a story of an unfortunate man n.
Skip this Video
Loading SlideShow in 5 Seconds..
A Story of an Unfortunate Man PowerPoint Presentation
Download Presentation
A Story of an Unfortunate Man

Loading in 2 Seconds...

play fullscreen
1 / 70

A Story of an Unfortunate Man - PowerPoint PPT Presentation

  • Uploaded on

A Story of an Unfortunate Man. …which coincidentally teaches some environmental nuggets. Are you sitting comfortably?. There once was a man called Jack. Jack was an avid reader. One day he was basking in the midday sun, reading his Roald Dahl book, when he realised he felt a bit hot….

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'A Story of an Unfortunate Man' - dyanne

An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
a story of an unfortunate man

A Story of an Unfortunate Man

…which coincidentally teaches some environmental nuggets

are you sitting comfortably
Are you sitting comfortably?

There once was a man called Jack. Jack was an avid reader. One day he was basking in the midday sun, reading his Roald Dahl book, when he realised he felt a bit hot…

jack had hyperthermia
Jack Had Hyperthermia.
  • Luckily a passing nurse found him and took him immediately to Auckland ED.
stage 1
Stage 1
  • Heat exhaustion
      • Volume and electrolyte loss as sweat, with inadequate replacement
      • Still have heat regulatory mechanisms and CNS not affected
stage 2
Stage 2
  • Heat stroke
    • Life threatening
      • Mortality <10% if treated, approaches 80% if not
    • T >40 degrees
      • >42 degrees  uncoupling of oxidative phosphorylation  cellular damage, failure of hypothalamic thermostat, inflammatory and coagulopathic stuff
    • Altered LOC (delirium, seizures, coma)
    • MOF
    • Not necessarily dehydrated

Classical heat stroke

    • Due to high environmental T
    • Young and elderly
    • Hot and dry
  • Exertional heat stroke
    • Due to physical activity
    • Athletes and military
      • To acclimatise must exercise 60-90mins/day; still takes up to 2/52 and max at 3/12
    • Hot and sweaty
    • Dehydration more common

80% hyperdynamic (ie. Incr CO),

  • 20% hypodynamic (ie. Distributive / high output shock)
  • Ataxia occurs early
  • Seizures, esp during cooling
  • lactic acidosis, respalkalosis, rhabdo, DIC, electrolyte disturbance
  • Organ failure
  • Prolonged QTc, ST changes
it s not only the sun
It’s not only the sun…
  • Jack could have:
    • Hypethyroidism, sepsis, DT’s, epilepsy, dermatological problem, spinal injury…
    • Anticholinergic / serotonin syndrome, malignant hyperthermia, neuroleptic malignant syndrome
what should auckland ed do1
What should Auckland ED do?
  • A+B: avoid sux
  • C: IVF resus only if dehydrated
    • If rhabdo: aim UO 50-100ml/hr
      • can use mannitol / frusemide to increase UO
      • consider urinary alkalinisation
    • Beware high output cardiac failure  puloedema
    • If need pressors avoid E+NE
      • Can cause vasoconstriction and hence prevent heat dissipation
    • Treat coagulopathy
  • D: can use sedatives / paralyse to decrease shivering
jack was made cool
Jack was made cool…
  • Evaporative
  • Ice water immersion
  • Ice packs
  • Cooling blankets
  • Cooled IV fluids
  • Gastric lavage etc…
jack recovered well
Jack recovered well…
  • Except for some residual ataxia (20% have a permanent residual neurological deficit)
  • The over-enthusiastic doctor was rather rigorous with the cooling…
  • He was found by a FED who came to offer him a sandwich.
the ssu nurse did a routine ecg
The SSU nurse did a routine ECG…

No prognostic significance

Osborn wave

Long QT

Wide QRS

AF with slow ventricular response in 50% with mod hypothermia

jack had hypothermia
Jack had Hypothermia.
  • Mild: <35 degrees
    • Shivering; ataxia, dyasthria, apathy
    • Incr HR / RR, resp alkalosis, peripheral vasoconstriction
  • Mod: <32 degrees
    • Failure of thermogenesis (no shivering, decr metabolism)
    • Initial cold-induced diuresis (don’t trust UO)
    • Decr LOC / HR / RR, resp acidosis, arrhythmia, stupor
  • Severe: <28 degrees
    • Loss of reflexes and voluntary motion, pupil dilatation, rigidity (initially the nurse thought Jack was dead…)
    • Puloedema, peripheral vasodilation, rhabdo, MOF, haemoconcentration and intravascular thrombosis
it s not only enthusiastic doctors
It’s not only enthusiastic doctors…
  • Drugs (eg. ETOH, sedatives), dermal disease, massive blood / fluid loss, elderly, neonates, hypothyroid / adrenal / glycaemia, neuropathies
  • …and cold weather / exposure

35 Mild hypothermia

  • Mod hypothermia: shivering stops

AF and other arrhythmias; 2/3 decr in HR and CO; Osborn waves common


Insulin resistance

31 Shivering stops (24-35, very variable)

30 O2 consumption and CO2 production decr by 50%

Incr myocardial irritability, ectopics; threshold for spontaneous bad arrhythmidefibrillation

and antiarrhythmics become ineffective

Double intervals between drug doses

29 Pupils dilated

VF may occur

28 HR 30-40


BMR decr by 55-65%; major acidosis

26 Areflexia

25 Risk of asystole; CO 45% normal

Cerebral blood flow 1/3 normal

24 Loss of vascular tone and cerebrovascular autoregulation

23 Absent corneal and oculocephalic reflex

22 Max risk of VF

20 HR 20

19 EEG flat, appears dead

18 Asystole

what did auckland ed do
What did Auckland ED do?
  • Filled out a risk pro
what should auckland ed do3
What should Auckland ED do?
  • Assess breathing and pulse for up to 1min to confirm
  • A+B: increased risk of gastric stasis
  • C:
    • T <30: most drugs / defib / pacing ineffective until…
    • T 30-35: give but double intervals between doses
    • Can try single shock + initial drugs for VF/VT, but then wait until >30 degrees
    • Warm IVF resus (42 degree 5% dextrose at 200ml/hr); will need large volumes
    • Only pace bradycardia if persists after warming
  • Most drug activity temperature dependent
  • Toxic doses required for effect
    • Leading to problems when rewarmed
  • Most arrhythmias revert with rewarming
  • VF treatment controversial
    • Bretylium
jack was made warm
Jack was made warm…
  • Rapidly rewarm to 30-34 degrees then slow
  • Passive rewarming
    • If mild; give the dude a blanket
  • Active external
    • If moderate / not shivering / CV compromise
    • Bair hugger, heat back etc…
  • Active internal
    • If severe
    • Humidified O2, blood warmer, lavages, haemodialysis, ECMO
rewarming research in general
Rewarming research in general
  • Paucity of RCTs esp in humans
  • Volunteer studies predominate, usually in shivering mild hypothermics
  • Methodological variations with same Rx
  • Questionable external validity
  • Limited clinical trials with small numbers
  • Many therapies ethically hard to study
scoring systems on hospital arrival
Scoring Systems on Hospital Arrival

The simple approach

Modell & Conn 1984 – in ED within 1 hr of rescue (paeds)




Obviously dead

luckily for jack
Luckily for Jack…
  • Rapid onset hypothermia and being young has better chance of survival

Here he is pictured with his discharge summary and the SMO On Call (Bernard?)

as jack was leaving auckland ed
As Jack was leaving Auckland ED…
  • He went to the toilet, washed his hands as his mother had taught him, and was electrocuted by the hand dryer (don’t ask me how).
  • He was found by a patient with a sore toe.
jack was frazzled
Jack was frazzled.
  • How frazzled depends on:
    • Voltage: high risk if >600V
      • Household voltage is 240V; lightening is >100 million V
    • Current type
      • Household is AC; lightening is DC
    • Current size
      • mAmps; >10mAmp  paralysis + tetany
    • Resistance
      • Bone > fat > tendon > skin > muscle > BV’s > nerve
    • Pathway
      • Vertical = bad for brain; 20% mortality
      • Horizonal = bad for heart + lungs; 60% mortality; 3x incr risk of VF
      • If ground current, more severe injury if legs apart
    • Duration
      • AC = longer (0.3-2secs) due to tetany
      • DC = shorter (millisecs) as thrown away
ac vs dc
AC vs DC
  • AC
    • Deep tissue damage
    • More likely to need fasciotomy / have rhabdo
      • 10% severe burns get ARF
      • Aim UO 1-2ml/kg/hr or use Parkland formula
    • Causes tetany prolonged apnoea (even after ROSC)
    • Causes VF (may cause asystole if high voltage)
  • DC
    • Superficial tissue damage (lightening can cause “flashover”)
      • Severe burns can be caused by high voltage arcs
    • BUT causes asystole
      • Cardiac arrest in 75% direct lightening strike injuries
      • Lightening strike mortality rate 10-30% (2/3 in 1st hour due to apnoea / arrhythmia); good prognosis unless significant 2Y injury
    • Blast injury (always look for TM rupture, hollow viscera)
    • Blunt trauma (high risk spinal #)
  • Look for entry and exit wounds
    • Do not signify depth
  • Skin
    • Cutaneous findings in 90%
    • Lichtenburg figures (extravasation of blood in subcutaneous tissue)
    • Look for clothing injury
  • Keraunoparalysis
    • Delayed onset transient paralysis + sensory disturbance + peripheral vasoconstriction
  • Always examine the eyes
    • Corneal burns, intraocular haemorrhage, retinal detachment, hyphema; late onset cataracts common
    • All require opthalmology review
    • Dilated pupils don’t mean they’re dead
  • Always examine the ears
    • 50% have TM rupture; sensorineural hearing loss
what did auckland ed do1
What did Auckland ED do?
  • Filled out a risk pro
yes and what else
Yes, and what else?
  • Jack seemed alright.
  • What did Auckland ED do with him?
to monitor or not to monitor
To monitor or not to monitor?
  • Do initial ECG
    • Monitoring is NOT indicated if asymptomatic and initial ECG normal
  • Indications for ECG monitoring (at least 12hrs)
    • High voltage injury (>1000V)
    • Abnormal ECG
    • LOC / seizures
    • Previous cardiac disease
    • Burns
to admit or not to admit
To admit or not to admit?
  • Discharge if:
    • 240V or less
    • Brief
    • No LOC / tetany / burns
    • Normal exam and asymptomatic
    • Normal ECG
  • Do urine (for myoglobin) and ECG if:
    • Minor wound / paraesthesia
  • Admit if:
    • >600V
    • Abnormal ECG or examination
    • Horizontal transmission
jack was ok
Jack was OK.
  • Jack had a normal ECG and examination. He felt great.

Jack was discharged home. Here he is, pictured with his discharge summary (Bernard had finished his shift).

jack wandered home
Jack wandered home.
  • He took a ferry to Waiheke, where he lived with some twits. Guess what happened next…
no he wasn t envenomated
No he wasn’t envenomated.

We’re not covering that cos we’re not bloody Australian.

jack almost drowned
Jack almost drowned.
  • He was found by a middle aged hippy.
  • He is choppered into Auckland ED. The noisy R40 tells us his GCS is 6 and the RTA is 10 minutes.
cardiovascular effects
Cardiovascular Effects
  • Hypotension
    • Shock, acidosis, hypovolemia (natriuresis), autonomic instability
  • Arrhythmias
    • Asystole (55%),
    • Ventricular tachycardia/fibrillation (29%)
    • Bradycardia (16%)
    • Brugada
    • Long-QT syndromes
  • It is the helicopter after all.
  • Pictured below is the resus team with Les Galler.
drowning resus
Drowning Resus
  • C: C spine immobilisation if
    • History of diving, use of water slide, MVA, signs of injury, ETOH
  • A+B: aggressive respiratory resus
    • Intubate if
      • Requiring FiO2 >40-60% to attain PO2 >70
      • Use PSV starting at 10cm, PEEP 5-7.5cm; wean ASAP to prevent barotrauma
  • C
    • N saline IVF resus (but beware puloedema)
    • Monitor electrolytes
    • Do 1hr CPR if persistent apnoea and asystole
  • D
    • Trt seizures; maintain normoG; rewarm if needed

Most text books will support a trial of NIV if blood pressure and GCS appropriate, however there are no literature to support its use

Start low and titrate up

volume support

Vt low – 6mls/kg

PEEP 5-10 cm H20 only if PaO2 < 60 on FiO2 <0.6

Ventilate for 24 hours to allow regeneration of surfactant

a note on rewarming
A note on rewarming…
  • Consider induced hypothermia
    • If comatose with spontaneous circulation
    • Do not actively warm to >32-34
    • Aim T 32-34 ASAP and maintain for 12-24hrs

Vandenet al. Part 12: cardiac arrest in special situations: drowning:2010 American Heart AssociationGuidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122:Suppl 3:S847-8

Guenether U et al.Extendedtheraeutic hypothermia for several days during extra-corporeal membrane-oxygenation after drowning and cardiac arrest: two cases of survival with no neurological sequelae. Resuscitation 2009;80:379-81

WARNER et al. Recommendations and consensus brain resuscitation in the drowning victim. Bierens JJLM, ed. Handbook on drowning: prevention, rescue and treatment. Berlin: Springer-Verlag, 2006:436-9

asymptomatic patient
Asymptomatic patient

No comorbidities

If at 4 - 6 hours:

CXR, ABG normal

Normal vitals on air

Remain ASx = discharge with advice

symptomatic patient
Symptomatic Patient

Consider foreign material in airway (approx. 50% of surf submersions)

Salbutamol / Ipratoprium nebs for bronchospasm

NG placement on free drainage may improve ventilatory distress

High risk for vomiting and gastric content aspiration

Suction +++

Most will require fluid resuscitation secondary to diuresis

Beware hypothermia and trauma

does it matter that it was salt water
Does it matter that it was salt water?
  • Nah, not really
  • Electrolyte abnormalities are theoretical
  • Abx if features of infection develop
    • Broad spectrum if grossly contaminated water
    • Anti-pseudomonal if in spa
    • Chemical pneumonitis if swimming pool
    • Sand pneumonitis if salt water
    • Fram neg, anaerobes, staph, fungi, algae, protozoa, aeromonas if freshwater)
which of the following factors is most relevant in history
Which of the following factors is most relevant in history?

Fresh Water/Salt Water/Polluted water

How many mls/kg does the average submersion injury aspirate ?

How many mls/kg aspirate of salt water causes alteration of

blood volume?


Orlowski et al instilled differing NaCl conc into dog ETT tubes

nasty water
Nasty Water
  • Pollutants
    • Hydrocarbons (Low viscosity /High Volatility)
    • Heavy Metals
    • Particulates
  • Microorganisms
    • Gram Negative
      • Pseudomonas, Aeromonas, Burkholderia, Legionella
    • Gram Positive
      • Streptococci and Staphylococci (from mouth)
  • Fungi
    • Pseudoallallescheria boydii
  • Prophylactic treatment not indicated (maybe if raw sewage)
other ineffective treatments
Other Ineffective Treatments

No head down positioning

No Heimlich maneuver

No diuretics 

No prophylactic antibiotics

No steroids

what s the prognosis doc
What’s the prognosis, doc?
  • <5mins to retrieval = good
  • <10mins to CPR = good
  • <30mins to spontaneous breathing = good
    • <10% significant neuro deficit; 60-120mins = 50-80% chance of serious neuro damage
  • ROSC before hospital = good
  • GCS on arrival
  • Prolonged submersion (>25mins) = bad
  • Asystole = bad
jack was fine
Jack was fine.
  • Here he is being discharged from DCCM.
jack got a new job
Jack got a new job.
  • He became a fireman.

I can’t bring myself to say what happened next. Let’s just skip over that part of the story.

  • PS. I think I’m getting rather attached to Jack.
  • PPS. This is Jack’s last environmental injury
  • PPPS. Don’t worry, he survives.
jack got burned
Jack got burned.
  • Minor: Partial thickness <15% (10% in <6yrs / >50yrs)

or Full thickness <2%

  • Moderate:Partial thickness 15-25% (10-20% as above)

or Full thickness 2-10%

  • Major: Partial thickness >25% (>20% as above)

or Full thickness >10%

Burns of special areas (hand, face, feet, ears, perineum,

crossing major jts)

Inhalational / electrical burns

Circumferential burns

Complicated by # / trauma

Burns in high risk pt

what s the admission criteria to the burn s unit
What’s the admission criteria to the Burn’s Unit?
  • Partial thickness >20%
    • >10% if <10/>50yrs, >15% if chemical
  • Full thickness >5%
  • Other major burn criteria
what about depth
What about depth?
  • Superficial: Epidermis only No blisters Red/pink Painful

Normal CRT

  • Superficial partial: Epidermis + papillary dermis Small blisters

Red, moist V painful

Normal CRT

  • Superficial deep: Above + reticular dermis May blister

Yellow, white, dry Variable pain

No blanching/bleeding

  • Full: Epidermis + dermis + subC tissue No blisters Pearl/charred, leathery Insensate

No CRT/bleeding

it s not just the skin
It’s not just the skin…
  • Consider blast injury
  • Consider inhalational injury
    • Steam can cause lung injury (12-24hrs)
    • What are the hallmarks of airway injury?
    • What are the indications for ETT?
    • Airway oedema can happen rapidly
  • Consider toxic gases
carbon monoxide
Carbon Monoxide
  • CO has 240x affinity for Hb binds Hb  shifts O2-Hb curve to L  Hb holds on to O2 that is can bind  cellular hypoxia
  • Cherry red skin but cyanotic
  • SaO2 falsly elevated
  • PaO2 probably OK
  • CO does not cause metabolic acidosis
who should i treat and how
Who should I treat and how?
  • Indications for HBO
    • impaired LOC at any time / any neuro Sx
    • COHb >15%
    • persistent Sx after 100% O2 for 4hrs (headache, weakness, visual disturbance, seizures, decr LOC)
    • angina or ECG evidence of myocardial toxicity
    • unexplained metabolic acidosis
    • >55yrs
cyanide poisoning
Cyanide Poisoning
  • Binds to Fe3+ in cytochrome oxidase system  Inhibits aerobic metabolism  cellular hypoxia, severe lactic acidosis
  • Lactate >10
  • SaO2 measure falsly high
  • PaO2 also high
  • No cyanosis
  • Cherry red macula, almond odour, headache, altered LOC
  • Treatment is with antidotes
    • Na thiosulphate, hydroxycobalamin (treatment of choice), di-cobalt EDTA (bad SE’s especially if not poisoned), amyl nitrite
brooke parkland formula
Brooke-Parkland Formula
  • 2-4ml/kg/% (+ maintenance volume if child)
  • Titrate to UO 0.5-1ml/kg/hr
  • 1sthalf in 8hrs N saline
  • 2ndhalf in 16hrs N saline
  • Always start IVF if >20% TBSA
jack made a miraculous recovery
Jack made a miraculous recovery
  • With extensive treatment he went from looking like this…
to this
To this…

Wait…Jack was now a woman????