The case
A 58-year-old man is on post-operative day three after a craniotomy for resection of a brain mass. No drain was placed. He was transferred from the ICU to the medical-surgical unit on post-op day two and has been awake, oriented, neurologically intact, and doing well since.
He gets up to have a bowel movement. Thirty minutes later, his nurse returns and finds him unresponsive.
- Eyes: no opening to any stimulus, including pain (E1)
- Verbal: no sounds (V1)
- Motor: arms flexing inward toward the chest, decorticate posturing (M3)
- GCS: 5
- Pupils: equal and reactive, not blown
- Airway and breathing: airway clear and patent, breathing unlabored with good air movement, 98–99% on 2 L nasal cannula
- Monitor: systolic 178 with a widened pulse pressure, heart rate in the 40s, slow irregular respirations. This is Cushing's triad.
CT is down the hall. Intubate first, or scan first? Commit to an answer, then work the questions.
| Earlier on med-surg | Found unresponsive | After osmotic therapy | |
|---|---|---|---|
| BP (mmHg) | 128/74 | 178/72 | 146/78 |
| Pulse pressure | 54 | 106 | 68 |
| MAP | 92 | 107 | 101 |
| Heart rate | 78 | 48 | 84 |
| Respiratory rate | 16, regular | 10, irregular | — |
| SpO2 | 97% on 2 L NC | 98–99% on 2 L NC | — |
| Temp (°F) | 98.6 | 98.8 | — |
| GCS | 15 | 5 (E1 V1 M3) | — |
| Pupils | Equal, reactive | Equal, reactive | — |
Questions
Q1 Airway: intubate now, or scan first?
Both are defensible, and the setting creates the decision. Here the airway was intact, he was ventilating well at 98–99% on 2 L, the scanner was immediately available, and the scan result would directly change the plan. That made CT-first a reasonable call. The reactive pupils bought the window.
CT-first is only safe if you bring the airway with you:
- An airway-capable team goes on the trip: the RN, the RT, and a provider who can intubate.
- Suction and airway equipment travel with him.
- Head of bed at 30°, head midline.
- Everyone is ready to intubate in the scanner if he deteriorates.
CT-first did not mean airway-never. After the scan he went directly to the ICU, where the airway was promptly secured. This was a question of sequence, not of whether to protect the airway.
Without rapid imaging, a GCS this low with posturing usually means securing the airway first. "GCS 8, intubate" is a useful rule of thumb, but airway protection is more than a number: oxygenation, secretion handling, and the risk of deteriorating in transport all count.
Q2 What are the posturing and the Cushing's response telling you, and what else could this be?
Decorticate posturing points to dysfunction above the midbrain: the cerebral hemispheres, internal capsule, or thalamus. Paired with Cushing's triad, it signals rising intracranial pressure. Watch for progression from decorticate (flexion) to decerebrate (extension), which means worsening herniation. Reactive pupils mean he has not passed the point of no return yet.
Keep the differential open while you move:
- Check the blood glucose level. Every unresponsive patient gets one, because hypoglycemia can mimic anything.
- Think seizure. A post-craniotomy patient found unresponsive could be postictal or in non-convulsive status epilepticus. CT answers the bleed question; EEG may still be needed.
Q3 What is the first-line treatment while you arrange definitive care?
- Call neurosurgery immediately.
- Give hyperosmolar therapy to temporize the ICP: hypertonic saline and/or mannitol, per protocol. In this case a 3% hypertonic saline bolus was given first, then stopped when mannitol was started.
- Head of bed at 30° with the head midline.
- Control blood pressure to the target neurosurgery sets.
As the ICP dropped, the Cushing's response reversed: heart rate came up and blood pressure came down. That reversal was the bedside proof the therapy was working. Osmotic therapy is a bridge, not the fix. It buys brain perfusion and time; it does not remove blood from a closed skull.
★ The reveal
CT confirmed hemorrhage at the resection site with midline shift. From CT he went directly to the ICU, where the airway was promptly secured. He then went immediately back to the OR for evacuation and came out stable.
The osmotic therapy kept his brain perfused and bought the window to reach the only definitive treatment: the neurosurgeon.
How mannitol works
It is an osmotic diuretic, and the key word is osmotic. Mannitol is a sugar alcohol that stays in the bloodstream. It cannot cross an intact blood-brain barrier, and the kidney does not reabsorb it. That "stays where you put it" quality is the whole mechanism.
What it does to the brain. Mannitol raises the osmolality of the blood above that of the brain tissue next to it. Water follows the osmotic gradient, so fluid moves out of the brain tissue and into the vessels across the intact barrier. Less water in a closed skull means lower intracranial pressure.
An early flow effect. In the first few minutes, mannitol expands plasma volume and lowers blood viscosity. Cerebral blood flow improves, and cerebral vessels can reflexively constrict slightly, which also nudges ICP down. You get a fast early effect and a sustained osmotic effect.
Then the diuresis. The kidney filters the fluid pulled into the vessels along with the mannitol. Because mannitol is not reabsorbed, it carries water into the urine, and the patient makes a lot of urine fast.
Why the vitals changed on this patient. As the ICP fell, the brain no longer had to fight for perfusion, so the Cushing's response switched off: heart rate came up and blood pressure came down.
What to watch for:
- Volume and the kidneys: brisk diuresis can push a patient toward hypovolemia and hypotension. High doses or existing kidney disease raise the risk of acute kidney injury. Track intake and output.
- Serum osmolality: follow it to guide re-dosing and keep it from climbing too high.
- Rebound: where the barrier is disrupted, as at a fresh resection bed or an active bleed, mannitol can leak into the tissue and reverse the gradient, pulling water back into the brain. One more reason it is a bridge, not a fix.
- Filter: give it through an in-line filter, because mannitol can crystallize.
Bedside takeaway: mannitol raises the osmolality of the blood above that of the brain, so water follows the gradient out of the brain tissue and into the vessels, and the kidneys clear it. Lower brain water, lower pressure, bought time.
Teaching points
- The suspected trigger was Valsalva. Bearing down raises intrathoracic pressure, impedes cerebral venous return, and drives ICP up, enough to start a bleed in a fresh surgical bed. In neurosurgical patients, the stool softener is a neuroprotective intervention.
- Cushing's triad is a late, ominous sign of rising ICP: hypertension with a widened pulse pressure, bradycardia, and irregular respirations.
- Posturing is a trend. Decorticate moving toward decerebrate means worsening herniation.
- Unresponsive means glucose and seizure are on the list. Check them every time.
- CT-first only works if the airway goes with you. Bring the team, the suction, and the equipment.
- Osmotic therapy is a bridge to the neurosurgeon, not a substitute.
Who does what
Physician / APP
Recognizes Cushing's, calls neurosurgery, makes the airway-versus-CT call, and orders hyperosmolar therapy.
RN
Finds him, calls the rapid response, gets vitals and a GCS, checks pupils and the blood glucose level, raises the head of the bed, and travels to CT ready for the airway.
RT
Brings airway equipment and suction to CT and is ready to bag or assist with intubation at any point.
Medic / flight
No scanner in the field. A GCS this low with posturing usually means securing the airway, avoiding hypoxia and hypotension, and moving fast to a neurosurgical center.
References
- Cook, A. M., Jones, G. M., Hawryluk, G. W. J., Mailloux, P., McLaughlin, D., Papangelou, A., Samuel, S., Tokumaru, S., Venkatasubramanian, C., Zacko, C., Zimmermann, L. L., Hirsch, K., & Shutter, L. (2020). Guidelines for the acute treatment of cerebral edema in neurocritical care patients. Neurocritical Care, 32(3), 647–666. https://doi.org/10.1007/s12028-020-00959-7
- Seifman, M. A., Lewis, P. M., Rosenfeld, J. V., & Hwang, P. Y. K. (2011). Postoperative intracranial haemorrhage: A review. Neurosurgical Review, 34(4), 393–407. https://doi.org/10.1007/s10143-010-0304-3
- Stevens, R. D., Shoykhet, M., & Cadena, R. (2015). Emergency neurological life support: Intracranial hypertension and herniation. Neurocritical Care, 23(Suppl. 2), S76–S82. https://doi.org/10.1007/s12028-015-0168-z
- Yadav, Y. R., Mukerji, G., Shenoy, R., Basoor, A., Jain, G., & Nelson, A. (2007). Endoscopic management of hypertensive intraventricular haemorrhage with obstructive hydrocephalus. BMC Neurology, 7, Article 1. https://doi.org/10.1186/1471-2377-7-1
Card image: representative CT of a thalamic hemorrhage, not this patient, resized. From “Endoscopic management of hypertensive intraventricular haemorrhage with obstructive hydrocephalus,” by Y. R. Yadav, G. Mukerji, R. Shenoy, A. Basoor, G. Jain, and A. Nelson, 2007, BMC Neurology, 7, Article 1 (https://doi.org/10.1186/1471-2377-7-1), via Wikimedia Commons. CC BY 2.0.
Educational content only, not medical advice. Cases are drawn from clinical experience; details are changed so no patient can be identified. Medications are named without doses; follow your facility's protocols and your local medical direction.
At the bedside
CAVN medical penlight with pupil gauge
Reactive pupils are what bought this patient his window. A penlight with a printed pupil gauge lets you measure size and reactivity the same way every check, and document it in millimeters instead of guessing.
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