The cellular asphyxiants are a diverse group of substances including carbon monoxide (CO), cyanide, sodium azide, methemoglobin-producing oxidizing agents, and hydrogen sulfide, all of which interfere with the cellular utilization of oxygen. Depending on the substance, the interference may occur at the level of hemoglobin, the electron transport chain, or both. In contrast with the simple asphyxiants, ambient oxygen concentrations are not affected.
CO is a colorless and odorless gas generated from the incomplete combustion of carbonaceous compounds. The affinity of CO for hemoglobin is 250 times greater than that of oxygen. Binding of CO to hemoglobin shifts the oxyhemoglobin dissociation curve to the left, further impairing tissue oxygen delivery. Symptoms of acute poisoning may range from headache to ischemic chest pain, seizures, and CNS depression. Up to 40% of poisoned patients develop delayed neurologic sequelae (DNS); most cases of DNS are associated with an initial loss of consciousness.
Although a nonspecific enzyme inhibitor, cyanide interferes with oxidative phosphorylation. Sources of cyanide include industrial and household chemicals, plants, and structure fires. Clinical manifestations reflect dysfunction of oxygen-sensitive organs, including the CNS and cardiovascular systems. A cyanide toxidrome has been described, consisting of altered mental status, mydriasis, respiratory depression, hypotension, tachycardia, and metabolic (lactic) acidosis.
Carbon Monoxide Poisoning. Venous blood samples with the bright red one (bottom sample) taken from a patient with acute carbon monoxide poisoning. The dark red venous blood (top sample) is a control sample from a patient with no carboxyhemoglobin. (Photo contributor: Daniel L. Savitt, MD.)
Management and Disposition
Immediate management focuses on airway stabilization and antidotal therapy. Carboxyhemoglobin levels should be obtained in patients with suspected CO poisoning. Pregnancy status should be determined in females presenting with suspected CO poisoning. Blood cyanide levels are not typically available in the immediate care setting. While 100% oxygen is the accepted antidote for acute CO poisoning, controversy persists regarding the mode of administration (normobaric oxygen versus hyperbaric oxygen). Potential indications for hyperbaric oxygen include syncope, altered mental status (especially with evidence of cerebellar dysfunction), acidosis, and pregnancy. Therapy for cyanide poisoning includes intravenous administration of hydroxocobalamin. Hydroxocobalamin has the advantage of raising blood pressure, but also causes intense red skin discoloration and chromaturia.
Skin Changes after Hydroxocobalamin. After administration of therapeutic dosing of hydroxocobalamin, the skin of the patient may exhibit a bright red color. (Reproduced with permission from Uhl W, et al. Safety of hydroxocobalamin in healthy volunteers in a randomized, placebo-controlled study. Clin Toxicol. 2006;44:17–28. Copyright © Informa Healthcare.)
Chromaturia after Hydroxocobalamin. Shortly after the intravenous administration of hydroxocobalamin, chromaturia may be evident. (Photo contributor: Saralyn R. Williams, MD.)