A Story of an Unfortunate Man
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Transcript of A Story of an Unfortunate Man
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…
Jack Had Hyperthermia.
• Luckily a passing nurse found him and took him immediately to Auckland ED.
Stage 1
• Heat exhaustion
• Volume and electrolyte loss as sweat, with inadequate replacement
• Still have heat regulatory mechanisms and CNS not affected
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, resp alkalosis, rhabdo, DIC, electrolyte disturbance
Organ failure Prolonged QTc, ST changes
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 do?
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 pul oedema– 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…
• Evaporative• Ice water
immersion• Ice packs• Cooling blankets• Cooled IV fluids• Gastric lavage
etc…
Jack recovered well…
• Except for some residual ataxia (20% have a permanent residual neurological deficit)
Unfortunately…
• 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…
Osborn wave
AF with slow ventricular response in 50% with mod hypothermia
Wide QRS
Long QT
No prognostic significance
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…)– Pul oedema, peripheral vasodilation, rhabdo, MOF, haemoconcentration and
intravascular thrombosis
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 hypothermia32 Mod hypothermia: shivering stops
AF and other arrhythmias; 2/3 decr in HR and CO; Osborn waves common Decr RR / LOC
Insulin resistance31 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 ineffectiveDouble intervals between drug doses
29 Pupils dilatedVF may occur
28 HR 30-40RigidityBMR decr by 55-65%; major acidosis
26 Areflexia25 Risk of asystole; CO 45% normal
Cerebral blood flow 1/3 normal24 Loss of vascular tone and cerebrovascular autoregulation23 Absent corneal and oculocephalic reflex22 Max risk of VF20 HR 2019 EEG flat, appears dead18 Asystole
What did Auckland ED do?
• Filled out a risk pro
Meanwhile Jack had a cardiac arrest…
What should Auckland ED do?
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
Pharmacology
• 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…
• 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
• 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
The simple approach
• Asymptomatic
• Symptomatic
• Critical
• Obviously dead
Modell & Conn 1984 – in ED within 1 hr of rescue (paeds)
Category Description GCS Neurologically Intact (%)
A Awake – fully orientated
14-15
100
B Blunted- rousable, purposeful to pain
8-13 100
C Comatose- not rousable, abnormal response to pain
6-7 >90
C1 Flexor response to pain
5 >90
C2 Extensor response to pain
4 >90
C3 Flaccid 3 <20C4 Arrested 3 <20
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…
• 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. • 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
– 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 #)
Lightening• 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
This is not Jack
What did Auckland ED do?
• Filled out a risk pro
Yes, and what else?
• Jack seemed alright.
• What did Auckland ED do with him?
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?
• 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 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.
• He took a ferry to Waiheke, where he lived with some twits. Guess what happened next…
No he wasn’t envenomated.
We’re not covering that cos we’re not bloody Australian.
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.
From Auerbach: Wilderness Medicine, 5th ed. ( Submersion or near-drowning) Fig 68.4.
Cardiovascular Effects• Hypotension
– Shock, acidosis, hypovolemia (natriuresis), autonomic instability
• Arrhythmias– Asystole (55%), – Ventricular tachycardia/fibrillation (29%)– Bradycardia (16%)– Brugada– Long-QT syndromes
What should Auckland ED do?
Wait…
• It is the helicopter after all. • Pictured below is the resus team with Les
Galler.
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 pul oedema)– Monitor electrolytes– Do 1hr CPR if persistent apnoea and asystole
• D– Trt seizures; maintain normoG; rewarm if needed
Ventilation• 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…• 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
Vanden et 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:S847-8Guenether U et al.Extended theraeutic 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
No comorbiditiesIf at 4 - 6 hours:
CXR, ABG normalNormal vitals on airRemain ASx = discharge
with advice
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?
• 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?
Fresh Water/Salt Water/Polluted waterHow many mls/kg does the average
submersion injury aspirate ? How many mls/kg aspirate of salt water causes
alteration ofblood volume?electrolytes?
Orlowski et al instilled differing NaCl conc into dog ETT tubes
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
• No head down positioning
• No Heimlich maneuver
• No diuretics • No prophylactic
antibiotics• No steroids
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.
• Here he is being discharged from DCCM.
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. • 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?
• Partial thickness >20% – >10% if <10/>50yrs, >15% if chemical
• Full thickness >5%• Other major burn criteria
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…
• 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
• 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?
• 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
What should I consider if there’s a metabolic acidosis?
Cyanide
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
• 2-4ml/kg/% (+ maintenance volume if child) • Titrate to UO 0.5-1ml/kg/hr
• 1st half in 8hrs N saline • 2nd half in 16hrs N saline• Always start IVF if >20% TBSA
And don’t forget tetanus
Jack made a miraculous recovery
• With extensive treatment he went from looking like this…
To this…
Wait…Jack was now a woman????
…and they all lived happily ever after