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Help needed - post traumatic status epilepticus
Karim Brohi karim at trauma.orgSat Aug 26 11:10:18 BST 2006
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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
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