Briefly discuss the information (including clinical features / investigations) that may help determine the prognosis of patients following cardiac arrest.
Prognostication after cardiac arrest may be very difficult and involve a number of modalities.
It involves consideration of:
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 after return of normothermia.
With new TTM trial suggesting 36C then 72 hours post arrest may again be appropriate.
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)
EEG: generalised suppression, burst suppression or generalised periodic complexes strongly associated with poor outcome.
SSEPs: Bilateral absence of N20 component of SSEP with median nerve stimulation within 1-3 days is strongly associated with poor outcome.
CT appearance – catastrophic changes with obvious pathology. Diffuse oedema has not been formally assessed as an indicator.
MRI may be more sensitive
Predictors of better outcome are:
Recovery of brainstem reflexes within 48 hours
Return of purposeful response within 24 hours
Hypothermia at the time of arrest
The tabulated summary below is based on the most recent ERC/ESICM statement (Sandroni et al, 2014). A vast and riduculous discussion of prognostication after cardiac arrest is also carried out in the Cardiac Arrest and Resuscitation section of this site.
|Predictive sign or investigation||Predictive utility||Confounding factors|
|Absent pupillary reflex||
0% false positive rate at 72 hours, irrespective of cooling
|Absent corneal reflex||0-15% false positive rate at 72 hours|
|Extensor motor response, or worse||May be associated with poor outcomes||
|Myoclonic status epilepticus||Persisting myoclonic status epilepticus has a 0% false positive rate within the first 24 hours||
|Somatosensory evoked potentials:
absence of the N20 component
|Absence of N20 predicts poor outcome with a0% 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 predicitive value;
cannot be used for prognostication.
|Absence of EEG reactivity||Low false positive rate (0-5%)||Confounded by sedation|
|Neuron-specific enolase||NSE over 33μg/L at 1-3 days post CPR predicts poor outcome with a 0% false positive 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 matter ratio in Hounsfield units was found in patients who failed to awaken after cardiac resuscitation. However, the predictive value of CT findings is not known||
If performed too early, the CT may not demonstrate any findings.
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