Smoke Inhalation and Carbon Monoxide Poisoning

Chapter 56

Smoke Inhalation and Carbon Monoxide Poisoning

Kevin C. Wilson and Arthur C. Theodore

Fires cause approximately 2500 deaths in the United States each year. Most are the result of smoke inhalation rather than burns. Smoke inhalation can cause death by several mechanisms, with carbon monoxide (CO) poisoning being the most common.

Fires are not the only cause of CO poisoning. Other potential causes include poorly functioning heating systems, improperly vented fuel-burning devices (e.g., furnaces, stoves, gasoline-powered electrical generators), and motor vehicles operating in poorly ventilated areas (e.g., parking garages). CO poisoning may also be intentional. Taken together, accidental and intentional CO poisoning causes 5000 to 6000 deaths in the United States each year.

Pathophysiology

Smoke inhalation may cause thermal injury, bronchopulmonary injury resulting from inhalation of toxins, oxygen depletion, or poisoning caused by CO, hydrogen cyanide, or other systemic toxins. Each is capable of inducing rapid systemic tissue hypoxia and death.

Thermal Airway Injury

Thermal injury occurs when heat from the fire and smoke injures the mucosa of the airways, causing erythema, edema, and ulceration. The edema typically becomes noticeable within 24 hours, lasts 3 to 5 days, and may be severe enough to compromise airway patency.

The supraglottic airway is the most common site of thermal injury. Although rarely occurring, thermal injury to the lower airways tends to be severe and is often associated with the inhalation of steam.

Toxin-Mediated Lung Injury

Smoke contains liquid droplets and elemental carbon that can adsorb toxic combustion products, such as acrolein, formaldehyde, phosgene, chlorine, perfluoroisobutylene, sulfur dioxide, nitrogen dioxide, and nitric oxide (Table 56.1). Inhalation of such toxins can directly injure the respiratory mucosa of the upper and lower airways, as well as the alveolar spaces. This can occur even in the absence of thermal injury.

TABLE 56.1

Toxic Products of Combustion

Chemical	Sources	Injury Produced
Aldehydes	Plastic from furniture	Upper airway injury and CNS depression
Acrolein	Acrylics from windows, wood finishes, or wall coverings	Diffuse airway and alveolar injury
Ammonia	Phenolics and nylon	Upper airway injury
Anhydrides	Chemical, paint, plastics	Airway injury, asthma, pulmonary hemorrhage with high-dose exposure
Carbon dioxide	Closed space fires (as high as 10% CO₂)	Respiratory acidosis, CNS depression
Cyanide	Carpets, upholstery, nylon, polyurethane products from isocyanates	Acidosis, shock, asthma, airway injury, hypersensitivity pneumonitis
Hydrogen chloride	Fabrics, polyvinyl chloride	Mucosal burns and edema, dysrhythmias, shock
Hydrogen fluoride	Polytetrafluoroethylene (Teflon) from pipes or kitchen utensils	Upper airway injury
Nitrogen dioxide	Nitrocellulose	Alveolar injury

CNS, central nervous system; CO₂ carbon dioxide.

Modified from Sheppard D: Noxious gases: pathogenetic mechanism. In Baum G, Wolinsky E (eds): Textbook of Pulmonary Diseases, 4th ed. Boston: Little, Brown, 1989, pp 840-841.

Chemical injury to the airways causes focal corrosion, neutrophilic airway inflammation, and disruption of mucociliary transport. Damage to the mucosal barrier can lead to increased susceptibility to respiratory infections. Alveolar injury occasionally results in the acute respiratory distress syndrome (ARDS), with increased alveolar and capillary permeability, interstitial and alveolar edema, impaired lymphatic flow, neutrophilic inflammation, hyaline membrane formation, and worsened ventilation-perfusion mismatching (see Chapter 73). Individuals who survive may develop fibrosis.

The extent and location of the injury depend on the duration of exposure, the patient’s minute ventilation, particle size, and water solubility of the toxins. A long duration of exposure or a high minute ventilation favors more severe bronchopulmonary injury. Small particles (<0.1 micron in diameter) are deposited primarily in the lung parenchyma, whereas larger particles (2 to 5 microns) are distributed throughout the respiratory tract.

Oxygen Depletion

During a fire, the air becomes hypoxic because the fire consumes ambient oxygen. Breathing hypoxic air decreases the alveolar oxygen concentration, which decreases the amount of oxygen available to bind hemoglobin or dissolve in the blood. The consequence is less oxygen delivery to the tissues and systemic tissue hypoxia.

Systemic Toxins

A variety of systemic toxins are inhaled during a fire, many of which can induce systemic tissue hypoxia via a variety of mechanisms. Examples include CO and hydrogen cyanide poisoning. CO forms carboxyhemoglobin (COHb) and impairs the delivery of oxygen to the tissues, whereas hydrogen cyanide binds to the mitochondrial cytochrome complex and interferes with the utilization of oxygen by the tissues. The effects of systemic toxins are frequently synergistic.

Carbon Monoxide

CO is a colorless, odorless, tasteless, nonirritant gas that is normally present at ambient concentrations of less than 0.001%. CO uptake into the lung is augmented when there is an increase in the ambient concentration of CO, the duration of exposure to CO, or the minute ventilation. In these situations, CO rapidly diffuses from the alveolus into the blood and binds hemoglobin, forming COHb. This competitively inhibits the formation of oxyhemoglobin, because CO binds to hemoglobin with an affinity that is 230 times greater than the affinity of oxygen for hemoglobin. The result is diminished oxygen delivery to the tissues and systemic tissue hypoxia.

Decreased oxyhemoglobin formation is not the only mechanism by which CO impairs oxygen delivery. Both CO poisoning and the respiratory alkalosis that commonly accompanies it shift the oxyhemoglobin dissociation curve to the left, which impairs the release of the oxygen to the tissues (see Figure A.1B in Appendix A). The shift of the oxyhemoglobin dissociation curve to the left is a consequence of a CO-induced conformational change of the hemoglobin, making it more oxygen avid.

Fetuses are particularly susceptible to the detrimental effects of CO poisoning because CO has significantly greater affinity for fetal hemoglobin than hemoglobin A. As a consequence, fetal demise often occurs in pregnant women who are otherwise successfully treated for CO poisoning.

Approximately 10% to 15% of the CO that diffuses from the alveolus binds to extravascular proteins (e.g., myoglobin, cytochrome-c oxidase, guanylate cyclase, nitric oxide synthase) instead of hemoglobin. This CO slowly dissociates from the extravascular proteins, creating a delayed phase of CO toxicity characterized by persistent derangements of oxidative metabolism, as well as myocardial and skeletal muscle function. Neurologic sequelae are due to perivascular neural injury caused by oxidative injury from oxygen-free radicals.

By the time the delayed phase occurs, COHb levels are often normal because the CO has dissociated from hemoglobin. The half-life of COHb is approximately 320 minutes when a patient is breathing ambient air with 21% oxygen concentration at sea level. This half-life is reduced to 60 minutes if the patient breathes 100% oxygen, and it is further reduced to 23 minutes if the patient breathes 100% oxygen under 2.5 to 3 atmospheres of pressure. The latter is referred to as hyperbaric oxygen (HBO). In addition to reducing the half-life of COHb, HBO can increase the amount of oxygen dissolved in plasma to a level sufficient to meet the basal oxygen requirements of tissues, even in the absence of functional hemoglobin.

Acceleration of CO excretion and augmentation of oxygen delivery are the primary rationales for HBO therapy in acute CO poisoning, which is discussed later. However, HBO therapy may also prevent the formation of oxygen species responsible for brain lipid peroxidation and thereby limit the extent and frequency of delayed neurologic sequelae.

Hydrogen Cyanide

Cyanide avidly binds to the ferric ion of cytochrome-c oxidase a3 (the final enzyme in the mitochondrial cytochrome complex) and other enzymes of the Krebs cycle, halting electron transport and the process by which hydrogen ions are converted to adenosine triphosphate (ATP). This cessation of aerobic metabolism forces the cell to convert to anaerobic metabolism in order to generate the ATP that is necessary for survival. The inability to utilize oxygen, even if amply supplied to tissues, is particularly deleterious to the cardiovascular and central nervous systems.

Cyanide poisoning may exacerbate central nervous system injury by numerous other mechanisms. First, inhibition of antioxidants (e.g., catalase, glutathione reductase, superoxide dismutase) leads to the accumulation of toxic oxygen-free radicals. Second, release of glutamate causes detrimental stimulation of N-methyl-d-aspartate (NMDA) receptors. Finally, inhibition of glutamic acid decarboxylase reduces the seizure threshold.

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Jul 7, 2016 | Posted by admin in CRITICAL CARE | Comments Off

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