Pool Prep Peril

By Lewis Nelson, MD

A 35-year-old man and his son mixed water into a plastic container of pool shock (a granular substance used to prepare swimming pools for their first use of the season) and reclosed the lid tightly. After several seconds, the container exploded, covering the man in a cloud of green smoke. He immediately felt a burning sensation in his eyes and throat, and went to the emergency department for evaluation. On arrival, he had a raspy voice and the mucosal surfaces of his mouth and eyes were erythematous. No stridor was present, and his lungs were clear. All vital signs were normal; oxygen saturation by pulse oximetry was 92% on room air.
 

DAMAGE FROM EXPOSURE TO IRRITANT GASES

Gases may be irritant in nature through two distinct mechanisms. Certain chemicals, such as those used as tear gas, enhance the neuronal release of substance P, the neurotransmitter involved in the pain response. When individuals are exposed to moderate doses of these chemicals, they experience pain as well as minimally visible changes to the body areas that come in contact with these agents. Alternatively, irritant gases dissolve in the mucosal water to form acids or alkali that injure the adjacent tissue.

In addition, some irritant gases generate reactive oxygen species that are also injurious. Once dissolved, these toxicologic mediators activate pain or irritant receptors and initiate an inflammatory response. They also directly injure the cell membranes of nearby tissue, producing clinical symptoms. In the eyes and oropharynx, this manifests as pain, erythema, injection, or induration; in the distal bronchopulmonary tree, it causes pulmonary capillary leak. The clinicopathologic syndrome associated with capillary leak is acute lung injury, which was formerly termed noncardiogenic pulmonary edema. Insight into the physicochemical nature of the irritant gas allows us to predict the expected clinical findings.

In general, irritant gases fall into one of three categories. These differ based on the solubility of the chemical in water. Examples of agents that are highly irritating in low concentration include ammonia, hydrogen sulfide, hydrogen chloride, and chloramine gas. Chloramine is of interest not because it is extremely toxic, but because it is the most commonly encountered problematic substance. In a misguided attempt to "superclean" a surface—such as a toilet—ammonia and a hypochlorite-containing product such as household bleach are used concurrently. The result of this inadvertent household chemistry experiment is the production of chloramine gas. In a closed space such as a bathroom, this gas may produce an immediate irritant response. Fortunately, such highly irritant gases are said to have good warning properties, since they produce burning in the eyes and throat immediately on exposure. More intense exposure—due either to highly concentrated gas or inability to escape—may result in dyspnea, stridor, bronchospasm, or upper airway obstruction.

Agents with poor water solubility are often nonirritating in moderate to high concentrations; some agents, in fact, may even be pleasant. Phosgene, the prototype of poorly soluble agents, has an odor akin to "freshly mown hay," and was used effectively as a gas during World War I because it lacked aversive qualities even at toxic doses. Because of these gases' low solubility, exposed individuals tend to remain in the toxic environment, and this prolonged exposure allows the gas to reach the alveoli. On dissolution, irritation of both the upper and lower respiratory epithelium occurs, which may lead to acute lung injury.

Other examples of poorly soluble gases include ozone and oxides of nitrogen such as nitrogen dioxide. Although initially asymptomatic, patients exposed to significant concentrations of these substances may develop pulmonary edema several hours to as late as 12 to 16 hours after exposure.

The agents with intermediate water solubility—of which chlorine is most representative—are irritating in high concentrations but may be quite tolerable at low levels. Very low-level exposure occurs poolside and, obviously, no significant toxicity occurs. The patient described above was exposed to a high concentration of chlorine gas released from the pool shock container, which typically contains either concentrated calcium hypochlorite or trichloro-s-triazinetroine, and suffered rapid mucosal irritation.

Because of the concentration of the gas, even a brief exposure allowed inhalation of enough gas to enter the bronchopulmonary tree. Chlorine releases both hydrochloric acid and reactive oxygen species, and both likely participate in the development of acute lung injury. In fact, the patient's chest radiograph revealed mild, diffuse, bilateral pulmonary infiltrates consistent with pulmonary edema.
 

EVALUATION AND MANAGEMENT STRATEGY

Because upper airway swelling may be profound and lead to stridor and glottic occlusion, aggressive airway management is the rule. Direct visualization of the vocal cords and supraglottic area is indicated in symptomatic patients. Although orotracheal or nasotracheal intubation is preferred, if needed, cricothyrotomy may become necessary. Corticosteroids should probably be used in patients with significant airway edema.

Pulmonary evaluation, including serial physical examination, pulse oximetry or blood gas analysis, and radiography, may be needed to adequately assess the extent of pulmonary damage. Supplemental oxygen should be used to prevent hypoxemia. Bronchospasm should be treated with beta-adrenergic agonist nebulizers at standard doses. There is no current role for the routine use of corticosteroids as prophylaxis or treament of acute lung injury, but their use in intractable bronchospasm is probably warranted.

Nebulized sodium bicarbonate has been shown to provide symptomatic relief in patients exposed to chlorine, and it is probably useful with all irritant gases that liberate acid. Through a neutralization reaction, the damaging effect of the acid is limited. Any heat or gas generated by this process should be readily dissipated by the bronchopulmonary system.

Nebulized sodium bicarbonate should be used in concentrations of less than 2% (which generally means about a 4:1 dilution of standard 8% sodium bicarbonate). Note that while symptoms may improve, there is no documentation that this regimen reduces complications or alters the natural history of the syndrome. This is certainly most concerning following exposure to irritant gases, such as chlorine or ozone, that liberate reactive oxygen species. Thus, patients who receive nebulized sodium bicarbonate should be observed for a prolonged period. Irritated eyes should be irrigated with copious amounts of normal saline. Fluorescein staining may reveal corneal abrasions, and ophthalmologic consultation or follow-up is recommended if symptom resolution is not rapid.

Observation is required for all patients exposed to irritant gases. Those exposed to highly soluble agents may be safely discharged if they do not become symptomatic within two to four hours of exposure, or after symptom resolution if exposure was not prolonged or intense. In such cases, delayed symptoms would not be expected. Hospital admission is required for all symptomatic patients who were exposed to intermediate or poorly soluble gases because the extent of toxicity is unpredictable. History of exposure will determine the need for admission of patients exposed to intermediate or poorly soluble gases who are not initially symptomatic. If exposure is extensive, or the patient's ability to return if symptoms develop is not guaranteed, 24 hours of hospital observation with continuous pulse oximetry is warranted.
 

PATIENT OUTCOME

Despite significant findings of hypoxemia—the initial arterial blood gas showed a pH of 7.47, pCO₂ of 30 mm Hg, and pO₂ of 65 mm Hg on supplemental oxygen—and clinical and radiographic evidence of acute lung injury, the patient's condition turned around rapidly and improved over the following 16 hours. His dyspnea resolved by the next morning. Although stridor did not develop, the throat irritation took two days to abate fully. The patient was discharged the following day.