Posters
Presenting Author Academic/Professional Position
Nida Asif
Academic Level (Author 1)
Resident
Discipline/Specialty (Author 1)
Internal Medicine
Academic Level (Author 2)
Resident
Discipline/Specialty (Author 2)
Internal Medicine
Academic Level (Author 3)
Resident
Discipline/Specialty (Author 3)
Internal Medicine
Academic Level (Author 4)
Resident
Discipline/Specialty (Author 4)
Internal Medicine
Academic Level (Author 5)
Faculty
Discipline/Specialty (Author 5)
Internal Medicine
Discipline Track
Patient Care
Abstract Type
Case Report
Abstract
Background: Phenytoin is the one of the oldest and widely prescribed anticonvulsant drugs with a narrow therapeutic index, exhibiting saturable metabolism at higher concentrations, hence small dose changes can disproportionately raise serum levels and precipitate toxicity. Chronic use can result in neurological toxicity (e.g., ataxia, nystagmus). Because these manifestations are often nonspecific, chronic phenytoin toxicity is frequently under-recognized or misattributed to other conditions especially in patients unable to report symptoms.
Case presentation: A 73-year-old female with past medical history of cerebral palsy with associated neurological complications including cognitive impairment, nonverbal status and childhood epilepsy maintained on long term phenytoin therapy presented to the emergency department for altered sensorium for one week. According to the family, she had experienced a ground level fall a few days prior due to unsteady gait, imaging studies performed at an outside hospital ruled out acute fractures or acute pathology. Her family reported that one week prior to presentation her phenytoin formulation had been changed from a suspension to tablet form 250 mg daily. On arrival vital signs were stable. Neurological examination revealed E4M4V1, normal deep tendon reflexes, inability to assess gait due to limited mobility. She exhibited no meningeal signs or focal neurological deficits. Additional physical exam findings included dry mucous membranes, capillary refill of 2-3 seconds, contractures of hands. Laboratory tests showed total phenytoin level was 40.9, normal range (10-20 microgram/ml), lactic acid of 3.49 mmol/L, other labs unremarkable. Patient was admitted for phenytoin induced encephalopathy and drug toxicity. Phenytoin was immediately discontinued, and supportive therapy was initiated. Neurology was consulted with recommendations starting levetiracetam and monitoring phenytoin levels every 4 hours until they decrease to therapeutic levels of (10-20 mcg/ml total phenytoin levels) at which point re-initiation at a reduced dose should be consider. Over the subsequent days phenytoin levels gradually declined to within therapeutic range, the patient’s neurological status improved, and phenytoin was reinitiated at a reduced dose.
Conclusion: This case underscores the importance of recognizing chronic phenytoin toxicity in long term phenytoin users with unexplained neurological deterioration. In cognitively impaired individuals such toxicity may go unrecognized. Regular therapeutic monitoring is also essential because phenytoin is highly protein bound; only free fraction is pharmacologically active. Thus, conditions like hypoalbuminemia and renal failure can lead to toxicity even when the total phenytoin levels appear “therapeutic” in such cases measuring the free phenytoin or using albumin corrected phenytoin calculations is recommended to guide dosing. The cornerstone of management in chronic toxicity is supportive care and temporary drug withdrawal, allowing excess drug to clear. An alternative anticonvulsant can maintain seizure control during the washout period. Early recognition and withdrawal of the drug can is curial and prevent long term complications.
Presentation Type
Poster
Recommended Citation
Asif, Nida; Zia, Sikandar; Durazo, Yareli; Fasehun, Oyinlola; and Suarez Parraga, Andres, "“Trapped in silence”: Chronic Phenytoin Toxicity in a Nonverbal Elderly with Cerebral Palsy" (2025). Research Colloquium. 76.
https://scholarworks.utrgv.edu/colloquium/2025/posters/76
Included in
“Trapped in silence”: Chronic Phenytoin Toxicity in a Nonverbal Elderly with Cerebral Palsy
Background: Phenytoin is the one of the oldest and widely prescribed anticonvulsant drugs with a narrow therapeutic index, exhibiting saturable metabolism at higher concentrations, hence small dose changes can disproportionately raise serum levels and precipitate toxicity. Chronic use can result in neurological toxicity (e.g., ataxia, nystagmus). Because these manifestations are often nonspecific, chronic phenytoin toxicity is frequently under-recognized or misattributed to other conditions especially in patients unable to report symptoms.
Case presentation: A 73-year-old female with past medical history of cerebral palsy with associated neurological complications including cognitive impairment, nonverbal status and childhood epilepsy maintained on long term phenytoin therapy presented to the emergency department for altered sensorium for one week. According to the family, she had experienced a ground level fall a few days prior due to unsteady gait, imaging studies performed at an outside hospital ruled out acute fractures or acute pathology. Her family reported that one week prior to presentation her phenytoin formulation had been changed from a suspension to tablet form 250 mg daily. On arrival vital signs were stable. Neurological examination revealed E4M4V1, normal deep tendon reflexes, inability to assess gait due to limited mobility. She exhibited no meningeal signs or focal neurological deficits. Additional physical exam findings included dry mucous membranes, capillary refill of 2-3 seconds, contractures of hands. Laboratory tests showed total phenytoin level was 40.9, normal range (10-20 microgram/ml), lactic acid of 3.49 mmol/L, other labs unremarkable. Patient was admitted for phenytoin induced encephalopathy and drug toxicity. Phenytoin was immediately discontinued, and supportive therapy was initiated. Neurology was consulted with recommendations starting levetiracetam and monitoring phenytoin levels every 4 hours until they decrease to therapeutic levels of (10-20 mcg/ml total phenytoin levels) at which point re-initiation at a reduced dose should be consider. Over the subsequent days phenytoin levels gradually declined to within therapeutic range, the patient’s neurological status improved, and phenytoin was reinitiated at a reduced dose.
Conclusion: This case underscores the importance of recognizing chronic phenytoin toxicity in long term phenytoin users with unexplained neurological deterioration. In cognitively impaired individuals such toxicity may go unrecognized. Regular therapeutic monitoring is also essential because phenytoin is highly protein bound; only free fraction is pharmacologically active. Thus, conditions like hypoalbuminemia and renal failure can lead to toxicity even when the total phenytoin levels appear “therapeutic” in such cases measuring the free phenytoin or using albumin corrected phenytoin calculations is recommended to guide dosing. The cornerstone of management in chronic toxicity is supportive care and temporary drug withdrawal, allowing excess drug to clear. An alternative anticonvulsant can maintain seizure control during the washout period. Early recognition and withdrawal of the drug can is curial and prevent long term complications.
