Raised Intracranial Pressure & Herniation Syndromes
Protect perfusion before the brain shifts
Physiology: a fixed box
Monro-Kellie doctrine. After the sutures fuse, the skull is a rigid container holding brain (about 80%), blood (about 10%), and CSF (about 10%). Any added volume, whether tumor, hematoma, abscess, edema, or trapped CSF, must be offset by removing something else. Early on, CSF is pushed into the spinal subarachnoid space and venous blood leaves the cranium, so ICP barely changes. Once this reserve is used up, compliance collapses and each small increment in volume produces a steep rise in pressure. Infants with open sutures instead show a bulging fontanelle, a growing head circumference, and sunsetting eyes.
Cerebral perfusion pressure. CPP = MAP − ICP. For example, a MAP of 80 with an ICP of 30 leaves a CPP of only 50 mm Hg. Healthy brain autoregulates, holding blood flow steady across a MAP of roughly 50–150 mm Hg, but injured brain becomes pressure-passive, so hypotension or rising ICP directly causes ischemia. Hypotension and hypoxemia are the major preventable causes of secondary brain injury.
Blood gases. PaCO₂ is the most potent regulator of cerebral vessel caliber: hypercapnia dilates arterioles and raises cerebral blood volume and ICP, whereas hypocapnia constricts them. Severe hypoxemia also causes vasodilation.
Recognizing raised ICP
- Headache worse lying flat, on waking, and with coughing or straining
- Vomiting, often without much nausea
- Visual symptoms: transient obscurations and blurring, with bilateral papilledema on fundoscopy
- Abducens (CN VI) palsy: horizontal diplopia; a false-localizing sign because the nerve's long course over the petrous apex is stretched by downward brainstem shift
- Declining consciousness, the most sensitive sign of worsening
Cushing reflex. Hypertension with a widened pulse pressure, bradycardia, and irregular respirations reflect brainstem ischemia: a sympathetic surge raises blood pressure to preserve CPP, and baroreceptors slow the heart. It is a late sign that herniation is imminent.
Papilledema takes hours to days to appear, so a normal fundus does not exclude an acute rise in ICP.
Imaging and monitoring. CT shows effaced sulci, compressed ventricles and basal cisterns, midline shift, or hydrocephalus. An external ventricular drain is the reference standard for measuring ICP and can also drain CSF; parenchymal monitors are an alternative. Monitoring is standard in severe TBI (GCS 3–8) with an abnormal CT.
Herniation syndromes
| Type | What moves | Structures compressed | Key signs |
|---|---|---|---|
| Subfalcine | Cingulate gyrus under the falx | Anterior cerebral artery (medial frontal infarct) | Most common; midline shift on CT; contralateral leg weakness |
| Uncal (lateral transtentorial) | Medial temporal uncus over the tentorial edge | CN III, cerebral peduncle, posterior cerebral artery | Ipsilateral fixed dilated pupil, contralateral hemiparesis, occipital infarct with contralateral homonymous hemianopia |
| Central (downward transtentorial) | Diencephalon and midbrain through the tentorial notch | Brainstem and basilar perforators | Small then fixed midposition pupils; decorticate then decerebrate posturing; Duret hemorrhages |
| Tonsillar | Cerebellar tonsils through the foramen magnum | Medulla | Neck stiffness, sudden respiratory arrest, cardiovascular collapse |
| Upward | Cerebellum up through the tentorial notch | Midbrain | Posterior fossa mass, sometimes after CSF overdrainage from above |
Uncal details. Pupillomotor parasympathetic fibers run on the outside of CN III, so the pupil dilates and stops reacting before ptosis and a down-and-out eye appear.
Kernohan notch. The herniating uncus can push the midbrain against the opposite tentorial edge, compressing the contralateral cerebral peduncle and causing hemiparesis on the same side as the mass. The blown pupil is the more reliable lateralizing sign.
Central herniation. Deterioration proceeds rostral to caudal: diencephalic (small reactive pupils, Cheyne-Stokes breathing, decorticate flexor posturing), then midbrain and upper pons (fixed midposition pupils, central hyperventilation, decerebrate extensor posturing), then lower pons and medulla (ataxic breathing, flaccidity, apnea). Decorticate posturing places the lesion above the red nucleus; decerebrate places it below, a worse sign. Stretching of basilar artery perforators produces Duret hemorrhages in the midbrain and pons.
Lumbar puncture in a patient with mass effect can precipitate tonsillar herniation. Obtain CT first when there is papilledema, a focal deficit, altered consciousness, a new seizure, or immunocompromise, but never delay antibiotics for suspected meningitis while waiting.
Tiered management
- Basic measuresHead of bed 30°, head and neck midline without tight tube ties or collars, analgesia and sedation to prevent coughing and ventilator dyssynchrony, normothermia, normoglycemia, seizure control, isotonic fluids only, and no hypotension or hypoxemia.
- Osmotherapy and CSF drainageMannitol or hypertonic saline boluses; an external ventricular drain, which is the treatment for acute hydrocephalus (intraventricular hemorrhage, posterior fossa mass).
- Bridge for impending herniationBrief hyperventilation to PaCO₂ 30–35 mm Hg while definitive therapy is arranged.
- Refractory ICPPentobarbital coma or decompressive craniectomy; evacuate any surgical mass.
| Feature | Mannitol | Hypertonic saline |
|---|---|---|
| Dose | 0.25–1 g/kg IV bolus | 3% boluses, or 23.4% through a central line |
| Volume effect | Osmotic diuresis; hypovolemia and hypotension | Expands intravascular volume |
| Main risks | AKI, electrolyte shifts | Hypernatremia, hyperchloremic acidosis, volume overload |
| Monitoring | Serum osmolality and osmolal gap before redosing | Serum sodium |
| Preferred when | Euvolemic and normotensive | Hypotensive or hypovolemic |
Why D5W is dangerous. Once its glucose is metabolized, D5W behaves as free water, which follows the osmotic gradient into brain tissue; other hypotonic solutions do the same.
Hyperventilation. Lowering PaCO₂ constricts cerebral arterioles and reduces ICP within minutes, but it also lowers cerebral blood flow and risks ischemia, and the effect fades within hours as CSF pH readjusts. It is a short bridge, never a prophylactic strategy.
Refractory therapy. Pentobarbital lowers cerebral metabolic demand and blood flow but causes hypotension and requires EEG monitoring. Decompressive craniectomy relieves pressure; in malignant MCA infarction, hemicraniectomy within 48 hours improves survival and functional outcome in patients 60 or younger; over 60 it still lowers mortality, but survivors often have major disability, so decide with the family.
Steroids and common pitfalls
Dexamethasone. Steroids shrink vasogenic edema, which follows a disrupted blood-brain barrier around brain tumors (metastases, glioma) and abscesses (given with antibiotics). They do not help the cytotoxic edema of ischemic stroke, provide no benefit in intracerebral hemorrhage, and increase mortality in TBI.
Do not give steroids for traumatic brain injury, do not hyperventilate prophylactically, and do not use prophylactic hypothermia; treat fever instead.