Inhaled Toxins

Foundations

Simple asphyxiants are inert and produce toxicity only by displacement of oxygen and lowering the fraction of inspired oxygen (Fi O ₂ ). Exposed patients remain asymptomatic if the Fi O ₂ is normal. Carbon dioxide and nitrogen are exceptions in that both can produce narcosis at elevated partial pressures, even though their predominant toxicological effect is simple asphyxiation. Since the introduction of catalytic converters, most deaths from the intentional inhalation of automotive exhaust result from simple asphyxiation, due to hypoxia, and not from carbon monoxide (CO) poisoning. Emerging methods of suicide secondary to gas inhalation are the inhalation of helium and charcoal burning.

Clinical Features

Acute effects occur within minutes of the onset of hypoxia and are manifestations of ischemia. A fall in the Fi O ₂ from normal, 0.21 (i.e., 21%), to 0.15 results in autonomic stimulation (e.g., tachycardia, tachypnea, and dyspnea) and cerebral hypoxia (e.g., ataxia, dizziness, incoordination, and confusion). Dyspnea is not an early finding because hypoxemia is not nearly as potent a stimulus to the medullary respiratory center as are hypercarbia and acidemia. Lethargy from cerebral edema occurs as the Fi O ₂ falls below 0.1 (10%), and life is difficult to sustain at an Fi O ₂ below 0.06 (6%). Because removal from exposure terminates the simple asphyxiation and allows restoration of oxygenation and clinical improvement, most patients present with resolving symptoms. Failure to improve suggests complications of ischemia (e.g., seizures, coma, and cardiac arrest) and is associated with a poor prognosis.

Differential Diagnoses

Because the presenting complaints offered by most exposed patients are nonspecific (e.g., dizziness, syncope, and dyspnea), the differential diagnosis is extensive. A consistent history, particularly of a setting in which asphyxia is expected to occur such as in an enclosed space, an appropriate spectrum of complaints and a rapid resolution on removal from exposure are generally sufficient to establish the diagnosis.

Diagnostic Testing

Minimally, symptomatic patients do not require chest radiography or arterial blood gas (ABG) analysis. There is no need for toxicology testing unless the asphyxiation was an act of deliberate self-harm, in which in this case, we recommend selected screening for acetaminophen and any other relevant toxin implicated by history, physical examination, or observation. A definitive diagnosis ultimately requires scene investigation by a trained and suitably outfitted team with personal protective equipment (PPE). Determination of the exact nature of the gas is of limited clinical value but may have important public health implications.

Management

Management rarely requires specific therapy other than removal from exposure, administration of supplemental oxygen, and supportive care. Neurologic injury or cardiorespiratory arrest should be managed with standard advanced cardiac life support (ACLS) resuscitation protocols. Psychiatric consultation is indicated when the exposure was an act of deliberate self-harm.

Disposition

Patients with manifestations of mild asphyxia, who recover after removal from the exposure can be discharged after 6 hours of observation if they are asymptomatic or minimally symptomatic with improvements. Patients at risk for complications of hypoxia, such as those presenting with significant signs or symptoms (e.g., altered mental status, coma, chest pain, electrocardiogram [ECG] changes) or with exacerbating medical conditions (e.g., cardiac disease, asthma), should be observed for 24 to 48 hours for the development or progression of post-hypoxic complications.

Foundations

The pulmonary irritant gases are a large and diverse group of agents that produce a common toxicological syndrome when they are inhaled in moderate concentrations. Although many of these gases can be found in the home, significant poisoning from consumer products is uncommon because of restrictions designed to reduce their toxicity. However, catastrophes such as the 1984 release of methyl isocyanate in Bhopal, India, which resulted in more than 2000 fatalities and 250,000 injuries, remain as an environmental risk. On a different scale, industrialization has increased ambient concentrations of sulfur dioxide, ozone, and oxides of nitrogen. These irritant gases frequently exacerbate chronic pulmonary disease.

Irritant gases dissolve in the respiratory tract mucus and alter the air-lung interface by invoking an irritant, or inflammatory response. When these gases are dissolved, most of them produce an acid or alkaline product, but several generate oxygen-derived free radicals that produce direct cellular toxicity ( Fig. 148.1 ). The clinical effects of pulmonary irritants can be predicted by their water solubility (see Table 148.1 ).

Clinical Features

Highly, water-soluble gases rapidly impact the mucous membranes of the eyes and upper airway causing lacrimation, cough and nasal burning. Although their pungent odor and rapid onset of symptoms tend to limit significant exposure, massive or prolonged exposure can result in life-threatening laryngeal edema, laryngospasm, bronchospasm, or acute respiratory distress syndrome (ARDS). In contrast, because poorly water-soluble gases do not readily irritate the mucous membranes at low concentrations and some have a pleasant odor (e.g., phosgene’s odor is similar to that of newly mown hay or freshly cut grass), prolonged breathing in the toxic environment allows time for the gas to reach deep into the alveoli. Even moderate exposure causes delayed irritation of the lower airway, alveoli, and parenchyma 2- to 24-hour after exposure. Initial effects may be mild, only to progress to overt respiratory failure and delayed ARDS during the ensuing 24 to 36 hours. 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.

Differential Diagnoses

The typical symptoms of pulmonary exposure to an irritant gas are bronchospasm, cough, chest tightness, and acute conjunctival irritation. Presentation may mimic non-toxicological causes of pulmonary disease, but the history generally confirms the exposure to the irritant ( Box 148.1 ). History may be particularly important if the patient presents with severe or advanced findings, such as ARDS, which can occur after many physiologic insults, including trauma and sepsis.

Diagnostic Testing

Inhalation of respiratory irritants may affect the upper airway, the lower airways and lungs, or both. Upper airway evaluation proceeds as described in the following Management section. Radiographic and laboratory studies are not useful in the evaluation of upper airway symptoms.

Oxygenation and ventilation are assessed by serial chest auscultation, pulse oximetry, and continuous capnography. Chest radiography is indicated for patients presenting with cough, dyspnea, hypoxia, or abnormal findings, such as rales or wheezes, on pulmonary examination. ABGs are reserved for patients who are more severely symptomatic, have hypoxia, or do not improve readily with oxygen therapy.

In general, it is neither possible nor necessary to test for the specific agent. There are no clinical tests that will differentiate the irritant to which a patient was exposed, although testing at the site by public health authorities may be performed for epidemiologic purposes. Knowing that an agent is highly water soluble will shorten the observation period for symptom development, whereas patients exposed to poorly water-soluble agents will require a more prolonged period of observation.

Management

Patients with no upper airway symptoms, normal voice, and no evidence of irritation (erythema) or burns on examination of the oral pharynx require no further upper airway evaluation but should be reexamined if symptoms or signs develop after the initial evaluation. Those with evidence of tissue irritation, such as oral or tongue edema, altered voice (raspy or muffled), stridor, or significant odynophagia or dysphagia require early examination by laryngoscopy and if severe, should undergo early intubation because rapid progression of these injuries is expected. Laryngoscopy may be performed using a flexible laryngoscope, rigid video, or conventional laryngoscope with appropriate topical anesthesia and sedation as indicated (see Chapter 1 ). Patients with evidence of mild irritation of the larynx or supralaryngeal area (erythema, no edema, normal glottis) may be observed. Those with more severe findings are considered not to require early intubation, such as erythema with mild edema, should undergo repeat examination from 30 to 90 minutes after the initial examination or earlier, if symptoms or signs are worsening.

Bronchospasm generally respond to inhaled beta-adrenergic agonists. Data regarding the use of corticosteroids are limited and do not support clinical benefits in humans. Therefore, corticosteroids are not recommended unless the patient has underlying reactive airways disease.

Patients exposed to chlorine or hydrogen chloride gas receive symptomatic relief from nebulized 2% sodium bicarbonate solution. This solution is prepared by diluting a given volume of standard 8.4% sodium bicarbonate solution with three equivalent volumes of sterile water and administering it in 3 to 5 mL aliquots with standard nebulizer equipment. There are no studies on the recommended dosing regimen, but if successful after its first use, providing it every 30 minutes as needed for symptom relief, for up to 6 hours, is a reasonable approach. Nebulized bicarbonate will not alter the inflammatory cascade so it will not have significant effect on the progression of pulmonary injury. ARDS, if identified, is managed as described in Chapter 2 .