EMS Protocol of the Week - Seizures

For this EMS protocol review, I wanted to focus on prehospital seizure treatment. Both the adult and pediatric algorithms are the same and utilize the same medications and weight based dosing. Paramedics are authorized to utilize 3 different benzodiazepines to treat active seizures:

Midazolam (Versed) 0.2mg/kg IV/IN/IM. If effect is not achieved, may be repeated after 5 minutes. Max single dose is 5mg and max cumulative dose is 10mg.

Lorazepam (Ativan) 0.1mg/kg IV/IN/IM. If effect is not achieved, may be repeated after 5 minutes. Max single dose is 2mg and max cumulative dose is 4mg.

Diazepam (Valium) 0.2mg/kg IV, infused over 1 minute. If effect is not achieved, may be repeated after 5 minutes. Max single dose is 5mg and max cumulative dose is 10mg.

The Medical Control Option for refractory seizures is to administer additional doses of any of these standing order medications. Some considerations for medication choice include availability, as Lorazepam requires refrigeration is not always carried, nor is IV Diazepam due to supply issues. Of these 3 medications, Midazolam is the fastest acting. With mounting doses of benzodiazepines, loss of spontaneous breathing should be a consideration, but typically can be outweighed by ceasing the seizure activity.

Finally, some patients with known seizure disorders, usually pediatrics, will have home prescriptions for PR diazepam, also known as Diastat. Occasionally, you will receive calls from EMS asking if they can administer this home medication. This formulation is not in the algorithm and has a much more erratic absorption than other routes of benzodiazepine administration. Because EMS is already present and has access to faster acting and more reliable medications like Midazolam, this should be administered instead.

Check out the RAMPART trial for a more in depth study on IM vs IV benzodiazepines and their efficacy!

TIA framework

I often have trouble wrapping my head around the concept of TIA. Thinking about it on a continuum with stroke, like the "unstable angina of the brain", caused by the same disease processes and modifiable risk factors as ischemic strokes, has helped me a lot. I have organized the main points into this graphic. I hope it helps you too.

1. TIA exists on a continuum with stroke:

-Even symptoms that resolve after 24 hrs may have abnormality on diffusion-weighted MRI (much more advanced imaging than we had when 24 hr cutoff was developed)

-think of it like “unstable angina of the brain”

-15% of pt’s with TIA go on to have a larger stroke in next 3 months (and HALF of those happen in the first 48 hrs – so start treatment right away!)

-Treatment is same for TIA as for small strokes – namely, to prevent major stroke in future

2. Alternative nomenclature:

• Stroke

  • Persistent deficits

  • Infarction on imaging

• Transient Symptoms with Infarction (TSI)

  • Deficits resolve

  • Infarction (stroke) on imaging

• Transient Ischemic Attack (TIA)

  • Deficits resolve

  • No Infarction (stroke) on imaging

3. Three key elements of TIA history:

-symptoms onset is SUDDEN

-symptom is a DEFICIT (or loss of something – such as sensation or strength)

– the presence of a paresthesia or abnormal smell etc. is more likely intracranial or migraine or seizure

-deficit is FOCAL and makes sense anatomically (correlates to a specific area of the brain or spinal cord – that’s right, the spinal cord can infarct too!)

            - multiple/generalized symptoms is usually something else.

4. Exam:

-always perform a complete neuro exam beyond just NIH scale

-thorough cardiac exam (afib? Pulse defecits?)

5. Unique stroke etiologies (other than most common atherosclerotic thromboembolic disease):

-Endocarditis > give IV Abx

-Carotid artery dissection > give AC

-Aortic arch dissection > CT surgery

-Temporal arteritis > corticosteroids

6. TIA mimics:

-focal/partial seizure

-todd’s paralysis

-complex migraine

-recrudescence triggered by other acute illness

-cardiac syncope

-metabolic (glucose, sodium, calcium)

-brain lesion

-demyelinating disease

-acute vestibular syndrome

-peripheral nerve lesion/neuropathy

-CNS infection

-psychogenic      

7. Initial evaluation/workup:

-Cardiac monitor (pick up Afib)

-EKG

-Labs (CBC, coags, often a troponin is warranted)

-CT head

-CTA head & neck for large vessel territory

-MRI (does not need to happen this second, but should be urgent, is often needed to confirm the diagnosis, which serves to encourage treatment (e.g. aspirin, statin, smoking cessation) so get it in the ER if you can)

8. Initial treatment in ER:

-162mg aspirin if no bleed on initial CT

                             -clopidogrel if ASA allergy

-neurology may recommend other anti-platelets (e.g. both ASA & plavix) but you dont have to start both yourself

-markedly elevated BP can be very slowly lowered (like really slowly. Like over days. PO meds not IV). Permissive hypertension is okay acutely because you want to make sure that ischemic brain gets perfused!

9. Who gets admitted?

-AHA says those who have symptoms <72 hrs ago, ABCD2 score >3, and those who are unable to get rapid evaluation as an outpt should be admitted

-Unfortunately, ACEP says that there is not adequate validation of ABCD2 score to make it a reliable SOLO tool for disposition, and I agree, but I figured I would still include it for you guys because it can be used in concert with other risk factors/circumstances (such as co-morbidities, access to quick followup) to determine who should stay to have their MRI/carotid doppler/echo/cardiac monitoring ASAP vs. who can followup w/neuro and cards in the office. 

10. Who gets anticoagulation?

-Afib

-ventricular thrombi on echo

-CHADS-VAsc 1 or more in men, 2 or more in women

11. Other treatment (not in ER):

-assess and treat modifiable risk factors (HTN, HLD, DM, smoking)

-carotid stenosis imaging can indicate need for carotid endarterectomy which greatly reduces future TIA/stroke risk, this is probably the most important f/u test to get!

-echo can find Left side thrombus that requires long-term AC.  Can also find PFO. 

References:

https://www.emrap.org/episode/c3tia/c3tia

Blum CA, Kasner SE. Transient Ischemic Attacks Presenting with Dizziness or Vertigo. Neurol Clin 33 (2015) 629–642. PMID: 26231276

Coutts SB. Diagnosis and Management of Transient Ischemic Attack. Continuum (Minneap Minn) 2017;23(1):82–92.PMID: 28157745

Lo BM, Carpenter CR.  Clinical Policy: Critical Issues in the Evaluation of Adult Patients With Suspected Transient Ischemic Attack in the Emergency Department Ann Emerg Med. 2016;68:354-370.PMID: 27568419

Tarnutzer AA, Lee S, et al.  ED misdiagnosis of cerebrovascular events in the era of modern neuroimaging. Neurology 2017;88:1468–1477.PMID: 28356464

Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack. Stroke. 2009 Jun 1;40(6):2276-93.PMID: 19423857

Prabhakaran S, Silver AJ, Warrior L, et al. Misdiagnosis of transient ischemic attacks in the emergency room. Cerebrovascular Diseases. 2008;26(6):630-5.PMID: 18984948

A common missed ED diagnosis

Q for all of You.

If i were to tell you that there is a disease entity that has-

• an estimated prevalence of 2% in the US 

• significant morbidity

• is easily treatable

• and that many of us have likely missed it in the ED

Would you know what it is?

Well. You're about to.

Wernicke Encepahalopathy. 

What is it?

• An encephalopathy that occurs secondary to thiamine (B1) deficiency

It's a disease only seen in alcoholics, right?

• ehhh, not quite.

• Wernicke most commonly is found in alcoholics (an estimated 12.5% of them), but has also been found in people who have bariatric surgery, hyperemesis gravidarum, and AIDS (one study found evidence of wernicke in 10% of autopsies in AIDS patients)

Well how does it present.

• Classically has a triad of ataxia ophthalmoplegia, and AMS

• though the full triad is only seen in <10% of patients

Is there a diagnostic tool available?

• Sure is, diagnosis is made with 2/4 of the following criteria

  • Dietary deficiencies

  • Oculomotor deficiencies

  • Cerebellar Dysfunction (ataxia)

  • AMS/mild memory impairment

Why is it important that I treat it?

• An estimated 60% of patients will have residual defecits

How do I treat it

• pretty simple.

• THIAMINE. 

• 500mg IV thiamine three times a day for 3 days, followed by 250mg IV for 2-3 days

  • there is conflicting evidence about the amount of thiamine to give. Yet all agree that thiamine is relatively harmless- basically just give a lot of thiamine

  • IV administration is important here. chronically malnourished patients (especially those with ethanol usage) do not absorb thiamine well in the GI tract.

  • co-administer magnesium IV - hypomagnesemia promotes thiamine resistance

• the 100mg we give in our bannana bags is preventative, and can provide sufficient thiamine for 1 week

So you're saying every confused alcoholic that's stumbling in the ED requires hospital admission for IV thiamine? That'll do great for our boarding issues in the ED

• Not quite.

• But if your drink patient is clinically sober and is then witnessed to have a wide based gait on their way out the ED. take a minute. have a conversation. do a brief ocular neuro exam. look for weird eyeball movements. 

• often times patients will have rapid improvement from an IV thiamine dose (within 30 minutes). While not specific, if this happens the patient should definitely be admitted for IV thiamine. 

How about that thiamine before glucose thing. Do i need to withhold glucose from a hypoglycemic alcoholic.

• Meh. NO!

• in theory, a glucose load increases thiamine requirements. The though was that giving a dextrose load can push the at risk patient into Wernicke. But studies have not shown this to be the case. 

• give your hypoglycemic patient glucose. just do it. Swoosh style. 

What's the pathophysiology behind it?

• Never thought you'd ask!

• Every ED docs favorite cycle - the Krebs cycle

• Thiamine is a co-factor for pyruvate dehydrogenase, which converts pyruvate --> Acetyl-CoA, which then enters the Krebs cycle and results in ATP production

• So no thiamine = no ATP

• no ATP = bad. 

That's all.

-Elly