Predicting neurological recovery post cardiac arrest

CLINICAL

-Myoclonic status from day 1 suggests no chance of neuro recovery (unless arrested from respiratory cause, or Lance-Adams syndrome - conscious with intentional myoclonus)

-Poor prognosis if 72hr post arrest:
-Absent pupillary / corneal reflexes

GCS< 4
But invalidated by therapeutic hypothermia (TH)
Poor prognosis after TH if GCS < 4 after 4 days off sedation

Confounding factors to assessment:

Organ failure - cardiac/hepatic/renal
Sedative drugs, muscle relaxants
Therapeutic hypothermia- slows drug clearance

ELECTROPHYSIOLOGICAL

- EEG

Always poor outcome if isoelectric in week 1
Generalised suppression and burst suppression poor signs
May reveal sub clinical seizures (can treat)

- BIS

Poor prognosis if BIS <22 or BSR > 48 (in cooled patients after 1st dose muscle relaxant)
But not reliable - incorrect in 10%

- Somatosensory evoked potential (SSEP)

Most reliable of EP tests
Absent N2O signal in primary somatosensory cortex bilaterally = poor prognosis (after ensuring PNS intact)

RADIOLOGICAL - CT

Exclude massive intracerebral catastrophe
Not evidence for prognostic value from loss grey-white differentiation on early CT

BIOCHEMICAL

All still research-based, not yet commercial in UK
Markers of cerebral damage
Blood and CSF neurone-specific enolase (NSE)
S-100 beta protein (from astrocytes) - insufficient evidence

RAISED ICP

Insufficient evidence as yet, possibly poor prognosis

OVERALL

-Still many uncertainties in prognostication
-SSEP may be best current, but not yet widely used

Scoring systems

Link: coma_clinician.pdf

Prognosis:

PAR (prognosis after resuscitation) score
OHCA score
Brain arrest neurological outcome scale (BrANOS) - based on arrest duration, CT and GCS. Not yet validated in therapeutic hypothermia.

Outcome:

Cerebral performance category ( 1= independent, can work. 5 = dead)
Glasgow Outcome Scale (1= dead, 5 = independent)

May be better outcomes with shorter no flow and low flow times, and initial rhythm VF/VT

BUT insufficiently reliable as prognostic factors

Then further injury when brain reperfused post arrest

ATP regenerated, free radicals formed
Apoptosis, cell necrosis
Disordered autoregulation
Cerebral oedema

Secondary cerebral injury

Therapeutic hypothermia (or ?avoiding hyperthermia) may reduce secondary cerebral injury

Brain rapidly affected by circulatory arrest

Unconsciousness < 20 secs (hypoxia)
Glucose and ATP stores eliminated < 5 min, resulting in disordered cellular calcium homeostasis / free radicals / protease release / onset of cell death