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PED-EM-L  August 1998

PED-EM-L August 1998

Subject:

Re: PED-EM-L Digest - 28 Aug 1998 to 30 Aug 1998

From:

Jeffrey Mann <[log in to unmask]>

Reply-To:

Jeffrey Mann <[log in to unmask]>

Date:

Mon, 31 Aug 1998 10:43:52 -0400

Content-Type:

text/plain

Parts/Attachments:

Parts/Attachments

text/plain (116 lines)

Automatic digest processor wrote:
>
> There is one message totalling 71 lines in this issue.
>
> Topics of the day:
>
>   1. mechanisms of braindeath
>
> For more information, send mail to [log in to unmask] with the message: info PED-EM-L
> The URL for the PED-EM-L Web Page is:
>   http://www.brown.edu/Administration/Emergency_Medicine/ped-em-l.html
>
> ----------------------------------------------------------------------
>
> Date:    Sun, 30 Aug 1998 02:55:32 +0000
> From:    "Dr. Nikolaus Lutz-Dettinger" <[log in to unmask]>
> Subject: mechanisms of braindeath
>
> Dear colleagues,
>
> I would like your comments on the following case and questions:
> Boy of 5 years has fever and complains of pain in abdomen and head.
> The same evening he is seen by the family physician, who diagnoses a
> viral disease and reassures the parents. Next morning the child seems
> fine without fever, but in the following hours the fever re-occurs,
> the parents see some petecchia and the child becomes somnolent. The
> child is brought to the ED of a community hospital at 1h30 pm, where
> bloodculture and LP are done and antibiotics are started. Initial lab
> shows clearly elevated inflammatory parameters, but is otherwise
> normal (no signs of circulatory compromise or organ dysfunction); LP
> shows 130 WBC, elevated protein and gram neg. diplococci. In the
> following hour, the neurologic situation of the child is described in
> varying terms, from "passive" to "not reacting to pain", but there is
> no clear evolution from better to worse. Temperature is 39.7 C,
> blood-pressure is rising in the course of that hour from normal to
> 180/110 mmHg, while pulse rate is remaining quite constant at 105/min;
> the child is breathing spontaneously (in room air ?). It is decided to
> do a CT of the brain, but ,while on the CT-table (about 3 pm), the
> child becomes apneic and is intubated without the use of medication;
> seemingly no circulatory instability even at that moment. The CT is
> interpreted as normal, although one could argue, the the ventricles
> where a little smaller than average (certainly not slitlike) and that
> corticomedullary differentiation was a bit less clear than usual.
> After the CT it becomes apparent, that the pupils are dilated and not
> reactive, while they where normal before. The elevated blood-pressure
> quickly returns to normal. Transfer to our institution is asked. From
> that moment to the eventual termination of intensive care about 21h
> later the general situation of the child remains perfectly stable,
> without a hint of circulatory disturbance (even without diabetes
> insipidus). The child remains flaccid with al signs of brain death.
> Because the child was very stable, we decided on arrival, to go
> immediately to the MRI-department (at about 5 pm). MRI showed some
> swelling of the mesencephalon (not impressive, the highest intensity
> on T2-weighted images symmetrically in the posterior parts of the
> thalamus) and possibly some sign of herniation through the foramen
> magnum;  MR-angio confirmed absence of brain circulation (Doppler of
> the a. cerebri media next morning showed the typical picture of
> negative diastolic flow equalling positive systolic flow). During the
> discussions of this case in our service, the following questions
> remained unresolved or contentious: 1) in the absence of systemic
> instability or other (toxic) systemic oxygen transport and delivery
> problems, is there another mechanism than herniation, that can result
> in brain death (i.e. cessation of bloodflow to any part of the brain?
> 2) It seems very probable, that the patient suffered brain death on
> the CT-table; why was the CT so unimpressive, merely hinting at some
> early signs of edema. 3) The rising blood-pressure before the CT seems
> most likely a sign of increasing ICP, but why than was this not
> associated by any reduction in pulse frequency. I'm looking forward to
> your ideas on these points,
>
> Nikolaus
>
> Dr. Nikolaus Lutz-Dettinger
> PICU
> Dept. of Intensive Care
> University Hospital Gent
> De Pintelaan 185
> B 9000 Gent
> Belgium
> tel.: **32 - 9 - 240 21 11
> fax: **32 - 9 - 240 49 95
> email: [log in to unmask]
>
> ------------------------------
>
> End of PED-EM-L Digest - 28 Aug 1998 to 30 Aug 1998
> ***************************************************
Dear Nikolaus,
 
Very interesting case!
 
I am not a neuroscientist - so I cannnot give you an 'informed' opinion.
However, I've heard that some patients with meningitis develop intense
vasopspasm of vessels passing through the subdural space. 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 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. 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 specfically caused that sub-group of bacterial meningitis patients
to deteriorate so rapidly. Could DIC and micro-infarcts from
micro-coagulation of brainstem and medullary arterioles and capillaries
be a possible etiological factor?
 
Did your patient have an autopsy?
 
Jeffrey.
 
For more information, send mail to [log in to unmask] with the message: info PED-EM-L
The URL for the PED-EM-L Web Page is:
  http://www.brown.edu/Administration/Emergency_Medicine/ped-em-l.html

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