Smoke Signals: Recognition and treatment of combustion-induced cyanide toxicity

 

 
 
 

John P. Benner, NREMT-PDavid Lawrence, DOWilliam Brady, MD | | Tuesday, September 29, 2009


The inhalation of combustion products, such as smoke from fires, is the leading cause of death from fire in the U.S. According to the National Fire Protection Agency (NFPA), there were more than 3,430 civilian fire-related deaths and 17,675 civilian fire-related injuries in 2007, with 50Ï80% attributed solely to the inhalation of smoke_s imbedded toxic chemicals. The danger of smoke inhalation is well demonstrated by several of this country_s large catastrophic fires. For instance, Boston_s Cocoanut Grove nightclub fire killed 491 people in 1942. Firefighters who entered the structure reportedly found bodies stacked near doorways and under tables, none of which had any evidence of burns.

Smoke is dangerous because of the toxicity of its suspended chemicals. Carbon monoxide and hydrogen cyanide form during the incomplete combustion of such common household products as plastics, synthetic polymers and polyurethane foam. Rapid treatment is necessary to reverse the toxicity caused by these agents. In the case of cyanide, treatment with certain antidotes, like sodium thiosulfate and hydroxocobalamin, is often necessary for the patient_s survival. Although EMS providers are typically well positioned to provide such care, they_re not usually equipped with the necessary medications to adequately treat cyanide poisoning. Let_s review combustion and smoke inhalation and cyanide toxicity and discuss the current EMS care in some regions of the U.S.

Combustion Byproducts

Consider the average home: Items commonly found inside include a plethora of organic and inorganic items, such as clothing, carpeting, upholstery/furniture, electronics, mattresses, refrigerators, cleaning supplies, painted walls, paper, etc. When these items are burned, the toxins can generate various lethal fumes. For example, when polyvinyl chloride (PVC) is burned, the common plumbing material is known to produce more than 75 different toxic chemicals.

An ordinary mattress and box spring set, containing wood, metal springs, cotton, polyurethane foam and other natural or synthetic polymers, can present a significant hazard. When rapid oxidation of the bed occurs, the wood and natural polymers can produce carbon monoxide (CO), acrolein, acetaldehyde, formaldehyde, acetic acid, formic acid and methane. The burning synthetic polymers can produce carbon monoxide, hydrogen chloride, phosgene, chlorine, ammonia, sulfur dioxide, hydrogen sulfide, isocyanates and hydrogen cyanide gas. As an illustration of the bed/mattress hazard, a tragedy occurred in 1990 at a Buenos Aires prison where inmates set ablaze an ordinary mattress containing polyurethane foam. The fumes produced by the burning mattress in the non-ventilated prison killed 35 inmates. An autopsy revealed that all the inmates_ blood contained highly elevated levels of cyanide at 2.7-7.2 mg/L; toxic levels of cyanide are within 0.5-1.0 mg/L, and lethal levels are > 3.0 mg/L, so it was determined that all inmates died of cyanide poisoning.

Each combustion-related toxin can be organized into one of the following categories: simple asphyxiants, chemical asphyxiants or irritants. Simple asphyxiants include carbon dioxide and methane, and work by displacing oxygen from a particular environment, including the "environment" in the lungs. Chemical asphyxiants include carbon monoxide, cyanide and hydrogen sulfide, which work by asphyxiation on the cellular level.

Acrolein, acetaldehyde, formaldehyde, acetic acid, formic acid, hydrogen chloride, phosgene, chlorine, ammonia, sulfur dioxide and isocyanates fall in the "irritant" category, because they cause illness/injury by burning and irritating the mucous membranes and lungs, eventually rendering the alveoli in the lungs useless for gas exchange. Each toxin category contains chemicals that are toxic to humans, but those typically found in concentrations considered immediately lethal to humans are the chemical asphyxiantsƒcarbon monoxide, hydrogen sulfide and cyanide.

Cyanide salts are commonly used in many industrial settings, like metal plating and paper manufacturing. In addition, many natural substances contain cyanide, including cassava root and the pits of peaches, apricots and apples. However, the most common environment in which EMS providers will encounter cyanide is during closed-space structure fires, when cyanide is produced as a gas secondary to the combustion of nitrogenous compounds, like plastics and polyurethanes.

The severity of cyanide toxicity is directly proportional to the specific tissues affected, and therefore, the route of exposure is critical. Due to the gaseous characteristic of the cyanide molecule and its weak acidity, it readily crosses all membranes, especially those of the alveoli in the lungs, which allows easy dissemination to the cells of all major organ systems. Consequently, fire-related inhalation can be a rapidly fatal route of exposure. Because the lethal cyanide dose for humans is approximately 200 mg, cyanide toxicity is dose-dependent and can be potentially lethal within seconds to minutes depending on the amount and concentration to which the victim is exposed.

Cyanide toxicity inhibits the body_s oxygen utilization and decreases the production of adenosine triphosphate (ATP), which is critical for the optimal functioning of the cardiovascular and central nervous systems.

Clinical Presentation

The clinical presentation of cyanide toxicity can take multiple forms. A complete and accurate history will be helpful in identifying a potentially toxic patient, but as with many emergency situations, time may not allow for an in-depth assessment. Certain clues regarding the nature and setting of the illness are important factors to consider. Therefore, consider cyanide in anyone presenting with: 1) soot in the nose or mouth and/or any non-specific symptoms following exposure to structure-fire smoke in an enclosed space for any duration, and/or 2) someone "found down" in any industrial setting.

It has been reported that the smell of "bitter almonds" is a hallmark of the presence of cyanide, either in the environment or in a patient_s exhaled air. However, only a small portion of the human population carries the gene for recognition of the bitter almond smell; therefore, this sign is considered unreliable.

A consistent clue of cyanide poisoning is the rapid development of symptoms with an onset closely following the duration of exposure to the toxin. The alert patient might present with non-specific complaints, such as headache, dizziness, nausea, vomiting, confusion/anxiety or difficulty breathing. In addition, patients may present with such neurological findings as an altered level of consciousness or seizures. Cardiovascular signs might include chest pain (myocardial ischemia/infarction), hypotension, dysrhythmias or cardiac arrest. In the mildly toxic patient, vital signs may be normal, but tachycardia, hypotension and tachypnea will typically be found in the moderately toxic patient.

Severe toxicity commonly presents with an altered level of consciousness, significant cardiovascular compromise and respiratory or cardiac arrest. In anyone presenting with an altered level of consciousness who has been exposed to closed-space smoke, assume cyanide poisoning until examination proves otherwise. In addition to cyanide toxicity, always remember to anticipate the signs of potential airway compromise in anyone recently exposed to smoke. Thermal injury from the inhalation of super-heated gases can cause upper airway edema and rapidly progress to complete airway obstruction. Therefore, early intubation should be considered.

EMS Treatment

Because potential routes of cyanide exposure include respiration, dermal absorption and ingestion, do not initiate care until you have taken adequate body substance isolation precautions and considered the proper personal protective equipment (PPE). If the toxin is suspected to be airborne, self-contained breathing apparatus and chemical protective clothing are required for the patient_s removal from the source. Continuous care of the patient should be continued while wearing PPE until decontamination has occurred. Proper decontamination includes the removal and isolation of the patient_s clothing and flushing of the skin with copious amounts of water. Bodily fluids, particularly vomit and respiratory secretions, should not be touched due to the possibility of dermal absorption by the EMS provider, and mouth-to-mouth resuscitation shouldneverbe performed without the proper pocket mask.

Treatment of cyanide secondary to smoke inhalation should, above all, include supporting airway, breathing and circulation. Never allow antidote administration to delay treatment of hypoxia, airway compromise or shock due to hypovolemia secondary to burns or other associated traumatic injuries. Adequate supportive care can, in some cases, save cyanide poisoned patients even without access to antidotal therapy. Aggressive oxygen therapy using any method necessary to protect and maintain an open airway, while supporting or providing adequate oxygenation and ventilation, is paramount. This can be synergistic with cyanide antidotes and is essential for treating carbon monoxide poisoning, which is also common in smoke inhalation patients. If the patient is in cardiac arrest, start CPR and perform treatment in accordance with local protocol and the American Heart Association 2005 ACLS guidelines.

In the case of a patient with a protected airway (either alert or intubated) with an ingestion exposure, activated charcoal administration should be considered following expert consultation. Activated charcoal doesn_t efficiently bind to cyanide, but given the extreme potency of the toxin, any amount of absorption by charcoal can be potentially lifesaving and should therefore be attempted. Benzodiazepines should be considered to correct seizures, and expert consultation should be considered to use sodium bicarbonate and vasopressors to correct metabolic acidosis and hypotension, respectively. In all cases of known or suspected cyanide poisoning from smoke inhalation, a poison control center should be contacted and expert consultation achieved.

Cyanide Antidotes

The prehospital empiric treatment of smoke-inhalation-related cyanide with antidotes has been quite controversial in the past few decades due to the inability to secure an accurate diagnosis in the field. Many hospitals can test cyanide levels through blood analysis; even those hospitals without on-site cyanide testing capabilities can typically identify lactic acidosis through basic lab values and co-oximetry, arterial blood-gas or venous blood-gas analysis. But without lab analysis technology available in the field for cyanide, the EMS provider can rely only on the circumstances of the patient_s environment and the clinical presentation. In addition, with the rapid deterioration commonly associated with a toxic patient_s condition, EMS providers have limited resources and may be too busy stabilizing the patient_s condition to consider an antidote.

Prior to the availability of the Cyanokit, the mainstay of antidotal treatment was the Cyanide Antidote Package (which is not recommended for prehospital use in the setting of smoke inhalation). However, now that the Cyanokit (hydroxocobalamin) is available in the U.S., empiric therapy for smoke inhalation provided by EMS providers is recommended, with the potential benefits of the drug far outweighing the risks of no treatment at all.

The classic cyanide antidote package, which has been marketed under such names as the Pasadena Kit and the Lilly Kit (Eli Lilly Company), and most recently, the Taylor Kit (Taylor Pharmaceuticals), requires a complex procedure and the administration of medications uncommon in the prehospital arena. The drugs contained in this kit include amyl nitrite pearls for inhalation, as well as sodium nitrite and sodium thiosulfate IV preparations. In this treatment method, the first step is to induce a condition known as methemoglobinemiaƒthe presence of methemoglobin in the blood. The development of methemoglobinemia is the first step in correcting cyanide poisoning. The methemoglobin allows for additional cyanide to be drawn from more vital cellular structures and eventually, with the aid of the next step, conversion to less toxic chemicals. The second step of this method involves administering sodium thiosulfate, which catalyzes hepatic rhodenase, an enzyme in the liver that metabolizes cyanide, combining the thiosulfate with the catalyzed cyanide to form thiocyanate, which is then sent to the kidneys for excretion.

The cyanide antidote package, while an effective treatment for known cyanide toxicity, has several limitations. Methemoglobinemia should not be induced in the known smoke inhalation patient due to the possibility of carbon monoxide being a concomitant toxin in the blood. Carbon monoxide in the blood forms a condition known as carboxyhemoglobinemia. This syndrome greatly reduces the hemoglobin molecule_s ability to successfully carry oxygen to the tissues. Methemoglobinemia induced in combination with existing carboxyhemoglobinemia can cause lethal hypoxia.

Further, the drugs in this kit can cause hypotension, which can exacerbate the hypotension effect from the cyanide. Because obtaining prehospital lab values isn_t currently an option, and the majority of cases of suspected cyanide exposure will be secondary to smoke inhalation, this method is inappropriate for the prehospital use.

Cyanokit is much easier to use in the field and has been used for decades in Europe with excellent results for known and suspected smoke-inhalation-induced cyanide poisoning. It was approved by the U.S. Food and Drug Administration in 2006 as an appropriate treatment for the U.S. market. Due to the safety profile and lack of serious side effects, the drug is suitable for use by EMS providers.

Hydroxocobalamin is an analog, or derivative, of vitamin B. In contrast with the cyanide antidote package, hydroxocobalamin does not induce methemoglobinemia and is easy to administer, which makes it readily appropriate for empiric therapy for suspected poisonings secondary to smoke inhalation. The only side effects are transient hypertension and red skin discoloration. The skin discoloration is of no clinical significance and will resolve in the 24Ï48 hours following administration. The transient blood pressure increase might be of great benefit because cyanide causes such profound hypotension in the symptomatic patient.

Conclusion

In the realm of treatment for cyanide toxicity from smoke inhalation, there is no direction to move but forward. EMS providers are in the critical role to provide swift treatment for emergent illnesses. With astute assessment and rapid treatment including modern antidotes, we can stamp out this common, lethal and often-overlooked illness.

John P. Benner,NREMT-P, is a practicing paramedic with the Charlottesville-Albemarle Rescue Squad, Madison County EMS, and special event medical management at the University of Virginia. He_s currently attending medical school in Virginia while he remains active in EMS.

David Lawrence,DO, is a practicing emergency physician and toxicologist at the University of Virginia. He_s a former EMT in various New Jersey agencies.

William Brady,MD, is a practicing emergency physician at the University of Virginia as well as operational medical director for the Charlottesville-Albemarle Rescue Squad, Madison County EMS, Seminole Trail Fire Department and special event medical management at the University of Virginia. Among other hospital duties, he also serves as the chair of the resuscitation committee at the University of Virginia Medical Center and medical director of paramedic education at the Peidmont Virginia Community College.

References

  1. Holstege CP, Kirk MA: "Smoke Inhalation." In Goldfrank_s Toxicologic Emergencies. McGraw-Hill. Columbus, Ohio, 2006.1749Ï57.
  2. Karter MJ: "Fire Loss in the U.S. 2007-A Full Report." NFPA Fire Analysis and Research, 2008. National Fire Protection Agency (NFPA).
  3. Morocco AP: "Cyanides." Critical Care Clinics. 21(4):691Ï705, 2005.
  4. Eckstein M, Maniscalco PM: "Focus on smoke inhalationƒthe most common cause of acute cyanide poisoning." Prehospital & Disaster Medicine. 21(2 Suppl 2):s49Ï55, 2006.
  5. Alarie Y: "Toxicity of fire smoke." Critical Reviews in Toxicology. 32(4):259Ï89, 2002.
  6. Fortin JL, Giocanti JP, Ruttimann M, et al: "Prehospital Administration of Hydroxocobalamin for Smoke Inhalation-Associated Cyanide Poisoning: 8 Years of Experience in the Paris Fire Brigade." Clinical Toxicology. 44(1 supp 1):37Ï44, 2006.
  7. Ferrari LA, Arado MG, Giannuzzi L, et al: "Hydrogen cyanide and carbon monoxide in blood of convicted dead in a polyurethane combustion: a proposition for the data analysis." Forensic Science International. 121(1Ï2):140Ï143, 2001.
  8. Holstege CP, Isom GE, Kirk MA: "Cyanide and Hydrogen Sulfide." In Goldfrank_s Toxicologic Emergencies. McGraw-Hill. Columbus, Ohio, 2006.1712Ï17247.
  9. Chyka PA, Seger D, Krenzelok EP, et al: "Position Paper: Single-Dose Activated Charcoal." Clinical Toxicology. 43(2):61Ï87, 2005.
  10. Nelson L: "Acute Cyanide Toxicity: Mechanisms and Manifestations." Journal of Emergency Nursing. 32(4, Supplement 1):S8ÏS11, 2006.
  11. Baud FJ: "Cyanide: critical issues in diagnosis and treatment." Human and Experimental Toxicology. 26(3):191Ï201, 2007.
  12. Borron SW: "Recognition and Treatment of Acute Cyanide Poisoning." Journal of Emergency Nursing. 32(4, Supplement 1):S12ÏS18, 2006.
  13. Koschel MJ: "Management of the Cyanide-Poisoned Patient." Journal of Emergency Nursing. 32(4, Supplement 1): p. S19-S26, 2006.
  14. Mlcak RP, Suman OE, Herndon DN: "Respiratory management of inhalation injury." Burns. 33(1)2Ï13, 2007.
  15. Barillo DJ: "Diagnosis and Treatment of Cyanide Toxicity." Journal of Burn Care and Research. 30(1):148Ï152, 2009.
  16. Lawrence DT, Kirk MA: "Chemical Terrorism Attacks: Update on Antidotes." Emergency Medicine Clinics of North America. 25(2):567Ï595, 2007.

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