Hi, guys. Thank you guys for coming. I know there's lots of sessions at 7 a.m. My name is Miriam Kaus. Thank you guys for joining in the session. So as you guys can imagine, it's a very broad topic that all of us are going to struggle to squeeze in all the time. I just wanted to go ahead and introduce some of our speakers. We have Dr. Steven Lipinski. He's going to be going through our first lecture. Carolyn D'Ambrosio is here as well, and Lisa Torres. Hold your questions until the very end, and hopefully this is going to be a good talk, and everyone's going to start thinking about any questions you guys have. As I said, it's a very broad topic, but we'll do our best to try to get everything in in an hour, and we'll get started right on time, in about two minutes. Okay, so just to keep the time going, we'll start right away. So I'm talking about physiological changes in pregnancy. I'm Steven Lipinski from Toronto, and I have no conflicts of interest relevant to this talk. So to begin with, just a brief case example to give you an idea of what we're talking about. So imagine you're seeing a 26-year-old woman, 28 weeks gestation. She comes in with hypoxic respiratory failure and bilateral infiltrates. This case was actually a pre-COVID example that I had, but this is also COVID. And there's her chest x-ray. So you can see the small lungs and the elevated diaphragms, the bilateral infiltrates. There's a lead apron across her abdomen. You can see the monitor showing saturation of 79%, and the blood gas, pH 7.29, PO2, 52 millimetres of mercury. So generally, I think the reaction of most people is something like this. And this is what we're going to cover today. So these are the session objectives listed, but mostly what you want to do is change your approach so you're not as anxious when you see this patient, and you can have a smiling face. So physiology. There are a number of anatomic and functional effects that take place, and the most important for us is upper airway edema and friability occurs, related to a number of hormonal changes. This is going to make intubation much more difficult and risky. You can have bleeding of the upper airway. If you stick tubes in the nose, they're likely going to bleed as well. And we'll hear more about the airway management later. The functional effects, there's an increased respiratory drive, mediated by progesterone, and this causes an increase in tidal volume rather than respiratory rate. This is a study of 1,000 women tracked through pregnancy, measuring their vital signs, and you can see the respiratory rate pretty much remains stable at about 14 per minute. 20 is the 90th percentile and 20 to the 97th percentile, so there's no increase in respiratory rate. And this is a much older slide showing a perhaps 10 percent increase in respiratory rate. Tidal volume increases by about 40 percent, and because the dead space is unchanged, all that tidal volume goes to the alveolus, so alveolar ventilation goes up by about 60 percent. There's a small change in total lung capacity, but there is a significantly reduced functional residual capacity, so less reservoir of air at the end of a breath. There's increased oxygen consumption and increased CO2 production, reaching about 25 percent above baseline. And these two facts, the reduced oxygen reserve and the increased oxygen consumption, mean the pregnant patient is going to desaturate much more quickly when they become apneic or if they hypoventilate, for example, during intubation. So blood gas in normal pregnancy shows a mild compensated respiratory alkalosis, pH slightly elevated. The CO2 runs at about 28 to 32, and the bicarb is down to about 20 to compensate. Now, during COVID, we called for a bunch of patients with blood gas looking like this, and the initial interpretation was a metabolic acidosis. The pH is down, the CO2 appears normal at 40, and the bicarb is low at 20. But remember, this is not a metabolic acidosis in the pregnant patient. This is a respiratory acidosis where the CO2 has risen and the bicarb hasn't had a chance to compensate. So these are patients with hypercapnic respiratory failure. So dyspnea in pregnancy, there is a physiological dyspnea of pregnancy. It's quite common, occurring in about three-quarters of women by the third trimester. And now, the mechanisms of dyspnea are too complicated for this talk, because I don't really understand them. And there are a lot of studies that have been done in dyspnea of pregnancy. So these two Canadians, Dennis O'Donnell and Dennis Jensen, a bunch of studies, and I'm not going to go through them either, because I don't understand them. But net effect is that mechanical and muscular factors don't play a role. It's not related to chemoreceptor sensitivity. It's not related to central drive. But it's really a normal awareness of the increased ventilation. And this causes the pregnant woman to be short of breath. It's an isolated symptom with an otherwise normal history and physical. It does not interfere with daily activities, but important to differentiate from other cardiorespiratory diseases. And often, these patients would need a brief workup to make sure there isn't a lung problem or a cardiac problem. Now, a question about fetal oxygenation. Us adult physicians worry a lot about the fetal oxygenation, I think far more than the maternal fetal medicine physicians. So let's talk about that. So oxygenation is determined by the placenta, and there's nothing we can do about that. And then, uterine oxygen delivery. And as with any organ, this depends on oxygen content, which is hemoglobin and percent saturation, and then blood flow. And the uterine blood flow is normally maximal and can be decreased by catecholamines, either endogenous or exogenous, by alkalosis, by hypotension, and by contractions. So what should we target the blood gases in pregnancy? So we often see suggested numbers like a set greater than 95%, for example, in this review here. But is this, in fact, true and necessary? When you look at the fetus, it works on very low oxygen saturation. So what's going to the fetus from the placenta has an oxygen at about 30 millimeters of mercury and returning at about 20 millimeters of mercury. And the fetus manages this by the left-shifted fetal oxygen dissociation curve of the fetal hemoglobin. So a woman with a PO2 of about 80 millimeters of mercury has a roughly similar oxygen content as a fetus with a PO2 of 30 millimeters of mercury. So that's one mechanism. Now remember, oxygen delivery depends on cardiac output, hemoglobin, and oxygen saturation. And when you think about it, the saturation is in a very narrow range, the hemoglobin less narrow. But the big effect is the cardiac output, which can increase by fivefold, making a big effect on delivery to the fetus rather than the actual saturation. The other factors that play a role as well. If the fetal oxygen saturation is low, there's an increased oxygen transfer. If the maternal PO2 is higher, there's an increased oxygen transfer. So the fetal PO2 and the fetal blood flow also play a significant role. Now is there data? There are a bunch of studies from the 70s and 80s looking at fetal growth restriction in rats and in sheep. But animals have very different physiology and anatomy. The gross anatomy of the placenta is different. The flow of blood in the placenta is different. And even a different number of cell layers separating the maternal and fetal circulation. So you really can't take anything from animal studies. In terms of human studies, very limited. There's one study I'm aware of where 10 women were subjected to 10% oxygen for 10 minutes during fetal monitoring. And there was no change noted in the fetal monitoring or in the middle cerebral artery Doppler, suggesting no concern to the fetus in this one study. Now remember, excess oxygen is dangerous as well. This is data in the non-pregnant patient showing that as you increase the oxygen, the cardiac index goes down related to an increase in total peripheral resistance. And when you look at the pregnant patient, the changes are even more marked. So giving excess oxygen to the pregnant patient may reduce oxygen delivery and actually make fetal oxygenation worse. And the American College of Obstetrics and Gynecologists suggested that you should not routinely apply oxygen when you get an abnormal fetal heart rate tracing, which was the practice previously, because it may have a deleterious effect. So hypoxia is likely dangerous to the fetus. The precise levels and duration unclear. Remember blood flow as well. We use similar targets to the non-pregnant patient. And remember that hyperoxia is also dangerous. So what about CO2 targets? So when you look at it, the low CO2 in the pregnant patient is to allow a gradient for excretion of CO2 from the fetus. There's also a transfer of bicarb across the placenta. And in some animal models, the bicarb does not cross the placenta, complicating the interpretation. So if you have a high CO2 hypercapnia, the effect is going to be fetal acidosis, which may right-shift the fetal hemoglobin curve, decreasing its oxygen-carrying capacity. And the net effect would be decreased fetal oxygen delivery. If you have a low CO2, that's going to cause uterine vasoconstriction we already mentioned. And the effect of that is going to be decreased oxygen delivery. So very high or very low is potentially bad for the fetus. Now there's, again, limited old data from the 70s and 80s in pregnant ewes, suggesting that moderate hypercapnia is safe. There are also reports during cesarean section in the good old days, before ethics was clear, where pregnant women undergoing C-section were allowed to have their CO2 rise. And in fact, the fetuses generally did better than ones where the CO2 was not allowed to rise. And there are case reports of asthmatics with CO2 up to 114 millimeters of mercury with good outcome. Now low CO2 is also bad for the fetus. Overventilation reduces utero-placental blood flow, but it also causes fetal cerebral vasoconstriction. So a double whammy on the fetus. So low CO2 potentially very bad. So low CO2 clearly dangerous. High CO2 unclear. Moderate levels may be well tolerated. Many of our COVID patients we ran had CO2s of 40 to 60. We didn't study the babies in detail, but everyone did fine. But really what it amounts to is it's a balance between injurious ventilation. So if you're going to get those CO2 levels down to 30, you're going to damage the mother's lungs. And balancing that with mild hypercapnia in the fetus. And I think we would prefer to not damage the mother's lungs and keep the mother alive through the episode of ARDS. So what about pulmonary physiology in disease? So just two quick examples. We previously looked at pregnant women with severe restrictive lung disease through pregnancy. And when you look at spirometry early and late in pregnancy, there's very little change. It doesn't change dramatically. Some women actually had an improved FVC. Some had a slightly decreased FVC. There wasn't really a trend related to whether this is parenchymal disease, kyphoscoliosis, or neuromuscular disease. But all actually did well with no major problems. Now ARDS, conventional wisdom would suggest that a decrease in chest wall compliance and increased ventilator pressures in pregnancy is a problem. But is this in fact true? So recently during COVID, this Argentinian group, Daniela Vasquez, had a large number of intubated patients with COVID and actually studied prospectively, collected data. And they compared it with non-pregnant patients with COVID. And the feeling was that there was actually no significant difference in mechanics in the pregnant patient. In the non-survivors, there were similar changes, like the increasing driving pressure in the right-hand graph was a problem and associated with poor outcome, but not a major difference in mechanics. So final point is ARDS and delivery. Is delivery beneficial to the mother? During COVID, many centers routinely delivered pregnant women as soon as they were on a mechanical ventilator. And is this the correct thing to do? So pre-COVID, we actually retrospectively reviewed 10 women who delivered while on a ventilator with ARDS. We looked at data three hours prior to delivery, then two to five hours after, and 12 to 15 hours after. We also used oxygenation index, which is really the inverse of the PTF ratio and includes mean airway pressure. And we estimated respiratory system compliance. And we found no major benefit in everyone. So some of the patients with the worst oxygen, two of them with the worst oxygenation index, had some improvement. One in the bottom left had an increased and improved compliance. But you couldn't be guaranteed a benefit in every patient. Some patients had a small benefit. Not all patients benefited. Now this is a study from Taiwan where they looked at 71 patients where they had a protocol of delivering within 48 hours of transfer to the ICU. They analyzed the patients as those with obstetric and non-obstetric causes for respiratory failure. And there was a very small improvement in those with obstetric causes, but no improvement for the patients with non-obstetric causes. And of course, COVID gave us a lot of opportunities. So this is a study from Argentina and one from Israel. The Argentinian prospectively looking at 47 patients who delivered, there was a small improvement in oxygenation, which really doesn't correlate with mortality, but no improvement in driving pressure and no improvement in compliance. And similarly, the Israeli study, a retrospective study in 13 ICUs of 80 pregnant women who delivered, and there was really no respiratory improvement. So in terms of delivery, really the mother's well-being should come first. And there are potential harms to delivery. The delivery results in an increased central circulation as the uterus returns blood flow to the circulation. And if you've got someone with bad ARDS and right ventricular strain, you can flood the lungs and you can overload the stressed right ventricle and cause hemodynamic collapse. Also, the general stress of surgery in a sick patient. And this needs to be weighed against very potential benefits of reducing oxygen consumption and perhaps simplifying management. So there may be a role in some patients, but this should be an individualized decision and not something with a routine protocol of delivering every pregnant woman in the ICU. And finally, just to sum the whole session up, this is from the UK EMBRACE report. To treat women who may become pregnant, who are pregnant, who have recently been pregnant, the same as a non-pregnant person, unless there's a very clear reason not to do so. Thank you very much. Thank you, Dr. Lipinski, for that excellent physiology review. Aloha. Good morning. Thank you for joining us so early today on this session on airway management of the pregnant patient. I'm Lisa Torres. I'm an assistant professor at Weill Cornell, New York Presbyterian Hospital, and I have no disclosures. So today, I'm going to discuss some key considerations when evaluating a critically ill pregnant patient for intubation and approaches to airway management. So first, let's think about which patient factors complicate airway management in pregnancy. So some of these Dr. Lipinski covered earlier, but there's changes in the nasal mucosa and oropharynx that will make airway management more challenging for us. So increase in estrogen circulating leads to increased production of tissue hyaluronic acid. And a lot of you have heard of hyaluronic acid in the context of moisturizers and the beauty industry. It works the same way in the tissues, and so it enhances tissue hydration. And that contributes to capillary congestion and increased tissue vascularization. And so over time, what happens is you get hyperplasia and hypersecretion of the mucous glands. So it's believed that all of these factors contribute to narrowing of the OP diameter. So malempati-4 scores increase at the end of gestation for some patients. So this was a study out of the UK where they looked at pregnant patients at 12 weeks and they graded their malempati score. And then they looked again at 38 weeks and did a repeat examination. And so what they found is that malempati-4 patients actually increased by 34%. And you can see that all the other malempati grades had a corresponding decrease. So some of these patients converted from whatever grade they were, 1 through 3, over to 4. And the authors postulated that this increase was due to weight gain. It correlated significantly with fluid retention and that type of weight gain. Other things to think about are that airway changes may be more severe in patients that have hypertensive disorders. And so I've listed some of the hypertensive disorders of pregnancy here, eclampsia being one of the more common ones. And so in this study, the authors wanted to look at the incidence of hypoxemia in patients that were pregnant with hypertensive disorders of pregnancy and those that didn't have that. And they had two cohorts. And so I'll just highlight here at the bottom that the entire cohort combined was 402 patients. And they found that patients that had hypertensive disorders of pregnancy had double the amount of hypoxemia. And they defined hypoxemia as occurring at induction with a SpO2 less than 90%. So patients with hypertensive disorders of pregnancy are prone to hypoxemia during induction of anesthesia. And they also postulated in this study that this was due to increased airway edema and pulmonary edema. In another study, they looked at whether there was an association between preeclampsia and airway hyperresponsiveness. And so in this study, they recruited a group of pregnant patients with preeclampsia and a group of controls. And they stratified further those two groups into non-asthmatic, non-atopic patients, those who had asthma and atopy, and those who had atopy that were non-asthmatic. Let me just get my pointer here. And so when they administered this methicoline challenge, you can see that the preeclamptic patients had much lower levels. They were significantly different between preeclamptic patients and controls for all subgroups. So the airway may become more difficult during the course of labor and warrant reassessment. So this is an image here of a patient pre-labor that had malampati 1. And post-labor, she had converted to malampati 3. And so it's important for patients that have prolonged labor, and that's defined as labor longer than 20 hours, to be reassessed. Because you may think going into their labor course that, oh, they're malampati 1. We're less worried. And they're laboring, laboring, bearing down, and everything becomes more edematous and swollen. So very important to reassess these patients, because the airway situation, if you have to manage it, can change very quickly. Other considerations is that there's an increased risk of aspiration of gastric contents due to hormonal and anatomic changes of pregnancy. So we see distortion of the gastric anatomy due to the enlarged uterus, we see lower esophageal sphincter incompetence, and we see delayed gastric emptying during labor and opioid administration. And that's actually true whether the patient receives neuraxial anesthesia or if they receive IV parenteral opiates. So important consideration, once they start receiving those opiates by different routes, it's going to delay their gastric emptying and put them at risk for regurgitation. Then finally, obstructive patients have less tolerance to periods of apnea. So they have reduced FRC, as Dr. Lipinski discussed, and they have increased oxygen consumption due to the fetus and the uterus. So in a patient that's developing acute hypoxemic respiratory failure, rapid and elective intubation is recommended. Okay, so now you've decided that you need to intubate this patient and you're preparing for airway management. This is certainly a sphincter tightening event for all of us, but there's a lot of things you can do to sort of maximize patient safety as best you can and maximize success. So one interesting piece of literature that I found discussed using sniffing position for non-obese pregnant patients and a ramped position for obese pregnant patients. And as I was reading more about this, I started to question it and found sort of other literature that questions this too, that ramped position offers several key benefits, irrespective of whether you're obese or not. So it facilitates laryngoscope insertion. And so if you just look at this sniffing position patient, you can see this angle here between the chin and the sternum. It's sort of a pointy, sharp, you know, acute angle. And if you compare that to this ramped position here, and this is a woman who's ramped to about 30 degrees head up position, you can see this angle between her chin and her sternum has opened up a bit more. Okay, so that facilitates insertion of your laryngoscope. Also this head up position helps you recruit a little bit more FRC than if you were in a supine sniffing position. So that's another benefit of ramped position. And then just being head up reduces the risk of gastric regurgitation. So it kind of makes you wonder, should we be ramping all of our pregnant patients this way? Throwing that out there for people to consider. So for pre-oxygenation, standard is really to give nasal cannula at 10 to 15 liters per minute. Now that we have high flow nasal oxygen, people have begun to study this. And it's been shown to prolong safe apnea time compared with face mask pre-oxygenation. So this group compared high flow nasal oxygen with standard face mask here. And they measured N-tidal O2 after intubation. And this is considered a really good surrogate marker for denitrogenation. So after that, so you could see there was a significant difference there in terms of the N-tidal oxygen. But when they looked at neonatal outcomes, there really were no differences. You can see the PaO2 in the uterine artery. This is the uterine vein. pH, PaO2, PaCO2, APGAR scores, they were all similar between the two groups. So unclear if there's really a benefit there in terms of outcome. So when there's no time, when the tube needs to go in and you don't have time to set up, you don't have time to roll over a high flow and get it, you know, initiated and set up, there is one maneuver we can do. And it's called the eight deep breaths over 60 seconds. Okay. And so in this study, what they did is they gave a hundred percent to be a non-rebreather mask to patients. And they had a group that did four deep breaths and they measured the N-tidal oxygen. Then they had the eight deep breaths group, which is this open circle. And then they had patients who were doing just regular tidal breathing for three minutes, okay, prior to intubation. And what they found was that the eight deep breaths group was able to achieve a 90% N-tidal oxygen in those 60 seconds, 76% of the time. So if you're really, you know, in a pinch, the patient is crashing, you need to get the tube in, have them take, if you can, over 60 seconds, eight deep breaths on a hundred percent. And that should be enough to kind of get them into a safe zone. So for induction, we usually use rapid sequence induction. We use this for patients who are greater than 20 weeks that require general anesthesia and who have GERD. So generally you use RSI without mask ventilation because you want to avoid inflating the stomach. In the past, there had been a lot of talk of using cricoid pressure, but that use, it hasn't been shown to increase, you know, intubation success in this population. There's been mixed data on it. And so use of cricoid pressure should really be individualized. So endotracheal tube intubation under general anesthesia remains the preferred mode of securing the airway. But sometimes you might need a tube that's smaller in an adult person than a 7-0. And some of those cases you might think about putting a smaller tube in would be someone who you know has airway edema, who has a history of a difficult airway, and who has a difficult view on the first attempt. You might just switch out the tube. In terms of the technique, it's unclear right now. The literature on the use of video laryngoscopy versus DL is limited. It seems now that people are moving towards using DL more consistently. And so here on this cartoon on the left, I'm just showing a patient in the sniffing position that's sort of giving this problem I alluded to earlier where the distance between the chin and the sternum is very narrow. And so if you try to put a normal handle laryngoscope, if that's what you're comfortable using, you may not be able to fit it well into that space. They've actually created a short handle laryngoscope for this purpose. It's called the DADA laryngoscope, D-A-T-T-A, created by Dr. Dada at Brigham and Women's. And so if you're a person that does DL, you could consider using this device and it would help you in the sniffing position. But if you put the patient in the ramp position, you may open up that space much more and not need to switch to a smaller handle. So repeated attempts at intubation should be avoided because they can cause trauma, bleeding, or edema. And so data suggests that complications increase when there are two or more attempts made. So between every attempt, you should be trying to re-optimize in some other way. And that's just an image of the short laryngoscope handle compared to a standard. So nasal hyperemia and polyps further increase the risk of bleeding with manipulation. So nasal pharyngeal intubation should generally be avoided. If you do need to do it and you have no other options, then you should think about using a topical vasoconstricting agent such as phenylephrine, epinephrine, or oxymetolazone. In terms of rescue, second-generation supraglottic airways allow passage of gastric tubes. So it might be kind of hard to appreciate here, but in this particular device there's an extra port here. And so you can pass a 14 French OG tube into the stomach using that port and go ahead and evacuate everything, which will hopefully sort of protect the patient from any other complications. So this is one device, there's another. These are all second-generation that have this port. So in the situation of cannot intubate, cannot ventilate, this often unfortunately requires an emergency invasive technique. And those would be cricothyrotomy, transtracheal ventilation, which is illustrated in this cartoon here, and can actually be attached to low-flow oxygen if you use that technique, or tracheostomy. But consider, you know, just familiarizing yourself with your institution's difficult airway algorithms. There's one that's actually specific to obstetric patients, which is created through the Obstetric Anesthetist Association and Difficult Airway Society. And then there's the general one we've probably all heard of, which is just the American Society of Anesthesiologists Difficult Airway Algorithm. And so that's for general patients, but both of those algorithms are appropriate for these difficult airways. So to summarize some take-home points, physiologic and anatomic changes of pregnancy make patients susceptible to hypoxemia and airway bleeding. Close attention should be given to patients with prolonged labor, and even postpartum, as the airway can become more edematous. We've definitely been called to airways after the baby was born, where the patient had some other complication, like bleeding or PE. And so you have to be cognizant that these airways can remain edematous for some time, even after delivery. Consider ramp position. I would love if somebody would study this, and like just do that and publish that, but ramp position during airway management offers key benefits that reduce the risk of hypoxemia and gastric regurgitation, should we be doing it more. And then finally, my advice would be intubate with the device with which you're most comfortable to minimize repeated attempts on the airway. If you're comfortable with DL, even though there's a movement to VL, use DL. Do what you're comfortable with, you know, to be successful. All right, thank you very much for your time. Okay, so I will be talking about the non-respiratory obstetric emergencies. We're going to, my name is Miriam Kaus, I'm from UT Houston. So this is a very, very broad topic, as I had mentioned before. I'm choosing the three major indications for ICU admissions for our pregnant patients, and that's going to be hypertensive disorders of pregnancy, hemorrhage, and infection. So that we're going to go through the common emergencies and also the management for these emergencies. So approximately about 2% of the patients actually end up, pregnant patients end up in the ICU, and when this happens, mortality becomes high. The most common indications, like I mentioned before, is hypertensive diseases, hemorrhage, and infections. Overall, the mortality rate related to pregnancy in the U.S. is about 17.3 deaths, but what's very concerning to all of us is that actually this mortality rate has been increasing since the 1980s, whereas worldwide pregnancy-related deaths have actually been decreasing. And some studies show that more pregnancy-related mortality is about, about 60% of those cases are preventable, so we all should be acting on making that possible, and I know that's why you guys are all here. So the leading cause actually in the U.S. is CV-related diseases related to pregnancy. So when you have a pregnant patient in your ICU, really the approach should be multidisciplinary. I know you guys will all save the MFM phone number and find their spectra and save it in your, in your call room. So really you should involve the MFM team, anesthesia, pharmacy, and then your ICU physician. The first thing, the next thing you want to do is determine if it's a medical or obstetric-related disorder. So many medical conditions can actually closely mimic obstetric condition, so you want to determine is it primarily an obstetric-related disorder that's causing the issue, or is it a medical disorder? And in this talk I'm focusing more mainly on the obstetric-related condition. If there's multiple, multiple organ system failure, what is the risk of continuing the pregnancy to the mother and the fetus, determining if it's possible or not. If you are going to deliver vaginal or C-section, is anesthesia going to be involved, and you want to optimize your patient for delivery. So this is just a chart kind of showing that many of the clinical syndromes can mimic both obstetric and medical causes, and it's very important for you to determine what is causing the, your patient to end up in the ICU. So first thing I'm going to talk about is the hypertensive disorder. So if you, if a patient is pre-20 weeks, then it's going to be chronic hypertension. After that, it's really your gestational hypertension. And preeclampsia sets in if your blood pressure is greater than 140 over 92 times, and you have proteinuria, or you have an organ dysfunction. So that can include simple things like headaches that won't relent, or renal insufficiency, or impaired liver function. So really, you don't have to have proteinuria to count as preeclampsia, and the most important thing is that preeclampsia can actually occur after delivery as well. So you don't want to forget that in a patient who may be just newly postpartum and in your ICU. So it actually, studies have shown that about 30 to 50 percent of patients, pregnant patients, who end up getting gestational hypertension can, will go on to develop preeclampsia. So that's why it's so important to not ignore patients who are pregnant and may have hypertension but not have proteinuria. And in the future, these patients also have an increased risk for having CV disease and stroke. So the incidence in the U.S. is about 1 in 25 pregnancies will have preeclampsia. The pathophysiology behind that is really thought to be related to abnormal placentation, and I'm not going to go into the detail behind that. But remember, when you see these patients, even though they look super volume overloaded, they're actually very intervascularly deplete. So if you have a patient who looks very volume overloaded, maybe going for the Lasix is not the first thing that you want to do. If you have development of seizures, then that upstages your diagnosis to eclampsia, and that can develop in about 1 in 50 patients who have severe patient features. But even in patients who don't have severe patient features, 1 in 400 will develop preeclampsia, eclampsia. So again, the management is really going to be recognizing the symptoms and diagnosing the hypertensive disorders, and then blood pressure control. And the biggest thing actually is seizure prevention and thinking about delivery for the fetus. So ACOG recommends that if your blood pressure, if the patient's blood pressure is over 160, over 110, that's when you really want to start thinking about using an agent to lower the blood pressure. And your blood pressure goals are not going to be super stringent in trying to lower it to systolics of 100. Your goal target is about 130 to 150, and they're happy with that. The agents to use will be labetalol, hydralazine, or nicotinamide. And mainstay of treatment for this is going to be a magnesium sulfate. Loading dose is about four to six milligrams and grams, and then your patient will stay on the magnesium drip, on a maintenance drip, till you have delivery and about 24 hours post delivery. Of course, as you can imagine, if it happens post delivery, then 24 hours of magnesium therapy is going to be essential. When the patient is on magnesium, it's very important that you do regular physical exams, especially in an ICU where obstetric conditions are not commonly seen. And the reason is that at high levels, magnesium toxicity can actually lead to cardiac arrest. So if you get to about 30 milligrams per deciliter, that's when you start seeing the respiratory depression and cardiac arrest. So if you have a patient who is just recently on magnesium and they undergo cardiac arrest, this is something that should be on your differential. And the antidote to that is calcium chloride, five to ten milliliters, ten percent solution, or calcium gluconate. So when should you think about delivering? Really, if a patient has severely uncontrolled blood pressure or any of the other signs where end organ perfusion or deficiencies are happening, that's when you want to think about delivering. If the patient is past 37 weeks, there really is no hesitation that the patient should be delivered. So ACOG has a strong recommendation for that. The hairy zone is kind of 34 to 37 weeks. And before 34 weeks, you really will see if expected management is possible or not, and if delivery is the right way to go. If delivery is supposed to happen before 34 weeks, you want to give the steroids, and that's going to be beta-methadone as a preferred agent. Okay, and the next thing that we're going to talk about is perian postpartum hemorrhage, as this is the second most common indication for ICU admission. So if the patient is antepartum, the most common causes are actually placental abruption and placenta previa, likely because there's a lot of cases of C-sections, and so this puts patients at risk for having this type of hemorrhage. Postpartum, it's reported to occur in about 1 to 3 percent of births, and this happens very commonly actually in the rest of the world. Uterine atony is the most common cause for postpartum hemorrhage, so something to think about. And these hemorrhages usually will happen within 24 hours after delivery. Less common causes will be uterine rupture and uterine inversion. So after you identify the cause, you want to arrest the bleeding and manage the hypovolemia. These patients can quickly develop DIC, so it's really important to determine if the patient is having significant enough blood. As you can imagine, there isn't a clear-cut way to measure how much is too much. So if a vaginal delivery, you think over 500 cc's, that's when you want to start getting concerned. With a C-section, it's about a liter, but as you can imagine, it's very visually what you're determining, and not a hard and fast. So you have to weigh your patient's condition and the appearance of the bleeding. For pharmacologic interventions, oxytocin is going to be first-line. Tranexamic acid, methyl argonavine, and misoprostol are the other agents that may be utilized as well. The nice thing is that most hospitals will have a management algorithm for postpartum hemorrhage, and you really want to follow that. Is there a clear consensus recommendation for how much blood products should be given to these patients? There's actually not, but if you have significant enough bleeding, eventually you'll follow your institution protocols, and generally they tend to be RBC to FFP to platelets at 1 to 1 to 1. But again, I took the picture out. There's a very long algorithm for every patient who's delivered, what you should give, and what you go next. So if the pharmacological interventions are not enough, what are some of the next steps that we can do at bedside, right? So I'm going to show some pictures that my husband was about to have me take out, but this is some of the things that you can do. So you can do intrauterine balloon packing or intrauterine massage. So the provider has one hand inside and applying pressure on the outside on the uterus. Or you can also do internal manual compression of the aorta if the patient had undergone a C-section. But as you can imagine, if that's being done, you want to relieve the pressure every few minutes to make sure that the extremities are still getting blood flow. Depending on how bad the bleeding is, some patients may need to undergo surgery or removal of the uterus, but you want to try to avoid that at all costs. Okay, so if your patient, you know, ends up having significant enough bleeding and ends up becoming unstable, one of the first things we tend to think about is that the patient should be placed in a left lateral decubitus position, right, if they're still pregnant. And this is really to help the aorta cable compression. But what if you end up having cardiac arrest? So this happens in about 1 in 12,000 admissions for delivery, okay? Overall, if you address it fast enough, actually the survival can be up to 59%. So it's really important for us to manage these patients appropriately. But if the cardiac arrest happens, this is where you want to leave your patient actually in the supine position. And how you're going to manage the aorta cable compression is actually to use manual left uterine displacement. And it is possible, and there's a lot of case studies kind of looking at how you can do that while CPR is ongoing. They looked at some studies where the patient was in a tilted position or kind of turned and they found that patients were more likely to slide off or actually not get good quality compressions. So better to manage the patient just like any other patient who is undergoing chest compressions but do manual displacement of the uterus. Again, so there's no modification for application of electric shocks if you need to do it. However, the other thing that you want to start thinking about is how gravid is your patient, right? So if it's within the institution, depending on the patient, if they're 23 or 24 weeks and above, is to start thinking about when you are going to evacuate the fetus, okay? And again, this is based on just kind of case series but what they look at is that the longer you wait to take out the fetus, the less likely they will be neurologically intact. So the idea is that you want to try to evacuate the fetus within four to five minutes of beginning CPR but as you guys can imagine, that's very, very quickly. So usually it looks like the median time ends up being about nine minutes but if you look at the difference between neurologically intact and not good neurologic outcome, it's really within five minutes to 15 minutes, most of the newborns will be neurologically intact so you don't want to wait too long. So of course, there isn't a hard and fast data behind this but it shows that the aortic cable compression maybe that's relieved after the fetus is removed and the fetus having better neurologic outcomes, you should think about doing C-section within a few minutes of starting CPR. So the last thing that I'm going to talk about is sepsis and septic shock in pregnancy. If the patient is coming in with sepsis while they're still pregnant, it tends to be septic abortions, intra-amniotic infections like chorioamnionitis and pyelonephritis postnatal, the most common is actually endometriitis. Usually tends to be polymicrobial in pregnancy and unlike the other conditions that I just discussed, in general, delivery is not indicated when a patient comes in with sepsis unless the fetus is the cause of the infection. So unless it's chorioamnionitis, really you're not thinking about delivery very fast in these patients. Because most of these patients, the progression to septic shock is rare. Of course, if it happens, then the patient is more at risk. Again, in general, they end up being more polymicrobial infections and group A strep is one of the most common ones. So which vasopressor should you use? Really, your targets are going to be the same as your general population. So you're still targeting a map of over 65 and norepi is still the vasopressor of choice. But yes, there is a lot of phenylephrine use in OB literature and there's a lot of data behind that, but it's really after you get neuroxula anesthesia. So I would still use norepinephrine and then you're doing continuous fetal monitoring really to see how your fetus is doing because the microvascular shunting and organ hyperperfusion that happens with vasoactive agents can be a little bit underreported. So overall, the case fatality rates for sepsis are about 3.2 to 4.4 in the US, but it's still a major contributor to maternal mortality. So we definitely want to think about it. Okay, sorry. Very, very rapid that I went through everything. So just to take home points would be that hypertensive disorders are a serious maternal mortality risk. If you have a patient who's undergoing cardiopulmonary resuscitation, really think about doing a perimortem C-section within a few minutes. And manual displacement is actually better than trying to tilt them. And sepsis is often polymicrobial in pregnancy. Thank you. Okay, everybody, I will get through this. Thank you so much. What a great crowd to start our day. So I'm going to talk about respiratory emergencies in pregnancy and I'm going to focus specifically on pulmonary embolism and ARDS. There are my disclosures. The most important ones for this talk was that I borrowed slides from two of the other speakers. So this is Serena Williams. If you remember nothing from my talk, remember her story. She's a top level athlete. I would argue the best athlete in the world at her peak. She, in 2011, had pulmonary emboli and was diagnosed with a hypercoagulable state, was on anticoagulants. A few years later, she went off those anticoagulants to have the C-section to deliver her daughter. The next day, she had acute shortness of breath and pain in her back. She was discarded. Nobody believed her. Hours went by. She finally got pain medicine. She was told she was just anxious. This is a top level athlete who's short of breath. She shouldn't have been short of breath no matter what we did to her. She finally advocated for herself enough that she got a CT scan and was diagnosed with, guess what, a bunch of PEs in her lungs. And then she got anticoagulation and bled from the anticoagulation, but she represents what we do wrong with pregnant patients in regards to PE. Her symptoms were discarded. She's an African-American woman, and although she's very intelligent and well-spoken and medically literate, she knew her disease. She had PEs before. People still didn't listen to her. And she was in a top facility. They just didn't listen to her. And so, remember her story. Pulmonary embolism in pregnancy, it's not that uncommon. One to two every thousand. Four to five times higher risk of venothromboembolism in pregnancy, so you should be thinking about it. Every patient who potentially could have a PE, increase your suspicion. Acute PE counts for one in 100,000 deaths, or one death per 100,000 deliveries, right, despite prophylaxis in high-risk patients. Even if we're prophylaxing the high-risk patients, we still have deaths from this. And the symptoms are very similar to physiologic changes that Dr. Lipinski went over, the dyspnea, the swollen lower extremities, and tachycardia. The risk factors are the same for everybody else. Hypercoagulable state, vascular damage, venous stasis. And one thing that I think I learned while doing this talk, is that, or I probably learned it 1.30 years ago, was that the right iliac artery crosses over the left iliac vein. And so you have this pulsating thing right on top of a deep vein, and then you have a gravid uterus on top of that. And so the majority of DVTs in pregnant patients are on the left side. 50% of the emboli occur during pregnancy, and 50% in the six weeks postpartum, which means postpartum is only six weeks long, so your average daily risk of a venothromba embolism is highest in the postpartum period, exactly what happened to Serena. In 2011, ATS came out with these guidelines, and similar to the Royal College in London, they said D-dimer has no role. Well, more data has come. There's varying recommendations for using a D-dimer in pregnancy. Everyone panics, like Dr. Lipinski said. Everyone goes, oh my gosh, when they have a pregnant patient in the ICU who's having respiratory failure. And they're so concerned about doing the normal diagnostic test, but what would you do if they weren't pregnant? We would probably check a D-dimer unless they had a C-section and they were postpartum. VQ scan versus a CTPA, everyone's worried about radiation to the fetus. Well, the exposure is less than 0.01. These are, it's like rats, right? It's the exposure of how much radiation is absorbed. But what is really risky for the fetus is actually 0.1. So it's far below what you should worry about. So go ahead and get that VQ scan or that CTPA if that's gonna help you with the patient. The only thing I would say about CTPAs, which I think we all know, being pulmonologists, is that the more CTs a female patient with breast tissue has the increased risk of breast cancer in her lifetime. So this study came out a few years ago, the year study that wasn't part of pregnancy, but they looked at these criteria for figuring out our risk for PE. And clinical signs of DVT, hemoptysis, and is the PE the most likely diagnosis? And by using that, actually having to get a CTPA was reduced 14% across all groups, males and females, but of course, pregnant patients were not included. So in 2019, the New England Journal of Medicine published this paper, which was pregnancy adapted criteria for the year's criteria, which is what I just mentioned. And so it just is a very nice algorithm. Again, if you take nothing away from this, this algorithm here you should have on your phone or you should look it up very quickly if you have a pregnant patient and you're worried about PE. It really walks you through, is there a sign of DVT? If the answer to that is no, you have to go look for the D-dimer. And it's really the level of the D-dimer and the clinical risk way down here that is incredibly helpful. So if you go all the way down here, you order a D-dimer, and they have none of those criteria that we mentioned, and the D-dimer's less than 1,000, PE's ruled out, you don't have to do anything else. If they have one to three of those year's criteria, the sign of a DVT, hemoptysis, or increased risk for PE, and the D-dimer is greater than 500, you need to get the CT and it's everything else in between. This is an incredibly helpful algorithm and I would say that is one thing I would have in my back pocket if you see pregnant patients in your ICU or if you're a consultant. And so there are a bunch of studies, this is a nice slide from Dr. Lipinski about the different studies that looked at D-dimer in evaluating PE in pregnancy, and you can see a bunch of them there. The one I just mentioned here is probably the best one, if I had to say. And that allowed for, by using that criteria, that algorithm I just showed, CT was avoided in 39% of the patients overall and 65% avoidance in the first trimester, which is when we worry the most about teratogenicity, excuse me. So predictive testing in pregnancy. There's only a few studies that really help us a lot, some of them more recent. The problem is because there just aren't that many patients out there, right? So the value of the studies out there are not that good because you don't have 1,000 pregnant patients included in them, right? D-dimer, a negative D-dimer is extremely helpful, right? And then it can be useful if it's below the threshold and you have a low risk. They asked some, they had a witness aspiration or something like that that really causes their shortness of breath or you know what it is. But the most important piece of this, a missed PE can be catastrophic, right? Because then they have the next one that can really kill them. So we always have to weigh the risk, we have to use the scales, risk of hemorrhage versus risk of recurrent PE. And I would say for the most part, unless you really, really are sure they don't have a PE and that D-dimer is really low, I would risk getting a definitive study or starting anticoagulation if that's easy, if they're too unstable to go. And then what do you treat the PE with? Unfractionated heparin or low molecular weight heparin depending on the situation. The DOACs and the vitamin K agonists are not recommended in this situation in pregnancy. Hemodynamically unstable pregnancy though is just like hemodynamically unstable PE in a non-pregnant patient, right? We only have a few case reports using TPA, but TPA is the one that's used the most. There's some major bleeding in these case reports, but overall fetal fatality is pretty low. So TPA or thrombolysis can be used and thrombectomy can actually be used. And there's case series again, but the better maternal outcomes, but some worse fetal outcomes. So you really have to make that decision in the moment is what is my risk here? ECMO, there again, we have a lot more information on ECMO in pregnant patients because of COVID, but in for ARDS than we do for PE, but ECMO is available. And if you are an institution that can do it or you can send the patient there and they're that unstable, you should think about it, right? So you can see here VA and VECMO outcomes, there's very little data in pregnancy, but there is higher than what I expected maternal survival, 64.7% and live births greater than 70%. So better than what I had originally anticipated when I was looking into this. So for PE in pregnancy, please increase your suspicions, four to five times more likely to have a VTE in pregnancy than not. Listen to your patient, remember Serena. D-dimer can be helpful if it's very low and you're using the year's criteria. And don't be afraid of the CT or the VQ scan. Unfractionated heparin, low molecular weight heparin is the treatment of choice, but also thrombolysis, thrombectomy and ECMO. Remember the pregnant person is the patient, treat the patient. If the patient isn't doing well, the fetus isn't doing well. And so you have to sort of keep your mind wrapped on that because everyone does panic and feels quite paralyzed when they have a pregnant patient in the ICU because it's so rare. So just try to keep your wits about you. Now, adult respiratory distress or acute respiratory distress syndrome and severe hypoxemia in pregnancy. Significant mortality associated with this. I know Dr. Lipinski already went over your O2 and your CO2 levels that you want during pregnancy if you can. The incidence of severe ARDS is increasing in the U.S. over time. And of course, the COVID pandemic really increased that dramatically. But it is 16 to up to 70 patients who are pregnant per 100,000, right? So it's not a minimal amount. There are definitely pregnant patients who get ARDS and the mortality can be as high as 14% in these studies. This is a really nice diagram from a review in seminars in fetal and neonatal medicine. And I'm just gonna highlight here the conditions during pregnancy that increase risk for severe ARDS. Obesity, smoking, asthma, diabetes, hypertension, preeclampsia and social determinants of health. I think we all know that, but I think that it's always a good reminder of who's at risk for ARDS and having more severe ARDS than somebody without those conditions. We already heard about sepsis, but the causes of ARDS, they can get it from sepsis, they can get it from overdoses, air embolism, pancreatitis, aspiration, which is the one that I have seen the most in my career. And then the things specific to pregnancy, amniotic fluid, severe preeclampsia, ovarian hyperstimulation syndrome, tocolytic pulmonary edema, and then septic abortion, which unfortunately I think we might be seeing more of. And then that's a nice diagram to remind all of us how dysregulated the capillary alveolus interaction occurs with ARDS. Everything, you get your inflammatory condition, you get your alveoli filled with protein, very difficult for gas exchange. Another great diagram from that review. So severe ARDS has a mortality rate that can approach 50%, and here's all the studies that we count on in our daily lives in the ICU. ARDSnet, Proceva, Acuras, they're all about low tidal volume ventilation, prone positioning, neuromuscular blockade, the ROSE trial, et cetera. So we do this with patients that come to the ICU. If they're pregnant, we try to get that lung protective strategy, the low tidal volume, but not well studied in pregnancy. We try to keep the plateau pressures below 30, but it can be quite challenging, especially the more advanced the pregnancy is because of the gravid uterus. There are recommendations to use esophageal pressure monitoring if you have that ability within your ICU in your facility, and the pregnancy itself can increase risk of barotrauma. So use of sedatives and paralytics. Neuromuscular blockade can cross the placenta in variable amounts, so in general, if you can avoid an infusion and just give intermittent dosing, that might be better for outcomes, but little is known about this long-term. Again, you only have a handful of patients who actually are this sick every year who are pregnant, and so trying to get good studies out of this is difficult. You want to displace the uterus laterally to avoid compressing the aorta. An inhaled nitric oxide, which we use sometimes with severe hypoxemia. Safety profile is in a case series, again, not well studied, but a case series showing that it is reasonable to use to reduce the pulmonary vascular resistance in pulmonary hypertension during pregnancy. Prone positioning, when to consider it, and remember, I'm talking about a pregnant patient here. When the PAO2 and FIO2 is less than 150 and the PEEP is between five and eight, you should start thinking about it. You want to increase your end-expiratory lung volume, better VQ matching. This is all the stuff that we do with other patients, right? And then look at all those trials listed at the bottom that I mentioned two or three slides ago. The exclusion criteria included pregnant patients, right? So that's the problem. We have case series, case reports. We don't have a lot of good measures, but we do know that prone positioning does work in patients who are not pregnant, and so it's worth giving it a try if your patient is not oxygenating well with severe ARDS. And again, another really nice slide from that review. This is for COVID, and so I Xed out the COVID treatment, but the rest of there, that's a great slide just sort of summarizing a lot of what I've already mentioned the lung protective volume, the unknown effects of neuromuscular blockade, sort of where the gravid uterus and the belly, how you do it. And then there is actually this diagram here, which is really nice, sort of showing it to you with a pregnant dummy that is used in putting the rolls above and below the gravid uterus. There's actually a YouTube video that Dr. Lipinski told me about that you can watch. So if you're ever in that situation, you can't remember this slide, look it up on YouTube. And then remember your ECMO, VV and VA ECMO for the following conditions that are listed there. But for severe ARDS with hypoxemia, you definitely want to consider it. And then of course, ECMO has its complication, hemorrhage being the number one, right, because we have to anticoagulate them for it. And DIC, thrombotic events, preterm delivery. But again, the patient is not gonna survive unless you try some of these things, if they're that sick. Their ARDS is that severe. So in my practice, we try it. Because if we don't try it, the patient's gonna die anyway. So let's give it a shot and see what we can do. And that's the way I approach the families, to talk to them about consent. There is some data on fetal outcomes in patients who've had ECMO while pregnant. There are lower APGAR scores. There's infants sometimes are born needing respiratory support. But in general, again, they're alive, right? And so I think that, and these are smaller studies, and there's some review papers here. With decent outcomes, with 77% survival, the patient and 61% survival of the fetus. So it's worth a try. And I know I'm right at the end. So I will summarize, ARDS has a high rate of mortality in pregnancy. We have very little data on it. The big trials excluded pregnant patients. And so we just do our best and try our best. But remember who the patient is. It's that mass of cells around the fetus. So you gotta take care of the patient. Anyway, thank you very much. Thank you.

physiological changes

medical emergencies

pregnancy

upper airway edema

respiratory drive

complications

airway management

video laryngoscopy

non-respiratory obstetric emergencies

postpartum hemorrhage