Isoniazid-Induced Acute Metabolic Acidosis and Neurotoxicity: A Case Report and Review of Literature
Isoniazid (INH) toxicity can lead to severe metabolic acidosis and neurologic manifestations. Recognizing overdose symptoms is critical for prompt treatment with pyridoxine and supportive therapy.
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Isoniazid induced Acute Metabolic Acidosis and Neurotoxicity A Case Report and Review of Literature Sumeet Prakash Mirgh, Jehangir Soli Sorabjee
Isoniazid (INH) is a crucial drug in the prevention and treatment of tuberculosis. INH is commonly known to cause derangements in liver function tests and peripheral neuropathy due to pyridoxine deficiency in slow acetylators. However, in toxic doses it is known to cause severe neurologic manifestations and acute metabolic acidosis. INH toxicity is characterized by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. Hence, the diagnosis of INH overdose should be considered in any patient who presents to Emergency medical services (EMS) with the triad. Though accidental overdose of anti-tuberculosis drugs have been reported in children and adults, acute toxicity is rare. When recognized, intravenous pyridoxine and correction of acidosis with sodium bicarbonate and supportive treatment is effective. The condition is easily treated with intravenous pyridoxine but if not treated in time could prove fatal. Unlike other poisonings, serum INH levels do not co-relate with either symptomatology or liver injury.
KEYWORDS Acidosis, Isoniazid (INH), Pyridoxine, Seizures, Toxicity.
INH has been reported to cause high anion gap metabolic acidosis and seizures as a manifestation of its toxicity. Pyridoxine, sodium bicarbonate and supportive therapy has shown to be effective for INH toxicity. As Tuberculosis is very common in India, it is very important for clinicians to know the manifestations and treatment of INH toxicity due to suicidal as well as accidental ingestion in children.
