Episode 81: Anesthesia for Craniotomies with Alyson Russo

Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Anesthesia and Critical Care Reviews and Commentary (ACCRAC) Podcast
Episode 81: Anesthesia for Craniotomies with Alyson Russo

In this episode, episode 81, I welcome Dr. Alyson Russo to the show to discuss how to prepare for and conduct anesthesia for craniotomy surgery.

CME: https://earnc.me/iM3y5w

10 thoughts on “Episode 81: Anesthesia for Craniotomies with Alyson Russo”

  1. Great episode,

    I’m a CA3 at a neuro anesthesia heavy program. Dr. Russian noted that she avoids giving midazolam for preoperative anxiolysis to avoid confounding mental status change. My experience is that most craniotomies for tumor resection, especially image guided, can last 6 to 9 hours which corresponds to 3 to 4.5 half lives. Can anyone comment on how sedated you’d expect the patient to be depending on how long the case lasts? We are judicious with premed as well but still give it at a decent proportion.

    Also any thoughts on using cisatracuriam to make the neuromuscular blockade more predictable and titratable to avoid movement in pins and hasten safe emergence?

    1. Hi there,

      Great questions. Dr. Russo’s response is below:

      Regarding midazolam: I know that some institutions do use it for patients undergoing craniotomies to help with anxiolysis, and it’s probably not wrong to use. As the resident points out, for a case lasting 6-9 hours, you are probably out of the window where it might confound the neuro exam at the end and I wouldn’t expect much, if any, sedation from the midaz at that point. For straight-forward cranis, however, the case may only be 3-4 hours long depending on your surgeon’s skill and the difficulty of the case, and that’s probably more of a gray zone. In addition, remember that if your patient is slow to emerge or there is some other issue with the neuro exam, the surgeon may want you to reverse the benzo with flumazenil– this could potentially lower the seizure threshold and also raise the ICP, both of which could be problematic for this patient population. That being said, I personally do a lot of crani procedures and never use benzos for these cases even for the longer ones. I find that engaging the patients, holding their hands, playing calming music, and getting them off to sleep quickly are all useful non-pharmacologic strategies that work very well in my experience.

      Regarding cisatracurium: I have used this both as bolus dosing and as an infusion for patients undergoing craniotomy procedures, but mostly if they have renal dysfunction. I do think it works well, but it is more expensive than rocuronium or vecuronium and that may be a consideration. The other factor to note is that it is not reversible with sugammadex (if you are using that at your institution). In my practice, I typically use vecuronium since I find it’s metabolism to be more predictable than rocuronium, and I tend to run an infusion- I’ll start at 3mg/hr for most craniotomy cases, and then increase the dose and give bolus doses of 1-3 mg depending on how many twitches the patient has on TOF monitoring. I try to titrate so that I have 2 twitches– when the case is finishing, you’ll be able to easily reverse when the patient is out of pins. Please note that some institutions/providers do not use paralysis at all for the crani cases, even when the patient is in pins.

  2. Great episode, and very thorough overview of neuroanesthesia and physiology! I have a question regarding strategies for bain swelling mgmt (“brain relaxation”). In both my training programs (residency and pediatric fellowship) we used mannitol, hypertonic NS (and hypernatremia), lasix, judicious hyperventilation, head of bed elevation, and of course avoidance of hypoxemia.
    But I recently came across an oral boards stem in which the surgeon requested therapeutic hypotension to assist with tumor exposure in a patient with a “full” brain. This to me sounds like a bad idea as low MAP will obviously compromise cerebral perfusion pressure (even though lower cerebral blood flow will reduce ICP), and in my mind (no pun intended) would place a patient at risk for cerebral ischemia. I was told by my faux-examiner (a co-fellow I was practicing with) that some surgeons and institutions DO in fact utilize therapeutic hypotension in their toolbox of brain relaxation techniques. Are my concerns valid? Can you please comment on this?
    (Just another anesthesiologist who dislikes hypotension a much as the next guy)

    1. Hi Matt,

      I’m sure there may be some surgeons who ask for therapeutic hypotension, but as you have correctly identified, there are major downsides to it. Just as with extreme hyperventilation, you will reduce blood flow to the brain and gain some reduced ICP transiently while causing cerebral ischemia. In a herniating patient where all other options have failed, for a very brief period of time it may be reasonable, though I certainly think it is risky and we don’t use the technique. If I were you and I got this question on oral boards, I would think they were testing my ability to disagree with a surgeon in a professional way and explain, as a consultant anesthesiologist, why I would prefer to use other methods to reduce ICP.

    2. Thanks Matt. Dr. Russo’s thoughts are below:

      From Dr. Russo on this question:

      Thank you for the question. I would say that I have the same concerns as you regarding hypotension for intracranial procedures. As you mentioned, we do typically use other means to decrease brain volume (mannitol, hyperventilation, hypertonic saline, Lasix, head of bed elevation), and in many cases, we try to maintain adequate blood pressures (no more than about 20% down from the patient’s baseline) in order to achieve good cerebral perfusion pressure to different parts of the brain. I take care of adult patients, many of whom have baseline hypertension, so the cerebral autoregulatory curve is shifted to the right at baseline, and I would be concerned about inadequate cerebral perfusion with deliberate hypotension. Many of those patients also probably have some degree of cerebrovascular disease, thereby increasing the risk of stroke with significant and prolonged hypotension. Therefore, I would not routinely use deliberate hypotension unless there was a strong reason to, and the benefit to the patient outweighed the risk of stroke.

      If the brain is still “full” despite all the afore-mentioned interventions, I suppose temporary hypotension could be considered, with the understanding that while it may improve surgical exposure, cerebral perfusion may be compromised (depending on the degree of hypotension induced). Remember that the ICP is effectively “0” while the dura is open and the brain is exposed, and CPP is MAP-ICP, so cerebral perfusion could be okay depending on the situation (though this is purely theoretical, and I would not rely on the numbers to say you are okay). A young and otherwise healthy patient may tolerate this for a short period of time (depends on the reason for the swollen brain– patients with TBI and hypotension have increased mortality compared to patients where the blood pressure is maintained), but I would be concerned with my adult patients and would need to have a discussion with the surgeon about risks and benefits of this maneuver.

      That being said, there may be a role for deliberate hypotension in aneurysm management. Surgeons who do not place temporary clips on an aneurysm may ask for hypotension in order to decrease blood flow into the aneurysm and allow for better placement of the permanent clip (I don’t know how common this is, honestly). Also, there may be a role with intraoperative aneurysm rupture in the case where the surgical team is unable to place a clip and stop the bleeding. Hypotension may need to be induced temporarily (with adenosine to cause BRIEF asystole) in that situation to allow for visualization of the ruptured vessel and placement of a clip. It is unclear to me how well carotid occlusion works in this setting, but is described as another maneuver to try. The surgeons at my institution routinely place temporary clips, so we will often raise the blood pressure to increase collateral flow. Also, with AVM’s, some degree of hypotension may help to decrease bleeding, but I think the risks of decreased perfusion still hold.

      The role of permissive and induced hypotension in current neuroanesthesia practice


  3. Dr. Russo mentioned using a subclavian CVP but what about a long arm CVP (multiple fenestrations etc) for patients at high risk for air embolism. Please comment on this and use of a precordial Doppler.

    1. Hi Deborah,

      Dr. Russo’s response is below. Thanks for the question!

      A multi-orifice catheter is certainly indicated in a sitting craniotomy or when there is a high concern for a venous air embolism (ie: operating in/near venous sinuses, for example). My understanding is that one would want to specifically use a multi-orifice catheter if there is concern for venous air embolism during a case. There may be more discussion of this in Dr. Mintz’s podcast on Venous Air Embolism.

      In addition, pre-cordial doppler, while it does not give the ability to treat a venous air embolism, it may be a way to detect one early. It is non-invasive, easy to place on the patient, and can be useful in determining if sudden hypotension during a craniotomy is secondary to an embolic event vs other causes (profound vagal response, sudden bleeding, anaphylaxis, etc.). The sensitivity for detecting a venous air embolism in order of greatest to least sensitive includes:

      precordial doppler
      Vital sign changes (blood pressure, EKG, pulse-ox)

  4. This was a great episode. At one point, during the discussion of hyperventilation, you mention that the respiratory alkalosis can lead to hypokalemia as a result of H+-K+ exchange. This has always felt like an oversimplification — at physiologic pH, hydrogen ions in the bloodstream are typically measured in the micromolar concentrations, while potassium ions are typically measured in the millimolar concentrations. To me, it doesn’t seem possible that this exchange could alter the potassium by multiple orders of magnitude. What am I missing?

    1. Hi Steve,

      If we have any biochemists in the audience maybe they can explain better than I can. There’s no question that the phenomenon is real, but whether it is oversimplified in the way it is usually explained I can’t tell you.

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