Neuroprognostication after Cardiac Death

Background and Context

During cardiac arrest, severe neurologic injury is common. It is important to know the extent of this to determine what the changes are that the patient might regain meaningful QOL/consciousness.

Competing interests: 1) Avoid prematuring terminating life support in patients who will survive 2) Avoid continuing life support in patients with poor neurologic outcomes

Approach to Neuroprognostication after Cardiac Death

Rule out Brain Death

This doesn't have to wait. If the patient is clearly brain dead (herniation, cerebral circulatory arrest) then you can declare it; guidelines recommend waiting at least 24 hours. Reminder that severe intoxication can mimic brain death (e.g. baclofen).

See Determination of Death.

Negative Prognostic Factors

• Mechanism of death: respiratory > cardiac
• Time: longer > shorter
• Unwitnessed > witnessed

Address Confounders

1. Sedating medications: midazolam, other BZDs, fentanyl (context-sensitive half-life). PPF has a half-life of about 40 minutes. Goal of sedation should be to prevent dangerous vent dyssynchrony or shivering.
   1. Ideally stick to more short-acting drugs: PPF, remifentanil
2. Temperature: normothermia facilitates earlier awakening and better neuroprognostication
3. Other: metabolic disturbances (electrolytes, renal, liver), multiorgan failure, seizure activity, TBI, deliriogenic medications, dysglycaemia

Timing of Evaluation(s)

• General recommendations are to wait 72 hours after normothermia (more if there are concerns about sedatives or confounders). This increases the test characteristics of the below variables (lower false positive rate).

Evaluation

1. Clinical examination (serial)
   1. Bilateral pupillary reflexes
   2. Bilateral corneal reflexes
2. Status myoclonus (continuous and generalised myoclonus persisting > 30 mins in comatose survivors of CA)
3. Bilateral absence of Somatosensory Evoked Potential (SSEP) N20 wave
4. EEG: Absence of EEG reactivity to external stimuli, presence of burst suppression or status epilepticus
5. Biochemistry: high Neuron-specific Enolase (>33-66)
6. Imaging:
   1. marked reduction in grey matter/white matter ratio or sulcal effacement on brain CT within 24 hours after ROSC
   2. presence of the extensive reduction in diffusion on brain MRI at 2-5 days after ROSC.

References

1. Neuroprognostication after cardiac arrest - EMCrit Project
2. Nolan JP, Sandroni C, Böttiger BW, et al. European Resuscitation Council and European Society of Intensive Care Medicine guidelines 2021: post-resuscitation care. Intensive Care Med. 2021;47(4):369-421. doi:10.1007/s00134-021-06368-4
3. https://criticalcarecanada.com/presentations/2016/neuroprognostication-after-resuscitated-cardiac-arrest.pdf
4. Neuroprognostication following Cardiac Arrest - RCEMLearning