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Washington University Experience | MYELIN (NON-IMMUNE MEDIATED) | Central Pontine Myelinolysis (CPM) | 8A0 Case 8 History
Case 8 History ---- The patient was a 43 year old man with no significant past medical history who was transferred from an outside hospital with anemia, thrombocytopenia and possible thrombotic thrombocytopenic purpura (TTP) on 1/24/95. The patient had been ill for two weeks with a three day history of icterus. Upon admission, physical examination showed significant scleral icterus, hepatomegaly, and marked edema. Vital signs showed no fever. Laboratory findings showed CBC hemoglobin 9.3 with hematocrit 25.9, MCV 111, WBC 4.8, platelet count 32,000, peripheral blood smear showed numerous macrocytes, occasional schistocytes, and acanthocytes. Urinary examination showed 2+ bilirubin with 2+ blood. Hypoalbuminemia was noted (albumin=2.7) which was accompanied by elevated liver enzymes (SGOT 128, LDH 4425). Direct and indirect Coombs' tests were negative. PT-PTT was 17.6-30.2. The hepatitis profile (hepatitis B core antibody, hepatitis A antibody, hepatitis B profile, and hepatitis C antibody) were all negative. Serum B12 less than 200 (normal=200-800) and, as a result, the patient was treated as B12 deficiency. Paracentesis showed ascites with 30,000 cells and 2200 nucleated cells with 86% neutrophils. The patient was placed on antibiotic Ceftriaxone for subacute bacterial peritonitis, even though the ascitic fluid culture was negative. On 1/25/95 the patient developed prerenal azotemia (no increasing BUN creatinine but low urine output). On 1/27 she was transferred to the MICU, at which time he was unresponsive. The CT scan of the abdomen and pelvis showed positive ascites, small cirrhotic liver, positive retroperitoneal varices, and prominent small bowel loops. On 1/27 he was intubated according to increasing respiratory distress. A head CT scan was normal. On 2/3/95 he was extubated and transferred out of the MICU. On 2/9 the chest x-ray showed bilateral lobar consolidation with underlying edema. His clinical course deteriorated despite the aggressive treatment. On 2/14/95 his renal function showed markedly increasing BUN and creatinine consistent with acute renal failure. Subsequently the patient developed hepatorenal syndrome which was unresponsive to treatment. An endoscopic retrograde cholangiopancreatography (ERCP) was performed and showed no evidence of biliary or pancreatic obstruction. On 3/1/95 the patient became unresponsive and was pronounced dead.
