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Raised Intracranial Pressure (ICP)

Emergency Neurological Life Support Intracranial Hypertension and Herniation Protocol Version 4.0. Last updated: Mar 2020.

Raised Intracranial Pressure (ICP)

Raised intracranial pressure (ICP) is an elevation of pressure within the cranial vault, usually defined as sustained ICP above 20–22 mmHg.

This updated UKMLA guide to raised intracranial pressure is based on Emergency Neurological Life Support guidelines, which cover relevant physiology, causes, symptoms, diagnosis, and management.

Relevant Physiology

The cranium is a rigid, non-expandable structure containing 3 main intracranial volume components:

  • Brain tissue
  • CSF
  • Blood

Monro-Kellie principle:

  • The Monro-Kellie principle states that the total intracranial volume must remain constant because the skull cannot expand
  • Therefore, if the volume of one component increases, e.g. due to haemorrhage, cerebral oedema, tumour, this must be offset by a compensatory reduction in another component
  • Early compensatory mechanisms include
    • Displacement of CSF into the spinal canal
    • Reduction in intracranial venous blood volume

Once the early compensatory mechanisms are exhausted, even a small further increase in intracranial volume can cause a rapid rise in ICP.

Why raised ICP is dangerous

The main danger of raised ICP is reduced cerebral perfusion pressure (CPP), meaning reduced blood flow to the brain.

  • CPP = pressure gradient driving cerebral blood flow
  • CPP = mean arterial pressure (MAP) – intracranial pressure (ICP)
  • As ICP rises, CPP falls. If CPP falls too low, cerebral blood flow becomes inadequate, causing cerebral ischaemia

Causes and Risk Factors

Structural causes (most important): [Ref]

Category Causes
Increase in brain tissue Space-occupying lesion (mass effect)

  • Tumour
  • Abscess
  • Haematoma
Cerebral oedema (increase in brain volume)

  • Encephalitis / meningitis
  • Trauma
  • Hypoxic ischaemic injury
  • Hypertensive encephalopathy
  • Metabolic / toxins (e.g. hyponatraemia, DKA, hepatic encephalopathy)
Increase in blood volume
  • Intracranial haemorrhage (EDH, SDH, SAH, ICH)
  • ↑ Cerebral blood flow
    • Hypercapnia
    • Aneurysms
    • AVMs
  • Venous obstruction (technically considered a secondary cause)
    • Cerebral venous sinus thrombosis
    • Jugular vein thrombosis
    • SVC syndrome
    • ↑ Central venous pressure (e.g. heart failure)
Increase in CSF
  • Obstructive hydrocephalus (→ reduced CSF absorption)
  • Choroid plexus tumour (→ increased production)

Other causes: [Ref]

  • Idiopathic intracranial hypertension (IIH)
  • Secondary causes of ↑ ICP [Ref1][Ref2]
    • Medications
      • Antibiotics: tetracyclines, fluoroquinolones
      • Retinoids / vitamin A derivatives
      • Hormones and steroids: corticosteroid withdrawal, anabolic steroids, growth hormone, oral contraceptives
      • Growth hormone
      • Lithium
    • Systemic and medical disorders
      • CKD, uraemia, OSA, COPD
      • SLE
      • Infections: HIV, Lyme disease, varicella, psittacosis, CNS infections, otitis media, mastoiditis
    • Endocrine disorder
      • Addison’s disease, adrenal insufficiency
      • Thyroid and parathyroid disorders
      • Cushing’s syndrome
    • Haematological disorders
      • Anaemia (including severe iron deficiency)
      • Thrombophilia
      • Polycythaemia vera
    • Syndromic / genetic conditions
      • Down syndrome
      • Turner syndrome
      • Craniosynostosis

Clinical Features

[Ref1][Ref2][Ref3]

Category Clinical features
General features of raised ICP
  • Headache
    • Often worse in the morning
    • Worse with lying flat, coughing, straining, sneezing
  • Nausea and vomiting
  • Papilloedema and visual disturbances
  • CN VI palsy (due to the long intracranial course / stretch) → horizontal diplopia
  • Pulsatile tinnitus (whooshing or humming sound that occurs with the heartbeat)
Late / advanced features of raised ICP
  • Cushing’s reflex – triad of hypertension (or wide pulse pressure) + bradycardia + irregular breathing
  • Abnormal posturing
  • Reduced consciousness
Features suggesting brain herniation
  • CN III palsy (classically seen in uncal herniation)
    • Asymmetrical pupils
    • Fixed, dilated pupil
    • Ipsilateral ptosis + “down and out” eye
  • Contralateral hemiparesis
  • Decorticate or decerebrate posturing
  • Apnoea (classically seen in tonsillar herniation, compressing the medulla)

Main types of brain herniation:

Type Description
Uncal herniation Herniation of the medial temporal lobe down the tentorium cerebelli, often compressing CN III
Tonsillar herniation Herniation of the inferior cerebellum down the foramen magnum, often causing brainstem compression (esp. medulla)
Subfalcine herniation Herniation of the cingulum of the medial frontal lobe, under the subfalcine falx

Investigation and Diagnosis

Clinical assessment: [Ref]

  • Comprehensive clinical history
  • Medication review (e.g. steroids, retinoids, tetracyclines, COCPs)
  • Ophthalmic and neurological examination
  • Measure blood pressure to assess for malignant hypertension / hypertensive emergency

Investigations: [Ref]

Investigation Description
1st line investigation: neuroimaging Non-contrast CT head is often performed initially to identify underlying causes of raised ICP

MRI may also be useful

Lumbar puncture Lumbar puncture should ONLY be performed after neuroimaging

  • Opening pressure >20 cm H₂O is suggestive of raised ICP
  • However, this is only supportive, not definitive confirmation of raised ICP
Definitive: invasive ICP monitoring Provides continuous, real-time measurements

Raised ICP is defined as a sustained (> 5 min) elevation of ICP to >22 mmHg

Raised ICP is often broadly defined as ICP >20 mmHg. However, modern guidelines commonly use sustained ICP >22 mmHg as a treatment threshold when invasive ICP monitoring is in place.

Do not perform lumbar puncture before neuroimaging if raised ICP is suspected, due to the risk of brain herniation if there is a space-occupying lesion.

If raised ICP is due to a space-occupying lesion, removing CSF from the spinal canal during lumbar puncture can create a pressure gradient between the skull and spinal canal. This can pull brain tissue downwards and cause brain herniation, especially tonsillar herniation, which can compress the brainstem and become rapidly fatal.

Management

Temporary Acute Management

There are different tiers of raised ICP management, aiming to reduce ICP and prevent brain herniation. If raised ICP or impending herniation is clinically suspected, acute ICP-lowering measures should not be delayed while awaiting investigations.

All ICP-lowering interventions should be viewed as temporising measures to prevent or reverse herniation while the underlying cause is identified and treated.

Management tier Component / description
Tier 0 – standard preventive measures The following should be performed in those who are at risk of raised ICP

  • Assess ABC, intubate if GCS ≤8
  • Elevate the head of the bed to >30°
  • Supportive care
    • Provide appropriate analgesia and/or sedation
    • Maintain normothermia (aggressively manage fever)
    • Avoid and correct hyponatraemia

High-dose corticosteroid should only be given in raised ICP due to vasogenic oedema, most commonly caused by brain tumours or abscess

Apart from brain tumour and abscess, corticosteroids are contraindicated in TBI and most other causes of raised ICP. [Ref]

Tier 1
  • Hyperosmolar therapy (both have equivalent efficacy)
    • Hypertonic saline (IV 2-23.4%), or
    • Mannitol (IV bolus)
  • Temporary controlled hyperventilation (for <2 hours)
Tier 2
  • Increase serum sodium goals for hyperosmolar therapy
  • Optimise sedation and analgesia (e.g. propofol)
  • Consider rescue decompressive surgery
Tier 3 For patients who are NOT a surgical candidate:

  • Sedation with pentobarbital (guided by ICP goal or until burst suppression on continuous EEG)
  • Hyperventilation
  • Moderate hypothermia (target core temperature 32–34°C)

Definitive Management

ICP-lowering measures (mentioned above) buy time, but definitive management is treatment of the underlying cause.

Some high-yield cause-specific management:

Cause of raised ICP Management
Intracranial tumour / metastasis Definitive tumour treatment options include neurosurgical resection, radiotherapy, chemotherapy

See the Brain Tumours in Adults article for more information

Brain abscess Aspiration + IV antibiotics

See the Brain Abscess article for more information

Hydrocephalus EVD in the acute setting
Extradural or subdural haematoma Urgent neurosurgical evacuation

See the Extradural Haemorrhage (EDH) and Subdural Haemorrhage (SDH) article for more information

Subarachnoid haemorrhage Neurosurgical clipping or endovascular coiling (if secondary to aneurysm)

See the Subarachnoid haemorrhage (SAH) article for more information

Intracerebral haemorrhage BP control, reverse anticoagulation if appropriate

See the Haemorrhagic Stroke article for more information

Cavernous venous sinus thrombosis Anticoagulation with heparin

See the Cerebral Venous Sinus Thrombosis (CVST) article for more information

Encephalitis / meningitis IV antimicrobials depending on the suspected cause.

See the Encephalitis and Meningitis article for more information

References

Related Articles

Papilloedema

Idiopathic Intracranial Hypertension (IIH)

Brain Abscess

Meningitis

Encephalitis

Brain Tumours in Adults

Head Injury in Adults

Extradural Haemorrhage (EDH)

Subdural Haemorrhage (SDH)

Subarachnoid haemorrhage (SAH)

Haemorrhagic Stroke

Cerebral Venous Sinus Thrombosis (CVST)

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