Intracranial pressure (ICP) is the pressure that exists within the cranium, including its compartments (e.g., the subarachnoid space and the ventricles). ICP varies as the position of the head changes relative to the body and is periodically influenced by normal physiological factors (e.g., cardiac contractions). Adults in the supine position typically have a physiological ICP of ≤ 15 mm Hg; an ICP of ≥ 20 mm Hg indicates pathological intracranial hypertension. ICP may be elevated in a variety of conditions (e.g., intracranial tumors) and can result in a decrease in cerebral perfusion pressure (CPP) and/or herniation of cerebral structures. Symptoms of elevated ICP are generally nonspecific (e.g., impaired consciousness, headache, vomiting); however, more specific symptoms may be present depending on the affected structures (e.g., Cushing triad if the brainstem is compressed). Findings from brain imaging (e.g., a midline shift) and physical examination (e.g., papilledema) can indicate ICP elevation but may not be able to rule it out. Therefore, ICP monitoring and quantification are vital in at-risk patients. Management usually involves expedited surgery of resectable or drainable lesions, conservative measures (e.g., positioning, sedation, analgesia, and antipyretics), and medical therapy (e.g., hyperosmolar therapy such as mannitol or hypertonic saline, or glucocorticoids). Treatment options for refractory intracranial hypertension include temporary controlled hyperventilation, CSF drainage, and decompressive craniectomy (DC), as well as other advanced medical therapies (e.g., barbiturate coma, therapeutic hypothermia).
Physiology of ICP 
- Physiological ICP is ≤ 15 mm Hg in adults (in supine position); children generally have a lower ICP.
- ICP varies depending on the position of the head relative to the rest of the body and is influenced by certain physiological processes (e.g., cardiac contractions, sneezing, coughing, Valsalva maneuver).
- Volume of intracranial contents 
- Brain: approx. 85%
- CSF: approx. 10%
- Blood: approx. 5%
Monro-Kellie principle: The sum of volumes of intracranial blood, CSF, and brain within the cranium is constant, which means that an increase in one component volume will be compensated for by a decrease in other(s). 
- Initial compensation allows for an increase in component volume with minimal change in ICP.
- Once the compensatory mechanisms are exhausted, ICP increases rapidly because of the skull's inability to expand and accommodate the increase in intracranial volume.
Physiology of cerebral blood flow
- Cerebral blood flow (CBF): the volume of blood (in mL) supplied to 100 g of brain tissue per minute 
- Cerebral autoregulation
Cerebral perfusion pressure (CPP): the effective pressure that delivers blood to the brain and is responsible for constant perfusion of brain tissue
- CPP = MAP - ICP
- A CPP of 0 equals the absence of brain perfusion.
- Cerebral perfusion is predominantly modulated by the partial pressure of carbon dioxide (pCO2).
- CPP linearly increases with pCO2 until pCO2 > 90 mm Hg. 
- Cerebral perfusion is, to a lesser degree, modulated by brain temperature through cerebral metabolism. 
- Partial pressure of oxygen (pO2) only modulates cerebral perfusion in severe hypoxic conditions when pO2 < 50 mm Hg.
Consequences of elevated ICP
- Decreased cerebral perfusion CPP
- Brain tissue herniation
- ↑ ICP → ↓ CPP → compensatory activation of the sympathetic nervous system → ↑ systolic blood pressure → stimulation of aortic arch baroreceptors → activation of the parasympathetic nervous system (vagus) → bradycardia 
- ↑ Pressure on brainstem → dysfunction of respiratory center → irregular breathing
- Most common type of cerebral herniation
- Mass effect due to affection of the ipsilateral frontal, parietal, or temporal lobes → medial displacement of the cingulate gyrus → herniation under the falx cerebri → compression of:
- Usually no pupillary involvement
Descending transtentorial herniation
Uncal herniation: mass effect caused by a supratentorial lesion → medial and downward displacement of the uncus at the tentorial incisure
- Early manifestations
- Ipsilateral posterior cerebral artery compression→ cortical blindness with contralateral homonymous hemianopia
- Ipsilateral oculomotor nerve compression → Hutchinson pupil (ipsilateral fixed and dilated pupil)
- Ipsilateral cerebral peduncle compression → contralateral hemiparesis
- Midline shift → altered consciousness
- Late manifestations
- Early manifestations
- Central herniation: mass effect caused by bilateral or midline supratentorial lesions or severe brain edema → downward displacement of the diencephalon, midbrain, and pons
Foramen magnum herniation
- Structures of the posterior fossa (e.g., cerebellar tonsils, medulla) herniate through the foramen magnum
- Symptoms include:
The following clinical features should raise suspicion for a cerebral herniation syndrome, which can be fatal if not treated promptly: acutely worsening level of consciousness (e.g., coma), pupillary changes (e.g., ipsilateral mydriasis, fixed dilated pupils), new focal neurological deficits (e.g., hemiparesis, decerebrate posturing), and cardiorespiratory compromise (e.g., bradycardia, apnea).
Neuroimaging (CT head/MRI head) 
Neuroimaging findings of intracranial hypertension: indirect indicators of elevated ICP and cerebral edema
- Midline shift
- Mass lesions
- Effacement of the basilar cisterns
- Effacement of cerebral sulci
- Evidence of brain herniation (e.g., uncal herniation or tonsillar herniation)
- Changes in ventricular size (e.g., enlarged with hydrocephalus, reduced with diffuse cerebral edema)
Invasive ICP monitoring
- Invasive monitoring is typically required for confirmation and accurate measurement of ICP.
- ICP should be evaluated in combination with CPP to guide therapeutic interventions and help prevent secondary brain injury and brain herniation. 
- There are no absolute contraindications for invasive ICP monitoring.
- Consider the risks versus the benefits in consultation with a specialist.
- Traumatic brain injury: ICP monitoring in severe TBI reduces in-hospital and two-week postinjury mortality. 
- Mass lesions: e.g., brain tumors, ICH, SAH, SDH, EDH
- Diffuse brain injury due to:
- Other: nonsurgical intracranial hemorrhages in patients who cannot undergo full clinical evaluation
Methods to monitor ICP 
Intraventricular catheters; with an external ventricular drain (EVD) and intraparenchymal catheters; (IPC) are most commonly used to monitor ICP, as they have the highest accuracy compared with other monitoring methods.
Intraventricular catheter: a monitoring device placed into the ventricles of the brain along with a CSF drainage system (i.e., an EVD) 
- Allows for continuous ICP monitoring and evaluation of intracranial compliance
- Useful in conditions in which CSF drainage is required for both diagnostic and therapeutic purposes
- The preferred monitoring method for intracranial lesions associated with hydrocephalus 
- Hemorrhage attributable to the placement of the device
- Malpositioning and/or accidental removal
- Blockage with blood or debris
- Intraparenchymal catheter: a fiberoptic device placed into the brain parenchyma without an accompanying CSF drainage system 
- Generally, ICP > 20 mm Hg indicates intracranial hypertension, which requires treatment. 
- ICP varies in a complex cyclical manner and is influenced by hemodynamic and metabolic factors.
- Monitor ICP along with to calculate using the formula CPP = MAP − ICP.
Do not use the ICP value in isolation as a prognostic marker or to inform therapeutic decisions. 
- Indications for ICP management
- Goals: Maintain (CBF) and prevent .
- Acute resuscitation and stabilization: Follow the .
- Consultation: Early involvement of neurosurgery and a neurocritical care specialist is essential.
|Stepwise ICP management (based on a multifactorial response) |
|Subsequent step|| |
|Elective temporizing step|
- General therapeutic targets: Base treatment decisions on trends identified using repeat assessments of ICP, CPP, and clinical status. 
Conservative therapy 
See also “Neuroprotective measures.”
- Patient positioning :
Sedation and analgesia 
- Prevents unnecessary spikes in ICP due to pain, agitation, and patient-ventilator dyssynchrony
- Combinations of benzodiazepines, opioid analgesics, and dexmedetomidine are generally used.
- Ketamine was previously contraindicated, but recent evidence suggests that it may be suitable for use.
- Propofol may be used but caution should be taken when using high doses because of the risk of hypotension. 
- Minimize waking patients up for neurological assessments.
- See “ ” for dosages and further information.
- Temperature management: : Maintain normothermia; fever should be treated with antipyretics.
- Fluid management: Target euvolemia and avoid serum hypoosmolarity.
- Seizure control
Medical therapy 
- Hyperosmolar therapy
|Overview of hyperosmolar therapies in ICP management |
|Therapeutic targets to consider |
|Adverse effects |
|Considerations || || |
Although hyperosmolar therapies can lower ICP, they have not been shown to improve neurological outcomes in patients with underlying TBI, acute ischemic stroke, ICH, SAH, or hepatic encephalopathy. 
Glucocorticoids: e.g., dexamethasone
- Recommended only if elevated ICP is caused by vasogenic edema secondary to: 
- Avoid in patients with ICH. 
- Not recommended in large hemispheric stroke 
- Contraindicated in TBI (associated with increased mortality) 
- Emergency surgery (if possible): e.g., resection of brain tumor, hematoma evacuation 
- Indications 
- Risks: hemorrhage, infection (e.g., ventriculitis, encephalitis, meningitis)
Decompressive craniectomy (DC): removal of a portion of the skull, which allows the brain to expand in volume, thereby reducing ICP 
- Primary DC: removal of a skull flap following evacuation or resection of an intracranial lesion (e.g., brain tumor)
- Secondary DC: removal of a skull flap without additional surgical procedures to treat refractory elevated ICP
- Recommended for (controversial): 
- Late refractory elevated ICP: reduced mortality, improved outcomes
- Early or late refractory elevated ICP: improved control of ICP, reduced neuro-ICU length of stay
- Large hemispheric stroke (e.g., malignant MCA infarction) in patients with an infarct > 12 cm and within 24–48 hours of symptom onset 
- Not recommended for patients with early refractory elevated ICP
- Recommended for (controversial): 
- Multiple approaches have been described in the literature (suboccipital, subtemporal, frontotemporoparietal, etc.) depending on the type and location of the brain lesion. 
- Lowers mortality in TBI without improving neurological or functional outcomes 
Nonsurgical therapy for refractory intracranial hypertension 
- Indications 
- Therapeutic targets
Controlled hyperventilation should only be used short-term and is not recommended routinely or for prophylaxis. Avoid excessive hyperventilation (PaCO2 < 30 mm Hg), prolonged hyperventilation, and hypoventilation of any kind, as CBF and perfusion may become compromised.
These are primarily reserved for patients with persistently refractory intracranial hypertension.
- Barbiturate coma: e.g., pentobarbital (off-label, not routinely recommended) 
Therapeutic hypothermia: highly controversial 
- No benefit has been observed when used prophylactically 
- Not recommended in TBI 
- Definition: excess accumulation of fluid within the brain parenchyma as a result of damage to the blood-brain barrier and/or the blood-CSF barrier 
|Overview of cerebral edema subtypes|
|BBB integrity|| || |
We list the most important complications. The selection is not exhaustive.