History
The diagnosis of phosgene toxicity depends largely on a history of exposure. [15] Consider phosgene toxicity in patients involved in the manufacture of dyes, resins, coal tar, and pesticides. Query patients regarding occupation and any exposure to chemicals, especially around sources of heat. [17] In the work setting and at home, phosgene can be produced by the combustion of methylene chloride (paint remover) or trichloroethylene (a degreasing solvent).
Although phosgene gas has the odor of newly mown hay, do not rely on the presence of that odor to substantiate a suspected phosgene exposure. Some persons cannot detect the smell of this agent, and the threshold for olfactory detection is well above dangerous exposure levels. The odor detection threshold concentration is approximately 0.5-1.5 ppm, which is at least 5 times the permissive exposure limit of 0.1 ppm set by the National Institute for Occupational Safety and Health (NIOSH). [4]
Patients typically have an asymptomatic period of 30 minutes to 72 hours after exposure, but in most cases of significant exposure the latent period is less than 24 hours. The duration and concentration of exposure determine the time to symptom onset. Phosgene toxicity is thought to be more severe with short-duration, high-concentration exposures than long-duration, low-concentration exposures. [18]
Phosgene toxicity can produce an immediate irritant reaction likely caused by the hydrolysis of phosgene to hydrochloric acid on mucous membranes. This reaction occurs only in the presence of high concentrations of phosgene (>3-4 ppm), typically lasts 3-30 minutes, and does not have any prognostic value for the timing and severity of later respiratory symptoms. The most important aspect of this stage is a laryngeal irritant reaction causing laryngospasm, which may lead to sudden death
The immediate irritant reaction to phosgene gas includes the following:
-
Lacrimation
-
Conjunctival irritation/burning
-
Burning sensation in mouth/throat
-
Throat swelling/changes in phonation - May reflect laryngeal edema
If the patient was sweating or wearing wet clothing at the time of exposure, the irritant reaction may also include a burning sensation on the skin. Like the airway reaction, this is caused by the breakdown of phosgene to hydrochloric acid.
Respiratory manifestations, which usually develop 4-24 hours postexposure, consist of the following signs and symptoms:
-
Cough - Initially dry, then increasing frothy white/yellow sputum
-
Chest tightness, chest pain, or substernal burning
-
Dyspnea - Exertional early on, subsequently becomes present at rest
-
Altered taste sensation - If the patient is a smoker, metallic or unpleasant taste to cigarettes
Other signs and symptoms of this phase, which result primarily from hypoxemia or volume depletion, include the following:
-
Lightheadedness
-
Angina
-
Headache
-
Anorexia
-
Nausea, and vomiting
-
Weakness
-
Anxiety and sense of impending doom
Physical Examination
Physical examination is useful with patients with active symptoms. Patients who relate a recent exposure may be in the latent phase and have no specific findings related to the exposure.
Head, ears, eyes, nose, and throat (HEENT) examination in patients with symptomatic phosgene toxicity may reveal the following:
-
Conjunctival injection and lacrimation
-
Nasal mucosa hyperemia associated with rhinorrhea
-
Oropharyngeal hyperemia and salivation
-
Altered phonation
Significant injury may occur to the lower airways without upper airway involvement. Respiratory findings may include the following:
-
Crackles on auscultation - Herald the onset of pulmonary edema
-
Cyanosis - Late finding
-
Thin, frothy white/yellow secretions
-
Wheezing
-
Tachypnea
-
Stridor
-
Accessory muscle use for respiratory effort
Cardiovascular findings may include the following:
-
Tachycardia
-
Hypotension - Late finding secondary to inflammation-mediated fluid diversion out of vascular system and into lung interstitium
Skin findings may include the following:
-
Cyanosis from pulmonary injury and resultant hypoxemia
-
Chemical burns from liquefied phosgene (although it also is considered a frostbite hazard in the compressed liquid form)
-
Anteroposterior portable chest radiograph in a male patient who developed phosgene-induced adult respiratory distress syndrome. Notice the bilateral infiltrates and ground-glass appearance Image courtesy of Fred P. Harchelroad, MD, and Ferdinando L. Mirarchi, DO.
-
British machine-gunners in anti-phosgene masks, Somme, 1915. Courtesy of the Imperial War Museum, London.
-
Phosgene structure.
-
The chest radiograph of a 42-year-old woman chemical worker 2 hours after exposure to phosgene. Dyspnea progressed rapidly over the second hour; PO2 was 40 mm Hg breathing room air. This radiograph shows bilateral perihilar, fluffy, and diffuse interstitial infiltrates. The patient died 6 hours postexposure. Used with permission from Medical Aspects of Chemical and Biological Warfare, Textbook of Military Medicine, 1997, p 258.
-
A lung section of the patient who died 6 hours after exposure to phosgene; the biopsy section was taken during postmortem examination. The section shows nonhemorrhagic pulmonary edema with few scattered inflammatory cells. Hematoxylin and eosin stain; original magnification X 100. Used with permission from Medical Aspects of Chemical and Biological Warfare, Textbook of Military Medicine, 1997, p 258.
