Acute isoniazid toxicity presenting with refractory seizures, severe metabolic acidosis, and rhabdomyolysis: a case report

Sai Samhitha Mogalapu; Akshay Balagopalan; Namicharan Nabirajan; Keerthana Prabhakaran; Roshan Raj; T. B. Umadevi; T. S. Santhi

doi:10.18203/2320-6012.ijrms20262207

Authors

Sai Samhitha Mogalapu Institute of Internal Medicine, Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai, Tamil Nadu, India
Akshay Balagopalan Institute of Internal Medicine, Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai, Tamil Nadu, India
Namicharan Nabirajan Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai, Tamil Nadu, India
Keerthana Prabhakaran Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai, Tamil Nadu, India
Roshan Raj Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai, Tamil Nadu, India
T. B. Umadevi Institute of Internal Medicine, Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai, Tamil Nadu, India
T. S. Santhi Institute of Internal Medicine, Madras Medical College and Rajiv Gandhi Government General Hospital, Chennai, Tamil Nadu, India

DOI:

https://doi.org/10.18203/2320-6012.ijrms20262207

Keywords:

Isoniazid toxicity, Pyridoxine therapy, Drug-induced seizures, High anion gap metabolic acidosis, Rhabdomyolysis

Abstract

Isoniazid remains widely used in India due to the high burden of tuberculosis and HIV, with toxicity being an important clinical concern. While peripheral neuropathy and hepatotoxicity are common, acute overdose presenting with seizures and rhabdomyolysis is uncommon and potentially fatal. A 21-year-old male presented following intentional ingestion of approximately 9 g of isoniazid, with two episodes of generalized tonic–clonic seizures. On admission, he was drowsy but arousable (GCS 12/15). Initial management included gastric lavage and activated charcoal. Laboratory findings showed elevated creatine phosphokinase (2556 U/l) and mild metabolic acidosis. Liver enzymes rose from day 2, peaked by day 5, and normalized by day 12. CPK levels peaked on days 5–6 and declined thereafter, correlating with generalized myalgia. The patient was treated with intravenous fluids, 5 g pyridoxine, and alkaline diuresis, with gradual clinical and biochemical recovery. He was discharged on day 14 after psychiatric evaluation. This case emphasizes the need to recognize isoniazid toxicity, classically characterized by seizures, metabolic acidosis, and altered sensorium. Early administration of pyridoxine and supportive care are essential for a favorable outcome.

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