Pulmonary Medicine

Thermal Injury and Smoke Inhalation

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What every physician needs to know:

Inhalation injury, including smoke inhalation, is common and potentially life-threatening, and it affects millions of people worldwide. Smoke is a combination of fumes (small, suspended particles to which irritants or cytotoxic chemicals adhere), mists (aerosolized irritants or cytotoxic chemicals), gases, and hot air. Exposure to smoke that arises from a burning environment may result in three types of injury: (1) direct thermal injury to the airways, particularly the upper airways; (2) chemical injury to the airways, including those of the lower respiratory tract, and lung parenchyma; and (3) systemic injury as a result of inhalation of toxic compounds. A wide variety of additional compounds may be generated in fires, many with potential toxicity (Figure 1).

Figure 1.

Oxyhemoglobin dissociation curve in the presence and absence of carbon monoxide.

Several well-publicized events, such as the fire at the Coconut Grove nightclub in Boston in 1942, the collapse of, the World Trade Center in New York in 2001, and the devastating nightclub fire in Rhode Island in 2005, highlight the possibility of mass casualties related to smoke inhalation. However, it is the prevalence of single home fires, each affecting relatively small numbers of people, that accounts for most fire-related inhalational injury in the United States.

This presentation focuses on thermal respiratory injury and the consequences of inhaling a selected number of respirable agents common in household and industrial fires.


Important Factors in Assessing the Potential Clinical Impact of Smoke Inhalation

Several environmental factors are key determinants of the clinical consequences of acute smoke inhalation: the source of the fire and resulting combustion products, the duration of the exposure, and ventilation of the environment.

Source of the fire and resultant combustion products - The degree of injury depends on the specific materials inhaled, their concentrations, their water solubility, and particle size, among other considerations. Water-soluble materials like acrolein and aldehyde damage the proximal airways. Less water-soluble substances like phosgene and nitrogen oxides are associated with a slower onset of injury to the more distal airways. Carbon monoxide and hydrogen cyanide produce systemic toxicity, rather than localized pulmonary injury.

Commonly employed building products have shifted from wood and organic substances to synthetics and petrochemicals, materials that burn more intensely and faster than wood and other natural products, increasing the likelihood that fire victims will inhale toxic materials in smoke before being able to escape the environment. (Table 1)

Table 1.

Examples of Potential Toxins and Their Sources in Inhaled Smoke

Duration of the exposure - Individuals exposed to smoke-filled environments for a more extended time will have greater cumulative exposure to the toxic materials generated. A number of factors influence total exposure per unit of time, including the victim's minute ventilation.

Ventilation of the exposure environment - More tightly enclosed environments are associated with greater intensity of toxin exposure.

Are you sure your patient has thermal injury or smoke inhalation injury? What should you expect to find?

The symptoms and signs of smoke inhalation can be divided into general findings in inhalational injury and those attributable to specific toxins, the most common of which are carbon monoxide and hydrogen cyanide. (Table 2)

Table 2.

Clinical Manifestations of Carbon Monoxide Poisoning

General Signs of Inhalational Injury

  • Burns of the neck and face

  • Singed nasal hair

  • Soot-laden oral and nasal secretions

  • Cough, dysphonia, and stridor

  • Tachypnea and cyanosis

  • Nausea and vomiting

  • Neurologic findings, including loss of consciousness

Clinical Manifestations of Carbon Monoxide Poisoning

With mild exposure, neurologic symptoms include headache, dizziness, myalgias, and neuropsychological impairment. More significant exposures are associated with confusion, loss of consciousness, and possible death. Tachycardia, increased cardiac output, arrhythmias, and cardiac ischemia may also be evident. Retinal hemorrhages and cherry-red skin color, the "classic" manifestations of carbon monoxide poisoning, are uncommon.

Signs of chronic carbon monoxide exposure may be subtle. These signs include chronic fatigue, behavioral changes, memory lapses, impaired sleep, changes in bowel habits, and a variety of peripheral neurologic findings.

Clinical manifestations do not correlate with carbon monoxide levels, suggesting that the resultant hypoxemia is not primarily responsible for the findings.

Clinical Manifestations of Hydrogen Cyanide Poisoning

Early signs include anxiety, confusion, headache, hypertension, dyspnea, and tachypnea. Subsequently, coma, seizures, pupillary dilatation, hypotension, bradycardia, and arrhythmias occur. Complete cardiovascular collapse may ensue.

Funduscopic examination may reveal "arterialization" of venous blood--that is, a bright red color that is associated with adequately oxygenated arterial blood. The finding reflects inhibition of oxygen consumption by poisoned tissues, resulting in an inappropriately high oxygen content of venous blood. The same phenomenon may be seen with inspection of a peripheral venous blood sample.

Beware: there are other conditions that can mimic thermal injury or smoke inhalation injury:

Not applicable.

How and/or why did the patient develop thermal injury or smoke inhalation injury?

Pathophysiologic Consequences of Thermal and Chemical Respiratory Injuries

Heat itself is rarely responsible for inhalational injury to the upper airways and tracheobronchial tree. Because of the low heat capacity of inhaled air and the highly efficient heat-exchanging capacity of the bronchial circulation, inspired gases rapidly equilibrate to body temperature in the upper airway before they pass through the thoracic inlet. An exception is steam inhalation, as steam has high latent heat and can induce significant direct thermal injury to the airways.

A variety of chemicals in inhaled smoke may induce substantial chemical injury to the airways. Many derivatives of these materials contain reactive nitrogen and oxygen species, acids, and aldehydes that induce a significant inflammatory response within the tracheobronchial tree.

As demonstrated in animal studies, increases in bronchial blood flow are seen within minutes of smoke inhalation. In humans, direct visualization of affected airways reveals hyperemia. Tissue injury and shedding of the airway epithelial lining, coupled with formation of protein-containing exudates and increased mucus production by goblet cells, result in an inflammatory medium that solidifies or mixes with blood clots in the airway lumen to form airway casts. The casts may completely occlude airways, including the upper airways, resulting in airway obstruction and hypoxemia.

Localized airway occlusion is associated with regional loss of hypoxic pulmonary vasoconstriction and produces increasing ventilation-perfusion mismatch, shunting, and hypoxemia. Significant airway obstruction may not occur immediately; up to twenty-four hours may be necessary for formation of mucosal edema sufficient to result in airway occlusion.

Ciliary dysfunction further impedes normal airway clearance mechanisms. As a consequence of ciliary damage, airways are at increased risk for obstruction and secondary bacterial infection.

Lung parenchymal injury following smoke inhalation is typically not seen immediately. Over the course of several hours, diffuse alveolar damage (DAD) and atelectasis develop, and loss of hypoxic pulmonary vasoconstriction and hypoxemia are seen. Increased procoagulant and decreased anti-fibrinolytic activity result in fibrin deposition in alveolar spaces. An influx of inflammatory cells also occurs.

Systemic responses to the exposure, including the systemic inflammatory response syndrome (SIRS), increased oxygen consumption, and release of inflammatory mediators into the lung that produce noncardiogenic pulmonary edema or acute respiratory distress syndrome (ARDS), may be observed. These changes may be delayed by 24-48 hours.

Effects of Specific Components of Toxic Smoke

Particulates - Normally, nasopharyngeal structures clear inspired air of particles suspended in smoke or air that have a particle diameter larger than 5 µ. In a fire environment, victims typically breathe through their mouths as a result of nasopharyngeal edema and dyspnea. Consequently, less filtering of large particles and more significant particle deposition occur in the airways, particularly proximally, with attendant airway injury.

Carbon Monoxide - Carbon monoxide (CO) is a colorless, odorless gas derived from incomplete combustion of wood, paper, and cotton. In addition to fires, environmental sources include malfunctioning furnaces and internal combustion engine exhaust. CO poisoning accounts for approximately 50,000 visits to emergency rooms annually in the United States.

At physiologic levels, CO serves as a neurotransmitter and modulates inflammation, cell proliferation, and programmed cell death (apoptosis). At toxic levels, CO induces inflammation and causes hypoxia. CO binds to hemoglobin with more than two hundred times the affinity of oxygen. With oxygen-binding sites occupied by CO, the sites are unavailable for oxygen. Since the vast majority of oxygen is transported in bound form, oxygen content and oxygen delivery are decreased. Inhalation of a 0.1 percent carbon monoxide mixture may produce a carboxyhemoglobin level greater than 50 percent.

CO shifts the oxyhemoglobin dissociation curve to the left, as reflected in a reduction in the P50. As a consequence, the unloading of oxygen from hemoglobin in peripheral tissues is reduced (Figure 1). CO binds to cytochrome c oxidase, inhibiting cell respiration, and induces generation of reactive oxygen species that produce apoptosis and neuronal cell death. CO also inhibits metalloproteins, decreasing oxygen utilization at the mitochondrial level, and avidly binds to cardiac myoglobin, resulting in decreased myocardial contractility, arrhythmias, and hypotension.

Hydrogen Cyanide - Hydrogen cyanide (HCN) is a colorless gas with the odor of bitter almonds. It has a half-life of 1-3 hours. HCN is produced from burning nitrogen-containing polymers, including furniture, upholstery, nylon, acrylics, silk, and wool. It is also found in plastics, glue removers, seeds, and plants. As a normal metabolite, cyanide may be detected at plasma levels of 0.3 mg/L in nonsmokers or 0.5 mg/L in smokers. Low-level detoxification occurs through metabolic conversion to thiocyanate. The vitamin B12 precursor, hydroxycobalamin, binds cyanide to form a nontoxic derivative, cyanocobalamin. At toxic levels, hydrogen cyanide inhibits cellular oxygen utilization, primarily through inhibition of cytochrome oxidase.

Others - A wide variety of additional compounds may be generated in smoke, including ammonia, phosgene, sulfur dioxide, hydrogen sulfide, formaldehyde, isocyanates, acrylonitriles, and acrolein.

Which individuals are at greatest risk of acquiring thermal injury or smoke inhalation injury?

See section on Classification.

What laboratory studies should you order to help make the diagnosis, and how should you interpret the results?

Laboratory Testing for Carbon Monoxide Exposure

Carboxyhemoglobin levels are measured using co-oximetry. Either arterial or venous blood samples are suitable for measurement. A carboxyhemoglobin level greater than 3 percent in a nonsmoker or 10 percent in a smoker confirms the diagnosis of CO poisoning. Initial levels measured in an emergency department will be influenced by the initial peak level, patient transport time from the fire scene, and prior administration of oxygen. Initial levels do not correlate with the presence, absence, or severity of symptoms. The CO level's not correlating with the clinical picture suggests that the inflammatory effects of CO, rather than the resultant hypoxemia, are responsible for the findings.

Traditional arterial blood gas analysis is misleading in CO poisoning. The standard measurement of oxygen saturation is based on a calculation using the measured PaO2. In the presence of CO, the oxygen-binding sites of hemoglobin are saturated predominately with CO, rather than oxygen. Furthermore, a normal PaO2 provides a false measure of reassurance, as the parameter no longer reflects the dynamic equilibrium between bound and unbound oxygen, but oxygen dissolved in plasma accounts for a very small fraction of blood oxygen content.

The wave lengths of light used in pulse oximeters do not distinguish between oxyhemoglobin and carboxyhemoglobin so pulse oximetry cannot be relied upon to assess the level of arterial oxygenation in the setting of CO poisoning.

Additional laboratory findings include metabolic acidosis (with an increased anion gap), elevated serum lactate, and possible rise in CPK because of muscle necrosis.

Laboratory Testing for Hydrogen Cyanide Exposure

A blood cyanide level greater than 0.5 mg/L is considered toxic. Anion gap-type metabolic acidosis, elevated serum lactate, and increased mixed venous O2 (as a result of inability to utilize oxygen at the cellular level) may be observed.

What imaging studies will be helpful in making or excluding the diagnosis of thermal injury or smoke inhalation injury?

Not applicable.

What non-invasive pulmonary diagnostic studies will be helpful in making or excluding the diagnosis of thermal injury or smoke inhalation injury?

Not applicable.

What diagnostic procedures will be helpful in making or excluding the diagnosis of thermal injury or smoke inhalation injury?

Not applicable.

What pathology/cytology/genetic studies will be helpful in making or excluding the diagnosis of thermal injury or smoke inhalation injury?

Not applicable.

If you decide the patient has thermal injury or smoke inhalation injury, how should the patient be managed?

General Management Principles in Smoke Inhalation

When a person is suspected of suffering from smoke inhalation, he or she should be removed from the source and transported to an emergency department while administering 100 percent oxygen via a nonrebreather facemask or, if indicated, through an endotracheal tube. Interventions made in the field, emergency department, or following hospital admission should include assurance of an adequate airway and an assessment of the effectiveness of ventilation and circulation (ABCs of resuscitation).

Patients with inhalational injury who require intubation should be identified promptly. One retrospective study demonstrated that several clinical features--including soot in the mouth, the presence of facial or body burns, and, on fiberoptic bronchoscopy, vocal cord edema--correlate with the need for intubation. The same study suggested that stridor, hoarseness, drooling, and dysphagia are not predictive of the need for intubation.

Consideration should be given to screening for other ingestions (e.g., alcohol, narcotics, etc.), especially if CO poisoning appears to be intentional.

A comprehensive patient evaluation should be performed, focusing on details of the exposure (duration, intensity, level of ventilation in the environment) and neurologic and cardiovascular manifestations. An ECG should be obtained and cardiac enzymes considered. 100 percent oxygen should be administered, bronchodilators should be considered, and adequate tracheal toileting measures must be ensured. The need for therapeutic bronchoscopy for evaluation of airway burns should be assessed, particularly if there is a copious amount of soot in the upper airway or if airway obstruction is suspected (as suggested by radiographic findings of lobar or whole lung atelectasis).

Intravenous fluids should be administered in accordance with hemodynamic indications and estimates of past and ongoing fluid losses. Aggressive volume resuscitation may be necessary, depending upon the extent of additional injuries, despite the possibility of enhanced edema formation in the lungs and airways.

Ventilator management, if indicated, is governed by principles of management of acute lung injury, including application of a low-stretch protocol.

Although the patient may be at significant risk for infection following acute injury, routine administration of prophylactic antibiotics is not advised.

At present, clinical data to support the use of nebulized anticoagulants or antioxidants are lacking.

Management of Carbon Monoxide Poisonin

100 percent oxygen should be administered until the carboxyhemoglobin level is less than 5 percent. Consideration should be given to administration of hyperbaric oxygen (HBO) The half-life of carboxyhemoglobin is reduced from 250 minutes while breathing room air to 40-60 minutes while breathing 100 percent oxygen under normobaric conditions, to 30 minutes under hyperbaric conditions of three atmospheres.

Although use of HBO in management of CO poisoning remains somewhat controversial, it can increase blood and tissue oxygen levels, accelerate the rate of CO elimination, and reduce oxidative stress and inflammation. Clinicians who have access to HBO should consider it under if there is any loss of consciousness, even transient; ongoing neurologic impairment; cardiovascular instability; high initial carboxyhemoglobin level (≥25%); severe acidosis; or exposure to CO for twenty-four hours or longer ,or if the victim is older than age thirty-five or pregnant. (Fetal mortality exceeds 50% in severe maternal CO poisoning.)

This recommendation regarding the use of HBO is based on a single center, prospective trial that demonstrated a lower incidence of cognitive sequelae in patients treated with three HBO sessions over twenty-four hours (25% incidence) compared with those treated with normobaric oxygen (46% incidence). Cognitive sequelae at one year post-exposure were also reduced in the HBO-treated group (18% versus 33% incidence). Patients treated with HBO had nearly normal carboxyhemoglobin levels prior to treatment, suggesting that the benefits of treatment are not primarily related to reductions in carboxyhemoglobin levels but to other mechanisms that may include increased ATP activity, reduction in lipid peroxidation, and beneficial effects on ischemia-reperfusion injury.

Although a Cochrane review (6 trials) did not support use of HBO for CO poisoning, the methodologies employed and the heterogeneity of the studies included in the analysis have been questioned. An additional concern about routinely referring patients for HBO is the need to transport critically ill patients to the HBO chamber.

Patients should be followed after discharge, as neurologic sequelae may persist or develop de novo weeks following the exposure.

Management of Hydrogen Cyanide Poisoning

Victims of hydrogen cyanide poisoning should be removed from the environment, 100 percent oxygen should be administered, and cyanide antidote(s) should be given. Cyanide antidotes include substances that generate methemoglobin, bind directly to cyanide, or serve as sulfur donors. Hyperbaric oxygen does not appear to affect blood cyanide concentrations in carbon monoxide poisoning. Methemoglobin generators include sodium nitrite and amyl nitrite. Nitrites convert the iron moiety in hemoglobin from the ferrous (+2) to the ferric (+3) state. The resulting methemoglobin serves effectively as a scavenger of free cyanide, converting it to cyanmethemoglobin.

Amyl nitrite is administered through inhalation of crushable pearls, each of which is inhaled for 15-30 seconds, with 30 seconds between pearls. Typically, amyl nitrite therapy results in generation of approximately 5 percent methemoglobin.

Sodium nitrite is administered intravenously at a dose of 300 mg over three minutes. A repeat dose of 150 mg may be administered two hours following the initial dose if cyanide toxicity persists and the resulting level of methemoglobinemia is acceptable. Methemoglobin levels usually remain under 20 percent. On a cautionary note, the resulting reduction in oxygen carrying capacity because of methemoglobin formation, coupled with carboxyhemoglobin levels resulting from CO exposure, may profoundly reduce the oxygen-carrying capacity of blood.

Sodium thiosulfate, which is administered intravenously, acts as a sulfur donor to the enzyme rhodenase and other sulfur transferases, and cyanide is converted to thiocyanate. The dose is 12.5 g intravenously over ten minutes. Administration of half the initial dose may be repeated after two hours in the setting of persistent cyanide toxicity. Thiocyanate toxicity may arise, particularly with reduced renal function, but thiocyanate is readily dialyzable.

Administration of hydroxycobalamin may be useful; 4-5 g of the agent is administered intravenously as a single dose.

What is the prognosis for patients managed in the recommended ways?

Neurologic Sequelae of Smoke Inhalation

Cognitive sequelae have been reported in nearly half of CO poisoning victims six weeks following exposure. A similar number of victims demonstrate affective disorders. Other sequelae include motor dysfunction, peripheral neuropathies, impaired hearing and balance (because of vestibular damage), dementia, and psychoses. As many as19 percent of patients may demonstrate cognitive problems as late as six years following exposure.

CNS imaging using MRI has demonstrated lesions of the basal ganglia and hippocampal atrophy years after the exposure.

What other considerations exist for patients with thermal injury or smoke inhalation injury?

See section on General Management Principles in Smoke Inhalation.

What’s the evidence?

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Baud, FJ, Barriot, P, Toffis, V. "Elevated blood cyanide concentrations in victims of smoke inhalation". N Engl J Med. vol. 325. 1991. pp. 1761-6.

Study showing that cyanide poisoning is not uncommon in victims of residential fires. Blood cyanide levels correlate with carbon monoxide concentrations. Elevated plasma lactate may be a useful indicator of cyanide toxicity in this setting.

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Concise summary of the pathophysiologic basis of, clinical findings in, and management and prognosis of carbon monoxide poisoning.

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Cummings, TF. "The treatment of cyanide poisoning". Occupational Medicine. vol. 54. 2004. pp. 82-5.

Concise summary of the management of cyanide poisoning, including discussion of the biochemical basis for the antidotes used.

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Gesell, LB. "Hyperbaric oxygen 2009: indications and results: the Hyperbaric Oxygen Therapy Committee report". Undersea and Hyperbaric Medical Society. 2008.

Hall, AH, Rumack, BH. "Clinical toxicology of cyanide". Ann Emerg Med. vol. 15. 1986. pp. 1067-74.

Review of toxicology, clinical manifestations, diagnosis, and management of cyanide poisoning.

Hampson, NB, Weaver, LK. "Carbon monoxide poisoning: a new incidence for an old disease". Undersea Hyperb Med. vol. 34. 2007. pp. 163-8.

Hardy, KR, Thom, SR. "Pathophysiology and treatment of carbon monoxide poisoning". J Toxicol Clin Toxicol. vol. 32. 1994. pp. 613-29.

Discussion of the pathophysiology and management of carbon monoxide inhalation with a focus on use of hyperbaric oxygen in selected patients.

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Kealey, GP. "Carbon monoxide toxicity". J Burn Care Res. vol. 30. 2009. pp. 146-7.

Discussion of the toxic effects of carbon monoxide and cyanide, along with metamphetamine.

Kwon, OY, Chung, SP, Ha, YR, Yoo, IS. "Delayed postanoxic encephalopathy after carbon monoxide poisoning". Emerg Med J. vol. 21. 2004. pp. 250-1.

Description of MRI changes that occur in the setting of delayed postanoxic encephalopathy following carbon monoxide poisoning.

Lawson-Smith, P, Jansen, EC, Hilsted, L, Hyldegaard, O. "Effect of hyperbaric oxygen therapy on whole blood cyanide concentrations in carbon monoxide intoxicated patients from fire accidents". Scandinavian Journal of Trauma, Resuscitation, and Emergency Medicine. vol. 18. 2010. pp. 32-37.

Prospective, controlled study that demonstrates the lack of changes in whole blood cyanide concentrations following hyperbaric oxygen therapy in patients with acute carbon monoxide poisoning.

Lo, C-P, Chen, S-Y, Lee, K-W, Chen, W-L. "Brain injury after acute carbon monoxide poisoning: early and late complications". AJR. vol. 189. 2007. pp. W205-W211..

Description of the patterns of neurologic injury induced by carbon monoxide poisoning using CT and MRI.

Madnani, DD, Steele, NP, deVries, E. "Factors that predict the need for intubation in patients with smoke inhalation injury". Ear Nose Throat J. vol. 85. 2006. pp. 278-80.

Report on the findings that predict the need for endotracheal intubation in patients with smoke inhalation injury: oral soot, facial and body burns, true or false vocal cord edema noted on bronchoscopy.

Mokhlesi, B, Leikin, JB, Murray, P, Corbridge, TC. "Adult toxicology in critical care: part II: specific poisonings: part II: specific poisonings". Chest. vol. 123. 2003. pp. 905-6.

Extensive presentation on a wide spectrum of toxidromes in adults, including cyanide and carbon monoxide.

Murakami, K, Traber, DL. "Pathophysiological basis of smoke inhalation injury". News Physiol Sci. vol. 18. 2003. pp. 125-9.

Review of underlying cellular and biochemical pathophysiologic basis of smoke inhalation injury.

Rehberg, S, Maybauer, MO, Enkhbaatar, P, Maybauer, DM. "Pathophysiology, management and treatment of smoke inhalation injury". Expert Rev Respir Med. vol. 3. 2009. pp. 283-97.

Comprehensive review of the pathophysiology and management of smoke inhalation, including an extensive bibliography.

Silver, S, Smith, C, Worster, A. "Should hyperbaric oxygen be used for carbon monoxide poisoning?". CJEM. vol. 8. 2006. pp. 43-6.

Review of the literature on the use of hyperbaric oxygen (HBO) in the treatment of carbon monoxide poisoning. The reviewers concluded that HBO is not indicated, in contradistinction to the recommendation of the Undersea and Hyperbaric Medical Society and others.

Thom, SR. "Antagonism of carbon monoxide-mediated brain lipid peroxidation by hyperbaric oxygen". Toxicol Appl Pharmacol. vol. 105. 1990. pp. 340-44.

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Thom, SR, Bhopale, VM, Han, ST, Clark, JM, Hardy, KR. "Intravascular neutrophil activation due to carbon monoxide poisoning". Am J Respir Crit Care Med. vol. 174. 2006. pp. 1239-48.

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Traber, DL, Enkhbaatar, P, Fishman, AP, Elias, JA, Fishman, JA, Grippi, MA, Senior, RM, Pack, AI. "Thermal lung injury in acute smoke inhalation". Fishman's pulmonary diseases and disorders. McGraw Hill. 2008. pp. 1053-61.

Concise review of smoke inhalation, with discussion of biochemical basis of lung and airway injury.

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Thorough review of carbon monoxide poisoning, including clinical manifestations, pathophysiologic basis, and use of hyperbaric oxygen in management.

Weaver, LK, Hopkins, RO, Chan, KJ. "Hyperbaric oxygen for acute carbon monoxide poisoning". N Engl J Med. vol. 347. 2002. pp. 1057-67.

Prospective, controlled trial demonstrating reduced risk of cognitive sequelae six weeks and twelve months following carbon monoxide poisoning in those treated with three hyperbaric oxygen sessions over twenty-four hours following exposure.

Weaver, LK, Hopkins, RO, Churchill, S, Deru, K. "Neurologic outcomes 6 years after acute carbon monoxide poisoning". Undersea Hyperb Med. vol. 35. 2008. pp. 258-259.

Weaver, LK, Valentine, KJ, Hopkins, RO. "Carbon monoxide poisoning: risk factors for cognitive sequelae and the role of hyperbaric oxygen". Am J Respir Crit Care Med. vol. 176. 2007. pp. 491-7.

Woodson, LC. "Diagnosis and grading of inhalation injury". J Burn Care Res. vol. 30. 2009. pp. 143-5.

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