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Episode 92 - INSIGHTS: Acute Ischemic Stroke Pt2

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Description

Listen to the fourth episode of NCS's INSIGHTS series on Acute Ischemic Stroke (part 2 of 2)

The INSIGHTS series is hosted by Casey Albin, MD and Salia Farrokh, PharmD, and covers different topics from Neurocritical Care ON CALL®, the only up-to-date, comprehensive resource to offer content exclusively dedicated to the practice of neurocritical care. Learn more about ON CALL®.

This episode is sponsored by Biogen.

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The NCS Podcast is the official podcast of the Neurocritical Care Society.

Contributors

  • Salia Farrokh, Pharm.D., BCPS, BCCCP

    Salia Farrokh, PharmD, BCPS, BCCCP is a neuro ICU clinical pharmacist specialist at Johns Hopkins Hospital. Dr. Farrokh received her PharmD degree from Saint John Fisher College, Wegmans School of Pharmacy in Rochester, NY. Her postgraduate training includes residencies in Critical Care and Pharmacy Practice at Yale-New Haven Hospital. Dr. Farrokh’s research interests include effective antiplatelet therapy in neuro intervention patients, optimal pain management in neuro ICU patients, and use of neurostimulants in this setting. Dr. Farrokh is passionate about training and precepting students and residents and is a certified ENLS trainer.

  • Casey Albin, MD

    Casey Albin, MD is an Assistant Professor at Emory University School of Medicine where she is a member of the department of Neurocritical Care. She completed both her neurology residency and a fellowship in Medical Simulation at Harvard Medical School/BWH/MGH. She completed Neurocritical Care fellowship at Emory. Dr. Albin’s research interests focus on educational innovations in acute neurologic emergencies and neurocritical care. In addition to running simulation courses, she is the editor of a best-selling textbook The Acute Neurology Survival Guide and is passionate about open access neurologic education through Twitter, blogs, and podcasts. She serves on the Education Committee of the Neurocritical Care Foundation.

  1. Hi everyone and welcome back. As a
  2. reminder this is the Insight podcast.
  3. Insight is a podcast that is diving in
  4. to sort of neurocritical care for a
  5. general intensivist for our trainees and
  6. helping to kind of bring exposure to
  7. neurocritical care topics for all. As a
  8. reminder we are so grateful for our
  9. sponsors Biogen and Cerebell and now we
  10. have a word from our sponsors before we
  11. dive right back in.
  12. Founded in 1978 Biogen is a leading
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  21. Biogen is advancing a pipeline of
  22. potential novel therapies across
  23. neurology, neuropsychiatry,
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  25. and remains acutely focused on its of
  26. serving humanity through science while
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  28. and equitable world.
  29. The acute phase of acute skimming stroke
  30. last time. And we talked about how we
  31. focus on thrombectomy and thrombolysis
  32. interventions such as alteplase versus
  33. tenectoplase and all those cool things.
  34. But beyond a stage really, the idea is
  35. what to do to reduce the recurrence and
  36. all the complications that can happen
  37. after this acute phase of stroke. So
  38. today, we're going to focus on all of
  39. that. What's going to happen after that
  40. acute phase of schematic stroke and how
  41. can we minimize all the complications?
  42. So, Casey, with that in mind, when
  43. you're admitting a patient with acute
  44. schematic stroke to your ICU, what are
  45. some of your considerations? So, when
  46. I think about kind of how we're going to
  47. tackle this admission, I think there
  48. are kind of three things to really think
  49. through. The first is just kind of
  50. blood pressure control, the most
  51. applicable thing in the first 24 hours.
  52. So we'll talk a little bit about how you
  53. manage that. The second thing I should
  54. sort of think about is, you know, is
  55. this a large stroke? And is this
  56. someone who potentially might need
  57. surgical intervention? So we'll talk
  58. about that. And then finally, it's
  59. kind of figuring out like, why did this
  60. stroke even happen? And like, what
  61. medications are we gonna put on board to
  62. prevent a recurrent stroke?
  63. And so to start with sort of the blood
  64. pressure goal, we know from the ASA
  65. guidelines that anyone who gets, I mean,
  66. who gets, um, lytic therapy, the
  67. blood pressure goal after you get either
  68. alteplase or tenecta place needs to be
  69. one, less than 180 over less than one
  70. of, uh, dialysis 105 of. And so I
  71. think a question was, you know,
  72. literature like is lower better, like
  73. if, if what we're doing is trying to
  74. prevent a reperfusion injury and
  75. hemorrhagic transformation of the stroke.
  76. And we think that that, you know, risk
  77. increases with higher blood pressure,
  78. is it better to lower the blood pressure
  79. more? Um, so Enchanted looked at this,
  80. this was a trial that was done some time
  81. ago published in the Lancet in 2019.
  82. And basically what it showed is that
  83. while we did prevent a couple more
  84. hemorrhagic transformations, we
  85. actually had no difference in the
  86. modified Rankin scale at 90 days with
  87. this intensive blood pressure of
  88. lowering group. So my takeaway from
  89. that is that yeah, maybe we've
  90. prevented some like very small
  91. hemorrhagic transformation that was
  92. probably not significantly significant.
  93. But at the same time, we reduced
  94. collateral circulation and our patients
  95. who rely on that collateral circulation
  96. weren't getting the perfusion that they
  97. needed. So I think the answer is up to
  98. 180 if the patient's auto-regulating
  99. below 180, just keep them there. We
  100. don't need to go crazy lowering their
  101. blood pressure.
  102. The kind of the next question that, you
  103. know, comes up in my practice is
  104. fortunately with life-saving treatment
  105. like, you know, lytic treatment, like
  106. mechanical thrombectomy in particular,
  107. a lot of our patients are not having
  108. these gigantic strokes anymore, and
  109. that's obviously fantastic. But I would
  110. say that there are still a reasonable
  111. number of patients that either don't
  112. qualify for treatment because they come
  113. in so late or that do get treated, but
  114. the treatment's just not successful.
  115. And so these patients end up having
  116. bigger strokes. The question is, is
  117. which of those patients are going to
  118. then develop malignant edema? So
  119. malignant edema is, you know, a mix of
  120. these eugenic edema, cytotoxic edema,
  121. ionic edema that causes the brain to
  122. swell, and that swelling, particularly
  123. in our young patients, can actually
  124. cause herniation and death So for some
  125. of these large territory infarctions,
  126. you know, the morbidity that can be up
  127. to you. I mean, the morbidity is very
  128. high and the mortality can be up to 80
  129. without any intervention. And so this,
  130. I think, is something that we really
  131. should be aware of. This is most an
  132. issue in our younger patients that have
  133. these large territory strokes. So what
  134. I mean by that is they have greater than
  135. 23 territory of the MCA being affected
  136. by early evidence of ischemia. That
  137. usually translates into someone having a
  138. non-dominant stroke of an NIH stroke
  139. scale greater than 15, or a dominant
  140. stroke scale greater than 20, right?
  141. So big strokes. We know in our younger
  142. patient population that that sort of
  143. stroke has a very high risk of
  144. progressing to herniation. And so
  145. decimal hamlet and destiny were sort of
  146. these first generation trials that were
  147. done in Europe looked at randomizing
  148. those patients to early surgical
  149. treatment And what they found was
  150. decompressive hemicranicectomy done in
  151. the
  152. 48 hours. So really ideally before
  153. there's any sort of evidence of
  154. herniation, like before the patient
  155. starting to look sleepy, very much
  156. before the patient has a blown pupil,
  157. that if we take the bone off and give
  158. those patients, you know, room for
  159. that swelling to occur going extra
  160. cramely, we're not only reducing the
  161. mortality, we're reducing morbidity.
  162. So the amount of patients who had a MRS
  163. of three, that was a much higher
  164. percentage of the patients who actually
  165. got the decompression. So I always,
  166. you know, when I'm talking to families
  167. about this, my personal practice is to
  168. say that our best chance at giving you
  169. the best possible functional outcome is
  170. to remove the bone and do this early.
  171. Now, I want to be clear that some
  172. patients are going to end up still in
  173. that sort of disabled category of having
  174. these, you know, severe disability
  175. after their stroke. And so this is,
  176. you know, this is a really important
  177. time for shared decision-making because
  178. some families will say, You know, my
  179. loved one wouldn't want to live if they
  180. were going to need a trachinopag and
  181. prolonged recovery. That's just not the
  182. type of care that it would be
  183. goal-comported for them. But it's
  184. really important to have those
  185. discussions upfront and to be an
  186. surgical capable hospital, right? So
  187. this is one of the big take home points
  188. for me is if you are not in a
  189. neurosurgical capable hospital and you
  190. have a young patient, less than 60
  191. years old, who has one of these big
  192. strokes, talk early about transferring
  193. them to someone that does have a
  194. neurosurgical capable facility. The
  195. data is really not as robust for our
  196. older patients, and so I think that
  197. becomes really a case-by-case scenario.
  198. Destiny too showed that, you know, in
  199. our older than 60 patients,
  200. decompressive hemichraniac to me did
  201. lead to a mortality benefit, but not so
  202. much a functional benefit. And so it
  203. really is a discussion to have with your
  204. neurosurgeons, to have with family,
  205. you know, this is not as clean and
  206. clear-cut.
  207. So, we've talked about blood pressure
  208. and control. We've talked about
  209. decompression for a large territory
  210. stroke. The next sort of thing is
  211. trying to figure out why they had the
  212. stroke. And we can certainly spend like
  213. a whole podcast talking about like
  214. different etiologies of stroke, how you
  215. work them up. And I think that that's
  216. going to get beyond the scope of what
  217. we're trying to cover here. So, what I
  218. wanted to leave you with is that very
  219. frequently as an intensive district
  220. going to get input from your vascular
  221. colleagues from your neurology consult.
  222. I think some of it is just being
  223. familiar with what agents are using to
  224. prevent secondary you know, ischemic
  225. events. So, Salia, you want to walk
  226. us through some of like what you're
  227. going to see with your team care of
  228. these, you know, post stroke patients?
  229. Sure. Yeah, a good point. I think the
  230. first maybe clarification here is that
  231. sometimes I get questions about should
  232. we put these patients on anti-thrombotic
  233. And I think I wanted to clarify what
  234. that even means because anti-thrombotic
  235. agents are kind of used as like one
  236. phrase without really understanding as
  237. simple as it sounds, what it means. So
  238. when we talk about anti-therambotic
  239. agents, that is this big umbrella of
  240. anti-quagulants and anti-platelet agents.
  241. So, and as you mentioned, you know,
  242. when these people have these acute
  243. episodes of Schimich stroke, almost all
  244. of our patients, unless they have a
  245. contraindication, they end up on an
  246. anti-therambotic agent, which means
  247. they're either gonna be on anti-platelet
  248. or anti-quagulation So the question is,
  249. who gets what? And can we actually give
  250. someone both agents, meaning an
  251. anti-platelet and an anti-quagulant? So
  252. I wanted to take some time to walk us
  253. through how we decide and who gets what.
  254. I think aspirin is pretty clear-cut here.
  255. It's
  256. the backbone of stroke prevention. We
  257. use that obviously commonly for patients
  258. with atherosclerosis disease. And it's
  259. usually started early on, after you get
  260. your stability, I had CT ideas that yes.
  261. patients on aspirin and that seems to be,
  262. I think, pretty straightforward. I
  263. think when we talk about DAPT or dual
  264. anti-platelet therapy, that's a very
  265. gray area in stroke. And what we know
  266. as of now is that patients who have
  267. minor stroke or TIA patients would high
  268. risk. If they have a very significant
  269. degree of phystinosis or high
  270. atherosclerotic patients, they may
  271. qualify for DAPT. Now, the earlier you
  272. start this dual anti-platelet therapy,
  273. the better off we are. And by early,
  274. we talk about 12 to 24 hours. So
  275. in prior trials, you know, we've seen
  276. that the earlier the better. And also
  277. other piece of this equation is that you
  278. don't want to keep these two
  279. anti-platelet agents forever. So there
  280. are again, studies that saw that if you
  281. kept it for a long duration, these
  282. patients had higher rates of bleeding.
  283. So because of that, The guidelines are
  284. talking about limiting it to 21 to 90
  285. days, so.
  286. So, yeah, how do you approach the fact
  287. that there are these sort of critical
  288. non-responders? I feel like every
  289. institution has a little bit of a
  290. different approach to trying to sort
  291. that out because obviously, the
  292. critical while there is more resistance
  293. to it is a much cheaper drug than
  294. Ticagro War. And so. Yeah, I think,
  295. Kagan, these cases are complicated,
  296. and I think what I can say is that we
  297. definitely have the capability of
  298. sending for P2Y12
  299. levels, although I have to say, that's
  300. never been proven to be as validated in
  301. neuro-critical care world as opposed to
  302. the cardiology world, but it is an
  303. available test,
  304. the P2Y12, to measure the amount of
  305. platelet inhibition with clopedic role.
  306. And I know that our institution, for
  307. example, to this state, we use that
  308. and put it in context with all the other
  309. things that are happening. I think what
  310. may be honest, even more helpful than
  311. looking at those levels is that if your
  312. patient was already on aspirin and they
  313. came in with another stroke, I think
  314. maybe it's time to think about the fact
  315. that they are resistant to control and
  316. we have to think about changing that age
  317. As far as anti-quagulation, I think,
  318. as we know, putting someone on
  319. anti-quagulation after a
  320. cute, skimmick stroke is very unique in
  321. a sense that these patients usually have
  322. AFib. These are patients that are high
  323. risk of cardiambolic stroke. As we all
  324. know, putting people on
  325. anti-quagulation really depends on
  326. patients with AFib who have the chads
  327. fast that require them to be on
  328. anti-quagulation I think the bigger
  329. question is when do you put patients on
  330. anti-quaglint after their acute skimmick
  331. stroke? Are you worried about their
  332. transformation to
  333. ICH? The answer is yes, we're always
  334. worried about this transformation and
  335. that's why I think these are very good
  336. discussions to have with your stroke
  337. team, with your neurocritical care team
  338. and your pharmacist, but what's been
  339. proposed in the guidelines is that if
  340. the risk of bleed is high, you really
  341. want to delay initiation of
  342. anticoagulation for the second
  343. for more than 14 days. So the earliest
  344. you wanna start in these high risk
  345. patients for ICHs to start at date 14.
  346. But if the risk is low, the
  347. guidelines or the American Heart
  348. Association guideline, I should say,
  349. talk about initiating it between day two
  350. to 14. So that's just something that's
  351. been proposed. Now, where do you pick
  352. in that big range of day 14? It's
  353. really up to your team and your risk
  354. factors for your patient and all the
  355. things that I think should be considered
  356. and it should be a multidisciplinary
  357. discussion.
  358. The final thing that I think is
  359. important when you have an inpatient
  360. stroke admission is like a lot of what
  361. prevents a secondary stroke is like just
  362. modifiable risk factors, right? So
  363. actually getting their diabetes under
  364. control, actually controlling their
  365. hypertension, working with a dietician
  366. to establish better dietary habits,
  367. you know, smoking cessation. So key,
  368. and I think these are often kind of
  369. overlooked because behavioral change is
  370. really hard, right? It is much easier
  371. for us to provide medications than it is
  372. for us to induce behavioral changes,
  373. but those behavioral changes are
  374. actually really what's going to prevent
  375. the secondary stroke. Okay, so this is
  376. a whirlwind tour of, you know,
  377. hospitalized acute stroke care. Big
  378. sort of takeaway points from sort of a
  379. clinical management, lower blood
  380. pressure is not better. Second takeaway
  381. point, if you have a patient who has a
  382. large ischemic stroke and they are young,
  383. less than 60. Think early and talk to
  384. it. a neurosurgical capable center
  385. really early in their course about
  386. decompressive hemecranicectomy. And
  387. then we have to kind of come up with
  388. like what caused this stroke and pick
  389. the right agent. And as Salia went
  390. through, there's a lot of complicated
  391. factors and choosing and what
  392. anti-thrombotic agent to use. Be
  393. thoughtful and take a multidisciplinary
  394. approach to this.