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Isoniazid Poisoning, Emergency Medicine


Basics


Description


  • Complexes with and inactivates pyridoxal-5 phosphate, the active form of pyridoxine (vitamin B6)
  • Inhibits pyridoxine phosphokinase, hindering the conversion of pyridoxine to its active form
  • Yields a net decrease in Ž ³-aminobutyric acid (GABA) production:
    • Depressed GABA causes cerebral excitability and seizures
  • Inhibits lactate dehydrogenase, decreasing the conversion of lactate to pyruvate:
    • Contributes to the profound anion gap metabolic acidosis
  • Chronic toxicity:
    • Interferes with synthesis of nicotinic acid (niacin)
    • May cause syndrome indistinguishable from pellagra after months of therapy (niacin deficiency)
  • Some actions similar to the monoamine oxidase inhibitors:
    • Reports of a tyramine-like reaction to isoniazid (INH)
    • Rare cases of mania, diaphoresis, depression, obsessive " “compulsive disorder, and psychosis
  • Pharmacokinetics:
    • Rapidly absorbed, peak levels within 1 " “2 hr
    • Volume of distribution is 0.6 L/kg and protein binding is low (10%)
    • Renally excreted within 24 hr after acetylation in the liver
    • Half-life is <1 hr in fast acetylators and 2 " “4 hr in slow-acetylating individuals

Etiology


  • High-risk groups include:
    • Immigrants
    • Homeless
    • HIV infected
    • Alcoholics
    • Lower socioeconomic status populations
  • Slow acetylators (60% of African Americans and Whites compared to 20% of Asians) are more prone to chronic effects/toxicity
  • LD50 estimated at 80 " “150 mg/kg
  • Ingestions <1.5 g lead to mild toxicity, and those of 10 g or more often result in fatality

Diagnosis


Signs and Symptoms


  • Acute toxicity:
    • Neurologic:
      • Altered mental status
      • Seizures refractory to standard therapy
      • Agitation
      • Coma
      • Dizziness
      • Ataxia
      • Hyper-reflexia
      • Slurred speech
      • Hallucinations
      • Psychosis
    • GI:
      • Nausea
      • Vomiting
    • Renal:
      • Anuria
      • Oliguria
    • Cardiovascular:
      • Hypotension
      • Tachycardia
      • Shock
      • Cyanosis
    • Metabolic:
      • Profound anion gap metabolic acidosis (elevated lactate)
      • Hyperthermia
  • Chronic toxicity:
    • Neurologic:
      • Peripheral neuropathy
      • Optic neuritis, optic atrophy
      • Psychosis
      • Insomnia
      • Vertigo
      • Pellagra
  • GI hepatitis:
    • Liver failure, hepatitis
    • Nausea, vomiting, constipation
    • Anorexia

Essential Workup


Without specific history of ingestion, initiate general workup for: ‚  
  • Altered mental status
  • Seizures
  • Metabolic acidosis

Diagnosis Tests & Interpretation


Lab
  • Arterial blood gas:
    • Profound metabolic acidosis
  • Electrolytes, BUN/creatinine, glucose:
    • Elevated anion gap acidosis
    • Hyperglycemia
  • CBC:
    • Acute toxicity:
      • Leukocytosis
      • Eosinophilia
    • Chronic toxicity:
      • Agranulocytosis
      • Eosinophilia
      • Hemolysis
      • Anemia

Imaging
  • CXR:
    • Evidence of tuberculosis increases suspicion for ingestion/toxicity.
    • Evaluate for aspiration pneumonia.
  • CT/lumbar puncture if indicated and questionable history

Differential Diagnosis


  • Toxins:
    • Tricyclic antidepressants
    • Salicylates (aspirin)
    • Theophylline
    • Methanol/ethylene glycol
    • Lithium
    • Carbon monoxide
    • Cocaine/cyanide
    • Agents that cause metabolic acidosis
  • CNS:
    • Cerebrovascular accident
    • Intracranial hemorrhage/mass/trauma/abscess
  • Hypoglycemia
  • Uremia
  • Thyrotoxicosis

Treatment


Pre-Hospital


Collect prescription bottles/medications for identification in the ED ‚  

Initial Stabilization/Therapy


  • ABCs:
    • Supplemental oxygen
    • Intubate if necessary for airway protection
    • Secure IV access
    • Cardiac monitor
    • 0.9% NS access
  • Naloxone, thiamine, D50W (Accu-Chek) if altered mental status

Ed Treatment/Procedures


  • Vitamin B6 (pyridoxine):
    • Specific antidotal treatment for INH toxicity
    • Goal: 1 g of pyridoxine for each gram of INH ingested (1 g q2 " “3min)
    • 5 g for unknown amount ingested
    • May repeat in 20 min for refractory seizures or persistent coma
    • If insufficient quantity of pyridoxine available, contact other hospital pharmacies and the regional poison control center to obtain more
    • If no parenteral pyridoxine available, crush tablets and give as a slurry via NG tube
  • Seizure control:
    • Pyridoxine restores deficiency in GABA
    • Benzodiazepines are synergistic with pyridoxine
    • Phenytoin has no role
  • Gastric decontamination after stabilization:
    • Consider gastric lavage only in life-threatening ingestions presenting within 1 hr with a protected airway (being aware of potential seizure activity and obtundation)
    • Activated charcoal (AC) dosed at 10:1 ratio (AC:drug)
  • Hemodialysis:
    • Persistent symptoms despite adequate therapy
    • Renal insufficiency in symptomatic patients
  • Sodium bicarbonate:
    • Acidosis usually resolves spontaneously after elimination of seizures

Medication


  • Dextrose: D50W 1 amp (50 mL or 25 g) (peds: D25W 2 " “4 mL/kg) IV
  • Diazepam (benzodiazepine): 5 " “10 mg (peds: 0.2 " “0.5 mg/kg) IV
  • Lorazepam (benzodiazepine): 2 " “6 mg (peds: 0.03 " “0.05 mg/kg) IV
  • Naloxone (Narcan): 2 mg (peds: 0.1 mg/kg) IV/IM initial dose
  • Pyridoxine (vitamin B6): 1 g IV for each gram of INH ingested (see above)
  • Thiamine (vitamin B1): 100 mg (peds: 50 mg) IV/IM

Follow-Up


Disposition


Admission Criteria
  • ICU admission for refractory seizures, severe acidosis, coma, altered mental status
  • Uncontrolled nausea/vomiting, unclear history of ingestion, or suicidal
  • Consult regional poison center:
    • (1-800-222-1222)

Discharge Criteria
  • Symptoms are usually observed within 45 min of an acute overdose but may be delayed for ≥2 hr
  • Discharge if asymptomatic after 6 hr

Followup Recommendations


Psychiatric referral for intentional overdoses or suicidal patients ‚  

Pearls and Pitfalls


  • Inadequate appreciation and management of INH poisoning:
    • Refractory seizures to standard treatments is a fundamental clue to INH poisoning
    • Severe acidemia with elevated lactate in altered patients with seizures
  • Never paralyze a seizing patient without the use of continuous EEG monitoring
  • Goal of pyridoxine therapy is gram for gram of INH
  • If pyridoxine adequately treats seizures, may give more if patient remains comatose

Additional Reading


  • Minns ‚  AB, Ghafouri ‚  N, Clark ‚  RF. Isoniazid-induced status epilepticus in a pediatric patient after inadequate pyridoxine therapy. Pediatr Emerg Care.  2010;26:380 " “381.
  • Osterhoudt ‚  KC, Henretig ‚  FM. A 16-year-old with recalcitrant seizures. Pediatr Emerg Care.  2012;28:304 " “306.
  • Tajender ‚  V, Saluja ‚  J. INH inducted status epilepticus: Response to pyridoxine. Indian J Chest Dis Allied Sci.  2006;48:205 " “206.

See Also (Topic, Algorithm, Electronic Media Element)


Seizures ‚  

Codes


ICD9


961.8 Poisoning by other antimycobacterial drugs ‚  

ICD10


  • T37.1X1A Poisoning by antimycobac drugs, accidental, init
  • T37.1X4A Poisoning by antimycobacterial drugs, undetermined, init

SNOMED


  • 67933004 Poisoning by isoniazid (disorder)
  • 291679008 Accidental isoniazid poisoning (disorder)
  • 291681005 Isoniazid poisoning of undetermined intent (disorder)
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