Author: Brandon O

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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