3015 Pancreatic Ascites: A Rare Complication of Chronic Pancreatitis

Abstract

INTRODUCTION: Pancreatic ascites is a rare complication of chronic pancreatitis. We present a case of recurrent pancreatic ascites refractory to medical management. CASE DESCRIPTION/METHODS: A 62-year-old man with alcohol related chronic pancreatitis thrombosis initially presented with abdominal pain which was treated as a chronic pancreatitis flare which was managed conservatively. CT showed a pseudocyst and a portal vein thrombus, for which he was started on therapeutic enoxaparin (Figure 1). EUS later showed the pseudocyst, along with calcifications and hypoechoic strands in pancreatic parenchyma (Figure 2). Subsequently, the patient had two more hospitalizations for chronic pancreatitis flares, but with new development of abdominal distention. CT confirmed the presence of a large intraabdominal and pelvic ascites. He underwent a diagnostic paracentesis revealing a SAAG less than 1.1, amylase level of 5954 U/L and a total protein of 3.1 mg/dl. Hence a diagnosis of pancreatic ascites was confirmed and portal hypertension was ruled out. The patient suffered rapid reaccumulation of ascites and required weekly paracentesis. He was treated with subcutaneous Octreotide, without improvement. Because of this, he underwent ERCP which showed leakage of contrast from the pancreatic duct (PD) (Figure 3). A PD stent was placed. After this he still developed ascites, but at a slower rate. Repeat paracentesis showed an amylase level of 291 U/L and subsequently 21 U/L. DISCUSSION: Minor PD injuries are common in acute pancreatitis resulting in peripancreatic fluid collections. The fluid collection is often contained and results in pseudocyst formation. Pancreatic fluid collections can also leak into the peritoneum leading to pancreatic ascites. The majority of cases occur in males in the 5th decade of life. Pancreatic ascites is primarily exudative with markedly raised ascitic amylase and protein content greater than 2.5 g/dl. Medical management includes diuretics and somatostatin analogs. If this fails, ERCP with PD stent placement is performed. This decreases intraductal pressure and diverts pancreatic secretion to the small bowel, thereby enhancing healing of the disrupted PD. Surgical therapy is recommended for patients with a lack of response to conservative therapy for 3-4 weeks or failure of endoscopic intervention. Our case report demonstrates the utility of endoscopic PD stent placement in patients with recurrent pancreatic ascites.