Chemical Disasters

Introduction

• Planning must take into account the chemical emergency near the centre of any release and chaos in surrounding areas through fear of exposure
• Must plan for large self-extricating population that self-present to ED

• Solids: 
  • Bulk, powders, dust or fumes
  • Dust particles
    • Visible if >100micrometres and invisible if smaller
    • 2.5-6micrometres deposit in bronchial mucosa
    • <2.5micrometre reach alveoli
  • Fumes <1micrometre
• Liquids
  • Liquids forced through small orifice under pressure can aerosolise
• Gas
  • Endothermic reaction can occur with release of gas from compressed cylinders causing hypothermic skin injury

• How deeply in the lungs a gas or vapor exerts its effects depends on degree of water solubility
  • High water solubility reacts with water in mucous membranes to cause irritation to eyes and upper airways e.g. ammonia, hydrogen chloride
    • Awake and ambulatory patients can leave the area as good warning properties
  • Low water soluble agents are less irritating, allowing greater duration of exposure and greater pulmonary penetration e.g. phosgene smells good, penetrates deep into alveoli and is there converted to hydrochloric acid
• Liquids above their boiling point are in gas form and vapor pressure = atmospheric pressure
  • The higher the vapor pressure for a gas, the more likely it is to volatilise into a gas
  • Can calculate concentration of a chemical as a vapor knowing its vapor pressure and atmospheric pressure to predict risk of toxicity

Chemical disasters

• EPA Acute Exposure Guideline Level (AEGL)
  • AEGL-1: Discomfort only
  • AEGL-2: Irreversible long-lasting effects
  • AEGL-3: Serious disease or death
• Exposure at AEGL-1 limits require public health and emergency responses to educate the public about minor effects expected and minimise ED visits
• Levels between AEGL-2 and 3 should require accurate and specific information to the public with sheltering in place, sealing of homes and self-decontamination
  • Highly susceptible (i.e. elderly, chronic lung disease or very young) may need priority evacuation
• AEGL-3 requires evacuation, field decontamination and triage

Scene HAZMAT planning guidelines

• Community risk assessment
  • Government level records of stored chemicals and usual amounts/release should be kept
  • Most commonly stored chemicals are anhydrous ammonia, chlorine, flammable mixtures, propane and sulfur dioxide
• Recognition of an event
  • Most industrial areas will have monitors for those agents without early warning properties
• Identification of substance involved
  • More important to recognise clinical syndrome manifesting in victims than specific substance
  • HAZMAT teams have multiple means of identifying substances
• Isolation and scene control
  • Incident command; hot, warm and cold areas; isolation process
  • Only those in fully encapsulating protective gear can enter hot zone to rescue victims
  • Warm zone for decontamination of victims + basic medical interventions e.g. open airway
  • Transfer to cold zone for more definitive triage and medical care with less cumbersome protective gear and less risk of secondary contamination

• Decontamination
  • Primary contamination of people and environment caused by direct contact with release
  • Secondary contamination by inadvertent contamination of rescue personnel or surrounding environment
    • Avoided by PPE and adequate decontamination of adherent solids and liquids on victims
  • Organophosphates can adhere to leather and be excreted in sweat (need to discard leather on primary responders and victims)
  • Remove clothing, brush off solids and wash and towel the face
  • Water is the universal decontaminant
    • 5 minutes of decontamination with warm water in warm zone is usually adequate
    • If direct contact with liquid or vapor, need to be hosed off, with focus on areas where fluids can pool/hide e.g. hair, skin folds, axilla, groin, toes and eyes

• Stabilisation and triage to cold zone
  • Cold zone should be upwind and uphill from hot zone
  • Evaluate for syndromic symptoms and need for antidotes
  • Airway, oxygen and bronchodilators are key
  • IV line placement priority in those with seizures, cardiac arrhythmias or hypovolaemia
  • Primary antidotes of benefit are hydroxocobalamin or atropine

• Must have hospital-wide plan for contaminated patient arrival
• Should be able to decontaminate multiple patients outside ED with warm water and proper PPE
• ED decontaminators should wear chemical-resistant gloves, coveralls and boots with air-purifying masks with filters designed for chemical threats

High-risk chemicals

• Toxic inhalants
  • Simple asphyxiants
    • Displace oxygen e.g. CO2, hydrogen, nitrogen, helium, beon, argon, krypton, xenon, radon, methane, butane and propane
    • At FiO2 <16% air hunger, tachypnoea and ALOC occur
    • At FiO2 <10%, LOC, seizures and vomiting can occur
    • Treatment is restoration of higher FiO2 and correction of underlying cause
  • Interfere with pulmonary diffusion
    • Highly soluble e.g. ammonia, chloramine (bleach and ammonia mixed together), sulfur dioxide and hydrogen chloride
    • Intermediate solubility e.g. chlorine gas and hydrogen sulfide
      • Chlorine reacts with water in upper airways to form hydrochloric and hydrochlorous acids
    • Less soluble irritants e.g. phosgene
      • Delayed onset severe acute lung injury from alveolar hydrochloric acid production
  • Interrupt oxygen transport e.g. CO and methaemoglobin-forming agents
    • Nitrites, benzocaine cause Fe2+ to Fe3+ conversion to form methaemoglobin
    • Headache, nausea, fatigue +- angina if fixed coronary occlusion
    • Treat with high FiO2 + methylene blue for methaemoglobin (electron donor and converts Fe3+ back to Fe2+
  • Interrupt oxygen utilisation at cellular level e.g. cyanide, hydrogen sulfide, phosphine and sodium azide
    • Bind to cytochrome oxidase a3, creatining intracellular acidosis
    • Hydroxocabalamin + sodium thiosulphate therapy for cyanide toxicity

• Organophosphates
  • Organophosphate agents bind to acetylcholinesterase in a two-stage process
    • First stage is reversible if pralidoxime is given
    • Second stage (ageing) is irreversible
  • Acetylcholinesterase breaks down Ach and its inhibition results in excessive cholinergic stimulation
    • Muscarinic: DUMBELS
      • Defecation, urination, miosis, bradycardia/bronchospasm, bronchorrhoea, emesis, lacrimation and salivation
    • Nicotinic:
      • Muscular fasciculation to profound muscular weakness and paralysis in dose-dependent fashion
    • Can get early paradoxical hypertension and tachycardia that is soon replaced by bradycardia from muscarinic stimulation
    • CNS seizures and coma
  • Treatment
    • Atropine – Reverses only muscarinic effects
      • Titrate to clearing of excess secretions (up to 20mg) (pupil size and HR are poor indicators of effective therapy)
    • Pralidoxime – Reverses nicotinic effects
      • 1-2g IV slowly over 20-30 minutes (if multiple victims can halve this to maximise number treated)
    • Benzodiazepines – Treat seizures (phenytoin not effective)
    • Avoid succinylcholine if intubating as will cause sux apnoea
    • If eye signs only, can give topical homatropine and monitor for 6-8 hours before discharge
    • Admit any patient requiring pralidoxime to ICU for repeat doses or infusion

• Incapacitating agents
  • Agents to immobilise victims can include ultra-potent opioids e.g. carfentanil, LSD, benzos, vomiting agents and mace
• Vesicants
  • Sulfur mustard gas, phosgene oxime
  • Damage eyes, skin, mucous membranes and potentially lungs if exposed to high enough concentrations
  • Sulfur mustard causes delayed blistering from 2-18 hours after exposure
  • Therapy is focused on copious irrigation with water and then serial eye exams, pulmonary monitoring and careful skin care
  • Can cause delayed marrow suppression and increased risk of infection 3-5 days after exposure

• Biotoxins
  • Clues to exposure
    • Disease or syndrome that rarely occurs naturally
    • Multiple victims of disease with no classic risk factors
    • Epidemiological statistical clues
    • Possible human and animal morbidity in same area
    • High mortality rate in otherwise healthy population
  • Many have very low LD50 (e.g. botulinum toxin, tetanus toxin, staph enterotoxin B, diphtheria toxin, ciguatoxin, ricin, tetrodotoxin)
  • Botulinum toxin
    • Early subtle cranial nerve palsies, difficulty swallowing and trouble speaking
    • Treatment with antitoxin will prevent progression but will not reverse paralysis so give as early as possible
    • Supportive care including ventilation may be required for up to 90 days
  • Ricin
    • Castor bean toxin and must be injected or inhaled as aerosol
    • Causes destruction of RNA and cell death
    • If inhaled, results in pulmonary symptoms after 8 hours with necrotising pneumonitis
    • After parenteral administration, get local pain then 15-24 hours later get vomiting, fever, localised lymphadenopathy
    • At 24 hours get sepsis-like syndrome
    • Needs aggressive supportive care

Last Updated on November 23, 2021 by Andrew Crofton