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Vesicant agents were first used as chemical weapons during World War I.[13] The best known is sulfur mustard, commonly known as mustard gas. It was used as a disabling agent and has a relatively long latency of 2 to 4 hours. Its successor, lewisite, is an arsenic-based compound (2-chlorovinyl dichloroarisine), is more volatile than sulfur mustard, has a short latency, and causes immediate eye pain in addition to its vesicant properties. Mustard agent is the most commonly encountered vesicant. Even though it is an early chemical warfare agent, it is still widely distributed around the world, and its relatively easy synthesis makes it a possible agent for use by terrorists.
A number of pathologic properties make it a concern for anesthesiologists. The overall management of mustard gas injury is the domain equally of the surgeon and specialized pulmonary physician.[48] [49] Intensive care unit (ICU) management presents longer-term problems, including respiratory problems. Eye and skin injuries fall within the aegis of other specialties.
Sulfur mustard (bis-2-chloroethyl sulfide) is a colorless or pale yellow, oily liquid that smells faintly of mustard. Its odor threshold is 1.3 mg/m3 , which is below the concentrations usually reached in a battlefield, and several minutes of detection are possible before incapacitating doses are reached. The LCt50 is about 1500 mg/min/m3 , and the LCt50 is between 200 and 1000 mg/min/m3 . Although the latency of action in cooler climates is about 4 hours, information from the Iran-Iraq War, the scene of its most recent use, indicates that the agent has a far shorter latency at higher ambient temperatures and causes significant respiratory damage apart from its classic action as a skin vesicant.
After exposure to mustard gas, there is a latent period of 4 to 12 hours, after which there are ocular symptoms of eye pain, blurred vision, and lacrimation that are accompanied by a diffuse erythema of exposed skin with edema and first-degree burns. The groin and genital areas are particularly susceptible. Exposure to high doses produces severe cutaneous injury with necrosis. The burns bear some resemblance to thermal burns but are very slow to heal and are prone to secondary infection. The bullae characteristic of exposure to mustard agent are filled with a fluid that is not itself corrosive ( Fig. 64-6 ). A feature of
Figure 64-6
Cutaneous vesication caused by mustard gas exposure.
(Courtesy of Her Majesty's Stationery Office, London, UK.)
The respiratory effects of mustard gas exposure are potentially serious, particularly when the ambient temperature is high.[50] [51] After exposure, there is an early tracheobronchitis with dry cough and hoarseness. Heavy exposure produces severe damage to the tracheal and main bronchial architecture, with necrosis, sloughing, and blcokage ( Fig. 64-8 ). A chemical bronchiolitis occurs at lower doses in high ambient temperatures and causes severe bronchospasm, requiring ventilation and intensive care.[49] Lung damage after mustard gas exposure can be severe and permanent, with chronic obstructive airways disease, bronchiectasis, and reactive airways dysfunction syndrome.
Sulfur mustard agent acts at a cellular level, forming highly reactive sulfonium ions that attack DNA by alkylation of sulfhydryl and amino groups. This causes the epithelial manifestations of exposure and long-term carcinogenesis, particularly of the skin, pharynx, and respiratory tract.
Figure 64-7
Eye injury caused by mustard gas exposure. (Courtesy
of Her Majesty's Stationery Office, London, UK.)
There is no specific treatment of mustard agent exposure, but animal studies have shown a combination of sodium thiosulfate, vitamin E, and dexamethasone can improve survival and reduce organ damage.[52] The key points of treatment are the need for decontamination, the latent period of action, and respiratory support for exposure affecting the respiratory tract. Willems[49] reviewed information on the clinical management of mustard gas casualties. The need for a proactive approach to airway management
Figure 64-8
Tracheal injury due to mustard gas. (Courtesy
of Her Majesty's Stationery Office, London, UK.)
The Iran-Iraq War during the 1980s saw the extensive use of sulfur mustard and produced a significant amount of clinical information about casualties. [53] Although the agent dates from World War I, it still produces a large number of casualties with cutaneous and respiratory injuries. The treatment given reflects the experience gained in the treatment of burn injuries since its first use. Decontamination was achieved early to limit the contact time with the agent. Because of the long latency of mustard, vesicle formation was often not present at this time. Affected areas were shaved, and the agent was diluted by irrigation. Management of the vesicles followed the pattern of aspiration, removal of necrotic tissue, and application of silver sulfadiazine cream. From the anesthetic standpoint, the respiratory effects found in the casualties were important and unprecedented from the use of mustard in the lower-temperature conditions of World War I. Chemical bronchiolitis giving rise to increased airway resistance was reported together with soiling of the larger airways due to sloughing. Intermittent positive-pressure ventilation with positive end-expiratory pressure was required with ICU support for the more seriously injured cases. Many of these were managed in hospitals around Europe, introducing chemical warfare injury to many anesthetists and intensivists for the first time. For the casualties who reached definitive hospital care, the recovery period was often long, and these patients had cachexia with significant negative nitrogen balance.
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