thank you for your suggestions.
> Could these vessels that were perfusing the brainstem and medulla have become so
> temporarily vaso-constriced, that the end-result was ischemia of the
> brainstem and medulla - and consequently brain death?
I think that damage to the brainstem played an important part in
this case, but I don,t think, that one can suffer braindeath, i.e.
total cessation of bloodflow to any part of the brain, without
herniation (or systemic unavailability of oxygen by respiratory,
circulatory or toxic mechanism).
>I do not know how this "vasospasm theory" was ever shown to actually
>occur in patients with meningitis and/or subarachnoid hemorrhage, and
>whether it is in fact a substantial phenomenon in patients with meningitis or
> subarachnoid bleeds.
It definitely plays a major role in subarachnoid hemorrhage, for
meningitis I am not sure.
>I have also been surprised when reading case
> reports re: Neisseriae meningitis in pediatric patients to discover how
> soon these patients can die after ED arrival, and I have also wondered
> what specifically caused that sub-group of bacterial meningitis patients
> to deteriorate so rapidly.
This evolution in fact is very unusual for meningococcal meningitis,
which usually is milder than pneumococcal meningitis. The patients
who die soon after ED arrival are patients with meningococcal sepsis,
where the meningitis component most often is minimal (these patients
are the prime example of the importance of an aggressive management
in the first hour, which can make a big difference)
> Did your patient have an autopsy?
No, the parents refused regrettably.
With kind regards,
Dr. Nikolaus Lutz-Dettinger
Dept. of Intensive Care
University Hospital Gent
De Pintelaan 185
B 9000 Gent
tel.: **32 - 9 - 240 21 11
fax: **32 - 9 - 240 49 95
email: [log in to unmask]
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