Rosen & Barkin's 5-Minute Emergency Medicine Consult (405 page)

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

• 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

Collect prescription bottles/medications for identification in the ED

• 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
  

• Vitamin B
  ₆
  (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
    

• 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 B
  ₆
  ): 1 g IV for each gram of INH ingested (see above)
  
• Thiamine (vitamin B
  ₁
  ): 100 mg (peds: 50 mg) IV/IM
  

FOLLOW-UP

• 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)
    

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

Psychiatric referral for intentional overdoses or suicidal patients

• 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
  

• 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

961.8 Poisoning by other antimycobacterial drugs

BASICS

• CNS depressant effect of isopropanol is 2 to 3 times as potent as that of ethanol.
  
• Many products that contain isopropanol also contain methanol, ethylene glycol, and ethanol.
  
• Rapidly absorbed following oral ingestion
  
• Ketogenic, but does not cause significant acidosis
  
• Metabolized by alcohol dehydrogenase to acetone (a CNS depressant):
  
  • Concomitant ethanol ingestion doubles half-life of isopropanol but not that of acetone.
    
  • Acetone eliminated by lung and kidney
    
• Half-life:
  
  • Isopropanol: 3–16 hr
    
  • Acetone: 7.5–26 hr
    

• Isopropanol (isopropyl alcohol): Clear, colorless, volatile liquid with faint odor of acetone and bitter taste
  
• Available as 70% rubbing alcohol solution:
  
  • May contain blue dye that was added to inhibit its abuse (“blue heaven”)
    
• Found in:
  
  • Various toiletries
    
  • Disinfectants
    
  • Window-cleaning solutions
    
  • Paint remover
    
  • Solvents
    
  • Jewelry cleaners
    
  • Detergents
    
  • Antifreeze
    
  • Hand sanitizers
    
• Typical adult patient: Chronic alcoholic who has been on drinking binge and recently depleted his or her ethanol supply
  
• Dermal and rectal administration can cause systemic toxicity.
  

DIAGNOSIS

• Usually occur within 30–60 min of ingestion
  
• Neurologic:
  
  • Lethargy
    
  • Weakness
    
  • Headache
    
  • Inebriation
    
  • Vertigo
    
  • Ataxia
    
  • Apnea
    
  • Coma
    
  • Initial excitation phase seen with ethanol ingestion is absent.
    
• GI:
  
  • Nausea/vomiting
    
  • Abdominal pain
    
  • Gastritis
    
  • Hematemesis
    
• Cardiovascular:
  
  • Hypotension
    
  • Tachycardia
    
  • Myocardial depression
    
  • Peripheral vascular dilation
    
• Pulmonary:
  
  • Respiratory depression
    
  • Hemorrhagic tracheobronchitis
    
• Dermatologic:
  
  • Skin irritation
    
  • Burns
    
• Ocular:
  
  • Irritation
    
  • Lacrimation