Title: Environment and Disaster

Q: Altitude at which altitude disorders begin?
A: 8000 ft or 2440m
(lower if comorbid illness)

Q: Altitude above which acclimitisation is impossible?
A: 5500m

Q: How does ventilatory acclimitisation occur?
A: 1. Carotid body senses reduced arterial oxygenation and signals respiratory centre to increase ventilation
2. Initial hyperventilation tampered by respiratory alkalosis
3. Renal excretion of bicarb normalises pH and allows ongoing hyperventilation

Q: How long does ventilatory acclimitisation take in high altitude?
A: 4-7 days

Q: How does acetazolamide aid acclimitisation to altitude?
A: Stimulates renal bicarb loss to combat respiratory alkalosis, normalise pH and allow ongoing hyperventilation

Q: Symptoms of acute mountain sickness
A: Headache, GI disturbance, dizziness, fatigue, sleep disturbance

Q: What indicates high altitude cerebral oedema?
A: Increasing severity of symptoms, vomiting with oliguria, lassitude and ataxia/ALOC

Q: DDx of acute mountain sickness
A: Hypothermia
CO poisoning
Pneumonia
CNS infection
Dehydration
Migraine
Exhaustion

Q: Treatment of mild acute mountain sickness?
A: Acetazolamide 250mg PO BD
Analgesics/antiemetics
Drop 300-1000m if refractory

Q: Treatment of moderate AMS
A: Low-flow O2 (1-2L NP overnight)
Acetazolamide 250mg PO BD
Dexamethasone 4mg PO q6h
Descend 300-1000m if refractory

Q: Treatment of high-altitude cerebral oedema?
A: Immediate descent or hyperbaric therapy
Titrate O2 to SpO2 90%
Dexamethasone 8mg PO/IV then 4mg q6h

Q: Treatment of high-altitude pulmonary oedema
A: Immediate descent
Target SpO2 90%
Nifedipine SR 30mg BD
Dexamethasone 4mg q6h if cerebral signs arise

Q: Is dexamethasone effective for high-altitude pulmonary oedema?
A: No

Q: How effective is acetazolamide in preventing high-altitude illness?
A: 75%

Q: What is the most lethal high altitude illness?
A: HAPE

Q: Hallmark of HAPE
A: Dyspnoea on exertion with dry cough progressing to dyspnoea at rest

Q: How does botulism present?
A: Foodborne: Gi symptoms then symmetric CN palsies and descending paralysis
Inhalational: Same but no GI symptoms

Q: Initial response to possible bioterrorism event
A: Pre-planned all hazards operation plan
Infection-control procedures including decontamination
Screening on arrival
Information to all staff
Supply management
Coordination of pre-hospital/hospital communication channels
Coordination of media messages
Public health notification

Q: When is decontamination warranted in suspected bioterrorism?
A: If recently exposed NOT if symptoms have arisen
Undress and soap/water adequate

Q: What size particles deposit in bronchi?
A: 2.5-6micrometres

Q: What size particles reach alveoli?
A: <2.5 micrometres

Q: Where do highly water soluble gases/vapors deposit?
A: React with water in mucous membranes to cause irritation to eyes and upper airways

Q: Management of organophosphate poisoning?
A: Remove any leather from patient + wash with warm water
Atropine 500mcg q1min up to 20mg titrated to clearing of respiratory secretions
Pralidoxime 2g IV slowly over 20min
Midaz for seizures
Do NOT use sux for intubation (Sux apnoea) as acetylcholinesterase inhibitor

Q: What is trench foot?
A: Direct soft tissue injury from prolonged cooling in wet conditions

Q: How does trench foot/immersion foot present?
A: Anaesthetic extremity
Pale, mottled, pulseless and immobile
No immediate change with rewarming
Hyperaemic phase hours after rewarming with reappearance of proximal sensation
Perfusion improves over 2-3 days

Q: What is pernio?
A: Chillblains

Q: How do chillblains present?
A: Mild inflammatory condition of extremities due to long-term intermittent exposure to damp, non-freezing conditions

Q: Management of chillblains?
A: Rewarm slowly in tepid water
Gently bandage
Elevate
Nifedipine/topical corticosteroids

Q: First-degree frostbite
A: Erythema, numbness, central pallor, no blisters

Q: Second-degree frostbite
A: Full-thickness skin freezing
Oedema, erythema, clear blisters
Desquamates to black eschars
Good prognosis

Q: Third-degree frostbite
A: Supdermal plexus involved
Haemorrhagic blisters
Skin necrosis
blue-grey discolouration of skin
Poor prognosis

Q: Fourth-degree frostbite
A: Subcut tissue, muscle, bone and tendon
Non-blanching cyanosis and deep black eschar
Very poor prognosis

Q: Treatment of frostbite
A: Dry and warm patient
Do not attempt rewarming until risk of refreezing removed
Analgesia, immobilise, elevated
Place extremity in gently circulating water at 37 degrees for 20-30 minutes
Anticipate severe pain with rewarming
ADT
Separate affected digits and wrap with dry gauze
Aloe vera to all blisters
Prophylactic Pen G 500 000 IV q6h

Q: All-hazards approach to disaster management
A: Risk assessment
On-scene and overall disaster command
Relief operations
Risk communication and media management
Reconstruction
Community recovery

Q: 4 triage categories in disaster
A: Immediate care - Critical with simple life-saving procedures e.g. jaw thrust
Delayed care - Significant injury but likely to survive hours to definitive care
Minimal care - Ambulatory
Expectant - Critical but requiring advanced resuscitation

Q: ED preparation for disaster
A: Clear non-critical patients
Discharge stable ward patients
Notify hospital executive
Amass equipment
Clear surgical theatres and ICU
Recall staff

Q: What is sieve and sort?
A: Sieve - Initial triage to identify order of transport to treatment area from scene
Sort - More detailed triage to determine order of transport to hospital

Q: Surge capacity components
A: 4S's
 - Staff
 - Stuff
 - Space
 - Structure (physical and management)

Q: What is Boyle's law?
A: P1V1=P2V2

Q: What is Dalton's law?
A: Total pressure exerted by mixture of gases = sum of partial pressures
Relevance - With increasing ambient pressure, partial pressure of nitrogen rises (0.79 x ambient pressure)

Q: What is Henry's law?
A: Quantity of gas in solution is proportional to partial pressure of gas
Relevance - Uptake of nitrogen into tissues at higher pressure

Q: Types of barotrauma on descent
A: Ear squeeze
External ear squeeze
Sinus barotrauma
Inner ear barotrauma
Face squeeze
Tooth squeeze

Q: How does external ear squeeze occur?
A: Occlusion of auditory canal with wax causes TM to bend outwards on descent

Q: How does inner ear barotrauma occur?
A: Forced Valsalva ruptures oval or round window

Q: How does inner ear barotrauma present?
A: Roaring tinnitus, sensorineural hearing loss and profound vertigo

Q: DDx of barotrauma of ascent
A: Alternobaric vertigo
Pulmonary barotrauma

Q: Does decompression illness occur with dives <10m depth?
A: Uncommon

Q: Classification of decompression illness?
A: Type I - Pain only (bends)
Type II - Pain + Vestibular (staggers), cardiopulmonary (chokes) and CNS
Type III - Above + CAGE

Q: Neurological symptoms in decompression illness
A: Truncal constriction
Woolly feeling in feet
Ascending paralysis

Q: Does arterial gas embolism occur from depths <10m?
A: Yes

Q: Clinical features of arterial gas embolism?
A: Cardiovascular collapse
Stroke symptoms
LOC
Seizure
Blindness
Parietal signs/symptoms often overlooked

Q: When does nitrogen narcosis occur?
A: At depths >30m

Q: Definition of drowning
A: Primary respiratory impairment due to immersion/submersion with liquid-air interface at airway.
Can live or die as a result

Q: Prognostication of drowning victims
A: CV stability and normal neurology - Do well
CV instability and coma - Do very poorly
In between difficult to prognosticate

Q: Do cerebral oedema control efforts and ICP management improve outcomes in drowning?
A: No

Q: Poor prognostic factors in drowning?
A: Submersion >10 min
Resus time >15 min
Time to effective CPR >10 min
GCS <5
pH <7.1 on arrival

Q: What is submersion vs. immersion?
A: Submersion is airway under water
Immersion is water splashed into airway e.g. waterboarding

Q: What is the most common heat-related illness?
A: Exercise-associated collapse

Q: Drugs associated with heat-related injury
A: Diuretics, anticholinergics, salicylates, stimulants, hallucinogenics

Q: DDx of heat stroke
A: Infection: Sepsis, meningoencephalitis, malaria
Endocrine: Thyroid storm, phaeo, DKA
Neuroleptic malignant syndrome
Serotonin syndrome
Hypothalamic stroke
Status epilepticus
Salicylate overdose
Stimulant overdose
Anticholinergic overdose
Malignant hyperthermia
Alcohol/benzo withdrawal

Q: When does exercise-associated collapse most commonly occur?
A: At end of race when venous return suddenly falls

Q: Management of prickly heat
A: Loose fitting clothing
Antihistamines for itch
Topical steroids
Chlorhex wash for sweat gland inflammation
1% salicylic acid TDS to desquamate skin if severe

Q: Heat exhaustion presentation
A: Headache, nausea, vomiting, malaise, cramps, tachycardia, orthostatic hypotension, near-syncope WITHOUT CNS impairment

Q: What is heatstroke?
A: Classic triad: Hyperthermia >41.5, CNS dysfunction, hot/dry skin

Q: Management of heatstroke
A: Ix - BSL, VBG, ECG, FBC, UEC, Coags
Aggressive cooling 0.1 degree/min
Target 38-39 (afterdrop >2)
Remove clothing, fine mist of tepid water with fanning
Ice packs
Ice-cold IV fluids
Treat seizures
Consider intubation/sedation/paralysis if not winning
Paracetamol/ibuprofen/dantrolene all CI

Q: Presentation of serotonin syndrome
A: CNS: Delirium, agitation, reduced LOC, seizures
Motor: Tremor, clonus, hyperreflexia
Autonomic: Hyperthermia, tachycardia, sweating, diarrhoea, HTN

Q: Treatment of serotonin syndrome
A: Mild - Benzos
Severe - I&V, paralysis
Cyproheptadine PO 8mg q8h
Chlorpromazine IV 50mg

Q: Causes of neuroleptic malignant syndrome
A: Any antipsychotic - Usually increased or new
Withdrawal of dopaminergic agents
Metoclopramide

Q: Four classic signs of NMS
A: Fever, rigidity, altered mental status, autonomic instability

Q: Treatment of NMS
A: Bromocriptine 10mg PO TDS

Q: Causes of malignant hyperthermia
A: Sux, volatile anaesthetics, ketamine

Q: Treatment of malignant hyperthermia
A: Change IV lines and cease any causative agent
Supportive therapy
Dantrolene 2.5mg/kg IV q15min up to 30mg/kg

Q: Mortality of heatstroke
A: 10%

Q: Causes of secondary hypothermia
A: Impaired shivering of any cause
Drugs - Alcohol, sedatives, vasodilators, narcotics
Metabolic - Ketoacidosis, hypoadrenalism, hypoglycaemia, hypopituitarism, hypothyroidism
CNS - Stroke, Spinal cord injury
Sepsis
Shock
Trauma

Q: Temp below which pupils fixed and dilated
A: <29

Q: Temp at which corneal reflexes disappear
A: <23

Q: Temp below which patient has risk of malignant arrhythmias
A: <32

Q: ECG changes in hypothermia
A: Bradycardia
Everything wider
 - Prolonged PR
 - QRS widening
 - QT prolongation
Osborn Waves <32
AF/A flutter
Asystole is common final arrhythmia

Q: What does an Osborne wave look like?
A: Hump at J point

Q: Where are Osborne waves best seen?
A: Inferolaterally

Q: DDx of Osborne waves?
A: BER
STEMI
Hypercalcaemia
Brugada
TBI
SAH
Vasospastic angina

Q: Severity of hypothermia (Swiss model)
A: Mild - 32-35 - Conscious, shivering
Moderate - 28-32 - Impaired consciousness +- shivering
Severe - <28 - Unconscious, vital signs present
HT IV - Arrest

Q: Which patients with hypothermia need ongoing core temperature monitoring?
A: HT II to IV (anything more than mild = <32)

Q: Can hypothermia cause arrest >32 degrees?
A: No. Look for other causes

Q: Clues to secondary hypothermia
A: Arrest >32 degrees
Areflexia/paralysis
Temp lower than expected by history
Failure of rewarming techniques
Tachycardia or tachypnoea (should have opposite if temp <32)

Q: Is empirical therapy for myxoedema/adrenal crisis warranted in hypothermia?
A: Not in absence of lab evidence

Q: Is empirical therapy for sepsis/intoxication warranted in hypothermia?
A: Yes

Q: When can death be declared in the hypothermic patient?
A: Obvious traumatic death e.g. decapitation
Valid ARP
Avalanche burial >35 min and airway packed with snow
Cardiac arrest prior to cooling
K >12

Q: Ix for hypothermic patient
A: BSL
ECG
VBG
FBC, UEC, LFT, Coags, BC, Lipase, TFT, random cortisol, ethanol/paracetamol/osmolar gap levels, CK

Q: Why might coagulopathy be missed in the hypothermic patient?
A: Labs warm samples so effect on coagulation is not evident in results

Q: Treatment of mild hypothermia
A: Warm environment, replace wet clothes, warm drinks, active movement

Q: Treatment of moderate hypothermia
A: Careful handling to avoid arrhythmia
Prevention of further heat loss - Replace wet clothes
Passive external rewarming - Warm environment
Active external warming - Bear hugger, blankets
Active minimally invasive warming - Warm IV fluids 40 degrees
Cardiac monitoring
Continuous core temperature monitoring

Q: When should head insulation be used in hypothermia?
A: In moderate-severe hypothermia (unless in cardiac arrest)

Q: Why are vasopressors contraindicated in early resus of hypothermia?
A: Hypothermia induces maximal vasoconstriction already and vasopressors increase arrhythmia risk

Q: Management of severe hypothermia (HT-III)?
A: Intubate
Passive external
Active external
Active minimally invasive - IV fluid 40 degrees, warm humidified ventilator gasses
Active invasive - 40 degree saline bladder lavage
ECMO/CPB (or ICC lavage if not available)

Q: Which hypothermic patients should be transferred to ECMO/CPB centre?
A: Stage III and IV (<28 degrees)
Hypotension out of proportion to temperature or ventricular arrhythmias

Q: Changes to ALS in hypothermia?
A: If <30 degrees
 - Standard ALS for 3 cycles, then defer further defib or adrenaline until temp at 30
30-35 degrees double dose interval of adrenaline
>35 degrees - Usual care

Q: NNT for CPB or ECMO in hypothermia?
A: 2 for survival

Q: What do centipedes cause?
A: Severe swelling and pain at bite site of short duration
Systemic envenoming does NOT occur

Q: Presentation of tick paralysis
A: Hours to days after attachment
Ataxic gait then progressive ascending paralysis with predominant CN involvement

Q: How is tick paralysis different from GBS?
A: Prominent CN involvement

Q: Management of symptomatic tick paralysis?
A: Remove tick ASAP
All need admission for 2 days as can worsen after removal

Q: Effects of blue-ringed octopus bite?
A: Rapid onset flaccid paralysis

Q: Effect of cone fish?
A: Rapid onset flaccid paralysis

Q: Which marine envenomations warrant PBI?
A: Sea snakes, blue ringed octopus and cone shell

Q: Which marine envenomations warrant hot water immersion?
A: Stinging fish, stingray, bluebottles, non-tropical jellyfish

Q: Do blue bottles benefit from hot water immersion or vinegar?
A: Hot water immersion

Q: Which marine envenomations benefit from vinegar?
A: Box jelly and Irukandji (tropical jellyfish)

Q: Does vinegar relieve pain of tropical jellyfish?
A: No. Prevents unfired nematocysts from injecting venom and allows removal of tentacles

Q: When to consider envenomation in differential?
A: Unexplained
 - Collapse
 - Paralysis
 - Respiratory failure
 - Coagulopathy
 - Myolysis
 - Renal damage
 - Convulsions
 - Ataxia

Q: Effects of sea snakes?
A: Rapid flaccid paralysis, myolysis

Q: Do sea snakes cause coagulopathy?
A: no

Q: Does polyvalent snake antivenom work for sea snakes?
A: Unsure. Tiger snake probably does

Q: Effects of box jellyfish envenomation
A: Sudden cardiorespiratory arrest
Severe pain

Q: Management of box jellyfish sting
A: Vinegar
Ice packs
MgSO4 10mmol over 15 min (5 min if unstable)
Analgesia
Antivenom
 - 1-6 vials as per instability
Burns therapy for sting

Q: Average delay of symptoms following Irukandji?
A: 20-40 min

Q: Management of Irukandji
A: ALS
Vinegar
Opioid
Midazolam
MgSo4
 - 0.15mmol/kg IV bolus then 0.15mmol/kg/hr infusion
 - Titrate up monitoring reflexes
 - Wean at 4-6 hours
GTN infusion up to 50mcg/min
ECG monitoring

Q: Indications for stonefish antivenom
A: Confirmed stonefish sting with intractable pain, systemic symptoms and/or oedema

Q: What is ionising radiation?
A: High energy, short wavelength particles that can remove electron from an atom and generate a charged particle

Q: What shields gamma and X-rays?
A: Concrete and lead

Q: Local radiation injury presentation
A: Week 1 - Erythema, hyperaesthesia, itch
Week 2 - Erythema with hair loss
Week 3 - Skin tenderness, swelling and itch
Week 4 - Desquamation and/or wet ulceration (higher Gy)
If >50Gy presents with immediate thermal burn

Q: Four phases of acute radiation syndrome
A: Prodrome
Latent phase
Manifest illness phase
Recovery

Q: Prodromal symptoms in acute radiation syndrome
A: Autonomic dose-dependent response with nausea, vomiting, anorexia, diarrhoea, hypotension, pyrexia, sweating and fatigue
 - High dose: Acute severe
 - Low dose: Delayed mild

Q: How long is the latent phase of acute radiation syndrome?
A: Hours to weeks depending on dose

Q: What are the three dose-dependent manifest illness syndromes in acute radiation syndrome?
A: GI, Haematopoietic and Cardio/CNS

Q: How long is the latent phase in haematopoietic acute radiation syndrome?
A: 1-3 weeks

Q: How does haematopoietic acure radiation syndrome present?
A: Peripheral lymphopaenia 1-3 weeks after prodromal symptoms

Q: Above what dose does haematopoietic syndrome occur in acute radiation syndrome?
A: >1.5Gy

Q: Above what dose does GI acute radiation syndrome occur?
A: >6Gy

Q: How does GI acute radiation syndrome present?
A: Acute GI prodromal symptoms, then 1 week of latency then recurrent GI symptoms

Q: Above what dose does CNS/CVS acute radiation syndrome occur?
A: >20Gy

Q: How does CNS/CVS acute radiation syndrome present?
A: Immediate hypotension and severe GI symptoms
CNS dysfunction within hours
Lymphocyte count falls to zero within hours

Q: Management of external contamination with radiation
A: cut and roll clothing away from face
Wash wounds with water
Do not scrub
Repeat washing until <2x background radiation on Geiger
Cover wounds with waterproof dressings

Q: How is radiation biologic dosimetry performed?
A: Rate and nadir of lymphopaenia + clinical symptoms/signs to ascertain dose range

Q: Initial bloods in snake bite
A: FBC, UEC, Coags, D-dimer, CK, LDH

Q: Serial bloods in snake bite
A: FBC, UEC, Coags, CK

Q: Examination in suspected snake bite
A: Ptosis, ophthalmoplegia, weakness
Peak flow
Dark urine
Bleeding gums
Prolonged bleeding from bite site/venepuncture

Q: When can PIB be removed after snake bite?
A: In resus, no clinical or lab evidence of envenomation, antivenom available

Q: Snakes in Australia that cause VICC?
A: Brown, Tiger, Taipan

Q: Snakes in Australia that cause anticoagulant coagulopathy?
A: Red-bellied black and black snakes

Q: Which Australian snakes cause a severe neurotoxicity?
A: Tiger, Taipan, Death adder, sea snake

Q: Do brown snakes cause neurotoxicity?
A: Mild and rarely

Q: Do black snakes cause neurotoxicity?
A: Rarely. Red-bellied do not

Q: Which snakes in Australia cause a myotoxicity?
A: Tiger snakes, black snakes (red-bellied is rare), taipans and sea snakes

Q: Do brown snakes cause myotoxicity?
A: No

Q: Which snake in Australia causes initial collapse?
A: Brown snake

Q: Which snakes in Australia causes MAHA?
A: Brown and Tiger
Brown tigers meow

Q: What do brown snakes cause?
A: VICC, collapse, MAHA, mild and rare neurotoxicity

Q: What do Tiger snakes cause?
A: VICC, neurotoxicity, myotoxicity, systemic symptoms and MAHA = EVERYTHING

Q: What do black snakes cause?
A: Anticoagulant coagulopathy, myopathy and systemic symptoms

Q: What do taipans cause?
A: VICC, neurotoxicity, myotoxicity, systemic symptoms = EVERYTHING (same as tiger but no MAHA)

Q: What do death adders cause?
A: Neurotox only

Q: What do sea snakes cause?
A: Neurotox + Myotox

Q: Do black snakes often cause systemic envenomation?
A: No

Q: How does VICC differ from anticoagulant coagulopathy?
A: Anticoagulant has raised APTT, minor INR elevation and normal D-dimer/fibrinogen vs.
INR +++, fibrinogen undetectable and D-dimer ++

Q: How is MAHA identified?
A: Microangiopathic haemolytic anaemia with schistocytes, thrombocytopaenia, rising creatinine, raised LDH and reduced haptoglobin

Q: Absolute indications for snake antivenom?
A: Any evidence of neurotoxicity
INR >1.3
Prolonged bleeding clinically
History of collapse/convulsions/arrest
Evidence of AKI

Q: Relative indications for snake antivenom?
A: Severe systemic symptoms
INR 1-1.3
CK >1000

Q: How should snake antivenom be given?
A: Dilute 1 in 10 N/saline (up to 10mL/kg for children)

Q: Can you re-start antivenom infusion if anaphylaxis occurs?
A: Yes. Must treat and then cautiously re-start at lower rate

Q: What is the rate of serious adverse reactions with snake antivenom?
A: 1%

Q: What proportion of patients suffer serum sickness after antivenom?
A: 30%

Q: How does serum sickness present?
A: Flu-like syndrome with arthralgia and rash 4-14 days after antivenom

Q: How is serum sickness treated?
A: prednisolone 50mg daily for 5 days
Consult with immunologist

Q: Management after snake antivenom delivery
A: Bloods at 6,12, 24 hours then daily until normalised

Q: How long does VICC take to respond to antivenom?
A: Up to 6 hours

Q: Management of VICC if active bleeding e.g. ICH?
A: Antivenom +- further dosing +- FFP with expert advice

Q: Is there a role for repeated antivenom dosing for myolysis?
A: Only if CK has second peak after initial fall

Q: Is there a role for repeated antivenom for neurotoxicity in snake bite?
A: No. Presynaptic toxins are not reversible and so symptoms can continue despite antivenom

Q: When can asymptomatic snake bite victim be discharged?
A: PIB removed, daylight hours, no signs of envenomation at any stage and normal labs at initial, 1 hour post-PIB removal, 6 and 12 hrs

Q: Discharge criteria post-antivenom for snake bite?
A: Clinical features resolved, normalising labs and at least 12 hours post-antivenom.
If VICC, need normalising coagulation profile.
Always daylight hours and education re: serum sickness

Q: Are funnel web spider bites painful?
A: Yes

Q: Presentation of funnel web envenomation?
A: Painful bite, perioral tingling, headache, abdo pain, neuroexcitatory

Q: Are red back spider bites painful?
A: Usually felt but may be painless

Q: Presentation of red back spider bite?
A: Local sweating, erythema, piloerection then significant local pain with gradual spread of pain to everywhere with gravitation to lower limbs irrespective of bite site

Q: What spider bites are PBI used for?
A: Funnel web

Q: When can funnel web spider bite patients be discharged?
A: Asymptomatic at least 4 hours post-bite and 2 hours post-PBI removal

Q: Do spider bites need assessment in hospital?
A: Only big black ones (possible funnel web) and red backs

Q: Indications for funnel web antivenom?
A: Any systemic symptoms

Q: Dose of funnel web antivenom?
A: 2 vials (4 if severe)

Q: When are repeat doses of funnel web antivenom warranted?
A: If ongoing or progressive symptoms, q15min 2 vials

Q: Indications for red back antivenom?
A: Severe pain syndrome if analgesia ineffective

Q: Dose of red back spider antivenom
A: 2 vials repeated at 2 hours if ongoing or progressive

Q: How much fluid must be aspirated to cause blood volume alterations?
A: >11mL/kg

Q: How much fluid must be aspirated to cause electrolyte disturbance?
A: >22mL/kg

Q: Normal non-fatal drowning victim aspiration?
A: 4mL/kg

Q: Disposition of drowning victims
A: GCS >12 and SpO2 >95%
 - Observe 4-6 hours and d/c if well
GCS <13
 - Admit all with ongoing support

Q: What do you do if drowning victim presents in arrest and normothermic?
A: Resuscitate but serious consideration to rapid cessation as recovery without profound impairment is very rare

Q: Temperature management for drowning victim
A: Actively rewarm if <34
Consider induced hypothermia 32-34 for 24 -72 hours (more important to prevent hyperthermia)

Q: What proportion of survivors of drowning with submersion time >15 minutes are neurologically intact?
A: 0%

Q: Survival after submersion >60 min
A: 0%

Q: Poor prognostic factors for drowning
A: Submersion >5 minutes (Most critical)
Resus time >25 minutes
Time to effective CPR >10min
GCS <5
pH <7.1
Persistent apnoea/CPR in ED
Asystole
Dilated non-reactive pupils and GCS <5 or pH <7.0

Q: What did RAVE-II trial show?
A: No benefit to IV redback antivenom vs. simple analgesia for lactrodectism

Q: Who performs initial sieve and sort triage?
A: First ambulance officer on scene

Q: 4S's of surge capacity
A: Staff
Stuff
Space
Structure (physical and management)

Q: Disaster response algorithm
A: CS-CATTT
 - Chain of command
 - Safety
 - Communication
 - Assessment
 - Triage
 - Treatment
 - Transport

Q: Mortality of heat stroke
A: 10-50%

Q: Therapeutic goal in heat stroke
A: Temp <42 degrees within 15 minutes of arrival
Aggressive cooling 0.1 degree per minute to 38 then monitor after drop of 2 degrees

Q: Treatment for heat stroke
A: Target <42 within 15 minutes
Target 38 then watch afterdrop
Remove all clothing
Tepid water spray fanning
Ice packs to axillae/groin
Ice bath if able
N/Saline 4 degrees resus fluid
Additional:
Diazepam 5-10mg IV
Chlorpromazine 25-50mg IV (second-line)
Maintain urine 2mL/kg/hr
NDMR paralysis and intubation
Invasive lavage and ECMO/CPB only for extreme cases refractory to above

Q: What proportion of drownings occur in children <5?
A: 50%

Q: What proportion of teenage drowning involve alcohol?
A: 25-50%

Q: How many more boys than girls drown?
A: 5x

Q: Phases of drowning
A: Voluntary breath holding
Laryngospasm
Respiratory efforts with laryngospasm
Hypoxia results in easing of laryngospasm and aspiration
Surfactant washout
Tissue hypoxia
MODS
Death

Q: What are the best predictors of poor neurological outcome in drowning?
A: Non-reactive pupils and GCS <5 on arrival to ICU

Q: What proportion of drowning survivors have good neurological outcome?
A: 75%

Q: What is the Orlowski scale?
A: Paediatric drowning prognostication
Age <3yo
Submersion >5 min
Delay to CPR >10min
GCS3 - Coma on arrival to ED
pH <7.1 on arrival to ED
<3 = 90% good outcome
>3 = 5% recovery

Q: What proportion of children that present comatose to ED after drowning will do well?
A: 45%

Q: Do children do better than adults in drowning?
A: No

Q: Describe the Conn and Modell classification?
A: Post-drowning prognostication and management guide
Cat A - Awake - GCS >13
Cat B - Conscious but obtunded - GCS 9-13
Cat C - Comatose - GCS <8
 - C1 - Decorticate
 - C2 - Decerebrate
 - C3 - Flaccid
 - C4 - Arrested

Q: When should Conn and Modell be performed post-drowning?
A: 2 hours post-immersion

Q: When should resuscitation be terminated in drowning?
A: K >11
>1 hour of CPR with asystole and apnoea if normothermic

Q: Describe the triage sieve?
A: Walking - Delayed
Dead - Not breathing despite airway opening
Immediate - RR <10/>30 or cap refill >2 seconds
Urgent - RR 10-30, cap refill <2 seconds

Q: Describe the triage sort?
A: Revised trauma score parameters (GCS, SBP, RR) to organise order of priority of transport to hospital

Q: Pathophysiology of HACE
A: Cerebral oedema secondary to prolonged hypoxia leading to capillary leakage and loss of autoregulation

Q: Pathophysiology of HAPE
A: Uneven pulmonary vasoconstriction secondary to alveolar hypoxia leads to increased flow to less constricted areas and subsequent capillary leak

Q: Benefits of sieve triage over sort?
A: Minimal training, rapid, simple and no equipment required

Q: Classic definition of heat stroke
A: CNS dysfunction, >40 and anhydrosis