Blister chemical agents

Background

  • Highly persistent
  • Skin primary route of exposure when in liquid form; pulmonary and GI tracts as routes in vapor form

Types

Pathophysiology

  • Alkylation of DNA, RNA, and protein causing cell death
  • Depletes glutathione causing cellular membrane breakdown

Clinical Features

  • Skin – Initially pruritus and stinging pain, superficial bullae appear over 24 hours. Blisters do not contain toxin
  • GI – abdominal pain, nausea, vomiting, diarrhea, and weight loss
  • Respiratory –
    • Usually only upper respiratory tract affected
    • Sinus congestion, sore throat, hoarseness. Rarely pulmonary edema
    • Epithelial sloughing and pseudomembranes causing inability to clear pathogens and dead tissue.
  • Mucous membranes and actively reproducing cells most vulnerable to severe damage
  • Ocular damage – occurs within 4-8 hours
    • conjunctivitis, chemosis, blepharospasm, and corneal perforation at even low level exposures
  • Bone Marrow – Leukopenia first (3-5 days), followed by anemia and thrombocytopenia
Bullae formation after blister chemical agent exposure (Wikimedia Commons).

Differential Diagnosis

Chemical weapons

Evaluation

Management

  • Immediate decontamination, 0.5% hypochlorite solution will inactivate sulfur mustard but not appropriate for pediatric patients
  • Supportive care, ABCs
  • Thermal burn-type care
  • Fluid losses less than with thermal burns
  • No antidotes for mustard agents
  • N-acetylcysteine, glutathione
  • G-CSF for patients with bone marrow suppression
  • British antilewisite (BAL) – chelating agent to reduce systemic effects from lewisite exposure.
    • Won’t alter the blistering effects on skin or airway.
    • Only used for patients with shock or severe pulmonary injury given BAL side effect
    • Relative contraindications to BAL: Renal disease, pregnancy

Disposition

See Also