Intracranial Hypertension (Elevated Intracranial Pressure)

Intracranial hypertension is defined as an intracranial pressure (ICP) >20mmHg. It is often a complication of head trauma or other neurological conditions and it may have lethal consequences.


The volume of the intracranial compartment is fixed. Changes in any of the components inside the compartment such as the brain parenchyma, cerebrospinal fluid and blood circulation, can cause changes on the intracranial pressure.

Elevation of the ICP reduces the cerebral perfusion pressure (CPP) and may cause neurological damage. The cerebral perfusion pressure is calculated by subtracting the intracranial pressure (ICP) from the mean arterial pressure (MAP):



Mass effect (tumor, blood)
Generalized brain swelling/Cerebral edema (hypoxic-ischemic encephalopathy, cerebral infarction, traumatic brain injury)
Increased venous pressure
Obstruction of CSF flow
Increased in CSF production


The classic Cushing`s triad (bradycardia, bradypnea and hypertension) may or may not be present.

Other clinical features of elevated ICP include headache, altered mental status (from confusion to coma), vomiting, cranial nerve palsies (VI), and papilledema.

Focal deficits may be present depending on the etiology of the elevated ICP (e.g. tumors, stroke) or the presence/absence of herniation.


The suspicion of intracranial hypertension should come through a suggestive history and physical examination.

A definitive diagnosis is made by ICP measurement (intraventricular, intraparenchymal, subarachnoid or epidural). There is still no clear evidence of who should receive ICP monitoring, but it may be indicated in patients who have a GCS <8 and other features suggestive of elevated ICP (physical examination, abnormal CT scan, Cushing`s triad).


The treatment should be focused on managing the underlying cause (e.g. tumor, hematoma, stroke) as well as keeping the ICP under control to avoid further neurological damage. The ICU is the proper setting for these cases due to the need of constant monitoring and sometimes the necessity of rapid intervention.

Acute elevations in ICP should be managed by temporary measures as follows:

  • Increasing the intravascular volume: Mannitol 20% bolus of 1g/kg. It may be repeated (0.25-0.5 g/kg) q6-8hr as needed. Hypertonic saline may be used as an alternative to mannitol if mannitol is not available.
  • Positional change to reduce pressure: Head elevation.
  • Inducing cerebral vasoconstriction by reducing serum CO2 concentration: Hyperventilation to a target PCO2 26-30mmHg. (Caution using this strategy with stroke patients).

Other important goals of the treatment include:

  • Maintain a proper MAP (continuous BP monitoring) to allow a good CPP (>60mmHg).
  • Sedation to keep a low encephalic metabolic rate: Pentobarbital 5-20mg/kg bolus followed by 1-4mg/kg/h. Continuous EEG monitoring is important.
  • Avoid fever to reduce metabolic demand. Continuous temperature monitoring is important. Therapeutic hypothermia (32-34C) may be useful in some cases, but it is not yet clear in the literature which group of patients with elevated ICP benefit from this treatment.
  • Avoid seizures: Antiepileptic therapy may be useful in some cases. Continuous EEG monitoring is, once again, relevant.

In addition to everything mentioned above, CSF removal through ventriculostomy may be used (1-2mL/minute for 2-3 minutes until ICP <20mmHg).

Decompressive craniectomy is also an option for some cases (e.g malignant hemispheric infarctions >50% of MCA in younger patients, )


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