Review Acute Chemical Emergencies

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Review Acute Chemical Emergencies
Stefanos N. Kales, M.D., M.P.H., and David C.
Christiani, M.D., M.P.H.

• Reporter ??? ??

From N Engl J Med Feb. 2004350800-8 Other
reference Up to date Chemical terrorism
Diagnosis and treatment of exposure to chemical
weapons
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Introduction

• Situation of Chemical Emergency
• Industrial disaster
• Occupational exposure
• Recreational mishap
• Natural catastrophe
• Chemical warfare
• Acts of terrorism

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Introduction

• The Classes of Substance
• Asphyxiants
• Cholinesterase Inhibitors
• Respiratory Tract Irritants
• Vesicants
• Difference from Biologic Agents

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General Principles Casualties

• Outdoors
• Move Upwind of contamination source
• Indoors
• Close the window and door
• Shut down the heating or cooling system
• Decontamination
• Remove Clothing decreased 85-90
• Shower

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General Principles A Mass Exposure

• The Majority of the affected persons ? Exposed
  minimally
• Affected by stress gt Affected physically
• ( From 51 to 161)
• Provide Psychological support

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General Principles Emergency Personnel

• Portable Radiation Detectors
• Appropriate Protective Equipment
• Early Decontamination before Transport
• Clinical Signs of severe chemical injury
• Altered mental status
• Respiratory insufficiency
• Cardiovascular instability
• A period of unconscious or Convulsions

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General Principles Emergency Personnel

• Initially Supportive Therapy
• Airway patency, Ventilation, Circulation
• Check any Trauma of injury
• Give Naloxone to AMS and Respiratory depression
  patient

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General Principles Emergency Personnel

• Early consultation the regional poison center
• The stock drugs of Chemical Emergency
• Diazepam
• Cyanide antidotes Kits
• Atropine and Pralidoxime

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Asphyxiants

• Substances that cause tissue hypoxia
• Symptoms
• Prominent Neurological and Cardiovascular sign
• Mild headache, fatigue, dizziness, and nausea
• Severe dyspnea, altered mental status, cardiac
  ischemia, and syncope to coma and seizure
• Respiratory failure CNS depression

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Asphyxiants

• Classification
• Simple asphyxiants (methane and nitrogen)
  physically displace oxygen in inspired air
• Chemical asphyxiants (carbon monoxide, cyanide,
  and hydrogen sulfide)
• Interfere with oxygen transport and cellular
  respiration
• ? Cause tissue hypoxia
• ? PaO2 decreased
• ? Anaerobic Metabolism
• ? Lactic acidosis

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Asphyxiants CO (Carbon monoxide)

• The most frequent cause of asphyxiant poisoning
• Incidence increased in Winter
• A diagnosis of CO poisoning
• Elevated carboxyhemoglobin level
• Low carboxyhemoglobin ???

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Asphyxiants CO (Carbon monoxide)

• 100 Oxygen
• HBO indication
• HbCO gt40
• Pregnancy or Child HbCO gt20
• Coma
• Had neurological sign
• Ischemia Heart ( EKG, chest pain)
• Delayed Neuropathy

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Asphyxiants Cyanide

• Rapid onset of symptoms ( Sudden collapse)
• Mild irritation to the eyes, nose and airways
• Skin flush
• Persistent Hypotension and acidemia despite
  adequate arterial oxygenation

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Asphyxiants Cyanide

• Nitrite
• Methemoglobin
• Cyanide Cyanomethemoglobin
• Free cytochrome oxidass
• Reserved for severe patient
• Monitor BP
• Thiosulfate
• ? Thiocyanate
• Accelerate the detoxification

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Asphyxiants Cyanide

• Dicobalt edetate (Europe, Australia)
• A Chelating agent
• Had potentially fatal adverse effect cardiac
  arrhythmia
• Hydroxocobalamin (Europe)
• Cyanide gt Cyanocobalamin ( Vit B12 )
• Need IV access

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Asphyxiants Hydrogen Sulfate

• Rapidly "knock down" both initially exposed
  persons and their would-be rescuers
• Highly irritating acute lung injury
• Monitored for ophthalmic toxicity ("gas eye")
• Palpebral edema, Bulbar conjunctivitis,
  Mucopurulent secretions
• Reduction in V.A
• Usually bilateral and seen in chronic
  intoxication
• Sodium Nitrite
• 100 Oxygen Hyperbaric oxygen

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Cholinesterase Inhibitors

• Included
• Organic phosphorus pesticides
• Carbamate pesticides
• Nerve Agent sarin, soman, tabun, and VX
• Inhibit acetylcholinesterase ? cholinergic
  overstimulation

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Cholinesterase Inhibitors

• Muscarinic symptoms
• Profuse exocrine secretions tearing, rhinorrhea,
  salivation, bronchorrhea, and sweating
• Ophthalmic symptoms miosis, dim vision,
  headache, eye pain
• May cause abdominal cramping, nausea, emesis,
  diarrhea, and fecal and urinary incontinence
• Nicotinic symptoms
• Muscular system muscles weakness,
  fasciculations, paralysis.
• Cardiovascular effects initially tachycardia and
  hypertension
• Central nervous system irritability, mild
  cognitive impairment, convulsions, coma

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Cholinesterase Inhibitors

• Multiple Mechanisms gt Respiratory failure
• Confirmed Diagnosis
• Cholinesterase activity test
• Absorption Routine
• Inhalation, through the skin, ingestion

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Cholinesterase Inhibitors

• Keep adequate airway and ventilation
• Antidotes
• Atropine
• Muscarinic sites
• Pralidoxime
• Nicotinic and Muscarinic sites
• CNS
• Diazepem
• Anticonvulsant Drug
• All patient with severe intoxication should use
• (Seizure, Loss of conscious, gt 2 organs
  involvement)

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Cholinesterase Inhibitors

• Organic phosphorus insecticides
• Oily, less volatile liquid
• Slower onset
• Effects lasting longer
• Large dose of Atropine
• Organophosphorus nerve agents
• Watery and Volatile
• Acting Rapidly and severely
• Effects lasting shorter
• Small dose of Atropine

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Cholinesterase Inhibitors

• Aging
• organophosphorusacetylcholinesterase binding
  becomes irreversibly covalent and resistant to
  reactivation by pralidoxime
• Soman Aging in minutes
• Sarin Aging in 3-5 hours

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Cholinesterase Inhibitors

• VX
• Minimal aging
• Oil, persistent in enviroment
• One drop can be lethal
• Organophosphorus insecticides
• Aging in slow rate, no clinical relevant
• gtPralidoxime should never be withheld

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Cholinesterase Inhibitors

• Carbamate insecticides
• More limited penetration of the central nervous
  system
• Inhibit acetylcholinesterase reversibly
• Result in a shorter, milder course
• Not need Pralidoxime

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Respiratory tract irritants

• Most frequently released in industrial accidents
• Determination of Clinical effects
• Direct tissue reactivity
• Reflex stimulation
• Water solubility
• Dose
• Highly soluble irritants
• absorbed in the upper respiratory tract, early
  warnings of toxicity
• Less soluble irritants
• more deeply and may cause acute lung injury with
  a delayed onset

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Respiratory tract irritants

• Tear gas ("lacrimators)
• Aerosolized solids
• Cause intense, immediate, and self-limited
  burning on exposed body surfaces, especially the
  eyes.
• Ammonia, hydrochloric acid, sulfuric acid,
  chloramines
• The chloramines Inappropriate mixing of ammonia
  and household bleach (hypochlorite)
• Highly soluble irritants to the upper respiratory
  tract

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Respiratory tract irritants

• Chlorine
• Intermediate solubility
• Small doses irritates the upper respiratory
  tract
• Larger doses bronchospasm and to acute lung
  injury
• Nitrogen dioxide
• Poorly soluble gas
• Silo-filler's disease
• gt Intense or prolonged exposure or the presence
  of underlying lung disease may result in
  bronchospasm or acute lung injury

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Respiratory tract irritants

• Phosgene
• The prototypical low-solubility irritant to
  mucosa
• Neither the irritation nor the odor provides an
  adequate warning of its presence
• As late as 15 to 48 hours after the exposure,
  acute lung injury may be manifested
• Dyspnea or CXR pulmonary edema within 4 hours
  after exposure indicated a worse prognosis and
  requires treatment in ICU.
• Asymptomatic or lungs appear clear on CXR
  obtained 8 hours after exposure, acute lung
  injury is unlikely to develop

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Respiratory tract irritants

• An assessment of the severity of the effects
• Particular substance or substances involved
• The duration of the exposure
• Exposed to the substance within a confined space
• Loss of consciousness

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Respiratory tract irritants

• Initially Management
• Administration of high-flow oxygen
• Decontamination
• May require endotracheal intubation
• Bronchodilators for bronchospasm
• Corticosteroids for severe airway reactivity
• Nebulized bicarbonate for chlorine derivatives???

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Respiratory tract irritants

• Acute lung injury
• Bed rest
• Corticosteroids
• For possible prophylaxis and as therapy
• The effects of exposure to phosgene is
  controversial
• Treatment of moderate-to-severe exposure to
  nitrogen dioxide.
• Positive end-expiratory pressure may be help in
  the presence of pulmonary edema.
• Diuretics should be avoided May aggravate
  intravascular hypovolemia.
• The prophylactic use of antibiotic drugs is not
  recommended

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Vesicants Skin caustics

• A blistering agents that extremely irritating to
  the eyes, skin, and airways
• Classification
• Simple acids or bases
• Blistering agent Mustard, Lewisite
• Mustard is the most important agent in this
  class.
• Had Caused the greatest number of casualties of
  all chemical warfare agents.

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Vesicants Skin caustics Mustard

• A radiomimetic alkylating agent that affects DNA
  chains and is an inflammatory activator
• A liquid at room temperature, but it becomes a
  vapor hazard as temperature rises.
• The typical period of latency of 4 -12 hours
• Within minutes, absorbed mustard becomes fixed in
  the dermis or penetrates the circulation.
• Decontamination is most effective when performed
  immediately after exposure.

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Vesicants Skin caustics Mustard

• Ophthalmic effects
• conjunctivitis, corneal damage, temporary or
  permanent loss of vision
• Dermatologic lesions
• Erythema, vesicles, bullae with a predilection
  for forming in intertriginous areas
• Airway involvement
• Within 24 hours after the exposure
• Epistaxis, Pharyngitis, Laryngitis, Dyspnea,
  Sputum production, hemorrhagic edema,
  pseudomembrane formation, mucosal sloughing with
  possible airway obstruction
• Pulmonary complications are the most common cause
  of death

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Vesicants Skin caustics Mustard

• High doses affect rapidly dividing cells
• Nausea and Vomiting
• Hematopoietic suppression ? leukopenia, within
  days to weeks
• High mortality
• Effects on the patient's airway within 6 hours
• Burns over more than 25 of the total body
  surface
• Absolute white-cell count lt 200 /cumm

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Vesicants Skin caustics Mustard

• Immediate decontamination and eye irrigation
• Pulmonary care
• Ophthalmic treatment
• Burn care
• Overhydration should be avoided have less fluid
  loss than patients with thermal burns
• Nonsteroidal antiinflammatory drugs may be
  beneficial
• Thiosulfate decrease systemic toxicity and
  mortality in animals
• Nonabsorbable antibiotics may prevent enteric
  sepsis.
• G-CSF for the treatment of severe neutropenia.

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Vesicants Skin caustics Mustard

• Medical Decontamination RSDL
• ( Reactive Skin Decontamination Lotion)
• July 31, 2003 had FDA approved
• Neutralizes the toxicity of nerve and blister
  agents by break down these molecules
• For VX, Mustard, Lewisite
• Acts within 3 minutes
• Had used in 1991 Gulf War
• May suitable for biologic agent
• Testing entire body, include eye, nose, mouth ??

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Vesicants Skin caustics Simple Acid and Bases

• Not vesicants
• No systemic toxicity
• The primary treatment is decontamination
• Hydrogen fluoride
• A component of some household rust removers and
  is used in certain industries
• A high affinity for calcium and magnesium
• ? Prevent life-threatening hypocalcemia and
  hypomagnesemia
• Dilute exposures result in delayed symptoms of
  severe pain and extensive burns and exposure

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Community Preparedness

• Successful outcome
• The Early extrication of casualties
• Immediate provision of basic life support
• Decontamination
• Follow-up with excellent supportive care
• Emergency planning should be applicable to both
  accidental and deliberate chemical releases.

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