Post-Cardiac Arrest Neuroprognostication

ABPN Neurocritical Care Study Guide Exam

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1 Chapter 1: Neurologic Examination & Coma Assessment in the ICU

Current Examination, Blueprint & Preparation Neurologic Examination in Critically Ill Patients Coma Evaluation & Consciousness Alterations Delirium & Toxic-Metabolic Encephalopathy in the ICU

2 Chapter 2: Cerebral Physiology & Intracranial Dynamics

Cerebral Blood Flow, Metabolism & Autoregulation Intracranial Pressure & Compliance Cerebral Edema & Herniation Syndromes

3 Chapter 3: Intracranial Hypertension & Cerebral Perfusion Management

Tiered ICP Management Protocols Hyperosmolar Therapy & Fluid Management Advanced & Refractory ICP Interventions

4 Chapter 4: Airway, Mechanical Ventilation & Pulmonary ICU Management

Emergency Airway Management & Neuro-Intubation Mechanical Ventilation Strategies in Acute Brain Injury Tracheostomy & Ventilator Weaning in Neurocritical Care Pulmonary Complications in the Neuro-ICU Obstructive Lung Disease, Pulmonary Hypertension & Bronchoscopy

5 Chapter 5: Hemodynamics, Shock & Cardiovascular Management

Hemodynamic Monitoring & Blood Pressure Targets Vasoactive Agents: Inotropes, Vasopressors & Antihypertensives Cardiac Complications of Brain Injury

6 Chapter 6: Neuropharmacology, Analgesia & Sedation

ICU Sedation & Analgesia Neuromuscular Blockade & Monitoring Propofol Infusion Syndrome & Drug Toxicities Antiseizure Drug Pharmacology in the ICU

7 Bleeding, Thrombosis & Hematologic Emergencies

Warfarin & Heparin Reversal Direct Oral Anticoagulant (DOAC) Reversal Antiplatelet Management & Platelet Dysfunction Venous Thromboembolism Prophylaxis & Management Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity

8 Chapter 8: Systemic ICU Care, Fluids, Electrolytes & Endocrine

Hyponatremia & Osmoregulation: SIADH vs Cerebral Salt Wasting Diabetes Insipidus, Hypernatremia & Endocrine Crises Critical Care Prophylaxis, Nutrition & Infection Prevention

9 Systemic Trauma & Environmental Injury

Polytrauma, Chest Injury & Abdominal Hemorrhage Burns, Electrical Injury & Hanging

10 Cardiac Emergencies & Mechanical Support

IABP, Ventricular Devices & ECMO Acute Coronary, Valvular, Rhythm & Aortic Emergencies

11 Kidney Injury, Acid–Base & Renal Replacement

Acute Kidney Injury & Renal Drug Clearance Acid–Base Disorders, Electrolytes & Renal Replacement

12 Systemic Infection & Endocrine Emergencies

Sepsis, Endocarditis & Antimicrobial Principles Thyroid, Adrenal & Dysglycemic Emergencies

13 Gastrointestinal & Hepatic Emergencies

Acute Abdomen, GI Bleeding & Abdominal Compartment Syndrome Acute Liver Failure, Cirrhosis & Hepatic Drug Effects

14 Chapter 9: Neuroimaging in the Neuro-ICU

Non-Contrast CT & CT Angiography CT Perfusion & Advanced Perfusion Imaging Magnetic Resonance Imaging in Critical Illness

15 Chapter 10: Electrophysiology & Neuromonitoring

Continuous EEG & ACNS Standardized Critical Care Terminology Invasive Neuromonitoring: ICP & External Ventricular Drains Multimodal Monitoring: PbtO2, Microdialysis & Transcranial Doppler

16 Angiography, Electrodiagnosis & CSF Analysis

Conventional Angiography & Cranial–Spinal Shunts EMG, Nerve Conduction & Acute Muscle Disease CSF Analysis: Infection, Inflammation & Hemorrhage

17 Chapter 11: Bedside Procedures, Ultrasound & Death by Neurologic Criteria

Critical Care Procedural Skills Critical Care Ultrasound & Echocardiography Determination of Death by Neurologic Criteria

18 Chapter 12: Acute Ischemic Stroke & Reperfusion Therapies

Acute Ischemic Stroke Management & Thrombolysis Endovascular Thrombectomy & Large Vessel Occlusion Malignant Hemispheric & Cerebellar Infarction

19 Chapter 13: Spontaneous Intracerebral Hemorrhage & Intraventricular Hemorrhage

Acute Intraparenchymal Hemorrhage Management Intraventricular Hemorrhage & Hydrocephalus Surgical Evacuation & Minimally Invasive Surgery in ICH

20 Chapter 14: Aneurysmal Subarachnoid Hemorrhage & Delayed Cerebral Ischemia

Aneurysmal Subarachnoid Hemorrhage: Acute Resuscitation & Securing Delayed Cerebral Ischemia & Cerebral Vasospasm Non-Aneurysmal Subarachnoid Hemorrhage & Vascular Malformations

21 Venous, Spinal & Traumatic Vascular Disease

Cerebral Venous Thrombosis & Spinal Cord Infarction Traumatic Dissection, Carotid–Cavernous Fistula & Penetrating Injury

22 Chapter 15: Traumatic Brain & Spinal Cord Injury

Severe Traumatic Brain Injury & Contusions Acute Traumatic Spinal Cord Injury & Neurogenic Shock Spine Trauma, Fractures & Cord Syndromes

23 Chapter 16: Status Epilepticus, Seizures & Neuromuscular Emergencies

Status Epilepticus: Convulsive & Non-Convulsive Refractory & Super-Refractory Status Epilepticus Acute Neuromuscular Respiratory Failure

24 Chapter 17: Post-Cardiac Arrest Care, CNS Infections & Encephalitis

Targeted Temperature Management & Post-Cardiac Arrest Care Post-Cardiac Arrest Neuroprognostication Acute CNS Infections, Encephalitis & Inflammatory Emergencies

25 Neuroinflammation & Neurooncology

Fulminant Demyelination & Autoimmune Encephalitis Brain, Spinal & Leptomeningeal Cancer Emergencies

26 Pregnancy, Transplantation & Pediatric Care

Pregnancy, Postpartum & Post-Transplant Neurologic Care Pediatric Neurocritical Care

27 Chapter 18: Neurosurgical & Perioperative Emergencies

Postoperative Neurosurgical Complications Device Complications: EVDs, Shunts & ICP Monitors Cerebral Hyperperfusion Syndrome & Post-Interventional Emergencies

28 Chapter 19: Ethics, Palliative Care & Organ Donation in the Neuro-ICU

Communication, Surrogate Decision-Making & Conflict Resolution Neuroprognostication Ethics, Withdrawal of Life Support & Palliative Care Organ Donation & Management of the Deceased Donor

Post-Cardiac Arrest Neuroprognostication

Key Takeaways Explain This Topic AI

Defer formal prognostic assessment until at least 72 hours after ROSC, or 72 hours after rewarming when hypothermia was used, and longer when confounders persist.

Bilaterally absent pupillary responses at the appropriate time and technically valid absent N20 responses at least 48 hours after ROSC are among the more reliable findings in the NCS guideline.

Absent corneal reflexes, poor motor response, early myoclonus without EEG, and an isolated NSE value are not reliable standalone predictors.

Use delayed EEG and imaging within supported time windows and interpret findings together.

An indeterminate prognosis warrants continued observation and communication consistent with patient goals.

Last updated: October 2026

Prognosis Is Different From Diagnosis of Death

Neuroprognostication estimates the likelihood of later functional outcomes after hypoxic-ischemic injury. It is not a determination of death by neurologic criteria and does not provide an exact personal forecast. Define the outcome and time horizon being discussed: survival, awareness, communication, independence, and need for assistance are different outcomes. A score of mRS 3 includes need for some help and should not be called complete functional independence.

The major methodological hazard is a self-fulfilling prophecy : a test seems to predict death when clinicians withdraw treatment because of that test. Studies with early treatment withdrawal, incomplete blinding, small samples, or poorly controlled confounders may overestimate certainty. Prefer validated findings and communicate both their evidential strength and their practical limits.

Timing and Confounders

The NCS 2023 guideline recommends deferring formal prognostic assessment until at least 72 hours after ROSC if hypothermia was not used, or at least 72 hours after rewarming if it was. This is a minimum framework, not a deadline to declare the prognosis hopeless. Sedative accumulation, kidney or liver dysfunction, seizures, metabolic disease, and systemic instability can require a longer period. Persistent coma at that point does not itself establish poor outcome.

Review drug dose, duration, clearance, active metabolites, temperature exposure, and residual neuromuscular blockade. A nominal half-life in healthy volunteers may underestimate the effect of a prolonged infusion in critical illness. Correct severe glucose, electrolyte, gas-exchange, endocrine, and acid–base disturbances. Examine repeatedly under appropriate conditions rather than interpreting one early assessment as final.

Communication can begin immediately. Explain uncertainty, the evaluation plan, known patient preferences, and what additional observation may resolve. A minimum prognostic waiting period is not a ban on family meetings or on considering a patient's established treatment limits. Decisions based on premorbid wishes or nonneurologic illness require their own explicit reasoning.

Clinical Examination and Evoked Potentials

Finding Interpretation in the appropriate setting

Bilaterally absent pupillary light response at least 72 hours after ROSC A reliable poor-outcome predictor under the guideline's assumptions; exclude ocular and technical confounders and confirm carefully

• Absent corneal reflexes alone Not sufficiently reliable as a standalone predictor
• Absent or extensor motor response alone Not sufficiently reliable as a standalone predictor

Bilaterally absent cortical N20 at least 48 hours after ROSC Reliable when peripheral and cervical responses are preserved and the study is technically adequate

Automated pupillometry can improve objectivity, particularly with small pupils, but no universal NPi cutoff should be advertised as producing zero false positives in every patient. Drugs and ocular pathology still require consideration. If manual testing suggests absent responses, confirm the observation using appropriate expertise and equipment where available.

For somatosensory evoked potentials , verify that stimulation reaches peripheral and cervical pathways and that artifact does not obscure the cortical response. A technically uninterpretable study is not an absent response. Severe hypothermia and other limitations matter. An absent N20 finding is a prognostic result, not proof of death or a substitute for the rest of the assessment.

EEG, CT, and MRI

Suppressed or burst-suppression EEG background, with or without periodic discharges, at least 72 hours after ROSC or rewarming and without sedation or other confounders is a moderately reliable poor-outcome finding in the NCS framework. Earlier patterns are useful for seizure assessment and trends but should not be assigned the same delayed prognostic meaning. Lack of reactivity, periodic discharges, or electrographic seizures alone do not justify a guaranteed outcome statement.

On CT obtained at least 48 hours after ROSC, diffuse loss of gray-white differentiation with sulcal effacement across vascular distributions can be moderately reliable. A normal early CT does not guarantee recovery. A gray-white ratio depends on acquisition and measurement methods; do not treat one universal decimal cutoff as an invariant biological boundary.

MRI showing diffuse restricted diffusion involving cortex and deep gray structures across vascular territories, assessed approximately 2–7 days after ROSC, can also be moderately reliable. Seizures and other causes of restriction must be considered. Quantitative ADC methods are not automatically interchangeable among scanners and studies. Transport and device safety determine whether the diagnostic benefit justifies obtaining MRI.

Biomarkers and Myoclonus

Neuron-specific enolase (NSE) can add information in selected multimodal approaches, but hemolysis, assay differences, and extracerebral sources complicate interpretation. NCS does not endorse a universal NSE threshold measured within 72 hours as a reliable standalone predictor. A value above 60 or 80 micrograms/L must not be represented as proving irreversible cortical necrosis with essentially no error.

Early myoclonus without EEG is not a reliable standalone marker of poor outcome. Assess whether movements have an electrographic correlate, the EEG background, sedation, and the evolving clinical state. Action myoclonus in an awake or recovering patient may represent Lance–Adams syndrome and can coexist with meaningful recovery. Timing alone does not perfectly separate these syndromes.

Integrate and Communicate

Seek concordant information from independent modalities, investigate disagreements, and avoid counting several manifestations of the same confounder as separate proof. If prognosis remains indeterminate, explain that uncertainty and consider extended observation when consistent with the patient's goals. Describe possible functional states concretely and avoid equating disability with death or assuming the family shares the clinician's valuation of dependency.

Source checked October 17, 2026: NCS 2023 neuroprognostication guideline and AHA 2025 post-arrest algorithm .