This article provides a clinical run-through of increased intracranial pressure for the USMLE step 2 examination. It defines raised ICP, runs through its pathophysiology, progression and special forms, diagnosis, differential diagnosis and treatment (management including patient monitoring).
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Computed tomography of human brain

Image: “Computer tomography of human brain, from base of the skull to top. Taken with intravenous contrast medium.” by Department of Radiology, Uppsala University Hospital. Uploaded by Mikael Häggström. License: CC0 1.0

Definition of Increased Intracranial Pressure

Intracranial pressure is usually less than or equal to 15 mmHg in the adult patient, and slightly lower in children. A raised intracranial pressure is defined as one above 20 mmHg.

Constant monitoring is needed for a true representation of ICP and intraventricular monitoring is considered the gold standard. However, raised ICP can be diagnosed via a thorough history and examination and often therapy will have to be started acutely before monitoring can be initiated and, as such, knowing how to identify raised ICP in clinical practice is incredibly important.

Pathophysiology of Increased Intracranial Pressure

Monroe doctrine says that because the brain is a defined “box” or incompressible space, the volume inside the cranium is fixed. There are a number of constituents to the inside of the cranium (blood, CSF, brain tissue) and increased in any one volume will decrease the volume of another.

The brain tissue (or parenchyma) usually makes up around 80% of the fixed internal volume (which itself is usually between 1,400 and 1,700 mL). The CSF makes up around 10% of total volume (around 150 mL) and blood the final 10%. As discussed previously, when any of these is increased, either the others must decrease or the intracranial pressure must increase (or both processes occur simultaneously).

Intracranial pressure is raised by a number of pathological processes, including masses (like tumors) abscesses and blood (hematomas). Impaired CSF flow can also cause a rise in intracranial pressure. This is because CSF is produced in the choroid plexus (amongst other areas) and is reabsorbed by arachnoid granulations back into the venous system. Blockages can stop the reabsorption of CSF increasing its volume and raising intracranial pressure.

Subfalcine herniation

Image: “CT scan of Subfalcine Herniation.” by RadsWiki. License: CC BY-SA 3.0

Herniation can occur when focal or global pressure force portions of the brain into the wrong area. For instance:

  • Subfalcine herniation
  • Uncal herniation
  • Tonsillar herniation

Progression and Special Forms

When the intracranial pressure increases beyond a certain point, herniation can occur. This can be:

  • Subfalcine (cingulate gyrus) herniation where the cingulate gyrus is displaced underneath the falx to the opposite side. This can cause compression of branches of the anterior cerebral artery.
  • Transtentorial (uncal, mesial temporal) herniation where the medial aspect of the temporal lobe is compressed against the tentorium cerebelli.
  • Tonsillar herniation where there is displacement of the cerebellar tonsils through the foramen magnum. This can cause compression of medullary respiratory centers.

Diagnosis of Increased Intracranial Pressure

A patient with raised intracranial pressure will usually have a headache. The current thinking is that this is the result of cranial nerve V pain fibers running along the dura and blood vessel. Patients may also have reduced consciousness; this can be from local lesions or from pressure pushing on the reticular formation (which is a structure in the brainstem involved in consciousness). Patients may also experience vomiting.


Image: “Papilledema is a swollen optic disc caused by increased intracranial pressure.” by Jonathan Trobe, M.D. – University of Michigan Kellogg Eye Center – The Eyes Have It. License: CC BY 3.0

On examination, funduscopy should be performed. Often raised ICP can be visualized as papilledema. A full cranial nerve examination should be conducted as cranial nerve VI palsies are common with raised ICP. (Cranial nerve VI, the abducens nerve, controls the lateral rectus muscle of the eye. Patients will present with eye resting in the adducted position. They may complain of double vision or “diplopia”).  If patients exhibit Cushing’s triad (bradycardia, respiratory depression and hypertension), then immediate intervention is needed.

Other symptoms and examination findings are localized and can be different dependent on the localization of the lesion. Herniation syndromes can also result in neurological deficits.

The only truly reliable diagnosis is investigation via IVP monitoring, although most diagnoses will rest on clinical findings and a good history.

Differential diagnosis

Below is a summary of major reasons for an increase in intracranial pressure. Usually, the differential for those with raised ICP will be much smaller than this list as patients don’t usually present with “raised intracranial pressure” and a diagnosis is more obvious given the total clinical picture. However, this is an important list to keep in mind if the immediate cause is unknown.


Image: “CT scan of a brain with hydrocephalus.” by Lucien Monfils – Own work. License: CC BY-SA 3.0

  • Space occupying lesions, i.e. a tumor or a hematoma
  • Edema
  • Increased CSF production
  • Decreased CSF absorption
  • Obstructive hydrocephalus
  • Obstruction of venous outflow
  • Idiopathic causes

Space occupying lesions are self-explanatory in that they are tumors or hematomas. Cerebral edema can be caused by a number of things, including traumatic brain injury, an infarction and ischaemic encephalopathy.

A choroid plexus papilloma can cause an increased CSF production, whilst decreased production can be the result of adhesions on the arachnoid granulations (typically the result of meningitis). An obstruction in the venous outflow can be from a venous sinus thrombosis or jugular vein compression.

Management of Increased Intracranial Pressure

Although early interventions will often be performed without direct monitoring of raised ICP, therapies are reversible and therefore a goal of treatment should be to place an ICP monitoring device. CT scans can show a raised ICP (i.e. with the presence of a tumor or a hemorrhage); however, they are unreliable and other methods to define ICP should be performed.

Intraventricular monitors are considered the gold standard. Infection risk is very high with this equipment and occurs in some 20% of patients. There is also a small, but substantial risk, of hemorrhage (at around 2%) – this risk is greater in those with coagulopathies.

Other methods of measuring ICP include intraparenchymal devices (that are inserted directly into brain parenchyma via a small bore hole in the skull), subarachnoid bolts or epidural monitoring devices.

Many simple end of the bed practices can make a massive difference. Raising the head of the bed by 45 degrees or not putting circumferential tape around the neck for securing ETT (jugular venous pressure).

Patients should be hyperventilated with around 25-30 mmHg of PCO2, although this is not absolute. Hyperventilation works because CO2 induces vasoconstriction and can decrease the volume of intracranial blood (reducing one of the three components determining intracranial pressure). It is useful in raised ICP as a result of cerebral edema, intracranial hemorrhage or tumor.

However, its use is not indicated in those with traumatic brain injury or acute stroke. This is because it reduces cerebral perfusion and can worsen neurological outcomes. As such, the underlying cause of raised ICP should be discussed before hyperventilation.

Patients can be given antiepileptic therapies. This is because patients are at an increased risk of developing seizures with a raised ICP and these can complicate the clinical picture. As such, antiepileptics should be prescribed in any individual where a seizure has happened or has been suspected to have occurred. Prophylactic treatment can also be given, but there are currently no clear guidelines as to when and where to give this.

In many cases where the underlying cause is not known or is untreatable, diuretics can be given to reduce blood volume and thus ICP. The first line diuretic is usually Mannitol at 2 g/kg (although some evidence suggests it should be given at 0.5 g/kg).

Hypertonic saline can be given to acutely lower the ICP. The volume of saline is governed by no guideline and will be different between hospitals. Some studies have suggested that hypertonic saline bolus is more efficacious than Mannitol.

In patients with a CNS neoplasia, IV steroids (glucocorticoids) are indicated and have a role in management. In hemorrhagic raised ICP and severe head injury induced increased ICP these therapies are associated with a worse outcome in large controlled trials and should not be used.

In some instances, CSF can be removed to relieve ICP. This is indicated in patients with hydrocephalus. CSF can be removed at a raise of 1-2 mL a minute for 2 minutes each procedure.

Patients may also undergo decompressive craniotomy, whereby the finite volume that can be housed in the skull is increased; therefore, reducing pressure on brain parenchyma etc. However, this surgery is not without complications and herniation can occur; infection of hemorrhage may worsen the clinical picture.

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