Skip to main content
  1. Courses
  2. NCS Podcast Series
  3. Episode 104: INSIGHTS - Sub...

Episode 104: INSIGHTS - Subarachnoid Hemorrhage Pt2.

Loading audio, please wait...

Description

Listen to the latest episode of NCS INSIGHTS series, this time on Subarachnoid Hemorrhage (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 ceribell.

Time is brain when it comes to seizures. Ceribell Point of Care EEG empowers the bedside team to detect or rule out seizure activity in minutes. To learn more, visit ceribell.com.

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. 00:00:19
    All right, everyone, welcome back.
  2. 00:00:20
    Again, this is another episode of the
  3. 00:00:22
    Insights podcast. As a reminder,
  4. 00:00:25
    Insights, the content we talk about
  5. 00:00:26
    here is based on the content from the
  6. 00:00:29
    on-call chapters published by the
  7. 00:00:31
    Neurocritical Care Society. This is a
  8. 00:00:33
    continually updated online guidebook
  9. 00:00:36
    that really provides just a rich wealth
  10. 00:00:40
    of content created by experts. And
  11. 00:00:43
    Sally and I are so excited to get to
  12. 00:00:45
    distill some of that content, but we
  13. 00:00:46
    really invite you to go and check out
  14. 00:00:48
    the chapters as well. We are so
  15. 00:00:50
    grateful to our sponsors Biogen and
  16. 00:00:52
    Sarah Bell, and now a word from one of
  17. 00:00:54
    our sponsors. Time is brain when it
  18. 00:00:56
    comes to seizures. Sarah Bell Point of
  19. 00:00:59
    Care EEG empowers the bedside team to
  20. 00:01:02
    detect or rule out seizure activity in
  21. 00:01:04
    minutes. To learn more, visit
  22. 00:01:06
    sarahbellcom Alright, so in the
  23. 00:01:10
    last episode, we sort of went through,
  24. 00:01:11
    you know, what are your, how do you
  25. 00:01:13
    approach a patient that you suspect
  26. 00:01:15
    might have some arachnoid hemorrhage.
  27. 00:01:17
    What is your sort of diagnostic
  28. 00:01:19
    algorithm? What are the things that
  29. 00:01:21
    you're worried about in that acute
  30. 00:01:22
    management for a patient who does have a
  31. 00:01:25
    very highly suspicious and urismo
  32. 00:01:27
    pattern in sub-ragnoid hemorrhage? This
  33. 00:01:29
    time, we're gonna spend a little bit
  34. 00:01:31
    more going through some of the medical
  35. 00:01:33
    management, not so much the surgical of
  36. 00:01:35
    clipping versus coiling, but the
  37. 00:01:37
    medical management of these patients
  38. 00:01:39
    once they get to a neuro ICU. These are,
  39. 00:01:42
    I think, some of the most challenging
  40. 00:01:45
    and engaging and just really rewarding
  41. 00:01:47
    patients to care for, just to kind of
  42. 00:01:49
    like think about this in sort of a broad
  43. 00:01:51
    perspective. You have sort of part one
  44. 00:01:53
    of an aneurysmal subarachnoid lifespan,
  45. 00:01:55
    which is just stabilization, preventing
  46. 00:01:59
    re rupture, treating herniation, I
  47. 00:02:02
    mean, preventing herniation and then
  48. 00:02:03
    treating
  49. 00:02:06
    hydrocephalus. Part two sort of starts
  50. 00:02:09
    once that aneurysm is secured, the
  51. 00:02:11
    hydrocephalus, if it's present, has
  52. 00:02:13
    been addressed And now we're really
  53. 00:02:15
    entering a phase that's going to last.
  54. 00:02:18
    you know, for that initial period all
  55. 00:02:20
    the way through 21 days where you think
  56. 00:02:23
    about trying to diagnose, screen,
  57. 00:02:26
    prevent delayed cerebral ischemia. So
  58. 00:02:30
    to be clear, vasospasm and delayed
  59. 00:02:34
    cerebral ischemia are not quite the same
  60. 00:02:36
    thing. We often talk about vasospasm
  61. 00:02:40
    and preventing vasospasm and treating
  62. 00:02:42
    vasospasm, but it's really important to
  63. 00:02:44
    know that vasospasm is one sort of
  64. 00:02:47
    biomarker of who's at risk for delayed
  65. 00:02:49
    cerebral ischemia. We know that this is
  66. 00:02:52
    a very complicated, complex phenomenon
  67. 00:02:55
    that involves cellular, misignally,
  68. 00:02:59
    cytokine release and sort of a much more
  69. 00:03:01
    complicated thing than just the blood
  70. 00:03:03
    vessels narrowing.
  71. 00:03:06
    However, it really is important that we
  72. 00:03:08
    screen and we look for vasospasm. And
  73. 00:03:11
    so one of the things that I really like
  74. 00:03:13
    about the new guidelines in the on-call
  75. 00:03:14
    chapter is that you get a sense for just
  76. 00:03:17
    how accurate of these screening
  77. 00:03:19
    techniques are. I think at many, many
  78. 00:03:22
    centers, transcranial dopplers are sort
  79. 00:03:25
    of the bread and butter of screening.
  80. 00:03:27
    The pulled estimates for TCDs to
  81. 00:03:29
    diagnose vasospasm have a pretty good
  82. 00:03:32
    sensitivity of almost 90. They're not
  83. 00:03:35
    quite as specific. So they're good at
  84. 00:03:37
    finding vasospasm. But again,
  85. 00:03:39
    vasospasm is just one biomarker of who's
  86. 00:03:43
    at risk for delayed cerebral ischemia.
  87. 00:03:47
    You know, this is helpful, and I think
  88. 00:03:49
    we use it because it's very sensitive.
  89. 00:03:53
    CTAs certainly have a higher sensitivity
  90. 00:03:56
    for detection of vasospasm when symptoms
  91. 00:03:58
    develop. And I think we're getting more
  92. 00:04:00
    and more data about using CT perfusion
  93. 00:04:03
    to kind of understand who is actually
  94. 00:04:05
    having dysregulated perfusion to parts
  95. 00:04:09
    of the brain that might be at risk of
  96. 00:04:11
    delayed cerebral ischemia. The final
  97. 00:04:14
    thing that we're using quite free or
  98. 00:04:16
    some centers use quite And I think there
  99. 00:04:18
    is evolving evidence for is using EEG.
  100. 00:04:22
    We know that patients who have a late
  101. 00:04:24
    onset epileptiform abnormalities
  102. 00:04:27
    probably have some perfusion abnormality
  103. 00:04:29
    going on to cause those late onset
  104. 00:04:32
    epileptiform abnormalities. And it
  105. 00:04:34
    seems like for those patients, there
  106. 00:04:36
    does seem to be a higher correlation of
  107. 00:04:39
    who goes on to develop delayed cerebral
  108. 00:04:41
    ischemia
  109. 00:04:51
    Now, we know that when patients develop
  110. 00:04:53
    symptoms, they benefit from often
  111. 00:04:55
    catheter-based therapy and angioplasty.
  112. 00:04:58
    But we as neurointensivists were really
  113. 00:05:01
    interested in trying to react before
  114. 00:05:05
    patients develop symptoms of DCI. So,
  115. 00:05:09
    yeah, I know kind of within our center,
  116. 00:05:10
    we're using more and more of
  117. 00:05:14
    IV no-renew Talk us through some of
  118. 00:05:18
    the like things that we should watch out
  119. 00:05:20
    for for those patients who get put on
  120. 00:05:22
    no-renew. Yeah, for sure. I think as
  121. 00:05:26
    you mentioned, Casey, we do have some
  122. 00:05:28
    patients that are refractory and
  123. 00:05:31
    bifractory, you know, we mean that
  124. 00:05:33
    even despite being on oral nemotopean,
  125. 00:05:36
    which is, you know, gold standard and
  126. 00:05:38
    our usual care in these cases, they
  127. 00:05:41
    still have. evidence of DCI, there is
  128. 00:05:44
    some evidence on TCD or CTA or CTP or as
  129. 00:05:49
    you said EEG. So these are the patients
  130. 00:05:51
    that are very complicated and these are
  131. 00:05:53
    the patients that we're looking for
  132. 00:05:55
    different strategies pharmacologically
  133. 00:05:58
    or non-pharmacologically to help them.
  134. 00:06:01
    So IV known as we all kind of know in
  135. 00:06:03
    critical care is an INO trope and the
  136. 00:06:05
    idea behind it is that by giving this
  137. 00:06:08
    agent you are going to improve and
  138. 00:06:11
    increase your cardiac output and the
  139. 00:06:13
    hope and the goal is that by improving
  140. 00:06:15
    your cardiac output, you're going to
  141. 00:06:17
    increase perfusion to the brain or
  142. 00:06:20
    cerebral perfusion. Now a couple of
  143. 00:06:22
    things when it comes to IV known just
  144. 00:06:24
    because I feel like we don't use as much
  145. 00:06:26
    as other, you know, agents, first
  146. 00:06:31
    thing is that it will have or it will
  147. 00:06:34
    cause a lot of hypotension. So it comes
  148. 00:06:36
    with that big price and we find
  149. 00:06:39
    ourselves usually at least in our
  150. 00:06:40
    institution that So we have
  151. 00:06:44
    IV, norepinephrine, and IV,
  152. 00:06:45
    noremonone kind of running at the same
  153. 00:06:46
    time. And then the other piece that is
  154. 00:06:49
    really important for people to note is
  155. 00:06:51
    that noremonone is rinnily cleared. So
  156. 00:06:55
    it will stick around if your patient has
  157. 00:06:57
    renal failure. You have to adjust it
  158. 00:06:59
    for a renal impairment. So it's not as
  159. 00:07:02
    clean as a lot of other invasive active
  160. 00:07:04
    agents, such as norepinephrine or
  161. 00:07:06
    phenylephrine or other agents.
  162. 00:07:10
    Absolutely I really do like this a lot.
  163. 00:07:12
    I think it - I've seen it be very
  164. 00:07:13
    helpful in preventing patients from
  165. 00:07:15
    needing catheter base therapy. Another
  166. 00:07:18
    one of my institution's favorite drugs
  167. 00:07:21
    of choice is intrathecal nichardibine.
  168. 00:07:24
    So walk us through a little bit about
  169. 00:07:26
    kind of what some of the studies show on
  170. 00:07:27
    that and maybe kind of the evidence that
  171. 00:07:30
    we have so far. We've done this from
  172. 00:07:33
    time to time. I think there is a role
  173. 00:07:36
    And I think, you know, where distance
  174. 00:07:38
    coming from is that. when we do calcium
  175. 00:07:41
    channel blockers, you know, like
  176. 00:07:43
    nemotopy, which is again, really the
  177. 00:07:44
    only agent that has been shown to have
  178. 00:07:46
    the most benefit when it comes to
  179. 00:07:49
    neurological improvement, you know,
  180. 00:07:51
    from early studies that's been done. I
  181. 00:07:55
    think the idea and the problem is that a
  182. 00:07:56
    lot of other calcium channel blockers
  183. 00:07:59
    like IV formulations will drop the blood
  184. 00:08:01
    pressure so much. There's always this
  185. 00:08:03
    concern that even in nemotopy, if you
  186. 00:08:06
    have a concern, right, that it's gonna
  187. 00:08:07
    drop your map is gonna come to that
  188. 00:08:09
    price and sometimes you have to choose
  189. 00:08:11
    between your augmentation of map and
  190. 00:08:13
    your, you know, nemotopy and we don't
  191. 00:08:15
    wanna get into that debate 'cause I know
  192. 00:08:16
    everyone does it differently. But I
  193. 00:08:20
    think the idea behind neikardipine
  194. 00:08:22
    intrathecal or intraventricular, which
  195. 00:08:24
    is some institutions do, is that you
  196. 00:08:28
    get the local benefit of a calcium
  197. 00:08:32
    channel blocker without the systemic
  198. 00:08:35
    side effect of it It's a lower dose. it
  199. 00:08:39
    is very targeted, it is easy to give.
  200. 00:08:43
    Again, like we typically do the
  201. 00:08:44
    intraventricular, which is you have the
  202. 00:08:46
    EVD, you put it in, you kind of let it
  203. 00:08:49
    sit there and then you basically drain
  204. 00:08:52
    after an hour or so. Now, the evidence
  205. 00:08:58
    behind this, there is to my knowledge,
  206. 00:09:00
    there is no randomized control trial.
  207. 00:09:02
    All that we know is observational
  208. 00:09:06
    studies And based on the observational
  209. 00:09:08
    studies, some of which are actually
  210. 00:09:10
    published in neurocritical care, there
  211. 00:09:12
    is some evidence that this could
  212. 00:09:14
    possibly be useful in this population.
  213. 00:09:16
    Absolutely. And I think again, the
  214. 00:09:18
    guidelines really emphasize that we
  215. 00:09:20
    really don't have enough data to include
  216. 00:09:22
    these. And it is sort of center
  217. 00:09:24
    specific and what centers are
  218. 00:09:25
    comfortable doing, what they've become
  219. 00:09:27
    accustomed to, how they use it in their
  220. 00:09:29
    protocols that are in place. One of the
  221. 00:09:31
    final thing that sort of has been
  222. 00:09:33
    interesting recently is the effect of
  223. 00:09:35
    lumbar drainage of the blood that's sort
  224. 00:09:37
    of sitting in the basal cistern. This
  225. 00:09:39
    in the guidelines, just said, there
  226. 00:09:42
    may be a role for lumbar drainage to
  227. 00:09:45
    prevent DCI. Right after the guidelines
  228. 00:09:48
    were published, early drain was just
  229. 00:09:50
    published recently. That maybe does
  230. 00:09:52
    show that there is a benefit of draining
  231. 00:09:54
    from below and trying to use the
  232. 00:09:56
    gravitational pull to get some of that
  233. 00:10:00
    cytotoxic blood out. But I think again,
  234. 00:10:03
    we need more experience, we're gonna
  235. 00:10:05
    need more evidence before that really
  236. 00:10:07
    makes it into the guidelines So, you
  237. 00:10:10
    know, these patients are in depth on a
  238. 00:10:11
    lot of drugs and emotipine being sort of
  239. 00:10:13
    the real evidence-based way to prevent
  240. 00:10:16
    or to improve functional outcomes.
  241. 00:10:20
    Magnesium, statin, salia, what's the
  242. 00:10:23
    final word on this? I think, you know,
  243. 00:10:25
    this could be a hot debate and we could
  244. 00:10:27
    talk about it for days, but the short
  245. 00:10:29
    answer is that not routinely recommended.
  246. 00:10:32
    And I think that's probably honestly the
  247. 00:10:33
    best answer. I mean, could you give
  248. 00:10:35
    magnesium for pain? Sure, could you
  249. 00:10:37
    keep someone's you know statin that are
  250. 00:10:39
    already taking from home. Yes, but I
  251. 00:10:40
    don't know that adding it with the
  252. 00:10:42
    intention that it's going to improve DCI
  253. 00:10:45
    is something that we know is, you know,
  254. 00:10:48
    going to be helpful, at least as of now
  255. 00:10:51
    with the evidence that we have.
  256. 00:11:01
    The other thing that the guidelines
  257. 00:11:03
    really shifted on and is that we're
  258. 00:11:05
    pulling back on who needs a continued
  259. 00:11:08
    anti-seizure medication. So what are we
  260. 00:11:11
    supposed to do about the patient who's
  261. 00:11:13
    not seizing in the ICU? You know, this
  262. 00:11:15
    is a person who's, we've never seen
  263. 00:11:17
    these, but someone said, like, oh,
  264. 00:11:20
    they have a seizure and onset. What are
  265. 00:11:23
    the guidelines saying about that and
  266. 00:11:24
    sort of anti-seizure recommendations in
  267. 00:11:26
    general, anti-seizure medication
  268. 00:11:28
    recommendations? Yeah, I think
  269. 00:11:32
    something that, you know, you and I
  270. 00:11:34
    kind of talked about a little bit of
  271. 00:11:35
    offline is that if you think that they
  272. 00:11:40
    seize, but there is, you know, no
  273. 00:11:41
    objective evidence that they seize, it
  274. 00:11:43
    looks like the recommendation is do
  275. 00:11:45
    seven days of anti-seizure medication,
  276. 00:11:48
    avoid fun and towing, and that's it.
  277. 00:11:50
    But I think we all agree that if you see
  278. 00:11:53
    someone seizing objectively on EEG, in
  279. 00:11:55
    your ICU, that's a different story.
  280. 00:11:58
    You hook them, you know. to EEG,
  281. 00:12:00
    you're gonna keep your anti-seizure
  282. 00:12:01
    medication and close monitoring and then
  283. 00:12:05
    future plans with the neurology or
  284. 00:12:08
    neurosurgery team as far as how many
  285. 00:12:10
    more days are they gonna get discharged?
  286. 00:12:12
    Are they not gonna get discharged? But
  287. 00:12:14
    I think if there is suspicious that they
  288. 00:12:18
    see these but not proven, you could do
  289. 00:12:21
    seven days of anti-seizure medication
  290. 00:12:23
    and kind of
  291. 00:12:26
    prevent all the confusion about, okay,
  292. 00:12:27
    like maybe even this seizure or
  293. 00:12:28
    something like that. But if we're
  294. 00:12:29
    actively seizing, I think that's a
  295. 00:12:31
    separate kind of discussion. Absolutely
  296. 00:12:34
    agree. I think we're gonna keep
  297. 00:12:35
    treating the patients that are seizing
  298. 00:12:36
    with their anti-seizure medications. I
  299. 00:12:38
    love it. Avoiding finitoad because of
  300. 00:12:40
    that drug, drug interaction with the
  301. 00:12:42
    mode of pain that we talked about last
  302. 00:12:43
    time and the fact that we know that this
  303. 00:12:45
    leads to poorer outcomes. But all of
  304. 00:12:48
    these patients, you know, when I round
  305. 00:12:50
    with students in the neuro ICU, I
  306. 00:12:51
    frequently hear, why is everyone
  307. 00:12:54
    febrile? And why does everyone have
  308. 00:12:55
    this low sodium? So what are we doing
  309. 00:12:59
    about all of these hyponatremic patients?
  310. 00:13:02
    And what do the new guidelines have to
  311. 00:13:03
    say about that? Yeah, so I think as a
  312. 00:13:07
    pharmacist, the first thing that I
  313. 00:13:08
    think about are there any medications
  314. 00:13:10
    that can do that? You know, that's why
  315. 00:13:12
    we typically don't allow any thizides
  316. 00:13:14
    for these patients or anything that
  317. 00:13:15
    could drop sodium that we can identify.
  318. 00:13:19
    I think, you know, just like anything,
  319. 00:13:21
    the question, the first question that
  320. 00:13:22
    comes up when we round is that why are
  321. 00:13:24
    they hyponatremic, right? Is this
  322. 00:13:26
    cerebral salt wasting, which I feel
  323. 00:13:28
    like in the majority of the cases, it's
  324. 00:13:30
    probably the likely diagnosis in these
  325. 00:13:32
    patients, or is this, you know, SIDH,
  326. 00:13:35
    or is it something else? Obviously, if
  327. 00:13:37
    you know what's happening, then it's
  328. 00:13:39
    easier. If it's, let's say, cerebral
  329. 00:13:41
    salt wasting, I think there is a lot of
  330. 00:13:43
    discussion about what about photocortic
  331. 00:13:44
    zone. And the guidelines, actually, I
  332. 00:13:46
    was really impressed that they said you
  333. 00:13:48
    could do photocortic zone. It will fix
  334. 00:13:50
    your number, it will fix your sodium,
  335. 00:13:52
    but guess what? It won't change your
  336. 00:13:54
    DCI outcomes And I think that was
  337. 00:13:56
    important to note. But the key point
  338. 00:13:58
    really is that if someone's hyponatremic
  339. 00:14:01
    and they're symptomatic because they're
  340. 00:14:04
    hyponatremic, I think we all agree that
  341. 00:14:05
    regardless of the ideology, you have to
  342. 00:14:07
    give them the hypertonic saline to get
  343. 00:14:09
    them to the goal that you have. So
  344. 00:14:11
    although, you know, working up why
  345. 00:14:14
    they're hyponatremic and let's say if
  346. 00:14:15
    they're SIDH, obviously, I think that
  347. 00:14:17
    becomes a little bit more tricky because
  348. 00:14:19
    food restriction in this population is a
  349. 00:14:21
    tough discussion to have We want to,
  350. 00:14:23
    you know, have them bubolemic because
  351. 00:14:24
    we know that's evidence-based to improve
  352. 00:14:27
    outcomes. So if you have to kind of
  353. 00:14:29
    have that discussion and see what
  354. 00:14:30
    direction we're going to go. But if
  355. 00:14:32
    it's cerebral salt wasting, I think
  356. 00:14:34
    food of cortisone is an option. You can
  357. 00:14:36
    still give them, you know, fluids and
  358. 00:14:38
    salts, meaning, you know, normal
  359. 00:14:40
    saline if they're very low, hypotonic
  360. 00:14:42
    saline, if they're very symptomatic,
  361. 00:14:45
    again, if they're
  362. 00:14:48
    permeating, obviously more concentrated
  363. 00:14:50
    sodium, like 234 I think knowing why
  364. 00:14:53
    their hyponatremate is important to fix
  365. 00:14:55
    that, but just like any neurological
  366. 00:14:57
    emergency, if they're actively
  367. 00:14:59
    symptomatic, then hypertonic saline is
  368. 00:15:02
    a very fair and reasonable a choice here.
  369. 00:15:13
    I feel like we could spend literally
  370. 00:15:16
    like the next four days talking about
  371. 00:15:18
    the guidelines, how fascinating these
  372. 00:15:20
    patients are, but I think this has been
  373. 00:15:23
    kind of a nice discussion for if you're,
  374. 00:15:25
    you know, rounding for the first time
  375. 00:15:27
    in the neuro ICU and you're seeing all
  376. 00:15:30
    of these complex management strategies
  377. 00:15:32
    play out. I mean, this is a place
  378. 00:15:34
    where there is still a lot of equipos
  379. 00:15:37
    about how do we best manage and prevent
  380. 00:15:40
    DCI, and all of this sort of neurologic
  381. 00:15:44
    complications and the systemic critical
  382. 00:15:46
    care illness that can go along with
  383. 00:15:48
    these very sick and complicated patients.
  384. 00:15:51
    I feel like this is what makes neuro ICU
  385. 00:15:53
    so fun. I agree. And I think, you
  386. 00:15:55
    know, when these guidelines came out,
  387. 00:15:57
    there's some, you know, discussion
  388. 00:15:59
    about, oh, like, it doesn't say do
  389. 00:16:01
    this and this and that. There's a lot
  390. 00:16:02
    of discussions about, well, we don't
  391. 00:16:04
    know, there is no evidence. But as you
  392. 00:16:06
    said, I think that's the fun part the
  393. 00:16:08
    beauty of this that you kind of do your
  394. 00:16:10
    own assessment. You read the literature
  395. 00:16:12
    and you can make that clinical judgment
  396. 00:16:15
    by looking at a patient as opposed to
  397. 00:16:16
    kind of following a recipe for every
  398. 00:16:18
    single patient. Totally agree. All
  399. 00:16:22
    right. Well, I think that brings us to
  400. 00:16:23
    the end of this episode. It has been so
  401. 00:16:25
    much fun. It's all you any parting
  402. 00:16:26
    words? I think we covered it all. We
  403. 00:16:29
    covered two different guidelines and
  404. 00:16:32
    hopefully people can learn something new
  405. 00:16:35
    or add comments if they wanted something
  406. 00:16:37
    more or different that we didn't talk
  407. 00:16:39
    about We definitely invite people to
  408. 00:16:41
    look at the on-call chapter, which has
  409. 00:16:43
    even more than we could possibly ever go
  410. 00:16:45
    into in these short episodes. All right.
  411. 00:16:48
    Well, thanks guys. It's been fun.
  412. 00:16:51
    Thank you. Bye.