Deteriorating Head-Injured Patient on the Ward

This is a secondary neurological deterioration with signs of uncal herniation (ipsilateral pupil dilation, contralateral hemiparesis) superimposed on a traumatic contusion/subdural collection. The Cushing response (hypertension with bradycardia and bradypnoea) signals raised intracranial pressure with impending brainstem compromise.

Priority sequence:

1. Airway and ventilation first - GCS 10 with a falling respiratory rate mandates intubation and controlled ventilation to target normocapnia (PaCO2 35–40 mmHg) and normoxia (SpO2 94–98%). Avoid prophylactic hyperventilation except as a bridge.
2. Osmotherapy - mannitol 0.5–1 g/kg or hypertonic saline, with attention to blood pressure and osmolality.
3. Head position and venous drainage - head up 30 degrees, neutral neck, loosen cervical collar if it impedes venous return, avoid compression of neck veins.
4. Blood pressure - maintain cerebral perfusion pressure; the Cushing response means the current hypertension is compensatory, so do not aggressively lower it.
5. Urgent repeat imaging and theatre - the deterioration plus new focal deficit and pupil change is a surgical emergency; do not wait for the repeat CT if the patient is herniating. Notify the consultant and prepare theatre.
6. Reversible causes - check arterial blood gas, glucose, sodium, seizure activity, and sedation/analgesia adequacy.

The key judgement is that a pupil change with a motor deficit after trauma is a herniation syndrome until proven otherwise; imaging should not delay decompression in a deteriorating patient.

The decision is driven by the lesion type and the clinical trajectory rather than by a single number.

• Mass lesion with shift and herniation signs - the dominant problem is a space-occupying contusion/subdural collection. Surgical evacuation of the hematoma and, where necessary, a decompressive craniectomy is indicated. An ICP monitor alone would not address the mass effect and would delay definitive treatment.
• ICP monitoring - appropriate when there is a traumatic brain injury with an abnormal CT and a GCS ≤ 8, or a normal CT with two or more risk factors. Here it is a useful adjunct after surgery, but not a substitute for decompression.
• Decompressive craniectomy - consider when there is refractory intracranial hypertension or a swollen hemisphere with herniation despite medical therapy. The evidence base (e.g., trials of decompressive craniectomy in severe TBI) shows that it reduces ICP and mortality but can increase the proportion of survivors with severe disability, so the decision must be individualized and discussed with the family.

Practical plan: proceed to theatre for evacuation of the hematoma and contusion, place an ICP monitor at the same time, and be prepared to extend to a decompressive craniectomy if the brain remains swollen. Postoperatively, manage in neurocritical care with sedation, normocapnia, normothermia, sodium and glucose control, seizure prophylaxis, and early repeat imaging.

Explain that the high blood pressure is likely a compensatory Cushing response to raised intracranial pressure: the brain is attempting to maintain cerebral perfusion. Lowering the blood pressure aggressively would reduce cerebral perfusion pressure and could worsen ischemia.

Management principles:

• Treat the cause (raised ICP) rather than the number.
• Maintain cerebral perfusion pressure (typically 60–70 mmHg in adults) with fluids and vasopressors if needed.
• Avoid antihypertensives unless there is a separate indication (e.g., hypertensive emergency unrelated to ICP), and never as a first response to the Cushing triad.
• Monitor for the full triad (hypertension, bradycardia, irregular respiration) as a warning sign of herniation.

Document the discussion with the family, emphasizing that the priority is decompression and control of intracranial pressure.