Intracranial Pressure (ICP) and Monroe-Kellie Hypothesis

1. Intracranial Pressure (ICP)

Intracranial pressure (ICP) is the pressure exerted by the contents of the skull on the brain tissue, blood, and cerebrospinal fluid (CSF).

Normal ICP Values

• Adults: 5-15 mmHg

• Children: 3-7 mmHg

• Neonates: 1.5-6 mmHg

• Critical ICP: > 20-25 mmHg → Requires intervention

ICP Measurement Sites

• Intraventricular catheter (EVD) – Gold standard

• Subdural bolt/sensor – Less invasive

• Parenchymal probe – Direct brain tissue measurement

• Epidural or subdural catheter – Less accurate

2. Monroe-Kellie Hypothesis

The Monroe-Kellie doctrine states that the total volume inside the skull is constant, as the skull is a rigid, non-expandable structure.

• It consists of three main components:

1. Brain parenchyma (~80%)

2. Cerebrospinal fluid (CSF) (~10%)

3. Blood (cerebral blood volume – CBV) (~10%)

• If one component increases, another must decrease to maintain normal ICP.

• Failure of compensation leads to raised ICP → brain herniation → death.

Compensatory Mechanisms

1. CSF Regulation

• ↓ CSF production (choroid plexus)

• ↑ CSF absorption (arachnoid granulations)

• CSF shifts to spinal subarachnoid space

2. Cerebral Blood Volume Regulation

• Vasoconstriction to ↓ blood volume

• Increased venous outflow

3. Brain Tissue Compliance

• Only minimal compensation possible

Once compensatory mechanisms fail → ICP rises rapidly → herniation risk.

3. Causes of Raised ICP

A. Increased Brain Volume (Cerebral Edema)

• Vasogenic edema: BBB disruption (tumors, infections, trauma)

• Cytotoxic edema: Cellular swelling (stroke, hypoxia)

• Interstitial edema: CSF accumulation (hydrocephalus)

B. Increased Blood Volume

• Hypercapnia (↑ CO₂) → Cerebral vasodilation

• Venous outflow obstruction (Jugular vein compression, head-down position)

• Hyperemia (Seizures, hyperthermia)

C. Increased CSF Volume (Hydrocephalus)

• Obstruction of CSF flow (Aqueductal stenosis, tumors)

• Decreased absorption (Meningitis, SAH, ↑ venous pressure)

• Overproduction (Choroid plexus tumors)

D. Space-Occupying Lesions (SOLs)

• Tumors, hemorrhage (SDH, EDH, SAH, ICH), abscess, cysts

4. Clinical Features of Raised ICP

A. Symptoms

• Headache – Worse in the morning, aggravated by Valsalva

• Vomiting – Often without nausea (projectile)

• Altered consciousness – Confusion, drowsiness → coma

• Seizures

• Diplopia (CN VI palsy) – Due to brainstem compression

B. Signs

• Cushing’s Triad (Late Sign, Brain Herniation)

• Hypertension (widened pulse pressure)

• Bradycardia

• Irregular respiration (Cheyne-Stokes, Biot’s breathing)

• Papilledema (optic disc swelling)

• Pupil changes (fixed, dilated in uncal herniation)

5. Management of Raised ICP

A. Immediate Measures (Rescue Therapy)

1. Head elevation (30°-45°) – Promotes venous drainage

2. Airway protection & ventilation

• Target PaCO₂: 30-35 mmHg (controlled hyperventilation)

3. Mannitol (0.25-1 g/kg IV) – Osmotic diuretic

4. Hypertonic saline (3% NaCl, 250 mL over 30 min) – Volume expansion, osmotic effect

5. Sedation & analgesia (Propofol, Dexmedetomidine) – Reduces metabolic demand

6. Neuromuscular blockade (Rocuronium, Vecuronium) – Prevents coughing, agitation

7. CSF drainage (EVD insertion) – Immediate ICP relief

Mannitol vs. Hypertonic Saline for Brain Relaxation

1. Introduction

Brain relaxation is crucial in neurosurgery and neurocritical care to reduce intracranial pressure (ICP) and improve cerebral perfusion. The two most commonly used hyperosmolar agents are mannitol and hypertonic saline (HTS).

2. Mechanism of Action

3. Comparison: Mannitol vs. Hypertonic Saline

4. Clinical Use Cases

 B. Definitive Management

• Treat underlying cause (tumor, hemorrhage, infection)

• Surgical decompression (craniotomy, decompressive craniectomy)

6. Brain Herniation Syndromes (Life-Threatening ICP Increase)