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Amantadine Toxicity: Uncovering a Rare Cause of Severe Encephalopathy
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A6912 - Amantadine Toxicity: Uncovering a Rare Cause of Severe Encephalopathy
Author Block: K. Albrektson1, A. Mandviwala1, C. Donatelli2, D. Soliman3, J. Lackamp3, C. V. Teba2; 1Internal Medicine, University Hospitals Cleveland Medical, Cleveland, OH, United States, 2Pulmonary, Critical Care, and Sleep Medicine, University Hospitals Cleveland Medical Center, Cleveland, OH, United States, 3Psychiatry, University Hospitals Cleveland Medical, Cleveland, OH, United States.
Introduction: Amantadine is a drug most commonly used in the United States for the treatment of Parkinson’s disease and drug-induced extrapyramidal symptoms. In other countries it is also used routinely for treatment of influenza A and post-stroke depressive symptoms. Toxicity with amantadine is seen in patients with renal failure and can present with varied neurologic symptoms, including confusion, ataxia, depression, and hallucination.
Case Presentation: We present a rare case of amantadine toxicity requiring intubation for severe encephalopathy in the absence of overt renal failure. A 57 year-old female physician with a past medical history of Sjogren’s syndrome and treatment-resistant depression was admitted to the ICU for acute hypoxemic respiratory failure secondary to progressively worsening encephalopathy. Creatinine was normal at 1.1 on admission. The patient’s encephalopathy was characterized by tremor, agitation, and subjective weakness. Home anti-depressive medications were notable for a five-drug regimen that included amantadine, protryptiline, donepezil, trazodone and duloxetine. These medications were prescribed by an out-of-state physician. Careful medication review revealed the patient’s amantadine dose had been briefly increased from 400 mg/day to 1000 mg/day in the weeks prior to hospitalization. This medication was held on admission and later restarted at a lower dose to avoid a potential withdrawal syndrome. The patient’s ICU course was complicated by progressive worsening of her encephalopathy and agitation, which resulted in prolonged mechanical ventilation after hypoxemia improved. The patient received a thorough work-up for her encephalopathy, including MRI brain, lumbar puncture, and EEG. These studies were unrevealing. The patient’s encephalopathy slowly improved after a week-long ICU stay and 30 day total hospitalization. The amantadine serum level taken on day 3 of her hospitalization was found to be elevated at 2400 ng/ml. Toxicity is generally thought to occur with levels over 1000 ng/mL.
Discussion: Amantadine toxicity in the absence of renal failure is a rare clinical entity and usually seen only in patients attempting suicide via toxic ingestion. More than 90% of this drug is excreted in the urine unchanged. In this case, the patient was taking an abnormally high dose of amantadine (400 -1000 mg/day) for an off-label indication of depression, which led to her toxicity. Amantadine recommended dosing does not exceed 400 mg/day in the treatment of Parkinson’s disease or Influenza A. This case illustrates a rare presentation of amantadine toxicity in a patient with normal kidney function.
Author Block: K. Albrektson1, A. Mandviwala1, C. Donatelli2, D. Soliman3, J. Lackamp3, C. V. Teba2; 1Internal Medicine, University Hospitals Cleveland Medical, Cleveland, OH, United States, 2Pulmonary, Critical Care, and Sleep Medicine, University Hospitals Cleveland Medical Center, Cleveland, OH, United States, 3Psychiatry, University Hospitals Cleveland Medical, Cleveland, OH, United States.
Introduction: Amantadine is a drug most commonly used in the United States for the treatment of Parkinson’s disease and drug-induced extrapyramidal symptoms. In other countries it is also used routinely for treatment of influenza A and post-stroke depressive symptoms. Toxicity with amantadine is seen in patients with renal failure and can present with varied neurologic symptoms, including confusion, ataxia, depression, and hallucination.
Case Presentation: We present a rare case of amantadine toxicity requiring intubation for severe encephalopathy in the absence of overt renal failure. A 57 year-old female physician with a past medical history of Sjogren’s syndrome and treatment-resistant depression was admitted to the ICU for acute hypoxemic respiratory failure secondary to progressively worsening encephalopathy. Creatinine was normal at 1.1 on admission. The patient’s encephalopathy was characterized by tremor, agitation, and subjective weakness. Home anti-depressive medications were notable for a five-drug regimen that included amantadine, protryptiline, donepezil, trazodone and duloxetine. These medications were prescribed by an out-of-state physician. Careful medication review revealed the patient’s amantadine dose had been briefly increased from 400 mg/day to 1000 mg/day in the weeks prior to hospitalization. This medication was held on admission and later restarted at a lower dose to avoid a potential withdrawal syndrome. The patient’s ICU course was complicated by progressive worsening of her encephalopathy and agitation, which resulted in prolonged mechanical ventilation after hypoxemia improved. The patient received a thorough work-up for her encephalopathy, including MRI brain, lumbar puncture, and EEG. These studies were unrevealing. The patient’s encephalopathy slowly improved after a week-long ICU stay and 30 day total hospitalization. The amantadine serum level taken on day 3 of her hospitalization was found to be elevated at 2400 ng/ml. Toxicity is generally thought to occur with levels over 1000 ng/mL.
Discussion: Amantadine toxicity in the absence of renal failure is a rare clinical entity and usually seen only in patients attempting suicide via toxic ingestion. More than 90% of this drug is excreted in the urine unchanged. In this case, the patient was taking an abnormally high dose of amantadine (400 -1000 mg/day) for an off-label indication of depression, which led to her toxicity. Amantadine recommended dosing does not exceed 400 mg/day in the treatment of Parkinson’s disease or Influenza A. This case illustrates a rare presentation of amantadine toxicity in a patient with normal kidney function.
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