What is the recommended acute management for an adult patient presenting with an acute cerebellar infarct?

Management of Acute Cerebellar Infarct

Immediately admit the patient to an intensive care or stroke unit with urgent neurosurgical consultation, even if the patient appears stable, as cerebellar infarcts can deteriorate rapidly and unpredictably within 72-96 hours, requiring emergent decompressive surgery. 1, 2

Initial Triage and Multidisciplinary Team Assembly

• Transfer to ICU or stroke unit is mandatory for all acute cerebellar infarcts to enable close neuromonitoring and rapid intervention 1, 2
• Assemble a team including neurointensivists, vascular neurologists, and neurosurgeons immediately upon diagnosis 1
• If your facility lacks neurosurgical capabilities or comprehensive stroke care, transfer the patient urgently to a higher-level center 1

Diagnostic Imaging Protocol

• Non-contrast CT is the first-line test but can be normal in up to 25% of cerebellar infarcts initially, particularly within the first 6 hours 1, 3
• MRI with diffusion-weighted imaging is superior for detecting cerebellar infarction and should be obtained if CT is negative but clinical suspicion remains high 4, 3
• Perform serial CT scans during the first 2 days to identify early swelling before clinical deterioration occurs 1, 2
• Obtain CT or MR angiography to identify vertebrobasilar occlusions or stenosis that may guide intervention 1

Critical Neurological Monitoring

The most reliable indicator of dangerous swelling is declining level of consciousness 1, 2. Monitor intensively for:

• Decreased arousal or Glasgow Coma Scale decline (earliest and most important sign) 1, 2
• Pupillary changes indicating brainstem compression 2
• Ophthalmoparesis and loss of oculocephalic responses from pontine compression 1, 2
• Breathing irregularities and cardiac dysrhythmias from brainstem involvement 1, 2
• Document neurological status, vital signs, oxygen saturation, temperature, and glucose at frequent intervals 1

Common pitfall: Truncal ataxia is frequently missed during bedside examination—specifically test truncal stability, gait, coordination, speech, and eye movements in all patients with dizziness or vertigo 1, 3

Medical Management

Supportive Care Measures

• Elevate head of bed 0-30 degrees to reduce intracranial pressure 2
• Maintain isotonic or mildly hypertonic fluid resuscitation—avoid hypoosmolar fluids that worsen cerebral edema 2
• Provide supplemental oxygen to hypoxic patients and maintain adequate oxygenation 1, 2
• Maintain normoglycemia with regular glucose monitoring and appropriate therapy; avoid hypoglycemia 1, 2
• Treat hyperthermia aggressively as fever worsens outcomes 2
• Screen for dysphagia within 24 hours before allowing oral intake to prevent aspiration 1

Blood Pressure Management

• Maintain adequate mean arterial pressure to ensure cerebral perfusion, though specific targets are not established 1, 2
• If blood pressure exceeds 220/120 mmHg, cautiously reduce by only 10-20% and monitor closely for neurological deterioration 1

Osmotic Therapy

• Administer mannitol or hypertonic saline for patients showing clinical deterioration from cerebral edema (Class IIa; Level of Evidence C) 2
• Monitor serum osmolality regularly with target of 300-310 mOsmol/kg when using osmotic agents 2

Medications to AVOID

• Do NOT use corticosteroids for cerebellar edema—they are ineffective and not recommended (Class III; Level of Evidence C) 2
• Do NOT use barbiturate coma or hypothermia—insufficient evidence supports their use 2
• Minimize sedation to allow accurate neurological assessment 2

Antiplatelet Therapy

• Administer aspirin 150-300 mg as soon as possible after imaging excludes hemorrhage, ideally within 48 hours 1

Thromboembolism Prophylaxis

• Initiate subcutaneous low-dose heparin or low molecular weight heparin for DVT prophylaxis 2

Airway Management

Indications for intubation include 1:

• Declining consciousness with inability to protect airway

• Persistent hypoxemia or hypercapnia

• Pooling secretions with upper airway obstruction

• Apneic episodes or respiratory failure

• Generalized seizures or recent aspiration

• Use rapid sequence intubation with standard agents 1

• Maintain normocapnia—avoid prophylactic hyperventilation as there is no evidence of benefit 1, 2

• Use short-acting sedatives (propofol or dexmedetomidine) in low doses if needed for ventilator synchrony 1

Surgical Intervention

Suboccipital decompressive craniectomy with dural expansion must be performed in patients who deteriorate neurologically despite maximal medical therapy (Class I; Level of Evidence B) 2

Timing and Indications

• Do not delay neurosurgical consultation—involve neurosurgery early even in stable patients, as deterioration can be sudden 1, 2
• Peak swelling occurs several days after onset, typically within 72-96 hours but sometimes 4-10 days 1
• Surgery is indicated for progressive decline in consciousness, signs of brainstem compression, or radiographic evidence of mass effect with hydrocephalus 1, 2, 5

Critical Surgical Pitfall

• Never perform ventriculostomy alone for hydrocephalus without decompressive craniectomy, as this can cause fatal upward herniation 2
• Ventriculostomy should only be combined with decompressive surgery 1

Post-Operative ICU Management

After decompressive surgery 2:

• Monitor intracranial pressure and maintain cerebral perfusion pressure >60 mmHg using volume replacement and/or vasopressors 2
• Obtain control CT at 24 hours or earlier if signs of intracranial hypertension develop 2
• Apply comprehensive ICU protocols including sepsis bundles, lung-protective ventilation, strict glucose control, and early enteral nutrition 2
• Begin DVT prophylaxis on postoperative day 2 after consulting neurosurgery 2
• Do NOT use prophylactic antiepileptic drugs—only treat if seizures occur 2
• Begin mobilization and rehabilitation after successful extubation and only in absence of intracranial hypertension 2

Prognosis and Complications

• Deterioration is more dependent on initial infarct volume than specific vascular territory involved 1
• Complications include obstructive hydrocephalus from fourth ventricle compression and brainstem compression from direct mass effect 1, 3, 6
• Hemorrhagic transformation can occur and may cause sudden rapid decline 1