Category: Cases

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References and resources

• Hyperammonemia cheatsheet from Prem:

• Kamel, A.Y., Shah, P., Pipek, L.Z. et al. Nutritional Emergencies. Curr Surg Rep 13, 30 (2025). https://doi.org/10.1007/s40137-025-00465-9:

Acute Liver Failure

Overall management of ALF

• Bernal, W. and J. Wendon, Acute liver failure. N Engl J Med, 2014. 370(12): p. 1170-1.
• Bernal, W., et al., Lessons from look-back in acute liver failure? A single centre experience of 3300 patients. J Hepatol, 2013. 59(1): p. 74-80.
• Kandiah PA, Nanchal R, Subramanian RM. Acute Liver Failure. In: Schmidt GA, Kress JP, Douglas IS. eds. Hall, Schmidt and Wood’s Principles of Critical Care, 5th Edition. McGraw Hill; 2023. Accessed August 09, 2023.

CRRT in ALF

• Warrillow S, Fisher C, Tibballs H, et al. Continuous renal replacement therapy and its impact on hyperammonaemia in acute liver failure. Crit Care Resusc 2020;22:158-165.
• Cardoso FS, Gottfried M, Tujios S, Olson JC, Karvellas CJ, Group USALFS. Continuous renal replacement therapy is associated with reduced serum ammonia levels and mortality in acute liver failure. Hepatology 2018;67:711-720.

Osmolar Shifts in ALF

• Liotta EM, Romanova AL, Lizza BD, Rasmussen-Torvik LJ, Kim M, Francis B, et al.
• Osmotic shifts, cerebral edema, and neurologic deterioration in severe hepatic encephalopathy. Crit Care Med. (2018) 46(2):280–9. doi: 10.1097/CCM.0000000000002831

Ammonia toxicity in Liver Failure

• Dasarathy S, Mookerjee RP, Rackayova V, Rangroo Thrane V, Vairappan B, Ott P, et al. Ammonia toxicity: from head to toe? Metab Brain Dis. (2017) 32(2):529–38. doi: 10.1007/s11011-016-9938-3
• Guo, R.M., et al., Brain MRI findings in acute hepatic encephalopathy in liver transplant recipients. Acta Neurol Belg, 2018. 118(2): p. 251-258
• Kumar G, Taneja A, Kandiah PA. Brain and the Liver: Cerebral Edema, Hepatic Encephalopathy and Beyond. Hepatic Critical Care. 2017 Aug 7:83–103. doi: 10.1007/978-3-319-66432-3_8. PMCID: PMC7122599.

Ammonia in Cirrhosis

• Gallego JJ, Ammonia and beyond – biomarkers of hepatic encephalopathy. Metab Brain Dis. 2025 Jan 15;40(1):100. doi: 10.1007/s11011-024-01512-7. PMID: 39812958; PMCID: PMC11735499.

Ammonia in in post bariatric surgery hyperammonemia

• Kamel AY, Shah P, Pipek LZ, Shah A, Kandiah PA. Nutritional Emergencies. Current Surgery Reports. 2025;13(1):30. DOI10.1007/s40137-025-00465-9

Post Lung Transplant Hyperammonemia

• Kamel, A.Y., et al., Hyperammonemia After Lung Transplantation: Systematic Review and a Mini Case Series. Transpl Int, 2022. 35: p. 10433.

Post cardiac arrest Hyperammonemia

• Nojima T et al. Can Blood Ammonia Level, Prehospital Time, and Return of Spontaneous Circulation Predict Neurological Outcomes of Out-of-Hospital Cardiac Arrest Patients? A Nationwide, Retrospective Cohort Study. J Clin Med. 2022 May 4;11(9):2566. doi: 10.3390/jcm11092566. PMID: 35566692; PMCID: PMC9105173.

Ammonia Bowel Ischemia

• Watari M et al. Ammonia determination as an early indicator in experimental superior mesenteric artery occlusion. Hiroshima J Med Sci. 1997 Dec;46(4):159-67. PMID: 9538566.

Study on undifferentiated causes of hyperammonemia

• Maquet J et al. Clinical, biochemical, and molecular findings in adults with hyperammonemia: A French bi-centric retrospective study. Mol Genet Metab. 2025 Sep-Oct;146(1-2):109223. doi: 10.1016/j.ymgme.2025.109223. Epub 2025 Aug 13. PMID: 40834544.

• Sakusic A, Features of Adult Hyperammonemia Not Due to Liver Failure in the ICU. Crit Care Med. 2018 Sep;46(9):e897-e903. doi: 10.1097/CCM.0000000000003278. PMID: 29985210; PMCID: PMC6095817.

Takeaway lessons

1. Effective ammonia clearance requires liver function, kidney function, gut function, and presence of skeletal muscles. It can also be compromised by A-V shunting bypassing the portal venous system (i.e. from enteric to systemic circulation; ask your radiologist to look for this as they may not otherwise report it).
2. Measuring the plasma ammonia level is not too technically difficult, but does have a time limit; allowing a sample to sit may falsely elevate the result. It’s therefore tough to do for outpatients. For inpatients, however, unless it gets forgotten on a table, it is generally not so difficult. Arterial vs venous doesn’t matter.
3. The peak ammonia on admission for cirrhotics is not as relevant as their cumulative ammonia burden over time (though of course this is not measurable). While difficult to interpret for those patients, a very high number is still very toxic, a very normal level probably absolves hepatic encephalopathy as a cause of altered mental status, and trending a number in between may help confirm response to therapy (eg the number should come down). A persistently elevated ammonia despite adequate catharsis may indicate need for a more aggressive regimen, or other attention to the underlying cause; a common cause would be a patient with GI bleeding, where persistent blood in the gut can cause persistent ammonia elevation.
4. Everyone agrees that ammonia should be followed in acute liver failure, where it correlates closely with risk of cerebral edema.
5. Checking ammonia in the patient without clear liver failure, but unexplained altered mental status, is reasonable—though an abnormal result will require a thoughtful approach to explaining it.
6. Cardiac arrest, especially with prolonged resuscitation, will reliably increase the ammonia level (if measured during or immediately after), as a direct effect of global ischemia.
7. Gut ischemia can elevate ammonia. Enterocytes require glutamine for energy; by interrupting this pathway, they may generate ammonia via anaerobic metabolism, much as other cells might generate lactate.
8. Medications, particularly valproate, can elevate ammonia.
9. Any elevated muscle activity or muscle breakdown, such as seizure or rhabdomyolysis, can generate nitrogen and hence transient hyperammonemia.
10. Any sarcopenia predisposes to hyperammonemia, as skeletal muscle is too sparse to reliably clear ammonia.
11. Inborn errors of metabolism involving the urease cycle are uncommon in adults but something to consider, especially if genetic testing is available to you.
12. Severe malnutrition, most often due to gastric bypass, can cause hyperammonemia. This is probably due to multifactorial causes, including sarcopenia and muscle catabolism, but malnutrition seems to induce a true hepatic steatosis is well (reversible if nutrition is restored). Radiographically and clinically this looks like MAFLD/MASH, but is not caused by metabolic syndrome or obesity, but the opposite state of malnutrition. (This phenomenon is also seen in Kwashiorkor.) Probably this is due to some synthetic dysfunction affecting beta oxidation and lipid metabolism, and/or absence of essential fatty acids—not clear.
13. Urease-producing bacteria can generate ammonia. This will usually be transient, since antibiotics will readily kill them. However, with a deep-seated infection such as an abscess, this may not be true and should be considered as an ongoing ammonia source. Examples include: Staph epidermidis and Staph saprophyticus, Helicobacter Pylori, Klebsiella, Nocardia, Cryptococcus, Pseudomonas spp., Corynebacterium, Proteus penneri, Providencia stuartii, and Morganella morganii
14. An especially important urease producer is ureaplasma, an atypical organism similar to mycoplasma, usually causing UTI or even STI. This will often not cause other signs of clinical infection, but can be a cause of ammonia production, and will not be grown on routine cultures (PCRs are needed on urine or BAL, or the Mayo Clinic has a blood PCR—all send-outs), nor covered with routine antimicrobials (atypical coverage, such as doxycycline, azithromycin, or levofloxacin is needed). This infection mostly occurs in the immunosuppressed, such as transplant patients, where it can cause occult pneumonia (an important and morbid cause of post-transplant hyperammonemia); consider it as well in anybody on rituximab or similar immunosuppression. It can also cause “sterile” joint effusions, so a patient on rituximab whose joint is tapped and grows inflammatory-but-aseptic fluid may be presumed to have progression of an underlying rheumatologic disease, have their immunosuppression escalated, and then end up with disseminated ureaplasma.
15. For the hyperammonemic due to malnutrition/gastric bypass: nourish with glucose and fats while limiting or holding protein completely in the acute period. This can be parenteral initially, as it’s easy to titrate protein in that fashion. Check and/or supplement everyone with micronutrients likely to be insufficient: high-dose thiamine, B6, L-carnitine, copper, zinc. Once ammonia stabilizes and clears, start to introduce protein cautiously, with the goal of eventually restoring an anabolic state to reverse the underlying steatosis. Go slow weaning everything to avoid rebounds.
16. Refractory hyperammonemia can be treated with dialysis (CRRT), though data is limited in this setting. Starting earlier may make sense, as osmolar clearance may be rapid once initiated and could precipitate cerebral edema if the osm load is already high. Some would add hypertonic saline with CRRT to try and mitigate this rapid osm drop, a common tactic in the ALF realm.
17. A common cause of proximal decompensation for these people is when micronutrient deficiencies starts to reduce gut motility, leading to poor tolerance of oral nutrition and anorexia. Once you fix these and the gut allows oral intake, their nutritional status can improve.
18. Lactulose and rifaximin can have some temporizing role in these patients, but a very short-acting one. They may also tend to worsen nutrition by accelerating gut transit time and filling the small-volume stomach.
19. The urease cycle scavengers sodium phenylacetate-sodium benzoate may help accelerate clearance of ammonia, if renal function is intact (they convert ammonia to PAGN which can be renally cleared). However, they are not a magic solution, take time to work, and do not address the underlying problem.

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References

• Extubation and the Myth of “Minimal Ventilator Settings”
• Why Physiology Is Critical to the Practice of Medicine: A 40-year Personal Perspective

Takeaway lessons

In Dr. Tobin’s opinion…

1. The common practice of pressure support trials on 5/5 cm H2O is unwise, because it’s too easy; even these “modest” amounts of support are much more than they will have after extubation, decreasing work of breathing by ~40%.
2. The idea that pressure support helps negate the resistance of the endotracheal tube is also erroneous; in the typical patient with a typical airway, the diameter of the native airway after extubation, and hence the work of breathing, will roughly approximate that of breathing through the ET tube (due to edema, etc). In other words, don’t try to negate that resistance; it will still be present later.
3. For Dr. Tobin, the sensible alternatives are T-piece or blow-by oxygen, or a 0/0 trial. He likes T-piece as it’s highly controllable for research, but those who prefer the patient to be attached to the ventilator can certainly do 0/0. (Note that no modern ventilator actually drops to zero pressure, usually offering about 1 cmH2O of support, but this is negligible.)
4. Each additional day on the ventilator increases the risk of VAP by about 1% and VAP has a mortality of about 70%. Getting off the vent ASAP is a vital goal.
5. Dr. Tobin thinks the idea of physiologic PEEP occurring in patients breathing on their own, including the obese, is a fallacy; once extubated, no PEEP is present.
6. There is no advantage in an SBT beyond 30 minutes; 30 will answer the question.
7. Respiratory muscle fatigue occurs in the vast majority of ICU patients, including after SBT; it has not been shown in fatigue studies using twitch stimulation of the phrenic nerve and similar work. If it does occur, it takes about 24 hours to recover.
8. The best marker of success on SBT is probably using esophageal manometry to assess work of breathing using the transpulmonary pressure. Short of this, look for clinical findings of work of breathing by visualization and palpation: any phasic contraction in the sternomastoids, phasic movement in the thyroid cartilage, and phasic recession in the intercostals/suprasternal fossa/supraclavicular spaces. Oxygenation is obvious from oximetry, and ventilation only needs to be queried if you have a concern about hypercarbia.
9. There is no role for the RSBI in evaluating SBT success. This tool was derived by Dr. Tobin as a screening tool for SBT readiness, i.e. a protocolized way to push clinicians to perform SBT earlier than they otherwise might by judgment alone. Patients should be screened by briefly placing them on 0/0 or T-piece, waiting about 1 minute to normalize breathing, then monitoring the RSBI for 1 minute. If <105, SBT can probably be done safely and has a good chance of success.
10. Transient apnea after transitioning to a spontaneous mode is usually not due to drugs, but stimulation of the Golgi tendon organs and mechanoreceptors caused by mechanical ventilation; this takes some time to reset.
11. The first treatment for a patient who appears agitated during an SAT/SBT is to speak to the patient, reassure them, and bring a level of calm. Dr. Tobin is not a fan of SBT with continued sedation as he would rather not muck with the medulla oblongata in these sensitive patients.
12. Dr. Tobin is not a huge fan of planned extubation to NIPPV except in niche cases; he would rather wait and see them failing, given the discomfort and risks associated with using CPAP/BiPAP. (Extubation to HFNC is no problem.)
13. In general, the SpO2 should be no higher than 90%. This places the patient on the steep portion of the oxyhemoglobin dissociation curve, making a fall in oxygenation immediate and obvious; a higher goal blunts the utility of this diagnostic tool.
14. For chronic vent weaning with a tracheostomy, trach collar trials are superior to a weaning pressure support strategy.
15. A protocolized approach to weaning is the only way to expedite the process; relying on clinician judgment and gestalt will always result in longer vent times.

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We explore the vagaries and nitty-gritty of drugs for seizure termination, including benzos and ASMs, with the great Tom Bleck, MD MCCM FNCS, neurointensivist, professor, and founding member of the Neurocritical Care Society.

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More reading

1. Status epilepticus in the ICU

Takeaway lessons

1. In the RAMPART study, IM midazolam (10 mg) achieved faster seizure control than IV lorazepam (4 mg), with most of the difference accounted for by the time needed to start the line. So if there’s no IV, use IM midazolam.
2. If there is an IV, there is no data on superiority of any benzo over any other. This makes it appealing to use lorazepam, simply because we have the most data surrounding its use. But use whatever.
3. It is often hard to truly know the timeline since seizures began, other than those already on EEG monitoring. Probably in many published populations, benzo non-responders may have been patients who were already seizing for some time. As soon as seizures begin, benzo-sensitive gaba A receptors immediately begin to be replaced by benzo-insensitive receptors (a phenomenon not seen when benzos are used for other applications).
4. Most seizures, even in the ICU, end in about 90 seconds. If you don’t witness the onset, you should probably plan to treat it. If you do, you should prepare to treat, but wait five minutes to see if it stops, our current cutoff for status epilepticus—most will stop before then. The caveat is that it’s not impossible some of these people who appear to stop convulsing have simply become non-convulsive… this generally takes longer (30+ minutes), but in critically ill patients all bets are off.
5. Meaningful respiratory dysfunction from benzos for seizures is vanishingly rare. Most patients who get intubated due to benzo-related sedation do so out of clinician preference, not true need. Consider a side-lying rescue position to maintain the airway, or an oral or nasal airway.
6. The VA Cooperative trial used a lorazepam dose of 0.1 mg/kg, one time, no cap. Most of the current guidelines now suggest giving a 4 mg dose, then repeating if necessary. If this still leaves you under 0.1 mg/kg, a third dose to finish it out is reasonable. Giving more than 0.1 mg/kg is probably not more effective. Six minutes between doses is sometimes recommended, but most would go closer to 4-5 minutes at most.
7. The goal is cessation of convulsions, or of any other clinical signs of seizure (twitches, eye deviation, etc). Ideally, the patient would then wake up promptly, but this is a rarity, especially in the ICU. This then leaves the question of whether the patient is still seizing, merely non-convulsively. This needs an EEG to answer, but the risk to the brain once convulsions cease is probably less, so you can probably wait for the EEG (rather than giving more empiric doses of benzos).
8. If not rousing, however, you should probably treat with an anti-seizure medication, unless rapid access to EEG can prove lack of ongoing seizure. The three studied in the ESETT trial were: levetiracetam 60 mg/kg, valproate at 40 mg/kg, or fosphenytoin at 20 mg/kg, all of which had about 40% response rate. This was used in patients still convulsing at the time, but efficacy can probably be extrapolated to non-convulsive patients (or prevention of the next seizure in delicate patients). The study was not powered to look at subgroups, and all three seemed equally effective.
9. Levetiracetam is most popular by dint of its ease of use, especially now that it’s available by IV push, and there are very few times it would be the wrong choice in this context. (Even in renal failure, the same load can be used; maintenance will simply be lower/less frequent.) For long-term use, it does sometimes cause behavioral problems, but that is not an acute issue.
10. 60 mg/kg is probably the right dose in most patients. Possibly less is effective in some cases, but it doesn’t seem to have toxicity at this dose, and higher doses probably reach adequate brain levels faster.
11. There is now some question whether introducing ketamine after the failure of the first benzo dose may decrease the chance of proceeding to require general anesthesia. This will be studied more in the upcoming KESETT trial.
12. When to intubate and induce general anethesia? For Tom, only if they’re still convulsing (after benzo + ASM), or proven to still be seizing by EEG. But it’s an open question. Rapid EEG devices are a great tool here. If there is absolutely no access to EEG, you should consider transfer to a center that has it, probably within an hour or so if not waking.
13. There may be some role for inducing “procedural sedation” with propofol without intubating, which will terminate seizures in some cases. But this is a challenge for most non-anesthesiologists.
14. Most induction meds for intubation have some anti-seizure effect, including etomidate, so there’s not much reason to use an unusual drug here. However, do use some kind of sedative, even if they’re already obtunded (please don’t merely paralyze).
15. If paralyzing with rocuronium (not a bad idea, due to the risk of hyperkalemia in some of these patients), consider reversing it after, if you plan to use clinical markers to monitor their status.
16. Once intubated, high dose benzo (usually midazolam) or propofol? No data on this, but benzos tend to cause more problems, such as long weans due to metabolites. Most ICU folks are more comfortable with high dose propofol.
17. If using midaz, use a loading dose of 0.2 mg/kg (loading propofol is probably not necessary though it was done in some trials), then start an infusion of 0.2 mg/kg/hr. As tachyphylaxis sets in fast, you may need to frequently increase the dose afterwards (hourly or so), tough to do without an EEG; propofol may be a better choice without continuous EEG.
18. Tom would empirically use about 80 mcg/kg/min propofol if hemodynamically tolerated, if EEG was unavailable.
19. Ketamine as an adjunct to general anesthesia has useful hemodynamic properties (e.g. added to propofol to combat hypotension), but also seems to have an effective anti-seizure effect on its own. It’s less clear about using it as monotherapy. For effective seizure therapy, go for a completely dissociative dose (e.g. 5 mg/kg).
20. Not all epileptiform activity on EEG needs to be treated by escalating therapy. This is pertinent to the rapid EEG devices that try to report seizure via algorithm, as they’ll generally alert for anything seizure-like, whereas not all of these truly need treatment.
21. Usually with propofol, barbituates, or inhalational anesthesia, the initial goal is burst suppression with 10 second suppression between bursts. (Even this may only control about 1/3 of patients, who may need complete flatline.) If using midazolam or ketamine, however, you may never achieve burst suppression (only around 1/5 ever will), yet you may still achieve seizure control.
22. Frequency of monitoring of continuous EEG depends somewhat on the situation, eg is the patient still trying to achieve seizure control/suppression or have they reached a fairly steady state. Note: an occasional self-terminating seizure (e.g. one a day) may not mean a patient is failing weaning, as an occasional seizure in the outpatient setting is not exactly an emergency.
23. Levetiracetam has been dosed as high as 6 g per day, which is usually tolerated, although behavioral problems are common. Adding additional agents is usually better than megadoses, but Tom prefers to add them one by one if seizures prove refractory; adding multiple agents at one makes it hard to pinpoint the cause of drug reactions. Clobazam is favored by some to help wean anesthesia.
24. Tom would most often use valproate as a second line. A single dose is safe even in pregnant women (pregnancy was not screened in ESETT, though it wouldn’t be continued in known pregnancy). Fosphenytoin is still reasonable, though has more complications, and was the most associated with intubation in ESETT.
25. Lacosamide is often underdosed; it’s best loaded with 10-13 mg/kg, monitoring the PR interval.
26. Phenobarbital is a good drug, especially in difficult to control patients, but start with an aggressive general anesthetic dose: 20 mg/kg load, usually hitting a serum level ~20 (then taper), and may need to go to 100-150 mg/kg to allow weaning of general anesthesia. Some patients will even wake up on these doses once they adapt. Halflife is around 120 hours, so if you make a change, give a load or expect to wait for steady state; pentobarbital is faster, but its cost has been exorbitantly raised, so if you use it, maybe load, then switch to phenobarb.
27. In new onset refractory status (NORSE), adding therapies fairly early like anakinra or tocilizumab (as they often have ample IL-1 or IL-6) can be wise. Treat vitamin deficiencies; vit D deficiency may be a marker that supplementation is beneficial. A ketogenic die can be tried fairly early, though it’s a lot of work for the dieticians and pharmacists to eliminate carbohydrates from meds (eg dextrose); the target beta-hydroxybutyrate level is not clear. Ganaxolone probably has little role now.
28. In general, partial/focal seizures probably do not need to be treated as aggressively as generalized seizures. There is likely a spectrum, based heavily on the extensiveness of seizure; complex partial seizures (focal with altered awareness) that persist past 10 minutes or so should probably be treated. Most would not intubate/induce general anesthesia for these, but would treat with ASMs, and benzos may not be needed. Absence status seems to cause no damage regardless of duration, though they can be terminated by benzos, and ethosuximide can be used.
29. If focal seizures arise from a foci such as intracranial hemorrhage, it’s usually worth using an ASM to try and prevent generalization, but understand that sometimes the focal seizures can’t be suppressed. (And if there’s a foci like a tumor, remove it—it will help.) Vagal nerve stimulators or direct brain stimulation may help with focal seizures too, and maybe transcranial current stimulation, all areas of research.
30. Don’t despair. About 35% of patients with super refractory status will return to their baseline. (35% will also die, but that’s not bad odds.)

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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