🚨 Raised Intracranial Pressure

Raised intracranial pressure (ICP) occurs when the volume of intracranial contents (brain, blood, CSF) exceeds the cranial vault's capacity, leading to brain compression and potential herniation. It's a life-threatening emergency requiring prompt recognition and management.

Classic 'Cushing's triad' (hypertension, bradycardia, irregular respirations) is a late and ominous sign. Early features include headache (worse on lying down), nausea/vomiting, altered mental status (irritability, confusion, decreased GCS). Papilloedema is a key fundoscopic finding.

ABCDE approach is critical. Secure airway and ensure adequate oxygenation and ventilation. Assess neurological status meticulously, paying close attention to GCS, pupillary size and reactivity, and focal deficits. Look for signs of herniation.

Rapidly deteriorating GCS, new pupillary asymmetry or unreactivity, new focal neurological deficits, posturing (decorticate/decerebrate), Cushing's triad. These indicate impending brain herniation and require immediate intervention.

Bedside: GCS, pupil assessment, vital signs, fundoscopy. Bloods: FBC, U&Es, glucose, coagulation screen, arterial blood gas. Imaging: Urgent CT head (non-contrast) to identify the cause (e.g., haemorrhage, mass lesion, hydrocephalus).

Elevate head of bed to 30 degrees. Maintain normocapnia (avoid hypercapnia). Ensure adequate oxygenation. Maintain normotension and normoglycaemia. Consider osmotic agents (e.g., hypertonic saline, mannitol) to reduce brain oedema. Administer sedatives/analgesics to reduce metabolic demand. Consider neuromuscular blockade if intubated.

Any suspicion of raised ICP, especially with neurological deterioration or signs of herniation. Urgent neurosurgical review is mandatory. Patients requiring intubation or with unstable vital signs need critical care involvement.

The Monro-Kellie doctrine explains the compensatory mechanisms for ICP. Cushing's triad indicates severe, late-stage raised ICP. Uncal herniation causes ipsilateral fixed and dilated pupil due to oculomotor nerve compression. Management focuses on reducing intracranial volume and maintaining cerebral perfusion pressure.