J.A. Garcia 1 ; 1 Wayne State University, Troy, MI (Tracking ID #74175) LEARNING OBJECTIVES: Physicians should be able to recognize early adverse events of commonly prescribed drugs. CASE INFORMATION: 56 y/o male, previously heatlhy presented to ER with fever, left calf pain and swelling which started after a brief hospitalization for a febrile illness. Lower extremity dupplex revealed thrombosis involving the Left popliteal and lesser saphenous veins. He was started on unfractionated heparin. Labs: WBC 10.2, Hemoglobin 11.7 and Platelets, 386k. Infectious work up was negative and he was eventually switched to coumadin and discharged. On the 4th day, he presented with fever and worsening left calf pain. A Lower extremity dupplex showed progression of the thrombus involving the posterior tibial vein. Heparin was restarted. WBC count 16.1, Hemoglobin 9.7 and platelets 240k . The fourth day of this admission Hb dropped to 6.5 with plts of 150k. On the 9th day, patient developed chest pain. EKG showed ST elevations and he had increased cardiac biomarkers compatible with acute lateral Myocardial Infarction. Cardiac catheterization revealed clean coronary arteries. On the 12th day, he complained of constipation, abdominal distension and pain. Abdominal Series showed ileus. Amylase 136, Lipase 73, ALT 21, AST 29, Alkaline Phosphatase 131, Tbili 0.9. WBC 27.2 Hemoglobin 11.7 and Platelets 72k. Because of the dropping platelets and the multiple thrombotic events, heparin was held, antibodies drawn, and liperudine was started. Heparin induced platelet aggregating antibodies were positive with ELISA. Abdominal CT showed focal areas of low attenuation with peripancreatic fat stranding compatible with necrotizing pancreatitis. IMPLICATIONS/DISCUSSION: Heparin is a widely used medication. Uncommon presentation of HITT should be early recognized to prevent unwarranted management. LEARNING OBJECTIVES: 1. Recognize the common toxicities of ecstasy 2. Diagnose water intoxication and its complications. CASE INFORMATION: KD is a 20-year old woman brought into the UCSF ED because she developed altered mental status after taking ecstasy. Seven hours prior to admission, she took 1.5 tablets of ecstasy, while her companion took 2 tablets of the same preparation. They remained at home and``drank lots of water.'' One hour prior to admission, KD complained of severe headache and multiple episodes of vomiting. She then``stopped making sense.'' In the ED, KD was alert and oriented to person and place but appeared agitated and confused. She then had a generalized tonic-clonic seizure, became apneic, and was intubated. A NCHCT showed bilateral uncal herniation with diffuse effacement of the sulci. Significant laboratory abnormalities included leukocytosis, serum sodium of 124, rhabdomyolysis, and evidence of SIADH. A urine toxicology screen was positive only for amphetamines. An ECG showed sinus tachycardia with diffuse ST elevations, and a chest radiograph showed bilateral patchy infiltrates consistent with pulmonary edema. Repeat physical exam three hours after admission documented the absence of brainstem reflexes. She expired 24 hours later, and her organs were harvested for transplantation. IMPLICATIONS/DISCUSSION: Ecstasy, or methylenedioxymethamphetamine (MDMA), is a recreational designer drug popular both for its pleasurable psychological effects and for its safe reputation. Acute adverse effects can range from nausea, headache, and myalgias to insomnia, paranoia, and depression. An ecstasy tablet often contains contaminants and other drugs. In addition, the dose of MDMA itself can range from 0 to 200 mg per tablet, and the toxic or even fatal dose range overlaps that of recreational use. The pattern of major physical toxicity is usually hepatic, cardiovascular, hyperpyrexic, or cerebral, although DIC, rhabdomyolysis, and acute renal failure also contribute to morbidity. Cerebral toxicity is manifested as seizures or cerebral edema, thought to result from hyponatremia. In most cases, the low sodium level is hemodilutional; users often sweat profusely and then drink large amounts of free water to rehydrate and to prevent overheating. Occasionally, SIADH contributes to hyponatremia in this setting. In addition to the physical toxicity, ecstasy can also lead to increased risk-taking behavior. Despite the widespread use of ecstasy and the range of potential toxicity, fatalities attributable to the drug are uncommon. KD's demise likely began with ingestion of MDMA, which led to water intoxication and SIADH. Hyponatremia followed, precipitating cerebral edema, increased intracranial pressure, and then uncal herniation. Respiratory arrest occurred with compression of the brain stem. The immediate cause of death was hypoxic encephalopathy. Several case reports suggest young women, such as KD, and children appear to be at the highest risk of poor outcomes associated with hyponatremia. This unfortunate case emphasizes the often overlooked and unpredictable morbidity and mortality associated with casual use of ecstasy.