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Isoniazid Toxicity

Isoniazid (INH) toxicity should be considered in any patient who has intractable seizures (typically associated with severe metabolic acidosis) and is unresponsive to standard antiepileptics. This is particularly true in patients from highrisk groups who are likely to have ready access to INH (e.g., AIDS patients, recent immigrants, Native Americans, homeless patients, and those patients who have tuberculosis or are living with someone who has tuberculosis). Empiric treatment with pyridoxine should be considered in such cases.

Causes

Few of the possible causes of Isoniazid Toxicity are included in the list below:

Emergence of multi-drug resistant tuberculosis
Emigration from Southeast Asia
American Indian descent
Inuit descent
Homelessness
Alcoholism
Overcrowded conditions

Symptoms

Anorexia
Nausea and vomiting
Dizziness
Elevated temperature
Altered mentation
Slurred speech
Photophobia and blurred vision
Symptoms usually occur within 2 hours of ingestion.

Signs

The classic triad of acute INH neurotoxicity is coma, metabolic acidosis, and refractory seizures.
Hyperpyrexia, hyperreflexia, tachypnea, tachycardia, hypotension, and altered mental status are common.
Other manifestations include nystagmus, mydriasis, ataxia, and cyanosis.
Seizures are usually generalized tonic-clonic seizures.

Treatment

Treatment of patients with evidence of toxicity involves managing immediate life threats, administering pyridoxine, and supportive care.
Ipecac syrup is contraindicated in patients with acute INH neurotoxicity because it may increase the risk of aspiration secondary to seizure.
Perform gastric lavage and administer activated charcoal as soon as possible, preferably within 2 hours of acute ingestion.

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