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Sat Aug 26 07:56:20 BST 2006

Thanks for the valproate information, Michael - there might be something
in that. We are giving 1 g tds enterally ie 3 g/day where 2 g should be
heaps, and we are struggling to stay in the bottom of the therapeutic
blood range. I will try to track down some IV valproate.

The seizures are not classic myoclonic but have rather more organised
clonus. In addition he has inducable clonus on clinical examination
(especialy ankle clonus).

Verbal report from the radiologist is 'totally normal MRI' yesterday. I
haven't laid eyes on the written report yet which hadn't come through by
the time I went home.

Cheers, Ian

>>> "Michael R Whitty" <mwhitty at bigpond.net.au> 26/08/2006 3:13pm >>>
Hi Ian,

>From what you have presented, I would also be reluctant to withdraw
treatment as a positive diagnosis has not been made.

>From a therapeutic standpoint, I would have thought 3 anticonvulsants
was
enough, but on the matter of valproate you say that he is on a
therapeutic
dose ... does this mean he has a therapeutic blood level?  Valproate
has a
short half life.  I've had patients on it that only have seizures prior
to
their next dose.  It is also not easy to maintain good 24/7 levels when
the
patient is being fed nasogastrically.  Recently, valproate has been
released
in an IV form in Australia.  If you are not already using this it might
be
worthwhile trying an infusion of 2 mg/kg/hr.  There are a few case
series of
success with IV valproate in status epilepticus.

What are the nature of his clonic seizures?  Are they ... myoclonic
(those
little jerky startled things you see with hypoxic-ischaemic brain
injury)?

Are his pupils reactive to light?

Without waiting for a reply, I would think that hypoxic-ischemic brain
injury is still the most likely cause.  He had a chest and facial
injury
(good potential for hypoxia) and who knows how long he was like that
before
he was found?  I would be dubious about what his GCS was at the time
of
intubation.  I would also be dubious about his absent ETCO2 episode.
Doctors lie to save their asses all the time.  This episode does raise
the
possibility of fat embolism, but I would expect that the MRI should now
be
abnormal if that was the aetiology of his current neurologic state.

How normal is his MRI?  Is there no increased white matter signal on T2
and
is/was the diffusion-weighted scan plum normal?

Kind regards,
Michael Whitty
Sydney, Aus.

-----Original Message-----
From: ccm-l-bounces at ccm-l.org [mailto:ccm-l-bounces at ccm-l.org] On
Behalf Of
Ian Seppelt
Sent: Saturday, 26 August 2006 1:27 PM
To: ccm-l at ccm-l.org; trauma-list at trauma.org 
Subject: ccml Help needed - post traumatic status epilepticus

Any good suggestions welcome, for a difficult management problem.

A 33 y/o was transferred to my ICU 15 days ago following a road
trauma.
Circumstances unclear - high speed crash into tree in rural area about
400km from here, with entrapment and difficult extrication. Apparently
conscious throughout and not hypoxic. Ambulance rendezvous with
helicopter team who described an agitated, injured man GCS 12, who was
electively intubated without difficulty. He was then transported to a
regional hospital for trauma assessment. Past history IV drug use, now
stable on a methadone programme, hepatitis C and essential
hypertension.
No prior history of epilepsy.

Injuries included sternal fracture, right lung contusion, undisplaced
fracture of right maxillary antrum, transverse midshaft fracture R
femur, comminuted right patellar fracture and multiple lacerations.
FAST
negative. CT brain, chest and abdomen otherwise normal. Spine normal.
To
theatre for ORIF of femur and wiring of patella. Intraoperatively the
only adverse event was a transient sudden loss of ETCO2.

Postoperatively he developed a generalised clonic status epilepticus.
He was loaded with phenytoin then clonazepam, a midazolam infusion,
magnesium and propofol. Repeat brain CT normal.

He was then transferred to my ICU for ongoing neurointensive care
management. The ongoing generalised clonic staus epilepticus was only
controlled with initially boluses of thiopentone and then a
thiopentone
infusion to burst suppression on continuous EEG. MRI/MRA/MRV normal.
Lumbar puncture normal. Fat embolism suspected but had none of the
usual
signs of fat embolism syndrome and there was no sign of right to left
shunt or pulmonary hypertension on TOE. 

After a number of days of burst suppression he has been allowed to
surface - again to a generalised clonic status. Triple anticonvulsants
with therapeutic doses of phenytoin and valproate and piracetam.
Bilaterally normal SSEPS. EEG again shows polyspike activity every
minute or so, maximally centrally and seen bilaterally. Repeat MRI
yesterday (14 days) still normal. Propofol to suppress seizures and
today I have loaded him with phenobarbitone (trying to avoid going
back
down the thiopentone coma route). 

He has had a tracheostomy and is getting over a nosocomial pneumonia
(probably caused by the thiopentone!). His wife is dejected and is
talking withdrawal of treatment. I am very uncomfortable with that on
the grounds that:

1. We don't know what the problem is [everybody is blaming hypoxia or
maybe cerebral fat embolism but there is no good evidence for either
of
these], 
2. We don't have control of his seizures unless we anaesthetise him,
and
3. Some people have suggested he might be responsive even when having
the seizures (a variant of Lance-Adams syndrome??)

While I agree the likely outcome is poor I have emphasized to his wife
that it is too early to write him off! She is adamant that he would
not
wish to survive unless it was in a very good functional state.

I welcome any advice or comments! What is the cause? What is the best
treatment? How do you prognosticate in this situation?

[Nb I have his wife's permission for this post, as he could well be
identifiable from the information I have given]

Best wishes, Ian

Ian Seppelt FANZCA FJFICM
Senior Staff Specialist
Dept of Intensive Care Medicine
The Nepean Hospital, PO Box 63 Penrith NSW 2751
Clinical Lecturer, University of Sydney

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ccml Help needed - post traumatic status epilepticus