Help needed - post traumatic status epilepticus

[Karim Brohi]

Ian,

These prolonged status cases do happen from time to time and are quite
distressing for all concerned.  There are some dramatic recoveries - even
after months of this - I remember one young girl (non-trauma) at UCSF like
this.  In general though functional outcome is often poor.

I would repeat the lumbar puncture - including looking for evidence of
meningitis/encephalitiis, especially fungal, viral, TB other wierdness (esp
with possible immunosuppression).  (Has he got/did he get an ICP monitor?)

In view of treatment I'm sure you've racked your brain about this but in the
prolonged status patient I've seen inhalational anaesthetics used
(isoflurane I think - though you'd think halothane would be better), and
also interestingly ECT.   People talk about Ketamine as well, but I have no
experience. Vagal nerve stimulation is also in vogue at the moment - and
there are case reports of its use in these situations.

I think it's probably too early to withdraw - but the prognosis for a good
functional outcome is poor.

Good luck

Karim



-----Original Message-----
From: trauma-list-bounces at trauma.org [mailto:trauma-list-bounces at trauma.org]
On Behalf Of Ian Seppelt
Sent: 26 August 2006 04:27
To: ccm-l at ccm-l.org; trauma-list at trauma.org
Subject: 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

######################################################################
Attention: 
This message is intended for the addresses named and may contain
confidential information. If you are not the intended recipient, please
delete it and notify the sender. Views expressed in this message are those
of the individual sender, and are not necessarily the views of Sydney West
Area Health Service.


This e-mail has been scanned for viruses
######################################################################
--
trauma-list : TRAUMA.ORG
To change your settings or unsubscribe visit:
http://www.trauma.org/traumalist.html