Pediatric emergency medicine trisk 4576 4576
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Because mustard penetrates tissue rapidly and binds to cellular components
within the first 2 to 5 minutes, the most important early intervention is immediate
decontamination, ideally within the first 2 minutes. Decontamination after a half
hour is unlikely to affect the eventual development of local effects, but even late
removal of agent can stop continuing absorption and limit the total internal dose.
As with nerve agents, RSDL is particularly effective for skin decontamination. In
contrast, soap and water often ends up simply smearing agent and increasing the
area for absorption. No specific antidotes to mustard poisoning are available.
Supportive care for skin lesions is analogous to that provided for burn injury,
although fluid requirements are usually far less than with comparable thermal
burns. Additional treatment of respiratory tract inflammation, ocular injury, and
immunosuppression associated with leukopenia may be required (see Chapters 93
Hematologic Emergencies , 99 Pulmonary Emergencies , 123 Ophthalmic
Emergencies ) and bone marrow stimulating factors may be needed.
Pulmonary Agents
Toxic inhalant agents, including chlorine and phosgene, may cause injury in
several ways, including simple asphyxia by displacing oxygen, topical damage to
airways or alveoli, systemic absorption through the pulmonary capillary bed, and
allergic hypersensitivity reactions. Both chlorine and phosgene were used in
battle in World War I, are commonly used for industrial purposes today, and are
reviewed briefly in this section.
Chlorine is a dense, acrid, yellow-green gas with intermediate water solubility
and chemical reactivity, whereas phosgene has low solubility and reactivity.
Because the initial irritant symptoms of gas exposure tend to correlate directly
with water solubility and chemical reactivity, low-dose exposures to chlorine and
even moderate exposures to phosgene might cause either no symptoms at all or
only mild irritation of mucous membranes. Victims could easily dismiss these
effects, thus prolonging exposure and the severity of the ultimate lung injury.
Phosgene (carbonyl chloride) also generates hydrochloric acid, contributing
particularly to upper airway, nasal, and conjunctival irritation at higher doses.
Also generated is a carbonyl group that participates in acylation reactions at the
pulmonary alveolocapillary membranes; the resulting leakage of fluid across
damaged membranes eventually leads pathologically to pulmonary edema and
clinically to acute lung injury (ALI), including its most severe form, acute
respiratory distress syndrome (ARDS). Phosgene lung injury may also be
mediated in part by an inflammatory reaction associated with leukotriene
production.
