Page 111 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

78 SECTION | I General

VetBooks.ir TABLE 5.3 LD 50 for Lewisite inhalation are similar to the lesions produced by mustard
gas exposures. Dogs that inhaled lethal doses died of
necrotizing pseudomembranous laryngotracheobronchitis
LD 50 (mg/kg)
Species
Route
(Goldman and Dacre, 1989). A thick membrane was noted
Mouse Dermal 12 in the nostrils, larynx and trachea with purulent bronchitis.
Rat Dermal 15 Edema, hemorrhage and emphysema were seen in the
lungs (Goldman and Dacre, 1989). Death can occur within
Subcutaneous 1
10 min with high concentrations (EPA, 1985a).
Oral 50
Unlike arsenic or mustard gas, Lewisite does not cause
Human Dermal 30 damage to the bone marrow or immunosuppression
(Sidell et al., 1997). Even though Lewisite is a substituted
Source: Data from RTECS, 2006. Registry of Toxic Effects of Chemical
Substances. National Institute for Occupational Safety and Health. arsine, it also does not appear to directly cause hemolysis
Cincinnati, OH (CD Rom Version). Edition expires 2006; provided by of the red blood cells (HSDB, 2005). Hypovolemia, sec-
Thomson MICROMEDEX, Greenwood Village, CO; Sidell, F.R., Takafuji,
E.T., Franz, D.R., 1997. Textbook of Military Medicine: Medical Aspects ondary to fluid loss, can be severe enough to cause renal
of Chemical and Biological Warfare. TMM Publications, Washington, dysfunction. Arrhythmias may occur as a result of hypo-
DC; DeRosa, C.T., Holler, J.S., Allred, M., et al., 2002. Managing
hazardous materials incidents. In Agency for Toxic Substances and volemia rather than a direct toxic effect of Lewisite on
Disease Registry. (Website: www.atsdr.cdc.gov). the myocardium. Lewisite was fetotoxic to rats and rab-
bits, but not teratogenic (Goldman and Dacre, 1989;
RTECS, 2006). It is a suspected carcinogen due to its
arsenic content.
Lewisite is similar to mustard gas in that it damages the Lewisite blood levels are not clinically useful, but an
skin, eyes and airways; however, it differs in that its clini- arsenic blood level below 7 μg/100 mL is considered nor-
cal effects appear within seconds of exposure and it is mal. Urine arsenic levels may be tested and levels of
about 10 times more volatile than mustard gas (Budavari, ,100 μg are considered normal (Proctor and Hughes,
2000). Exposure to Lewisite is very painful, in contrast to 2004). Concentrations between 0.7 and 1.0 mg/L indicate
mustard. See Table 5.3 for LD 50s of various species by a potentially harmful exposure.
different routes of exposure.
Dermal contact results in immediate pain. Both vapor
and liquid Lewisite can penetrate skin. Reddening of the Treatment
skin becomes evident within 15 30 min after exposure
(EPA, 1985a; Sidell et al., 1997). Evidence of tissue Move animals to fresh air and monitor for coughing and
destruction (grayish epithelium) will be present within respiratory distress. Monitor blood gases and SpO 2 in
minutes of skin contact (Goldman and Dacre, 1989; Sidell patients with significant exposures. If coughing or diffi-
et al., 1997). Severe blisters develop within 12 h after culty breathing develops, administer oxygen and assist
exposure. The blisters may rupture, usually about 48 h ventilation as needed. Bronchospasm should be treated
after occurrence, with copious amounts of fluid seeping with inhaled beta agonists and possibly corticosteroids.
from the site. With dermal exposure, as little as 0.5 mL Monitor electrolytes and PCV as animals can become
may cause severe systemic effects, and 2 mL may be hemoconcentrated. Crystalloids should be given with cau-
lethal. Severe edema can be seen due to the Lewisite’s tion not to overhydrate the patient (Goldfrank et al.,
increased capillary permeability. Dermal burns are gener- 1998). Consider urinary alkalinization and maintain good
ally deeper than those with mustard gas. Healing occurs urine output. Monitor for liver and kidney failure and sec-
much faster than with sulfur mustard-induced lesions and ondary infection.
is generally complete within 4 weeks. Emesis is not recommended due to the irritant and
Ocular contact causes immediate pain, lacrimation, and vesicant nature of Lewisite. Dilute oral ingestions with
blepharospasm. Permanent blindness may occur if eye milk or water. Perforation and stricture formation may
exposure occurs for more than 1 min without rapid decon- occur after ingestion as severe irritation or vesication
tamination (EPA, 1985a). A small droplet (1 μL) can (blistering) of the esophagus or gastrointestinal tract is
cause perforation and loss of vision (Sidell et al., 1997). likely to occur. Endoscopy may be used to determine the
Inhalation of the Lewisite vapor may result in irrita- extent of injury.
tion to nasal passages, profuse nasal discharge and violent Flush eyes with copious amounts of tepid water for at
sneezing (HSDB, 2005). Inhalation of 6 ppm can be lethal least 15 min. A 5% BAL (dimercaprol, British Anti-
(USACHPPM, 2001c). Following inhalation of vapor, Lewisite) compounded ophthalmic ointment applied
coughing and hemoptysis commonly occurs (Sidell et al., within 2 min may prevent a significant reaction.
1997; HSDB, 2005). Lesions following Lewisite Treatment at 30 min will lessen the ocular reaction but