Prognosis After Cardiac Arrest

Reviewed and revised 26 January 2014

OVERVIEW

Prognosis involves consideration of:

  • the underlying cause of cardiac arrest (e.g. overdose vs dilated cardiomyopathy)
  • presence of co-morbidities (e.g. metastatic cancer, dementia)
  • use of targeted temperature management (therapeutic hypothermia)
  • features of the the cardiac arrest and cardiovascular assessment
  • neurological assessment

NEUROLOGICAL ASSESSMENT

Clinical

  • no sedation or neuromuscular blocking agents required (poor sign)
  • pupillary response to light at 72h (absent = poor sign)
  • corneal reflex at 72h (absent = poor sign)
  • best motor response at 72h (absent or extensor response = poor sign)
  • presence of myoclonic status epilepticus (MSE)
    • Generalised and repetitive myoclonus is strongly associated with poor outcome, with a reported false positive rate of 0%.
    • Conversely, single seizures and sporadic myoclonus, do not accurately predict poor outcome.

Biochemical evidence of damage (neurone specific enolase, protein S-100, CSF CKBB)

  • NSE: Serum neuron-specific enolase levels > 33 microg/L at days 1-3 strongly associated with poor outcome
  • S100, CSF CKBB:  not considered accurate enough for prognostication.

Electrophysiological evidence of damage (EEG, SSEPs)

  • EEG: EEG patterns of generalised suppression, burst suppression, or generalised periodic complexes are strongly associated with poor outcome, but the prognostic accuracy is not considered as high as SSEP
  • SSEPs: Bilateral absence of N20 component of SSEP with median nerve stimulation within 1-3 days post CPR is strongly associated with poor outcome.

Imaging (CT/ MRI brain)

  • Imaging may reveal catastrophic intracerebral cause for the arrest.
  • Diffuse swelling on CT scan is common, but predictive power not known
  • role of MRI/PET also unclear

CARDIOVASCULAR ASSESSMENT

Cardiovascular factors are much less useful than neurological assessment

  • response to therapy
  • witnessed?
  • downtime (time to return of spontaneous circulation < 10min)
  • whether CPR performed, delay to CPR and quality of CPR
  • shockable (better) or non-shockable rhythm (worse)
  • successful revascularisation of STEMI (if underlying cause)
  • EF (less -> poor prognostic sign)

CONFOUNDING FACTORS

  • Induced Hypothermia – majority of studies carried out before induced hypothermia widely used. Evidence that cooling may alter interpretation of these results, but to what extent remains unclear
  • Time of assessment: Period of at least 72 hours post CPR recommended. Unclear how hypothermia effects this.
  • CT scan done too early may not show changes
  • Sedatives and neuro- muscular blockers
  • Metabolic derangements
  • Presence of shock
  • Organ failure
  • Role of “self-fulfilling prophecy” in interpreting studies

AAN GUIDELINES

AAN Guidelines 2006 state:

  • “Pupillary light response, corneal reflexes, motor responses to pain, myoclonus status epilepticus, serum neuron-specific enolase, and somatosensory evoked potential studies can reliably assist in accurately predicting poor outcome in comatose patients after cardiopulmonary resuscitation for cardiac arrest.”
  • “Prognosis cannot be based on the circumstances of CPR.”
  • “Burst suppression or generalized epileptiform discharges on EEG predicted poor outcomes but with insufficient prognostic accuracy”
  • “These predictors may be confounded by therapeutic hypothermia”

Predictors of poor prognosis

  • absent pupillary response at 72 hours
  • absent corneal reflex at 72 hours
  • no motor response or extension to pain at 72 hours (i.e. worse than flexion)
  • myoclonic status epilepticus (MSE); ie. generalized myoclonic convulsions in face and extremities and continuous for a minimum of 30 min
  • bilateral absence of cortical SSEPs (N20 response) at 1 to 3 days
  • serum neuron-specific enolase >33 μg/L at 1 to 3 days

Less useful:

  • no CPR for > 8 minutes
  • time to ROSC > 30 minutes
  • duration of anoxic coma > 72 hours
  • Burst suppression or generalized epileptiform discharges on EEG

Predictors of better prognosis:

  • recovery of brainstem reflexes within 48 hours (papillary, corneal, oculocephalic)
  • return of purposeful response within 24 hours
  • primary pulmonary event leading to hypoxaemia
  • hypothermia at time of arrest (emersion)
  • young age

THERAPEUTIC HYPOTHERMIA

  • has potential to confound prognostication
  • AAN 2006 guidelines were largely based on studies from the pre-therapeutic hypothermia era
  • appropriate approach remains controversial
  • a conservative approach is to delay prognostication until 72 hours post-normothermia (i.e. after rewarming)
  • This will be come less of an issue if (as expected) T36C is widely adopted as the target for post-arrest care in the wake of the TTM trial

NEUROLOGICAL PROGNOSTICATION PROTOCOL USED IN THE TTM TRIAL

The TTM trial (Nielsen et al, 2013) used a standardised protocol for neurological prognostication to guide decisions regarding treatment withdrawal following targeted temperature management post-cardiac arrest:

  • All patients in the trial were actively treated until a minimum 72 hours after the intervention period, i.e. after rewarming, when neurological evaluation was done on patients not regaining consciousness.

Exceptions from this rule were

  1. patients with myoclonus status in the first 24 hours after admission and a bilateral absence of N20-peak on median nerve somatosensory evoked potentials (SSEP)
  2. patients who became brain dead due to cerebral herniation, and
  3. because of ethical reasons described below.

At that time-point, limitations in and withdrawal of therapy could be instituted by the treating physicians. The neurological evaluation was based on:

  • clinical neurological examination (including Glasgow Coma Scale (GCS), pupillary and corneal reflexes)
  • SSEP and electroencephalogram (EEG)
  • Biomarkers for brain damage were not used for operational prognostication

Findings allowing for discontinuation of active intensive care:

  • Brain death due to cerebral herniation
  • Severe myoclonus status in the first 24 hours after admission and a bilateral absence of N20-peak on median nerve SSEP
  • Minimum 72 hours after the intervention period: persisting coma with a Glasgow Motor Score 1-2 and bilateral absence of N20-peak on median nerve SSEP.
  • Minimum 72 hours after the end of the intervention period: persisting coma with a Glasgow Motor Score 1-2 and a treatment refractory status epilepticus (see TTM trial supplement for definition)

Patients with Glasgow Motor Score 1-2 at 72 hours or later who had retained N20-peak on the SSEP, or patients in hospitals where SSEP was not  available were:

  • re-examined daily
  •  the limitations/withdrawal of intensive care considered if GCS-Motor did not improve and metabolic and pharmacological affection was ruled out

Active treatment could be withdrawn prior to 72 hours after the intervention period for ethical  reasons

  • for instance: previously unknown information about disseminated end-stage cancer  or refractory shock with end-stage multiorgan failure
  • However assumptions of a poor  neurological function were not allowed be the sole reason for withdrawal of active treatment  prior to 72 h after the intervention period (exception: brain death and early myoclonus status including a negative SSEP)

AN APPROACH

  • perform TTM at T36C for cardiac arrest survivors
  • prognosticate at day 5 post-cardiac arrest
  • use the protocol as otherwise described in the TTM trial

References and Links

LITFL

Journal articles

  • Friberg H, Rundgren M, Westhall E, Nielsen N, Cronberg T. Continuous evaluation of neurological prognosis after cardiac arrest. Acta Anaesthesiol Scand. 2013 Jan;57(1):6-15. doi: 10.1111/j.1399-6576.2012.02736.x. Epub 2012 Jul 26. Review. PubMed PMID: 22834632. [Free Full Text]
  • Nielsen N, et al; the TTM Trial Investigators. Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest. N Engl J Med. 2013 Nov 17. [Epub ahead of print] PubMed PMID: 24237006. [Free Full Text]
  • Oddo M, Rossetti AO. Predicting neurological outcome after cardiac arrest. Curr Opin Crit Care. 2011 Jun;17(3):254-9. doi: 10.1097/MCC.0b013e328344f2ae. Review. PubMed PMID: 21346563.
  • Rossetti AO, Oddo M, Logroscino G, Kaplan PW. Prognostication after cardiac arrest and hypothermia: a prospective study. Ann Neurol. 2010 Mar;67(3):301-7. doi: 10.1002/ana.21984. PubMed PMID: 20373341.
  • Thömke F. Assessing prognosis following cardiopulmonary resuscitation and therapeutic hypothermia-a critical discussion of recent studies. Dtsch Arztebl Int. 2013 Mar;110(9):137-43. doi: 10.3238/arztebl.2013.0137. Epub 2013 Mar 1. PubMed PMID: 23533554; PubMed Central PMCID: PMC3601284.
  • Wijdicks EF, Hijdra A, Young GB, Bassetti CL, Wiebe S; Quality Standards Subcommittee of the American Academy of Neurology. Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2006 Jul 25;67(2):203-10. Review. PubMed PMID: 16864809. [Free Full Text]

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

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