Decontamination lewisite exposure

Similar to the mustard agents, exposure prevention is the first line of defense against lewisite. Rapid decontamination is especially relevant to lewisite exposure due to the rapid development of pain (1-2 min) associated with lewisite exposure. Unlike other vesicants, an effective antidote for lewisite toxicity exists in the form of British anti-lewisite (BAL 2,3-dimercaptopropanol) which binds with arsenicals, thereby countering the lewisite-induced damage. Such chelation therapy is associated with notable side effects (e.g. renal effects) and requires carefiil medical management. More effective analogs of BAL have been developed with less significant side effects. 

Immediate eye pain and blepharospasm result from lewisite exposure, followed by conjunctival and lid edema. Severe exposures can produce necrotic injuries of the iris with depigmentation, hypopion, and synechia development. In contrast, very low levels may only involve the conjunctivae (McManus and Huebner, 2005). The eye lesions produced by lewisite are particularly serious blindness will follow contamination of the eye with liquid lewisite unless decontamination is prompt. 

Lewisite-exposed patients arriving at the hospital within 30-60min of exposure will likely have pain or irritation. Patients without symptoms most likely did not snfifer Lewisite exposure, and they can go home, with instructions to return immediately if they develop symptoms. After decontamination. Lewisite-exposed patients with respiratory symptoms require placement in a critical care unit. Patients withont symptoms, including those sent home, require observation for 18-24h. The sooner after exposure symptoms develop, the more likely they are to progress (24). 

Lewisite is a vesicant and toxic lung-irritant that is absorbed into tissues. If inhaled in high concentrations, it can be fatal in as little as 10 minutes the body is unable to detoxify itself from lewisite exposure. Routes of entry into the body include the eyes, skin absorption, and inhalation. Eye contact results in pain, inflammation, and blepharospasm (spasms of the muscles of the eyelid), which leads to closure of the eyelids, comeal scarring, and iritis (inflammation of the iris). If decontamination of the eyes occurs quickly after exposure, damage may be reversible however, permanent injury or blindness can occur within one minute of exposure. 

Appropriate PPE must be worn by members of emergency services treating casualties of lewisite exposure. Inadequate decontamination may result in secondary cases from exposure to primary cases. 

Decontaminate the casualty ensuring that all the vesicants have been removed. Rapid decontamination of any exposure is essential. If vesicants have gotten into the eyes, irrigate the eyes with water or 0.9% saline solution for at least 15 minutes. BAL (British-anti-Lewisite, dimercaprol) solution or ophthalmic ointment may be beneficial if administered promptly. Irrigate open wounds with water or 0.9% saline solution for at least 10 minutes. 

Lewisite Shock Pulmonary injury Blisters Decontamination soap, water, no bleach Antidote BAL-dimercaprol may decrease systemic effects of lewisite Pulmonary management BAL 3-5 mg/kg deep IM q4 h X 4 doses (dose depends on severity of exposure and symptoms) Skin management BAL ointment Eye management BAL ophthalmic ointment... 

Pediatric exposures to vesicants can be quite toxic however, in contrast to nerve agent exposures, HD causes significantly greater morbidity than mortality. While mustard did not cause many deaths in WWI, death from HD exposure is usually due to massive pulmonary damage complicated by infection (bronchopneumonia) and sepsis. Children often show a quicker onset and greater severity of toxicity. Skin and eye toxicity occurs in the form of blisters or irritation that can result in blindness for the most severe cases. Except for lewisite, vesicant exposures must be managed with supportive care and rapid decontamination. 

To prevent or lessen lewisite damage, early decontamination within minutes after exposure must be instituted. Unlike mustard, lewisite does not cause damage to the hematopoietic organs, but fluid loss from increased capillary permeability necessitates careful attention to fluid balance. 

Medical personnel should follow the same principles for managing Lewisite skin, eye, and airway lesions that they follow for managing mustard lesions. A specific antidote, BAL (dimercaprol), will prevent or greatly decrease the severity of skin and eye lesions if applied topically within minutes after the exposure and decontamination (however, preparations of BAL for use in the eyes and on the skin are no longer available). Given intramuscularly, BAL will reduce the severity of systemic effects. BAL binds to the arsenic of... 

Lewisite and phosgene oxime (GX) are also vesicants but are different from sulfur mustard and have never been used militarily. In liquid or vapor form they produce immediate pain and injury. Because of the immediate pain, the victims tend to run away from the exposure and immediately begin self-decontamination. 

Almost 100 years after the first use of mustard gas (HD) in warfare, there is stiU no available antidote, although there is an antidote (British anti-Lewisite) to the vesicant Lewisite, an arsenical compound developed in 1919. Treatment is therefore based on early recognition of the exposure and immediate decontamination to prevent further injury. This is particularly important in the case of the eyes. 

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