It's now ICU day 10. Through this time, the patient's neurologic exam has remained suboptimal-- she opens her eyes to voice, has a weak cough, and has a best motor response of localizing with her left arm, nothing with her right. TCDs have shown mild-moderate vasospasm over the past few days, though her exam has remained stable. Head CTs have been obtained as EVD adjustments have been made; there's been a small stable left convexity subdural fluid collection. Her EVD remains in place, and is currently open to drain at 10cmH2O at the tragus. She's draining about 5-10mL of CSF per hour. After discussion with her surrogate decision-makers, we proceed with performing a bedside tracheostomy.
On ICU day 12, she has a sudden decline in her exam. She no longer opens her eyes to voice, and her best motor response is that of withdrawal bilaterally. She's only intermittently been on low-dose dexmedetomidine gtt since the tracheostomy.
While our team was pretty confident about the basilar tip aneurysm being secured, it's still possible for it to have re-ruptured if there has been even a small residual neck or dome that has been slowly expanding. We also have to remind ourselves that the patient had another aneurysm-- at the right ophthalmic-- that's pretty small, but present and non-secured. That could bleed. This could include intraventricular extension, which would then cause worsening hydrocephalus. So, really, our first thought is: is there new blood? A possibly helpful single data point is whether or not the patient's EVD output has suddenly become bloodier. (In this patient's case, fortunately not.)
If not new blood, then there are still other key possibilities we have to consider. This patient does have an aneurysmal SAH, so we have to think about whether she's developed clinical vasospasm. While the most common teaching is that vasospasm and delayed cerebral ischemia (DCI) occur between post-bleed days 3-14, it is less common, though very much possible, for this to happen even out to day 21. Patients don't always follow the textbooks. Her TCDs up to this point have only demonstrated isolated sonographic vasospasm; there haven't been any clinical manifestations. Maybe she's developed worsening vasospasm and this is now the clinical manifestation.
Intracranial hypertension is a possibility. Luckily, we do have a functioning EVD, which could confirm or refute that concern. (Though at this point, her cerebral compliance is likely impaired, so a relatively normal ICP in general might still be too high for her.) If there's suddenly worsening ICPs, we could consider whether that's due to more blood (as discussed above) or something else, like infection. Ventriculitis can impair ventricular compliance, causing more significant effects to relatively higher ICPs.
Seizure is a possibility, whether directly or indirectly (increase in cerebral metabolic demand leading to higher ICPs as the more proximate problem). Cortical spreading depolarization is another possibility that is likely underappreciated, though it's hard to identify.
You check the EVD setup-- stable serosanguinous drainage. Her ICP is currently 9mmHg. The ICP waveform is normal.
You send the patient down to the CT scanner (they're stable enough) first, and obtain a non-contrast HCT, CTA head/neck, and CT perfusion. You plan to connect to cEEG afterwards if this is unrevealing.
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