Stroke And TIA – Help From MCHD Paramedic Podcast, EMC Podcast, And emedicine.medscape.com

Today, I’m reviewing three resources on Stroke and TIA. The first are from MCHD Paramedic Podcast. The second are from Emergency Medicine Cases, and the third are from emedicine.medscape.com.

First are two stroke podcasts linked below from the MCHD Paramedic Podcast  The podcasts are from the Montgomery County Hospital District EMS

These two podcasts are brief state of the art review of the paramedic diagnosis and treatment of stroke. They are outstanding. They contain a new approach to field treatment of stroke and are of interest to all clinicians not just ems clinicians (paramedicts and emts)

Here are the links:

MCHD Paramedic Podcast – Episode 9 – The State Of EMS Stroke Care In 2018

MCHD Paramedic Podcast – Episode 10 – Stroke Systems Of Care Featuring Dr. Peter Antevy

And here is the summary with references from the show notes:

In the past 24 months, stroke care has evolved in the way we evaluate strokes in the pre-hospital space and how they are worked up and treated in the hospital. Large vessel Occlusion (LVO) stoke is a large caliber vessel clot causing stroke symptoms. New techniques and devices in endovascular retrieval of these clots along with intravenous Tpa has shown great success in five randomized trials published in 2015.(1) The number we need to treat for one improved neurologic outcome at 90 days according to data from these trials is 2.6 patients. This is a massive breakthrough in the way we approach acute stroke care. Improved outcomes in these trials are directly associated with times to reperfusion therapy and EMS must change the way we diagnose and rank stroke patients in order to get them an endovascular capable facility when appropriate. In the first podcast our team will review all of the pertinent data from these trials and suggest how EMS should approach this LVO stroke diagnosis. In the second part of our stroke awareness series we talk with Dr. Peter Antevy, an EMS medical director from Florida who is an expert of developing regional systems of care for these LVO stroke patients. He will discuss development of their system and exciting new data that demonstrates a treatment benefit up to 24 hours after onset of symptoms in some subsets of these stroke patients. (2, 3)

References

1.Hermes Collaboration: Lancet 2016
www.thelancet.com/journals/lancet/…00163-X/abstract
2. Dawn Trial: NEJM 2018
www.nejm.org/doi/full/10.1056/NEJMoa1706442
3. DEFUSE 3 Trial: NEJM 2018
www.nejm.org/doi/full/10.1056/NEJMoa1713973

Next are  two podcasts from Emergency Medicine Cases. Both should be listened to and, as always, the shownotes are outstanding:

TIA Diagnosis And Management, Episode 117 From Emergency Medicine Cases – With Additional Resources.
Posted on November 23, 2018 by Tom Wade MD [I linked to my post because it has additional resources that I think are important for me to remember.] Here is the introduction from the show notes of the podcast:

Much has changed in recent years when it comes to TIA risk stratification, workup and antiplatelet therapy. In this podcast we use the overarching theme of timing to elucidate how to distinguish true TIA from the common TIA mimics, the importance of timing in the workup of TIA, why the duration of therapy with dual antiplatelet therapy and timing of starting anticoagulation in patient with atrial fibrillation, contributes to the difference between preventing catastrophic strokes and causing intracranial hemorrhage. Remember that stroke is a leading cause of adult disability and is the third leading cause of death in Canada. It’s time we paid more attention to TIA…

Ep 120 ED Stroke Management in the Age of Endovascular Therapy from Emergency Medicine Cases, January 2019. And here is the introduction:

According to the Global Burden of Disease Study published in NEJM in December 2018 the estimated lifetime risk for a 25 year old during their remaining lifespan is 25% [1]. Stroke is the 3rd leading cause of death and 1st leading cause of major disability in North America. As we transition from the relatively simple era of systemic thrombolytics under 3 hours vs “ASA and admit” for over 3 hours, decision making has become much more complicated and varied, depending on where you work. Which patients need what type of scanning? Where should that scanning be done – at the stroke center or at the peripheral center? Which patients should get systemic thrombolytics? Which patients should get endovascular therapy? In this EM Cases main episode podcast, a follow up to our episode on TIA released in November 2018 with Walter Himmel and David Dushenski, we try to simplify the confusing time-based and brain tissue-based options for stroke management…

And finally there are many useful articles on stroke and TIA on emedicine.medscape.com. I have listed ones that I have read and found useful:

Transient Ischemic Attack
Updated: Dec 03, 2018 from emedicine.medscape.com
Author: Ashish Nanda, MD

Imaging of the brain should be performed within 24 hours of symptom onset, as follows [14:

  • Magnetic resonance imaging (MRI) with diffusion-weighted imaging (preferred)

  • Noncontrast computed tomography (CT; ordered if MRI is not available)

The cerebral vasculature should be imaged urgently, preferably at the same time as the brain. Vascular imaging for TIA includes the following:

  • Carotid Doppler ultrasonography of the neck

  • CT angiography (CTA)

  • Magnetic resonance angiography (MRA)

POINT: Success at Last for Dual Antiplatelet After Stroke, TIA
Sue Hughes May 17, 2018 from emedicine.medscape.com

GOTHENBURG, Sweden — A combination of clopidogrel plus aspirin reduced major ischemic events, including ischemic stroke, myocardial infarction, or death from ischemic vascular causes, compared with aspirin alone in patients with minor ischemic stroke or high-risk transient ischemic attack (TIA) in the POINT trial.

Although the dual antiplatelet therapy was associated with an increased bleeding risk, the authors say the benefits outweigh the risk.

“If dual antiplatelet therapy is given for just 30 days, then this results in 19 major ischemic events being prevented per 1000 patients treated at the cost of two extra major bleeds,” he reported.

“In addition, we didn’t see any increase in fatal or intracranial bleeding. The additional bleeds were systemic — mainly gastrointestinal, which we can treat — and most were reversible,” he added.

Imaging in Carotid and Vertebral Artery Dissection
Updated: Jul 17, 2018 from emedicine.medscape.com
Author: Jeffrey P Kochan, MD

Vertebrobasilar Atherothrombotic Disease
Updated: Oct 05, 2016 from emedicine.medscape.com
Author: Eddy S Lang, MDCM, CCFP(EM), CSPQ

Vertebrobasilar atherothrombotic disease (VBATD) deserves special attention among emergency physicians because it is difficult to diagnose and important not to misdiagnose. Signs and symptoms of VBATD overlap those of other more common benign entities (eg, labyrinthitisvestibular neuronitisbenign paroxysmal positional vertigo).

Approximately one fourth of strokes and transient ischemic attacks (TIAs) occur in the vertebrobasilar distribution. [1]

  • Brainstem infarctions have been reported in autopsy series at a rate of 2 per 1000 cases. One clinical study has suggested that the disease occurs 25% as frequently as occlusions of the carotid artery and its branches.

  • Recent developments in neuroimaging provide new perspectives about the disease’s prevalence. Some studies using MRI suggest that 40% of patients with vertebrobasilar TIAs have evidence of brainstem infarction.

    Vertebrobasilar ischemic disease encompasses a vast spectrum of clinical syndromes, extending from subclinical to lethal brainstem infarctions.

    Of patients who suffer infarctions in the vertebrobasilar territory, 50% report TIAs in the days or weeks (rarely months) prior to onset of the permanent deficit. A systematic review suggests that although overall mortality is no different than anterior territory ischemia, the early risk (within 7 d) of recurrent stroke or TIA progression to stroke is higher with VBATD. [1]

    Basilar artery syndrome, which presents as a locked-in state, is caused by complete occlusion of the intracranial portion of vertebrobasilar circulation. It is a devastating disease with a mortality rate of 75-85%.

Vertebrobasilar TIAs typically have shorter duration than attacks involving the carotid territory, lasting 8 minutes on average compared with 14 minutes for carotid TIAs.

Classic symptoms of posterior region ischemia include the following [29:

  • Vertigo

  • Visual field defects (diplopia, hemianopia)

  • Auditory phenomena (sudden sensorineural hearing loss)

  • Facial numbness or paresthesias

  • Dysphagia, dysarthria, hoarseness

  • Syncope (drop attacks)

  • Hemisensory extremity symptoms (eg, contralateral to facial component)

Vertigo is the hallmark symptom of patients experiencing ischemia in the vertebrobasilar distribution. Many patients describe their vertigo as nonviolent or more of a swimming or swaying sensation. Exact incidence of vertigo is unknown, yet as many as one third of patients with VBI may experience vertigo as the sole manifestation of their illness.

Causes

Atherosclerosis is by far the most common cause of VBI, making VBI most common among patients with cardiovascular risk factors such as age, hypertension, diabetes mellitus, smoking, dyslipidemias, and family history of premature coronary artery disease (men < 55 years old, women < 65). VBI may result from any disease process that has an impact on the arterial supply to the posterior fossa, including the following:

Fibromuscular dysplasia

Rotational occlusion (Bow hunter’s stroke) – Mechanical occlusion or stenosis of the vertebral artery at the C1-C2 level caused by lateral flexion

Vertebral artery dissection

Vertebrobasilar aneurysms

Dolichoectasia of basilar artery

 

 

 

 

Additional References:

Large Vessel Occlusion in Acute Stroke: Cortical Symptoms Are More Sensitive Prehospital Indicators Than Motor Deficits Pub [PubMed Abstract] [Full Text HTML] [Full Text PDF]. Stroke. 2018 Oct;49(10):2323-2329. doi: 10.1161/STROKEAHA.118.022253.

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