L 0 to 190 weight loss, which he had attributed to altering his Blood urea nitrogen 10 mg/dL 6 to 20 diet to find meals that did not exacerbate his pain or Creatine – serum 0.7 mg/dL 0.8 to 1.4 nausea. His medical history was significant for gas- Prothrombin time 13.9 sec 11.7 to 14.2 troesophageal reflux disease diagnosed 4 years ear- INR 1.1 1.0 lier. He has smoked one-half of a pack of cigarettes Partial thromboplastin time 30 sec 24 to 36 per day and has drank 2 to 3 glasses of beer on the AST, aspartate transaminase; ALT, alanine aminotransferase; weekends for the last 3 years. The patient denied GGT, gamma glutamyltransferase; INR, international normal- having any previous surgeries nor was he taking any ized ratio. medications at the time of presentation. His family history was noncontributory, specifically for bowel biliary colic. The ultrasound demonstrated a nor- copyright. disease or bowel cancer, and negative for any his- mal-appearing liver and gallbladder but was signif- tory of bleeding or clotting disorders. icant for an enlarged spleen with an apparent small On physical examination, the patient was noted to be afebrile with a normal blood pressure and a portal vein and several serpiginous vessels, sugges- heart rate of 56, which was thought to be physio- tive of PVT with cavernous transformation. This logic per the patient’s aerobic fitness level. Specific finding was further confirmed with a triphase liver examination findings were sparse spider angiomas computerized tomography (CT) scan which involving the upper chest and neck and some mild showed a decrease of opacification in the main http://www.jabfm.org/ tenderness to palpation over the periumbilical and portal vein with several collateral vessels in the epigastric region. The patient did not have an ap- splenic hilum as well as the porta hepatis. The scan preciably enlarged liver or spleen on palpation. He further described thrombosis into the superior did not demonstrate signs of icteric or pale sclera mesenteric vein as well (see Figure 1). nor did he have jaundiced appearance or pale pal- In light of the finding of PVT with the prior mar creases. He did not have signs of asterixis. A history of hematemesis and melena, the patient rectal examination was negative for gross blood and underwent esophagogastroduodenoscopy, which on 30 September 2021 by guest. Protected was also negative for occult blood. Laboratory revealed Grade II–III nonbleeding esophageal var- studies in general showed sings of hypersplenism ices in the distal esophagus. Variceal band ligation with a mildly decreased white blood cell count and (VBL) was performed for suspected recurrent thrombocytopenia and also demonstrated a mild bleeding and as secondary prophylaxis. With an transaminitis. His blood cell lines did not suggest a unknown etiology for PVT, additional laboratory severe blood loss given his history, nor did they serum studies were performed to search for hyper- suggest an infectious, inflammatory, or malignant coagulable disorders as well as evidence of intrinsic process in regards to his chief complaint. See Table hepatic disease. The ensuing laboratory studies 1 for initial laboratory results. were normal, with the exception that the patient A right upper quadrant ultrasound was per- was determined to be heterozygous for the pro- formed to evaluate for cholelithiasis because the thrombin 20210G/A gene mutation (see Table 2). history of post-prandial pain was concerning for This genetic mutation has been shown to be a risk 238 JABFM May–June 2008 Vol. 21 No. 3 http://www.jabfm.org J Am Board Fam Med: first published as 10.3122/jabfm.2008.03.070157 on 8 May 2008. Downloaded from venous system. After 2 weeks, the severity and fre- quency of the patient’s post-prandial pain and nau- sea had decreased significantly. He was completely asymptomatic by 1-month postdischarge. A repeat CT of the abdomen is currently pending to evalu- ate resolution of the thrombus. The patient will remain on warfarin therapy with an INR goal of 2.0 to 2.5 for 6 to 12 months. Discussion PVT as the etiology of abdominal pain in an oth- erwise healthy young adult is an uncommon occur- rence and raises several questions. What are the etiologies for and prevalence rates of PVT, espe- cially in a noncirrhotic patient? What is the signif- icance of the prothrombin 20210G/A mutation and the impact on relative risk of thrombosis? What are Figure 1. Selected computed tomography image with the treatment options for a patient with noncir- arrow indicating thrombosis within the portal vein and rhotic PVT and the prothrombin gene mutation as evidence of cavernous formation.
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