EM SAQs · Raised intracranial pressure
Raised intracranial pressure — assessment and emergency management
An ACEM-style SAQ on the recognition and emergency management of raised intracranial pressure.
On this page
Study tools
Target exams
Model answer
Reveal model answerShowHide
Recognition. The combination of progressive morning headache with vomiting, papilloedema and a decreased conscious level is raised intracranial pressure. The blood pressure of 180/95 with a heart rate of 48 and irregular respiration is the Cushing triad — a late, pre-terminal sign meaning cerebral herniation is imminent or underway. Act now.
Airway. The patient is drowsy with an irregular respiratory pattern — protect the airway. Intubate early (rapid-sequence induction with a neuroprotective agent) if the GCS is 8 or below or the airway or oxygenation cannot be maintained.[1]
Breathing. Ventilate to normocapnia — a PaCO2 of 35 to 40 mmHg. Do NOT prophylactically hyperventilate. Maintain the oxygenation at or above 95 per cent (or PaO2 ≥80 mmHg).[2]
Circulation. Defend CPP at 60 to 70 mmHg. BTF 4th-edition SBP floors are age-stratified: ≥100 mmHg if aged 50 to 69 years, ≥110 mmHg if aged 15 to 49 or over 70. The Cushing hypertension does NOT mean you lower the pressure. Positioning and tier-1 measures. Elevate the head to 30 degrees with the head neutral to aid the venous drainage. Ensure sedation and analgesia, normothermia, normoglycaemia, and seizure control.[12]
Osmolar therapy. Give mannitol 0.5 to 1 g per kg intravenously (2.5 to 5 mL/kg of 20%) OR hypertonic saline (3 per cent, or 23.4 per cent 30 to 60 mL) immediately as a bridge to definitive treatment. A historical caution is to watch osmolarity because mannitol may precipitate AKI above 320 mOsm per L.[1]
Investigation. An urgent CT head (once intubated and stable for transfer) to identify the cause — a tumour, haematoma, abscess, or hydrocephalus — and to show the midline shift and the effaced basal cisterns. NEVER perform a lumbar puncture when raised ICP is suspected.[1]
Disposition. Call the neurosurgeon immediately. Admit to a neurosurgical or intensive-care bed with an intracranial-pressure monitor. For a tumour with vasogenic oedema, add dexamethasone (4 to 8 mg/day if mild symptoms; 16 mg/day or more if severe mass effect — Ryken, metastases) — but do NOT give steroids if the cause is trauma (CRASH: 21.1% vs 17.9% 2-week mortality).[16][4]
References5ShowHide
- [1]Carney N, Totten AM, O'Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery, 2017.PMID 27654000
- [2]Godoy DA, Seifi A, Garza D, Lubillo-Montenegro S, Murillo-Cabezas F. Hyperventilation Therapy for Control of Posttraumatic Intracranial Hypertension. Frontiers in Neurology, 2017.PMID 28769857
- [4]Roberts I, Yates D, Sandercock P, et al. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet, 2004.PMID 15474134
- [12]Kim H. Anesthetic management of the traumatic brain injury patients undergoing non-neurosurgery. Anesthesia and Pain Medicine, 2023.PMID 37183278
- [16]Ryken TC, McDermott M, Robinson PD, et al. The role of steroids in the management of brain metastases: a systematic review and evidence-based clinical practice guideline. Journal of Neuro-Oncology, 2010.PMID 19957014