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

EMS Protocol of the Week - Seizures

So, you’re having a seizure. What do you do? 

Well nothing, I guess; you’re having a seizure. 

But paramedics can do stuff! And with this brilliant and natural segue, we’re on to Protocol 513 – Seizures.

The ALS protocol for seizures does what it can to diagnose and treat within the confines of the paramedic’s scope of practice. They should be checking a 3-lead for any concerning arrhythmias that may be mimicking as seizure activity, as well as assessing for hypoglycemia that may need to be reversed. Notice that there is a note included that reminds providers to account for a relative hypoglycemia for diabetic patients who may be euglycemic by non-diabetic standards. Similar to other protocols where hypoglycemia is mentioned, ALS will respond by giving dextrose IV/IO or glucagon IM if unable to obtain vascular access.

From here, the protocol discusses benzos, offering separate IV/IO and IM/IN dosing strategies to account for the time and safety concerns that often come with attempting to secure vascular access in a patient that is actively thrashing about. Check the protocol for specifics, but broadly, ALS providers are allowed to administer up to two doses of lorazepam OR up to two doses of diazepam OR a single dose of midazolam by Standing Order. As an OLMC physician, you can authorize repeat doses of any of those as you see fit.

That’s it! Stop the seizure! Don’t forget that benzos will require a Tracking Number (MMC-####), but don’t be alarmed if the crew asks to call back for the number after they’ve controlled the seizure in front of them; they won’t leave you hanging! While you wait for their call back, you can brush up on the protocols at www.nycremsco.org or with the protocol binder!

Dave

Acute vision loss in the ER

Acute monocular vision loss is often an ophthalmologic emergency! Use this nifty graphic to help you differentiate between the most dangerous pathologies, and to remind you how to initiate their medical management!

These are the key take-homes for today's pearl:

-Ophtho should be consulted for all 6 of these pathologies of monocular vision loss. However, it is IMPERATIVE that they be consulted ASAP for CRAO, CRVO, and retinal detachment. That is because the only treatments we have for these pathologies are administered by ophtho, not by the ER.

• Ocular chamber paracentesis, intra-arterial tpa, or intra-ocular antihypertensives may be administered by ophtho for CRAO

• Depending on exam findings (they may also ask for "fluorescein angiography" to differentiate ischemic vs. nonischemic) in suspected CRVO, ophtho may give intra-ocular steroids, hypotensive agents, biologic agents, or even perform surgery.

  • EM used to give ASA to these pts. Antiplatelet agents have since been found to be harmful. The only thing you need to do while waiting for your opthalmologist is to try to control their hypertension.

• We may have all learned that "mac-on" retinal detachment is more of a surgical emergency than "mac-off" (which is technically true, but will only differentiate whether the pt goes to the OR today vs. in 3 days - so they are still both often operative!) however our US and exam is not as good at differentiating the the two, so play it safe, and consult ophtho assuming it is "mac-on" every time... in case it is.

  • On a similar tangent, if you believe you note posterior vitreous detachment on your POCUS, but no retinal detachment, they should still see an ophtho ASAP, because there is a large co-incidence of the two, and often PVD proceeds RD by just a few days.

-For the painful monocular vision losses (glaucoma, optic neuritis, and GCA) we can feel a little less helpless and start treatment before ophtho arrives!

• High dose methylpred for suspected GCA w/vision loss (500-1000mg IV )

• High dose methylpred for suspected optic neuritis (dosing per neurology)

• For suspected angle closure glaucoma, give topical optic beta blockers (timolol) and alpha agonists (such as brimonidine or apraclonidine). We can also start systemic (PO or IV) acetazolamide (if ok kidney function, chose methazolamide if poor kidney function) if the IOP is not coming down with topicals. Next step after that would by IV mannitol/glycerol, but your friendly ophthalmologist will guide you on that.

  • We should avoid giving pilocarpine which can exacerbate certain ocular conditions

  • Also note that if the pt has had cataract surgery in the affected eye, he/she cannot possible be in angle closure (a helpful tip as these pts may have the "steamy" cornea we associate w/acute angle closure glaucoma).