Note on lewisite – properties , mechanism of action and clinical effects and clinical diagnosis

Lewisite: Overview

Lewisite is a blister agent (vesicant) developed as a chemical weapon. It is a highly toxic organoarsenic compound that has seen limited use due to the severe damage it causes upon exposure.

Properties of Lewisite:

  • Chemical Name: 2-chlorovinyldichloroarsine
  • Appearance: Colorless to brown liquid
  • Odor: Geranium-like odor
  • Volatility: Volatile at room temperature, producing highly toxic vapors.
  • Solubility: Slightly soluble in water but highly soluble in organic solvents such as alcohol.
  • Persistence: Less persistent than mustard gas, but under cool and humid conditions, it can remain active for hours or days.

Mechanism of Action:

Lewisite primarily affects tissues through direct contact or inhalation. It is rapidly absorbed by the skin, mucous membranes, and respiratory tract. The arsenic component of Lewisite plays a key role in its toxicity.

  • Enzyme inhibition: Lewisite binds to sulfhydryl groups in enzymes, inactivating them and disrupting cellular metabolism.
  • Cellular damage: By inhibiting critical enzymes like pyruvate dehydrogenase, Lewisite disrupts cellular respiration, leading to metabolic failure. This results in tissue damage and necrosis.
  • Vascular damage: Lewisite causes capillary leakage and damage, contributing to blistering and inflammation in the affected tissues.

Clinical Effects:

The clinical effects of Lewisite vary based on the route of exposure (inhalation, skin contact, or ocular exposure) and the dose. The effects are rapid compared to other chemical warfare agents like mustard gas.

  1. Skin exposure:
  • Immediate pain: A burning sensation and pain occur within seconds of exposure.
  • Blistering: Redness (erythema) develops, followed by the formation of fluid-filled blisters within 12–24 hours.
  • Necrosis: In severe cases, the skin may undergo necrosis, resulting in deep tissue damage.
  1. Inhalation:
  • Respiratory distress: Inhalation of vapors causes irritation of the nose, throat, and lungs, leading to coughing, wheezing, and shortness of breath.
  • Pulmonary edema: In severe cases, lewisite exposure can lead to life-threatening pulmonary edema (fluid accumulation in the lungs), resulting in hypoxia.
  1. Ocular exposure:
  • Eye irritation: Intense burning and tearing are experienced within minutes of exposure.
  • Corneal damage: Prolonged exposure can cause corneal damage, leading to temporary or permanent blindness.
  1. Systemic toxicity:
  • Arsenic poisoning: Systemic absorption of lewisite leads to symptoms of arsenic poisoning, including gastrointestinal distress (nausea, vomiting), cardiovascular collapse, and multi-organ failure.

Clinical Diagnosis:

Diagnosing lewisite exposure is based on a combination of clinical signs, symptoms, and history of potential exposure to chemical warfare agents. Key diagnostic considerations include:

  • Rapid onset of symptoms: The characteristic early-onset pain and burning sensation distinguish lewisite from mustard gas, which causes delayed pain.
  • Blistering patterns: The development of blisters, especially if they occur rapidly after exposure, is indicative of vesicant exposure.
  • Laboratory confirmation: Detection of lewisite or its metabolites in biological samples (e.g., blood or urine) can confirm exposure. Special testing for arsenic or lewisite-specific metabolites may be used in suspected cases.
  • Differential diagnosis: Other causes of skin blistering, such as burns or other vesicant agents, should be considered to rule out alternative causes.

Early identification of lewisite exposure and prompt medical intervention is crucial to minimize tissue damage and systemic toxicity. Treatment generally focuses on decontamination, supportive care, and specific antidotes such as British anti-lewisite (BAL), which chelates arsenic to neutralize its effects.

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