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Episode 96: INSIGHTS - Increased Intracranial Pressure

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Description

Listen to the sixth episode of NCS' INSIGHTS series, this time on Increased Intracranial Pressure.

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.

Science that transforms patient lives. Science that seeks to solve societal problems. Science that acts with purpose. Science that is inspired by the diversity and passion of our people. Discover where science meets humanity at Biogen.

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. 00:00:20
    Hi, everyone. Welcome back to the
  2. 00:00:21
    Insights Podcast. I'm here with Salia,
  3. 00:00:23
    and we're going to do another 10 to 15
  4. 00:00:25
    minutes update about things that you can
  5. 00:00:27
    bring to the bedside for neurologic
  6. 00:00:29
    emergencies. As a reminder, all of our
  7. 00:00:31
    content comes from the on-call chapters
  8. 00:00:35
    in the Neuro Critical Care website. So
  9. 00:00:37
    we really invite you to go to
  10. 00:00:38
    neurocriticalcareorg and check out the
  11. 00:00:40
    content there under the Educational
  12. 00:00:42
    Resources. And as another reminder, we
  13. 00:00:45
    are so grateful for the sponsors of the
  14. 00:00:49
    podcast, Biogen and Cerebell. And now
  15. 00:00:50
    a word from our sponsor. Founded in
  16. 00:00:54
    1978, Biogen is a leading global
  17. 00:00:56
    biotechnology company that has pioneered
  18. 00:00:58
    multiple breakthrough innovations,
  19. 00:01:00
    including a broad portfolio of medicines
  20. 00:01:02
    to treat multiple sclerosis, the first
  21. 00:01:05
    approved treatment for spinal muscular
  22. 00:01:07
    atrophy, and two co-developed
  23. 00:01:09
    treatments to address a defining
  24. 00:01:11
    pathology of Alzheimer's disease.
  25. 00:01:14
    Biogen is advancing a pipeline of
  26. 00:01:16
    potential novel therapies across
  27. 00:01:18
    neurology, neuropsychiatry,
  28. 00:01:20
    specialized immunology, and rare
  29. 00:01:22
    diseases, and remains acutely focused
  30. 00:01:25
    on its purpose of serving humanity
  31. 00:01:27
    through science while advancing a
  32. 00:01:29
    healthier, more sustainable, and
  33. 00:01:31
    equitable world. All right, hi, Casey,
  34. 00:01:35
    it's good to be here and talk about ICP
  35. 00:01:38
    crisis. I know that would promise us to
  36. 00:01:40
    our audience, so it's really exciting
  37. 00:01:42
    to be back and talk about this really
  38. 00:01:44
    fun topic, but also really essential to
  39. 00:01:47
    neuro-cortical care, management of our
  40. 00:01:49
    patients. So to start with, I think
  41. 00:01:52
    we're gonna do two different discussions.
  42. 00:01:54
    One is gonna focus on diagnostic piece
  43. 00:01:57
    of this, how do we manage, or how do
  44. 00:02:00
    we diagnose ICP and what do we consider,
  45. 00:02:02
    and then how do we manage these patients
  46. 00:02:04
    and pharmacological management, which
  47. 00:02:06
    I'm really excited to talk about So,
  48. 00:02:10
    Casey, when do you consider ICP? in
  49. 00:02:15
    your patients? Yeah, this can be
  50. 00:02:17
    tricky. I mean, I think there are
  51. 00:02:18
    certain ones that you walk into your
  52. 00:02:20
    room and you see that a patient has a
  53. 00:02:22
    blown pupil and they're appended and
  54. 00:02:23
    you're like, No, that's no brainer.
  55. 00:02:25
    They probably have some horrible ICP
  56. 00:02:27
    crisis going on. But I think the most
  57. 00:02:29
    of our patients who have elevated
  58. 00:02:31
    interprenal pressure and they're
  59. 00:02:33
    becoming more and more similar. And,
  60. 00:02:36
    you know, the problem with that in the
  61. 00:02:38
    neuropatient population is that there
  62. 00:02:39
    can be a lot of reasons while our
  63. 00:02:41
    patients are sleepy And one of the
  64. 00:02:43
    things that I think is really important
  65. 00:02:45
    to tease out is using the neuroimaging
  66. 00:02:49
    to sort of guide does this person have
  67. 00:02:52
    risk factors for having an elevated ICP?
  68. 00:02:56
    And, you know, things that cause
  69. 00:02:58
    damage to the brainstem, things that
  70. 00:02:59
    cause damage to the xalami, things that
  71. 00:03:01
    result in bilateral cerebral hemisphere
  72. 00:03:03
    dysfunction, all of those things can
  73. 00:03:05
    make you sleepy. So what we're looking
  74. 00:03:07
    for, usually with our screaming head C2
  75. 00:03:09
    when someone comes in the door, Is this
  76. 00:03:12
    person? have evidence of a big mass
  77. 00:03:15
    lesion, something that's causing their
  78. 00:03:16
    dying shift, maybe creeping herniation,
  79. 00:03:19
    trans-torial herniation, uncle
  80. 00:03:21
    herniation, you know, herniation
  81. 00:03:23
    syndrome because of the focal lesion.
  82. 00:03:26
    And that might be because, you know,
  83. 00:03:28
    they have traumatic brain injury.
  84. 00:03:30
    They've had an intracranial hemorrhage.
  85. 00:03:32
    They have noignant ischemic cerebral
  86. 00:03:35
    edema after they've had a large middle
  87. 00:03:37
    MCA stroke. And then the problem could
  88. 00:03:40
    also be that they have global cerebral
  89. 00:03:42
    edema. And so that's, you know, a
  90. 00:03:44
    thing that we can think about in our
  91. 00:03:46
    patients that have traumatic brain
  92. 00:03:47
    injury or encephalitis or even venous
  93. 00:03:49
    sinus plombosis or anoxic injury. So
  94. 00:03:52
    there are so many neuropathologies that
  95. 00:03:55
    can result in increased intracranial
  96. 00:03:58
    pressure.
  97. 00:04:00
    The other thing that could cause
  98. 00:04:01
    increased intracranial pressure is that
  99. 00:04:03
    the patient has an accumulation of fluid
  100. 00:04:06
    in the brain such as hydrocyclists And I
  101. 00:04:09
    think of these as kind of two different
  102. 00:04:11
    baskets. that have a focal lesion, the
  103. 00:04:15
    patients who have global cerebral edema,
  104. 00:04:18
    and then the patients that have
  105. 00:04:19
    hydrocephalus, all of those things can
  106. 00:04:21
    cause elevated intracranial pressure,
  107. 00:04:23
    but they're managed a little bit
  108. 00:04:24
    differently. So I think the first thing
  109. 00:04:27
    that I'm doing when I walk in the room
  110. 00:04:29
    is trying to think about, is the
  111. 00:04:31
    patient sleepy or heading towards
  112. 00:04:34
    somulants, comatose, and then do they
  113. 00:04:37
    have radiographic evidence of something
  114. 00:04:38
    that would mechanistically make sense to
  115. 00:04:41
    cause elevated intracranial pressure.
  116. 00:04:52
    Let's say you are deattending taking
  117. 00:04:54
    care of this really sick patient with
  118. 00:04:57
    ICH and then you realize that there is a
  119. 00:05:01
    significant midline shift. Can you walk
  120. 00:05:04
    us through how again you suspect ICP
  121. 00:05:07
    crisis and how you would go about your
  122. 00:05:09
    management of this patient? Yeah, I
  123. 00:05:12
    think that's one of the most common
  124. 00:05:13
    things that we see these patients who
  125. 00:05:14
    come in, they've got a giant bleed and
  126. 00:05:17
    the bleed itself is not actually in one
  127. 00:05:19
    of the structures that would cause, you
  128. 00:05:21
    know, just alter mental status. Let's
  129. 00:05:23
    say this is like mostly just in the
  130. 00:05:24
    basal ganglia, but it's causing some
  131. 00:05:26
    midline shift, it's causing compression
  132. 00:05:28
    and trans-intorial herniation that we
  133. 00:05:30
    can see on the head CT we just got,
  134. 00:05:33
    like all other emergencies, like we're
  135. 00:05:34
    still starting with ABCs. The thing
  136. 00:05:38
    about this patient, you said they
  137. 00:05:39
    already have an midline shift, they've
  138. 00:05:41
    got a big ICH. Already I'm sort of
  139. 00:05:43
    thinking this patient is on the road to
  140. 00:05:45
    maybe an intubate shift And so walk into
  141. 00:05:48
    the room for this. patient. The first
  142. 00:05:50
    thing I assess are ways that we can
  143. 00:05:52
    optimize the patient just from like a
  144. 00:05:55
    bedside management thing. Like, sit
  145. 00:05:57
    the patient up. Then we have to think
  146. 00:05:59
    about, you know, is their neck king to
  147. 00:06:01
    one side and that's preventing venous
  148. 00:06:03
    return. So again, just getting the
  149. 00:06:05
    neck midline and sitting the patient up.
  150. 00:06:07
    That can at least help temporize while
  151. 00:06:09
    you're trying to better assess what's
  152. 00:06:11
    going on. If the patient is agitated
  153. 00:06:14
    and having or having a lot of pain,
  154. 00:06:16
    that's also causing them to be combated.
  155. 00:06:18
    That can read their blood pressure. We
  156. 00:06:20
    know that blood pressure and interest
  157. 00:06:22
    removal pressure have a injured patient,
  158. 00:06:25
    so sort of linear relationship. And so
  159. 00:06:28
    that's another thing that we can just
  160. 00:06:29
    kind of address trying to calm patients
  161. 00:06:31
    down, make sure they're not in pain,
  162. 00:06:32
    not agitated. All of those are just
  163. 00:06:35
    good things that we can do easily at the
  164. 00:06:37
    bedside before even having to initiate
  165. 00:06:39
    sort of higher tiers of increased
  166. 00:06:42
    intracranial pressure management
  167. 00:06:45
    So that's really what I'm thinking as I
  168. 00:06:47
    walk in the rooms, like how can we
  169. 00:06:49
    optimize this patient? while we're
  170. 00:06:50
    probably setting up to get the patient
  171. 00:06:53
    into baby. Innovation in patients with
  172. 00:06:54
    interpreneal pressure issues really is a
  173. 00:06:57
    unique situation where you have to be
  174. 00:07:00
    very mindful of the patient's blood
  175. 00:07:02
    pressure, right? We know that they,
  176. 00:07:06
    you know, you could worsen in their
  177. 00:07:07
    bleed if their pressure is too high,
  178. 00:07:10
    but you could also cause
  179. 00:07:11
    perihematolendema and you could also
  180. 00:07:13
    cause, you know, even low cerebral
  181. 00:07:16
    perfusion pressure if you let their
  182. 00:07:18
    blood pressure get too low So I try to
  183. 00:07:20
    be like really hemodynamically neutral
  184. 00:07:22
    in that situation. So that brings us to
  185. 00:07:25
    kind of what I'm doing beyond that,
  186. 00:07:29
    which is pharmacology management of
  187. 00:07:30
    their integration to cranial pressure.
  188. 00:07:40
    Celia, walk us through like salty or
  189. 00:07:43
    sweet or hyperhytic saline, manatol,
  190. 00:07:46
    which I'm not giving and in what
  191. 00:07:48
    situations and what should I be looking
  192. 00:07:50
    for as I give those drugs? Yeah,
  193. 00:07:53
    excellent question, I get this every
  194. 00:07:56
    single time, sweet or salty. So the
  195. 00:07:59
    truth is, whatever you have available
  196. 00:08:02
    and is fastest for you and your
  197. 00:08:04
    institution, I think that's the answer,
  198. 00:08:07
    but I think it can walk us through,
  199. 00:08:09
    okay, what to consider, what is
  200. 00:08:11
    usually actually faster, what is
  201. 00:08:12
    usually more available. So, you know,
  202. 00:08:15
    when we talk about, see, we talk about
  203. 00:08:17
    manatol, which is an hyperosmal agent
  204. 00:08:19
    and we talk about salty, we're talking
  205. 00:08:21
    about hypersonic saline, it goes from 3
  206. 00:08:24
    to 234. Let's talk about maybe manatol
  207. 00:08:29
    first and then we talk about hypersonic
  208. 00:08:30
    saline.
  209. 00:08:39
    So, one of the things that is nice
  210. 00:08:40
    about Manateal is that it can be given
  211. 00:08:43
    peripheral. So, again, if your
  212. 00:08:45
    patient does not have a central line and
  213. 00:08:48
    you don't want to waste time giving or
  214. 00:08:50
    putting in a central line, then that is
  215. 00:08:52
    awesome. Manateal dosing is usually 05
  216. 00:08:56
    to 2 grams per kilogram. I can tell you
  217. 00:08:58
    that because it's such an acute
  218. 00:09:01
    situation when they ask me, I usually
  219. 00:09:03
    talk about 50 to 100 grams to make it
  220. 00:09:05
    kind of easy Some institutions have the
  221. 00:09:08
    vials, some institutions have the
  222. 00:09:10
    infusion bags, again, it doesn't
  223. 00:09:12
    matter what concentration you have, the
  224. 00:09:14
    20 infusion bags or the 25 vials. The
  225. 00:09:17
    idea is that you get 50 to 100 grams,
  226. 00:09:20
    that's usually sufficient for most
  227. 00:09:22
    patients. And then although you do not
  228. 00:09:25
    need a central line, you always need a
  229. 00:09:28
    filter. Sometimes I get questions about
  230. 00:09:31
    this is an emergency, can I give it
  231. 00:09:32
    without a filter? Absolutely not you
  232. 00:09:35
    need a filter because of personalization,
  233. 00:09:37
    sometimes you don't see these crystals
  234. 00:09:39
    and you don't want to obviously infuse
  235. 00:09:40
    crystals. Now, what do we monitor for?
  236. 00:09:44
    Remember that manatol actually can cause
  237. 00:09:47
    hypertension. It can make people die a
  238. 00:09:50
    race.
  239. 00:09:52
    It's something that, again, like we
  240. 00:09:54
    know about emergencies and all that,
  241. 00:09:55
    but we try not to use manatol and
  242. 00:09:58
    patients with renal failure just because
  243. 00:09:59
    of the risk of accumulation and the fact
  244. 00:10:01
    that it can cause rebound ICP issues if
  245. 00:10:04
    it accumulates in the body You want to
  246. 00:10:06
    repeat abuses, the one gram per
  247. 00:10:09
    kilogram. You could repeat that based
  248. 00:10:11
    on your ICP. If you wanted to kind of
  249. 00:10:15
    get a sense of how much more you could
  250. 00:10:16
    repeat manatol, you can always look at
  251. 00:10:19
    your osmolar gap. Osmolar gap of 20 is
  252. 00:10:22
    the threshold. So if your osmolar gap
  253. 00:10:23
    is less than 20, that means that you
  254. 00:10:25
    have room to give more manatol. So
  255. 00:10:27
    that's, you know, all about manatol,
  256. 00:10:29
    which I think, a lot of institutions
  257. 00:10:31
    are comfortable with giving it. It is,
  258. 00:10:33
    you know, pretty available.
  259. 00:10:35
    for a line and all that.
  260. 00:10:44
    I think hypertonic saline is unique in
  261. 00:10:48
    the sense that not only it helps, you
  262. 00:10:50
    know, with the ICP crisis, but if your
  263. 00:10:52
    patient requires sodium augmentation,
  264. 00:10:54
    that's a beauty of this agent. Again,
  265. 00:10:58
    the 23 point for a person, I think, is
  266. 00:11:01
    the agent of choice if you are dealing
  267. 00:11:03
    with acute emergencies. Again, if
  268. 00:11:05
    you're bumping to sodium or if you don't
  269. 00:11:06
    have that concentration, you can
  270. 00:11:08
    definitely give the 3, which talk about
  271. 00:11:10
    giving 500 mLs of the 3 over 30 minutes
  272. 00:11:14
    as a bolus until you have more access.
  273. 00:11:17
    The 3, remember, can be actually given
  274. 00:11:20
    peripherally. Now, if you have enough
  275. 00:11:22
    studies to say that the 3 is actually
  276. 00:11:26
    safe, peripheral administration is safe.
  277. 00:11:29
    But then the 23 point for a percent,
  278. 00:11:32
    although there are some reports talking
  279. 00:11:36
    about its administration peripherally.
  280. 00:11:38
    I have to say that we have not changed
  281. 00:11:40
    our practice yet. We're still very much
  282. 00:11:42
    so talking about giving it centrally
  283. 00:11:44
    only because of the risk of extra
  284. 00:11:46
    conversations. It's very, very
  285. 00:11:47
    hyperosmolar. Now if you don't have a
  286. 00:11:50
    central line, you can actually,
  287. 00:11:52
    traditional central line, you can give
  288. 00:11:54
    it as IO. As far as the do sync with
  289. 00:11:56
    the, we talked about how with the three
  290. 00:11:58
    person, we talked about 500 moboluses,
  291. 00:12:00
    which can get your sodium up. But if
  292. 00:12:02
    you wanted to use a 234, it's the 30 ml,
  293. 00:12:05
    which is the usual do sync Again, I
  294. 00:12:09
    think back in today, we used to give it
  295. 00:12:11
    a longer administration time of 15 to 20
  296. 00:12:14
    minutes. Now, we know that it can be
  297. 00:12:16
    given faster, so now we're doing it as
  298. 00:12:18
    an IV push. The risks are that you have
  299. 00:12:22
    to have the appropriate line and also
  300. 00:12:25
    hypotension can happen. So again,
  301. 00:12:28
    making sure that you are hemodynamically
  302. 00:12:29
    monitoring your patient, making sure
  303. 00:12:29
    that
  304. 00:12:32
    you are supporting the blood pressure
  305. 00:12:34
    with vasoactive agents, if you have to,
  306. 00:12:37
    obviously sodium check should be done
  307. 00:12:40
    after that. And we talk about every
  308. 00:12:44
    four to six hours of checking sodium to
  309. 00:12:46
    make sure that we're not losing track of
  310. 00:12:48
    how much we're giving and we're not
  311. 00:12:50
    getting, we're not ending up with super,
  312. 00:12:52
    super high sodium numbers. That's such
  313. 00:12:55
    an awesome advice. I think one of the
  314. 00:12:57
    things that I've like a pearl that I've
  315. 00:12:58
    learned since, almost everyone, I
  316. 00:13:01
    think actually everyone has code card by
  317. 00:13:03
    card. And so if you are practicing in a
  318. 00:13:06
    place where you can't actually get
  319. 00:13:08
    mannehthal or 3, a little good pearl is
  320. 00:13:12
    that the code card by card actually has
  321. 00:13:14
    about 50 milli equivalents of sodium.
  322. 00:13:17
    So pushing two of those is roughly equal
  323. 00:13:20
    to about 200 cc of that 3 saline. So
  324. 00:13:24
    nice little pearl if you're practicing
  325. 00:13:26
    somewhere where you don't have access to
  326. 00:13:28
    some of these other traditional
  327. 00:13:30
    high-brow small regions.
  328. 00:13:39
    And so, we've given this treatment,
  329. 00:13:42
    you know, whether you're giving the
  330. 00:13:46
    hypertonic saline or manotol, get one
  331. 00:13:48
    of them in, just as Sally will say,
  332. 00:13:49
    like, Which infrared one is faster that
  333. 00:13:51
    you can get? Give that. The thing,
  334. 00:13:53
    then, that you have to kind of decide,
  335. 00:13:55
    I think, in sort of this trajectory of
  336. 00:13:57
    your sick patient, is this a patient
  337. 00:13:59
    who's going to benefit from invasive
  338. 00:14:01
    neuromonetary, or do we have to
  339. 00:14:03
    estimate what their ICPA is based on
  340. 00:14:05
    sort of non-invasive monitors? So
  341. 00:14:08
    really, the guidance for who gets
  342. 00:14:09
    invasive neuromonetary is all based on
  343. 00:14:12
    the TBI guidelines. You know, the
  344. 00:14:14
    recommendation is for a traumatic brain
  345. 00:14:15
    injury if a patient is in a coma, so a
  346. 00:14:18
    GCS of three to eight, and have an
  347. 00:14:21
    abnormal scan, or if they're in a coma
  348. 00:14:24
    with a normal scan but have some
  349. 00:14:26
    concerning features like motor posturing
  350. 00:14:28
    or their hypotensive or their shoulder
  351. 00:14:32
    than 40, then it's appropriate to use
  352. 00:14:34
    invasive monitoring and that situation.
  353. 00:14:38
    may get an EVD because they have a
  354. 00:14:40
    concurrent hydrocephalus issue. So a
  355. 00:14:43
    lot of our ICHs will also have IVH, and
  356. 00:14:46
    they get an EVD placed for drainage of
  357. 00:14:49
    that IVH. Same thing with our subarach
  358. 00:14:52
    patients. Frequently they will have
  359. 00:14:54
    EVDs. And those are really nice 'cause
  360. 00:14:55
    they actually give us a number, right?
  361. 00:14:57
    We can go by that. For other patients
  362. 00:15:00
    in the unit, especially those with the
  363. 00:15:02
    global problems that are not trauma
  364. 00:15:04
    patients, we're really using
  365. 00:15:05
    non-invasive monitors, and that can
  366. 00:15:07
    include just the non-compensities that
  367. 00:15:10
    we're getting, and that can include
  368. 00:15:12
    peopleometry, optic nerve sheath
  369. 00:15:14
    diameter, and even the pulsatility
  370. 00:15:16
    index from our transcranial couplers.
  371. 00:15:18
    So there are a lot of ways that we can
  372. 00:15:20
    estimate if a patient's ICP is up or not,
  373. 00:15:23
    and you either still have concern for
  374. 00:15:25
    increased ICP, or you actually have a
  375. 00:15:27
    number that's showing you that you do
  376. 00:15:29
    have increased ICP, then we have to get
  377. 00:15:32
    into higher tiers of ICP management.
  378. 00:15:43
    That could include mildly hypovinolating
  379. 00:15:46
    the patient. Again, we don't want to
  380. 00:15:48
    get sort of below a PACO2
  381. 00:15:52
    of 32, but sort of in that mild range,
  382. 00:15:55
    that's okay. I tend to think about real
  383. 00:15:58
    hyperventilation only for the patients
  384. 00:16:00
    who are like on their way to the OR as a
  385. 00:16:04
    temporizing measure.
  386. 00:16:04
    Neuromostoaparalysis also has the
  387. 00:16:06
    ability to be efficacious and lowering
  388. 00:16:08
    ICP. I usually try that first, I
  389. 00:16:11
    actually give a bolus and see like did
  390. 00:16:12
    that help the patient and only commit
  391. 00:16:14
    patients if it actually was helping them.
  392. 00:16:17
    And then we have to really assess where
  393. 00:16:18
    patients are on sort of their cerebral
  394. 00:16:20
    auto-regulation curve. And that's a
  395. 00:16:22
    little bit tricky, so we're not gonna
  396. 00:16:24
    get too deep in the weeds on that.
  397. 00:16:26
    Beyond those interventions, then we're
  398. 00:16:28
    really looking at a little bit of
  399. 00:16:30
    cooling, so mild type of fermia, 35 to
  400. 00:16:32
    36 degrees, and then surgical
  401. 00:16:35
    interventions. You know, if a
  402. 00:16:37
    patient's not a surgical candidate for a
  403. 00:16:40
    decompressive kidney craniectomy, then
  404. 00:16:43
    really I think coming in the sort of
  405. 00:16:45
    last blind medical treatment we have is
  406. 00:16:47
    a barbiturate coma. And so Salia, walk
  407. 00:16:50
    us through, if you actually do get
  408. 00:16:51
    there, what are some of the things that
  409. 00:16:53
    you have to keep in mind? This is kind
  410. 00:16:55
    of a high risk medication. So what
  411. 00:16:57
    should we know? Yeah, exactly. As you
  412. 00:17:01
    mentioned, QC this is, really, I
  413. 00:17:02
    think, the last resort. I think this
  414. 00:17:04
    is when you get here, you've really
  415. 00:17:05
    done everything else. You've exhausted
  416. 00:17:07
    all the other options. Really, the way
  417. 00:17:10
    this works out, at least from my
  418. 00:17:11
    experience, is that we have people on
  419. 00:17:13
    purple fall initially, but then, as
  420. 00:17:15
    you know, there's a lot of issues with
  421. 00:17:17
    purple fall when you give it at such a
  422. 00:17:19
    high dose for ICP crisis, that we know
  423. 00:17:21
    that it's not sustainable because of the
  424. 00:17:23
    purple fall related infusion syndrome
  425. 00:17:25
    complications and risk of cardiac
  426. 00:17:29
    arrhythmia is really, which is really
  427. 00:17:30
    ultimately gets people into trouble with
  428. 00:17:32
    the purple fall related infusion
  429. 00:17:33
    syndrome. So when we talk about
  430. 00:17:36
    pentabar, number one is that there
  431. 00:17:38
    should be a discussion with the family
  432. 00:17:40
    because this is This is an agent that is
  433. 00:17:43
    going to mask your neuro exam very much
  434. 00:17:46
    significantly for days One piece of
  435. 00:17:49
    clarification is that your pupil exam
  436. 00:17:52
    will still be Unchained so that's really
  437. 00:17:54
    the only exam that you have in that
  438. 00:17:56
    setting Everything else will probably be
  439. 00:17:59
    gone And the idea is that if you ever
  440. 00:18:03
    wanted to reconsider or have a family
  441. 00:18:04
    meeting You have to do that before
  442. 00:18:06
    putting someone on punch of our because
  443. 00:18:07
    again because of the half-life the drug
  444. 00:18:09
    will be in the system for days So you
  445. 00:18:12
    always want to have that discussion of
  446. 00:18:13
    the family before you put them on the
  447. 00:18:15
    pent of our coma
  448. 00:18:25
    Now, just like what we talked about
  449. 00:18:26
    with hemodynamics, this one is huge,
  450. 00:18:28
    right? This is a huge negative inotrove
  451. 00:18:32
    and can cause significant hypotension,
  452. 00:18:34
    bradycardia. Almost all these patients
  453. 00:18:37
    end up on vasoactive agents. I usually,
  454. 00:18:39
    when I see people reaching for pentobarb
  455. 00:18:41
    and wanting to start that, I get the
  456. 00:18:44
    norepine fusion from our pixis machine
  457. 00:18:45
    before even they start
  458. 00:18:51
    a pentobarb because I know that it's
  459. 00:18:51
    going to be needed, especially with the
  460. 00:18:52
    boluses that we give You basically have
  461. 00:18:53
    to also think about how to monitor your
  462. 00:18:56
    management, sending pentobarb levels.
  463. 00:18:58
    Really has not been shown to be very
  464. 00:19:00
    effective. We look at clinical signs,
  465. 00:19:02
    we look at ICP crisis, and then also
  466. 00:19:06
    EEG. A lot of these patients are hooked
  467. 00:19:07
    to EEG, so birth suppression is
  468. 00:19:09
    typically what we think about when we
  469. 00:19:11
    have people on pentobarb for treating
  470. 00:19:14
    these complications. There's all the
  471. 00:19:17
    other side effects, you know, we
  472. 00:19:18
    commonly talk about with all the barbit
  473. 00:19:19
    rates, people, and usually with Elias,
  474. 00:19:21
    which is really complicated. And, you
  475. 00:19:23
    know, I've had people with
  476. 00:19:27
    ballastchemia, it's a common side
  477. 00:19:28
    effect, unfortunately. It happens a
  478. 00:19:29
    lot, but it's a price that sometimes we
  479. 00:19:32
    feel like we have to pay if we can get
  480. 00:19:34
    people over this hump. And then the
  481. 00:19:35
    other piece is that, when do you send
  482. 00:19:38
    for levels, right? I think when you
  483. 00:19:39
    are done with your pentobarb coma, and
  484. 00:19:42
    you're still not getting an exam from
  485. 00:19:45
    your patient, I think that's when you
  486. 00:19:46
    think about, okay, let's send
  487. 00:19:47
    pentobarb levels to see if this is,
  488. 00:19:50
    this is because of the brain damage, or
  489. 00:19:53
    this is because of pentobarb kind of,
  490. 00:19:55
    still kind of lingering in the system.
  491. 00:19:58
    Obviously, drug interactions, remember
  492. 00:19:59
    that barbecues are all a sip-and-ducer,
  493. 00:20:01
    so if you suspect significant
  494. 00:20:03
    interactions, something to keep in mind.
  495. 00:20:06
    So, those are some of the pearls, I
  496. 00:20:08
    would say, with pentobarb, again, a
  497. 00:20:09
    lot of discussions to have with the
  498. 00:20:11
    family, with the team, making sure
  499. 00:20:13
    they know about the side effects,
  500. 00:20:15
    making sure that they're protected human
  501. 00:20:16
    dynamically, they're intubated, You
  502. 00:20:19
    know, we talk about eye care for these
  503. 00:20:20
    people also to make sure that, you know,
  504. 00:20:22
    their eyes are moist and because they're
  505. 00:20:23
    going to be close and just making sure
  506. 00:20:26
    they're comfortable and then, again,
  507. 00:20:28
    not sending levels while they're on it,
  508. 00:20:30
    but rather looking at the EEG for birth
  509. 00:20:31
    suppression
  510. 00:20:41
    So, I think that's pretty much our
  511. 00:20:42
    algorithm, you know, starting from
  512. 00:20:44
    just walking in the door making sure
  513. 00:20:45
    their positioning is optimized, that
  514. 00:20:47
    they're not hyper-ventilated, and then
  515. 00:20:50
    looking to this sort of, you know, the
  516. 00:20:52
    foundation of this management, which is
  517. 00:20:53
    our hyper-asmolar, and then graduating
  518. 00:20:56
    into some of these more extremes, like,
  519. 00:20:59
    paralyzing, dating, cooling, and then
  520. 00:21:01
    this pentabarb coma. I think with that,
  521. 00:21:03
    we can wrap it up, Salia, any last
  522. 00:21:05
    girls to leave people with? I think the
  523. 00:21:07
    most important thing is that, what do
  524. 00:21:09
    you have available in your institution
  525. 00:21:11
    to use that first, as far as
  526. 00:21:12
    hyper-asmolar agents, you know,
  527. 00:21:14
    hyper-tonic saline versus manatol, as
  528. 00:21:16
    far as which ones were effective? We
  529. 00:21:18
    don't really know. I mean, right now,
  530. 00:21:20
    there is no evidence to say one is
  531. 00:21:22
    better than the other, I think. Just
  532. 00:21:24
    having access and knowing to do-saying
  533. 00:21:26
    and knowing to side effects. And then
  534. 00:21:27
    if you need to escalate to pentabarb,
  535. 00:21:29
    just knowing to side effects and how to
  536. 00:21:32
    monitor and how to titrate, those are
  537. 00:21:34
    some of the pearls that I hope that this
  538. 00:21:36
    talk gave you and helped with your
  539. 00:21:39
    future management. All right, until
  540. 00:21:41
    next time guys, thanks so much. Bye.
  541. 00:21:44
    Thank you. Bye guys.