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.

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INTRODUCTION: Sodium polystyrene sulfonate (kayexalate) combined with sorbitol is a resin that exchanges sodium for potassium primarily in the colonic mucosa to treat hyperkalemia. It has been associated with ischemic colitis. CASE DESCRIPTION/METHODS: We present a case of a 78-year-old female with a medical history of renal disease requiring hemodialysis and heart failure, admitted with an ischemic right lower limb. She was started on an intravenous heparin drip as per vascular surgery recommendations. Overnight her potassium level was noted to be 5.9 mg/dL for which she was medically treated with dextrose solution, regular insulin along with three doses of oral 15 mg kayexalate. The next morning she complained of sudden onset abdominal pain. CT imaging showed pneumatosis along with asymmetric mural thickening of the cecum, concerning for cecal ischemia. The patient underwent emergent exploratory laparotomy which revealed ischemia of the cecum and ascending colon. A right hemicolectomy was done and the patient eventually made a complete recovery. Later, pathology revealed findings of ischemic colitis with detached purple refractile material in the colon consistent with kayexalate crystals. DISCUSSION: Colonic necrosis after the use of kayexalate is a rare and an under-recognized complication. Incidence of colonic necrosis is reported to be around 0.27% which increases to 1.8% in uremic patients. It often presents with nonspecific symptoms such as constipation, fecal impaction, obstruction, gastrointestinal bleeding, bezoars and rarely, acute abdomen as in our patient. Previously addition of sorbitol to kayexalate was thought to be the main culprit leading to colonic necrosis but cases have been reported in patients taking sorbitol free kayexalate. The exact mechanism of action remains unclear with a few possibilities such as a direct toxic effect, elevated prostaglandin levels and hyperreninemia in patients with renal insufficiency, leading to nonocclusive mesenteric ischemia, have been suggested. Endoscopically it presents as ulcerated lesions with a definitive diagnosis made after seeing kayexalate crystals on the histological exam. Patients without signs of peritonitis are usually managed medically with intravenous fluid resuscitation, use of supplemental oxygen, bowel rest and broad-spectrum antibiotics. Clinicians must be cautious in prescribing kayexalate to patients and keep kayexalate induced colitis in one of the differentials in patients presenting with signs and symptoms of colitis.

INTRODUCTION: Carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA 19-9) are validated and well-known tumor markers for colorectal and pancreatic malignancies but data concerning these markers in bladder carcinoma are limited. We report a rare case of bladder carcinoma with metastasis to the bone marrow producing very high serum levels of CEA and CA 19-9. CASE DESCRIPTION/METHODS: A 68-year-old man with a medical history of hypertension, COPD presented with altered mental status. The patient further reported anorexia, unintentional weight loss of 50 lbs and intermittent hematuria over the last few months. He was confused but hemodynamically stable on presentation. Initial laboratory data showed pancytopenia, ALP of 712 U/L with normal transaminases and bilirubin, urine microscopy showed >100 red blood cells/HPF. A CT scan of the abdomen showed bilateral hydronephrosis with thickening of the urinary bladder and diffusely abnormal bone marrow. Bone marrow biopsy showed poorly differentiated metastatic carcinoma with positive immunohistochemical (IHC) stains for cytokeratin (CK)7 and CK20. In addition, very high levels of tumor markers CA19-9 42,635 U/ml, CEA 347 ng/ml raised a possibility of origin from the gastrointestinal or pancreatobiliary system. Subsequently, upper endoscopy, colonoscopy, EUS, and magnetic resonance cholangiopancreatography (MRCP) were performed and results were unremarkable. Finally, a cystoscopy was performed showing multiple papillary tumors throughout the bladder. Unfortunately, the patient died before any further workup and therapeutic interventions were initiated. DISCUSSION: Elevated levels of CEA and CA19-9 have been demonstrated in TCC of the bladder. The specificity of CEA for diagnosis of colorectal cancer is 89 percent while the specificity of CA 19-9 for pancreatic cancer goes up to 85% at a serum level >37 U/ml but neither are useful tools in the primary diagnosis of TCC. The pattern of staining with the CK20 and CK7 may be helpful in narrowing the diagnostic spectrum, but both can show positivity in pancreatobiliary and urothelial cancers. IHC allows limited determination of the tissue of origin in poorly differentiated carcinomas due to atypical staining patterns. In conclusion, when CEA and CA19-9 serum levels are elevated, a gastrointestinal malignancy should be excluded and one should be mindful of the existence of CEA and CA19-9 producing TCC and thus examine the urologic tract.

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