Neurocritical Care – Fundamentals & ICP Management

Neurocritical Care – Fundamentals & ICP Management

Case Example

• 27 y/o male, high-speed MVC

• GCS 6 (no eye opening, no speech, withdrawal on R side only)

• Concern: TBI with elevated ICP → risk of secondary brain injury

Core Physiology

• Monro–Kellie Doctrine: Skull = fixed box (brain + CSF + blood).

  • If volume ↑ in one component, others must ↓ or ICP rises.

  • Compensation: CSF shunting to spinal canal, ↑ venous outflow.

  • Once exhausted → ICP rises → risk of herniation.

• Cerebral Perfusion Pressure (CPP)

  • CPP = MAP – ICP

  • Brain autoregulates CBF between CPP ~50–150 mmHg.

  • Danger zone: CPP < 50 → cerebral ischemia.

Why ICP Matters

1. ↓ CPP → secondary ischemic injury

2. Herniation syndromes (life-threatening)

   • Uncal: ipsilateral blown pupil, contralateral hemiparesis.

   • Central (transtentorial): coma (RAS compression).

   • Subfalcine: ACA compression → ipsilateral leg weakness.

   • Tonsillar: brainstem compression → flaccid paralysis, resp arrest.

Clinical Red Flags

• GCS < 8 after trauma

• Unilateral dilated pupil

• Abnormal posturing

• Late: Cushing’s triad (HTN, bradycardia, irregular respirations)

Management Goals

• Prevent secondary injury (hypotension, hypoxemia).

• Maintain adequate MAP/CPP.

• Reduce ICP.

• Keep the brain in “normal” environment: normoxia, normotension, normoglycemia, normothermia.

ICP Management – Tiered Approach

Tier 0 – Universal Measures

• Sedation/analgesia (avoid agitation & vent bucking).

• Head elevation (30°), midline positioning.

• Avoid tight cervical collar compression.

• Target RASS ~ -2 (light sedation).

Tier 1 – First-line Therapies

• Hyperosmolar therapy

  • Mannitol (1 g/kg, excreted in ~3h). Watch osm gap & diuresis.

  • Hypertonic saline (3%, 7.5%, 23.4%). Watch serum Na (<160).

  • Hypertonic bicarbonate can substitute if no access to above.

  • Choice depends on comorbidities (hypovolemia → avoid mannitol; CHF → avoid hypertonic saline).

• Hyperventilation

  • Short-term, target PaCO₂ 30–35 mmHg.

  • Induces vasoconstriction → ↓ CBF volume.

• CSF diversion (e.g., EVD).

Tier 2 – Escalation

• Deep sedation (ICP-targeted)

  • Propofol: ↓ cerebral metabolism, rapid on/off; watch hypotension.

  • Midazolam: longer half-life, delirium risk.

  • Dexmedetomidine: light sedation, unreliable ICP effect.

  • Ketamine: neutral effect on ICP, preserves BP.

• Do not abruptly stop sedation in ICP crisis.

Tier 3 – Rescue Therapies

• Neuromuscular blockade: Prevent coughing/straining, short duration (use train-of-four, ensure deep sedation).

• Hypothermia: Limited evidence; emphasis on preventing fever.

Systemic Neuroprotective Care

• Blood pressure

  • Avoid hypotension (especially in TBI).

  • Some pathologies:

    • Ischemic stroke → permissive HTN.

    • ICH → cautious BP lowering.

  • Arterial line monitoring recommended.

• Volume status

  • Maintain euvolemia.

  • Anticipate mannitol-induced diuresis.

  • Watch for diabetes insipidus in severe brain injury.

• Glycemic control

  • Avoid both hypo- & hyperglycemia.

  • Insulin drip protocols if needed.

• Temperature

  • Prevent fever.

  • Therapeutic hypothermia = weak evidence, not routine.

• Seizure control

  • Prevent seizures → avoid metabolic demand spikes.

Take-Home Principles

• Herniation = clinical diagnosis (don’t wait for imaging).

• ICP crisis signs: coma + unilateral blown pupil.

• Treat ICP in tiers: start with basics → escalate carefully.

• Always balance CPP = MAP – ICP.

• Goal = prevent secondary injury and keep brain in homeostasis.