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A Story of an Unfortunate Man A Story of an Unfortunate Man

A Story of an Unfortunate Man - PowerPoint Presentation

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A Story of an Unfortunate Man - PPT Presentation

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 ID: 714588

high jack auckland injury jack high injury auckland risk water ecg burns normal hypothermia thickness acidosis degrees shivering loc decr drowning blood

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Slide1

A Story of an Unfortunate Man

…which coincidentally teaches some environmental nuggetsSlide2

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…Slide3

Jack Had Hyperthermia.

Luckily a passing nurse found him and took him immediately to Auckland ED. Slide4

Stage 1

H

eat exhaustion

Volume and electrolyte loss as sweat, with inadequate replacement

Still have heat regulatory mechanisms and CNS not affectedSlide5

Stage 2

Heat stroke

Life threatening

M

ortality <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 dehydratedSlide6

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 sweatyDehydration more commonSlide7

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 changesSlide8

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 syndromeSlide9

What should Auckland ED do?Slide10

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 UOconsider 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 shiveringSlide11

Jack was made cool…

Evaporative

Ice water immersion

Ice packs

Cooling blankets

Cooled IV fluids

Gastric lavage etc…Slide12

Jack recovered well…

Except for some residual ataxia (20% have a permanent residual neurological deficit)Slide13

Unfortunately…

The over-enthusiastic doctor was rather rigorous with the cooling…

He was found by a FED who came to offer him a sandwich. Slide14

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 significanceSlide15
Slide16

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 thrombosisSlide17

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 / exposureSlide18

35

Mild hypothermia

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

ineffective

Double

intervals between drug doses

29

Pupils dilated

VF may

occur

28

HR

30-

40

Rigidity

BMR

decr by 55-65%; major

acidosis

26

Areflexia

25

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 AsystoleSlide19

What did Auckland ED do?

Filled out a risk proSlide20

Meanwhile Jack had a cardiac arrest…Slide21

What should Auckland ED do?Slide22

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 volumesOnly pace bradycardia

if persists after warmingSlide23

Pharmacology

Most drug activity temperature dependent

Toxic doses required for effect

Leading to problems when rewarmedMost arrhythmias revert with rewarmingVF treatment controversial

BretyliumSlide24

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

, ECMOSlide25

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 studySlide26

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

<20

C4

Arrested

3

<20Slide27

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?)Slide28

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. Slide29

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

PathwayVertical = bad for brain; 20% mortalityHorizonal = 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 awaySlide30

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 1

st

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 #)Slide31

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 commonAll require opthalmology reviewDilated pupils don’t mean they’re dead

Always examine the ears

50% have TM rupture;

sensorineural

hearing lossSlide32

This is not JackSlide33

What did Auckland ED do?

Filled out a risk proSlide34

Yes, and what else?

Jack seemed alright.

What did Auckland ED do with him?Slide35

To monitor or not to monitor?

Do initial ECG

M

onitoring 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

BurnsSlide36

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:

>600VAbnormal ECG or examinationHorizontal transmissionSlide37

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).Slide38

Jack wandered home.

He took a ferry to

Waiheke

, where he lived with some twits. Guess what happened next… Slide39

No he wasn’t envenomated.

We’re not covering that

cos

we’re not bloody Australian.Slide40

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. Slide41

From Auerbach: Wilderness Medicine, 5th ed. ( Submersion or near-drowning) Fig 68.4.Slide42

Cardiovascular Effects

Hypotension

Shock, acidosis,

hypovolemia (natriuresis

), autonomic instability

Arrhythmias

Asystole

(55%),

Ventricular tachycardia/fibrillation (29%)

Bradycardia

(16%)

Brugada

Long-QT syndromesSlide43

What should Auckland ED do?Slide44

Wait…

It is the helicopter after all.

Pictured below is the

resus team with Les Galler. Slide45

Drowning Resus

C:

C spine

immobilisation ifHistory

of diving, use of water slide, MVA, signs of injury,

ETOH

A+B:

aggressive respiratory

resus

Intubate if

R

equiring

FiO2 >40-60% to attain PO2 >70Use PSV starting at 10cm, PEEP 5-7.5cm; wean ASAP to prevent barotraumaC N saline IVF resus (but beware pul oedema)

Monitor electrolytesDo 1hr CPR if persistent apnoea and asystoleD Trt seizures; maintain normoG; rewarm if neededSlide46

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 H

2

0 only if PaO

2

< 60 on FiO

2

<0.6Ventilate for 24 hours to allow regeneration of surfactantSlide47

A note on rewarming…

Consider induced hypothermia

If comatose

with spontaneous circulation

D

o

not actively warm to >32-

34

A

im 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;80:379-81WARNER et al.

Recommendations and consensus brain resuscitation in the drowning victim.

Bierens

JJLM, ed. Handbook on drowning: prevention, rescue and treatment. Berlin: Springer-

Verlag

, 2006:436-9Slide48

Asymptomatic patient

No comorbidities

If at 4 - 6 hours:

CXR, ABG normal

Normal vitals on air

Remain

ASx

= discharge with adviceSlide49

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 traumaSlide50

Does it matter that it was salt water?

Nah, not really

Electrolyte abnormalities are theoretical

Abx if features of infection develop

B

road

spectrum if grossly contaminated

water

A

nti

-pseudomonal if in

spa

Chemical pneumonitis if swimming poolSand pneumonitis if salt waterFram neg, anaerobes, staph, fungi, algae, protozoa, aeromonas if freshwater)Slide51

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?

electrolytes?

Orlowski

et al

instilled differing NaCl conc into dog ETT tubes Slide52

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)Slide53

Other Ineffective Treatments

No head down positioning

No Heimlich maneuver

No diuretics 

No prophylactic antibiotics

No steroidsSlide54

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 arrivalProlonged submersion (>25mins) = badAsystole = badSlide55

Jack was fine.

Here he is being discharged from DCCM. Slide56

Jack got a new job.

He became a fireman.Slide57

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. Slide58

Jack got burned.

Minor:

Partial thickness <15% (10% in <6yrs / >50yrs)

or

F

ull

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 ptSlide59

What’s the admission criteria to the Burn’s Unit?

P

artial

thickness >20% >10% if <10/>50yrs, >15% if

chemical

Full

thickness >5

%

Other

major burn criteria

Slide60

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/bleedingSlide61

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 gasesSlide62

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 acidosisSlide63

Who should I treat and how?

Indications for HBO

impaired

LOC at any time / any neuro SxCOHb >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>55yrsSlide64

What should I consider if there’s a metabolic acidosis?

CyanideSlide65

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 LOCTreatment is with antidotesNa thiosulphate, hydroxycobalamin (treatment of choice), di-cobalt EDTA (bad SE’s especially if not poisoned), amyl nitriteSlide66

Brooke-Parkland Formula

2

-4ml/kg/% (+ maintenance volume if child)

Titrate to UO 0.5-1ml/kg/hr

1

st

half in 8hrs N saline

2

nd

half in 16hrs N

salineAlways start IVF if >20% TBSASlide67

And don’t forget tetanusSlide68

Jack made a miraculous recovery

With extensive treatment he went from looking like this…Slide69

To this…

Wait…Jack

was now a woman????Slide70

…and they all lived happily ever after