QJM Advance Access published August 11, 2012

Q J Med doi:10.1093/qjmed/hcs151

Clinical picture
Unusual cause of bleeding in liver cirrhosis patient
A 42-year-old man presented to the emergency department with 2 weeks history of fatigue and dark tarry stool. He had past medical history significant for primary sclerosing cholangitis with liver cirrhosis, complicated with ascites and small nonbleeding esophageal varices. He denied nausea, vomiting, abdominal pain, weight loss or change in appetite. He also denied excessive use of non-steroid anti-inflammatory drugs (NSAIDs). On presentation he was on spironolactone, furosomide, omeprazole and nadalol. On exam, he appeared pale with stable vitals signs. Skin examination revealed spider angiomata and palmar erythema. Abdomen was non-distended with no abdominal tenderness or organomegaly. There was no asterixis. Initial blood work revealed hemoglobin of 5.8 g/dl (normal 13.517.5 g/l) down from his baseline of 13 g/dl. Platelet count was 87/ml (normal 150 000400 000/ml). Prothrombin time and INR were 15.2 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 blood cells and two units of fresh frozen plasma. Continuous intravenous esomeprazole and octreotide were started soon after admission. The patient underwent esophagogastroduodenoscopy (EGD). This revealed duodenal bulbar varices without stigmata of bleeding (Figure 1). Endoscopic ultrasound (EUS) showed a submucosal anechoic lesion corresponding to the endoscopic finding in the second portion of the duodenum (Figure 2). Color Doppler imaging revealed a vascular lesion. Patient hemoglobin responded well to blood transfusion and remained stable. Liver vascular ultrasound showed patent hepatic vasculature. Echocardiogram showed normal right ventricular size and function. The patient underwent transjugular intrahepatic portosystemic shunt (TIPS) procedure which resulted in a decrease in the porto-systemic pressure gradient from 23 to 5 mmHg. He was discharged home few days later in a stable condition. Patients with liver cirrhosis have an increased risk of mortality and morbidity due to their susceptibility

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

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

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 bleeding 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 severe and often life threatening.4 This prompts early diagnosis and treatment. Although esophageal varices are easily diagnosed with EGD alone, the submucosal location and the lack of red color signs of duodenal varices pose a diagnostic challenge.5 Any cirrhotic patient with GI bleed should undergo a thorough endoscopic evaluation of the duodenum. When the diagnosis is in doubt, EUS, is a valuable tool in confirming the diagnosis. There are multiple 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 by case 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.

Photographs and text from: Shadi Al Halabi, Digestive Disease Institute, Cleveland Clinic, Cleveland, OH, USA; M. Chadi Alraies, Clinical Assistant Professor of Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Department of Hospital Medicine, Cleveland Clinic, Cleveland, OH, USA; Abdul Hamid Alraiyes, Department of Pulmonary Diseases, Critical Care & Environmental Medicine, Tulane University Health Sciences Center, New Orleans, LA, USA; Ibrahim Hanouneh, Digestive Disease Institute, Cleveland Clinic, Cleveland, OH, USA; William D. Carey, Professor of Medicine, Cleveland Clinic Lerner College of Medicine of Case, Western Reserve University, Center for Continuing Education and Digestive Disease Institute, Cleveland Clinic, Cleveland, OH, USA. email: alraiec@ccf.org Conflict of interest: None declared.

References
1. 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 liver: a nationwide cohort study in Denmark. J Clin Epidemiol 2003; 56:8893. 2. Graham DY, Smith JL. The course of patients after variceal hemorrhage. Gastroenterology 1981; 80:8009.

Acknowledgements
All authors had access to the manuscript and a role in writing the manuscript.

3. Hashizume M, Tanoue K, Ohta M, Ueno K, Sugimachi K, Kashiwagi M, et al. Vascular anatomy of duodenal varices: angiographic and histopathological assessments. Am J Gastroenterol 1993; 88:19425.

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4. Amin R, Alexis R, Korzis J. Fatal ruptured duodenal varix: a case report and review of literature. Am J Gastroenterol 1985; 80:138. 5. Matsui S, Kudo M, Ichikawa T, Okada M, Miyabe Y. The clinical characteristics, endoscopic treatment, and prognosis for patients presenting with duodenal varices. Hepatogastroenterology 2008; 55:95962. 6. Haruta I, Isobe Y, Ueno E, Toda J, Mitsunaga A, Noguchi S, et al. Balloon-occluded retrograde transvenous obliteration (BRTO), a promising nonsurgical therapy for ectopic varices: a case report of successful treatment of duodenal varices by BRTO. Am J Gastroenterol 1996; 91:25947.

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