Increased ICP NGN Case Study

The trajectory cue above all: GCS 15 → 12 in under two hours. A falling GCS is the earliest and most reliable sign of rising ICP — level of consciousness deteriorates before anything else does.

The lateralizing cue: a newly unequal, sluggish right pupil on the side of the impact — pressure is squeezing the third cranial nerve on that side. New anisocoria in a head-injured patient is a neurosurgical emergency cue.

The pattern cues: the “talk then deteriorate” story is the classic lucid interval of an epidural hematoma (temporal impact — middle meningeal artery territory); projectile-style vomiting without nausea and worsening headache complete the picture. Restlessness is early ICP, not anxiety.

Noted, not yet alarming: HR 64 and BP 142/84 — watch these; where they go next matters enormously.

Epidural hematoma (most supported): temporal impact + lucid interval + rapid deterioration + ipsilateral pupil change. Arterial bleeding fills the epidural space fast — which is why the decline is measured in minutes to hours and why this is among the most operable, most survivable emergencies in neurotrauma when caught.

Also possible: subdural hematoma (venous, usually slower — but acute subdurals exist), expanding contusion with edema, or diffuse injury. The CT sorts them; every one of them is managed first as “rising ICP.”

The physiology underneath: the skull is a closed box (Monro-Kellie): blood accumulating means brain and CSF must yield — first compensation (what bought him the lucid interval), then decompensation (what’s happening now), then herniation (what you are racing). Cerebral perfusion pressure = MAP − ICP: as ICP climbs, the brain’s blood supply falls.

1. Expanding intracranial hemorrhage heading toward herniation — the unilateral blown pupil is uncal herniation announcing itself. Definitive treatment is surgical evacuation; everything nursing does now is about buying time to the OR.

2. Secondary brain injury — hypoxia, hypercapnia, hypotension, fever, and pain each independently worsen outcomes. The injured brain tolerates none of them.

The too-late sign: Cushing’s triad — hypertension with widening pulse pressure, bradycardia, irregular respirations — is a late, pre-herniation finding. His HR 64 with a creeping systolic deserves suspicion now; waiting for the full triad is waiting for the cliff.

Immediately: stat call to provider/neurosurgery and escalate the CT to now — this scan is the most important transport in the hospital tonight, and a nurse goes with him. Head of bed 30°, head and neck midline (venous drainage is free ICP relief), continuous monitoring, oxygen to keep saturations high-normal, and neuro checks with pupils every few minutes — the trend is the monitor.

Protect against the spikes: minimize stimulation, treat pain and nausea per orders (vomiting and agitation both spike ICP), keep him from Valsalva (straining, coughing hard), normothermia.

Anticipate: hyperosmolar therapy (mannitol or hypertonic saline) as a bridge, intubation for airway protection if GCS keeps falling (≤8 = airway), reversal of any coagulopathy, and rapid OR mobilization for evacuation. Keep him NPO — he’s a surgical patient as of this assessment.

Flat is wrong, full stop: lowering the head of bed impairs venous drainage and raises ICP — he stays at 30° with his head midline even while agitated. Pad and protect rather than flatten.

Sedation is a provider decision with a trade-off: agitation genuinely spikes ICP, so calming him matters — but sedation erases your neuro exam, the one monitor you have before the OR, and can depress respirations (CO₂ retention dilates cerebral vessels and raises ICP further). If sedation is ordered, it’s short-acting, titrated, with airway readiness — never a casual “something to settle him.”

Also reconsider the agitation itself: it may BE the rising pressure — or a full bladder, pain, hypoxia. Check the fixable causes fast while escalating. And recheck those pupils: any further change goes straight to neurosurgery, not into a note.

Improving: GCS recovered from 12 to 14, pupils equalized — the compressing clot is out and the third nerve released. The speed from recognition to evacuation is why this story ends well; epidural hematomas reward fast nurses.

Still watching: re-bleeding and post-op swelling (the next 24–48 hours of hourly neuro checks are not ceremonial), seizure risk (prophylaxis per orders), sodium and fluid status, pain control without over-sedation, and the same ICP-protective care — HOB 30°, midline, quiet, normothermic.

The honest answer for his wife: the dangerous clot is out and he’s recovering well, and the team watches closely for days, then weeks — concussion-spectrum symptoms (headaches, fatigue, concentration trouble, irritability) are common after a real brain injury and deserve follow-up, not toughing out. Recovery is a trajectory, and tonight it turned the right way.