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LEWISITE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Lewisite is a substituted arsine and is a vesicant (blister-causing) liquid with potential use as a terrorist or war agent. It is a liquid and can be dispersed through a bursting charge of explosive. It was synthesized in the early 20th century and is similar to mustard gas in that it damages the skin, eyes, and airways; however, it differs in that its clinical effects appear within seconds of exposure.
    B) Military Classification: Blister Agent
    C) Military abbreviation: L

Specific Substances

    1) Arsine, dichloro(2-chlorovinyl)-
    2) (2-Chloroethenyl)arsonous dichloride
    3) 1-Chloro-2-di-chloroarsinoethane
    4) 2-Chlorovinyldichloroarsine
    5) Arsine, (2-chlorovinyl)dichloro-
    6) Arsonous dichloride, (-chloroethenyl)-
    7) beta-Chlorovinylbichloroarsine
    8) Chlorovinylarsine dichloride
    9) Dichloro(2-chlorovinyl)arsine
    10) L
    11) Lewisite (arsenic compound)
    12) Molecular Formula: C2-H2-As-Cl3
    13) CAS 541-25-3
    1.2.1) MOLECULAR FORMULA
    1) C2-H2-As-Cl3

Available Forms Sources

    A) FORMS
    1) Lewisite can be dispersed in air as very fine droplet sprays, through a bursting charge of explosive (Grant & Schuman, 1993).
    B) SOURCES
    1) Lewisite (b-chlorovinyldichloroarsine) was first synthesized in 1918 by a research team headed by U.S. Army Captain W.L. Lewis (Sidell et al, 2000).
    2) Synthesis of Lewisite involves the addition of arsenic trichloride to acetylene, using aluminum chloride as a catalyst. This results in a mixture of L-1 (2-chlorovinyldichloroarsine, Lewisite) with an optimum yield of 20%, L-2 (di-(2-chlorovinyl)-chloroarsine), L-3 (tris- (2-chlorovinyl)-arsine), and an explosive component. A yield of 80-85% of L-1 can be obtained using mercuric chloride as a catalyst, although the catalytic solution is very corrosive (Goldman & Dacre, 1989; Lewis, 1997).
    3) No verified use of Lewisite on a battlefield exists, although Japan may have used it against China between 1937 and 1944 (CDC, 2001; (Sidell et al, 2000).
    4) The U.S. manufactured the chemical during World War I; however, the war ended while the shipment was being transported and the vessel carrying it sank before reaching its destination. U.S. stockpiles must be destroyed before April 2007, as mandated by the Chemical Weapons Convention. Currently several countries may have a stockpile of this chemical warfare agent (CDC, 2001; (Sidell et al, 2000).
    C) USES
    1) Lewisite is an arsenical vesicant warfare poison used by the military as a respiratory and systemic poison. In ambient air, Lewisite is about 10 times more volatile than mustard gas, and can be used as an irritant vapor over large distances. (Budavari, 2000; Goldman & Dacre, 1989; (HSDB, 2001); Lewis, 1998; Lewis, 2000; Sidell et al, 2000).
    2) It may be mixed with sulfur mustard to lower the freezing point of mustard (Sidell et al, 2000).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Lewisite is a vesicant or a blistering-type military poison that is extremely toxic by all routes of exposure. As a chemical warfare agent it can cause severe blistering and chemical burns, but may also act systemically to produce: diarrhea, restlessness, hypothermia, weakness, acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) and hypotension. The main route of absorption that results in systemic toxicity is through the respiratory tract, however, systemic effects may be seen after ingestion or through dermal contact.
    B) Lewisite acts first as a vesicant (since first contact is usually through dermal exposure), then as a pulmonary irritant and finally as a systemic poison. It can cause violent sneezing, severe pain and terror. It has similar toxic effects to mustard gas in that its main target organs are the skin, eyes and airways (the main organs affected); however, it differs in that its clinical effects appear within seconds of exposure. Data on human exposure is few; most information on its clinical effects is based on animal studies.
    C) After inhalation, mucous membranes are affected, causing severe irritation. Vocal cord paralysis and chemical pneumonitis may result. After severe inhalation exposures, acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) and death due to respiratory failure may occur. Systemic absorption can result in increased capillary permeability, causing loss of fluid from the vasculature, resulting in hemoconcentration, shock, and death.
    D) Dermal contact results in immediate stinging and burning sensations, and erythema within 30 minutes. Formation of sharply circumscribed, painful blisters, may occur in 2 to 13 hours after exposure. As little as five minutes of dermal exposure may result in a gray area of dead epithelium similar to that seen with corrosive burns. Itching and irritation may occur for about 24 hours, whether or not a blister is seen.
    E) Severe burns can result from dermal exposure. Skin burns are generally deeper than those with mustard gas. Skin penetration can result from contact with either liquid or vapor forms. Very small amounts (0.5 mL) can produce systemic effects; as little as 2 mLs can be fatal.
    F) Eye exposure results in rapid damage. Contact causes an immediate stinging and burning sensation. Blepharospasm may occur instantly, however, conjunctival and lid edema, iris inflammation, and corneal haziness occurs over several hours.
    G) Temporary blindness due to blistering and swelling of the eyelids and mucous membranes can occur. Erosion of the corneal epithelium may heal spontaneously, however, corneal scars may develop after initial recovery and reduce visual acuity. Moreover, permanent blindness is possible without prompt decontamination (within 1 minute).
    0.2.3) VITAL SIGNS
    A) Hypotension, tachycardia, and hypothermia may develop.
    0.2.4) HEENT
    A) Lacrimation, burns and/or strong irritation may occur after eye exposure. A geranium-like odor may be detectable on the victim.
    0.2.5) CARDIOVASCULAR
    A) "Lewisite shock" (refractory hypotension) may result due to increased capillary permeability and subsequent leakage following Lewisite exposures.
    0.2.6) RESPIRATORY
    A) Severe respiratory irritation leading to acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) and chemical pneumonitis may occur following acute exposure to Lewisite.
    0.2.7) NEUROLOGIC
    A) Restlessness and weakness may occur following systemic absorption.
    0.2.8) GASTROINTESTINAL
    A) Nausea, vomiting and salivation may occur with exposure to Lewisite.
    B) Gastroenteritis, sometimes with watery or bloody diarrhea, may occur after acute exposure to Lewisite.
    0.2.9) HEPATIC
    A) Hepatic necrosis has been reported in exposed animals.
    0.2.10) GENITOURINARY
    A) Acute toxic exposures may result in renal dysfunction.
    0.2.12) FLUID-ELECTROLYTE
    A) Significant intravascular volume depletion may occur.
    B) Electrolyte abnormalities may occur in conjunction with fluid losses.
    0.2.13) HEMATOLOGIC
    A) Hemolytic anemia due to "Lewisite shock" with subsequent hemoconcentration has been reported in one case. Lewisite does NOT cause bone marrow damage.
    0.2.14) DERMATOLOGIC
    A) Severe blistering and chemical burns have occurred following liquid and vapor exposure to Lewisite.
    0.2.19) IMMUNOLOGIC
    A) Unlike mustard gas, Lewisite does NOT produce immunosuppression.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no human reproductive studies were found for Lewisite.
    0.2.21) CARCINOGENICITY
    A) Lewisite is considered a suspect carcinogen because of its arsenic content.

Laboratory Monitoring

    A) Quantitative 24 hour urine collections are the most reliable laboratory measure of arsenic excretion following Lewisite exposures.
    B) Monitor cell blood counts and electrolytes in all symptomatic exposures.
    C) Monitor respiratory rate, pulse oximetry, and chest radiography in patients with significant exposures. If abnormal, check and monitor arterial blood gases and pulmonary function tests. Acute lung injury is a major toxic effect of Lewisite.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) Do NOT induce emesis.
    B) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    C) Consider insertion of a small, flexible nasogastric tube to aspirate gastric contents soon after a significant ingestion. The risk of worsening mucosal injury must be weighed against the potential benefit of removal of this systemic toxin.
    D) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    E) Monitor serum electrolytes and administer replacement therapy as indicated.
    F) Chelation with dimercaprol (BAL) or succimer (DMSA) or DMPS should be initiated in patients exhibiting systemic effects or patients with large areas of dermal burns or patients with liquid Lewisite contamination over greater than 5% of their body surface area. The 24-hour urine arsenic level should be less than 50 mcg/L before stopping chelation therapy. Organic dietary arsenic (normally found in seafood) may account for some urinary arsenic, and when in question, it should be speciated to determine organic and inorganic concentrations. Furthermore, any dietary seafood should be avoided during therapy because of this reason.
    G) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    0.4.3) INHALATION EXPOSURE
    A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    B) Monitor serum electrolytes and administer replacement therapy as indicated.
    C) Chelation with dimercaprol (BAL) or succimer (DMSA) or DMPS should be initiated in patients exhibiting systemic effects or patients with large areas of dermal burns or patients with liquid Lewisite contamination over greater than 5% of their body surface area. The 24-hour urine arsenic level should be less than 50 mcg/L before stopping chelation therapy. Organic dietary arsenic (normally found in seafood) may account for some urinary arsenic, and when in question, it should be speciated to determine organic and inorganic concentrations. Furthermore, any dietary seafood should be avoided during therapy because of this reason.
    D) ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
    E) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    F) Hemodialysis should be performed in the presence of renal failure.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    B) BAL - If applied within a few minutes of contact, it may prevent permanent damage.
    C) All patients with significant eye exposure should be carefully monitored for possible development of systemic signs and symptoms. Follow treatment recommendations in the INHALATION EXPOSURE section where appropriate.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) Prompt decontamination is extremely important. Any exposed skin (as well as exposed clothes) should be irrigated/washed with a 5% solution of sodium hypochlorite (diluted liquid household bleach), as soon as possible (preferably within one minute). Wash contaminated skin with soap and water afterwards. Topical 5% BAL ointment or solution may decrease blistering effects.
    2) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    3) Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.
    4) Monitor serum electrolytes and administer replacement therapy as indicated.
    5) Chelation with dimercaprol (BAL) or succimer (DMSA) or DMPS should be initiated in patients exhibiting systemic effects or patients with large areas of dermal burns or patients with liquid Lewisite contamination over greater than 5% of their body surface area. The 24-hour urine arsenic level should be less than 50 mcg/L before stopping chelation therapy. Organic dietary arsenic (normally found in seafood) may account for some urinary arsenic, and when in question, it should be speciated to determine organic and inorganic concentrations. Furthermore, any dietary seafood should be avoided during therapy because of this reason.
    6) COOLING - In one animal study, it was determined that cooling of Lewisite-exposed skin for 2 hours, followed by 1 hour of DMSA topical application was effective in reducing skin injury compared to either therapy alone.
    7) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If hypotension persists, administer dopamine (5 to 20 mcg/kg/min) or norepinephrine (ADULT: begin infusion at 0.5 to 1 mcg/min; CHILD: begin infusion at 0.1 mcg/kg/min); titrate to desired response.
    8) Hemodialysis should be performed in the presence of renal failure.

Range Of Toxicity

    A) As little as 0.5 mL, absorbed through the skin, may cause severe systemic effects, and 2 mL may be lethal. Inhalation of as little as 6 ppm may be lethal. Major routes of entry into the body include ocular, percutaneous, and inhalation.

Clinical Effects

Summary Of Exposure

    A) Lewisite is a vesicant or a blistering-type military poison that is extremely toxic by all routes of exposure. As a chemical warfare agent it can cause severe blistering and chemical burns, but may also act systemically to produce: diarrhea, restlessness, hypothermia, weakness, acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) and hypotension. The main route of absorption that results in systemic toxicity is through the respiratory tract, however, systemic effects may be seen after ingestion or through dermal contact.
    B) Lewisite acts first as a vesicant (since first contact is usually through dermal exposure), then as a pulmonary irritant and finally as a systemic poison. It can cause violent sneezing, severe pain and terror. It has similar toxic effects to mustard gas in that its main target organs are the skin, eyes and airways (the main organs affected); however, it differs in that its clinical effects appear within seconds of exposure. Data on human exposure is few; most information on its clinical effects is based on animal studies.
    C) After inhalation, mucous membranes are affected, causing severe irritation. Vocal cord paralysis and chemical pneumonitis may result. After severe inhalation exposures, acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) and death due to respiratory failure may occur. Systemic absorption can result in increased capillary permeability, causing loss of fluid from the vasculature, resulting in hemoconcentration, shock, and death.
    D) Dermal contact results in immediate stinging and burning sensations, and erythema within 30 minutes. Formation of sharply circumscribed, painful blisters, may occur in 2 to 13 hours after exposure. As little as five minutes of dermal exposure may result in a gray area of dead epithelium similar to that seen with corrosive burns. Itching and irritation may occur for about 24 hours, whether or not a blister is seen.
    E) Severe burns can result from dermal exposure. Skin burns are generally deeper than those with mustard gas. Skin penetration can result from contact with either liquid or vapor forms. Very small amounts (0.5 mL) can produce systemic effects; as little as 2 mLs can be fatal.
    F) Eye exposure results in rapid damage. Contact causes an immediate stinging and burning sensation. Blepharospasm may occur instantly, however, conjunctival and lid edema, iris inflammation, and corneal haziness occurs over several hours.
    G) Temporary blindness due to blistering and swelling of the eyelids and mucous membranes can occur. Erosion of the corneal epithelium may heal spontaneously, however, corneal scars may develop after initial recovery and reduce visual acuity. Moreover, permanent blindness is possible without prompt decontamination (within 1 minute).

Vital Signs

    3.3.1) SUMMARY
    A) Hypotension, tachycardia, and hypothermia may develop.
    3.3.3) TEMPERATURE
    A) Hypothermia may occur following acute exposure to Lewisite (EPA, 1985; (Anon, 1996)).
    3.3.4) BLOOD PRESSURE
    A) Hypotension may be noted following exposure to large amounts of Lewisite (Sidell et al, 2000).
    3.3.5) PULSE
    A) Tachycardia may occur following exposure to large amounts of Lewisite secondary to hypovolemia and/or pain (Sidell et al, 2000).

Heent

    3.4.1) SUMMARY
    A) Lacrimation, burns and/or strong irritation may occur after eye exposure. A geranium-like odor may be detectable on the victim.
    3.4.3) EYES
    A) BURNS - Profuse tearing and blepharospasm, resulting from eye exposure, may protect the eyes from exposure to vapor, but not from direct contact with the liquid (Grant & Schuman, 1993; (Goldman & Dacre, 1989; (Anon, 1999)). Severe pain and conjunctivitis develop early, followed by corneal scarring and iritis in severe cases (Grant & Schuman, 1993; ((Anon, 1999)).
    1) Permanent loss of sight may occur if eye exposure occurs for more than one minute without rapid decontamination (EPA, 1985; Sittig, 1991; Karalliedde et al, 2000; (Anon, 1999)). A small droplet (0.001 mL) can cause perforation and loss of vision (Sidell et al, 2000).
    2) BAL (dimercaprol) can prevent permanent damage to the eye if it is instilled within minutes of exposure (Grant & Schuman, 1993).
    B) CONJUNCTIVITIS - Photophobia, dimness of vision, diplopia, and lacrimation may occur (Heyman et al, 1956) Grant & Schuman, 1993; (Sidell et al, 2000).
    C) MIOSIS - This is an early effect (Sidell et al, 2000).
    D) EDEMA - In rabbit studies, exposure to Lewisite resulted in almost immediate edema of the eyelids, conjunctiva, and cornea. Early and severe involvement of the iris and ciliary body also occurred. This in turn was followed by gradual depigmentation and shrinkage of the iris stroma (Sidell et al, 2000).
    E) SEVERE INJURIES - Acute, severe eye injuries may be persistent (Sidell et al, 2000).
    3.4.5) NOSE
    A) BURNING - A sensation of burning, dryness and constriction of the oral and nasal cavities may occur (Sidell et al, 2000; HSDB , 2000).
    3.4.6) THROAT
    A) Vocal cord paralysis may result following a large exposure to the vapor ((Anon, 2000)).

Cardiovascular

    3.5.1) SUMMARY
    A) "Lewisite shock" (refractory hypotension) may result due to increased capillary permeability and subsequent leakage following Lewisite exposures.
    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) "Lewisite shock" may be seen following exposure to large amounts of Lewisite. This is caused by protein and plasma leakage from the capillaries (reduced plasma volume) with subsequent hemoconcentration and hypotension. In extreme exposures, all capillaries may be affected, resulting in protein and plasma leakage from the circulation into the periphery with resultant hypovolemic shock (Sidell et al, 2000; Goldman & Dacre, 1989; (Anon, 1999)).
    2) Acute systemic poisoning from large skin burns can result in hypotension ((Anon, 1996); (Anon, 1999)).
    B) CONDUCTION DISORDER OF THE HEART
    1) Dysrhythmias may potentially occur as a result of hypovolemia and electrolyte imbalance following Lewisite exposures. Dysrhythmias are a secondary effect of electrolyte abnormalities rather than a direct toxic effect of Lewisite on the myocardium (Sidell et al, 2000).
    C) INCREASED CAPILLARY FRAGILITY
    1) The major systemic toxic effect of Lewisite is on the capillaries and pulmonary capillaries are the most sensitive (Goldman & Dacre, 1989; (Anon, 1999)). Following exposure to large amounts of Lewisite, protein and plasma leakage from systemic capillaries into the periphery may occur, with subsequent hemoconcentration and hypotension. Small amounts of Lewisite on the skin may cause local edema due to local capillary effects. Pulmonary capillaries may be affected with large exposures to vapor, resulting in edema and acute lung injury (ALI) (Sidell et al, 2000; Sidell et al, 1998; (Anon, 1999)).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) DYSRHYTHMIA
    a) Lewisite poisoning has resulted in a rapid, weak pulse in dogs and other species. A profound bradycardia with deficient diastolic relaxation occurs. The heart gradually ceases beating or terminates in ventricular fibrillation (Goldman & Dacre, 1989).

Respiratory

    3.6.1) SUMMARY
    A) Severe respiratory irritation leading to acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) and chemical pneumonitis may occur following acute exposure to Lewisite.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE LUNG INJURY
    1) Lewisite is a severe irritant. Inhalational exposure (depending on concentration) may be lethal in as little as 10 minutes (EPA, 1985). Severe inhalational exposures can result in acute lung injury and death due to respiratory failure (Karalliedde et al, 2000).
    2) Following a large inhalational exposure, progressive acute lung injury results. Persons who survive an initial exposure may develop acute lung injury (EPA, 1985; Sidell et al, 2000; HSDB , 2000). Acute systemic poisoning from large skin burns as well as vapor inhalation can result in acute lung injury ((Anon, 1996); (Anon, 1999)). Acute lung injury is frequently accompanied by pleural fluid.
    B) IRRITATION SYMPTOM
    1) Lewisite is a pulmonary irritant and vesicant (blister-causing) that causes immediate signs and symptoms. It is extremely irritating to the lower airways and mucous membranes. Following prolonged inhalation of the vapor, marked spasmodic coughing with frothy or blood-stained sputum commonly occurs. Severe damage to the respiratory system also may occur, with symptoms of dyspnea and chest pain (Sidell et al, 2000; HSDB , 2000; (Anon, 1999)).
    a) Airway lesions following Lewisite exposures are similar to the lesions produced by mustard gas exposures (Sidell et al, 2000).
    C) PNEUMONITIS
    1) Chemical pneumonitis may result following mucous membrane irritation from the vesicant action of Lewisite ((Anon, 2000)). Chronic exposure to Lewisite may cause sensitization and chronic lung impairment ((Anon, 1999)).
    D) RHINITIS
    1) Inhalation of the Lewisite vapor may result in irritation to nasal passages and a burning sensation followed by profuse nasal secretions and violent sneezing (HSDB , 2000; (Anon, 1999)).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RESPIRATORY DISORDER
    a) In a rabbit study comparing intravenous toxicity of Lewisite with sodium arsenite, severe pulmonary damage was reported in Lewisite treated animals but not in the arsenic treated group (HSDB , 2000). Intravenous injections in rabbits resulted in acute lung injury in cases of severe toxicity; death was due to respiratory failure (Karalliedde et al, 2000).
    b) Dogs that inhaled lethal Lewisite doses died of necrotizing pseudomembranous laryngotracheobronchitis (Goldman & Dacre, 1989).
    2) PNEUMONIA
    a) DOGS - Following prolonged exposure to high concentrations of Lewisite vapor, dogs were reported to have labored breathing, inflammation of the entire respiratory system, and acute lung injury. Bronchopneumonia followed this stage with termination in death. Autopsy revealed a thick membrane in the nostrils, larynx, and trachea with purulent bronchitis. Hemorrhage, edema, and emphysema of the lungs were also noted (Goldman & Dacre, 1989).

Neurologic

    3.7.1) SUMMARY
    A) Restlessness and weakness may occur following systemic absorption.
    3.7.2) CLINICAL EFFECTS
    A) FEELING NERVOUS
    1) Restlessness and weakness may occur following acute systemic poisoning from large skin burns ((Anon, 1996)).

Gastrointestinal

    3.8.1) SUMMARY
    A) Nausea, vomiting and salivation may occur with exposure to Lewisite.
    B) Gastroenteritis, sometimes with watery or bloody diarrhea, may occur after acute exposure to Lewisite.
    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) Nausea, vomiting and salivation may occur after exposure (EPA, 1985; Goldman & Dacre, 1989).
    B) GASTROENTERITIS
    1) Excretion of oxidized Lewisite products into the bile by the liver may result in injury to the intestinal mucosa. Acute systemic poisoning from large skin burns results in diarrhea (sometimes bloody) ((Anon, 1996)).
    3.8.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) VOMITING
    a) DOGS - Following prolonged exposure to high concentrations of Lewisite vapor, retching, vomiting and intense salivation have been reported (Goldman & Dacre, 1989).

Hepatic

    3.9.1) SUMMARY
    A) Hepatic necrosis has been reported in exposed animals.
    3.9.2) CLINICAL EFFECTS
    A) HEPATIC NECROSIS
    1) Excretion of Lewisite oxidation products into the bile by the liver caused focal necrosis of the liver in animal studies. Necrosis of biliary vessel mucosa with peribiliary hemorrhages has occurred and may be expected in severe human exposures ((Anon, 1999); (Anon, 1996)).

Genitourinary

    3.10.1) SUMMARY
    A) Acute toxic exposures may result in renal dysfunction.
    3.10.2) CLINICAL EFFECTS
    A) RENAL FAILURE SYNDROME
    1) Toxic exposures may result in sufficient fluid loss to cause secondary renal dysfunction and hypotension (Sidell et al, 2000; HSDB , 2000).

Hematologic

    3.13.1) SUMMARY
    A) Hemolytic anemia due to "Lewisite shock" with subsequent hemoconcentration has been reported in one case. Lewisite does NOT cause bone marrow damage.
    3.13.2) CLINICAL EFFECTS
    A) HEMOLYSIS
    1) Arsines are noted to cause hemolytic anemia. Hemolysis is a primary toxic effect of arsine gas. Lewisite, a substituted arsine, does NOT directly cause hemolysis of red blood cells (HSDB , 2000). There is little data examining the relationship of Lewisite exposures directly resulting in hemolysis. Hemolysis of erythrocytes has occurred in nonfatal cases, with resultant hemolytic anemia ((Anon, 1999); Goldman & Dacre, 1989).
    2) One case of true or hemolytic anemia due to "Lewisite shock" (protein and plasma leakage from capillaries and subsequent hemoconcentration and hypotension) has been reported. The bone marrow in this case revealed no degenerative changes (Sidell et al, 2000; Goldman & Dacre, 1989).
    B) LACK OF EFFECT
    1) Unlike arsenic or mustard gas, Lewisite (substituted arsine) does NOT cause damage to the bone marrow (Sidell et al, 2000; Sidell et al, 1998).

Dermatologic

    3.14.1) SUMMARY
    A) Severe blistering and chemical burns have occurred following liquid and vapor exposure to Lewisite.
    3.14.2) CLINICAL EFFECTS
    A) SKIN IRRITATION
    1) An immediate stinging sensation is felt after exposure. Erythema (reddening) becomes evident within 15 to 30 minutes after exposure (EPA, 1985; Sittig, 1991; Sidell et al, 2000; (Anon, 1999)). Evidence of tissue destruction (grayish epithelium) will be present within minutes of skin contact (Sidell et al, 1998; Goldman & Dacre, 1989). Pain following exposure intensifies, even after removal from the source. Onset of symptoms occurs sooner after liquid contact than vapor. Dermal absorption occurs within 3 to 5 minutes, especially following liquid exposures (Sidell et al, 2000).
    B) BULLOUS ERUPTION
    1) Lewisite produces severe vesication or blisters on the skin, generally evident within 12 hours after exposure (EPA, 1985; Sidell et al, 2000; Goldman & Dacre, 1989; (Anon, 1999)). It can penetrate rubber (Budavari, 1996; HSDB , 2000). The blister begins as a small vesication in the center of the erythematous area, which expands to include the entire inflamed site. Blisters may rupture, usually about 48 hours after occurrence, with copious amounts of fluid seeping from the site (Goldman & Dacre, 1989). Healing of the lesions occurs much faster than with sulfur mustard-induced lesions and is generally complete within 4 weeks (Sidell et al, 2000; Goldman & Dacre, 1989).
    a) Fluid from a Lewisite-induced blister is non-irritating, but does contain 0.8 to 1.3 mg/mL of arsenic and many leukocytes (Sidell et al, 2000; Goldman & Dacre, 1989).
    C) DISCOLORATION OF SKIN
    1) A grayish epithelium, due to tissue destruction, becomes evident within minutes of exposure (Sidell et al, 1998; Sidell et al, 2000; Goldman & Dacre, 1989).
    D) EDEMA
    1) Dermal exposure may result in edema due to local effects on affected capillaries (Sidell et al, 2000; Goldman & Dacre, 1989).

Immunologic

    3.19.1) SUMMARY
    A) Unlike mustard gas, Lewisite does NOT produce immunosuppression.
    3.19.2) CLINICAL EFFECTS
    A) LACK OF EFFECT
    1) Unlike mustard gas, another vesicant agent, Lewisite does NOT cause immunosuppression with overwhelming infection following systemic absorption (Sidell et al, 2000). Secondary infections are uncommon following exposure to Lewisite.

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no human reproductive studies were found for Lewisite.
    3.20.2) TERATOGENICITY
    A) ANIMAL STUDIES
    1) FETOTOXICITY
    a) Fetal death has been reported in the offspring of rats administered Lewisite (RTECS , 2000).
    b) Lewisite was not teratogenic in either rats or rabbits (Goldman & Dacre, 1989). Arsenic compounds have typically induced birth defects in experimental animals with high doses, which may have also been maternally toxic (OTA, 1985).
    c) Teratogenic potential is suspected, but there are no definitive studies.
    d) Lewisite was fetotoxic, but not teratogenic, in rats; it was not a teratogen in rabbits (RTECS, 1993; (Goldman & Dacre, 1989).
    3.20.3) EFFECTS IN PREGNANCY
    A) PREGNANCY DISORDER
    1) Arsenic in general has been implicated in adverse effects on human reproduction. Increased miscarriages and birth defects were reported in employees and women living near a smelter in Sweden, but mixed exposures were involved (Nordstrom et al, 1979). Increased miscarriages were also reported in Finland, but there were mixed exposures (Hemminki et al, 1980).
    B) ANIMAL STUDIES
    1) FETOTOXICITY
    a) Lewisite, administered orally between days 7 and 15 of pregnancy, was toxic to the fetus in rabbits and rats (RTECS , 2000). Fetotoxicity was seen in rats and rabbits exposed to 2 mg/kg/day and 0.6 mg/kg/day, respectively, but maternal toxicity was also evident (Hackett et al, 1987). It had no adverse effects on male or female fertility or on the unborn at oral doses up to 0.6 mg/kg/day in a two-generation study in rats (Sasser et al, 1989).
    3.20.4) EFFECTS DURING BREAST-FEEDING
    A) BREAST MILK
    1) Arsenic is transferred across the placenta and into breast milk (Barlow & Sullivan, 1982). There may be some risk to nursing infants of mothers exposed to arsenic. Japanese children who drank arsenic-contaminated powdered milk may have suffered problems in later brain development (Barlow & Sullivan, 1982).

Carcinogenicity

    3.21.1) IARC CATEGORY
    A) IARC Carcinogenicity Ratings for CAS541-25-3 (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004):
    1) Not Listed
    3.21.2) SUMMARY/HUMAN
    A) Lewisite is considered a suspect carcinogen because of its arsenic content.
    3.21.3) HUMAN STUDIES
    A) CARCINOMA
    1) Lewisite is considered a suspect carcinogen due to its arsenic content ((Anon, 1999)) but there is no available scientific evidence to support this label (Goldman & Dacre, 1989; Sidell et al, 2000).
    B) SKIN CARCINOMA
    1) One case of Bowen's disease (intraepidermal squamous cell carcinoma) has been reported to occur many years after exposure to Lewisite (Krause & Grussendorf, 1979), but a causal relationship is unsubstantiated.
    C) PULMONARY CARCINOMA
    1) Occupational exposure to Lewisite has been associated with lung cancer in former poison gas workers (Wada et al, 1963; Nishimoto et al, 1986; Nishimoto et al, 1987).
    a) This study has been criticized because of mixed exposures (Goldman & Dacre, 1989).

Genotoxicity

    A) Lewisite was inactive in the Ames Salmonella assay and proved inconclusive in D melanogaster for sex-linked lethal mutations assay.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Quantitative 24 hour urine collections are the most reliable laboratory measure of arsenic excretion following Lewisite exposures.
    B) Monitor cell blood counts and electrolytes in all symptomatic exposures.
    C) Monitor respiratory rate, pulse oximetry, and chest radiography in patients with significant exposures. If abnormal, check and monitor arterial blood gases and pulmonary function tests. Acute lung injury is a major toxic effect of Lewisite.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) An arsenic blood level below 7 mcg/100 mL is considered in the normal range. Lewisite blood levels are not clinically useful.
    2) Monitor fluid and serum electrolyte status in patients with significant vomiting, diarrhea, or hypotension from fluid third spacing. Resultant renal dysfunction can occur.
    B) HEMATOLOGIC
    1) Lewisite exposures can cause hemoconcentration; follow the hematocrit in all suspected exposures.
    C) ACID/BASE
    1) Monitor venous or arterial blood gases in patients with significant exposures or those developing systemic symptoms.
    4.1.3) URINE
    A) URINARY LEVELS
    1) 24-hour urine collections for total arsenic excretion or spot specimens measured as concentration of arsenic (in micrograms or milligrams) per gram of urinary creatinine are generally the preferred samples, as they balance out the effects of varying urine volume and concentration.
    2) A method for a quick urine spot test (Reinsch test) has been described (Grande et al, 1987) but its clinical utility is uncertain. Even with chelation, an unexposed individual should not have more than 100 mcg of arsenic per 24 hour total urine output. Urinary arsenic may be elevated up to 200 to 1700 mcg/L within 4 hours after eating some seafood (Baselt, 2000; Proctor et al, 1988).
    a) Urinary concentrations between 700 and 1000 mcg/L (0.7 to 1.0 mg/L) may indicate potentially harmful exposure (Proctor et al, 1988).
    b) Urine levels are generally below 100 mcg/gram of creatinine, and generally below 20 mcg/gram of creatinine in unexposed individuals (Hathaway et al, 1996).
    c) A recommended maximum permissible value for arsenic in the urine of exposed workers is 220 microgram/gram of creatinine (HSDB , 2000).

Radiographic Studies

    A) ABDOMINAL RADIOGRAPH
    1) Arsenic is radiopaque and an abdominal film should be obtained whenever Lewisite ingestion is suspected (Hilfer & Mendel, 1962; Gousios & Adelson, 1959).
    B) CHEST RADIOGRAPH
    1) Monitor the chest radiograph in patients following significant Lewisite exposures.

Methods

    A) OTHER
    1) There is no specific laboratory test for Lewisite. Urinary arsenic excretion may be helpful in identifying possible exposure to Lewisite. An arsine evolution-electrothermal atomic absorption method has been reported for the determination of ng/mL concentrations of total arsenic in the urine. This method has a detection limit of 6 ng/mL, a sensitivity of 1 ng/mL, and is linear from 0 to 110 ng/mL for arsenic derived from an organic arsenic compound (HSDB , 2000).
    B) MULTIPLE ANALYTICAL METHODS
    1) Gas chromatography combined with multiple ion detection mass spectrometry and hydride generation-heptane cold trap technique has been reported for the detection of inorganic and methylated arsenic compounds in human urine. A relative limit of detection for arsines generated by reduction of a 50 mL sample is reported to be 0.2 to 0.4 mg arsenic/mL for arsenate and arsenic compounds (HSDB , 2000).
    2) An electron-capture gas chromatographic technique can be used to differentiate organic from inorganic arsenic in the urine (Baselt & Cravey, 1989).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Quantitative 24 hour urine collections are the most reliable laboratory measure of arsenic excretion following Lewisite exposures.
    B) Monitor cell blood counts and electrolytes in all symptomatic exposures.
    C) Monitor respiratory rate, pulse oximetry, and chest radiography in patients with significant exposures. If abnormal, check and monitor arterial blood gases and pulmonary function tests. Acute lung injury is a major toxic effect of Lewisite.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) EMESIS/NOT RECOMMENDED
    1) Ipecac-induced emesis is NOT recommended because of the irritant and vesicant nature of Lewisite.
    B) ACTIVATED CHARCOAL
    1) Activated charcoal is of unknown benefit in Lewisite ingestion, but should be considered after significant ingestions.
    2) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    C) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    D) INHALATION EXPOSURE
    1) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
    E) DERMAL EXPOSURE -
    1) Prompt decontamination is of UTMOST IMPORTANCE. Immediately wash skin and clothes with 5% solution of sodium hypochlorite or diluted liquid household bleach, within one minute if possible. Wash contaminated skin with soap and water afterwards. Topical 5% BAL compounded ointment or solution may decrease vesicant effects.
    F) EYE EXPOSURE
    1) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    2) A 5% BAL compounded ophthalmic ointment or solution applied within 2 minutes may prevent permanent eye damage.
    6.5.2) PREVENTION OF ABSORPTION
    A) EMESIS/NOT RECOMMENDED
    1) EMESIS is to be AVOIDED, because of the irritant and vesicant nature of this material.
    B) DILUTION
    1) DILUTION: If no respiratory compromise is present, administer milk or water as soon as possible after ingestion. Dilution may only be helpful if performed in the first seconds to minutes after ingestion. The ideal amount is unknown; no more than 8 ounces (240 mL) in adults and 4 ounces (120 mL) in children is recommended to minimize the risk of vomiting (Caravati, 2004).
    C) GASTRIC LAVAGE
    1) Consider insertion of a small, flexible nasogastric tube to aspirate gastric contents soon after a significant ingestion. The risk of worsening mucosal injury must be weighed against the potential benefit.
    D) ACTIVATED CHARCOAL
    1) Although arsenic is commonly listed as being effectively adsorbed to charcoal, there is not much data to support adsorption of Lewisite to activated charcoal.
    2) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    3) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) BURN
    1) Severe irritation or vesication (blistering) of the esophagus or gastrointestinal tract is likely to occur following liquid Lewisite ingestion. Observe patients with ingestion carefully for the possible development of esophageal or gastrointestinal tract irritation or burns. If signs or symptoms of esophageal irritation or burns are present, consider endoscopy to determine the extent of injury.
    2) Perforation, bleeding, and late stricture formation may result after ingestion. If severe irritation or burns of the esophagus or gastrointestinal tract are suspected, surgical consultation is advised.
    B) GENERAL TREATMENT
    1) Treatment guidelines for patients sustaining systemic effects following significant oral exposure may be found in the INHALATION EXPOSURE treatment section.

Inhalation Exposure

    6.7.1) DECONTAMINATION
    A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
    B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
    C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.
    6.7.2) TREATMENT
    A) SUPPORT
    1) Monitor respiratory rate, pulse oximetry, chest radiography and fluid-electrolyte status in patients with significant exposures. If abnormal, check and monitor arterial blood gases and pulmonary function tests. Administration of supplemental oxygen, fluid and electrolyte replacement therapy, and antibiotics for secondary infection may be required.
    B) CHELATION THERAPY
    1) INDICATIONS - for systemic treatment include: (1) cough with dyspnea and frothy sputum and signs of pulmonary edema; (2) skin burn the size of the palm of the hand or larger caused by liquid Lewisite and not decontaminated within the first 15 minutes; and (3) skin contamination by liquid Lewisite covering 5% or more of the body surface in which there is evidence of immediate skin damage or erythema within 30 minutes ((Anon, 1996)).
    a) A series of 3 recommended chelators (DMPS, DMSA, and BAL) has shown that DMPS has the highest capacity to reverse or prevent pyruvate dehydrogenase inhibition by sodium arsenite. Conversely, BAL had the least capacity to reverse or prevent pyruvate dehydrogenase inhibition by sodium arsenite ((Anon, 1996)).
    2) THERAPEUTIC END-POINT - Repeat courses of chelation therapy should be prescribed in severe poisonings until the 24-hour urine arsenic level falls below 50 micrograms/liter (Goldfrank et al, 1998; AMA, 1986). BAL has been shown to increase urinary arsenic concentration by about 40%, with maximum excretion occurring within 2 to 4 hours after BAL dosing (Goldfrank et al, 1998). Organic dietary arsenic (normally found in seafood) may account for some urinary arsenic, and when in question, it should be speciated to determine organic and inorganic concentrations. Furthermore, any dietary seafood should be avoided during therapy because of this reason.
    C) DIMERCAPROL
    1) EFFICACY - Dimercaprol (BAL) is an effective arsenic chelator, but has the disadvantages of requiring painful deep intramuscular injections and having numerous side effects. In the presence of arsenic-induced liver damage, BAL is not very effective and is contraindicated. Use BAL with caution in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency as it may cause hemolysis (Howland, 2002).
    2) ADVERSE EFFECTS - Typical side effects which are dose-dependent include hypertension, tachycardia, nausea and vomiting, headache, burning sensation of lips, feeling of chest constriction, conjunctivitis, lacrimation, rhinorrhea, sweating, muscle aches, burning and tingling of extremities, and anxiety. Adverse effects are maximal within 10 to 30 minutes and usually subside within 30 to 50 minutes (Howland, 2002; (Anon, 1996)).
    3) DOSE - The maximum dosage of BAL is 3 mg/kg (200 mg for an average person) given as a deep intramuscular injection and repeated every 4 hours for 2 days, then given every 6 hours on the third day, and every 12 hours for up to 10 days. Avoid subcutaneous leakage ((Anon, 1996)). Doses above 5 mg/kg result in adverse effects in 50% of patients. Unless the adverse effects are unduly severe or prolonged, they do NOT contraindicate the full course of treatment.
    D) SUCCIMER
    1) EFFICACY - 2,3-Dimercaptosuccinic acid (DMSA) appears to be a very effective experimental arsenic chelator in animals (Graziano et al, 1978) and man (Lenz et al, 1981; Kosnett MJ & Becker CE, 1987; Fournier et al, 1988; Aposhian et al, 1982). DMSA has the advantage of being an oral agent as well as being relatively non-toxic. Hemolytic anemia has been reported following succimer therapy in a patient with glucose-6-phosphate hydrogenase deficiency. Thus this chelator should be used with caution in these patients (Gerr et al, 1994).
    2) SUCCIMER/DOSE/ADMINISTRATION
    a) PEDIATRIC: Initial dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days (Prod Info CHEMET(R) oral capsules, 2011).
    1) The dosing interval is then increased to every 12 hours for the next 14 days. A repeat course may be given if indicated by elevated blood levels. A minimum of 2 weeks between courses is recommended, unless blood lead concentrations indicate the need for prompt retreatment.
    2) Succimer capsule contents may be administered mixed in a small amount of food (Prod Info CHEMET(R) oral capsules, 2011).
    b) ADULT: Succimer is not FDA approved for use in adults, however it has been shown to be safe and effective when used to treat adults with poisoning from a variety of heavy metals (Fournier et al, 1988a). Initial dose is 10 mg/kg or 350 mg/m(2) orally every 8 hours for 5 days (Prod Info CHEMET(R) oral capsules, 2011).
    1) The dosing interval then is increased to every 12 hours for the next 14 days. A repeat course may be given if indicated by elevated blood levels. A minimum of 2 weeks between courses is recommended, unless the patient's symptoms or blood concentrations indicate a need for more prompt treatment (Prod Info CHEMET(R) oral capsules, 2011).
    3) MONITORING PARAMETERS
    a) The manufacturer recommends monitoring liver enzymes and complete blood count with differential and platelet count prior to the start of therapy and at least weekly during therapy (Prod Info CHEMET(R) oral capsules, 2011).
    b) Succimer therapy did not worsen preexisting borderline abnormal liver enzyme levels in a prospective evaluation of 15 children with lead poisoning (Kuntzelman & Angle, 1992).
    E) UNITHIOL
    1) A related compound to DMSA, the sodium salt of 2,3-dimercapto-1-propanesulfonic acid (DMPS), was also effective in protecting rabbits from the lethal effects of Lewisite. However, it was less stable than DMSA upon storage in water (Aposhian et al, 1982).
    2) DMPS/INDICATIONS: Chelating agent for heavy metal toxicities associated with arsenic, bismuth, copper, lead and mercury (Blanusa et al, 2005).
    3) DMPS/DOSING
    a) ACUTE TOXICITY
    1) ADULT ORAL DOSE:
    a) 1200 to 2400 mg/day in equally divided doses (100 to 200 mg 12 times daily) (Prod Info DIMAVAL(R) oral capsules, 2004).
    2) ADULT INTRAVENOUS DOSE (Arbeitsgruppe BGVV, 1996; Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013):
    a) If oral DMPS therapy is not feasible or in severe toxicity, it may be given intravenously.
    b) ADMINISTRATION: DMPS should be injected immediately after breaking open the ampule and should not be mixed with other solutions. DMPS should be injected slowly over 3 to 5 minutes. The opened ampules cannot be reused.
    c) First 24 hours: 250 mg intravenously every 3 to 4 hours (1500 to 2000 mg total).
    d) Day two: 250 mg intravenously every 4 to 6 hours (1000 to 1500 mg total).
    e) Day three: 250 mg intravenously every 6 to 8 hours (750 to 1000 mg total).
    f) Day four: 250 mg intravenously every 8 to 12 hours (500 to 750 mg total).
    g) Subsequent days: 250 mg intravenously every 8 to 24 hours (250 to 750 mg total).
    h) Depending on the patient's clinical status, therapy may be changed to the oral route.
    3) PEDIATRIC ORAL DOSE (Arbeitsgruppe BGVV, 1996; Blanusa et al, 2005):
    a) There are insufficient clinical data regarding the pediatric use of DMPS. It should be used only if medically necessary.
    b) Initial dose: 20 to 30 mg/kg/day orally in many equal divided doses.
    c) Maintenance dose: 1.5 to 15 mg/kg/day.
    4) PEDIATRIC INTRAVENOUS DOSE (Arbeitsgruppe BGVV, 1996; Blanusa et al, 2005; Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013):
    a) There are insufficient clinical data regarding the pediatric use of DMPS. It should be used only if medically necessary.
    b) If oral DMPS therapy is not feasible or in severe toxicity, it may be given intravenously.
    c) ADMINISTRATION: DMPS should be injected immediately after breaking open the ampule and should not be mixed with other solutions. DMPS should be injected slowly over 3 to 5 minutes. The opened ampules cannot be reused.
    d) First 24 hours: 5 mg/kg intravenously every four hours (total 30 mg/kg).
    e) Day two: 5 mg/kg intravenously every six hours (total 20 mg/kg).
    f) Days three and four: 5 mg/kg intravenously every 8 to 24 hours (total 5 to 15 mg/kg).
    b) CHRONIC TOXICITY
    1) ADULT DOSE
    a) 300 to 400 mg/day orally (in single doses of 100 to 200 mg). The dose may be increased in severe toxicity (Arbeitsgruppe BGVV, 1996; Prod Info DIMAVAL(R) oral capsules, 2004).
    c) DMPS/ADVERSE REACTIONS
    1) Chills, fever, and allergic skin reactions such as itching, exanthema or maculopapular rash are possible (Hla et al, 1992; Prod Info DIMAVAL(R) oral capsules, 2004). Cardiovascular effects such as hypotension, nausea, dizziness or weakness may occur with too rapid injection of DMPS. Hypotensive effects are irreversible at very high doses (300 mg/kg) (Prod Info DIMAVAL(R) oral capsules, 2004; Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013).
    4) SOURCES
    a) DMPS is not FDA-approved, but is available outside of the US from Heyl Chem-pharm Fabrik in Germany (Prod Info Dimaval(R) intravenous intramuscular injection solution, 2013; Prod Info DIMAVAL(R) oral capsules, 2004). In the US it may be obtained from some compounding pharmacies.
    F) ACUTE LUNG INJURY
    1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
    2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).
    a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
    3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
    4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
    5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
    6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
    7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
    G) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    H) HEMODIALYSIS
    1) Hemodialysis should be performed in renal failure, as the main route of excretion will be inhibited if this occurs. As the serum creatinine falls, urinary arsenic may increase (Giberson et al, 1976). Dialysance of arsenic in two patients was 76 and 87 milliliters/minute (Vaziri et al, 1980). This may be greater than renal clearance in the presence of oliguria or renal failure.
    2) Hemodialysis may be needed to remove BAL-metal complexes in cases of renal failure (Howland, 2002).
    I) HEMOLYSIS
    1) Maintain urine output of at least 1 to 2 milliliters/kilogram/hour with appropriate hydration and diuretics if necessary.
    J) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) A 5% BAL compounded ophthalmic ointment or solution applied within 2 minutes may prevent a significant reaction; application at 30 minutes will lessen the ocular reaction but does not prevent permanent damage (Goldfrank, 1998).
    B) Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If significant eye irritation is present, prolonged early flushing and early ophthalmologic consultation are advisable.
    6.8.2) TREATMENT
    A) GENERAL TREATMENT
    1) SYSTEMIC TOXICITY - No cases of systemic Lewisite poisoning following only eye exposure have been reported. All patients with significant eye exposure should be carefully monitored for possible development of systemic signs and symptoms. Follow treatment recommendations in the INHALATION EXPOSURE section where appropriate.
    2) CONSULTATION - If significant eye irritation is present, prolonged early flushing and early ophthalmologic consultation are advisable.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) Any exposed skin (as well as exposed clothes) should be irrigated/washed with a 5% solution of sodium hypochlorite (diluted liquid household bleach) as soon as possible (preferably within one minute). Wash contaminated skin with soap and water afterwards ((Anon, 1999)).
    2) Topical application of a 5% BAL ointment or solution within 15 minutes of an exposure has been reported to be effective in diminishing the blistering effects of Lewisite (Smith & Dunn, 1991). Wash off any protective ointment prior to applying topical BAL.
    3) COOLING - In one animal study (hairless guinea pigs), cooling of Lewisite exposed skin at approximately 10 degrees C for as little as 30 minutes post-exposure resulted in a significant decrease in both the size and severity of the skin lesions, with 4 hours of cooling almost completely eliminating skin injury. Even when cooling was delayed for as long as 2 hours post-exposure, significant protection was also observed. Cooling of Lewisite-exposed skin for 2 hours, followed by 1 hour of DMSA topical application, was more effective in reducing skin injury compared to either therapy alone (Nelson et al, 2006).
    4) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    6.9.2) TREATMENT
    A) BURN
    1) APPLICATION
    a) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.
    2) DEBRIDEMENT
    a) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
    b) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
    c) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).
    3) TREATMENT
    a) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
    b) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
    c) WOUND DRESSING:
    1) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
    2) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.
    d) DRESSING CHANGES:
    1) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
    2) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.
    e) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.
    4) TETANUS PROPHYLAXIS
    a) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.
    B) GENERAL TREATMENT
    1) Treatment guidelines for patients sustaining systemic effects following significant dermal exposure may be found in the INHALATION EXPOSURE treatment section.
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Range Of Toxicity

Summary

    A) As little as 0.5 mL, absorbed through the skin, may cause severe systemic effects, and 2 mL may be lethal. Inhalation of as little as 6 ppm may be lethal. Major routes of entry into the body include ocular, percutaneous, and inhalation.

Minimum Lethal Exposure

    A) ADULT
    1) Lewisite is not detoxified in the body. High concentrations can cause death within 10 minutes (USACHPPM , 2001).
    2) Lewisite at 150 mg/min/m(3) causes 1% lethality (USACHPPM , 2001).

Maximum Tolerated Exposure

    A) OCCUPATIONAL
    1) The TWA for the workplace is 0.003 mg/m(3). This is currently based on the technologically feasible detection limits. To date, OSHA has not promulgated a permissible exposure concentration for lewisite (CDC, 2001; SBCCOM, 1999; (USACHPPM , 2001).
    2) The 72-hour TWA for the General Population is 0.003 mg/m(3) (CDC, 2001; (USACHPPM , 2001).
    3) No deaths occur at 100 mg/min/m(3) (USACHPPM , 2001).
    B) ROUTE OF EXPOSURE
    1) Vesication may occur with 14 mcg of liquid on the skin. Blister fluid due to Lewisite exposure is non-irritating, but does contain 0.8-1.3 mg/mL of arsenic (Sidell et al, 2000).
    2) Nasal irritation occurs at concentrations of 8 mg/min/m(3), but Lewisite odor is not detected until concentrations reach about 20 mg/min/m(3) (U.S. Army, 1996).

Workplace Standards

    A) ACGIH TLV Values for CAS541-25-3 (American Conference of Governmental Industrial Hygienists, 2010):
    1) Not Listed

    B) NIOSH REL and IDLH Values for CAS541-25-3 (National Institute for Occupational Safety and Health, 2007):
    1) Not Listed

    C) Carcinogenicity Ratings for CAS541-25-3 :
    1) ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed
    2) EPA (U.S. Environmental Protection Agency, 2011): Not Listed
    3) IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
    4) NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed
    5) MAK (DFG, 2002): Not Listed
    6) NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

    D) OSHA PEL Values for CAS541-25-3 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
    1) Not Listed

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) References: Lewis, 2000 RTECS, 2001 Sidell et al, 2000; SBCCOM, 1999; USACHPPM, 2001 U.S. Army, 1997
    1) ICt50- (OCULAR)HUMAN:
    a) <300 mg/min/m(3) (SBCCOM, 1999; USACHPPM, 2001)
    2) LD50- (SKIN)HUMAN:
    a) 2.8 g/kg (liquid) (U.S. Army, 1996)
    b) 30 mg/kg (Sidell et al, 2000)
    3) LD50- (SKIN)MOUSE:
    a) 12 mg/kg
    4) LD50- (ORAL)RAT:
    a) 50 mg/kg
    5) LD50- (SKIN)RAT:
    a) 15 mg/kg
    b) 15-24 mg/kg (SBCCOM, 1999)
    6) LD50- (SUBCUTANEOUS)RAT:
    a) 1 mg/kg

Pharmacology Toxicology

Toxicologic Mechanism

    A) Lewisite applied to skin results in local edema due to increased capillary permeability. Increased capillary permeability occurs following systemic absorption, through the skin, the respiratory tract (primary route), or ingestion. This may result in a sequence of physiological events, similar to that of shock observed in severe burns, hence the term "Lewisite shock". It is not clear which factor is directly responsible for increased capillary permeability, although there are several possibilities. Etiologic agents may include Lewisite or Lewisite oxide, a capillary dilating material released from skin or tissue. Alternatively, enhanced capillary permeability may result from an interference with the metabolism of capillary endothelial cells (Goldman & Dacre, 1989).
    1) If the concentration of Lewisite is high enough, all capillaries of the body are sensitive to damage. Lung capillaries appear to be more readily damaged because of absorption via the respiratory tract and first passage through the lungs following skin contact. Following exposure to large amounts of Lewisite, protein and plasma leakage from systemic capillaries into the periphery may occur, with subsequent hemoconcentration and hypotension. Small amounts of Lewisite on the skin may result in local edema due to effects on local capillaries. Pulmonary capillaries may be affected with large exposures to vapor, resulting in edema at the site and acute lung injury or acute respiratory distress syndrome (Sidell et al, 2000; Sidell et al, 1998).
    B) Hemolysis is a primary toxic effect of arsine gas. Lewisite, a substituted arsine, does NOT appear to directly cause hemolysis of the red blood cells (HSDB , 2000). There is little data concerning Lewisite exposures directly resulting in hemolysis. Hemolysis of erythrocytes has occurred in nonfatal cases, with resultant hemolytic anemia ((Anon, 1999)). Reduction in plasma volume due to increased capillary permeability has resulted in a secondary anemic condition, a hemolytic anemia with no degenerative changes in the bone marrow. No corrective response occurs with iron injections and the reticulocyte response of bone marrow gives rise to new red blood cells which are normal in appearance (Goldman & Dacre, 1989).
    C) The vesicant toxicity of Lewisite, causing immediate pain and irritation, is due to its ability to combine with thiol groups which are essential for activity of a number of enzymes. It is speculated that binding to dihydrolipoic acid, a component of the pyruvate dehydrogenase complex, results in many of the effects of Lewisite. This reaction prevents the formation of acetyl coenzyme A from pyruvate (Karalliedde et al, 2000).
    D) Ocular injuries following Lewisite exposure are due in part to the liberation of hydrochloric acid resulting in: localized superficial opacity of the cornea and deep penetration of Lewisite into the cornea and aqueous humor causing rapid necrosis (Goldfrank et al, 1998).

Physicochemical

Physical Characteristics

    A) Lewisite, is an oily, liquefied gas with a characteristic odor of geraniums. Freshly distilled or pure lewisite is a colorless liquid, but impurities and age cause the color to range from amber to black or from violet to brown, or an olive-green. At lower temperatures Lewisite remains a liquid and is persistent in colder climates. Lewisite hydrolyzes rapidly, thus maintaining a biologically active concentration on a humid day is difficult (AAR, 2000; ((HSDB, 2001); Lewis, 2000; Sidell et al, 2000).
    B) Synthesized Lewisite is composed of cis- and trans- isomers at a 10:90 ratio (Munro et al, 1999).
    C) Lewisite has several impurities: bis(2-chlorovinyl) chloroarsine, tris- (2-chlorovinyl)arsine and arsenic trichloride (Munro et al, 1999).
    D) The vinyl double bond and dichloroarsine group stabilizers are normally added to prevent decomposition (Munro et al, 1999).

Molecular Weight

    A) 207.32

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