Smoke Inhalation Injury Medication

Updated: Nov 06, 2018
  • Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS  more...
  • Print

Medication Summary

The primary treatment of smoke inhalation injury is oxygen. Bronchodilators may be of benefit in patients displaying bronchospasm. In addition, specific antidotes are methylene blue for methemoglobinemia and thiosulfate/sodium nitrite for cyanide (CN) poisoning. Certain patients with carbon monoxide (CO) toxicity may require hyperbaric oxygen therapy (HBO).

Oxygen is used for any suspected significant inhalation injury. Treat with high concentrations of humidified oxygen en route to the hospital.

Humidified oxygen

Use of high oxygen flow rates and a nonrebreathing-type face mask with a tight seal facilitates delivery of high levels of supplemental oxygen, which helps reverse the oxygenation defect created by ventilation-perfusion mismatch. Inhaled oxygen also helps in the displacement of CO from hemoglobin, decreasing the half-life of carboxyhemoglobin from 4-6 hours in room air to 40-60 min in 100% fractional concentration of oxygen in inspired air (FiO2).

Hyperbaric oxygen therapy

HBO therapy also displaces CO from intracellular stores and may improve mitochondrial function. HBO requires special facilities that are not available at all centers, resulting in a delay in treatment while the patient is transported to facility with HBO.

Hyperbaric therapy should be considered in those patients who have high carboxyhemoglobin levels greater than 25%, who are unconsciousness, have other neurologic findings, or have severe metabolic acidosis (ph < 7.1). The benefit of treating patients 12 hours or more after CO exposure remains unproven.


Beta2 Agonists

Class Summary

These agents relieve reversible bronchospasm by relaxing smooth muscles of the bronchi. Increased resistance from airway edema and reflex bronchoconstriction from irritation of airway receptors contribute to airway obstruction.

Bronchodilators are important in the treatment of bronchoconstriction and bronchorrhea. Toxic smokes can cause bronchoconstriction, especially if the exposed individual has underlying asthma or chronic obstructive pulmonary disease (COPD). In patients with profound bronchoconstriction and wheezing, subcutaneous epinephrine has been helpful in stabilizing mast cells and halting or reversing potentially fatal bronchoconstriction.

Albuterol (Proventi HFAl, Ventolin HFA, VoSpire ER, ProAir HFA)

Albuterol is a beta-agonist that is useful in treatment of bronchospasm refractory to epinephrine. It relaxes bronchial smooth muscle by acting on beta2-receptors, while having little effect on cardiac muscle contractility. Airway resistance is decreased, and ventilation is improved.

Epinephrine racemic (AsthmaNefrin, S2)

Racemic epinephrine alleviates airway edema and reflex bronchospasm. Although it has not been directly studied in smoke inhalation, inhaled racemic epinephrine can theoretically provide relief from both airway edema and reflex bronchospasm in this setting.


Terbutaline is used for severe bronchoconstriction, especially in patients with underlying reactive airways disease. This agent acts directly on beta2-receptors to relax bronchial smooth muscle, relieving bronchospasm and reducing airway resistance.

Epinephrine (Adrenalin, EpiPen, Adrenaclick)

Epinephrine is used for severe bronchoconstriction, especially in patients with underlying reactive airways disease. This agent has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. The beta-agonist effects of epinephrine include bronchodilation, chronotropic cardiac activity, and positive inotropic effects.


Antidotes, Other

Class Summary

Several CN antidotes exist, which work by different mechanisms of action. Hydroxocobalamin binds to CN to form cyanocobalamin. Amyl nitrite and sodium nitrite convert a portion of circulating hemoglobin to methemoglobin. Sodium thiosulfate allows the production of thiocyanate.

Sodium thiosulfate

After formation of methemoglobin and production of cyanomethemoglobin, thiosulfate acts as a sulfur donor to the endogenous enzyme rhodanese. This enzyme removes CN from the cyanomethemoglobin complex and forms thiocyanate, which is excreted renally. CN also is removed directly from cytochrome oxidase and is converted to thiocyanate in the presence of thiosulfate via the enzyme rhodanese.

Methylene blue (ProvayBlue)

Methylene blue is used to convert methemoglobin to oxyhemoglobin. It contains a tetramethyl thionine chloride moiety that is reduced (it is an electron acceptor) in the presence of nicotinamide adenine dinucleotide phosphate–oxidase (NADPH) and methemoglobin reductase to leukomethylene blue. Leukomethylene blue then becomes available to reduce methemoglobin to oxyhemoglobin.

Methylene blue may be ineffective in treating patients with glucose-6-phosphodiesterase (G-6-PD) deficiency because, in the hexose monophosphate shunt, G-6-PD is essential for the generation of NADPH. Without NADPH, methylene blue cannot act as a reducing agent in the transformation of methemoglobin to oxyhemoglobin.

Hydroxocobalamin (Cyanokit)

Hydroxocobalamin is a vitamin B-12 precursor that contains a cobalt ion, which has greater affinity for cyanide than does cytochrome oxidase. Binding of cyanide to the cobalt ion results in the formation of cyanocobalamin, which is excreted renally. Hydroxocobalamin has few adverse effects and has the following advantages over other cyanide treatments:

This agent is safe to use in victims of smoke inhalation. [59, 60] Cyanocobalamin is a pigmented compound, and interferes with spectrophotometric tests. Any necessary blood samples should be drawn prior to administration of antidote if possible, because it will not be possible to obtain accurate results for most blood tests afterward.

Amyl nitrite

In the presence of nitrites, hemoglobin is converted to methemoglobin, which has a higher binding affinity for CN than does the cytochrome oxidase complex. Administration of amyl nitrite produces a methemoglobin level of 5% and subsequent formation of cyanomethemoglobin, allowing electron transport and cellular respiration to continue. This medication is given until an IV line is established and sodium nitrite can be administered.

Sodium thiosulfate & sodium nitrite (Nithiodote)

In the presence of nitrites, hemoglobin is converted to methemoglobin that has a higher binding affinity for CN than does the cytochrome oxidase complex. Administration of sodium nitrite produces a methemoglobin level of 20-30% and subsequent formation of cyanomethemoglobin, allowing electron transport and cellular respiration to continue.



Class Summary

Whether corticosteroids are beneficial in toxic smoke inhalation is a matter of some debate, but many experts consider these agents helpful in this setting. Corticosteroids are considered especially useful in metal fume fever, which is believed to be mediated by an inflammatory cascade of events involving cytokines and histamine release.

Methylprednisolone (Medrol, Depo-Medrol, Solu-Medrol, A-Methapred)

Methylprednisolone decreases inflammation by suppressing the migration of polymorphonuclear neutrophils (PMNs) and reversing increased capillary permeability.

Dexamethasone (Dexamethasone Intensol)

Dexamethasone decreases immune reactions. It provides a local anti-inflammatory effect while minimizing some of the gastrointestinal and other risks associated with systemic medications. Dexamethasone suppresses the migration of polymorphonuclear leukocytes (PMNs) and reduces capillary permeability.



Class Summary

No reports exist as to the efficacy of chelating agents; however, dimercaprol and edetate calcium disodium (CaEDTA) have been suggested because of their ability to reduce serum zinc levels. Zinc toxicity may be treated with a combination of dimercaprol and CaEDTA or with EDTA alone. Nausea, vomiting, and elevated liver enzymes occur more commonly with combination therapy.

Dimercaprol (BAL in Oil)

Dimercaprol is the drug of choice for treatment of mercury toxicity; although not formally indicated for zinc toxicity, its use has been suggested in the setting of severe zinc oxide inhalation injury, since it lowers serum zinc levels. It is administered by deep intramuscular injection.

Edetate calcium disodium

Although edetate calcium disodium is used mostly in lead chelation, for which it is a second-line agent, treatment with this agent has been associated with lowering of serum zinc levels. Begin therapy 4 h after giving dimercaprol. The IV route is used exclusively, and continuous infusion is recommended.



Class Summary

Adjunctive therapy may be useful in patients with eye irritation accompanying smoke inhalation injury. These agents relax ciliary muscle spasm, which can cause deep aching pain and photophobia.

Atropine ophthalmic

This agent acts at parasympathetic sites in smooth muscle to block the response to acetylcholine of the sphincter muscle of the iris and the muscle of the ciliary body, causing mydriasis and cycloplegia.


Alkalinizing Agents

Class Summary

These agents are indicated for topical treatment of patients who have experienced cutaneous exposure to sulfur trioxide or titanium tetrachloride.

Sodium bicarbonate

Rinse affected skin thoroughly before applying sodium bicarbonate solution. Potential exists for exothermic reaction (burns) whenever a base is mixed with an acid; therefore, after titanium chloride or sulfur trioxide exposure, rinse affected skin thoroughly and copiously with water or saline.

Pharmacists at Walter Reed Medical Center recommend using a 5% solution of sodium bicarbonate to rinse over the affected area, followed by rinsing copiously with water or saline. The author believes that copious irrigation alone with water or saline should be sufficient, along with proper wound care, rather than introducing another chemical onto an already irritated area of skin.

Nebulized sodium bicarbonate may be helpful in cases of chlorine gas inhalation. It should not be used for inhalation of other gases.