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Smoke Inhalation Injury Medication

  • Author: Keith A Lafferty, MD; Chief Editor: Joe Alcock, MD, MS  more...
 
Updated: Sep 25, 2015
 

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 >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.

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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 (Proventil, Ventolin, VoSpire ER, ProAir)

 

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

 

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.

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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

 

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-PD0 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 nitrite

 

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.

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Corticosteroids

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, Medrol Dosepak, Depo-Medrol, Solu-Medrol, A-Methapred)

 

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

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Chelators

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)

 

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 (Calcium Disodium Versenate)

 

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.

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Cycloplegics/Mydriatics

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 (Isopto-Atropine, Atropine Care)

 

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.

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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 feels 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.

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Contributor Information and Disclosures
Author

Keith A Lafferty, MD Adjunct Assistant Professor of Emergency Medicine, Temple University School of Medicine; Medical Student Director, Department of Emergency Medicine, Gulf Coast Medical Center

Keith A Lafferty, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Denise Serebrisky, MD Associate Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director, Division of Pulmonary Medicine, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center/North Central Bronx Hospital; Director, Jacobi Asthma and Allergy Center for Children, Jacobi Medical Center

Denise Serebrisky, MD is a member of the following medical societies: American Thoracic Society

Disclosure: Nothing to disclose.

Keisha Bonhomme, MD Resident Physician, Department of Internal Medicine, St Vincent’s Medical Center

Disclosure: Nothing to disclose.

Claudia V Martinez, MD Resident Physician, Department of Emergency Medicine, State University of New York Downstate College of Medicine

Claudia V Martinez, MD is a member of the following medical societies: American Academy of Emergency Medicine, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Chief Editor

Joe Alcock, MD, MS Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Joe Alcock, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Michael R Bye, MD Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Charles Callahan, DO Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center

Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Heidi Connolly, MD Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center

Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Robert G Darling, MD, FACEP Adjunct Clinical Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Associate Director, Center for Disaster and Humanitarian Assistance Medicine

Robert G Darling, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Telemedicine Association, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US

Disclosure: Nothing to disclose.

Harry J Goett, MD Assistant Professor of Emergency Medicine, Department of Emergency Medicine, Temple University Hospital

Harry J Goett, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Mark Keim, MD Senior Science Advisor, Office of the Director, National Center for Environmental Health, Centers for Disease Control and Prevention

Mark Keim, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Emily B Nazarian, MD Assistant Professor of Pediatrics, Fellowship Director, Pediatric Critical Care, Golisano Children's Hospital at Strong

Emily B Nazarian, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Girish D Sharma, MD Professor of Pediatrics, Rush Medical College; Senior Attending, Department of Pediatrics, Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush University Medical Center

Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

James Steven Walker, DO, MS Clinical Professor of Surgery, Department of Surgery, University of Oklahoma College of Medicine

James Steven Walker, DO, MS is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, and American Osteopathic Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Smoke inhalation in pediatric victims. Note the many hallmarks of smoke inhalation complexed with burn injury (ie, facial burns, carbonaceous particles in the nasal cavity, periorbital edema, hair singeing). Early endotracheal tube placement is necessary to secure patency of the upper airways and adequate ventilation.
Table. Inhalants [1, 25]
Type Inhalant Source Injury/Mechanism
Irritant gases Ammonia Fertilizer, refrigerant, manufacturing of dyes, plastics, nylon Upper airway epithelial damage
Chlorine Bleaching agent, sewage and water disinfectant, cleansing products Lower airway epithelial damage
Sulfur dioxide Combustion of coal, oil, cooking fuel, smelting Upper airway epithelial damage
Nitrogen dioxide Combustion of diesel, welding, manufacturing of dyes, lacquers, wall paper Terminal airway epithelial damage
Asphyxiants (mitochondrial toxins) Carbon monoxidea Combustion of weeds, coal, gas, heaters Competes for oxygen sites on hemoglobin, myoglobin, heme-containing intracellular proteins
Hydrogen cyanideb Burning of polyurethane, nitrocellulose (silk, nylon, wool) Tissue asphyxiation by inhibiting intracellular cytochrome oxidase activity, inhibits ATP production, leads to cellular anoxia
Hydrogen sulfidec Sewage treatment facility, volcanic gases, coal mines, natural hot springs Similar to cyanide, tissue asphyxiant by inhibition of cytochrome oxidase, leads to disruption of electron transport chain, results in anaerobic metabolism
Systemic toxins Hydrocarbons Inhalant abuse (toluene, benzene, Freon); aerosols; glue; gasoline; nail polish remover; typewriter correction fluid; ingestion of petroleum solvents, kerosene, liquid polishes CNS narcosis, anesthetic stats, diffuse GI symptoms, peripheral neuropathy with weakness, coma, sudden death, chemical pneumonitis, CNS abnormalities, GI irritation, cardiomyopathy, renal toxicity
Organophosphates Insecticides, nerve gases Blocks acetylcholinesterase; cholinergic crisis with increased acetylcholine
Metal fumes Metal oxides of zinc, copper, magnesium, jewelry making Flulike symptoms, fever, myalgia, weakness
a Major component of smoke.



b Smells like almonds, component of smoke from fires.



c Smells like rotten eggs.



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