Inhaled toxins anesthesia key anoxic brain injury

Table 159-1

Common inhaled toxins






Irritant, highly soluble


Fertilizer, combustion

Irritant, highly soluble

Carbon dioxide

Fermentation, complete combustion, fire extinguisher

Simple asphyxiant; systemic effects

Carbon monoxide

Incomplete combustion, methylene chloride

Chemical asphyxiant


Mixed cleaning products (e.G., hypochlorite bleach and ammonia)

Irritant, highly soluble


Swimming pool disinfectant, cleaning products

Irritant, intermediate solubility

Chlorobenzylidene malononitrile (CS), chloroacetophenone (CN)

Tear gas (mace)

Pharmacologic irritant

Hydrogen chloride

Tanning and electroplating industry

Irritant, highly soluble

Hydrogen cyanide

anoxic brain injury

Combustion of plastics, acidification of cyanide salts

Chemical asphyxiant

Hydrogen fluoride

Hydrofluoric acid

Irritant, highly soluble; systemic effects

Hydrogen sulfide

Decaying organic matter, oil industry, mines, asphalt

Chemical asphyxiant; irritant, highly soluble


Natural gas, swamp gas

Simple asphyxiant



Chemical asphyxiant


Mines, scuba diving (nitrogen narcosis, decompression sickness)

Simple asphyxiant; systemic effects

Nitrous oxide

Inhalant of abuse, whipping cream, racing fuel booster

Simple asphyxiant

Noble gases (e.G., helium)

Industry, laboratories

Simple asphyxiant

Oxides of nitrogen

Silos, anesthetics, combustion

Irritant, intermediate solubility


Medical use, hyperbaric conditions

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Irritant, free radical; systemic effects


Electrostatic energy

Irritant, free radical


Combustion of chlorinated hydrocarbons

Irritant, poorly soluble


Hydration of aluminum or zinc phosphide (fumigants)

Chemical asphyxiant

Smoke (varying composition)


Variable, but may include all classes

Sulfur dioxide

Photochemical smog (fossil fuels)

Irritant, highly soluble

Clinical features

Highly water-soluble gases have their greatest impact on the mucous membranes of the eyes and upper airway. Exposure results in immediate irritation, with lacrimation, nasal burning, and cough. Although their pungent odors and rapid symptom onset tend to limit significant exposure, massive or prolonged exposure can result in life-threatening laryngeal edema, laryngospasm, bronchospasm, or acute respiratory distress syndrome (ARDS) (formerly known as noncardiogenic pulmonary edema). 4 poorly water-soluble gases do not readily irritate the mucous membranes at low concentrations, and some have pleasant odors (e.G., phosgene’s odor is similar to that of hay).Anoxic brain injury because there are no immediate symptoms, prolonged breathing in the toxic environment allows time for the gas to reach the alveoli. Even moderate exposure causes irritation of the lower airway, alveoli, and parenchyma and causes pulmonary endothelial injury after a 2- to 24-hour delay. Initial symptoms consistent with acute respiratory distress syndrome may be mild, only to progress to overt respiratory failure and acute respiratory distress syndrome during the ensuing 24 to 36 hours. 5

Gases with intermediate water solubility tend to produce syndromes that are a composite of the clinical features manifested with the other gases, depending on the extent of exposure. Massive exposure is most often associated with rapid onset of upper airway irritation and more moderate exposure with delayed onset of lower airway symptoms. 6

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Diagnostic strategies and differential considerations

The evaluation of upper airway symptoms is usually done through physical examination but may require laryngoscopy. After exposure, swelling may occur rapidly or may be delayed, so normal findings on oropharyngeal or laryngeal evaluation may not exclude subsequent deterioration. Radiographic and laboratory studies have little role in the evaluation of upper airway symptoms.

Oxygenation and ventilation are assessed by serial chest auscultation, pulse oximetry, and capnometry supplemented as needed by chest radiography and abgs in patients with cough, dyspnea, hypoxia, or abnormal findings on physical examination. No clinical test can identify the specific irritant, and identification is not generally necessary for patient care, although knowing the causative agent may allow refinement of the observation period.Anoxic brain injury

Bronchospasm, cough, chest tightness, and acute conjunctival irritation frequently follow allergen exposure, but the history generally suggests the diagnosis. ARDS occurs after many physiologic insults, including trauma and sepsis, highlighting the need for accurate history taking. 5


Signs of upper airway dysfunction (e.G., hoarseness and stridor) mandate direct visualization of the larynx and immediate airway stabilization, if necessary. Given the potential rapidity of airway deterioration, early and frequent reassessment should be performed.

Bronchospasm generally responds to inhaled beta-adrenergic agonists; the role of ipratropium is not yet defined. Other than as a standard treatment of a comorbid condition, such as asthma, there is no clear indication for corticosteroids. 7

anoxic brain injury

Patients exposed to chlorine or hydrogen chloride gas receive symptomatic relief from nebulized 2% sodium bicarbonate solution. 6 because the inflammatory cascade is not altered, however, the component of lung injury mediated by free radicals probably continues and causes delayed deterioration. Patients receiving inhalational bicarbonate therapy require extensive discharge instructions for signs and symptoms of pulmonary irritation or admission to the hospital.

Diagnosis of acute respiratory distress syndrome indicates the need for aggressive supportive care, including manipulations of the patient’s airway pressures (e.G., continuous positive airway pressure and positive end-expiratory pressure).Anoxic brain injury exogenous surfactant and nitric oxide may have a beneficial role in toxin-induced acute respiratory distress syndrome, despite little support for use in other forms of the syndrome.

Clinical features

Most smoke-associated morbidity and mortality relate to respiratory tract damage. Thermal and irritant-induced laryngeal injury may produce cough or stridor, but these findings are often delayed. Soot and irritant toxins in the airways can produce early cough, dyspnea, and bronchospasm. Subsequently, a cascade of airway inflammation results in acute lung injury with failure of pulmonary gas exchange. The time between smoke exposure and the onset of clinical symptoms is highly variable and dependent on the degree and nature of the exposure.Anoxic brain injury singed nasal hairs and soot in the sputum suggest substantial exposure but are neither sufficiently sensitive nor specific to be practical. 8

CO inhalation should be routinely considered in these patients. Patients who are exposed to filtered or distant smoke (e.G., in a different room) or to relatively smokeless combustion (e.G., engine exhaust) inhale predominantly CO, cyanide, and metabolic poisons and do not sustain smoke exposure.

Diagnostic strategies and differential considerations

With the obvious exposure history, the differential diagnosis is limited. Although it is often unclear whether inhalational injuries are thermal or irritant, the differentiation is clinically irrelevant. CO and cyanide should be considered in every case.Anoxic brain injury

Early death is caused by asphyxia, airway compromise, or metabolic poisoning (e.G., CO). Airway patency should be evaluated early. If evidence of significant airway exposure is present, such as carbonaceous sputum or hoarse voice, the airway should be examined by direct or fiberoptic laryngoscopy. Simply observing the patient for deterioration can result in airway compromise requiring rapid and, by then, very difficult airway intervention. Signs of alveolar filling or hyperinflation on chest radiography, abnormal flow-volume loop or diffusing capacity for CO on pulmonary function testing, or abnormal distribution and clearance of radiolabeled gas on ventilation scans can help predict lower airway injury. 9

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Metabolic acidosis, particularly when it is associated with a serum lactate level greater than 10 mmol/L, suggests concomitant cyanide poisoning. 10 oxygenation should be assessed by co-oximetry because blood gas analysis and pulse oximetry may be inaccurate in CO-poisoned patients (see later).