Algorithm for a seizure code

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Here's the scenario: It's midnight, I'm the intern on call, and our IM team gets paged to a code. When we get there, there's a 45 year old surgery patient s/p who knows what having a grand mal seizure.

Where would I find algorithms on how to treat this? Is it just lorazepam 2-4 mg IV until s/he stops? I feel pretty comfortable with the ACLS algorithms, but it's the non-cardiac codes that I'd appreciate a little more structure around.

I haven't had to run these codes just yet, but let's just say I want to be ready.

Any advice/resources would be appreciated.

 

[Pir8DeacDoc]

2mg IV ativan will stop him in his tracks. repeat PRN....

 

[mpp]

link

 

[mlw03]

Check any decent neurology text for more details, but it's not just IV ativan - that's only the first step. here's an algorithm we were taught:

1. IV lorazepam or diazepam; i hear mostly lorazepam is used, up to 8 mg
2. loading dose of phenytoin - 1 gram given at 50 mg/min; you need this because even though the benzo will stop the seizure, without an anticonvulsant on board the seizure will resume as soon as the benzo wears off (which is pretty soon if you use valium instead of ativan). the phenytoin helps stabalize those membranes.
3. if seizures continues give phenobarbitol 1-1.5 grams at 50 mg/min
4. if seizure still haven't stopped you have to induce anesthesia with midazolam or pentobarbitol and intubate to provide respiratory support.

goal is you have to get the seizure stopped pretty quick or the patient is going to cook their brain by this point. also give sugar in the form of 50% dextrose, but make sure to give thiamine 100 mg first to not precipitate Wernicke's encephalopathy.

despite what step 1 books say about 30 minutes being required for a diagnosis of status epilepticus, most neurologists treat any seizure that lasts more than 5 minutes as SE and start pumping benzos and dilantin to try and stop the seizure.

 

[deleted109597]

Even if the person is paralyzed and intubated, the seizure doesn't stop. You must keep treating it, because the brain doesn't depolarize the same way muscle does.

You must consider a few other causes...hyponatremia, for which the treatment is 3% saline, pyridoxine deficiency, for tuberculosis patients on INH.

 

[Apollyon]

Even if the person is paralyzed and intubated, the seizure doesn't stop.

This is the meat of this whole thread. The paralyzed pt is still seizing away and burning up brain wholesale. Likewise, a paralyzed but not sedated patient that is otherwise intact is black-letter malpractice (it's torture - literally).

 

[gutonc]

Even if the person is paralyzed and intubated, the seizure doesn't stop. You must keep treating it, because the brain doesn't depolarize the same way muscle does.

Benzos, barbituates and other anestheisa magic drugs treat you the physician, not the person having the seizure. They will decouple the neuro- from the -muscular component of the seizure and make things look less crazy but will not actually fix anything and, as mentioned, grey matter will continue roasting until you actually break the neuro component of the seizure.

Give ativan so you can safely approach the pt., load w/ phenytoin (or fosphenytoin), intubate (if indicated) and get your neuro colleagues down there ASAP.

 

[napoleondynamite]

During my 8 years in EMS, there were a few times I had a status epilepticus pt in the field and no line to push Ativan. Remember that in this instance, with an actively seizing pt (and in my case-in the back of a bumpy ambulance going lights and sirens!) obtaining IV access can be difficult at best! It is a good trick to know that you can give RECTAL Valium in this case. I have done this a couple of times, and it worked just as good as IV Ativan. Just thought I'd throw in my two cents..

Also, don't forget about BLS stuff. Place the patient on his/her side, suction secretions, pad their head, place a bite-block if possible. That sort of stuff that will prevent further injury to your patient.

 

[a_ditchdoc]

Benzos, barbituates and other anestheisa magic drugs treat you the physician, not the person having the seizure. They will decouple the neuro- from the -muscular component of the seizure and make things look less crazy but will not actually fix anything and, as mentioned, grey matter will continue roasting until you actually break the neuro component of the seizure.

Give ativan so you can safely approach the pt., load w/ phenytoin (or fosphenytoin), intubate (if indicated) and get your neuro colleagues down there ASAP.

I was under the impression that benzos and barbituates actually stop the seizure as they are not paralytics and act on the memberane channels. Am I wrong? I have seen pentobarb used in ICU's by neurologists for long term status control...it certainly knocked out the epileptiform activity on the eeg.

 

[docB]

Are we really 9 posts in and no one has mentioned checking a glucose?

I agree with those who have mentioned that a paralyzed patient may still be seizing. That's a good reason to use sux to tube those pateints as it will dissipate in ~5 minutes and then if they're still seizing you'll know it.

 

[mlw03]

i said to give IV dextrose and thiamine. the algorithms i've read say to do that without bothering to check the glucose level first - even if they're euglycemic or a bit high it's not going to hurt, and you're giving the thiamine before or concurrently to prevent Wernicke's. i've never heard a good argument for checking the glucose rather than just giving the thiamine/dextrose empiracally, but if i'm mistaken please let me know.

 

[augmel]

Benzos, barbituates and other anestheisa magic drugs treat you the physician, not the person having the seizure. They will decouple the neuro- from the -muscular component of the seizure and make things look less crazy but will not actually fix anything and, as mentioned, grey matter will continue roasting until you actually break the neuro component of the seizure.

Give ativan so you can safely approach the pt., load w/ phenytoin (or fosphenytoin), intubate (if indicated) and get your neuro colleagues down there ASAP.

Doesn't the GABA agonism of benzos and phenobarb decrease the brain activity that is causing the seizure? Seems like treating the patient to me. Its also not a bad idea to treat that muscular component anyway and prevent rhabdo (admittedly not usually severe.) I think we have all seen the folks who get a single mg of ativan and respond quite nicely. I agree that loading dilantin is the next step if they are refractory or you think they are likely to seize again based on the underlying etiology.

 

[Anasazi23]

Benzos, barbituates and other anestheisa magic drugs treat you the physician, not the person having the seizure. They will decouple the neuro- from the -muscular component of the seizure and make things look less crazy but will not actually fix anything and, as mentioned, grey matter will continue roasting until you actually break the neuro component of the seizure.

Give ativan so you can safely approach the pt., load w/ phenytoin (or fosphenytoin), intubate (if indicated) and get your neuro colleagues down there ASAP.

This isn't quite true. Benzodiazepines were originally developed for the purpose of seizure abortion.

1. Stabilize vitals. Maintain airway, administer O2, maintain BP
2. Check glucose, chem-7, CA, Mg. Get CBC and tox screen. Start an IV line and give 100mg Thiamine followed by 50ml of 50% glucose (debatable). Some start loading doses here if the cause of the status is known from a neurological standpoint.
3. Start Lorazepam 0.1mg/kg at 2mg/min to total dose of about 8mg
4. If this fails to abort the seizure, give fosphenytoin in loading dose of 20mg/kg. May give additional doses of 10mg/kg. Beware of hypotension here.
5. Consider ET tube if still seizing. Start Phenobarb 20mg/kg at 50-100mg/min.
6. If this fails, consider pentobarb and continue treating.

Of course, do not mix dextrose containing solutions with Phenytoin, as it precipitates in solution.

 

[deleted109597]

Benzos, barbituates and other anestheisa magic drugs treat you the physician, not the person having the seizure. They will decouple the neuro- from the -muscular component of the seizure and make things look less crazy but will not actually fix anything and, as mentioned, grey matter will continue roasting until you actually break the neuro component of the seizure.

Give ativan so you can safely approach the pt., load w/ phenytoin (or fosphenytoin), intubate (if indicated) and get your neuro colleagues down there ASAP.

Uh, ativan is a benzo.
Benzos are first line. Barbs work on a different receptor, and are second line if benzos don't work. You can load with dilantin after you break the seizure, or load during the seizure. Different people do different things. Always start with a benzo though.

 

[docB]

i said to give IV dextrose and thiamine. the algorithms i've read say to do that without bothering to check the glucose level first - even if they're euglycemic or a bit high it's not going to hurt, and you're giving the thiamine before or concurrently to prevent Wernicke's. i've never heard a good argument for checking the glucose rather than just giving the thiamine/dextrose empiracally, but if i'm mistaken please let me know.

True. I often just give a D50 if no one can find a glucometer quickly.

 

[swpm]

Uh, ativan is a benzo.
Benzos are first line. Barbs work on a different receptor,

No, benzodiazepines and barbiturates both act on GABA receptors. IIRC, benzos increase the frequency with which the Cl- channels open; barbiturates increase the duration they stay open.

Open Cl- Channel = hyperpolarized membrane = higher threshold for the neuron to fire = less brain cooking.

 

[deleted109597]

No, benzodiazepines and barbiturates both act on GABA receptors. IIRC, benzos increase the frequency with which the Cl- channels open; barbiturates increase the duration they stay open.

Open Cl- Channel = hyperpolarized membrane = higher threshold for the neuron to fire = less brain cooking.

Yes, Benzos and barbs work differently, they potentiate each other. But I wouldn't call the protein a GABA receptor, as does this image. This is terribly poor from a biochemical standpoint. Receptors are binding sites, not chloride channels. But you get the point. I say receptors, you (and they) say binding sites.

I'm not saying you're wrong, just that the terminology is incorrect. But I knew what you were saying.