Deteriorating Head-Injured Patient on the Ward
A 34-year-old man is admitted after a motorcycle crash with a Glasgow Coma Scale (GCS) score of 14 (E4 V4 M6), a right frontal contusion on CT, and no anticoagulation. Six hours later the nurse calls: GCS is now 9 (E2 V2 M5), the right pupil is 5 mm and unreactive while the left is 3 mm and reactive, and blood pressure is 168/94 mmHg with a heart rate of 58/min. He is intubated for airway protection. Repeat CT shows the contusion has expanded to 4 cm with 8 mm midline shift and effacement of the basal cisterns. There is no intracranial pressure (ICP) monitor in place, and the nearest operating theatre is 15 minutes away.
1. Interpret the clinical trajectory and explain the physiological basis of the vital signs. What is your immediate management priority before and during transfer?
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The picture is a right uncal herniation syndrome: ipsilateral pupillary dilation from third nerve compression, a progressive GCS fall, and Cushing physiology. Hypertension with bradycardia reflects the Cushing reflex - rising ICP reduces cerebral perfusion pressure, triggering a sympathetic pressor response with a vagally mediated bradycardia; it is a late, pre-herniation warning sign, not a benign finding.
Priority is preventing secondary injury while arranging decompression:
- Secure airway and ventilate to normocapnia (PaCO2 35–40 mmHg); brief hyperventilation to 30–35 mmHg only as a bridge if herniation is imminent, since sustained hypocapnia causes ischaemia.
- Head up 30 degrees, neutral neck, loosen cervical collar straps if they compress venous drainage.
- Osmotherapy now: 20% mannitol 0.5–1 g/kg or hypertonic saline, with a urinary catheter and electrolytes monitored.
- Maintain MAP to keep CPP ≥60 mmHg; do not treat the hypertension reflexively.
- Urgent surgical decompression - do not delay for an ICP monitor. The expanding mass with midline shift and clinical herniation is the indication; ICP monitoring would only confirm what is already apparent.
2. The on-call registrar asks whether to give steroids and whether to hyperventilate to a PaCO2 of 25 mmHg for the transfer. Justify your answer.
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Both are wrong in this setting.
Steroids: the CRASH trial showed increased mortality with corticosteroids in traumatic brain injury, and they are contraindicated outside specific indications (e.g., spinal cord injury protocols, where evidence is also debated). They do not reduce contusion oedema.
Aggressive hyperventilation: PaCO2 of 25 mmHg produces arteriolar constriction and reduces cerebral blood volume, but also reduces cerebral perfusion globally and can cause ischaemia in injured tissue. It is reserved for acute herniation as a short bridge (target 30–35 mmHg) with the lowest effective level, never as a routine transfer strategy.
For transfer, the safer package is normocapnia, adequate sedation/analgesia, osmotherapy, haemodynamic stability, and rapid transport to theatre. A brief period of modest hyperventilation is acceptable only if the pupil remains fixed and dilated during movement.