ACEM2011 Day 3

Resuscitation Update
Discussed the changing landscape of resuscitation guidelines

Paul Middleton – 2010 ARC guidelines
Chair of Australian Resusc council NSW Branch

Discussion of “Non-evidence based guidelines”
“Eminence based” – used old world examples of:
Trepanning
Phrenology
Apothecary/Homeothpaothy
Lithtrite – to crush bladder stonrd
Tropical enema
Spermatohhoea ring… ouch!

Talked about the historical methods of resuscitation which had no evidence (barrel, horse, fumigation, bellows, freezing, silvester, holger-neilson)
And the father of resuscitation: Peter Safar, who sedated/paralyzed med students & did EAR on them!

Guidelines:
1980 – 55 pages 240 references – has been MASSIVELY expanded over following 25 years

Guidelines produced by ILCOR
Now: ANZCOR – produces Australian guidelines
Aim to update every 5 years

Went through method by which ANZCOR analysed evidence

RECENT CHANGES TO GUIDELINES:
Acronym: DRSABCD
S = send for help
C: compressions (30:2)
D = emphasized – get early defib (AED)
Flowchart emphaisies Compression only CPR

No rescue breaths
Except: drowning, paeds

“signs of life” = removed
Now: “unresponsive, not breathing normally” (allows for agonal resps)
Start with compressions
Compression only if unwilling/unable to do EAR
Being used by telephone instrcutors/000 operators

Quality of CPR emphasized
Immediate
Constant: high quality
Continuous – minimize breaks – max break 10 secs
Change rescuers every 2-4 mins
Rate > 100
Depth 1/3 chest (or 5cm)
Waveform capnography (not color change)
Detects tube placement, quality of CPR & ROSC

Algorithm has been greatly simplified

MAIN CHANGE TO ALS:
= charge defib while CPR is going
Stopping for even a few seconds – de-oxygenates myocardium & makes successful defib less likely
Minimises interruptions to CPR

Single shock
Stacked shocks only in witnessed monitored arrest (with defib < 10secs)
Adrenaline & Amiodarone = only drugs
(atropine only for bradycardia)

Emphasis for intra-osseus access

Post resuscitation care is now “the norm”. Everyone should get it.

Therapeutic hypothermia for all including non-shockable rhythms and in hospital arrests.

Paeds:
Dx of arrest – same
Max 10sec pulse check for healthcare providers
BLS: 30:2 ratio 100/min
ALS: 15:2 100/min

When tubed: 12-14breaths/minute

Single dose shock: 4J/kg
Adrenaline & Atropine

“Disco can save lives”

Strong recommendation that all ED Physicians & nurses undergo formal training in ACLS
www.arcnsw.org.au

Peter Kas: Guideline Schmidelines

OPALS Study: Steil NEJM 2004
ALS vs no ALS – no difference to intact survival

Defib increases survival in VF/VT
Cardiac output with good CPR < 50% normal (15-40%)
Playing around with airway may be detrimental
Cooling works

AIRWAY:
To intubate or not…

Circulation 2009 (119) Garza, Gratton
Improved survival with a modified resuscitation protocol

Does intubation make a difference?
No studies looking at best time to intubate during a resusc
It interrupts CPR
False +ve & false –ve (PE, APO)
Is there an optimal rate? Need to balance interruptions to CPR vs oxygenation
“hyperventilation kills”
Increases intrathoracic pressure, decreases venous return and decreases coronary perfusion pressure
Decreased cerebral perfusion pressure
Several studies show ventilation rate > 10/min assoc with no survival
Push hard & fast, bag gently & slowly
Study showing: If you bag during a compression – coronary perfusion pressure falls

Volumes of 600ml are appropriate
We give 100% FiO2, but is that optimal? May generate free radicals… – but no real evidence

LMA benefits:
Blind insertion
Doesn’t interrupt CPR
Regurgitation less than with BVM
But: Can’t rely on EtCO2 to predict survivial with an LMA (compared to accurate ETCO2 with an ETT)

CHEST COMPRESSIONS:
Certain pressure needs to be generated
Diastolic of 35-40 needed to get coronary perfusion

PULSE CHECK “during cpr” = useless
“femoral pulse” during CPR = retrograde venous flow
Palpable pulse doesn’t equate to vital organ perfusion
Wastes a lot of time

Duty Cycle:
Amount of time compressing vs recoil – should be 50%
Too fast – don’t get diastolic filling

Showed videos of The Bee Gees “Stayin alive”  & Queen “Another one bites the dust” simultaneously with a video of someone doing optimal CPR. The rates really are 100/minute for these songs!

“Autopulse” – a new CPR machine: “equivalent to high quality manual cpr”

ARCTIC STUDY:
18% overall survival, 72% post VF arrest!!!

Take home points:
BE AGGRESSIVE
BE VIGILANT – CONTINUOUS CPR:
Including During transfer from Ambo bed to trolley/handover

USE INTRA-OSSEOUS OR FEMORAL ACCESS

TIM GREEN: When to stop resuscitation
Resuscitation defines us as crit care physicians

NEED TO GET CLEAR INFO ABOUT: Duration of CPR prior to arrival

Ethical/social/Cultural issues/financial isses
Sudden vs Trauama vs paeds
Do you continue while waiting for parents to arrive?

What is futility?
ILCOR 2005 definition: key determinants are length and & quality of life
EMA 2011 (23) 640-643: Emergency medicine & futile care

“Life is a sexually transmitted disease with 100% mortality”

When not to start:
Advanced care directives, end of life decision making

We have a great opportunity to get DNR orders –when they come in alive

People have the right to die

Dignity: or indignity of death in resuscitation room – we have a lot of control over this.

Often difficult to predict the futility of CPR at the time it’s started…
Stories of successful prolonged resus color our judgement

Medico-legal issues: perhaps overstated/overplayed in our thinking

Should we offer resus to all: essentially yes until clearly futile or authentic Advanced directive sighted.

Quality of life:
May be clear-cut, but often not
Risk of persistent vegetative state

Family presence during resusc – led by paeds colleagues, extrapolated to adult. Definitley beneficial, needs a dedicated staff member

Resource use: waste, cost, value for money…
Things like balloon pumps, ECMO etc are VERY expensive…

Risks to staff:
Biological fluids, stress/burnout, personal factors

Breaking bad news:
Need to be good at it.

Such a poor prognosis procedure, may lead to feelings of clinical impotence

Prolonging resus so staff can practice?
Not necessarily bad:
Time to get Echo out
Get a line in
Med students doing cpr during handover
Professional courtesy & repsect for paramedics (ie don’t just call it as the walk in
the door, they’ve been busting their guts to get the patient to you!)

Organ donation:
Is ED the best place to address this? There are donations that can be made after cardiac death (eg corneas)

Unrealistic expectations: of families
NEJM study (TV resus): 75% survived resus, 67% to discharge

Survivial no better from 1977-2001
15 vs 17%

Holland:
Overall 6%
Witnessed at home: 8%
Witnessed outside home: 18% – moral – if you don’t feel well at home – go for a walk!

USA:
All comers – 8%
(4-14%)Bystander witnessed VF/VT – 22%

In hospital: better outcomes
BUT, if longer than 10-15 mins – often futile

Survival by time:
5% decline per minute = theoretically no survival after 12 mins!

FUTILE IF:
No BLS within 8mins
No defib within 12mins

Terminatng in ED:
   20-30mins with no ROSC
   Any rosc “resets the clock”, but take other things into account
Contorversy:
Hypothermia, toxicological arrests

Survivial of those who arrive arrested is universally dismal:
= 0.6%!!

Hypothermia
VF resistant < 30 degrees
But dead people are cold: in Australia unless at the snow, “dead & cold” is just that: dead.  You don’t need to actively warm them.

Trauma
Blunt: If found apneic/pulseless – don’t start
See slides for other guidelines…

Thoracotomy:
Stanford algorithm

Paeds:
Prognosis – poorer
Can prolong resus for parents/staff

Neonatal: longer than 10mins – futile
(2 cycles of ACLS predicts futility)

PREPARING FOR RESUSC: THE BAT PHONE RINGS:
Prepare relatives room
Prepare resus room: staff, drugs, equipment
AS SOON AS PATIENT ARRIVES: ESTABLISH DOWNTIME
– Get ambos to check with control if necessary (what time call was received) & if any ROSC since
Continue CPR during handover
Check rhythm, paramedic tubes/lines

Terminate resuscitation if:
ACLS > 20-30 mins
Blunt – asap after arrival
Traumatic – cease

Informing family – see slides

OK to give family senior ED docs phone number
Tim’s given his card to 200+ families, and has only had 2 calls
Empowering for families.

DNR tattoos are not legally binding!!

TOXICOLOGY FORUM:

Andis Graudins
Use of Intralipid Emulsion in poisoning:
MOA: many mechanisms… They still don’t really know how it works, or if it even works…
? Different mechanisms for different drug classes
Numerous animal studies
Better than adrenaline at reversing asystole in bupivacaine poisoned
rats & dogs

Effect may be better for bupivicane than for other LA’s:
Has been compared to: Ropivicaines, Mepivicaine
Also studied in toxicity with:
TCA: clomipramine – improvement shown
Propranolol – no effect on BP
Improved other haemodynamics
Increases toxic dose causing death
Increased blood drug concentrations

Issues with studies:
Higher lipid doses
Short term outcomes/measurements only (ie minutes, not hours/days)
IV toxins (most humans take things orally)
Rarely studied compared to standard Rx

Human studies
IV vs oral toxin
No prospective studies
Case series/reviews
Case reports – mostly positive, some negative

LA Toxicity:
> 20 case reports
Time to response – often 30secs to minutes, can be longer ie it’s highly variable
“End of the needle” responses = uncommon
Few cases have checked drug levels to confirm exposure
Seen in: propranolol, Carvedilol, Dothiepin, Amitryptiline
Most had had standard Rx: pressors, insulin, bicarb,
Alkalinisation not well described
Most had response within 5mins-1hr
Also all have had standard Rx at same time (eg CPR)
Most have been CVS studies, some CNS toxicity as well

Harvey et al (EMA 2011)

Indications – really not clear
Symptomatic toxicity vs CVS/CNS collapse
Has been used in sedative/hypnotic OD’s
Eg: Quetiapine, sertraline
Some with benefit to GCS, some with no effect
Has been shown to reduce QTc (but this isn’t really a good thing to measure in a patient who is tachycardic, and doesn’t really have any correlation with outcome)
One case series (of 9) – didn’t really make any difference in need for intubation or GCS

Downsides:
Few reports of toxicity from the ILE itself
One iatrogenic accidenal overdose – patient got 2 litres of lipid emulsion!
? Acute lung injury – but not clear if this was from ILE
Hyperviscosity – hi dose only
Decreased O2 transfer
Can affect biochemical assays for many (ie need to let lab know that patienyt has had lipid emulsion for following 12-16 hours as it’ll affect the analysis of their bloods)
Fat emobilsm – uncommon
Coagulopathy
Pancreatitis – theoretical

Oral Overdoses:
Issues:
Usually Mixed O.D’s
Lipophillic & non lipophillic drugs
Immediate vs sustained release – benefit really not clear from case reports

Dose Of Intralipid
Many different dosing regimens
1.5m/kg
then 05ml/kg/hr infusion
(as per www.lipidrescue.org )

Bolus + infusion seems to have better effect on BP/MAP than bolus alone

CONCLUSION:
Still don’t really know how it works
More logical in IV toxin exposure cf oral (due to delayed absorption etc in oral OD)
Lipid sink may explain some of effect, may be related to overcoming Na+ channel blockade
Dosing regimen – varied & not consistent

Use may be refined to severe toxicity, once other standard treatments have been maximized. Eg
TCA
Lipophillic B-blockers
Liphilic Local anaesthetics
Role in SR drug toxicity  – even more unclear

DEFINITELY NOT 1st LINE Rx IN CVS COLLAPSE or COMA
Do not used for drug induced coma, or to avoid intubation
Still use all standard toxicological treatment for all OD’s
Bicarb
Hyperventilate
Hypertonic saline for Na-blockers
Insulin – takes 30-60mins to work
If given, collect blood for assay pre& post ILE to see if it has an effect.

Is it a fad or a universal antidote?
Will there ever be an RCT?
Who knows…

Geoff Isbister
SNAKES, ANTIVENOM & DOING LESS

Best managed in ED Observation unit – ICU just adds to length of stay (unless they’re intubated or need dialysis)

Snake distribution – if you know what snakes are in your area, that plus analysis of the clinical condition of the patient will be just as useful in determining which anti-venom to use as a VDK (and will possibly be more accurate)

Syndromes: On average
Venom Induced Consumptive Coagulopathy (VICC) 75%
Systemic Syx 10%
Myotoxicity 5%
Neurotoxicity 5%

Deaths:
Brown snakes only, from early out of hospital arrests

Australian Snakebite Project – ASP (2004-2011)
Prospective study
(Side studies: Use of FFP & Tiger antivemon for Red belly black snake in RCT’s)

60 definite bites, 56 envenomated
Tiger snakes mainly in VIC, some in TAS

Brown vs Tiger:
Tiger – more neuro/myo, less coags

VDK:
75% +ve
FALSE +ve rate (brown) in 5/44 cases – were given wrong antivenom!
But that’s OK because all antivenom is polyvalent…

TAKE HOME MESSAGE
VDK swabs have high false +ve rate!!
Need to sit & WATCH it to see what well changes first
Best done by lab staff
Expire every 3-6months
Cost $300 each!
Can cost $10-20,000 pa just to be stocked, often only use it once/twice a year

VDK – Adds little to geography + clinical
Source: wound site – best
Urine – high false +ve
Overall false pos & negs occur
Only useful in envenomed patients

Geoff showed some great evidence, in which they measured venom levels after increasing doses of antivenom. It showed no difference in outcome in 1 vs 2 vials of antivenom when post Rx levels of venom were checked…

LOCATION/GEOGRAPHY
Darwin: Mulga, death adder, brown snake
Eastern: brown, tiger
Vic: Tiger
Take home message – familiarize yourself with your local snakes!

CLINICAL FEATURES
COAGULOPATHY: Brown & tiger

NEURO ONLY: Death adder

DOSE: How much antivenom should you give?
& How often?!

Old school of thought:
Unrecordable INR = severe, so you need need increasing doses, and titrate: repeat coags every 1-3hrs,
fibriniogen = best test
But what do you correct the coags to?!
Do you need a normal INR/finrinogen/D-dimer?

In their study: In vivo binding after 1-2 vials given: No venom detected!
ie Effect lasts longer than than the venom hangs around for
Venom wipes out factors 3/5/8 ie it’s CONSUMPTIVE, it consumes all the factors so you have to wait until the liver can re-synthesis them.

Takes time to resynthesise clotting factors: Anti-venom DOES NOT speed that up!
Giving more antivenom does not make it happen faster!
Fibrinogen takes longest to recover (can be days)
Median time to recovery of INR < 2 = 14HOURS!!  (This assumes no ongoing absorption of venom) So why do serial coags?
Previously: to decide on re-dosing antivenom
Now:
Asymptomatic: Disposition decision
Actively bleeding post antivenom = give FFP

Neurotoxicity:  Antivenom reduces intubation rates

Myotoxicity:
Once CK goes up (which tends to happen LATE) – there’s no venom left in circulation so antivenom wont help reverse the rhabdo
If you give antivenom EARLY – you can prevent the myotoxicity

Mx OF SUSPECTED SNAKE BITE:
Syx may be just due to feeling scared/worried/vagal!
Which lab tests? Over how long?
You need to measure 4 things: aPTT, INR, CK, neuro exam
When these 4 factors were studied in envenomed patients:
97% +ve by 6hrs
99% +ve by 12 hours
If all negative at 12hours – send them home, BUT if you can only manage to convince them to hang around for 6hours, you’ll only miss 3%

ED OBSERVTION UNITS & snakebite:
Admit those with:
Coagulopathy: observe 24-36hrs, serial INR’s, then d/c
Suspected snakebite

ICU
For ventilated or needs dialysis
Often then d/c to med ward, and then hang around for 1-3 days unnecessarily if they only have coagulopathy = unnecessary extension of LOS.

Australian Snakebite Project  – to recruit patients into study, call Geoff
1800 676 944

NICK BUCKLEY
Anti-cholinsterase pesticide poisoning update
Relatively uncommon in Aus
Very very Common in developing world: 3-400,000+ suicides from pesticides worldwide!

Photos & videos (some were quite confronting) from hospital in Sri Lanka where Nick has worked

Organo-phosphates (OP’s)
Not as bad for environment compared to organo-chlorides as they don’t hang around as long in environment, so are more popular/easier to get
Wide range of anti-cholinetersases as OP’s
Most are pro-poisons – need conversion in liver, can take DAYS = delayed onset toxicity
Some undergo ageing: = irreversible binding
Carbamates = reversible
Some are neuro-pathic – not clear which ones

Average mortality = 15% (varies depending on agent 1%-30%)

Diagnosis = not hard
Foaming at mouth, fasciculations, pinpoint pupils, resp paralysis/disordered breathing (CNS/muscle related & from crap in lungs), tachycardia, pinpoint pupils

What do they die of?
25% = resp failure
Also:
CVS Shock
Pneumonia
Best predictor of death = GCS (if you’re on a coma you’re likely to die)

MYTHS:
Health workers need PPE to protect them from poisoning
NO EVIDENCE THAT any healthcare worker has ever been poisoned by not having PPE
May alter if NERVE agent is suspected, but again, risk is overstated
In wards in Sri_lanka – patients share beds and don’t make non-poisined patients sick!

Indication for Atropine
Pinpoint pupils, sweating, resp difficulty
Look well – 0.6mg
Sick: up to 25mg
Keep giving Until Bradycardia, Hypotension & bronchospasm resolves

Then give 10% of max dose per hour
Give the initial amount quickly eg over 15mins
Double the dose with each dose, every 2 minutes.

LAST PRIORITY = decontamination
Skin – do after atropine

GI decontamination: Possibly slight benefit, but NOT a high priority

OTHER OPTIONS:
Oximes – pralidoxime
No use once OP has aged
Does of toxin may be higher/outlast dose of oxime
Need high/multiple doses, variable responses
Never really been shown to work…
In RCT – increased mortality in Pralidoxime group when compared to placebo! May make toxicity worse
If already intubated – no difference
May be related to WHO recommended dosing…

In some studies – higher doses work better…
Optimal dose = unclear

ATROPINE IS ONLY FOR MUS
CARINIC EFFECTS

Rx FOR NICOTINIC EFFECTS
Which is often a delayed onset & prolonged problem (mainly resp failure)
Benzos – can help (in animal studies, mainly related to nerve agents with CNS effects).
Mg – can help
Clonidine – can help

NMJ blockers –may prevent OP-induced NMJ failure, or protect the NMJ from OP

If patient is intubated – paralysis is OK, and may be beneficial

MYTHS ABOUT MASS POISONINGS
Emergency services will identify the chemical
Patients will arrive decontaminated
You need to stockpile anti-dote

Because:
People who die, die at scene
Those who survived to hospital live

Remember:
Healthcare workers won’t get contaminated
Universal precautions are enough