So a couple of days ago my colleague Ian Ajmo asks me to take a look at one of our patients for a second opinion. It’s a 75 year old male who had surgery for an incarcerated inguinal hernia during the night and was left intubated, but, despite his last sedation being during surgery (4 am), he still hasn’t woken up (11 am). He is known for a cerebellar glioblastoma but was functional living at home and had been given a one year prognosis.
So Ian was concerned, rightly so, and took the savvy initial step, after noting a GCS of 5 (some minimal reaction to pain), of looking at his optic nerve sheaths (ONS), and found them to be over 6 mm. For those unfamiliar, an optic nerve sheath dilation (ONSD) of 5.7mm (normal <4mm) generally corresponds to an ICP over 2o mmhg.
So this astute finding (as the requisition for a CT was being done) prompted me to do a little further neuro-ultrasound. Here is the distal carotid doppler:
internal carotid
external carotid
So this is done in the upper neck, just distal to the bifurcation, so while extra cranial, the internal carotid nonetheless represents a view into the relationship between arterial flow and intracranial hemodynamics. It takes virtually no experience to see the radical difference in flow between the internal and the external carotid. The EC shows a beautiful systolic peak and diastolic flow. On the other hand, the IC shows a small systolic peak, a bit of retrograde flow, and essentially minimal or no diastolic flow. That is telling us, physiologically, that the ICP elevation has radically limited diastolic flow. This isn’t good.
Next, I do trans-cranial doppler (TCD):
Now despite good visualization of brain tissue, specifically brainstem (sometimes difficult in men), I struggle to find any blood flow, and finally manage to see what looks like the basilar artery, and has very poor flow, similar to the EC, with a small systolic peak, retrograde flow and little diastolic flow.
This right away tells us there is a massive ICP elevation explaining the lack of awakening, and a dismal prognosis.
CT:
Confirms a huge RT MCA stroke with 15mm midline shift and foci of hemorrhage. While waiting for the CT his urine output was > 6 liter, prompting the attending to give some DDAVP and fluids to preserve hemodynamics (at least until the scan).
We withdrew therapy in view of the prognosis.
This case illustrates the usefulness and rapidity of bedside ultrasound to assess functional intracerebral dynamics, which can help diagnosing or ruling out an elevated ICP as a cause for a change in neuro status, or a “non-waking” patient, which is usually due to sedation accumulation, but now always…
cheers,
Philippe
thinking critical care 
Great case presentation into ruling out some of the other cases of prolonged emergence from general anesthestics. Interesting use of several U/S techniques in order to arrive at this – all before the CT head!
Great case presentation of the use of various U/S “views” to work through the DDx of patients who have prolonged emergence from general anesthestics! Looks like TCD is a difficult technique at the best of times.
[…] Rola presents a fascinating case of POCUS for neurological assessment. Really thought-provoking stuff. […]
This is a brililant diagnosis! I admit that our routine intervention would be a urgent CT scan and no TCD. A colleague of mine is collecting data since a few years comparing optic nerve dilation and intracranial hypertension in patients with one ore more ICP monitoring, but the correlation is not so strong so far.
Just a question: I suppose your patient wasn’t a potential organ donor because of his cancer, in that case do you routinely withdraw therapies even when a patient is already (or nearly) brain dead, or you declare brain death (since he’s already intubated)?
Thanks Marco! I’m curious about your colleague’s correlations, however, as it seemed to me quite established that there is a strong correlation between ONSD and elevated ICP, with a 5.7mm-20mmhg point, excluding of course local orbital or periorbital processes…
In terms of your question, since TCD is not yet formally used as an unequivocal test for brain death, we would still have to do the rest (apnea, etc) to declare brain death for the purpose of donation, but in terms of withdrawal, I consider it sufficient to establish a dismal prognosis.
I’m about to put up a second neuro case and will also put up a nice review on TCD.
thanks for reading!
hi. i am dr ajay – pediatric intensivist in pune-India,. we dont have facility to measure invasive icp .
i have read the article of ica and eca flow difference in raised icp.
can you thrwo some light on my following queries
can internal and external carotid doppler be used to predict and monitor raised icp and also to check response to treatment .
can ijv doppler be used for the same and how
can Central retinal vein velocity and central retinal artery RI be used for predicting raised icp and monitor response.
tahnks
waiting for reply