Course Toxic Exposures

Carbon Monoxide

Carbon monoxide (CO) poisoning is frequently seen after any type of natural disaster. Faulty or insufficient exhaust systems with the use of damaged furnaces, generators, camp stoves, or wood fires can be a prevalent hazard following an acute disaster. Since CO is colorless and odorless, patients do not realize that they are being exposed. Standard universal precautions applicable to all patients should be used. Victims will not exhale CO but carbon dioxide, so there is no risk of secondary contamination. Symptoms of CO exposure vary from fatigue, headache, ataxia, and nausea, to total loss of consciousness (based on seriousness of exposure). CO binds avidly to hemoglobin, creating carboxyhemoglobin. Carboxyhemoglobin does not readily release oxygen when compared with normal oxyhemoglobin. This results in tissue and cellular hypoxia. Consequently, in severe exposures patients may lose consciousness secondary to hypoxia and if not removed from the exposure will eventually die. CO is also directly cardio and neurotoxic. When CO poisoning is suspected, the most important initial treatment is removing the patient from the exposure and allowing him or her to breathe uncontaminated air. Administer supplemental oxygen via face mask, if available. Once in the hospital, certain laboratory tests may be useful. Measuring carboxyhemoglobin leads to a definitive diagnosis. Hemoglobin/hematocrit values can be used to detect underlying anemia, which can contribute to decreased oxygen carrying capacity. Remember that peripheral saturation (pulse oximetry) gives a falsely normal (or low normal) result, since COHb has a light spectrum quite similar to oxyhemoglobin. Hyperbaric oxygen therapy (HBO) have been used with severe exposures to decrease half-life of carboxyhemoglobin (330 minutes to 20 minutes) and prevent delayed neurologic sequelae. However, clear evidence for benefit has not been proven. Limited availability and critical illness also limits use of HBO and probably will not be of much use in disaster situations.

Cyanide

Cyanide is released from combustion of plastics, wool, silk, nylon, synthetic rubber, paper, and melamine resins. Consider cyanide exposure if synthetic materials are involved in the fire or in patients with carbon monoxide poisoning and severe metabolic acidosis. Cyanide disrupts mitochondrial oxidative metabolism, and affects all tissues, particularly those most metabolically active, such as brain and heart. Early findings include tachypnea and hyperpnea, tachycardia, dizziness, headache, nausea and vomits. More severe exposures are associated with CNS depression, coma and seizures. Respiratory depression can occur.

Recommendations for on site management include decontamination of victims, particularly those exposed to the liquid agent, including removal of wet clothes and skin washing. Administer 100% oxygen supplementation and respiratory support as needed. Give antiepileptic agents, such as benzodiazepines, for seizures, and crystaloid infusion if the victim is hemodynamically unstable.

After arrival to the hospital, certain laboratory tests may be useful in the management of these patients. Laboratory abnormalities include severe metabolic acidosis and hyperlactatemia.

There are specific therapeutic measures available for cyanide poisoning, however would not return to affect acute clinical care.

Hydroxocobalamin should be considered the first line antidote. It is administered intravenously and is considered to be relatively safe. It may cause hypertension which is temporary. It causes a deep red coloration of bodily fluids which may interfere with certain laboratory tests and pulse oximetry.

Alternative or older cyanide treatment consists of nitrates and sodium thiosulfate. Amyl nitrate and sodium nitrate induce methemoglobinemia which dissociates cyanide from cytochrome oxidase. Caution is required, since this agent can cause hypotension and overproduction of methemoglobin, thus compromising oxygen transport capacity in patients with already comprised state (ie CO toxicity). Sodium thiosulfate transforms cyanide to thiocyanate which is renally excreted.

While recovery is rapid if cyanide poisoning is well and timely treated, without proper management, it can cause rapid death. Because cyanide levels are usually not readily available, consider empiric treatment for cyanide toxicity in a patient with severe acidosis, hyperlactatemia and hypotension who was exposed to a house/ industrial fire.

Poisons

Animal displacement after a large-scale natural disaster can also lead to unexpected, secondary toxin exposures. Be aware of what type of poisonous animals are prevalent in the community. Snakes are a particular problem, and rescue and medical staff should be knowledgeable about treatment of such problems. In the past, incision of the bite, putting ice on the wound, and placing a tourniquet was recommended. Currently, none of these recommendations are in place. Instead, wash the bite with soap and water, immobilize the extremity, and keep it below the level of the heart. Then transfer the patient to the hospital as fast as possible. It is estimated that up to approximately 30% of snake bites contain little or no venom. Ideally, the patient is observed for signs and symptoms of poisoning in a setting in which antivenom is immediately available. Administer antivenom upon signs of patient distress. Antivenom can also be administered by transport service with proper knowledge, especially if the patient is coming from a remote location.