Prognostication after OOHCA

Stuart Lane

Background

• Outcomes from cardiac arrest are poor

• Usually significant neurological sequalae if the patient survives

• Prognostication is difficult• It is a core business for ICM• An obsession with 72 hours being the

time to prognosticate

What are the useful parameters?

• Absent pupillary light or corneal reflex at 72 hours

• Extensor or no response to central painful stimuli at 72 hours

• Myoclonic status epilepticus (MSE)• Bilateral absent cortical responses on

Somatosensory evoked potentials at 72 hours

• Serum neuron-specific enolase > 33µgl-1

Pupil & corneal reflexes at 72hrs

• Very rarely completely absent unless patient– Brain dead– Not officially brain dead– Obviously a poor prognosis

• Levy JAMA 1985– Almost 30 years old

• These parameters predated the widespread use of therapeutic hypothermia

Extensor or no response to central painful stimuli at 72 hours

• GCS not validated outside TBI• Huge variation in clinicians interpretation of

GCS motor score– The GCS, especially motor score is done very

badly in the CICM fellowship exam

• Significant proportion of patients with m=2 whose outcome is not poor

• Use of long-acting sedatives when renal function has been impaired and TH been used

• Remi and propofol better?

Myoclonic status epilepticus (MSE)

• MSE after a circulatory arrest on day 1 is a poor prognostic sign

• Seen less frequently due to TH and paralysis• What about the Lance-Adams Sydrome?

• Was actually cardiac arrest and airway obstruction• Evidence that hypoxia is not so bad as ischaemia and

hypoxia• Usually is intention myoclonus after 48 hours• The history usually gives the story

• Overdiagnosis if outlook is poor is bad• Underdiagnosis if outlook is good is bad• History and clinical examination

SSEP’s

• Bilateral absence of the N20 component of the SSEP with median nerve stimulation recorded on days 1 to 3 or later after CPR accurately predicts a poor outcome.

• Not usually available at many institutions• Timing is unclear• Not usually completely absent• EEG’s fare worse

• Are more affected by drugs / metabolism• Burst suppression or generalised epileptiform activity are

poor prognostic signs• Little accuracy

Serum neuron-specific enolase > 33µgl-1

• Levels quoted are before the advent of TH

• TH can lower the NSE level compared to non-TH patients in OOHCA

• Does this just demonstrate decreased neuronal injury because of TH

• Needs validation

Others

• Neuroimaging not helpful• But we do this all the time• For families?• For primary teams?

• Circumstances of CPR• Witnessed• Bystander CPR• VF/VT arrest• Early defibrillation• ‘down-time’ / ROSC

Confounding factors

• Multi-organ injury, both initial and reperfusion

• Major metabolic derangement• Multiple sedative agents• Therapeutic hypothermia• Family dynamics

Thoughts

• The context of the patient has been lost• These parameters are guidelines for patients• What is the patients background?• What is a good outcome for them?

• Should not come to ICU?• But they often do• ‘They will have a good outcome because

they had PPCI and TH’• ‘It may not be as bad’

Thoughts

• The basics should not be forgotten– Good history and examination– Open and honest discussion with the

family

• If there is really a risk of unacceptable badness, is this what they would want?

• Do not use a single parameter to give you the answer– Obsession with motor score at 72 hours

Finally

• The greatest ally of the physician is time• If a patient requires it, then let them have it.• If they don’t then don’t prolong it• Families are ordinary people in extraordinary

circumstances• They need our guidance and direction• Not our academic debate and confusion• You can withdraw treatment on day 1• But it may require longer to reach that

conclusion