Neurological prognosis after cardiac arrest

This weeks question

With regards to neuroprognostication after cardiac arrests:

– Is myoclonus universally believed to be a strong enough marker of poor prognosis that decisions regarding withdrawal can be made based predominantly on its presence?

– After considering confounding factors (e.g. TTM, sedative medications) are people comfortable to consider abnormal motor score of GCS sufficeint evidence of poor prognosis? If so after what time period?

– Are there any other markers people recommend or advise caution with?


A

This meta-analysis from the US in 2006 may be helpful when considering the questions.

This meta-analysis says that there is Level B evidence that myoclonus status epilepticus is invariably associated with in-hospital death and “poor outcome”, it does however say that sporadic focal myoclonus does not predict poor outcome.

With regard to motor score they report no false positives GCS motor score of 2 or less after 72 hours as a predictor of poor outcome or death. (I’m not sure what the numbers involved were though).

B

Prognostication is incredibly difficult. Myoclonus is not sufficient to indicate a bad outcome.

There were new guidelines out last year (I’m away at the mo so can’t forward it) [I presume you mean these – JB]. They suggest a combined approach using gcs/ct head/EEG and somatosensory evoked potentials (ssep’s).

Ssep’s can be done early at 24-48 hours but unfortunately at the moment we don’t have access to them….we are trying to get them. Ssep’s seem to be the only investigation that gives a definitive answer so it is unfortunate that we can’t access them!

There is also a move to use MRI but logistically this is problematic. There is also research into things like neuron specific enolase but no clinical use for it yet.

We used to withdraw quite early on these patients but we tend to leave it longer and longer and use a range of modalities to prognosticate.

We also had a case a couple of years ago that we withdrew on at day 7 based on poor gcs/EEG/ct findings and put the patient down the dcd donation pathway. The patient woke up 36 hours later! We have therefore started waiting a bit longer!

We are trying to get ssep’s to help us and allow us to use multimodal investigations to aid in prognostication.

The key thing I think is that it is very difficult and that we need to allow a lengthy period of time to prognosticate.

C

The AAN review from 2006 which A mentioned is unfortunately now 9 years old and references, almost exclusively, studies published before the advent of widespread therapeutic hypothermia (and subsequently TTM), which has thrown everything into confusion. As Claire says, even myoclonus is little use any more.

D

Does anybody feel that they can reliably identify myoclonus purely clinically?

I see things that look ‘a bit jerky’, but I am rarely convinced, particularly when they are so paroxysmal and the EEG invariably only records in a quiescent period.

E

It sounds like the evidence is not robust enough and it would concern me relying on individual markers to decide on prognosis….sort of like only using CVP to assess fluid status.

I think we should use a combination of clinical history, examination, neuro-imaging and electrophysiology to construct as good a ‘picture’ as possible regarding prognosis. The real question for me (and maybe others) is how long I.e when to do the tests and when to assess/wait for recovery. Does anyone have any views or advice?

F

Good topic.

Beware misdiagnosis. See this case report on Lance – Adams syndrome!

The time window in which myoclonic status epilepticus is the likely diagnosis is reported as very short.

G

I guess now that we have changed our approach from therapeutic hypothermia to targeted temperature management the confounding effect of this will need to be considered less frequently?

It seems agreed that occasional myoclonic jerks have little prognostic value in patients suffering from HIE.  But it does seem from the literature that post arrest day 1 myoclonic status (therefore very unlikely to be Lance-Adams) is associated “with a hopeless neurological prognosis” – however the references for this in multiple sources all reference the same papers – another paper by the author A linked (Wijdicks Ann Neurol 1994)  and a 1998 Lancet paper by Zandbergen. But I suppose this doesn’t make it less valid? Again as D said assuming we get the diagnosis correct!

H

A‘s review is an excellent one.

SSEP’s and biomarkers can definitely help. So can extensor posturing and no motor response along with upper brainstem areflexia – fixed pupils,  absent corneal reflexes. Myoclonic STATUS is also a hard sign, but as A points out focal myoclonus is not the same thing (we’ve had a survivor go off to neurology with intact higher function but uncontrolled hemi-myoclonus) and there is also non-epileptic myoclonus – the jerkiness D talks about – which is non-central in origin. So everything that jumps is not myoclonus. 

Time frames do need to get longer, the AAN review is quite clear that 72 hours is long enough when you haven’t been cooled, but if you have God knows. And C‘s right its 9 years old anyway.

But CT, alpha coma (stuff we practically rely on) aren’t discriminatory. 

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