Unusual Cause of Bleeding in Liver Cirrhosis Patient

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    Clinical picture

    Unusual cause of bleeding in liver cirrhosis patient

    A 42-year-old man presented to the emergencydepartment with 2 weeks history of fatigue anddark tarry stool. He had past medical history signifi-cant for primary sclerosing cholangitis with livercirrhosis, complicated with ascites and small non-bleeding esophageal varices. He denied nausea,vomiting, abdominal pain, weight loss or changein appetite. He also denied excessive use ofnon-steroid anti-inflammatory drugs (NSAIDs). On

    presentation he was on spironolactone, furosomide,omeprazole and nadalol. On exam, he appearedpale with stable vitals signs. Skin examinationrevealed spider angiomata and palmar erythema.Abdomen was non-distended with no abdominaltenderness or organomegaly. There was no asterixis.Initial blood work revealed hemoglobin of 5.8 g/dl(normal 13.517.5g/l) down from his baseline of13g/dl. Platelet count was 87/ml (normal 150000400 000/ml). Prothrombin time and INR were15.2 s (normal 9.913 s) and 1.8 (normal 0.91.2),respectively. His Childs Pugh Score was 7 (Class B),Model of End-Stage Liver Disease (MELD) score was 8.

    The patient received two units of packed red bloodcells and two units of fresh frozen plasma.Continuous intravenous esomeprazole and octreo-tide were started soon after admission. The patientunderwent esophagogastroduodenoscopy (EGD).This revealed duodenal bulbar varices without stig-mata of bleeding (Figure 1). Endoscopic ultrasound(EUS) showed a submucosal anechoic lesion corres-ponding to the endoscopic finding in the second

    portion of the duodenum (Figure 2). Color Dopplerimaging revealed a vascular lesion. Patienthemoglobin responded well to blood transfusionand remained stable. Liver vascular ultrasoundshowed patent hepatic vasculature. Echocardiogramshowed normal right ventricular size and function.The patient underwent transjugular intrahepaticportosystemic shunt (TIPS) procedure which resultedin a decrease in the porto-systemic pressure gradientfrom 23 to 5 mmHg. He was discharged home fewdays later in a stable condition.

    Patients with liver cirrhosis have an increased riskof mortality and morbidity due to their susceptibility

    Figure 1. (A) EGD showing duodenal bulbar varices without stigmata of bleeding (arrow). (B) Normal duodena mucosa.

    ! The Author 2012. Published by Oxford University Press on behalf of the Association of Physicians.All rights reserved. For Permissions, please email: [email protected] Page 1 of 3

    Q J Meddoi:10.1093/qjmed/hcs151

    QJM Advance Access published August 11, 2012

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    to a variety of complications.1 Variceal bleeding is

    one of the most life-threatening complications in

    cirrhotics, with mortality up to 30% for each bleed-

    ing episode.2 The prevalence of duodenal varices in

    cirrhotic patient has been reported at about 0.4%.3

    Bleeding duodenal varices is known to be severeand often life threatening.4 This prompts early diag-

    nosis and treatment. Although esophageal varicesare easily diagnosed with EGD alone, the sub-

    mucosal location and the lack of red color signs of

    duodenal varices pose a diagnostic challenge.5 Anycirrhotic patient with GI bleed should undergo a

    thorough endoscopic evaluation of the duodenum.

    When the diagnosis is in doubt, EUS, is a valuabletool in confirming the diagnosis. There are mul-

    tiple therapeutic options in the management of

    duodenal varices which include: (i) non-selective

    beta blockers; (ii) TIPS procedure; (iii) endoscopic

    management of varices with ligation and glue

    injection; and (iv) balloon-occluded retrograde

    transvenous obliteration.5,6 However, a case bycase management decision has to be made taking

    into consideration the experience of the physician

    and available therapeutic options. In our patient, he

    underwent TIPS with no further bleeding on

    subsequent follow-ups.

    Acknowledgements

    All authors had access to the manuscript and a rolein writing the manuscript.

    Photographs and text from: Shadi Al Halabi,Digestive Disease Institute, Cleveland Clinic,Cleveland, OH, USA; M. Chadi Alraies, ClinicalAssistant Professor of Medicine, Cleveland ClinicLerner College of Medicine of Case WesternReserve University, Department of HospitalMedicine, Cleveland Clinic, Cleveland, OH, USA;Abdul Hamid Alraiyes, Department of PulmonaryDiseases, Critical Care & Environmental Medicine,Tulane University Health Sciences Center, New

    Orleans, LA, USA; Ibrahim Hanouneh, DigestiveDisease Institute, Cleveland Clinic, Cleveland, OH,USA; William D. Carey, Professor of Medicine,Cleveland Clinic Lerner College of Medicine ofCase, Western Reserve University, Center forContinuing Education and Digestive DiseaseInstitute, Cleveland Clinic, Cleveland, OH, USA.email: [email protected]

    Conflict of interest: None declared.

    References1. Sorensen HT, Thulstrup AM, Mellemkjar L, Jepsen P,

    Christensen E, Olsen JH, et al. Long-term survival and

    cause-specific mortality in patients with cirrhosis of the

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    hemorrhage. Gastroenterology1981; 80:8009.

    3. Hashizume M, Tanoue K, Ohta M, Ueno K, Sugimachi K,

    Kashiwagi M, et al. Vascular anatomy of duodenal varices:

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    Gastroenterol1993; 88:19425.

    Figure 2. EUS showing anechoic lesion corresponding to the endoscopic finding of the duodenum consistent with vascularlesion (arrow).

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    4. Amin R, Alexis R, Korzis J. Fatal ruptured duodenal varix: a

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