Critical Care Scenarios

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We chat about neuromuscular blockade, monitoring, and reversal in the ICU, including why sugammadex isn’t more widely used, with Sara J Hyland, PharmD, BCCCP, FCCP, researcher and clinical pharmacist in perioperative and emergency medicine.

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Takeaway lessons

1. Aminosteroids (rocuronium, vecuronium) can be reversed by neostigmine + glycopyrrolate (the latter to mitigate peripheral cholinergic effects of neo), or sugammadex. Benzylisoquinoliniums (e.g. cisatracurium) can only be reversed by the neostigmine option.
2. Neostigmine is an acetylcholinesterase inhibitor; in other words, it doesn’t directly antagonize the effect of the paralytic, it simply helps boost the supply of ACH at the neuromuscular junction to overcome it. This means its reversal effect is indirect and imperfect.
3. Neo is completely ineffective when blockade is deep. In fact, it can have a paradoxical effect of prolonging paralysis when used in these situations. It should really only be used when the train-of-four is 4 twitches. It is also slower acting than sugammadex, and even given with glyco, has inevitable risk of cholinergic toxicity (e.g. bradycardia).
4. Neo + glycopyrrolate costs around $30 for a dose, versus around $150-200 for a sugammadex approach. (This does not take into consideration broader system costs from a less effective and less efficient reversal method.) Overall cost with sporadic ICU use will always pale in comparison to high-volume perioperative use, though.
5. Sugammadex is a direct binder of the rocuronium/vecuronium molecule, and can attract even already-bound compound from its receptor; hence, it can function at any level of blockade (even very deep).
6. A large number of our patients who appear to have cleared their paralysis (seeming clinically “strong,” TOF 4) still have a significant continuing effect of neuromuscular blockade. This may contribute to failures of extubation and other complications. In one ICU study of random ICU patients, >40% had active neuromuscular blockade to a degree that would have precluded extubation by anesthesia standards.
7. As a result, the international, guideline-directed gold standard for reversal of neuromuscular blockade is now using quantitative, objective neuromuscular monitoring (before and after reversal agents) to confirm resolution to a >90% TOF ratio.
8. What’s that? Normal train-of-four devices (qualitative peripheral nerve stimulators) are inadequate; 4 out of 4 twitches may be present despite 70% of nicotinic ACH receptors still blocked. Better devices (with accelerometers, myometers, EMG, etc) can measure the actual twitch strength and compare the ratio of first to last twitch—i.e. does it fade or maintain strength? The fourth twitch should be >90% the strength of the first before extubation. (All four twitches must be present to even attempt this technique; other techniques can be used at levels of blockade deeper than this.)
9. Although sugammadex will be effective at any degree of block, it is dosed differently at different levels, so pre-drug assessment is still important. (It may also reveal the option of using neostigmine, if desired.) Post-drug assessment is then needed to confirm adequate response.
10. “Recurarization,” or recurrence of paralysis after reversal, is a known phenomenon. It is rare after sugammadex, and tends to occur when it was underdosed; the immediate effect may be good but the paralytic may outlast the reversal. This phenomenon should be considered in a patient with unexpected weakness/coma or respiratory failure after reversal, and either neuromuscular testing or empiric sugammadex should be considered.
11. There is an anaphylaxis risk with sugammadex, as the molecule type is also found (and could have induced sensitization) in many everyday cosmetic compounds. But the risk is extremely low (well under 1%)—lower than rocuronium, and in fact, anaphylaxis to rocuronium potentially could be treated with sugammadex.
12. There is a small risk of mild bradycardia and hypotension after sugammadex, as well as rare reports of sudden unexplained cardiovascular collapse. The cause of these is not well understood, and in many cases may be mere confounders.
13. Why isn’t sugammadex widely used in the ICU, as it is in the perioperative world? Unclear; we may not realize how common residual paralysis is (i.e. very), and over-rely on insensitive clinical assessments (squeezing hands, tidal volumes, lifting the head, etc). This was the situation in anesthesia two decades ago and we may be lagging behind.
14. In some cases rocuronium may be having residual effects hours to days later; the duration of effect on the package insert is defined as median time to >25% of first twitch height reemerging, a standard far below what clinically-relevant paralysis might entail. This residual effect might cause failures of extubation, especially in tenuous patients.
15. Even in intubated patients, persistent paralytic effect may be a cause of distress and PTSD if sedation has been inadvertently weaned (i.e. awake paralysis).
16. In the absence of quantitative monitoring, a good clinical assessment, confirmation of four twitches on TOF, and at least an eyeball assessment of twitch strength is a reasonable starting point.
17. In a patient remaining intubated (e.g. reversed to facilitate neuro exams), the demands for monitoring are less; an empiric low-dose sugammadex (e.g. 200 mg) titrated to a patient who can engage in your exam is probably fine—they don’t need complete strength. Even simple “bugzapper” TOF devices can rule out deep blockade in these situations.
18. In a failed airway situation, give a hefty dose empirically. A post-sugammadex check may still be appropriate, though. Don’t expect this to rescue you in a crashing patient. Note that if you gave sugammadex, it may linger in the body for days, making it difficult to reparalyze with an additional dose of rocuronium if your airway approach requires that. (You may need to use a higher roc dose later, or succinylcholine, or cisatracurium.) Tell anesthesia if they’re taking a patient to the OR, or reattempting an RSI, if you previously gave sugammadex.
19. The paralytic/sugammadex complex circulates in the blood until it’s renally cleared. With a low GFR, this can take a long time; there is a theoretical risk of the complex dissociating at some later point and re-paralysis occurring. In a dialysis-dependent patient, in fact, it may not clear very efficiently with lower-flux filters, such as during CRRT. For these reasons, in the past, renal failure was a contraindication to sugammadex, but data and clinical experience has since shown it to be generally safe.

References

1. Ross J, Ramsay DP, Sutton-Smith LJ, Willink RD, Moore JE. Residual neuromuscular blockade in the ICU: a prospective observational study and national survey. Anaesthesia. 2022 Sep;77(9):991-998. doi: 10.1111/anae.15789. Epub 2022 Jul 15. PMID: 35837762.
2. Grabitz SD, Rajaratnam N, Chhagani K, Thevathasan T, Teja BJ, Deng H, Eikermann M, Kelly BJ. The Effects of Postoperative Residual Neuromuscular Blockade on Hospital Costs and Intensive Care Unit Admission: A Population-Based Cohort Study. Anesth Analg. 2019 Jun;128(6):1129-1136. doi: 10.1213/ANE.0000000000004028. PMID: 31094777.
3. Frenkel M, Lien CA. Eliminating residual neuromuscular blockade: a literature review. Ann Transl Med. 2024 Aug 1;12(4):65. doi: 10.21037/atm-23-1743. Epub 2024 May 14. PMID: 39118951; PMCID: PMC11304418.
4. Blum FE, Locke AR, Nathan N, Katz J, Bissing D, Minhaj M, Greenberg SB. Residual Neuromuscular Block Remains a Safety Concern for Perioperative Healthcare Professionals: A Comprehensive Review. J Clin Med. 2024 Feb 1;13(3):861. doi: 10.3390/jcm13030861. PMID: 38337560; PMCID: PMC10856567.
5. Renew, J.R., Ratzlaff, R., Hernandez-Torres, V. et al. Neuromuscular blockade management in the critically Ill patient. j intensive care 8, 37 (2020). https://doi.org/10.1186/s40560-020-00455-2
6. Thilen SR, Weigel WA, Todd MM, Dutton RP, Lien CA, Grant SA, Szokol JW, Eriksson LI, Yaster M, Grant MD, Agarkar M, Marbella AM, Blanck JF, Domino KB. 2023 American Society of Anesthesiologists Practice Guidelines for Monitoring and Antagonism of Neuromuscular Blockade: A Report by the American Society of Anesthesiologists Task Force on Neuromuscular Blockade. Anesthesiology. 2023 Jan 1;138(1):13-41. doi: 10.1097/ALN.0000000000004379. PMID: 36520073.
7. Linn DD, Renew JR. Neuromuscular monitoring: A tutorial for pharmacists. Am J Health Syst Pharm. 2025 Feb 20;82(5):e242-e251. doi: 10.1093/ajhp/zxae287. Erratum in: Am J Health Syst Pharm. 2025 Jun 16:zxaf124. doi: 10.1093/ajhp/zxaf124. PMID: 39425960.
8. Bologheanu R, Lichtenegger P, Maleczek M, Laxar D, Schaden E, Kimberger O. A retrospective study of sugammadex for reversal of neuromuscular blockade induced by rocuronium in critically ill patients in the ICU. Sci Rep. 2022 Jan 18;12(1):897. doi: 10.1038/s41598-022-04818-7. PMID: 35042888; PMCID: PMC8766455.
   https://pubmed.ncbi.nlm.nih.gov/35042888/
9. Gartner HT, Rech MA. Sugammadex Use Outside of the Postoperative Setting. Annals of Pharmacotherapy. 2024;58(11):1117-1121. doi:10.1177/10600280241232660 
10. Hallisey SD, Prucnal CK, Ilg AM, Seethala RR, Jansson PS. Use and Outcomes of Sugammadex for Neurological Examination after Neuromuscular Blockade in the Emergency Department. West J Emerg Med. 2025 Mar;26(2):347-352. doi: 10.5811/westjem.29328. PMID: 40145930; PMCID: PMC11931695.
11. Hyland SJ, Pandya PA, Mei CJ, Yehsakul DC. Sugammadex to Facilitate Neurologic Assessment in Severely Brain-Injured Patients: A Retrospective Analysis and Practical Guidance. Cureus. 2022 Oct 19;14(10):e30466. doi: 10.7759/cureus.30466. PMID: 36407180; PMCID: PMC9673186.
    https://pubmed.ncbi.nlm.nih.gov/36407180/
12. Rech MA, Gottlieb M. SUGAMMADEX SHOULD BE USED TO REVERSE ROCURONIUM IN EMERGENCY DEPARTMENT PATIENTS WITH NEUROLOGIC INJURIES. Ann Emerg Med. 2025 Jan;85(1):78-79. doi: 10.1016/j.annemergmed.2024.04.015. Epub 2024 Oct 16. PMID: 39412465.
13. Harlan SS, Philpott CD, Foertsch MJ, Takieddine SC, Harger Dykes NJ. Sugammadex Efficacy and Dosing for Rocuronium Reversal Outside of Perioperative Settings. Hosp Pharm. 2023 Apr;58(2):194-199. doi: 10.1177/00185787221126682. Epub 2022 Sep 29. PMID: 36890961; PMCID: PMC9986574.
    https://pubmed.ncbi.nlm.nih.gov/36890961/
14. Winant M, Engel H, Dubois P, Halenarova K, De Backer D. Reversal of rocuronium-induced fixed pupillary dilation by sugammadex in ICU patients with COVID-19. Br J Anaesth. 2024 Mar;132(3):627-629. doi: 10.1016/j.bja.2023.12.011. Epub 2024 Jan 12. PMID: 38218692.
15. Lemus R, Guider W, Gee SW, Humphrey L, Tobias JD. Sugammadex to Reverse Neuromuscular Blockade Prior to Withdrawal of Life Support. J Pain Symptom Manage. 2021 Aug;62(2):438-442. doi: 10.1016/j.jpainsymman.2021.03.001. Epub 2021 Mar 5. PMID: 33677073.
    https://pubmed.ncbi.nlm.nih.gov/33677073/
16. Hristovska AM, Duch P, Allingstrup M, Afshari A. Efficacy and safety of sugammadex versus neostigmine in reversing neuromuscular blockade in adults. Cochrane Database of Systematic Reviews 2017, Issue 8. Art. No.: CD012763. DOI: 10.1002/14651858.CD012763.
17. Renew JR, Linn DD. Pro: The Use of Sugammadex Does Not Preclude the Need for Objective Neuromuscular Monitoring. J Cardiothorac Vasc Anesth. 2025 Jul;39(7):1878-1881. doi: 10.1053/j.jvca.2025.04.001. Epub 2025 Apr 5. PMID: 40307132.
18. Todd MM, Kopman AF. Sugammadex Is Not a Silver Bullet: Caveats Regarding Unmonitored Reversal. Anesthesiology. 2023 Jul 1;139(1):1-3. doi: 10.1097/ALN.0000000000004587. PMID: 37279102.
19. Bowdle TA, Haththotuwegama KJ, Jelacic S, Nguyen ST, Togashi K, Michaelsen KE. A Dose-finding Study of Sugammadex for Reversal of Rocuronium in Cardiac Surgery Patients and Postoperative Monitoring for Recurrent Paralysis. Anesthesiology. 2023 Jul 1;139(1):6-15. doi: 10.1097/ALN.0000000000004578. PMID: 37027807.
20. Linn DD, Renew JR. The impact of sugammadex dosing and administration practices on potential cost savings for pharmacy departments. Am J Health Syst Pharm. 2024 Sep 23;81(19):e575-e583. doi: 10.1093/ajhp/zxae124. PMID: 38725325.
21. Lin CJ, Eikermann M, Mahajan A, Smith KJ. Restrictive versus unrestrictive use of sugammadex for reversal of rocuronium: a decision analysis. Br J Anaesth. 2024 Feb;132(2):415-417. doi: 10.1016/j.bja.2023.11.037. Epub 2023 Dec 15. PMID: 38104004.

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We explore the world of thrombectomy for acute ischemic stroke with Justin F. Fraser (@doctorjfred), MD, FAANS, FAHA, Professor and Vice-Chair of Neurological Surgery and Director of Cerebrovascular Surgery and Neuro-interventional Radiology at University of Kentucky, where he specializes in cerebrovascular, endovascular, skull base, and endoscopic transsphenoidal surgery.

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Takeaway lessons

1. In the opinion of Dr. Fraser, thrombectomy for qualifying patients with acute ischemic stroke is the current standard of care. Patients in non-thrombectomy centers should be transferred. Failure to do so is potentially negligent.
2. Dr. Fraser feels there are few true contraindications to thrombectomy (as long as the patient’s goals are concordant), and the current indications should probably be most strokes <24 hours with a large vessel occlusion on CTA – i.e. ICA (including with a tandem extracranial carotid occlusion), MCA, ACA, or basilar. He no longer feels most cases need perfusion imaging as even large or older infarcts seem to benefit.
3. The main current question is the utility of thrombectomy in “medium vessel occlusions,” such as M2 and more distal vessels.
4. Radial artery access is growing in popularity, similar to its growth in cardiovascular interventions, now that devices have shrunk enough to fit. The right wrist is preferred.
5. In general, qualifying patients should still receive systemic thrombolytics as soon as possible prior to performing thrombectomy, at least with the state of the evidence in 2025. This also helps manage any particles that embolize into more distal vessels during aspiration of a larger thrombus.
6. Generally, thrombectomy is merely a process of aspirating an embolus. However, if thrombosis also involved an intracranial atherosclerotic narrowing, there may still be unstable stenosis afterwards, so about a third of cases also require stent placement. (Carotid occlusions are a different story and usually need stenting, just as with elective endarterectomies.) When stents are placed for this reason or for a carotid lesion, dual antiplatelet inhibition is usually needed; this may be started during the procedure with an intra-arterial agent if DAPT is not already on board.
7. Thrombectomy can be performed under local anesthesia only, or under deeper sedation; the practice for Dr. Fraser’s group is to put everybody under general anesthesia. Anesthesia’s efforts are performed simultaneously to the interventional prep and should not delay it.
8. Post-procedure blood pressure targets are controversial. Fraser targets SBP <160 for 24 hours to limit reperfusion hemorrhage.
9. Post-procedure MRI is usually appropriate to delineate infarct size and to appreciate the degree of edema, potentially requiring decompressive craniectomy (large hemispheric or cerebellar stroke). If MRI is delayed, CT is appropriate, perhaps dual-energy CT to differentiate hemorrhage from contrast staining.
10. Expanding thrombectomy to more patients in smaller hospitals requires more trained neurointerventionalists, but this is not a completely simple matter, as it must be balanced against adequate volume to maintain proficiency for the proceduralists and their teams. Smaller centers also need a link to a larger center that can support them for scheduling gaps and complications.

Resources

Society of Neurointerventional Surgery

Get Ahead of Stroke