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Neurology · Topic 5 of 22

Increased Intracranial Pressure & Herniation

Neurology · neurocritical care

Increased Intracranial Pressure & Herniation

The skull cannot expand: as ICP rises, brain perfusion falls. Keep CPP at least 60, treat ICP above 22 in tiers, and catch herniation early.

Key numbers
CPP = MAP − ICPCPP ≥ 60 mmHg
Treat ICP above 22 mmHgICP > 22 mmHg
01 · CalculateCPP = MAP − ICP

Cerebral perfusion pressure = MAP − ICP; as ICP rises or MAP falls, CPP drops, and below about 50 mmHg the brain becomes ischemic — keep CPP at least 60 mmHg in severe TBI.

02 · Defined byTreat ICP above 22 mmHg

Treat sustained ICP > 22 mmHg — the Brain Trauma Foundation threshold adopted by the SIBICC algorithm; many protocols still use 20 mmHg.

03 · GiveHypertonic saline or mannitol for raised ICP

Give hyperosmolar therapy as boluses: hypertonic saline (3% or 23.4%; suggested over mannitol in TBI and ICH) or mannitol 0.5–1 g/kg IV, keeping serum osmolality 295–320 mOsm/kg.

01

Presentation

What you'll see
Cushing triad signals impending herniation must knowCushing triad — hypertension with a widened pulse pressure, bradycardia, and slow irregular respirations — signals markedly raised ICP and impending herniation.
Blown pupil: uncal herniation must knowUncal (transtentorial) herniation compresses the ipsilateral third nerve first — a dilated, unreactive pupil — then the cerebral peduncle, causing hemiparesis (usually opposite the pupil), coma and abnormal posturing.
02

Diagnosis & monitoring

Work-up
GCS ≤ 8: intubate and monitor ICPA GCS of 8 or less after head injury suggests the need for intubation and ICP monitoring; monitor ICP and CPP whenever ICP is raised.
03

Do right now

In this order
First moves
1
Sedate; intubate by rapid sequence
→
2
Head of bed 30°, head midline
→
3
Normal PaCO₂; hyperventilate only as a bridge
→
4
Hypertonic saline or mannitol for raised ICP
→
5
Drain CSF through a ventricular drain
Why each step
Sedate; intubate by rapid sequenceControl pain, agitation and coughing with sedation; when herniation is suspected or the airway is unprotected, intubate by rapid-sequence orotracheal intubation, not nasotracheal.
Head of bed 30°, head midlineElevate the head of the bed to 30° with the head midline and the neck neither rotated nor flexed to improve venous outflow, and limit tracheal suctioning.
Normal PaCO₂; hyperventilate only as a bridgeTarget a normal PaCO₂ (about 38–42 mmHg); hypocapnia lowers ICP by vasoconstriction but causes ischemia, so hyperventilation is only a brief bridge for herniation — never routinely below 30.
Hypertonic saline or mannitol for raised ICPGive hyperosmolar therapy as boluses: hypertonic saline (3% or 23.4%; suggested over mannitol in TBI and ICH) or mannitol 0.5–1 g/kg IV, keeping serum osmolality 295–320 mOsm/kg.
Drain CSF through a ventricular drainWith an external ventricular drain in place, CSF drainage is a first-tier ICP treatment (removed slowly); with only a parenchymal monitor, consider placing a ventriculostomy.
04

Management

Orders
Isotonic fluids only — no free waterKeep the patient euvolemic with isotonic fluids; free water (D5W, 0.45% saline) worsens cerebral edema and is avoided.
Refractory ICP: escalate to higher tiersIf ICP stays high, escalate: neuromuscular blockade or mild hyperventilation (PaCO₂ 32–35), then pentobarbital coma, decompressive craniectomy, or mild hypothermia (35–36 °C).
Avoid hypotension to protect CPPCorrect hypotension promptly and treat systemic hypertension only when severe, because MAP must stay high enough to hold CPP as ICP rises.
05

Red flags & don'ts

Avoid harm
Steroids only for vasogenic edema avoidGlucocorticoids such as dexamethasone help vasogenic edema around tumors or abscesses but not cytotoxic edema from stroke or trauma, where they raise glucose; routine steroids are not used in TBI.
06

Vasogenic or cytotoxic edema?

Commonly confused
MechanismBlood–brain barrier disruption
Typical causesTumor, abscess
GlucocorticoidsEffective (dexamethasone)
07

More detail

Reference
Show 7 reference facts
SIBICC "do not use" list: continuous mannitol infusion, scheduled hyperosmolar dosing, lumbar CSF drainage, furosemide, routine steroids, hypothermia below 35 °C, and routine PaCO₂ < 30 mmHg.
Herniation types: subfalcine (cingulate gyrus under the falx; most common, may infarct anterior cerebral territory), central, upward from a posterior-fossa mass, and tonsillar through the foramen magnum.
Kernohan notch: compression of the contralateral cerebral peduncle against the tentorium produces hemiparesis on the same side as the lesion — a false-localizing sign.
During mannitol therapy the Neurocritical Care Society suggests following the osmolar gap rather than an osmolality threshold for AKI risk; with hypertonic saline, avoid severe hypernatremia and hyperchloremia.
A single 30–60 mL dose of 23.4% saline reversed clinical transtentorial herniation in about 75% of cases in one cohort.
Raised ICP comes from mass lesions (tumor, abscess, hematoma), diffuse edema (for example acute liver failure), venous outflow obstruction, or blocked CSF flow (hydrocephalus).
Barbiturate coma is titrated to ICP control, not to serum levels or burst suppression; hypotension is its main hazard and must be avoided.
Pearl

CPP = MAP − ICP: lower the ICP or support the MAP — but never let the MAP fall.

Sources · Merck Manual Professional — Brain Herniation (updated Jul 2026) · Merck Manual Professional — Traumatic Brain Injury (TBI) · Hawryluk GWJ et al. A management algorithm for patients with intracranial pressure monitoring: the Seattle International Severe TBI Consensus Conference (SIBICC). Intensive Care Med 2019 (PMC6863785) · Cook AM et al. Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients (Neurocritical Care Society). Neurocrit Care 2020 (PMC7272487) · Starter sheet built from the verified AGACNP fact map (facts reviewed 2026-10-15).