Study guide
Malignant Hemispheric & Cerebellar Infarction
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
Malignant Hemispheric & Cerebellar Infarction
Key Takeaways Explain This Topic AI
Large hemispheric infarctions require close surveillance for declining consciousness, mass effect, and herniation, with early neurosurgical referral.
In selected patients aged 60 or younger, decompression within 48 hours substantially improves survival and shifts functional outcomes.
DESTINY II supports a survival benefit in older patients, with frequent substantial dependency; mRS 3 is not full independence and mRS 5 is not vegetative state.
Cerebellar infarction with symptomatic hydrocephalus may need ventriculostomy; deterioration from brainstem compression requires urgent consideration of suboccipital decompression.
Last updated: October 2026
Malignant Hemispheric & Cerebellar Infarction
Malignant ischemic infarction occurs when complete occlusion of a major cerebral or cerebellar arterial trunk leads to massive, space-occupying edema. Without timely neurosurgical decompression, progressive tissue displacement forces uncal, central, or tonsillar herniation, terminating in secondary brainstem infarction and death.
Pathophysiology & Biomechanics of Malignant Edema
Malignant middle cerebral artery ( M C A MCA MC A ) infarction affects approximately 10 % 10\% 10% of all supratentorial ischemic strokes, most commonly stemming from an acute thromboembolic occlusion of the internal carotid artery ( I C A ICA I C A ) terminus or proximal M C A M 1 MCA\text{ }M1 MC A M 1 segment.
The Two-Phase Edema Cascade
Cytotoxic Edema (Hours 0 – 24 0\text{--}24 0 – 24 ): Acute cessation of blood flow depletes intracellular ATP, arresting the N a + / K + Na^+/K^+ N a + / K + ATPase pump. Sodium, chloride, and water pour into astrocytic foot processes and neurons, causing cellular swelling while total brain tissue volume remains initially constant.
Vasogenic Edema (Hours 24 – 96 24\text{--}96 24 – 96 ): Endothelial cell death, up-regulation of matrix metalloproteinases ( M M P - 9 MMP\text{-}9 MMP - 9 ), and breakdown of capillary tight junctions (zonula occludens) compromise the blood-brain barrier. Plasma water, albumin, and macromolecules leak into the extracellular parenchymal space, generating massive tissue expansion.
Temporal Peak: In malignant infarction, cerebral edema typically peaks between day 2 and day 4 (48 to 96 hours post-stroke) . Under medical therapy alone (hyperosmolar therapy, sedation, hyperventilation), mortality reaches 70 – 80 % 70\text{--}80\% 70 – 80% , primarily driven by uncal transtentorial herniation compressing the midbrain, stretching paramedian perforating vessels (Duret hemorrhages), and extinguishing brainstem function.
Early Predictors of Malignant Progression
Recognizing impending malignant edema before irreversible clinical deterioration occurs is vital for timely surgical referral.
Predictor Domain High-Risk Features for Malignant Edema Progression
Patient Demographics Younger age ( < 60 years < 60\text{ years} < 60 years ): Absence of age-related cerebral atrophy leaves minimal intracranial CSF reserve to buffer swelling
Neurological Deficit Baseline NIHSS > 15 – 20 > 15\text{--}20 > 15 – 20 for non-dominant hemispheric stroke; baseline NIHSS > 20 > 20 > 20 for dominant hemispheric stroke within 6 hours
Early CT Hypodensity Hypodensity involving > 50 % > 50\% > 50% of the MCA territory or ASPECTS ≤ 4 \le 4 ≤ 4 within 12 hours of onset
Vascular Territories "MCA-plus" syndrome: Concomitant infarction in adjacent anterior cerebral artery ( A C A ACA A C A ) or posterior cerebral artery ( P C A PCA PC A ) territories
Mass Effect / Midline Shift Septum pellucidum displacement ≥ 5 mm \ge 5\text{ mm} ≥ 5 mm or pineal gland displacement ≥ 3 mm \ge 3\text{ mm} ≥ 3 mm within 24–48 hours
Vascular Imaging Absence of pial collateral circulation on CTA; carotid T-occlusion; TCD pulsatility index > 1.5 > 1.5 > 1.5
- Decompressive Hemicraniectomy for Supratentorial Stroke
- Surgical Technique and Timing
A sufficiently large frontotemporoparietal decompression with dural expansion is important to relieve swelling and avoid constriction at the bone edges. Common operative dimensions are approximately 12–15 cm or larger depending on anatomy. This is a specialist technical principle rather than a universal contraindication defined by one measured diameter. Refer before irreversible deterioration; osmotherapy and brief rescue ventilation can bridge to definitive assessment, but do not replace indicated decompression.
- Landmark Randomized Trial Evidence
- Patients Aged ≤ 60 \le 60 ≤ 60 Years: The Pooled Analysis
The European pooled analysis of three prospective randomized trials— DECIMAL , DESTINY , and HAMLET —evaluated decompressive hemicraniectomy within 48 hours in patients ≤ 60 \le 60 ≤ 60 years of age with malignant MCA infarction:
Mortality Reduction: Surgery reduced 1-year mortality from 71 % 71\% 71% to 22 % 22\% 22% (absolute risk reduction of 49 % 49\% 49% , N N T = 2 NNT = 2 NNT = 2 ).
Survival with mRS at most 3: Surgery doubled the proportion of patients achieving survival with no worse than moderate disability, which may still require help ( 43 % 43\% 43% vs 21 % 21\% 21% , N N T = 4 NNT = 4 NNT = 4 ).
Outcome counseling: mRS 5 denotes severe dependency, not vegetative state. Describe the entire outcome distribution and the patient’s values rather than equating survival with independence.
Patients Older Than 60: DESTINY II
Among patients aged 61–82 treated within 48 hours, six-month mortality was 33% with surgery versus 70% with medical treatment. No patient achieved mRS 0–2. The respective mRS distributions were 7% versus 3% at mRS 3, 32% versus 15% at mRS 4, and 28% versus 13% at mRS 5. Thus surgery improved survival but many survivors needed substantial help. mRS 3 allows walking without another person's assistance while requiring some help; mRS 4 means inability to walk or attend bodily needs without assistance, and mRS 5 means severe dependency with constant care. None of these scores by itself defines consciousness or quality of life.
Discuss these possible outcomes with the surrogate in relation to the patient's preferences and baseline function. Age alone does not resolve the decision, and trial group averages do not determine an individual's outcome. State the timing and population of the study rather than applying one percentage to every large infarction.
Malignant Cerebellar Infarction & Posterior Fossa Decompression
Malignant infarction of the cerebellum—most frequently resulting from posterior inferior cerebellar artery ( P I C A PICA P I C A ) or superior cerebellar artery ( S C A SCA SC A ) occlusion—presents unique mechanical dangers due to the tight confines of the posterior fossa.
Posterior Fossa Compartment Dynamics
The infratentorial compartment is bounded superiorly by the rigid, non-compliant tentorium cerebelli and inferiorly by the foramen magnum. Expanding cerebellar edema triggers a sequential cascade:
Effacement of the fourth ventricle and perimedullary / prepontine cisterns.
Acute obstructive (non-communicating) hydrocephalus from fourth ventricle or cerebral aqueduct occlusion.
Downward tonsillar herniation: Cerebellar tonsils impact into the foramen magnum, causing direct medullary compression, respiratory arrest, and death.
Upward transtentorial herniation: Swollen cerebellar vermis herniates upward through the tentorial incisura into the ambient cistern, compressing the midbrain and posterior cerebral arteries.
Neurosurgical Interventions & The EVD Trap
Definitive treatment for malignant cerebellar infarction with fourth ventricle compression, brainstem distortion, or altered consciousness is emergent suboccipital decompressive craniectomy ( S D C SDC S D C ) with expansile duraplasty, foramen magnum decompression, and resection of non-viable necrotic cerebellar tissue.
Warning
Ventriculostomy is recommended for symptomatic obstructive hydrocephalus after cerebellar infarction. Selected patients can improve with careful CSF diversion alone, while neurologic deterioration from brainstem compression despite medical treatment requires suboccipital decompression. Avoid uncontrolled drainage and reassess urgently: hydrocephalus, infarct size, brainstem compression, clinical trajectory, and response determine whether decompression is also needed. EVD monotherapy is not universally a fatal error.