Smoke Inhalation Medication

  • Author: Keith A Lafferty, MD; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: Jun 30, 2010
 

Medication Summary

Oxygen is the primary medication used in the treatment of smoke inhalation. Bronchodilators may be of benefit in patients displaying signs of bronchospasm. After this, specific antidotes of methylene blue for methemoglobinemia and thiosulfate/sodium nitrite for CN poisoning are indicated. Certain patients with CO toxicity may require hyperbaric therapy.

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Bronchodilators

Class Summary

These agents act to decrease the muscle tone in the small and large pulmonary airways.

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Albuterol (Proventil, Ventolin)

 

Beta-agonist that is useful in treatment of bronchospasm refractory to epinephrine. Relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility. Airway resistance is decreased, and ventilation is improved.

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Vitamin, Water Soluble

Class Summary

This agent binds to CN to form cyanocobalamin, which is renally excreted.

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Hydroxocobalamin (Cyanokit)

 

B-12 precursor that minds cyanide to its cobalt ion forming cyanocobalamin. The cobalt ion has greater affinity for cyanide than does cytochrome oxidase. Cyanocobalamin is excreted renally. Has few adverse effects and has several advantages over other cyanide treatments including ease of administration, rapid onset of action, good safety profile, no effect on the oxygen carrying capacity of blood, and is safe in victims of smoke inhalation.[31, 32] Low-dose hydroxocobalamin in combination with sodium thiosulfate used successfully to prevent cyanide toxicity due to prolonged sodium nitroprusside infusions.

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Antidotes

Class Summary

These agents convert a portion of circulating hemoglobin to methemoglobin.

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Amyl nitrite (Isoamyl 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 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 produces a methemoglobin level of 20-30% and subsequent formation of cyanomethemoglobin, allowing electron transport and cellular respiration to continue.

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Sulfur compounds

Class Summary

These agents provide a sulfur moiety to rhodanese, allowing the production of thiocyanate, which subsequently is excreted by the kidneys.

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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.

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Reducing agents

Class Summary

These agents are used in order to convert methemoglobin to oxyhemoglobin.

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Methylene blue

 

Tetramethyl thionine chloride moiety that is reduced (it is an electron acceptor) in the presence of NADPH and methemoglobin reductase to leukomethylene blue. Leukomethylene blue then becomes available to reduce methemoglobin to oxyhemoglobin.

May be ineffective in treating patients with 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.

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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, and Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

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.

Specialty Editor Board

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.

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.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

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