Category: Cases

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We dive into fluid resuscitation in sepsis, with Dr. Jon-Emile Kenny, pulmonary and critical care physician, author of the physiology textbook Heart-lung.org, and inventor of the FloPatch device.

Disclosures: Dr. Kenny appears here as both a clinician as well as a representative of his company and product, and should be presumed to retain a degree of bias in this discussion. However, his appearance is not part of a commercial relationship with our show; no compensation was provided, and neither he nor his company have any input in the episode’s content, nor the right to review it (or prevent its publication) after recording.

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Takeaway lessons

1. Before giving IV fluids, ask: 1) Is there an indication to give fluids? 2) Is giving fluids safe? 3) Will giving fluids be effective?
2. One of the most common misconceptions is that safety and efficacy are opposite ends of a spectrum, and efficacy necessarily implies safety. This is not so. Think instead of fluid like a drug, which could be effective, yet also dangerous (e.g. anaphylaxis), or vice versa. A volume overloaded patient could be fluid responsive, but giving fluid could be a poor idea.
3. Interpreting heart function and cardiac output is difficult in sepsis, particularly on the venous or filling side. Many have some degree of diastolic dysfunction, which sepsis itself can induce.
4. Kenny likes to phenotype patients into a 4-quadrant grid, similar to the traditional Diamond-Forrester heart failure classification, characterizing a patient as either wet/dry and normal/low cardiac output. POCUS can be used to assess both of these; LVOT VTI >17-20 is a normal-ish stroke volume and IVC is a surrogate for preload.
5. The only phenotype likely to benefit from fluid is the cold, dry patient (warm patients don’t need fluid, wet patients are unlikely to respond and maybe shouldn’t have it even if they will), although in sepsis, 20-30% of even this group are not fluid responsive and fluid will simply congest them.
6. Using BP response to fluid challenge is insensitive; in a significant number of patients, cardiac output will increase but BP will not. A marker of flow, e.g. doppler ultrasound, is more sensitive.
7. The FloPatch is a wireless, wearable, continuous-wave doppler ultrasound. It adheres over the neck and continuously monitors both the carotid and jugular vessels. The jugular provides a CVP-like waveform for qualitative clinician inspection, while the carotid is used to automatically measure the systolic flowtime duration, which is associated with stroke volume (better evidence than calculating a stroke volume).
8. The height of the carotid waveform may change with alterations in inotropy, afterload, and other factors, but if those are consistent, fluid responsiveness is best associated with the duration alone (base of the triangle).
9. An increase in flowtime duration of >7 milliseconds after a preload challenge (Trendelenburg position or ~250-300 ml rapid fluid bolus) is associated with 10% increase in stroke volume. (This cutoff is meant to match existing literature on fluid responsiveness.)

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We discuss propofol infusion syndrome (PRIS) and propylene glycol toxicity from lorazepam infusions, with medical toxicologist Dr. Jerry Snow, director of the toxicology fellowship at Banner University Medical Center in Phoenix.

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Takeaway lessons

1. PRIS is a defect in the electron transport chain leading to a failure of ATP production and fatty acid metabolism. There seems to be a susceptibility in some part of the population, but not a clearly understood or monofactorial one. People with mitochondrial disorders are at higher risk, but there is no definitive testing for PRIS risk.
2. PRIS has mostly been described with infusions greater than ~67 mcg/kg/min infusions, running for >48 hours.
3. The most common presentation is some combination of: elevated lactate, rhabdomyolysis, and new cardiac changes (which may be varied, including new bundle branch block, bradycardia, Brugada-like ST elevations, and changes in function on echo). Trending lactate and CK periodically on high-dose propofol is not a bad idea.
4. Triglyceride elevation probably has some association with PRIS, as it is also associated with high propofol doses, but there is not a direct link.
5. The primary treatment is stopping propofol and supportive care. There have been some case reports of ECMO being used.
6. It is not clear whether patients might be treated by dose-lowering propofol rather than stopping entirely, but it would be a fairly bold move; a safer option might be discontinuation and later rechallenge, but many experts recommend avoiding propofol in the future. Data is limited, but it should probably be added to allergy lists.
7. Propylene glycol is a toxic alcohol used as diluent for lorazepam, diazepam, and phenobarbital infusions. It is lower amounts in the latter two, and they are less often used, so toxicity is almost always in lorazepam, and almost always in infusions (not intermittent boluses).
8. It is associated with higher infusion rates for prolonged periods. This is probably above >6-7 mg/hr, or >0.1 mg/kg/hr, or >1mg/kg/day, depending on who you ask.
9. Propylene glycol is an alcohol, which behaves similarly to other toxic alcohols like ethylene glycol; it creates an elevated osmolar gap, and is metabolized via alcohol dehydrogenase (ADH) to lactate, creating a lactic acidosis.
10. Presentation is predominantly an unexplained lactic acidosis. An elevated osmolar gap will help confirm. Mental status can be affected as well. Trending a daily lactate and/or osmolality is not a bad idea on high-dose lorazepam infusions.
11. There is no common confirmatory testing, although some centers can probably obtain propylene glycol levels.
12. Treatment of propylene glycol toxicity is predominantly stopping or weaning the drip and supportive care. In the most severe cases, it can be treated similarly to other toxic alcohols, including fomepizole and/or renal replacement therapy (especially in patients with renal failure who are more likely to accumulate the compound and its metabolites). It probably does not need to be listed as an allergy/drug reaction.

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Brandon and Bryan mock up a goals of care discussion for a critically ill patient, and reflect on the right and wrong ways to execute this complex procedure.

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Resources

Center to Advance Palliative Care

The Conversation Project

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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

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We learn about the basics of fetal monitoring in the critically ill pregnant woman and how to integrate them into our ICU workflows, with Stephanie Martin, MFM obstetrician and host of the Critical Care Obstetrics podcast and teacher at the Critical Care Obstretrics Academy.

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Takeaway lessons

1. A fetus is considered potentially viable at 23-24 weeks gestational age, with 22-23 weeks being occasionally viable in specific circumstances and highly specialized centers. “Potentially viable” does not mean guaranteed survival, as fetal mortality is still quite high. In other words, at 23 weeks and above, intervention to promote fetal survival make sense. Every additional day of gestation improves outcomes.
2. A conversation should occur preemptively between the mother, ICU, and obstetric teams to clarify what options will be considered—in some circumstances, early delivery (via C-section) is not desired due to the risk to the mother, and should not be assumed to be the contingency in all viable pregnancies. On the flip side, delivery of a non-viable fetus could still be appropriate for the mother’s health, such as in uterine infection or hemorrhage.
3. If a fetus will not be delivered early, there may be no role for fetal monitoring.
4. Fetal monitoring is therefore relevant at viable gestational ages. However, it is also more difficult for early pregnancies; the monitors can easily wander off a tiny fetus, and the strips are harder to interpret.
5. Fetal monitors essentially monitor 1. Fetal heartrate (via Doppler), and 2. Uterine contraction. Heartrate is monitored primarily to determine variability, i.e. how much the rate changes from its average baseline in response to stimulus, particularly uterine contraction (which causes fetal stress of sorts). Poor variability with markers like late decelerations can be a sign of fetal acidosis and ischemia, particularly to the brain, which can increase the risk of fetal demise or birth defects such as cerebral palsy. Prematurity creates particular vulnerability to this.
6. Maternal sedation leads to fetal sedation, which can make interpreting the heart rate more difficult.
7. Uterine contractions rarely turn into labor, but they provide a natural stress test to the fetus.
8. Much of the interpretation of “fetal distress” comes down to the context—for instance, maternal acidemia will always cause fetal acidemia, but in a rapidly reversible setting such as DKA, the best solution may simply be resuscitating the mother.
9. Fetal distress is often an early marker of shock and other systemic stress, as uterine perfusion is sacrificed fairly early by the body in favor of other organs. This often manifests as uterine contractions.
10. Any pregnant woman with a gravid uterus up to the umbilicus, or >20 weeks, who is critically ill, should not lie supine; the uterus will compress the great vessels and may cause shock. Elevate the head of the bed or tilt them laterally at all times. (During CPR, assign someone to manually displace the uterus to the left, as tilting the entire patient is challenging.)
11. There is relatively little role for ultrasound or other tools for fetal monitoring; the gold standard is fetal heart rate monitoring.
12. Paroxysms of vital sign changes (tachycardia, hypertension, etc) in a pregnant woman could be a subtle marker of contractions.
13. With regards to ionizing radiation, generally, do whatever test you would do in a non-pregnant woman. Birth defects are generally established by the end of the first trimester, so in a viable pregnancy, it should not be a concern at all. While appropriate attention should be paid to avoiding needless radiation, if an important diagnosis needs to be made, do the x-ray or CT scan (or even fluoroscopy, likely the highest risk).
14. In the post-partum patient, the longer it’s been since birth, the less likely a maternal illness is pregnancy-related. In the first week, assume it’s pregnancy related. In the first six weeks, consider it, especially hypertension complications. Cardiac problems (e.g. peripartum cardiomyopathy) can occur even later, especially as the diagnosis may be delayed. A common presentation is post-partum “asthma,” actually pulmonary edema, as the fluid bolus of delivery overloads a cardiomyopathic heart. The most hypercoagulable period in pregnancy is actually the first six weeks post-partum, so VTE is an important concern.

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We discuss the basics of EEG in the ICU, including when to do it, selecting the appropriate study, and the basics of bedside interpretation, with Carolina B Maciel, MD, MSCR, FAAN, triple boarded in neurology, neurocritical care, and critical care EEG.

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Takeaway lessons

1. There is little to no role for a very short (<2 hour) EEG in the critically ill patient, who generally has “less of everything”; to determine the presence of seizure activity or other electrical disease, more data is usually necessary.
2. Long-term or continuous EEG is usually defined as >12 hours. 2-12 is a middle ground (both clinically and for billing purposes). In most ICU cases, a “middle” study of a few hours can be done, then the findings used to inform the need for a longer study; validated scores exist for this, such as 2HELPS2B.
3. Don’t forget the non-seizure diagnoses that can be made/supported from EEG, such as brain death, cefepime-induced encephalopathy, sudden clinical changes due to osmotic shifts, etc. In reality, EEG readers, particularly in the community, may or may not be making great efforts to appreciate these things. You will get better reads if you communicate your questions to the reader, and consulting neurologists/neurointensivists may be able to glean more from a non-specific EEG report as well. Critical care EEG folks like Carolina may be the most helpful, but there are very few training programs for this.
4. Basic filters on the EEG include the high and low pass filters (should be LFF of 1 hz, HFF ~7–8 hz), and potentially a notch filter for 60 hz (in the US) or 50 hz (in Europe) to filter out AC electrical noise.
5. Dark vertical lines on the strip occur every 1 second. With normal scale there should be about 3 centimeters (around your thumb’s length) between them.
6. Odd numbered leads are on the left side of the head. Even numbers are on the right. Z-numbered leads are in the sagittal midline.
7. Do you see intermittent bursts of something pointy, like it will hurt to sit on? These may be muscular artifact, which can be hard to distinguish (look at the patient to see if they’re moving/twitching), but if not, this may be an epileptic discharge; similar to a PVC, or someone coughing in the symphony audience, it’s an inappropriate interruption in brain activity. This may be focal or global (all leads), and focal may be higher risk. They may be repetitive, occurring somewhat regular intervals, which are also more concerning. Ultimately, the concern is always whether they are going to evolve/organize into full seizures, so if no evolution ever occurs, that is also more reassuring.
8. When to treat epileptogenic discharges on EEG is always a judgment call and must be put in context of the patient. More abundant discharges with a more malignant appearance are more concerning, but the clinical correlation matters too; EEG findings with no clinical correlate are less worrisome. Convulsive seizures are a medical emergency (especially with continuous tonicity), but non-convulsive electrical activity, even non-convulsive status, usually has room and time to weigh the risks versus the benefits of therapy. Talk to experts and make a thoughtful decision.
9. Carolina hates fosphenytoin due to the cardiotoxic effects. Lacosamide is quite benign.
10. The ictal-interictal spectrum is an electrical finding (not meeting the arbitrary definition of unequivocal status epilepticus) that may be important or not; you must consider the patient. If there is a clinical alteration in mental status that may be due to the activity, you should challenge them with a loading dose of a fast-acting, minimally sedating anti-seizure medicine and see if it helps their EEG and clinical status. Carolina dislikes benzos for this (sedating), thinks levetiracetam is only okay (too slow to reach peak brain concentration, ~90 minutes); brivaracetam (5 mins) and valproic acid (5-10 mins) are good.

References

Training modules for ACNS 2021 ICU EEG terminology

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A roundup from members of the SCCM’s ICU Liberation committee, recorded at SCCM Congress 2025.

Included:

• Heidi Engel
• Kali Dayton
• Kristina Betters
• Stacey Williams
• Jessica Anderson
• Jenna Domann
• Sergio Zanotti
• Erika Setliff
• Brian Peach

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We discuss the basics of evaluation for tracheostomy placement, periprocedural care, and post-procedure complications with Vinciya Pandian, PhD, ACNP, FCCM, tracheostomy nurse practitioner and researcher.

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We discuss assessment, monitoring, medical stabilization, and when to consider transplant of the patient with acute liver failure. We are joined by Dr. Sergio Navarrete, anesthesiologist and intensivist with fellowship training in transplant anesthesia.

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Takeaway lessons

1. Transaminases rising into the many hundreds or thousands (especially with pre-existing liver disease), or a MELD in the low teens (from baseline normal) should raise concern for a concerning degree of liver injury, usually due to shock liver, congestion, or infection. This should also prompt consideration for transplant evaluation, and usually a phone call to your transplant center.
2. Reversible causes, such as acetaminophen toxicity or portal vein thrombosis, must be ruled out.
3. Optimization of perfusion should include not only the left-sided systemic circulation, but also the right-sided system and venous congestion; congestive hepatopathy (from volume overload or RV failure) can absolutely cause severe liver injury. Echo, potentially with tools like VEXUS scoring, can be a great help here.
4. N-acetylcysteine has a clear indication for treating acetaminophen poisoning, but not much data for other causes of liver failure. However, many clinicians believe it may provide some benefit, and there is probably no harm—other than administering a fair amount of volume.
5. Hypoglycemia and hypothermia are both relatively late and ominous findings in the ALF patient (put them on a dextrose infusion and hourly glucose checks). Transaminase levels reflect hepatocyte injury but not liver function. Synthetic function as measured by INR or fibrinogen are helpful. Bilirubin is usually too slow and non-specific to be actionable. Trend this stuff every 6 hours or so.
6. Mental status is a key monitoring tool as a marker of cerebral edema. The clinical exam, ammonia level, potentially serial CT scans, and maybe invasive ICP monitoring (Sergio prefers a bolt over EVD) may all be needed in high-risk cases.
7. The highest risk patients for cerebral edema are those with truly acute/hyperacute liver failure. Trend ammonia, which has some correlation with herniation risk, but the neuro exam is more useful. Neurosonography could be used as well.
8. Lactulose should be used, and in extremis hyperosmolar therapy considered, although data for this is less clear than in other neurologic emergencies.
9. Liver ischemia and death will reliably cause a systemic inflammatory state with resulting distributive shock; this can persist even after transplant, due to persistent elements of the dying liver. Treat this like any SIRS/distributive shock state.
10. Bleeding and clotting can both occur; numbers usually suggest coagulopathy, but hemostatic rebalancing is often present, at least until something perturbs the balance (e.g. a procedure). Labs like the INR are a marker of disease severity, not bleeding risk. Fibrinogen is a little better, but TEG is probably the most useful marker of bleeding status, as many of these people are actually hypercoagulable.
11. Some would use CRRT relatively early in a liver failure patient; Sergio would not. However, he would consider it in the volume overloaded patient to manage congestion (if diuresis proved inadequate).
12. Liver-specific extracorporeal organ support using various devices (MARS, “liver dialysis,” albumin dialysis, etc) are interesting/promising therapies that largely have not shown convincing benefit in studies. They tend to be sporadically available and highly institution-specific.
13. In all cases, earlier consultation to liver transplant specialists is better than later (this may involve an interfacility phone call or transfer). Several days are usually needed for transplant evaluation, many aspects of which are not directly medical, such as assessment of social support, insurance, pre-transplant workup, etc. Waiting too long may mean a patient dies before the process can be completed.
14. All truly acute liver failure should be referred for transplant evaluation.
15. Typical rule-outs for transplant include uncontrolled metastatic malignancy, age (often >75; every center has a different cutoff), and severe unrepairable cardiac dysfunction. Infections such as active bacteremia are a concern. Much of this is a judgment call and up to the transplant team, and their culture and policies.
16. Alcohol use is not necessarily a rule-out for transplant; some (not all) centers will consider these patients. The social milieu is more important. It is not unreasonable to refer a patient to a more distant center that has broader eligibility criteria than a nearer one that rules them out.
17. Some critically ill patients may be transplant candidates, particularly if most of their problems are deemed secondary to their liver failure and hence potentially reversible. Liver transplant is a procedure that can and often should be performed in the setting of multi-organ failure, shock, respiratory failure, etc. But each center has its own risk tolerance.

References