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EM SAQsRaised intracranial pressure

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.

10 marks10 min2 min readSource-verified ·

Target exams

ACEMFRCEMABEM
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Target exams

ACEMFRCEMABEM
Prompt
A 60-year-old woman presents with a 2-week history of progressive early-morning headache and vomiting. In the department she becomes drowsy. Her blood pressure is 180/95, heart rate 48, and her respiratory pattern is irregular. Outline your assessment and immediate management, including the airway, the ventilation, the osmolar therapy and the disposition. (10 marks)

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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]

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References5ShowHide
  1. [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. [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
  3. [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
  4. [12]Kim H. Anesthetic management of the traumatic brain injury patients undergoing non-neurosurgery. Anesthesia and Pain Medicine, 2023.PMID 37183278
  5. [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
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