ccml Help needed - post traumatic status epilepticus

[Ian Seppelt]

Good news!

After phenytoin, difficulties with valproate absorption (and we can't
get the IV at present - only stock in Australia is past its use by
date!), piracetam, phenobarbitone and propofol, yesterday's EEG was
finally quiet and we are starting to back off on the anticonvulsants.

Just to make things even more interesting the last few days have also
included big problems managing a neurogenic fever. He had been cruising
on 39 C since admission but for the last few days it had been 40 going
on 41 C. No success with paracetamol, cold air surface cooling, ice
packs, a proprietary set of cooling packs with cerebral cool cap
[Hornsby], cold saline bladder and gastric lavage, dantrolene, or an
extracorporeal circuit (CVVH machine with tubing sitting in iced water).
Then MAGIC - we got access to an endovascular cooling catheter
(InnerCool) and got temperature control within 2 hours. I've never used
one before (basically a big heat exchanger you put up the IVC and
perfuse countercurrent with temperature controlled fluid) but am very
impressed. Unfortunately the disposables cost AU$2000 so it is not for
routine use.

And even more magic - he is now awake and communicating with his wife!

I will keep you informed as he comes off the ventilator

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

>>> John Lambert 29/08/2006 1:21pm >>>
I just reviewed the anaesthetic record (he was anaesthetised at my
institution), and I have the following to add...

>From the automated record the period of reduction in CO2 was LESS THAN
2 minutes.

The SpO2 record did not even show a dip at that time, and the immediate
responses of the anaesthetist are clearly visible (reduction of nitrous,
increase of FiO2, bagging...)

The episode was approximately half an hour AFTER the femoral nailing,
although there was mild hypoxia peri-nailing (down to SpO2 90%)

There was a less than 10% increase in HR and BP peri-episode...

Although clearly an event happened at that time, it would be a complete
stretch and highly unreasonable to think that it caused cerebral hypoxia
in my humble opinion.

It is far more likely that the original insult has caused a diffuse
shear injury, or possibly a hypoxic injury.  Alternatively his brain is
unhappy it is not getting its normal dose of methadone!  :-)

John



Dr John F. Lambert
Director of Intensive Care,  Orange Base Hospital
Area Director of Critical Care Services,  Mid Western Area Health
Service
Orange  NSW  Australia
Phone: (02) 6393 3201
Facsimile: (02) 6393 3207 (not private)
Mobile/Cell Phone: (0428) 236 740

>>> prasannasimha <prasannasimha at gmail.com> 26/08/06 15:53:13 >>>
Fall in ETCO2 - air /fat embolism or more likely disconnected
ventilator 
with alarms off intraoperatively or a slipped out ET tube ? sounds 
suspicious - maybe hypoxic encephalopathy.
Prasanna

Michael R Whitty wrote:
> 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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