ALPHA-INTERFERON THERAPY AND DELIRIUM. D. Misra 1 , S. Young 1 , C. Schleupner 1 ; 1 New Hanover Regional Medical Center, Wilmington, NC (Tracking ID #75477) LEARNING OBJECTIVES: Recognize delirium as one of the neuro-psychiatric adverse effects of alpha interferon therapy. We intend to share our experience because it may pose as a diagnostic challenge for clinicians. CASE INFORMATION: We present the case of a 57 yr old caucasian male who had previously been diagnosed with malignant melanoma. He had undergone local excision and was found to have positive lymph nodes. He was started on adjuvant alpha interferon therapy, initially at a dose of 40 million units a day which he could not tolerate primarily because of constitutional symptoms. His symptoms included severe arthralgias, myalgias and headaches. He received this dosage for only 4 days, which was then discontinued and subsequently started back on a reduced dose of 20 million units a day after a drug free interval of one week. He tolerated the lower dose without any side effects. The following week, he was started back on 40 million units a day of interferon which he received for five days. Within a couple of days, pt was experiencing severe headaches along with myalgias and arthralgias. This became worse and patient presented with delirium, agitation and combativeness. He required intravenous sedation and eventually endotracheal intubation for airway protection. His workup including blood counts, basic metabolic panel; urinalysis, drug screen, CT scan of the head and CSF examination were all within normal limits. Serum transaminases were mildly elevated but this was unchanged since the beginning of interferon treatment. His stay in the intensive care unit lasted 24 hours. The following day, he was back to his baseline cognitive level and was discharged home. IMPLICATIONS/DISCUSSION: Alpha interferon is a glycoprotein produced by leukocytes which has broad spectrum antiviral, immunologic and antiproliferative properties. Therefore, it is commonly used in treatment of hairy cell leukemia, hepatitis, renal cell carcinoma and malignant melanoma. The spectrum of side effects is wide and depends on various factors including the dose of the drug, age of the patient and the type of interferon. Our literature search revealed very few case reports of interferon induced delirium. Neuro-psychiatric adverse effects occur with doses higher than 30 million units per day. The temporal relationship of the onset of delirium with high dose interferon treatment in our patient stands out prominently. We believe that this occurrence should be brought to the notice of physicians prescribing interferon so that patients presenting with neuro-psychiatric manifestations are diagnosed and managed appropriately. A 51 year-old man with an ischemic cardiomyopathy presented to the emergency department after experiencing multiple shocks from his automatic implantable cardiac defibrillator (AICD). In the ED, the patient developed ventricular tachycardia at a rate of 162 bpm with a BP of 132/102. His AICD began antitachycardia pacing and DC countershocks without success. The patient was loaded with amiodarone and placed on a 2mg/ min infusion of amiodarone. Sinus rhythm was restored. Lab values included normal liver function tests and a creatinine of 2.1. The patient stabilized. After 24 hours, the amiodarone infusion was reduced to 1 mg/min. Twelve hours later, the patient developed confusion and severe dyspnea. Lasix was given without improvement. The patient developed fever, hypotension, and became lethargic. The exam showed a quiet, tender abdomen. The HCO3 had fallen to 6 meq/L, and the creatinine had risen to 3.2 mg/dl. The ALT was 1947 U/L, the AST was 2629 U/L, the bilirubin was 4.2, and the PT was 16.9s (INR 2.8) . The patient was diagnosed with fulminant hepatic failure. Dopamine and a bicarbonate infusion were begun. Antibiotics were started. The patient was intubated and vitamin K was given. Amiodarone was considered to be a possible cause of the fulminant liver failure. Thus, 72 hours after admission, the amiodarone infusion was stopped despite persistent ventricular ectopy. The patient's status declined and he died on the fifth day from complications from a liver biopsy. IMPLICATIONS/DISCUSSION: Fulminant hepatic failure develops in less than 2 weeks after an insult to the liver. The diagnosis of liver failure should be entertained in the presence of encephalopathy associated with jaundice, coagulopathy, acidosis, fever and hypotension. In this patient, clinical suspicion was confirmed by the rapid change in the liver function tests. The viral hepatidities and drug/toxin exposure are the most common etiologies of fulminant liver failure. In this patient, the leading considerations were ischemic and drug/toxin exposure. A review of the literature revealed at least twenty fatalities from acute hepatic failure following the administration of high dose parenteral amiodarone over the last twenty years. The chronology of exposure and onset of hepatic failure were consistent with amiodarone induced hepatotoxicity in this patient. Regardless of the cause, the treatment of acute liver failure requires removal of the exposure and supportive care for the expected complications. Despite aggressive support, mortality remains at 60-90% without transplantation. LEARNING OBJECTIVES: To recognize that brown recluse spider bites may cause pyoderma gangrenosum and pathergy due to persistent neutrophil mediated injury. CASE INFORMATION: A 47 year-old woman presented with a six month history of recurrent, painful, nonpruritic ulcers on the dorsa of both wrists and the right calf. Past history revealed that six months prior, while cleaning debris from an old tavern, she was bitten on the hand by a spider. The spider was captured and identified as a brown recluse spider. Within hours she was ill with nausea, vomiting, malaise and fever. She improved with supportive treatment. The lesion cleared but weeks later, began to reoccur following minor trauma such as that caused by mosquito bites. On physical examination we discovered pyoderma gangrenosum like lesions that were confirmed by biopsy. Long-term therapy with dapsone was started. IMPLICATIONS/DISCUSSION: Pyoderma Gangrenosum was first described by Brunsting et al in 1930. The etiology is unknown in fifty percent of the cases but associated with Ulcerative Colitis and Behcet's Disease. Spider bites rarely lead to pyoderma gangrenosum and even more rarely lead to recurrent lesions and pathergy. Brown recluse venom has been purified and studied and is known to persist in some wounds for a relatively long time. The precise mechanism of the lesions is not known although neutrophil inhibitors such as nitrogen mustard and dapsone can mitigate or prevent the reaction. The development of new lesions at distant sites from the inciting lesion is unexplainable and suggests an immune mediated response and not a local reaction. The observed clinical response to dapsone suggests an ongoing neutrophil mediated injury. Currently dapsone is being carefully tapered. It is unknown if the lesions will persist and argue for a permanent ongoing cell mediated injury or cease and suggest a self limited condition as remaining venom is cleared.