Seizure activity during re-warming phase of hypothermia

[Sugarcoma, RN]

I am relatively new to hypothermia and have only rewarmed twice. Both developed what I interpreted to be seizures but what docs told me was myoclonic jerks. Increasing paralytic did not suppress these but did help to make them less pronounced. As the patients got closer to goal temp they become more pronounced.

The docs did not really treat as I would have expected for possible seizure activity and they said it was because this was not really seizure activity. I gave Ativan push to one with no real change. Was told to continue paralytic as per the train of four but to not try to titrate to suppress the activity with either the paralytic or Versed. No other treatment was ordered.

I have been doing some research which has only left me more confused. I have found that there is a condition called post hypoxic myoclonus and that it is an ominous sign during rewarming. I have also read that seizure activity is common in post arrest patients and these articles have included some treatment recommendations.

I was left feeling bad and like I wasn't doing enough for my patients. My thoughts were that we are doing this (hypothermia) to save their brain, we cannot really accurately assess neuro status until they are warmed, and finally continuous seizure activity is detrimental to neuro status. I guess I was expecting aggressive treatment. Am I overthinking this?

My questions are:

How do you tell the difference between post hypoxic myoclonus and seizures? Especially without EEG? Are there any clues that I, as the bedside nurse can use to differentiate between the two?

Have you seen PHM? Do you treat it? If so how do you treat it? I read one study where propofol was effective.

I should add that both times it happened fairly close to shift change and I am not aware of what the day team may have done for treatment.

[ICUNurseStat]

It's been my experience that with myoclonus, you tend to see a very rhythmic generalized twitching. With seizures associated with an anoxic injury, they are often focal, rather than generalized tonic clonic.

Our therapeutic hypothermia patients are normally on propofol so the neurologist sometimes has us titrate it to keep down the myoclonus. Then of course we get an EEG with no sedation if possible. Sometimes if the neurologist feels like it's myoclonus rather than seizures they do not start anticonvulsant drug therapy.

As you said, myoclonus is usually an indicator of a very poor prognosis. It is related to the injury to the brain rather than just the rewarming process.

[silentRN]

If it becomes uncontrollable, you can try propofol, and if that doesn't work you put them on a pentobarbital coma, but you would definitely need an EEG...problem with pentobarbital coma, is that it takes forever to clear the system. There's other drugs that can be tried first too, like Keppra and phenytoin that may help with the seizures, but from experience if the patient continues to be in status then they're gonna need a continuous gtts of something.

If it's twitching because of an anoxic brain injury, then ya, there's really not much you can do for them but do the propofol...but you can't keep someone on propofol for the rest of their life...and as the prior person commented before, it's an indicator of a poor prognosis.

[MunoRN, RN]

Myoclonus can have multiple causes, with anoxic brain injury being one them and can be a poor prognostic indicator. But it can also be due to the severe electrolyte shift that occur, particularly during rewarming.

Aggressive antiseizure treatment isn't necessarily indicated with myoclonus as it is with other types of seizures. Symptom control is usually done with benzos, since antiepileptic drugs are only effective against cortical myoclonus, while benzos are effective against all origins of myoclonus.

Do you use paralytics throughout therapeutic hypothermia or just during cooling?

[umcRN, BSN, RN]

All our cooling kiddos are kept on continuous EEG throughout the cooling and rewarming. Seizures can be seen even if the patient is paralyzed. I guess I assumed all cooling patients were monitored with EEG

[jduvallRN]

I went to Charlotte Davis's Nursing Innovation CCRN review 2-day class three weeks ago with Nursing Innovation in Atlanta. The instructor went in-depth with Therapeutic Hypothermia for both cardiac arrest - post v fib, and also for TBI's. She was one of the most interesting speakers I have ever listened to and really broke down the concepts for me. What she highlighted was the electrolyte imbalances and fluid shifts during the rewarming phase. She also mentioned reperfusion injuries both neurologically and to the heart. Do you think this might be the issue? That the clonus or seizure activity was part of the reperfusion because she said was common.

[Sugarcoma, RN]

Basically the research I have done has said that myoclonus is probably a combination of subcortical and cortical, and that it is a result of severe hypoxia. Nothing that explains why it happens specifically during re-warming. I am hoping to pin down our neuro intensivist one morning just to help my understanding as my research has left me more confused. There is a lot of info on it in regards to peds, but not much for the adult population.

To answer the questions: We use the paralytic through the cooling and re-warming phase, until the pt. reaches 35 degrees then we turn it off and allow them to passively re-warm. Our patients do not get an EEG until they are completely warmed.

I honestly do not know if this clonus activity is a reperfusion injury or if the warming and reperfusion simply unmasks the severe anoxic damage that was done during the arrest.

[dah doh, BSN, RN]

We use paralytics both in cooling and warming phases. Seizures and myoclonus are more likely to be observed during rewarming. We use paralytics, propofol, Ativan, keppra, and other seizure meds as treatment. One of our neurologists likes depakote to suppress the jerking since it bothers the families. We get an EEG ASAP! We do not use pentobarbital due to the lengthy half-life. Usually observation of either of these activities is a bad sign of hypoxia and/or anoxia and a generally poor prognosis.

[glycine45]

obtain, most likely, accurate answer by asking a board certified physician in neurology, please.