How to manage a post-cardiac arrest patient with severe brain injury in a facility where therapeutic hypothermia (TH) is not available?

Management of Post-Cardiac Arrest Patients Without Therapeutic Hypothermia

When therapeutic hypothermia is unavailable, focus on preventing secondary brain injury through strict fever control (maintain temperature <37.5°C), avoiding hyperoxia and hyperventilation, maintaining hemodynamic stability, and delaying prognostication for at least 72 hours. 1, 2

Critical Temperature Management Without Cooling Equipment

Fever prevention is mandatory and nearly as important as active cooling. Even without specialized cooling devices, you must aggressively prevent hyperthermia, which exacerbates brain injury. 2

• Maintain core temperature below 37.5°C for at least 72 hours using basic measures: antipyretics (acetaminophen, NSAIDs), cooling blankets, ice packs to groin/axilla/neck, and fans 2
• Treat any infectious source of fever immediately 1
• Monitor temperature continuously with core temperature measurement (esophageal, bladder, or rectal probe) 3

Respiratory Management to Prevent Cerebral Injury

Avoid both hyperventilation and hyperoxia, as both worsen neurological outcomes. 1, 2

Ventilation Strategy:

• Target normocarbia: PETCO2 35-40 mmHg or PaCO2 35-45 mmHg 1, 2
• Hypocapnia causes cerebral vasoconstriction and reduces cerebral blood flow, worsening ischemic injury 1, 2
• Set initial ventilator rate at 10 breaths/minute and titrate based on capnography 1

Oxygenation Strategy:

• Titrate FiO2 to achieve arterial oxygen saturation of 94% (not 100%) 1, 2
• Hyperoxia generates free radicals that exacerbate neurological injury 1, 2
• Once stabilized, wean FiO2 aggressively to avoid prolonged hyperoxemia 2

Hemodynamic Management

Maintain systolic blood pressure >100 mmHg to ensure adequate cerebral perfusion. 1

• Avoid hypotension at all costs, as it compounds ischemic brain injury 1
• Use vasopressors (norepinephrine preferred) to maintain adequate mean arterial pressure 1
• Target MAP ≥65 mmHg, higher if patient has chronic hypertension 1

Metabolic Control

Maintain normoglycemia, as both hypoglycemia and hyperglycemia worsen brain injury. 2

• Do NOT implement tight glucose control (80-110 mg/dL) - this increases hypoglycemia risk and worsens outcomes 1
• Target glucose 140-180 mg/dL using insulin infusion protocols 1
• Check glucose every 1-2 hours initially, then every 4 hours once stable 2

Seizure Detection and Management

Perform EEG monitoring as soon as possible, as seizures occur in 5-20% of comatose survivors and are often subclinical. 1, 2

• Continuous EEG monitoring is ideal; if unavailable, perform serial EEGs daily for first 3 days 1, 2
• Post-cardiac arrest seizures are frequently refractory to standard anticonvulsants 1
• Use standard status epilepticus protocols: benzodiazepines first-line, followed by levetiracetam, valproate, or phenytoin 1
• Consider propofol or midazolam infusions for refractory seizures 1

Coronary Intervention

Perform early coronary angiography if cardiac etiology is suspected, particularly with ST-elevation on ECG. 2

• Up to 50% of cardiac arrest patients have acute coronary occlusion 4
• Absence of ST-elevation does NOT exclude acute coronary occlusion 4
• Do not defer catheterization due to coma alone 2

Prognostication: The Most Critical Pitfall to Avoid

Do NOT perform prognostication before 72 hours, as premature withdrawal of care is the leading cause of death (50% of cases) and many predictors are unreliable without therapeutic hypothermia data. 4, 2, 5

At 72 Hours Post-ROSC (Without Therapeutic Hypothermia):

Document these clinical findings daily starting at 72 hours: 4

• Pupillary light reflexes (bilateral absence at 72 hours predicts poor outcome with 0% false positive rate, 95% CI 0%-9%) 4
• Corneal reflexes (bilateral absence at 72 hours with absent pupillary reflexes: 0% false positive rate) 4
• Glasgow Coma Scale motor score (score of 1 at 72 hours: 5% false positive rate) 4
• Vestibulo-ocular reflexes (absence ≥24 hours: 0% false positive rate, 95% CI 0%-14%) 4

Additional Testing (If Available):

• Somatosensory evoked potentials: Bilateral absence of N20 component at 24-72 hours predicts poor outcome (0% false positive rate, 95% CI 0%-13%) 4
• EEG findings: Generalized suppression <20 μV, burst-suppression pattern, or diffuse periodic complexes on flat background suggest poor prognosis (3-11% false positive rate) 4
• Serum biomarkers: NSE and S100 protein may help, but cutoff values vary and should not be used alone 4

Critical Caveats:

• No single test reliably predicts outcome within first 24 hours 4
• Myoclonus alone is NOT reliable (some patients with myoclonus have complete recovery; false positive rate 0%, but wide confidence interval 0%-40%) 4
• GCS motor score ≤2 at 72 hours has 14% false positive rate 4
• Case reports document unexpected neurological recovery 9-24 hours after normothermia in patients initially deemed to have grave prognosis 6

Transfer Considerations

If your facility lacks post-cardiac arrest care capabilities, strongly consider early transfer to a comprehensive cardiac resuscitation center. 2

• Centers with therapeutic hypothermia, 24/7 cardiac catheterization, and specialized protocols have significantly better outcomes 4, 2
• Transfer should occur as soon as patient is stabilized for transport 2
• Do not delay transfer for prognostication 2

What NOT to Do

• Never hyperventilate (worsens cerebral ischemia) 1, 2
• Never allow hyperoxia (generates free radicals) 1, 2
• Never implement tight glucose control 80-110 mg/dL (increases hypoglycemia risk) 1
• Never prognosticate before 72 hours (leads to premature withdrawal of care) 4, 2, 6
• Never allow fever (exacerbates brain injury) 2
• Never allow hypotension (compounds ischemic injury) 1