Rosen & Barkin's 5-Minute Emergency Medicine Consult (404 page)

• Inhaled nebulized β
  ₂
  -adrenergic agonists (albuterol) for bronchoconstriction
  
• Inhaled/IV/PO corticosteroids: Beclomethasone, methylprednisolone, prednisone:
  
  • Controversial
    
  • No controlled trials that document benefit of acute corticosteroids after irritant gas inhalation.
    
• Nebulized sodium bicarbonate (3.75% solution) after chlorine gas exposure:
  
  • Reported to improve oxygenation in several case reports/series.
    
• Nebulized calcium gluconate after acute hydrogen fluoride inhalation:
  
  • Reported, but with no proven benefit
    
• Hydroxocobalamin or cyanide antidote kit if hydrogen cyanide is suspected (see “Cyanide Poisoning”)
  
• Oxygen or hyperbaric oxygen therapy if carbon monoxide poisoning documented
  

• Albuterol: 0.5 mL (peds: 0.03 mL or 0.15 mg/kg/dose) of 0.5% solution diluted in NS to 3 mL aerosolized
  
• Beclomethasone MDI: 1–2 sprays (40–80 μ/spray) BID
  
• Calcium gluconate: Nebulized (2.5–3% solution) prepared by adding 0.15 g of calcium gluconate to 6 mL of NS
  
• Methylprednisolone: 80–125 mg (peds: 1–2 mg/kg) IV
  
• Prednisone: 40–80 mg (peds: 1–2 mg/kg) PO
  
• Sodium bicarbonate: Nebulized (3 mL of 8.4% sodium bicarbonate mixed with 2 mL of NS to prepare 5 mL of 5% solution)
  

FOLLOW-UP

• ICU admission:
  
  • Intubated patients
    
  • Significant respiratory insufficiency or potential upper airway obstruction
    
• Persistently symptomatic with bronchospasm or oxygen requirement
  
• Exposure to irritant gases that affect peripheral airways:
  
  • Delayed pulmonary edema and respiratory failure may occur.
    
• Conservative treatment for children, pregnant women, elderly patients, or those with pre-existing chronic obstructive pulmonary or coronary disease
  

• Mild exposures that respond well to supportive care and have no oxygen requirement or bronchospasm after 4–6 hr of observation
  
• Follow-up chest radiograph during observation and prior to discharge, especially if any symptoms are present or clinically worsening
  

Intensive care for patients with early evidence of acute lung injury

• Occupational medicine referral for work-related exposures.
  
• Pulmonary follow-up for repeated symptomatic exposures.
  

• Beware of delayed onset of low-solubility agents. These exposures may require 23-hr observation for delayed respiratory symptoms.
  
• Avoid exposure of agent to first responders, with appropriate decontamination.
  

• Bosse GM. Nebulized sodium bicarbonate in the treatment of chlorine gas inhalation.
  J Toxicol Clin Toxicol
  . 1994;32:233–241.
  
• Rorison DG, McPherson SJ. Acute toxic inhalations.
  Emerg Med Clin North Am
  . 1992;10:409–435.
  
• Taylor AJ. Respiratory irritants encountered at work.
  Thorax
  . 1996;51:541–545.
  
• Vinsel PJ. Treatment of acute chlorine gas inhalation with nebulized sodium bicarbonate.
  J Emerg Med
  . 1990;8:327–329.
  
• Weiner AL, Bayer MJ. Inhalation: Gases with immediate toxicity. In: Ford MD, Delaney KA, Ling LJ, et al., eds.
  Clinical Toxicology
  . Philadelphia, PA: WB Saunders; 2001.
  
• Weiss SM, Lakshminarayan S. Acute inhalation injury.
  Clin Chest Med
  . 1994;15:103–116.
  

See Also (Topic, Algorithm, Electronic Media Element)

• Carbon Monoxide Poisoning
  
• Cyanide Poisoning
  

CODES

• 986 Toxic effect of carbon monoxide
  
• 987.7 Toxic effect of hydrocyanic acid gas
  
• 987.9 Toxic effect of unspecified gas, fume, or vapor
  

BASICS

• Complexes with and inactivates pyridoxal-5 phosphate, the active form of pyridoxine (vitamin B
  ₆
  )
  
• Inhibits pyridoxine phosphokinase, hindering the conversion of pyridoxine to its active form
  
• Yields a net decrease in γ-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
    

• 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

• 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
    

Without specific history of ingestion, initiate general workup for:

• Altered mental status
  
• Seizures
  
• Metabolic acidosis
  

• 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