ARREST AND RESUSCITATION

ANSWER PAPER

SUNDAY 24/01/2016

Deranged Physiology » Home » CICM Fellowship Exam » Past Papers » 2011, Paper 2 SAQs

Outline the important management principles in treating a patient who has been admied to your ICU

intubated and ventilated immediately following successful resuscitation from an out of hospital cardiac

arrest.

[ Hide Answer ]

Post-resuscitation care has an impact on overall outcome and consists of ongoing resuscitation and

organ support, neuroprotection, treatment of the cause of the cardiac arrest and management of

underlying co-morbidities.

Check adequacy of airway, ETT position, ventilation and circulatory statusAppropriate monitoring and intravenous accessVentilation:

Control CO2Avoid hypoxia and hyperoxia

Circulation:

Stabilise circulation with fluid therapy and vasoactive drugsConsider early echoDiagnosis / treatment of acute coronary syndrome with angiography/PTCA orthrombolysisEvaluation for pacemaker or ICD if primary dysrhythmiaMechanical support - use of IABP for cardiogenic shock in acute MI has recently beenquestioned.Some centres may consider use of ECMO

Neurological:

erapeutic hypothermia at 32-34oC for 12-24 hr appears to be neuroprotective withimproved neurological outcome although the optimal method and timing of cooling isstill to be determined.Treatment of seizures

Diagnosis and management of precipitating event

Let us deconstruct this answer. is question interrogates the candidate's ability to approach a post-

arrest patient in a systematic manner. Of course, the natural tendency of any ICU trainee would be to

immediately start ranting about therapeutic hypothermia (hard to blame them, of course - it is indeed

an exciting topic). And then to strat ranting about family discussions. e savvy candidate will note

that there is no mention of family discussions in the model answer.

estion 24

e answer is organised in a familiar A-B-C-D of resuscitation. I have both a brief summary of post-

resuscitation care, and a prolonged elaboration of this topic. In brief, a structured answer would

resemble the following:

e comatose patient should be intubated, and the ETT secured.

Mechanical ventilation (mandatory mode) should be commencedNo unique recommendation - standard ventilationAim for normoxia and normocapnea.Avoid hyperoxia.Anticipate aspiration pneumonia, pneumothorax, pulmonary oedema, pulmonarycontusions, and ARDS.

Anticipate distributive shock, potentially with cardiogenic shockVasopressor support, inotropes and fluids as required to maintain a MAP >65Urgent coronary angiogram, if there is no obvious non-cardiac cause of arrest.Urgent TTEWatch for QTc prolongation

erapeutic hypothermia to 32-24° if the patient remains comatose;Targeted temperature management is a valid alternative, and may be preferredAvoid hyperthermiaSedation and neuromuscular blockade; avoid benzodiazepines.EEG

Watch for hypokalemiaReplace electrolytes to prevent arrhythmias

Renal function may deteriorate due to hypoxic injuryHypothermia may result in hyperviscosity; use crystalloidAnticipate a vigorous diuresis with hypothermia

Normoglycaemia maintained with an insulin-dextrose infusionNo need to start feeds until aer rewarming

Avoid invasive procedures while hypothermicPlatelet dysfunction coagulopathy and thrombocytopenia of hypothermia are reversible.If the patient has ongoing uncontrolled bleeding, therapeutic hypothermia iscontraindicated.

Most common complication is pneumonia (staphylococcal)Most common bacteraemia is gram negative (bacterial translocation from the gut)In hypothermia, leucocyte migration and phagocytosis are impaired, predisposing toinfection.

Airway support:

Breathing:

Circulation

Disability (.. or prevention thereo)

Electrolytes

Fluids and renal function

Gastrointestinal and nutritional support

Haematological issues

Infectious complications

First, the college wants you to acknowledge that the patient is intubated, and that you are concerned

about their ETT position. is, as a maer of general principle, is never wrong.

Secondly, the college wants you to acknowledge that you would pursue normoxia and normocapnea.

TTE, angiography, fluids and vasopressors are mentioned - again, this is consistent with the AHA

guidelines.

erapeutic hypothermia is mentioned, and it would be amiss to write an answer to this question

without discussing this.

Overall, the model answer expects nothing suprising or inventive from the candidate. e only

unusual feature is the mention of ECMO, which (unlike the rest of the answer) does not have strong

evidence behind it in post-resuscitation care.

 

Kilgannon, J. Hope, et al. "Association between arterial hyperoxia following resuscitation from cardiac

arrest and in-hospital mortality." JAMA: e Journal of the American Medical Association 303.21

(2010): 2165-2171.

Peberdy, Mary Ann, et al. "Part 9: Post–Cardiac Arrest Care 2010 American Heart Association

Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular

Care." Circulation 122.18 suppl 3 (2010): S768-S786.

Stub, Dion, et al. "Post Cardiac Arrest Syndrome A Review of erapeutic

Strategies." Circulation 123.13 (2011): 1428-1435.

 

Deranged Physiology » Home » CICM Fellowship Exam » Past Papers » 2015, Paper 1 SAQs

Critically evaluate the use of therapeutic hypothermia in intensive care practice.

[ Hide Answer ]

Maintenance of a target temperature to provide neuroprotection. A range of different temperatures

employed with ‘mild hypothermia’ traditionally 32-34oC; more recently 36oC post TTM trial.

Rationale:

Hypothermia may lessen the brain injury through a number of mechanisms:

Cerebral metabolic rate decreases by ~6-10% per degree Celcius drop in temperatureReduced release of excitatory amino acids / glutamate which mediate neuronal injuryReduced ischaemia reperfusion induced reactive oxygen species releaseReduced inflammation – both cellular response and cytokine expressionReduced apoptosisPreservation of blood brain barrier (reduced NO, aquaporin 4, metallo-proteinases)

Clinical utility and evidence:

Post cardiac arrest:

Standard of careHACA and Bernard studies in 2002 cooled VF/VT patients to 32-34 for 12-24 hrs.TTM trial 2013 showed no difference between target 33 and 36 in patients with outof hospital arrest of presumed cardiac cause. Fever avoided for 72 hrs in TTM.Current ARC/ILCOR guideline remains 32-34 but either approach reasonable.Avoidance of hyperthermia may be more important than hypothermia.ILCOR dra guidelines for 2015 recommend 32-36 for all arrests withunresponsiveness post ROSC for 24 hours (weak recommendation, very low qualityevidence.)Prehospital cooling with crystalloid confers no benefit with increased APOStudies that suggest benefit of TTM in patients with cardiac arrest post hangingHYPERION trial underway to evaluate TTM 32.5 – 33.5 in non-shockable cardiacarrest survivors

Traumatic brain injury:

Multiple studies have looked at TH to treat severe TBI i.e. prophylaxis.Meta-analysis of trials spanning over 20 yrs suggests a beneficial effect on mortalityand favourable outcome.When limited to higher quality trials no significant mortality benefit.BTF guidelines level III recommendation for prophylactic hypothermia with nosignificant decrease in mortality but association with higher GOSCooling associated with lower ICP and higher incidence of pneumonia

estion 9

Most trials using 32-35 degrees for at least 48 hrsPOLAR awaited – TH for severe TBIEurotherm 3235 awaited – TH for Intracranial hypertensionTH commonly used to treat intracranial hypertension rather than as prophylaxis.Contemporary data evaluating this practice is lacking

 

Other potential uses

Hepatic encephalopathy

Intracranial hypertension common in grade III/IV encephalopathy related to ALFSome advocate cooling as a treatment of strategy to manage intracranial HTControversialNo RCTs

Meningitis

Evidence of potential harm

Stroke

Fever associated with two-fold risk of death aer haemorrhagic or ischaemic strokePharmacologic methods of fever control have not shown improved outcomeNINDS and European (EuroHYP-1) funded trials looking at inducedhypothermia underway

Seizures

Case reports with HYBERNATUS trial underway evaluating TH for refractory SE

SAH

No good data to support the use of TH in SAH.Small studies have looked at TH in patients with intracranial HTFever associated with worse outcomes

Neonatal encephalopathy

Results of RCTs recommend cooling 33-34 for 72hr

Adverse effects:

Bradycardia / ArrhythmiasIncreased SVR and venous return with cold diuresisHypokalaemia during cooling and rebound hyperkalaemia during rewarmingImmunosuppression / infectious ComplicationsCoagulopathyAltered drug metabolism / reduced clearance sedative drugsRequirement for sedation +/- paralysisConcern regarding rebound intracranial hypertension during warming phaseChallenge of achieving and maintaining target temperature

Practice:

Reasonable statement of candidates practice re TH

Additional comments: Candidates  mentioned  detail  that  was  not  requested,  such  as  methods of  cooling.  Candidatesalso showed poor breadth of knowledge related to the potential use of hypothermia in conditionssuch as TBI / SAH / CVA.

Rationale for therapeutic hypothermia:

erapeutic hypothermia has been advanced a a means of improving survival and good

neurological outcome following cardiac arrest.It has also been offered as a means of controlling intracranial hypertension which isrefractory to other modalities.erapeutic hypothermia modulates the activity of body proteins and electrolytes.is modulation is thought to have some beneficial effects in scenarios whereinflammatory damage is anticipated.is also involves the down-modulation of the overall metabolic rate, which decreases themetabolic demands of the organism in situations where supply of metabolic substrate maybe compromised.Decrease in oxygen consumption matches decreased demand with decreased supply in"penumbra" areas, at the watersheds, where hypoxic injury has caused oedema.\

Advantages of therapeutic hypothermia

Decreased granulocyte migration into tissueDecreased cerebral oedemaIntrinsic anticonvulsant effects of hypothermia

Well-accepted indications:

Mild therapeutic hypothermia for survivors of cardiac arresterapeutic hypothermia for traumatic brain injury

Evidence for use in cardiac arrest:

Pseudorandomised unblinded trial in 1996 - promising resultsBernard et al  demonstrated a survival benefit in out of hospital VF arrest survvors A recent Cochrane review supports the use of therapeutic hypothermia, finding a 1.35 riskreduction for mortality.e recent TTM trial  has demonstrated non-inferiority of a more conservativehypothermia (36℃) with standard temperature goals, in terms of mortality.

Evidence for use in traumatic brain injury

EUROTHERM 3235 trial (2015): 387 patients; hypothermia was used as a second-linetherapy to reduce ICP.No survival benefit was observed.Recruitment was suspended early owing to safety concerns.ICP control was in fact beer in the hypothermia group (they required rescue therapiesless frequently)e meta-analysis mentioned by the college is possibly  this 2013 review by Georgiou et al;except there was no benefit in mortality when only high quality trial were included.

Extended indications:

erapeutic hypothermia in cooling of a hyperthermic patient

Hyperthermia is associated with substantial harm, particularly if the temperature increasesbeyod 41℃Causes of such hyperthermia may be numerous, including sepsis, malignant hyperthermia,anticholinergic drug poisoning, heat stroke, and so on and so forth.In brief, these causes all have specific management strategies which may take time towork.In the interim, the temperature must be managed, so that organ damage does not occurInduction of hypothermia (or maintenance of controlled normothermia) by cooling thepatient can be viewed as one of the indications.

erapeutic hypothermia for subarachnoid haemorrhage

eoretically, TH may be protective in SAH in the same way that it is supposed to beprotective in traumatic brain injury. Areas affected by ischaemia in the context ofvasospasm may benefit from having a lower metabolic rate.TH certainly  seems to decrease the flow velocity in the MCA of subarachnoidhaemorrhage patients (Seule et al, 2014), suggesting that the metabolic rate is indeedaffected enough to influence cerebral blood flow.Animal studies have also demonstrated that hypothermia reverses vasospasm (in rats)In patients with "poor-grade" SAH, good functional outcome was achieved in 48% with thecombination of barbiturate coma and hypothermia to 33-34℃ (Gasser et al, 2003)

A more recent case series (Seule et al, 2010) found good outcomes in 57% of  severe SAHpatients who developed vasospasm.In contrast, Karnatovskaia et al (2014) found no difference in neurological outcome withintheir case series.No recommendation in favour of this use of TH can be made with a straight face.

erapeutic hypothermia for super-refractory status epilepticus

Hypothermia is known to have antiepileptic effects.Case series (eg. Corry et al, 2008) have demonstrated its feasibility in humans (targettemperature: 31–35℃)Neurocritical care society guidelines for status epilepticus (Brophy et al, 2012) identifiedonly 4 articles in the literature, and were unable to make very strong recommendations.e HYBERNATUS trial mentioned in the college answer is apparently ongoing, but nolonger recruiting participants.

erapeutic hypothermia for severe sepsis

Anti-inflammatory effects of hypothermia were studied in an animal model of severesepsis (Kwang et al, 2012).e hypothermic rats (30–32 ℃) did beer in terms of acute lung and liver injury.Human applications of this are limited by concern that …firstly, a fever is an antibacterialphysiological response, and secondly, that the haemodynamic instability of septic shockwill be exacerbated by hypothermia.

erapeutic hypothermia for meningitis

Evidence of potential harm mentioned by the college in their answer was found by a 2013RCT (Mourvillier et al). e investigators found a higher mortality in the hypothermiagroup.

erapeutic hypothermia for neonatal asphyxia

Following on from the success of TH in adult cardiac arrest, this modality has been appliedto neonatal hypoxic-ischaemic encephalpathy.Shankaran et al (2005) performed an RCT; the group of neonates who were cooled 33.5℃for 72 hours; the rate of cerebral palsy was reduced from 19% to 15%, and mortalityimproved from 37% to 24%. In the long term, there was no increase in disability amonghypothermia-exposed survivors when compared to surviving controls (Shankaran et al,2012)TOBY trial (2014) confirmed that both survival and neurological outcome is improved

erapeutic hypothermia for stroke

e college answer points out that fever is associated with two-fold risk of death aerhaemorrhagic or ischaemic stroke. Pharmacologic methods of fever control have notshown improved outcome in stroke.In animal models of stroke, , mild or moderate hypothermia has been shown to decreaseinfarct size and lead to functional improvement when cooling was initiated within a fewhours of ischemia onset (Clark et al, 2008). But… ese were rats, and they were cooled to24℃

erapeutic hypothermia for acute hepatic encephalopathy

is use of TH is an extension of the observation that TH reduces cerebral oedema inpatients with traumatic brain injury.Some authors (Stravitz et al, 2008) have suggested that TH may be an effective bridge toliver transplant.Human case series support this assertion (Jalan et al, 1999); during their treatment therewas no significant relapse of increased intracranial pressure.ere are no RCTs, but a large-scale retrospective cohort (Karvellas et al, 2014) did not findany survival benefit.

erapeutic hypothermia in ARDS :

Recent studies (Zhicheng et al, 2012) have confirmed that mild hypothermia improves gasexchange, lung compliance, duration of ventilation and the levels of IL-6 in local lungtissue.

Of particular interest is the use of hypothermia to reduce the whole-body oxygen demandin situations where even veno-venous ECMO is powerless to oxygenate the patient (Hayeket al, 2015)

Intraoperative therapeutic hypothermia

Cardiothoracic surgery, routinely in use (including DHCA).Neurosurgery for aneurysm clipping: IHAST trial, 2005; no benefit ("good-grade" SAHpatients)Vascular surgery, to protect the spinal cord during prolonged aortic cross-clamp

Suspended animation for delayed resuscitation

In essence, this is a practice of stopping the circulation with deep hypothrmia, so as to buytime to the definitive management of the cause of the cardiac arrest.Animal studies have demonstrated success with up to 90 minutes of no-flow (Safar et al,2002)Wu et al (2006) subjected dogs to rapid haemorrhage, and then used a 2℃ saline aorticflush to achieve a brain temperature of 10℃. e dogs remained on ice for 2 hours, andwere then revived on cardiopulmonary bypass.  Intact neurological outcome was achievedin 4 out of 6 dogs.

Andrews, Peter JD, et al. "Hypothermia for intracranial hypertension aer traumatic brain injury." NewEngland Journal of Medicine 373.25 (2015): 2403-2412.

Georgiou, A. P., and A. R. Manara. "Role of therapeutic hypothermia in improving outcome aer

traumatic brain injury: a systematic review." British journal of anaesthesia (2013): aes500.

Polderman, Kees H. "Application of therapeutic hypothermia in the ICU: opportunities and pitfalls of a

promising treatment modality. Part 1: Indications and evidence." Intensive care medicine 30.4 (2004):

556-575.

Seule, M., et al. "erapeutic hypothermia reduces middle cerebral artery flow velocity in patients with

severe aneurysmal subarachnoid hemorrhage." Neurocritical care 20.2 (2014): 255-262.

Gasser, Stefan, et al. "Long‐Term Hypothermia in Patients with Severe Brain Edema Aer Poor‐Grade

Subarachnoid Hemorrhage Feasibility and Intensive Care Complications." Journal of neurosurgicalanesthesiology 15.3 (2003): 240-248.

Karnatovskaia, Lioudmila V., et al. "Effect of prolonged therapeutic hypothermia on intracranial

pressure, organ function, and hospital outcomes among patients with aneurysmal subarachnoid

hemorrhage." Neurocritical care 21.3 (2014): 451-461.

Kim, Jong Youl, and Midori A. Yenari. "Hypothermia for treatment of stroke." Brain Circulation 1.1

(2015): 14.

Todd MM, Hindman BJ, Clarke WR, Torner JC; Intraoperative Hypothermia for Aneurysm Surgery

Trial (IHAST) Investigators. Mild intraoperative hypothermia during surgery for intracranial

aneurysm. N Engl J Med 2005;352:135-45.

Clark, Darren L., et al. "Comparison of 12, 24 and 48 h of systemic hypothermia on outcome aer

permanent focal ischemia in rat." Experimental neurology 212.2 (2008): 386-392.

Shankaran, Seetha, et al. "Whole-body hypothermia for neonates with hypoxic–ischemic

encephalopathy." New England Journal of Medicine 353.15 (2005): 1574-1584.

Shankaran, Seetha, et al. "Childhood outcomes aer hypothermia for neonatal encephalopathy." NewEngland Journal of Medicine 366.22 (2012): 2085-2092.

Azzopardi, Denis, et al. "Effects of hypothermia for perinatal asphyxia on childhood outcomes." NewEngland Journal of Medicine 371.2 (2014): 140-149.

Mourvillier, Bruno, et al. "Induced hypothermia in severe bacterial meningitis: a randomized clinical

trial." JAMA 310.20 (2013): 2174-2183.

Rim, Kwang Pil, et al. "Effect of therapeutic hypothermia according to severity of sepsis in a septic rat

model." Cytokine 60.3 (2012): 755-761.

Corry, Jesse J., et al. "Hypothermia for refractory status epilepticus." Neurocritical care 9.2 (2008): 189-

197.

Villar, Jesus, and Arthur S. Slutsky. "Effects of induced hypothermia in patients with septic adult

respiratory distress syndrome." Resuscitation 26.2 (1993): 183-192.

White, H. D., C. D. Spradley, and A. Hayek. "erapeutic Hypothermia For Refractory Hypoxia In

Acute Respiratory Distress Syndrome Undergoing Extracorporeal Membrane Oxygenation." Am JRespir Crit Care Med 191 (2015): A4570.

Zhicheng, Fang, et al. "Effect of mild hypothermia treatment on mechanical ventilation of acute

respiratory distress syndrome." Modern Journal of Integrated Traditional Chinese and WesternMedicine 29 (2012): 002.

Stravitz, R. Todd, et al. "erapeutic hypothermia for acute liver failure: toward a randomized,

controlled trial in patients with advanced hepatic encephalopathy." Neurocritical care 9.1 (2008): 90-96.

Jalan, Rajiv, et al. "Moderate hypothermia for uncontrolled intracranial hypertension in acute liver

failure." e Lancet 354.9185 (1999): 1164-1168.

Karvellas, C., et al. "A multicenter retrospective cohort analysis of therapeutic hypothermia in acute

liver failure." Critical Care 18.Suppl 1 (2014): P200.

Wu, Xianren, et al. "Induction of profound hypothermia for emergency preservation and resuscitation

allows intact survival aer cardiac arrest resulting from prolonged lethal hemorrhage and trauma in

dogs." Circulation 113.16 (2006): 1974-1982.

 

Deranged Physiology » Home » CICM Fellowship Exam » Past Papers » 2008, Paper 2 SAQs

Outline  the advantages and limitations of the various sites for measuring body temperature in

critically ill patients.

(You may tabulate your answer).

[ Hide Answer ]

Advantages Limitations

PAC Considered gold standard,

continuous measurement

Invasive, needs

a PA

catheter

Bladder Continuous measurement,

minimally invasive, stable measurements

regardless of urine flow rates

Costly, needs a

monitor for

display.

Rectal probe Intermient or continuous

measurements

Few tenths of

a degree

higher than

core

temperature,

intrusive, may

be difficult

with patient

positioning in

ICU, risk of

spread of

pathogens,

rectal trauma

Oesophageal Provide continuous readings Probe position

difficult to

confirm as

they are not

estion 8

always radio-

opaque, risk of

oesophageal

trauma or

perforation,

uncomfortable

in

spontaneous

or alert

breathing

patients

Tympanic Reflects hypothalamic and

core temperature.

Poor

agreement

with other

methods,

presence of

wax

or ear

pathology may

distort

measurements.

Nasopharyngeal Similar to oesophageal Sinusitis, can’t

be used in

BOS #.

Accuracy

depends on

position

Oral safe, convenient, and

familiarity

Needs

cooperative

patients,

presence of ET

and oro gastric

tubes may

limit this in

ICU patients,

mouth

breathing,

drinking hot

or cold fluids

may distort

measurements.

Forehead Dot technique, non-invasive Poor

agreement

with PAC

in ICU

patients,

intermient

Axillary Non-invasive Less than core

body

temperature,

intermient

data

e answer table from the college is a comprehensive response, and it is difficult to improve upon it

without a swamp of useless detail.

e key point is that the PA catheter is the gold standard, and everything else is measured against it.

e general trend can be described thus: the closer your probe gets to the heart, the more accurate

your measurement to the temperature of intracardiac blood.

It would make sense that intracardiac blood should be a good measure of body temperature, as the

blood has been circulating all around the body, exchanging heat everywhere. However, not all agree

that this is a valid viewpoint. Some have suggested that the beer temperature to be guided by is the

temperature of the hypothalamus, because it is the organ which is responsible for regulating

temperature.

Methods of Measuring Body Temperature in the ICU

Advantages Limitations

PAC Considered gold standard,continuous measurement

Invasive.PAC has a number of seriouscomplications associated with itsuse

Bladder Continuous measurement,minimally invasive,stable measurementsregardless of urine flowratesNot as accurate as PAC,but beer than rectal andsurface methods

Costly,needs a monitor for displaySource of infection

Rectal probe Intermient or continuous

measurements

Bacterial metabolism renders the

rectum slightly hoer than core

temperature

Invasive

Risk of traumatic insertion

Potential source of bacteraemia

Oesophageal Provide continuous readings Position-dependentRisk of oesophageal trauma

Not as accurate as PAC,

but beer than rectal and

surface methods

Uncomfortable

Tympanic Reflects hypothalamic and

core temperature.

Poor agreement with othermethodsEar canal obstruction or earpathology may distortmeasurements.

Nasopharyngeal Similar to oesophageal Risk of sinusitisContraindicated in base of skullfracturesPosition-dependentMay erroneously measure thetemperature fo the humidifiedgas in the ETT

Oral safe, convenient, and

familiar

Accurate - next best thing to

the PA catheter

Needs cooperative patientsPresence of ET and oro gastrictubes may limit this in ICUpatientsMouth breathing, drinking hotor cold fluids may distortmeasurements.

Forehead Dot technique, non-invasive Poor agreement with PAC in ICU patientsIntermient data

Axillary Non-invasive Less than core body temperatureIntermient data

Giuliano, Karen K., et al. "Temperature measurement in critically ill orally intubated adults: a

comparison of pulmonary artery core, tympanic, and oral methods." Critical care medicine 27.10 (1999):

2188-2193.

Lefrant, J-Y., et al. "Temperature measurement in intensive care patients: comparison of urinary

bladder, oesophageal, rectal, axillary, and inguinal methods versus pulmonary artery core

method." Intensive care medicine 29.3 (2003): 414-418.

NIERMAN, DAVID M. "Core temperature measurement in the intensive care unit." Critical care

medicine 19.6 (1991): 818-823.

WEBB, GEORGE E. "Comparison of esophageal and tympanic temperature monitoring during

cardiopulmonary bypass." Anesthesia & Analgesia 52.5 (1973): 729-733.

 

Deranged Physiology » Home » CICM Fellowship Exam » Past Papers » 2015, Paper 1 SAQs

Briefly discuss the information (including clinical features / investigations) that may help determine

the prognosis of patients following cardiac arrest.

[ Hide Answer ]

Prognostication aer cardiac arrest may be very difficult and involve a number of modalities.

It involves consideration of:

History

Underlying cause of the arrestCo-morbiditiesUse of therapeutic hypothermiaFeatures of the arrest – down time, CPR, ROSC

Clinical assessment

Timing:

Neurological assessment timing will be determined by the use of therapeutic hypothermia and the

duration and type of medication for sedation but is most reliably performed day 3 without therapeutic

hypothermia – probably day 5 with TH. Suggestion is to wait 72 hours aer return of normothermia.

With new TTM trial suggesting 36C then 72 hours post arrest may again be appropriate.

 

Examination:

Clinical – off sedation and neuromuscular blocking agents

Cranial nerve abnormalities – absence of pupillary response and corneal reflexes are bad prognostic

indicators.

Best Motor response at 72 hours with absent or extensor response associated with poor outcome.

Status / Generalised and repetitive myoclonus (as opposed to sporadic myoclonus)

Biochemical parameters

Neurone specific enolase >33mcg/L at days 1-3 indicates poor outcomeS100, CSF CKBB not accurate enough for prognostication

Electrophysiological features

EEG: generalised suppression, burst suppression or generalised periodic complexes strongly associated

with poor outcome.

estion 20

SSEPs: Bilateral absence of N20 component of SSEP with median nerve stimulation within 1-3 days is

strongly associated with poor outcome.

Imaging

 CT appearance – catastrophic changes with obvious pathology. Diffuse oedema has not been formally

assessed as an indicator.

MRI may be more sensitive

Predictors of beer outcome are:

Recovery of brainstem reflexes within 48 hours

Return of purposeful response within 24 hours

Hypothermia at the time of arrest

Young age

e tabulated summary below is based on the most recent ERC/ESICM statement (Sandroni et al,

2014). A vast and riduculous discussion of prognostication aer cardiac arrest is also carried out in the

Cardiac Arrest and Resuscitation section of this site.

Predictors of Poor Outcome in Comatose Survivors ofCardiac Arrest

Predictive sign orinvestigation

Predictive utility Confoundingfactors

Absent pupillary reflex  0% false positive rate at 72 hours,

irrespective of cooling

SedationHypothermiaParalysisPresence ofshockMetabolicderangements,eg. acidosis

Absent corneal reflex  0-15% false positive rate at 72 hours

Extensor motor response,or worse

May be associated with poor outcomes High falsepositive rate(~50%)

Myoclonic statusepilepticus

Persisting myoclonic status epilepticus hasa 0% false positive rate within the first 24hours

Interpreter-dependentFindings maybe subtleParalysisinterfereswithinterpretation

Somatosensory evokedpotentials: absence of the N20component

Absence of N20 predicts poor outcome witha0% false positive rate.

Presence of N20 does not rule out a poor

outcome.

N20 responses

may disappear

on repeat

testing.

N20 responses

may reappear,

but this does not

suggest a good

prognosis.

Burst suppression on EEG May be associated with poor outcome  Poor predicitivevalue;  cannot be usedforprognostication.

Absence of EEG reactivity Low false positive rate (0-5%) Confounded bysedation

Neuron-specific enolase NSE over 33μg/L at 1-3 days post CPRpredicts poor outcome with a 0% falsepositive rate

NSE may be

elevated for

reasons other

than brain

injury; for

instance, it may

be secreted by

neuroendocrine

tumours

CT brain On CT, an inversed gray/white maer ratioin Hounsfield units was found in patientswho failed to awaken aer cardiacresuscitation. However, the predictive valueof CT findings is not known

If performed too

early, the CT

may not

demonstrate any

findings.

Engdahl, Johan, et al. "Can we define patients with no and those with some chance of survival when

found in asystole out of hospital?." e American journal of cardiology 86.6 (2000): 610-614.

Bunch, T. Jared, et al. "Outcomes and in-hospital treatment of out-of-hospital cardiac arrest patients

resuscitated from ventricular fibrillation by early defibrillation." Mayo Clinic Proceedings. Vol. 79. No.

5. Elsevier, 2004.

Levine, Robert L., Marvin A. Wayne, and Charles C. Miller. "End-tidal carbon dioxide and outcome of

out-of-hospital cardiac arrest." New England Journal of Medicine 337.5 (1997): 301-306.

Rea, omas D., et al. "Temporal Trends in Sudden Cardiac Arrest A 25-Year Emergency Medical

Services Perspective." Circulation 107.22 (2003): 2780-2785.

Carew, Heather T., Weiya Zhang, and omas D. Rea. "Chronic health conditions and survival aer

out-of-hospital ventricular fibrillation cardiac arrest." Heart 93.6 (2007): 728-731.

Goldberger, Zachary D., et al. "Duration of resuscitation efforts and survival aer in-hospital cardiac

arrest: an observational study." e Lancet (2012).

Wijdicks, E. F. M., et al. "Practice Parameter: Prediction of outcome in comatose survivors aer

cardiopulmonary resuscitation (an evidence-based review) Report of the ality Standards

Subcommiee of the American Academy of Neurology."Neurology 67.2 (2006): 203-210.

Rogove, Herbert J., et al. "Old age does not negate good cerebral outcome aer cardiopulmonary

resuscitation: analyses from the brain resuscitation clinical trials."Critical care medicine 23.1 (1995):

18-25.

LEVY, DE, et al. "Predicting Outcome from Hypoxic-Ischemic Coma." Survey of Anesthesiology 30.2

(1986): 93.

Sandroni, Claudio, et al. "Prognostication in comatose survivors of cardiac arrest: an advisory

statement from the European Resuscitation Council and the European Society of Intensive Care

Medicine." Resuscitation 85.12 (2014): 1779-1789.

 

Deranged Physiology » Home » CICM Fellowship Exam » Past Papers » 2014, Paper 2 SAQs

a) What are short-latency (N20) somatosensory evoked potentials (SSEPs)?

b) Describe how SSEPs can be used for prognostication in patients with hypoxic-ischaemic brain

injury.

c) Explain whether, and if so how, induced hypothermia impacts on the validity of SSEP results.

[ Hide Answer ]

a)

Evoked potentials are the electrical signals generated by the nervous system in response to sensory

stimuli.

Somatosensory evoked potentials (SSEPs) consist of a series of waves that reflect sequential

activation of neural structures along the somatosensory pathways.

Somatosensory evoked potentials are usually derived from the median nerve and the tibial nerve

SSEP components typically are named by their polarity and typical peak latency in the normalb

population. N20 is a negativity that typically peaks at 20 milliseconds aer the stimulus.

b)

SSEP is the most reliable test to predict poor outcome in this patient group.

SSEP does not predict good outcome.

Pre-test probability for poor outcome essential: use test only in patients who remain unconscious

following hypoxic-ischaemic insult (M score ≤ 3).

Validated to use as early as 24 hours aer cardiac arrest.

SSEP not influenced by sedatives, analgesics, paralysing agents or metabolic insults.

Bilaterally absent short latency peaks (N20 peaks) have 100% predictive value for poor outcome

(death or severe disability), with false positive rate nearly 0% and narrow confidence intervals.

c)

Hypothermia affects SSEP test results: mainly delayed peaks (prolongation conduction times);no

consistent effect on voltages (amplitudes).

Aer rewarming of the patient SSEPs have comparable test characteristics as compared with studies

done before therapeutic hypothermia and as such have been validated for prognostication following

hypoxic-ischaemic brain injury aer rewarming with similar low false positive rate.

estion 11

Peripheral nerve stimulation should evoke a central response even in the presence ofsedation or hypothermiae absence of such a response suggests severe damage to the cortexBilateral absence of response suggests global rather than focal damageErgo, SSEP should act as sensitive diagnostic tool to detect severe brain injury aer cardiacarrest

Both median nerves are stimulated at the wrist with a bipolar surface electrodeAlternative site is the tibial nerveStimulus repeats at 2-5 Hz, with a duration of 0.2msecSurface electrodes read cortical activity at the scalpEvoked potentials are peaks of electrical activity which follow the peripheral stimulus witha predictable latency.e responses are named aer their polarity (N for negative, P for positive) and theirlatency.N20 indicates a negative response over primary somatosensory cortex at ∼20 ms poststimulation.

Non-invasivePortableLess confounded by sedation or hypothermia than EEG (in fact, not influenced bysedatives, analgesics, paralysing agents or metabolic insults)Bilaterally absent N20 SSEP during hypothermia is a good predictor for absent N20SSEP aer rewarming, which means you can do SSEPs during the period of hypothermia(Bouwes et al, 2010)ReproduceableInterpretation is guided by specific criteria, rather than subjective expertise.

Bilaterally absent short latency peaks (N20 peaks) have 100% predictive value for pooroutcome (death or severe disability), with false positive rate nearly 0% and narrowconfidence intervals.Recent (2014) consensus statement on prognostication following cardiac arrest suggestedthat SSEPs are prognostic at > 72 hours in cooled patients and at >24 hours in non-cooledpatientsAmong a total 287 patients with bilaterally absent N20 SSEPs, only one was a false positiveresult (Young et al, 2005)Post hoc analysis by independent interpreters has suggested that the false positive wassimply interpreted inaccurately in the first instance.

Guérit, J-M., et al. "Consensus on the use of neurophysiological tests in the intensive care unit (ICU):

electroencephalogram (EEG), evoked potentials (EP), and electroneuromyography

(ENMG)." Neurophysiologie Clinique/Clinical Neurophysiology 39.2 (2009): 71-83.

Tjepkema-Cloostermans, Marleen Catharina, J. Horn, and M. J. A. M. Puen. "e SSEP on the ICU:

Current applications and pitfalls." Netherlands journal of critical care 17.1 (2013): 5-9.

 

Rationale for the use of somatosensory evoked potentials in the comatose survivor of cardiac arrest

Practice of somatosensory stimulation and evoked potential measurement

Advantages of somatosensory evoked potentials

Evidence supporting the prognostic value of SSEPs

Deranged Physiology » Home » CICM Fellowship Exam » Past Papers » 2012, Paper 2 SAQs

With regards to the determination of brain death:

a) Apart from identifying evidence of sufficient intracranial pathology, list the preconditions that must

be met prior to the determination of brain death by clinical criteria:

b)What is the recommended minimum time for observation in cases of hypoxic-ischaemic brain injury,

prior to performing clinical testing of brain-stem function?

c)For each of the following brainstem reflexes, list the cranial nerves that are tested:

a. Cough reflex

b. Vestibulo-ocular reflex

c. Pupilary light reflex

d. Corneal reflex

e. Gag reflex

d) List three contraindications to performing apnoea testing:

e) List the acceptable imaging techniques that may be used to demonstrate brain death as an

alternative to clinical testing as recommended by the ANZICS Statement on Death and Organ

Donation.

[ Hide Answer ]

a)

Minimum period of 4 hours in which the patient is observed to have unresponsive coma,unreactive pupils, absent cough/tracheal reflex and no spontaneous respiratory effortNormothermia (temp >35oC)Normotension (SBP >90 mmHg, MAP >60 mmHg in adult)Exclusion of sedative drugsAbsence of severe electrolyte, metabolic or endocrine disturbanceIntact neuromuscular functionAbility to examine the brainstem reflexes including at least one ear and one eyeAbility to perform apnoea testing

estion 17

b)

24 hours

c)

a. Cough reflex cranial nerve X

b. Vestibulo-ocular reflex cranial nerve III,IV,VI,VIII

c. Pupilary light reflex cranial nerve II & III

d. Corneal reflex cranial nerve V & VII

e. Gag reflex cranial nerve IX & X

(for each part of this question ALL cranial nerves are required in order to receive the 5 marks, nomarks should be given for an incomplete response)

d)

1. 1. Concomitant high cervical cord injurySevere hypoxaemiaHaemodynamic instability

e)

Four vessel intra-arterial catheter angiography with digital subtraction (preferred)Radionuclide imaging with Tc-99m HMPAO and single photon emission computerisedtomography (SPECT) (preferred)CT angiography (limited experience to date) (acceptable)

is question tests the candidate's detailed knowledge of the ANZICS Statement on Death and Organ

Donation (I have linked to Version 3.2, from 2013).

a) Apart from identifying evidence of sufficient intracranial pathology, list the preconditions that must

be met prior to the determination of brain death by clinical criteria:

e below answer is taken directly from the Statement.

NormothermiaNormotensionExclusion of the effects of sedating drugsAbsence of severe electrolyte, metabolic or endocrine disturbanceIntact neuromuscular functionAbility to adequately examine brainstem reflexesAbility to perform apnoea testing

b)What is the recommended minimum time for observation in cases of hypoxic-ischaemic brain injury,

prior to performing clinical testing of brain-stem function?

Again, quoting ANZICS:

"ere must be a minimum of four hours observation and mechanical ventilation during whichthe patient has unresponsive coma "

c)For each of the following brainstem reflexes, list the cranial nerves that are tested:

a. Cough reflex Vagus (CN X)

b. Vestibulo-ocular reflex CN III, IV, VI, and VIII

c. Pupilary light reflex CN II, CN III

d. Corneal reflex CN V, CN VII

e. Gag reflex CN IX, CN X

In this list the college have omied the test for pain in the trigeminal nerve distribution (CN V and VII)

d) List three contraindications to performing apnoea testing:

Hemodynamic instabilitySevere hypoxic respiratory failureHigh cervical cord injury

e presence of any brainstem reflexes is also a contraindication. Apnoea testing must be carried out

only aer the brainstem reflexes have been tested, and if any of them were found to be positive any

further braindeath testing cannot continue.

e) List the acceptable imaging techniques that may be used to demonstrate brain death as an

alternative to clinical testing as recommended by the ANZICS Statement on Death and Organ

Donation.

Four-vessel digital subtraction arterial angiographyTc-99m HMPAO (technetium 99m radiolabelled hexamethyl propylene amine oxime)SPECTCT angiography

ANZICS Death and Organ Donation Commiee, THE ANZICS STATEMENT ON DEATH AND

ORGAN DONATION Edition 3.2 2013

 

Deranged Physiology » Home » CICM Fellowship Exam » Past Papers » 2009, Paper 1 SAQs

. Prior to the determination of brain death by clinical examination,

a)  list the preconditions that must be met before formal testing can begin

b)  What are the indications for ancillary tests for brain death (ie tests that demonstrate the absence of

intracranial blood flow)?

c)  What are the 2 imaging techniques  currently recommended by ANZICS for determining the

absence of intracranial blood flow:

[ Hide Answer ]

Preconditions

a) A known cause of coma (check terminology in new ANZICS guidelines)

b) Minimum of 4 hour period observation

c) neuro-imaging consistent with acute brain pathology which could result in brain death;

d) temperature > 35C;

e) normotension (as a guide, systolic blood pressure > 90 mmHg, mean arterial pressure (MAP) >

60 mmHg in an adult);

) exclusion of effects of sedative drugs: the time taken for plasma concentrations of sedative drugs to

fall below levels with clinically significant effects depends on

the dose and pharmacokinetics of drugs used, and on hepatic and renal function. If there is any doubt

about the persisting effects of opioids or benzodiazepines, an appropriate drug antagonist should be

administered;

g) absence of severe electrolyte, metabolic or endocrine disturbances. ese include marked

derangements in plasma concentrations of glucose, sodium, phosphate or magnesium, liver and renal

dysfunction and severe endocrine dysfunction;

h) intact neuromuscular function. If neuromuscular-blocking drugs have been administered, a

peripheral nerve stimulator or other recognised method (e.g. electromyography) should always be used

to confirm that neuromuscular conduction is normal;

What are the indications for ancillary tests for brain death?

°     Inability to adequately examine the brain-stem reflexes. It must be possible to examine at least one

ear and one eye;

°     Inability to perform apnoea testing. is may be precluded by severe hypoxic respiratory failure or

estion 28

a high cervical spinal cord injury.

What are the 2 imaging techniques  currently recommended by ANZICS for determining the absence

of intracranial blood flow:

Four vessel intra-arterial catheter angiography, with digital subtraction; Tc-99 HMPAO SPECT

radionuclide imaging

CT angio with certain caveats may be acceptable. Do not recommend MR angio

is question resembles several other questions in the past papers:

estion 17 from the second paper of 2012 and estion 12.1 from the second paper of2010 ask about pre-conditions for brain death testing.estion 12.2 from the second paper of 2010 discusses imaging modalities to assess theintracranial blood flow.

e pre-conditions for clinical brain death testing are:

Normothermia (over 35 degrees)Normotension( MAP >60)Not sedatedNot paralyzedNot in a state of electrolyte or metabolic derangement (eg. hypoglycaemia)Possessing at least one intact eye and one ear (to examine brainstem reflexes)Able to breathe (to test for apnoea; i.e. high C-spine injury may disqualify you)Unresponsive comaA suitable explanation for why the patient is comatose, which would be consistent withthe diagnosis of brain death

Otherwise, this current paper asks one original question: when must one resort to imaging?

Well. e ANZICS Statement on Death and Organ Donation suggests several distinct scenarios when

one cannot perform clinical brain death testing:

Inability to adequately examine the brain-stem reflexes:

One ear and one eye are not intactSedation, hypothermia, paralysis

Inability to perform apnoea testing:

Severe hypoxic respiratory failureHigh cervical spinal cord injury

ANZICS Death and Organ Donation Commiee, THE ANZICS STATEMENT ON DEATH AND

ORGAN DONATION Edition 3.2 2013

 

Deranged Physiology » Home » CICM Fellowship Exam » Past Papers » 2012, Paper 1 SAQs

Outline the Intensive Care management of a 25-year-old male who has fulfilled brain death criteria and

is awaiting surgery for organ donation.

[ Hide Answer ]

College Answer

Temperature Maintenance:

Hypothermia is common due to: cold fluids, heat loss through exposure, inability tovasoconstrict or shiver, reduced metabolic rate.

Maintain normal core temperature

Cover patientWarm roomWarming blanketWarm fluids especially high volumeHumidification

Respiratory support:

Aim to avoid fluid overload

Aim for adequate Sp02 and normocarbia with lowest Fi02 and limit tidal volumes

Bronchoscopy for persisting collapse

Chest physiotherapy may be helpful

Circulatory Support:

Immediately prior to brain death there is oen a period of sympathetic hyperactivity with associated

tachycardia and hypertension. is is lost following brain death commonly resulting in vasodilation

and hypotension

Maintain adequate mean arterial pressure. Use judicious volume expansion and low doseinotropes (usually noradrenaline)

Monitor peripheral perfusion and urine output regularly

Continue maintenance fluids

Metabolic haematology and biochemistry:

Diabetes insipidus is common and if not recognized and treated can quickly lead to hypernatraemia

and hyperosmolality

Measure electrolytes and creatinine regularly and treat as appropriate to maintain normalranges

Treat Diabetes insipidus with desmopressin (DDAVP) 4-8µgrams intravenously and repeatif necessary, or low dose vasopressin

estion 1

Start low dose insulin infusion if blood glucose persistently above 12mmol/L

Stop bleeding, correct coaguloapthy, thrombocytopaenia and anaemia

Avoid hypernatraemia

Other electrolyte abnormalities – K, PO4, Ca, MgConsider thyroxine replacement

Communication:

Family - counsel, explain, keep updated

Liaison with donor coordinator and surgical retrieval teams

 

Discussion

is is a straightforward question about the care of the brain-dead organ donor. A summary exists on

this site, which was derived directly from the recent ANZICS guidelines. If one were to rearrange the

answer to fit some sort of primitive alphabetical template, it could resemble this:

Non-clinical issues: (presumably, these have been dealt with now that the patient is "awaiting surgery

for organ donation"

Early involvement of the transplant coordinatorNon-coercive sensitive family discussion re opportunity for donationTissue typing, viral screen, further organ function testsFacilitate family time at bedsideEnsure aercare of donor family

A. e circuit should be humidified.B. Normoxia and normocapnea must be maintained.

ere will be periodic requests for ABGs on 100% FiO2 from the donor coordinator, butaerwards the FiO2  must be minimised to prevent oxidative stress damage to the lungs.

C. Haemodynamic instability is to be expected: - e initial autonomic storm should be managed with nitroprusside and esmolol - e subsequent collapse should be treated with noradrenaline and/or vasopressin - Bradycardia will be resistant to atropine (no vagus to block); catecholamines or pacingwill be required -ough they do not make a direct statement to this effect, ANZICS tacitly support CPR inthe brain-dead organ donor; "cardiopulmonary resuscitation may result in recovery ofcardiac function and successful transplantation".

D. Normoglycaemia must be maintained.E. Normothermia must be maintained by warming externally, and by using warmed fluids.

Electrolytes need to be maintained within normal laboratory ranges; particular aention needs to be paid to the sodium. DDAVP may be required as a hormone replacement. Other "endocrine support" (T3, hydrocortisone) should be considered in the followingcircumstances: - haemodynamic instability - an ejection fraction of less than 45% - heart donation is being considered

F. Fluid resuscitation should be conservative if you plant to donate lungs,  aggressive if youplan to donate kidneys, and an intelligent compromise if both organs are being considered.

G. Nutrition must continue. Good nutrition (or rather, the absence of malnutrition) has been associated with improvedra function (Singer et al, 2005)

H. Coagulopathy must be observed and corrected; if worsening coagulopathy or DIC develop,organ retrieval should be expedited.

References: 

Summarized from the ANZIC statement on Brain Death and Organ Donation, Version 3.2

Dujardin, Karl S., et al. "Myocardial dysfunction associated with brain death: clinical,

echocardiographic, and pathologic features." e Journal of heart and lung transplantation 20.3

(2001): 350-357.

Totsuka, Eishi, et al. "Influence of high donor serum sodium levels on early postoperative gra

function in human liver transplantation: effect of correction of donor hypernatremia." LiverTransplantation and Surgery 5.5 (1999): 421-428.

Novitzky, D., D. K. C. Cooper, and B. Reichart. "Hemodynamic and metabolic responses to hormonal

therapy in brain-dead potential organ donors." Transplantation 43.6 (1987): 852-854.

Phongsamran, Paula. "Critical care pharmacy in donor management." Progress in Transplantation 14.2

(2004): 105-113.

RANDELL, TARJA T., and KRISTER AV HöCKERSTEDT. "TRIIODOTHYRONINE TREATMENT IN

BRAIN-DEAD MULTIORGAN DONORS-A CONTROLLED STUDY." Transplantation 54.4 (1992): 736-

737.

Goarin, Jean-Pierre, et al. "e effects of triiodothyronine on hemodynamic status and cardiac function

in potential heart donors." Anesthesia & Analgesia 83.1 (1996): 41-47.

Follee, David M., Steven M. Rudich, and Wayne D. Babcock. "Improved oxygenation and increased

lung donor recovery with high-dose steroid administration aer brain death." e Journal of heart andlung transplantation: the official publication of the International Society for Heart Transplantation17.4 (1998): 423-429.

Lisman, T., et al. "Activation of hemostasis in brain dead organ donors: an observational study."

Journal of rombosis and Haemostasis 9.10 (2011): 1959-1965.

Lim, H. B., and M. Smith. "Systemic complications aer head injury: a clinical review." Anaesthesia 62.5

(2007): 474-482.

Dalle Ave, Anne L., Dale Gardiner, and David M. Shaw. "Cardio‐pulmonary resuscitation of brain‐dead

organ donors: a literature review and suggestions for practice." Transplant International (2015).

Singer, Pierre, Haim Shapiro, and Jonathan Cohen. "Brain death and organ damage: the modulating

effects of nutrition." Transplantation 80.10 (2005): 1363-1368.