Abstract

INTRODUCTION: Non-cirrhotic portal hypertension (NCPH) is a rare manifestation of non-cirrhotic etiology, with gastric varices reported to occur in less than 10% of cases. Current literature hopes to identify cases in order to specify future diagnosis modalities and treatment. We present the second patient in the english literature to present with NCPH causing isolated Gastric Varices (IGV) in the absence of an identifiable etiology. CASE DESCRIPTION/METHODS: A 53 year old male with past medical history of diverticulitis presented to the emergency department with hematemesis and melena. He denied alcohol abuse or NSAID use. Physical exam showed BP 81/49 mmHg and non-radiating epigastric tenderness. Labs showed Hb10.4, platelet count 144,000, and BUN 39. Lipase, liver function and coagulation panel were normal. Ethanol, tylenol, and drug screen were negative. Viral hepatitis panel was negative. Patient was started on IV fluids, PPI, octreotide, and transfused two units PRBC. Emergent esophagogastroduodenoscopy (EGD) showed no bleeding source with adherent clot in fundus of stomach. Computed tomography (CT) of the abdomen with contrast showed a patent portal vein. Repeat EGD later showed moderate-sized IGV type I in fundus and GE junction ulceration. The varices were banded and ulceration clipped. Patient was treated with IV ceftriaxone, octreotide, and PPI. MRI of the abdomen showed 1.9 cm nodule in posterior hepatic dome, with portal hypertension. A nuclear scan of liver and spleen showed no colloid shift. Ultrasound of hepatic vessels showed no evidence of portal vein thrombosis with hepatopetal flow. Patient responded well to therapy, was initiated on beta blockers, and given appropriate outpatient follow up. DISCUSSION: Isolated Gastric Varices (IGV) are typically associated with thrombosed splenic vein, and occur most commonly in patients with portal hypertension. There are two main subtype: IGV1 located in the fundus, and IGV2 located in pylorus, body, and cardia. It is important to consider all possible etiologies attributable to portal hypertension when evaluating gastric varices on EGD. Despite the fact that they occur more frequently than esophageal varices, IGV carry a higher likelihood of mortality. Current treatment modalities include: airway protection, hemodynamic stabilization, somatostatin analogues, prophylactic antibiotics, and early endoscopic intervention. Additional studies are needed to further advance the knowledge of IGV, and establish a consensus on appropriate treatment modalities.

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