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Sat Aug 26 04:26:50 BST 2006

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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Help needed - post traumatic status epilepticus