Management of Raised Intracranial Pressure
Clinical Recognition
Raised ICP should be suspected clinically in any patient with neurological injury who develops worsening headache, progressive alteration in consciousness, new vomiting, visual changes, or focal neurological signs. The classic Cushing’s triad — hypertension, bradycardia, and irregular respirations — represents brainstem compromise from raised ICP and impending herniation. It is a pre-terminal sign that demands immediate intervention.
Papilloedema on fundoscopy indicates chronically raised ICP (it takes hours to days to develop) and will not be present in the acute phase of ICP elevation — its absence does not exclude raised ICP. Pupillary changes — initially ipsilateral dilatation and loss of reactivity — indicate compression of cranial nerve III by transtentorial herniation and are a neurosurgical emergency.
Stepwise Management of Raised ICP
ICP management follows a stepwise approach, escalating through interventions in order of invasiveness and risk:
| Step | Intervention | Mechanism and Notes |
| 1 | Head-up 30°, head midline | Facilitates venous drainage from the cranium via the internal jugular veins. Ensure ETT ties or cervical collars are not compressing the neck veins. |
| 2 | Optimise MAP and CPP | If hypotensive, vasopressors to achieve MAP ≥65–70 mmHg. Adequate CPP is the first priority. |
| 3 | Normocapnia (PaCO2 4.5–5.0 kPa) | Avoid hypercapnia — even mild CO2 retention causes significant cerebrovascular vasodilation and ICP rise. |
| 4 | Adequate sedation and analgesia | Agitation, coughing, and pain all cause ICP spikes. Ensure adequate sedation depth in ventilated patients. |
| 5 | Treat fever | Every 1°C of fever increases CMRO2 by ~7% and worsens cerebral oedema. Target normothermia with paracetamol and cooling measures. |
| 6 | Osmotherapy — Mannitol 20% | 0.5–1 g/kg IV over 15–20 minutes. Reduces ICP within 15 minutes; effect lasts 2–6 hours. Monitor serum osmolality (stop if >320 mOsm/kg) and electrolytes. Can repeat every 4–6 hours. |
| 7 | Osmotherapy — Hypertonic saline | 3% NaCl or higher concentrations. Effective alternative or adjunct to mannitol. May be preferred if hypovolaemic. Monitor sodium (target 145–155 mmol/L). |
| 8 | Acute hyperventilation | Target PaCO2 3.5–4.0 kPa for maximum 30–60 minutes as a bridge to definitive treatment. Causes cerebral vasoconstriction; reduces ICP rapidly but risks ischaemia if sustained. |
| 9 | CSF drainage | Via external ventricular drain (EVD). Most effective ICP management available; also allows ICP monitoring. Requires neurosurgical placement. |
| 10 | Decompressive craniectomy | Surgical removal of a section of skull to allow brain expansion. Reduces mortality in malignant MCA infarction (DESTINY II) and refractory TBI. Neurological outcomes vary. |
| Pitfalls in ICP Management • Dexamethasone is NOT indicated in TBI — the CRASH trial showed increased mortality, but it is indicated in cerebral oedema surrounding tumours and in bacterial meningitis (before or with the first dose of antibiotics) • Hyperventilation is a temporising measure only — do not use it as definitive ICP management • High PEEP (>10–12 cmH2O) impairs venous return from the cranium and raises ICP — minimise where possible in patients with raised ICP • Avoid tight ETT ties or tracheostomy tapes that compress the internal jugular veins • Mannitol causes a rebound rise in ICP if the osmolality rises above 320 mOsm/kg — monitor carefully |