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Symptoms and signs of raised intracranial pressure

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Suspected intracranial pressure crisis

Falling consciousness, a new unequal or poorly reactive pupil, new focal weakness or posturing, seizure without recovery, or abnormal breathing can indicate expanding mass effect and impending brain herniation.

Action: Call emergency, anaesthetic and neurosurgical help now; stabilise airway, oxygenation and circulation, keep the head elevated and midline when safe, repeat a documented neurological examination, and arrange immediate brain imaging without delaying resuscitation.

Synopsis

Recognise raised intracranial pressure across acute and slower presentations, interpret age-dependent symptoms and examination changes, and escalate threatened herniation before late cardiovascular signs appear.

  • Raised intracranial pressure is a physiological state with many causes; headache and vomiting may suggest it, but deterioration in consciousness, pupils, motor responses or breathing determines emergency urgency.
  • Do not wait for the complete Cushing triad: hypertension, bradycardia and irregular breathing commonly appear together only late in an intracranial pressure crisis.
  • Age changes the presentation: infants may show head enlargement, a tense fontanelle and irritability, while older children and adults more often report headache, vomiting, transient visual obscurations or diplopia.

Key red flags

A new reduction in alertness, agitation or abnormal behaviour, especially when the motor component of the Glasgow Coma Scale worsens.

A newly dilated, unequal or less reactive pupil, new gaze abnormality, facial asymmetry, hemiparesis or extensor or flexor posturing.

Severe or rapidly increasing headache with repeated vomiting, collapse, seizure, visual obscurations or diplopia from impaired ocular movement.

Irregular respirations, apnoea, systemic hypertension with bradycardia or loss of protective airway reflexes are late signs and demand immediate treatment.

In an infant, a tense fontanelle, accelerating head circumference, separated sutures, persistent vomiting, lethargy, irritability or downward deviation of the eyes.

Papilloedema or suspected optic-disc swelling requires urgent cause-finding and visual assessment even when central visual acuity remains apparently normal.

Consciousness and behaviour

Look for slowing, confusion, irritability, agitation, drowsiness and reduced GCS. Record eye, verbal and motor components separately and compare with a reliable baseline. A small sustained motor decline can be more consequential than an unchanged total score suggests.

Pupils and motor signs

Measure pupil size and light response, eye position, facial movement and limb power. New unilateral pupillary dilation with reduced consciousness and opposite-sided weakness is a cardinal transtentorial herniation pattern, although atypical or bilateral findings occur.

Late physiological response

Systemic hypertension, often with widened pulse pressure, bradycardia and irregular respiration or apnoea represents brainstem compromise. The full Cushing response is uncommon and late, so its absence cannot reassure after earlier neurological deterioration.

Reasoning priorities

01
Serial structured neurological observations

Detect clinically meaningful change in consciousness, pupils, limb movement and cardiorespiratory physiology rather than relying on one examination.

In traumatic head injury, NICE specifies GCS components, pupil size and reactivity, limb movements, respiratory rate, heart rate, blood pressure, temperature and oxygen saturation. Any confirmed deterioration triggers urgent medical reassessment and consideration of immediate CT.

Worked reasoning

Worked case: acute deteriorationHeadache, vomiting and declining consciousness

A patient becomes drowsier with a new pupil or focal motor change, with or without a known intracranial lesion.

  1. Recognise an intracranial pressure crisis from the trajectory, call senior emergency, anaesthetic and neurosurgical teams, and perform simultaneous airway, breathing and circulation assessment with continuous oxygen saturation and blood-pressure monitoring.
  2. Protect the airway when indicated, avoid hypoxaemia and hypotension, elevate the head more than 30 degrees and keep it midline if spinal and circulatory safety permit, while documenting GCS components, pupils and limb responses.
  3. Obtain immediate non-contrast CT as soon as the patient can be positioned safely; do not send an unstable patient away from resuscitation or delay presumptive herniation treatment for a complete classic triad.
  4. Treat the identified cause with the neurocritical and neurosurgical team, reassess after every intervention, and escalate persistent herniation signs to hyperosmolar, CSF-diversion or operative pathways matched to aetiology and age.
  5. Verify response through repeated examination, cardiorespiratory physiology, imaging and ICP data when present; continued decline overrides an initially reassuring result.
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Sources and review status4 sources · checked 13 Sept 2026 · clinical review pending
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 13 Sept 2026; clinical approval remains outstanding.

Authoring stateRapid draftClinical stateAwaiting reviewJurisdictionUnited Kingdom