A 57 year-old man with HTN was initially found down outside. He was brought to the ED by EMS. Initial neurologic exam was notable for GCS 7. He was intubated by the ED team for airway protection. Non-contrast head CT revealed an acute right thalamic IPH with IVH. A right frontal EVD was placed by neurosurgery, with elevated opening pressure noted. EVD was set to be open at 15cmH2O at the tragus. He was subsequently admitted to the NCCU for further management.
In the NCCU, sedation requirements were minimal due to persistent markedly depressed neurologic exam. His ICPs generally remained < 20mmHg without intervention, with only ~40mL CSF drained per day. Nicardipine gtt was titrated off and oral antihypertensives adequately achieved his goal BP.
On day 8 of his ICU admission, he began experiencing frequent spikes in his ICPs up to 50mmHg, requiring treatment with hypertonic saline and mannitol. You look at his EVD setup, and there has been no change in character of his CSF drainage. You look up at the monitor, and see the following ICP waveform tracing:
Recall that P1 represents the influx of arterial blood. P2 represents the reverberation of this resultant pressure across the parenchyma. P3 is the dicrotic wave, caused by the sudden closure of the aortic valve. Normally, P1 > P2 > P3.
Here, however, the second peak of the waveform, P2, is higher than the first peak, P1, and third peak, P3. This indicates that the patient's cerebral compliance is impaired.
It can be helpful to think of the intracranial compartments, and which pathologies may affect each one.
In the parenchyma, a new structural disturbance such as new/progressive hemorrhage due to the underlying uncorrected cause, or worsening cerebral edema instigated by the blood products, can impair compliance. Either of these could also disrupt CSF outflow, contributing to obstructive hydrocephalus physiology.
In the ventricles, worsening ventricular hemorrhage can also impair compliance, and may also compromise the function of the EVD due to clot clogging the catheter. Infection can also cause inflammation of the ependyma, reducing CSF absorption and thus contributing to non-obstructive hydrocephalus physiology.
In this patient's case, he developed a fever and his CSF was analyzed, with studies confirming a diagnosis of bacterial ventriculitis. This explained the sudden need for intracranial hypertension management whereas it was not a problem earlier in his admission. He initially had multiple ICP crises per day, though this frequency improved over the following few days as his ventriculitis was treated.
Copyright © 2024-2025 Andrew M. Nguyen, M.D. For educational use only.
This work is licensed under
CC BY-NC-SA 4.0.
