CBRN Flashcards
What is a HAZMAT spill?
Accidental release of hazardous material e.g. At a chemical plant or nuclear power station
Give an example of secondary contamination
Airborne chemical weapon that infiltrates into food and water sources to cause secondary contamination of population
If a chemical weapon is incorporated into an explosive devise, how would the number of case fatalities be affected?
Number of people affected by the chemical weapon would probably decrease as the chemical disintegrates with the high temperature however number of fatalities still very high from the explosion related trauma
Considering the factors that affect the casualty rates of CBRN attacks (deployment, climate & population) describe an attack that would result in the maximum number of casualties .
Aerosolised weapon that’s released by line deployment (e.g. Via a plane) perpendicular to a gentle upward breeze, targeting a major unprepared population
What three processes are central to the management of CBRN incidents ?
Triage, decontamination and protection of hospital staff
What is the purpose of triage ?
Determination of the best use of available resources by estimating the survivability of patients injuries
How is secondary triage different to primary triage?
Secondary triage occurs at hospital whereas primary triage occurs at the site of a disaster
Define the four categories of triage
Expectant- death inevitable
Immediate- life saving treatment required urgently
Delayed- life saving treatment can be delayed without causing interim harm
Minor- the walking wounded
What is decontamination?
Removal or neutralisation of CBW to limit human exposure
Ideally, how should victims of CBW be decontaminated ?
Ideally the victims would remove all their clothes and jewellery themselves and then wash with water and soap (or other chemical agent e.g. Hypochlorite solution). This should be done before arriving in hospital and any staff at the scene should wear Level C personal protective equipment.
In reality, to preserve patients dignity it is acceptable to allow patients to remain dressed if privacy can’t be assured
How can we reduce the likelihood of hospitals becoming contaminated after a CBW incident ?
Decontaminate patients before arriving at hospital
CBW patients should be isolated
Ensure all hospital staff wear protective clothing e.g. air humidifiers and chemical resistant clothing
Vaccinations
Post exposure prophylaxis
Follow universal procedures as before e.g. Correct disposal of chemical waste
Be rigorous with basic hygiene technique
What is the difference between a chemical and a biological weapon?
Chemical weapons do not rely replication in the human body to have their effect
List 5 categories of chemical weapon
Toxins, blood agents, choking agents, blistering agents and nerve agents
What bacteria is the Botulinum toxin derived from?
Clostridium botulinum
What are the symptoms of botulinum exposure? How long does it take these symptoms to develop?
Botulinum toxin produces symptoms 1-4 days after exposure (more gradual than nerve agents). Victims get a progressive, symmetrical paralysis involving bulbar palsy (dysarthria,dysphonia,dysphagia), ocular palsy (ptosis, diplopia) and eventually can die from respiratory muscle paralysis.
What are two differential diagnoses of botulinum toxicity?
Myasthenia gravis and guillian barré syndrome
How does botulinum toxin result in flaccid paralysis?
Binds to presynaptic receptors at cholinergic synapses which prevents acetylcholine from being released. Neuromuscular junctions are a type if cholinergic synapse so botulinum toxin prevents muscle contraction
Why does botulinum toxin result in mydriasis?
Botulinum toxins cause pupil dilatation by preventing the release of acetylcholine. Reduced AcH uptake into the parasympathetic neurons at the level of the ciliary ganglion or the parasympathetic neuromuscular junctions in the sphincter pupillae of the iris can result in mydriasis.
NB- toxin can also affect sympathetic innervation as preganglionic sympathetic nerves are involved in cholinergic synapses
Where is ricin sourced from?
Waste products of castor oil
Guess the toxin: patient presents confused with a GCS 8. In hospital they are constantly in and out of sleep. Dies 2 days later from a cardiac arrest
Ricin - in high doses rapidly fatal in low does causes confusion, drowsiness, coma and weakness. Cause of death normally cardio/respiratory collapse within 36-72 hours
Guess the chemical weapon: man in mid 40s on holiday in south of France. At seafood buffet wife notices his speech is funny and he struggles to drink his G&T. Starts to get chest pain and becomes SOB so rushed to local A&E
Saxitotoxin
Concentrated in shellfish, inhibits sodium ion channels, rapidly fatal with bulbopalsy.
Death caused by cardio and respiratory arrest
Treatment is organ support
List four nerve agents
Sarin, soman, VX gas, tabun
How do nerve agents work?
Acetylcholinesterase inhibitors
Irreversibly binds to AChE , forming covalent bonds with the neurotransmitter via a process called ageing.
This prevents the breakdown of acetylcholine in cholinergic synapses e.g. Neuromuscular junctions
What are the signs and symptoms of nerve agent toxicity ?
Apart from sludge BBB, ere are other very important signs and symptoms. EYE PAIN can be observed from a distance and occurs because of ciliary body spasm. In addition increased acetylcholine in the CNS can lead to seizures and in the PNS MUSCLE FASCICULATIONS
SLUDGE BBB Salivation Lacrimation Urination Defeacation Gastric Emesis- Vomiting
Killer Bs
Bradycardia
Bronchospasm
Bronchorrea
What might someone’s face look like who has been exposed to a nerve agent ?
Eyes-miosis and red from painful ciliary body spasm. Lacrimation visible
Mouth- excessive saliva, vomit
Explain these post NA signs:
HR 170
BP 150/100
Tachycardia and hypertension due to sympathetic stimulation of the adrenal medulla
How quickly do NA tend to act?
Very quickly- victim can become incapacitated in 1-10 minutes and death normally occurs between 1-15 minutes.
Which NA takes longer to kill its victim?
VX gas- 4-24 hours
What do victims of NA tend to die from?
Bronchoconstriction, paralytic respiratory failure, bradycardia or seizures
If possible , what should be given immediately to a patient with suspected nerve agent toxicity ?
An OXIME
Nerve agent binds to one side (esteric side) of the AChE and will commence irreversible ageing process.
Oximes can be given before the ageing process is complete. Oximes bind to the other side of the AChE (anionic side) and this binding results in a change of AcHE conformational shape, releasing it from the nerve agent. The oxime then unbinds from the now functioning acetylcholinesterase
When is pralidoxime indicated? What dose and route should be used?
Suspected nerve agent toxicity. Pralidoxime should be administered asap by slow IV route. Give 30mg/kg slow IV which is approximately 2g
In addition to an oxime, what else can be given for nerve agent toxicity? What route and dose should be given ?
Atropine- 2mg at 5-10 minutes until pupils have dilated and ‘atropinisation’ has occurred
How does atropine work in nerve agent toxicity ?
Antagonises cholinergic side effects of the nerve agents, effectively drying up secretions
What should be suspected if a patients paralysis worsens following pralidoxime admin?
Re-inhibition of re-activated ACHE
Which nerve agent has the quickest ageing process?
Soman
A soldier takes ‘pyridostigmine bromide’ before entering a suspected nerve agent agent. Why? How does it work?
Pyridostigmine is an acetylcholinesterase inhibitor. It acts as a reversible competitive antagonist of acetylcholinesterase which creates a reservoir of temporarily inactivated AChE that the nerve agent is unable to bind to. Later dissociation of the pyridostigmine can then deactivate the enzyme which is able to hydrolyse acetylcholine in a cholinergic crisis (with the help of other drugs such as atropine and oximes)
Apart from atropine and oximes, what other drugs and interventions may be useful in a nerve agent agent?
Ventilators support to prevent respiratory failure
Magnesium- reduces pre synaptic ACH
Clonidine- reduces CNS cholinergic symptoms
Diazepam- anticonvulsant
How does hydrogen cyanide cause death?
Histotoxic hypoxia (inability of cells to take up oxygen from bloodstream despite normal delivery) occur as hydrogen cyanide binds to IRON on CYTOCHROME OXIDASE ENZYMES which interrupts cellular respiration.
Where is cyanosis poisoning common?
In house fires, hydrogen cyanide vapour is created through burning nitrites found in plastics
What does hydrogen cyanide typically smell and look like?
Almonds, colourless
What would you expect an ABG of a cyanide victim to look like?
Metabolic acidosis
Hyperlactataemia
Low arteriovenous oxygen difference
You’re treating a patient in a supposed gas attack. They are breathing rapidly and appear confused. They are not choking. Suddenly the patient collapses and starts shaking rapidly. What gas do you suspect?
Cyanide. Difficult to diagnose as symptoms not very specific .
Tend to present with confusion, tachypnea, dizziness which can result in coma, convulsions and cardiorespiratory arrest
What is the recommended antidote for cyanide poisoning?
Sodium thiosulphate (IV) Sodium Nitrate (IV) Hydroxycobalamin (IV)
How does hydroxycobalamin work as an antidote?
Binds to cyanide to form non toxic cyanocobalamin which is urinated out
Why is sodium nitrate given to cyanide victims?
Converts haemoglobin to methaemoglobin. The latter can then bind to cyanide which forms a non toxic product Cyanomethaemoglobin
What is dicobalt edetate?
Second line treatment of cyanide poisoning that is only given if cyanide poisoning if definite. It’s a chelating agent that combines with cyanide to form a non toxic product
A veteran tells you about his experience in the war. As he speaks to you, you notice he’s quite out of breath.
He says that he was once a victim of chemical weaponry. He thought he’d escaped it but 4 hours later he got horrendous symptoms. He remembers getting painful blisters underneath his armpits, severe eye pain and blurry vision. He couldn’t breathe at the time and started coughing lots. Initially the cough was dry and then he began producing red mucus
1) what chemical agent do you suspect caused these symptoms?
2) why is is currently out of breath?
3) what symptoms can result in death?
1) mustard gas
2) COPD/bronchiectasis- long term complication of exposure caused by distal airway collapse and tracheobronchitis
3) respiratory symptoms as mentioned above cause tracheobronchitis and distal airway collapse with potential pulmonary haemorrhage and failure
Bone marrow suppression can also cause death with leukopenia several days after exposure. This can lead to secondary infection and bleeding
What eye symptoms are seen in mustard gas poisoning?
Pain , blurred vision, lacrimation
Reduced visual acuity due to oedema of cornea and vesication.
How can nerve agents be differentiated from blistering agents?
Blistering agents tend to have a latency period
Name two choking agents
Chlorine and phosgene gas
What are the symptoms of chlorine gas poisoning?
Eye pain, lacrimation, blepharospasm (forced closure of eye lids)
Long term tissue damage
What is the characteristic smell of phosgene gas? What colour is it?
Colourless gas (chlorine yellow/green) that’s meant to smell like newly moved hay
Where is phosgene gas most concentrated?
Close to the ground because of its high density
What effect does phosgene gas have on the respiratory system?
Irritated distal airways causing alveolar necrosis and haemorrhage
Why do choking agents cause death?
Irritation of the eyes and nasopharyngeal mucosa can lead to larygospasm, pulmonary oedema, hypoxaemia and ischaemia. Not just respiratory system therefore affected can result in multi organ failure
How do you manage a patient who has been exposed to a choking agent?
IV/inhaled corticosteroids, B2 agonists, prophylactic antibiotics as at risk of secondary infection
What is anthrax?
Type of biological weapon. Bacteria ‘bacillus anthracis’
What are the characteristic skin changes seen with anthrax poisoning?
Small, painless, itchy papilla that form vesicles that can rupture to form ‘black Escher’ (anthrax=coal =appearance of ruptures)
When do symptoms of anthrax poisoning manifest?
1-4 days after exposure
What are the initial clinical features of anthrax poisoning?
Non specific - fever, malaise, fatigue , myalgia, non productive cough
What is the term that describes the symptoms of chest pain, SOB and strider seen when anthrax in inhaled ?
Necrotising haemorrhaging mediastinitis
What does oedema factor do? (One of three proteins in anthrax)
Converts ATP->cAMP which increases intracellular oedema
How can anthrax poisoning be confirmed?
ELISA testing (enzyme linked immunosorbent assay) which tests to see if anthrax toxins list in the blood. Detected 36 hours after exposure
What species does the plague come from?
Yersina Pestis
What is the typical incubation period for the plaque?
2-3 days
What form of plague is formed from inhalation?
Pneumonic plague
How is pneumonic plague treated?
IM streptomycin 30mg/kg given immediately + maintenance dose every 12 hours for 10 days
What type of biological weapon is ebola?
Viral haemorrhage fever
What causes the symptoms associated with viral haemorrhage fevers?
Endothelial damage by RNA viruses result in massive internal and/or external haemorrhage. Symptoms begin as non-specific symptoms of infection
What is the treatment for viral haemorrhage fevers?
Supportive treatment of patient who should be isolated. May require mechanical ventilation, prothrombin should be avoided unless signs and symptoms suggestive of DIC. Fluid resuscitation can aggravate pulmonary oedema.
Give three examples of viral encephaltitis’
VEE= venuzualan equine encephalitis EEE= Easter " " WEE= " "
What are the symptoms of viral encephalitis?
Fever, headache, vomiting (inc. ICP)
When do features of WEE and EEE develop in relation to exposure?
Prodrome of up to 11 days so symptoms progressive
How are viral encephalitis’ managed?
Supportive treatment, often ICU. Neurological impairment minimised by giving anticonvulsants, anti epileptics and ventilation
Are vaccines available for viral encephalitis’ ?
yes
Patient who presented post bacterial weapon complaining of fever, malaise, anorexia, non-productive cough. What would you suspect?
Tularaemia (may also think about plague)
What is the treatment for tularaemia? Is there a vaccine available?
Streptomycin/gentamycin . vaccine is available
Rash all over body that went from being maculopapula->pustular->scabs. Diagnosis? What other symptoms would you expect?
Small pox
Fever, malaise, rigors,headache
What type of virus is small pox? How is it diagnosed?
Variola virus. PCR
How is small pox treated?
Cidofovir
What are the three forms of Glanders seen?
Septicaemia form
Pulmonary form
Oropharyngeal form
How long does it take for the septicaemia form of glanders to develop post exposure?
10-14 days
What are the features of pulmonary glanders? What might be seen on CXR?
Bilateral pneumonia, pulmonary nodular necrosis and miliary shadowing on CXR.
How does oropharyngeal glanders present?
Blood streaked, mucopurulent substance from mouth, nose and eyes
How is glanders treated?
Organ support with the antibiotics co-amoxiclav and sulfadiazine. No vaccine available
What organism is glanders?
Burkholderia mallei
How can anthrax poisoning be confirmed?
ELISA testing (enzyme linked immunosorbent assay) which tests to see if anthrax toxins list in the blood. Detected 36 hours after exposure
What species does the plague come from?
Yersina Pestis
What is the typical incubation period for the plaque?
2-3 days
What form of plague is formed from inhalation?
Pneumonic plague
How is pneumonic plague treated?
IM streptomycin 30mg/kg given immediately + maintenance dose every 12 hours for 10 days
What type of biological weapon is ebola?
Viral haemorrhage fever
What causes the symptoms associated with viral haemorrhage fevers?
Endothelial damage by RNA viruses result in massive internal and/or external haemorrhage. Symptoms begin as non-specific symptoms of infection
What is the treatment for viral haemorrhage fevers?
Supportive treatment of patient who should be isolated. May require mechanical ventilation, prothrombin should be avoided unless signs and symptoms suggestive of DIC. Fluid resuscitation can aggravate pulmonary oedema.
Give three examples of viral encephaltitis’
VEE= venuzualan equine encephalitis EEE= Easter " " WEE= " "
What are the symptoms of viral encephalitis?
Fever, headache, vomiting (inc. ICP)
When do features of WEE and EEE develop in relation to exposure?
Prodrome of up to 11 days so symptoms progressive
How are viral encephalitis’ managed?
Supportive treatment, often ICU. Neurological impairment minimised by giving anticonvulsants, anti epileptics and ventilation
Are vaccines available for viral encephalitis’ ?
yes
Patient who presented post bacterial weapon complaining of fever, malaise, anorexia, non-productive cough. What would you suspect?
Tularaemia (may also think about plague)
What is the treatment for tularaemia? Is there a vaccine available?
Streptomycin/gentamycin . vaccine is available
Rash all over body that went from being maculopapula->pustular->scabs. Diagnosis? What other symptoms would you expect?
Small pox
Fever, malaise, rigors,headache
What type of virus is small pox? How is it diagnosed?
Variola virus. PCR
How is small pox treated?
Cidofovir
What are the three forms of Glanders seen?
Septicaemia form
Pulmonary form
Oropharyngeal form
How long does it take for the septicaemia form of glanders to develop post exposure?
10-14 days
What are the features of pulmonary glanders? What might be seen on CXR?
Bilateral pneumonia, pulmonary nodular necrosis and miliary shadowing on CXR.
How does oropharyngeal glanders present?
Blood streaked, mucopurulent substance from mouth, nose and eyes
How is glanders treated?
Organ support with the antibiotics co-amoxiclav and sulfadiazine. No vaccine available
What organism is glanders?
Burkholderia mallei
What is found in a nerve agent combopen?
Atropine, pralidoxime and diazepam
Why are poppers stored in cyanide gas masks?
Poppers convert haemoglobin into methaemoglobin which has an affinity for cyanide
