JEMS Clinical Review Feature
Asphyxiant: Any gas capable of causing death due to oxygen displacement.
Decompensation: The failure of a system.
Hypoxia: Decreased oxygen in the cells. Symptoms include cyanosis, tachycardia and altered levels of consciousness.
Ischemia: Poor blood supply to an organ or part, often marked by pain.
Phosgene: Toxic, colorless gas causing severe pulmonary edema by destruction of alveolar tissue.
>> Identify the four mechanisms of toxic inhalation.
>> Recognize the injuries caused by the inhalation of toxic chemicals.
>> Determine the treatment for cyanide poisoning and other inhalation injuries.
You’re dispatched to the rear of a suburban shopping center for an unresponsive person inside a vehicle. While responding, you receive additional information: The caller reports a second patient who’s lying on the ground next to the vehicle, coughing forcefully and thrashing around.
Moments later, dispatch tells you that additional 9-1-1 callers and first arriving police officers report a vehicle “parked at an odd angle and not running” behind the shopping center. And there’s an odd odor emanating from the vehicle. Dispatch informs you that they’ve also requested the fire department and a hazmat team to respond.
You arrive on location to find the vehicle parked in an unusual manner, with cigarette butts and other debris on the ground next to the driver’s door. It appears as if someone was in the vehicle for a while. As you do a scan of the entire scene, you notice someone on the ground next to the passenger side of the vehicle. The police officer reports that he drove up to the vehicle when he arrived and saw some odd notes taped on the driver’s side window. As he approached the vehicle, he saw three separate notes that read, “Call 9-1-1,” “Do not enter,” and “You will die.” The officer says he could hear the person next to the car moaning but didn’t think it was safe for him or others to approach and remove the victim from the area because of the odor in the air and notes on the car window.
You return to your ambulance and locate your binoculars. As you glance at the vehicle, you’re able to read the notes clearly and confirm what the officer had already reported. It appears this was a double suicide attempt by the car’s occupants, but one may have changed his mind and attempted to get away from the vehicle. You can see that the male patient lying on the ground next to the vehicle is attempting to crawl away. Then you also begin to notice an odd smell.
Your partner asks, “Does that smell like rotten eggs?”
A fire officer arrives on scene, and you brief him on what you and the police have seen and detected so far. He immediately states that you’re too close and need to retreat to a more distant location.
After relocating to an upwind position, a joint command post is established and initial air monitoring is conducted by fire personnel. The hazmat crew arrives, dons their suits and approaches the vehicle. As they approach the vehicle, they report back to command that their meters are showing dangerously high levels of hydrogen sulfide (H2S) in the area. They also report that the patient lying on the ground is breathing poorly and is in need of medical attention as soon as they can extricate him from the area and decontaminate him.
The hazmat crew begins decontaminating the patient with a standard solution of soap and water, and you prepare your equipment to care for him. In addition to the patient’s respiratory problems, he may be hypothermic because the ambient temperature outside is 28º F, and you don’t know how long he was lying on the ground.
Your partner turns the heat in the patient compartment on high, turns the defroster on high and places towels along the dashboard to warm them. As your partner leaves the ambulance, he gathers all the hot packs he can carry to warm the patient.
The hazmat crew advises that the female inside the vehicle is obviously deceased, and the crew sees several empty chemical containers inside. They also report extremely high levels of H2S inside the vehicle.
The patient outside the vehicle is finally brought to you after he’s been thoroughly decontaminated. He appears to be in his late teens or early 20s. The first thing you note is his bright red skin and a stream of frothy, orange emesis coming from his nose and mouth. The patient has snoring respirations and is unresponsive to all stimuli.
You immediately begin ventilating the patient with a bag-valve mask (BVM), and you’re able to easily insert an oropharyngeal airway. You load the patient into your ambulance and begin rapid transport to the hospital.
You continue to ventilate the patient as you obtain baseline vital signs. You find the patient is tachycardic and has a slow respiratory rate. Pulse oximetry shows 86% saturation of peripheral oxygen. You initiate IV access, begin administering warmed normal saline and wrap him in a thermal blanket.
Again, the patient begins to vomit frothy, orange emesis. You suction copious amounts of it out of his mouth and nose and are now having a hard time ventilating him. You elect to intubate the patient and do so without difficulty while continuing suction. You attach a digital end-tidal carbon dioxide (EtCO2) device and continue ventilation. As you near the hospital, you suddenly notice that you have a headache unlike any you’ve ever had before. Your eyes begin to tear. Your throat begins to feel sore, and you start coughing.
You ask your partner to hurry up in getting to the hospital because you now feel nauseated and think you’re going to vomit and pass out. As you arrive at the hospital, all your symptoms worsen. You transfer care to the emergency department (ED) staff and are subsequently admitted for evaluation.
You’re diagnosed as having been exposed to low levels of H2S. Your supervisor tells you a few hours later that your patient died from his high level exposure and inhalation.
The initial approach to any toxic inhalation situation is the same. First, scene safety is paramount. The rescuer is at unequivocal risk to fall victim to the same inhaled agent(s) as the patient. Use of appropriate hazmat resources, personal protective equipment—including self-contained breathing apparatus—and decontamination are mandatory when managing patients with toxic inhalations.
Once the patient is safely accessible for the EMS provider, the mainstay of patient treatment is supportive care, with high-flow, 100% oxygen, BVM ventilation and endotracheal intubation (ETI) as needed. In certain toxic inhalations, the more specific treatments described below may also be indicated.
Inhaled agents manifest their toxic effects by four different mechanisms: physical particulates, simple asphyxiants, chemical irritants and chemical asphyxiants. Additionally, if the inhalation occurs in the setting of a fire, heat can cause life-threatening upper airway burns.
Physical particulates are small, solid particles that are carried by gases or atmospheric air into the body through inhalation (e.g., dust or combustion soot). In general, these small particles cause physical irritation to the upper airways. In some cases, extremely small particles may even be carried down to the alveolar level and cause mechanical problems, such as impairing proper gas exchange. Physical particulates may act as vehicles that carry toxic chemicals, such as organic acids, throughout the respiratory system. This situation is encountered most commonly with cases of smoke inhalation.
The signs and symptoms of physical particulant exposure are the result of irritation of the respiratory system. This usually includes excessive coughing and some degree of shortness of breath. If the affected patient has a history of underlying pulmonary disease, such as asthma or chronic obstructive pulmonary disease (COPD), then these effects can be greatly magnified and even cause decompensation, which results in severe respiratory distress.
Management is supportive: Remove the patient from the source of the physical particulates, and administer oxygen. Patients with signs of reactive airway disease (e.g., wheezing and poor air flow) should be treated with nebulized bronchodilators, such as albuterol.
Simple asphyxiants cause injury by merely being present in an environment and displacing the normal levels of atmospheric oxygen. These gas agents include carbon dioxide (CO2), nitrogen, methane and natural gas. Simple asphyxiants are encountered when the environmental atmosphere becomes abnormally loaded with one of these gases at such high concentrations that they significantly or completely push the normal oxygen out. Simple asphyxiants have no inherent toxic or metabolic effect on the body’s cells, other than causing hypoxia by default due to lack of adequate oxygen.
The signs and symptoms of exposure to a simple asphyxiant depend on the specific agent involved and the relative concentration of the agent in the atmosphere (i.e., how severe the lack of atmospheric oxygen is). Patients will exhibit such classic signs of hypoxia as agitation, which may rapidly progress to unconsciousness and then cardiac arrest. If the simple asphyxiant is CO2, patients may experience a narcotic-like sleepiness as the initial effect of exposure.
The mainstay of simple asphyxiant management is gaining safe access to the patient, followed by high-concentration oxygen administration and cardiopulmonary support as indicated.
Chemical irritants express their toxic effects by chemical reaction with the mucus membranes of the eyes and respiratory system. Two general classes of chemical irritants: those that react readily with water and those that don’t. Chemical irritants that are highly reactive with water are called hydrophilic (“water loving”) chemicals. Hydrophilic inhaled agents include hydrochloric acid and ammonia.
These agents react quickly with the moist membranes of the eyes and the upper respiratory tree, causing immediate intense burning and pain. Because non-hydrophilic agents don’t readily react with the moist membranes of the upper respiratory tract, they can pass more deeply into the lungs and cause direct lung injury. Sometimes these effects are delayed, and a patient may be relatively stable for a while and then decompensate with respiratory failure due to acute lung injury. An example of a non-hydrophilic chemical irritant is phosgene gas.
Treatment of chemical irritant exposures should include supportive care and irrigation of eyes with water or saline. As with particulate irritants, patients with underlying asthma or COPD will likely benefit from nebulized albuterol treatments if bronchospasm is evident during physical examination.
Simply stated, chemical asphyxiants cause injury by asphyxiating patients at the cellular level by massively deranging normal cellular utilization of oxygen. The most common example of a chemical asphyxiant is carbon monoxide (CO). A product of combustion, CO rapidly displaces oxygen from the hemoglobin, forming carboxyhemoglobin (COHgb). Other examples of inhaled chemical asphyxiants are cyanide gas (HCN) and, as seen in the case presented earlier, H2S. Both HCN and H2S block the effective use of oxygen within the cell. This causes rapid body-wide ischemia, which results in a severe metabolic acidosis.
Signs and symptoms of inhaled chemical asphyxiant exposure depend on which specific agent the patient has been exposed to. CO poisoning often has a gradual, even insidious, onset of symptoms, which may include headache, chest pain and decreasing mental status. Frequently, the patient progresses to coma and death.
Patients exposed to H2S and HCN tend to have a very rapid onset and progression of symptoms. The treatment for CO poisoning is supportive care with high-flow oxygen via a non-rebreather mask or ET tube for the comatose patient. High-concentration oxygen helps “push” the CO off the stricken patient’s hemoglobin and allow the return of normal oxygen transport by the red blood cells. CO-exposure patients with high blood levels of COHgb or those who are pregnant, have signs of cardiac ischemia or have a loss consciousness are all candidates for hyperbaric oxygen therapy.
H2S poisoning has several unique features, including the characteristic “rotten egg” smell that was noted in our scenario. At high concentrations, however, the appreciation of this characteristic odor may be rapidly lost. H2S is also unique because it possesses its primary chemical asphyxiant and chemical irritant properties, resulting in eye and upper airway irritation and burning. At high concentrations, H2S can cause can cause death after just a few breaths. The treatment for H2S exposure includes supportive care with high-concentration oxygen and ETI if indicated.
The “off ventilation” of exhaled H2S from the contaminated patient’s pulmonary tree may be significant enough to cause some level of toxicity to the EMS provider. For this reason, adequate ventilation of the patient compartment during transport is essential. Additional advanced therapies for the H2S-poisoned patient may include the use of the nitrite component of the standard cyanide kit and hyperbaric oxygen therapy.
Cyanide is the final, major chemical asphyxiant agent. Rapid intervention by ALS providers plays a critical, life-saving role in the management of patients suffering from cyanide poisoning. The seriously poisoned cyanide victim classically presents with unresponsiveness, hyperventilation and hypotension without evident cyanosis. Once cyanide poisoning is suspected, either based on this clinical presentation or hazmat information provided on the scene, EMS providers should immediately initiate cyanide antidote therapy.
The typical cyanide antidote kit has been the standard of emergency care for more than 50 years. The kit contains three drugs designed to be administered in the following sequence: inhaled amyl nitrite, IV sodium nitrite and IV sodium thiosulfate. More recently, a safer cyanide antidote has become available in the U.S. IV hydroxocobalamin, combined with sodium thiosulfate, has been used successfully in Europe for many years and avoids the side effects (e.g., hypotension and derangement of normal hemoglobin) of nitrite therapy used in the standard cyanide kit. As with all toxic inhalations, supportive care with 100% oxygen should be used in all cyanide inhalations. Indeed, high-flow oxygen has been shown to enhance the effectiveness of IV cyanide antidotes.
Although we presented a chemical suicide, toxic inhalations are also frequently encountered in industrial settings. It’s only a matter of time before an emergency responder falls victim to someone’s failed or actual suicide attempt by way of H2S or other chemical irritants or asphyxiants. Remember, scene safety is and must be your No. 1 priority. It’s paramount to your survival and overall success. Maintaining a high index of suspicion for potential injury, coupled with a strong knowledge base, will lead to your success. JEMS
1. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice. Mosby: St. Louis, Mo. 2010.
2. Tintinalli J, Kelen G, Stapczynski J: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill: New York. 2010.
This article originally appeared in May 2011 JEMS as “Toxic Transport: Treating inhalation injuries without becoming a patient.”