Head and Neck · 6 min read
Intracranial Pressure and Herniation
Intracranial Dynamics
The Monro-Kellie doctrine states that the skull is a fixed box containing brain tissue (about 80%), blood (about 10%), and cerebrospinal fluid (about 10%); an increase in one component must be offset by a decrease in another. Early compensation displaces CSF into the spinal canal and venous blood out of the skull. Once compensation is exhausted, compliance falls and small additions of volume produce steep rises in pressure.
Normal intracranial pressure (ICP) in adults is about 5–15 mmHg. Cerebral perfusion pressure (CPP) = MAP − ICP. BTF guidelines recommend treating ICP > 22 mmHg and maintaining CPP 60–70 mmHg; CPP above 70 with aggressive fluids and vasopressors increases the risk of ARDS and is avoided. For example, a MAP of 80 mmHg with an ICP of 25 mmHg yields a CPP of 55 mmHg, which requires intervention on both sides of the equation.
ICP Monitoring
ICP monitoring is indicated in salvageable patients with severe TBI (GCS 3–8 after resuscitation) and an abnormal CT (hematomas, contusions, swelling, herniation, or compressed basal cisterns). With a normal CT, monitoring is considered when two or more of the following are present: age over 40, unilateral or bilateral motor posturing, or SBP < 90 mmHg.
| Device | Advantages | Limitations |
|---|---|---|
| External ventricular drain (EVD) | Gold standard accuracy; allows therapeutic CSF drainage; can be recalibrated | Highest infection risk (ventriculitis); hard to place with compressed ventricles |
| Intraparenchymal fiberoptic or strain-gauge | Easier placement; lower infection risk; reliable waveform | Cannot drain CSF; cannot be re-zeroed after insertion (drift) |
| Subdural or epidural sensors | Less invasive | Less accurate; rarely used |
An EVD transducer is leveled at the tragus of the ear (approximating the foramen of Monro) and re-leveled with every position change. Drainage is set to a prescribed height or pressure threshold; clamp the drain before moving or repositioning the patient to prevent over-drainage, which can cause subdural hemorrhage or upward herniation. Monitor hourly drainage volume, color, and clarity, and maintain a closed system to reduce infection.
The normal ICP waveform has three peaks. P1 (percussion wave) reflects arterial pulsation, P2 (tidal wave) reflects brain compliance, and P3 (dicrotic wave) follows aortic valve closure. When P2 exceeds P1, compliance is reduced and the brain is poorly able to accept additional volume. Sustained plateau (Lundberg A) waves indicate critically low compliance.
Tiered Management of Intracranial Hypertension
Management proceeds in tiers, escalating only when a lower tier fails. Before escalating, exclude a surgical lesion with repeat CT and correct reversible causes: hypoxia, hypercarbia, fever, agitation, pain, seizure, hyponatremia, and venous outflow obstruction from a tight cervical collar or endotracheal tube tie.
| Tier | Interventions | Nursing points |
|---|---|---|
| General (all patients) | HOB 30°, head midline, normothermia, analgesia and sedation, SpO2 ≥ 90%, normocarbia | Loosen collar ties; avoid hip flexion > 90°; cluster care |
| Tier 1 | Intermittent CSF drainage via EVD; hyperosmolar bolus (mannitol or hypertonic saline) | Check Na+ and osmolality; confirm EVD leveling |
| Tier 2 | Deeper sedation, neuromuscular blockade trial, mild hyperventilation to PaCO2 32–35 with monitoring | Monitor for pneumonia and ischemia; train-of-four if paralyzed |
| Tier 3 | Barbiturate coma, decompressive craniectomy, or mild hypothermia for refractory ICP | Barbiturates cause hypotension; EEG for burst suppression |
Hyperosmolar Therapy
Mannitol (0.25–1 g/kg IV bolus) creates an osmotic gradient that draws water out of brain tissue and improves blood rheology. It is an osmotic diuretic: expect brisk diuresis, avoid it in hypotensive or hypovolemic patients, place a urinary catheter, and hold further doses when serum osmolality approaches 320 mOsm/kg or the osmolar gap widens. Administer through an in-line filter because crystals can form.
Hypertonic saline (for example 3% infusion or bolus, or 23.4% bolus through a central line) reduces ICP while expanding intravascular volume, which makes it preferred in the hypotensive or hypovolemic patient. Monitor serum sodium frequently; protocols commonly cap sodium at about 155–160 mEq/L. Watch for volume overload and hyperchloremic acidosis.
Hyperventilation and Refractory Measures
Hyperventilation lowers ICP within minutes by causing hypocapnic cerebral vasoconstriction, but it also reduces cerebral blood flow and can cause ischemia, especially in the first 24 hours when flow is already low. Prophylactic hyperventilation (PaCO2 ≤ 25 mmHg) is not recommended. Brief hyperventilation is used only as a bridge for signs of active herniation while definitive therapy (osmotherapy, surgery) is arranged.
High-dose barbiturates (pentobarbital) reduce cerebral metabolic demand and are reserved for ICP refractory to maximal medical and surgical therapy; they are not given prophylactically. Monitor for hypotension, myocardial depression, and immunosuppression, and titrate to EEG burst suppression. Decompressive craniectomy removes a bone flap to allow the brain to expand; the flap may be stored in the abdominal subcutaneous tissue or a bone bank, and a helmet protects the defect. Prophylactic hypothermia is not recommended by BTF; mild hypothermia is at most a rescue measure for refractory ICP, while fever must be treated aggressively.
Herniation Syndromes
Herniation is the displacement of brain tissue across a rigid dural fold or through the foramen magnum. Recognizing the pattern early guides emergent interventions: elevate the head of bed, give a hyperosmolar bolus, briefly hyperventilate as a bridge, and prepare for emergent CT and neurosurgery.
| Type | Displacement | Key findings |
|---|---|---|
| Uncal (lateral transtentorial) | Medial temporal lobe (uncus) over tentorial edge | Ipsilateral dilated pupil (CN III), then contralateral hemiparesis; decerebrate posturing late |
| Central transtentorial | Both hemispheres downward through tentorial notch | Decreasing LOC, small reactive pupils, Cheyne-Stokes breathing, then midposition fixed pupils |
| Subfalcine (cingulate) | Cingulate gyrus under the falx cerebri | May compress anterior cerebral artery: contralateral leg weakness |
| Tonsillar (foramen magnum) | Cerebellar tonsils into foramen magnum | Medullary compression: apnea, cardiovascular collapse; most immediately lethal |
| Upward (transtentorial) | Posterior fossa contents upward | Posterior fossa mass or excessive CSF drainage; rapid decline |
In uncal herniation, a Kernohan notch phenomenon occasionally produces weakness on the same side as the lesion because the opposite cerebral peduncle is compressed against the tentorium; the dilated pupil remains the more reliable localizing sign. Respiratory patterns progress from Cheyne-Stokes (diencephalon) to central neurogenic hyperventilation (midbrain), apneustic breathing (pons), and ataxic breathing (medulla) as herniation descends.
- CPP = MAP − ICP; treat ICP > 22 mmHg; target CPP 60–70 mmHg.
- Monitor ICP in severe TBI with abnormal CT, or normal CT with ≥ 2 of: age > 40, posturing, SBP < 90.
- Level EVD at the tragus; clamp before repositioning; P2 > P1 = poor compliance.
- Mannitol diureses (avoid in hypotension; osm < 320); hypertonic saline preferred when hypovolemic.
- Hyperventilation only as a brief bridge for herniation; never prophylactic.
- Barbiturates and craniectomy are for refractory ICP; prophylactic hypothermia is not recommended.
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