1970 Spontaneous Page Kidney as a Cause of Gastric Variceal Bleed

Abstract

INTRODUCTION: Gastric variceal bleeding occurs in 15–50% of patients with non-cirrhotic portal venous thrombosis but can also occur in cases of splenic vein thrombosis (SVT) due to the formation of isolated gastric varices (IGV). We present the first reported case of a page kidney causing splenic vein compression, thrombosis, and subsequent gastric variceal bleeding. CASE DESCRIPTION/METHODS: A 31-year-old stuntman presented with epigastric pain and worsening exertional dyspnea over 3 weeks. History was notable for melena and anemia with no reported ulcers on endoscopy. On admission, he had hemoglobin of 4.1 g/dl with severe iron deficiency and elevated reticulocyte count. There was no serologic evidence of hepatic or renal disease. A computed tomography (CT scan) of the abdomen revealed a large left-sided perirenal collection consistent with page kidney, splenomegaly and decreased caliber of the mid and distal splenic vein suggestive of nonocclusive SVT. His liver was normal. Initial endoscopy revealed an IGV type 1 and mild portal hypertensive gastropathy (Figure 1). CT angiography did not reveal a splenorenal shunt to pursue a balloon retrograde transvenous obliteration (BRTO). While admitted, he developed hematemesis and worsening anemia. Ultimately, underwent IR splenic vein stenting with a bare-metal stent and subsequent decompression of the gastric varices with brisk flow of the portal vasculature (Figure 2). DISCUSSION: Gastric varices are classified primarily by location with most involving the gastroesophageal junction due to portal hypertension. The incidence of bleeding is highest in IGV, typically associated with SVT. Common etiologies of SVT include pancreatitis, malignancy or trauma. Our case described an extrinsic splenic vein compression and subsequent thrombosis due to a sub-capsular renal hematoma possibly of unclear etiology. Treatment for GV often depends on local expertise, but commonly consists of cyanoacrylate injection, banding (especially in type 1 gastro-esophageal varices), transjugular intrahepatic portosystemic shunt (TIPS) placement, BRTO, and even splenectomy. More recently, in cases of IGV due to isolated SVT, splenic vein stenting has been increasingly utilized. In our case, TIPS would not address the pre-hepatic portal hypertension and cyanoacrylate was not available. Splenic vein stenting was thus chosen to decompress the IGV with excellent response seen on subsequent follow-up (Figure 1).