It was a head injury patient on a busy ward. Vitals had been stable for two hours. Then the nurse noticed something: the patient's heart rate had dropped and blood pressure had climbed. By the time the team arrived, one pupil was blown. They went straight to CT and found a massive extradural haematoma with significant midline shift.
That sequence — the slowing heart rate, the rising blood pressure, the late pupil change — is the story of raised intracranial pressure (ICP). Recognising it early, before the pupil blows, is what separates a good outcome from a catastrophic one.
Why Does ICP Rise?
The skull is a rigid box. Inside it sit three components: brain tissue (~80%), cerebrospinal fluid (~10%), and blood (~10%). This is the Monro-Kellie doctrine — the total volume inside the skull is fixed. If one component expands (a haematoma, oedema, a tumour), the others must compensate or pressure rises.
Normal ICP is 5–15 mmHg. Above 20 mmHg is considered raised. Above 40 mmHg is life-threatening. The brain initially compensates by shunting CSF into the spinal canal and compressing venous blood. But once those buffers are exhausted, small volume increases cause dramatic pressure spikes.
Brain + Blood + CSF = constant. If one goes up, the others must come down — or ICP rises. This is the foundation of everything that follows clinically.
The Clinical Signs — In Order of Appearance
Raised ICP produces signs in a predictable sequence. The earlier you catch it in that sequence, the better the outcome.
Early signs
Headache — typically worse in the morning (ICP naturally rises during sleep) and worsened by coughing, straining, or lying flat. A patient who says their headache is worst when they first wake up should raise your suspicion.
Nausea and vomiting — often described as projectile and not preceded by nausea in acute cases. This is from direct pressure on the vomiting centre in the medulla.
Papilloedema — swelling of the optic disc on fundoscopy. This is a reliable sign but takes hours to days to develop — it tells you ICP has been raised, not that it's rising right now.
Intermediate signs
Deteriorating conscious level — a falling GCS is one of the most important signs. Any patient whose GCS drops by 2 or more points needs urgent reassessment. Do not attribute confusion to pain medication without ruling out neurological deterioration.
Cushing's Triad — the classic but late sign of dangerously elevated ICP: hypertension, bradycardia, and irregular breathing. This occurs because the brainstem is being compressed. It is a pre-terminal sign — if you are seeing this, the window for intervention is closing fast.
Cushing's Triad = Hypertension + Bradycardia + Irregular respirations. This is a neurosurgical emergency. Do not wait for imaging if this is present — call for help immediately while arranging urgent CT.
Late signs — herniation
When ICP is critically elevated, the brain herniates — it is pushed through openings in the skull or tentorium under pressure. The most important patterns:
Herniation Syndromes
- Uncal herniation: The uncus (medial temporal lobe) herniates through the tentorial notch, compressing CN III. You see a fixed, dilated pupil on the ipsilateral side — "blown pupil." This is a surgical emergency. Contralateral hemiplegia follows as the cerebral peduncle is compressed.
- Central herniation: Downward displacement of the diencephalon. Bilateral small pupils early, then bilateral fixed midposition pupils. Decorticate then decerebrate posturing.
- Tonsillar herniation: Cerebellar tonsils pushed through the foramen magnum, compressing the medulla. Causes sudden respiratory arrest. This is what happens when you LP a patient with raised ICP — never do an LP without ruling out raised ICP first.
Your Bedside Assessment
Every head injury or altered conscious patient deserves a structured assessment for raised ICP. At the bedside, do this systematically:
Quick Bedside Check for Raised ICP
- GCS — document it properly: E+V+M. Trend matters more than a single reading.
- Pupils — size, symmetry, and reaction to light. An asymmetric or unreactive pupil is a red flag.
- Vital signs trend — is BP climbing? Is HR falling? Look at the trend, not just the current reading.
- Posturing — decorticate (flexion) or decerebrate (extension) posturing indicates deep dysfunction.
- Fundoscopy — look for papilloedema if subacute presentation.
When charting observations on a head injury patient, always chart GCS and pupils together with the time. A nurse who documents "GCS 14, pupils equal and reactive" at 10pm and "GCS 12, left pupil sluggish" at 11pm has just told you something critically important — the trend is your early warning system.
What to Do While Awaiting Imaging
While you arrange urgent CT, these measures can buy time:
Head positioning: Nurse at 30 degrees head-up to promote venous drainage. Keep the neck neutral — no tight collars or ties compressing jugular veins.
Oxygenation: Hypoxia worsens cerebral oedema. Target SpO2 ≥94%. Avoid hypercapnia — CO2 is a potent cerebral vasodilator and will worsen ICP.
Osmotherapy: Mannitol 0.25–1g/kg IV or hypertonic saline can acutely reduce ICP by drawing water out of the brain. This buys time for definitive treatment — it is not a substitute for surgery when surgery is needed.
Avoid: Hypotension (CPP = MAP − ICP; dropping BP kills the brain), excessive fluids, and hyperthermia.
The Bottom Line
Raised ICP kills through herniation — and herniation happens fast. Your job as the intern is to recognise the early warning signs before the pupil blows, act on the trend rather than a single set of observations, and escalate early. A blown pupil is not the beginning of raised ICP — it is near the end.
Know the sequence. Monitor the trend. Act early.
Early signs: headache (worse mornings), vomiting, papilloedema, falling GCS. Cushing's triad (hypertension + bradycardia + irregular breathing) = late, dangerous sign. Blown pupil = uncal herniation = surgical emergency. Never LP without ruling out raised ICP. Head-up 30°, oxygenate, consider osmotherapy while arranging imaging.
