DELAYED DIAGNOSIS OF PERFORATED SIGMOID STERCORAL ULCER. M. Kasubhai 1 , M. Singh 1 , T. Saleem 1 , A. Singh 2 , V. Dimitrov 1 ; 1 Lincoln Medical and Mental Health Center., Bronx, NY; Cornell University LEARNING OBJECTIVES: 1) Recognize that stercoral ulcers result from pressure necrosis of the mucosa by the direct effect of a mass of retained feces. 2) Fecal Impaction is commonly diagnosed and rapid and gentle care can prevent this morbid complication CASE INFORMATION: 67 year old male presented with history of seizures, lower abdominal pain and constipation. Past history was relevant for seizure disorder, diabetes, stroke and bilateral above knee amputation. He was afebrile and hemodynamically stable. Left lower quadrant tenderness was noted. Rectal examination revealed fecal impaction and was manually disimpacted. The hemotocrit was 40 with leucocytosis. X-rays of chest and abdomen were normal. The patient subsequently developed fever and was treated for diverticulitis. Fever resolved with antibiotics. CT scan revealed thickening of the wall of the rectum and sigmoid, colonic dilatation and small bowel ileus. Colonoscopy performed two weeks later to evaluate the cause of constipation revealed an ulcer at the recto-sigmoid junction with biopsy revealing dysplastic changes. The other considerations of the ulcer being viral, bacterial, fungal or tuberculous were excluded by biopsy and culture. A stercoral ulcer was also considered and treated conservatively. After two weeks a repeat colonoscopy showed a persistent ulcer with acute and chronic inflammatory exudate. An exploratory laparotomy was performed because of persistent colonic dilatation and ileus. A sigmoid tear was noted over the ulcer, which was plugged by matted loops of small bowel. Sigmoid resection and colostomy was done. The patient recovered completely and was discharged home. DISCUSSION: Stercoral ulcers are usually found in the rectum and sigmoid. Their size is variable and margin usually irregular. When symptomatic, they usually reveal themselves by bleeding or perforation. Relieving the fecal impaction manually can result in perforation of the ulcer. Fever and leucocytosis, as in our patient, should suggest perforation. Our patient also had unexplained localised ileus and colonic dilatation, which should have led to an early exploratory laparotomy. Fecal impaction is commonly diagnosed and the rapid and gentle care can prevent its morbid complications HYPOKALEMIC PARALYSIS: PURSUING A DIAGNOSIS. J. Kent 1 , W.P. Moran 1 , L.B. Jones 1 , J. Stopyra 1 ; 1 Wake Forest University School of Medicine, Winston-Salem, NC LEARNING OBJECTIVES: 1) Recognize an uncommon presentation of SjÐgren's Syndrome. 2) Use a literature search as a diagnostic aid. 3) Demonstrate the importance of pursuing a diagnosis to the end. CASE INFORMATION: A 69 yo w female with past medical history of gastroesophageal reflux disease, hypertension, anxiety, arthritis and hypokalemic paralysis presented to the emergency department with a one-week history of progressive right-sided weakness. Her symptoms included difficulty using her right hand, impairment of gait, and a decrease in appetite. She had a history of right-sided paralysis due to hypokalemia nine months earlier requiring hospitalization, which had resolved with aggressive potassium replacement. She received neurologic and endocrine workups at that time without any etiology found, and she was discharged on oral potassium and spironolactone. With this second episode, her CT scan was negative for an acute CVA, and her potassium level was found to be 2.1. On exam, her oral mucous membranes were dry. Her lab values were suggestive of renal tubular acidosis. After doing a MEDLINE search with keywords including hypokalemia, paralysis, and acidosis, it was found that there have been over 20 case reports of patients with SjÐgren's syndrome presenting with a hypokalemic paresis or paralysis. Upon further questioning, the patient did note that her eyes and mouth had felt unusually dry for the past year. Diagnostic testing included a positive Schirmer's test and a minor salivary gland biopsy that was strongly suggestive of Sjo È gren's syndrome. The hemiparesis completely resolved with replacement of her potassium, and she was discharged on potassium supplementation with spironolactone, as well as artificial tears and lozenges for treatment of her Sjo È gren's symptoms. DISCUSSION: This patient's episode of hemiparesis/ paralysis due to hypokalemia was the second such episode within 9 months. During her first episode, it was also noted that she had symptomatic dryness of mouth and eyes and that her mucous membranes were dry. Sjo È gren's syndrome itself was not mentioned in a differential diagnosis. The main clinical problem appeared to be the hypokalemia and hemiparesis, which are not traditionally associated with Sjo È gren's. When the patient's hypokalemia and paralysis resolved, she was discharged with outpatient follow up. During this second episode, the patient's main symptoms were again relieved before a diagnostic etiology was found. However, the diligent search for a reason for her hypokalemia by the team resulted in the discovery of her underlying problem, Sjo È gren's Syndrome, which then allowed for more complete treatment. The use of a literature search and its finding of a series of case reports was a significant aid to the team in reaching the diagnosis. An 86 year old woman with no significant past medical history and taking no medications was admitted to the intensive care unit after a one day history of weakness, dizziness, nausea and vomiting. The patient was hypotensive with a blood pressure of 90/50 mmHg, without orthostatic changes. The pulse was 64; she was afebrile, and had dry oral mucosa. The remainder of the physical examination was normal. Laboratory workup was significant for pyuria and mild anemia (Hgb = 11.4 g/dL). Intravenous fluids were started and antibiotics were given for her urinary tract infection. During the hospital stay, the patient developed disorientation, hallucinations, and incoherent speech interpreted as delirium secondary to her infection and ICU psychosis. When her delirium did not resolve with hydration, antibiotics and transfer to a regular floor, a hepatic profile was ordered as part of the workup for metabolic causes for her delirium. This testing revealed an isolated elevated alkaline phosphatase (650 U/L). Abdominal ultrasound showed marked dilation of the common bile duct and subsequent abdominal CT scan showed no masses in the area of the gall bladder and liver. A 1.5 cm common bile duct stone was successfully extracted by endoscopic sphincterotomy and her mental status returned to baseline. DISCUSSION: The causes of delirium include medication side effects or withdrawal, dehydration, infections, hypoxia, hypoglycemia, and other metabolic abnormalities. Many systemic illnesses may produce delirium in elderly patients, especially in combination with new medications, fever, or sleep deprivation. In this patient, a comprehensive evaluation for metabolic causes of delirium (despite lack of localizing symptoms or signs on physical examination led to a diagnosis of unsuspected common bile duct stone and institution of appropriate treatment. Since delirium is associated with adverse outcomes, making the correct diagnosis is important. It is essential to do a complete workup for delirium in order to determine all treatable causes, particularly in hospitalized elderly patients.