What are the typical presentation and immediate management steps for a cerebellar intracerebral hemorrhage in an adult, especially in middle‑aged to elderly patients with hypertension, anticoagulant use, or chronic alcohol abuse?

Cerebellar Intracerebral Hemorrhage: Presentation and Immediate Management

Clinical Presentation

Cerebellar hemorrhage presents with a distinct constellation of symptoms that differ from supratentorial bleeds, requiring urgent recognition due to the confined posterior fossa space and risk of rapid deterioration. 1

Cardinal Symptoms

• Sudden onset of severe headache (typically occipital), often accompanied by nausea and vomiting due to increased intracranial pressure 1
• Ataxia and gait disturbance – patients cannot walk or stand without support, distinguishing cerebellar from supratentorial hemorrhage 2
• Vertigo and dizziness – often severe and disabling 2
• Altered level of consciousness – ranging from drowsiness to coma, particularly when brainstem compression or hydrocephalus develops 1
• Cranial nerve palsies – especially sixth nerve palsy (diplopia) and facial weakness from brainstem compression 1

High-Risk Features Requiring Immediate Intervention

• Neurological deterioration with declining Glasgow Coma Scale score 1
• Signs of brainstem compression – abnormal respiratory patterns, pinpoint pupils, extensor posturing 1
• Hydrocephalus from ventricular obstruction – rapidly progressive obtundation 1
• Cerebellar hemorrhage volume ≥15 mL – strong predictor of need for surgical intervention 1

Risk Factor Assessment

The history must rapidly identify predisposing conditions:

• Chronic hypertension – the most common cause of deep cerebellar hemorrhage 1, 3
• Anticoagulant use (warfarin, DOACs) – associated with larger hematomas and higher mortality 1
• Antiplatelet therapy (aspirin, clopidogrel) – increases bleeding risk 1
• Chronic alcohol abuse – associated with coagulopathy and hypertension 1
• Sympathomimetic drug use (cocaine, amphetamines) – particularly in younger patients 1, 4

Immediate Emergency Management

Airway and Breathing (First Priority)

• Endotracheal intubation is indicated for Glasgow Coma Scale ≤8, inability to protect airway, or signs of impending herniation 5, 2
• Use slow induction (approximately 20 mg propofol every 10 seconds) to avoid rapid hemodynamic shifts 5
• Maintain oxygen saturation >94% and avoid hypoxia, which worsens secondary brain injury 1

Blood Pressure Management (Critical Time-Sensitive Intervention)

For patients presenting within 6 hours of symptom onset with systolic BP >150 mmHg and no immediate surgical plan, reduce blood pressure in a controlled manner to a target of 140 mmHg (range 130-150 mmHg). 1, 6

• Initiate treatment within 2 hours of symptom onset and achieve target within 1 hour of starting therapy 6
• Never lower systolic BP below 130 mmHg – associated with worse outcomes and increased mortality 6
• Maintain cerebral perfusion pressure ≥60 mmHg at all times 1, 6
• Avoid dropping systolic BP by >70 mmHg within 1 hour – increases risk of acute kidney injury 6

Preferred Antihypertensive Agents

• Intravenous nicardipine – preferred due to easy titration (start 5 mg/hr, increase by 2.5 mg/hr every 5-15 minutes to maximum 15 mg/hr) 6
• Intravenous labetalol – small boluses (10-20 mg) or continuous infusion if no contraindications 1, 6
• Use continuous arterial line monitoring for patients requiring IV antihypertensives 6

Reversal of Coagulopathy (Urgent)

Anticoagulation must be reversed immediately – the need to arrest intracranial bleeding outweighs all other considerations. 7

For Warfarin-Associated ICH

• Prothrombin complex concentrate (PCC) – preferred over fresh frozen plasma due to rapid reversal with minimal fluid volume 1, 7
• Vitamin K 10 mg IV – administer in addition to PCC for sustained reversal 1
• Target INR <1.4 within 1 hour of presentation 1

For Direct Oral Anticoagulants (DOACs)

• Idarucizumab for dabigatran reversal 1
• Andexanet alfa for factor Xa inhibitor reversal (rivaroxaban, apixaban) 1

Fluid Management

• Use 0.9% saline as the crystalloid of choice – the only isotonic solution that prevents increased brain water 1, 5
• Avoid hypotonic solutions (Ringer's lactate, Ringer's acetate, gelatins) – these worsen cerebral edema 1, 5
• Maintain euvolemia through repeated hemodynamic assessment 5
• Avoid volume overload while preventing hypovolemia 1

Neuroimaging (Immediate)

• Non-contrast CT head is the initial imaging modality of choice – rapidly identifies hemorrhage location, volume, and complications 1
• CT angiography should be considered to identify underlying vascular malformations, especially in younger patients or non-hypertensive elderly 1
• Calculate hematoma volume – volumes ≥15 mL mandate neurosurgical consultation 1
• Assess for hydrocephalus and brainstem compression – both require urgent intervention 1

Surgical Decision-Making (Time-Critical)

For patients with cerebellar ICH who are deteriorating neurologically, have brainstem compression and/or hydrocephalus from ventricular obstruction, or have cerebellar ICH volume ≥15 mL, immediate surgical removal of the hemorrhage with or without external ventricular drain is recommended in preference to medical management alone to reduce mortality. 1

Indications for Immediate Surgery

• Neurological deterioration with declining GCS 1
• Brainstem compression on imaging 1
• Obstructive hydrocephalus 1
• Hematoma volume ≥15 mL 1

Critical Pitfall to Avoid

External ventricular drain (EVD) alone may be insufficient or potentially harmful when basal cisterns are compressed – surgical evacuation is required 1

Monitoring Requirements

• Admit to neurocritical care unit – associated with reduced mortality compared to general ICU 1, 7
• Neurological assessment every 15 minutes until stable, using Glasgow Coma Scale and National Institutes of Health Stroke Scale 1
• Blood pressure monitoring every 15 minutes until target stabilized, then every 30-60 minutes for first 24-48 hours 6
• Continuous cardiac monitoring – elevated troponin and ECG abnormalities are associated with worse outcomes 1

Additional Acute Management

• Maintain normoglycemia – hyperglycemia associated with worse outcomes 1, 7
• Fever control – temperature >37.5°C for 24 hours correlates with poor outcomes and ventricular extension 1, 7
• Seizure prophylaxis is NOT routinely recommended unless clinical or electrographic seizures occur 1
• Venous thromboembolism prophylaxis with intermittent pneumatic compression devices starting at admission; pharmacologic prophylaxis can begin 24-48 hours after hemorrhage stability is confirmed 7

Prognostic Indicators

The most powerful predictors of 30-day mortality include:

• Glasgow Coma Scale score on admission 1
• Hematoma volume 1
• Presence of intraventricular hemorrhage 1
• Hydrocephalus 1
• Infratentorial location (cerebellar) 3

Key Clinical Pitfalls

• Delaying surgical consultation in patients with cerebellar hemorrhage ≥15 mL or any signs of brainstem compression – these patients require immediate neurosurgical evaluation 1
• Using EVD alone without hematoma evacuation when basal cisterns are compressed – this may worsen herniation 1
• Aggressive BP lowering below 130 mmHg systolic – increases mortality 6
• Using fresh frozen plasma instead of PCC for warfarin reversal – slower reversal and excessive fluid volume 1, 7
• Administering hypotonic IV fluids – worsens cerebral edema 1, 5
• Failing to recognize hematoma expansion – occurs in 38% of patients scanned within 3 hours, associated with 5-fold increase in clinical deterioration 1