Welcome to the 51st Critical Care Congress. In this session, we'll talk about postpartum non-hemorrhagic complications, specifically focusing on amniotic fluid embolism. I'm an affiliated professional at Northside Hospital in the Critical Care Unit. Also, I'm an adjunct faculty at Georgia Baptist College of Nursing, Mercer University. I've worked in critical care for over the last 20 years, with the most recent 15 years in specialization and focus on resuscitative efforts and maternal quality improvement efforts with maternal resuscitation at our facility. In this session, we're going to discuss amniotic fluid embolism, the identification, and some focused initial supportive measures for amniotic fluid embolism. Our outcomes will include identifying the major elements of amniotic fluid embolism, discussing the treatment of amniotic fluid embolism, and implementation of management strategies of amniotic fluid embolism. When we look at the Center for Disease Control causes of pregnancy-related death in the United States between 2014 and 2017, we see that amniotic fluid embolism ranks about 5.5% of pregnancy-related deaths. Amniotic fluid embolism is something that is very rare. Most practitioners will see one, maybe two cases over the decades of their career. The incidence of amniotic fluid embolism ranges from 1.9 to 6.1 per 1000 births. A recent population-based study demonstrated an overall mortality rate of approximately 20%. Prior to this population-based study, historically, amniotic fluid embolism has been reviewed or studied based upon case study reports. Those mortality rates range between 0 and 100%. In the population-based study, it was found that 70% of amniotic fluid embolism occurs during delivery, with 11% specifically after vaginal delivery and 19% after cesarean delivery. Amniotic fluid embolism is a rare syndrome. Classic characterization or presentations are encompassing of cardiorespiratory collapse, increased pulmonary vascular resistance, and disseminated intervascular coagulation. This triad typically occurs during and up to 30 minutes after delivery. Although amniotic fluid embolism is rare, it should be continued to be considered in the differential in any peripartum cardiac arrest patient, inclusive of other differentials of pulmonary embolism, acute myocardial infarction, iatrogenic complications of anesthesia, and other differentials that are included. Risk factors for amniotic fluid embolism are surrounding situations where maternal and fetal fluids are potentially exchanged. These include operative situations of vaginal and cesarean delivery, placenta previa, placenta accreta, or abruption. Typical presentation for amniotic fluid embolism is sudden hypoxemia, hypotension, and coagulopathy. The diagnosis of amniotic fluid embolism is a clinical diagnosis. It generally occurs in relation to labor and delivery, and amniotic fluid embolism is considered in the differential in patients that are pregnant and or immediately postpartum with sudden cardiovascular collapse, sudden cardiac arrest, the development of seizures, the development of severe respiratory distress, and the development of severe hypoxemia, especially if these events are followed by coagulopathy without another explanation for the development of coagulopathy or disseminated intravascular coagulation. A little bit deeper dive in that clinical presentation, specifically looking upstream at the mental status perspective. These patients classically have periods of anxiety, changes in mental status, and a sense of impending doom. And these mental status changes or mental status alterations generally precede cardiovascular collapse. And very commonly, these patients will have cardiovascular collapse, including pulseless electrical activity or PEA, asystole, or VTAC, VFib. So when we look at proposed pathophysiology for amniotic fluid embolism, there's still a lot of discussion in the literature and a lot of conversation out there about the exact pathophysiology of amniotic fluid embolism. So there's kind of three big pieces. So you have this disruption of maternal-fetal interface. You have increased pulmonary vascular resistance. You have acute respiratory failure. And you have factor VII and platelet aggregation. The increased pulmonary vascular resistance is thought to be secondary to endothelium activation and mechanical obstruction. And the mechanical obstruction subsequently leads to the RV failure or the acute RV failure, leading to the symptoms of the patient. The acute respiratory failure drives the severe hypoxemia. And the factor VII and platelet activation drives the DIC, which contributes to the hemorrhagic complications that are associated with amniotic fluid embolism, up to and including hemodynamic instability. There is a lot of conversation around this being more of an anaphylactoid type of response as opposed to a truly embolic response, hence the endothelial activation as a part of the proposed pathophysiology. When we think about the treatment of amniotic fluid embolism, treatment is really focused on stabilization and supportive care. And this is done best with a multidisciplinary approach, inclusive of critical care medicine, maternal-fetal medicine, and obstetrics working together to care for this patient. Management is focused on rapid management of hemodynamics and supportive care. The early identification or the early placement of emphasis on amniotic fluid embolism for patients that have cardiovascular collapse and cardiac arrest is essential for initiating treatment strategies and management strategies early on. When we take a look at the supportive measures for patients with suspected amniotic fluid embolism, there are a series of things that come into play. And so we have a patient that has suspected amniotic fluid embolism. They have a cardiopulmonary arrest. We want to obviously rescue that patient. We want to provide the appropriate resuscitation with high-quality CPR. Some key things around high-quality CPR, our hand position is the same for pregnant versus non-pregnant patients. The other significant piece is left uterine displacement, which we will talk about in a little bit more detail later on. Considering early delivery, so cesarean section or vaginal delivery, this is where the collaborative multi-professional team approach comes into play. We'll talk a little bit about perimortem c-sections or resuscitative hysterotomies for the patients of amniotic fluid embolism. And then early phases of amniotic fluid embolism show elevated RV pressures that are significantly, bedside echo is very helpful here, subsequently leading to a second or a late phase of LV failure and cardiogenic pulmonary edema, and then the addition of the coagulopathy, which may be immediate or delayed, requiring massive transfusion and the treatment of uterine atony that may develop. The following few slides, we're going to dig in detail into the supportive measures a little bit more specifically. We're going to focus on the initial resuscitation and management. I know that this may not be the direct piece of amniotic fluid embolism, but managing the initial resuscitation is going to help facilitate time to work through your differential diagnosis, as well as provide some potential improvements in return of spontaneous circulation for mother and some outcomes for baby. So the mainstay for cardiopulmonary resuscitation, even in pregnant patients, is the initiation of high quality chest compressions. And an important factor here is noting the kind of the start time. And the reason that the start time is beneficial is the decision to make about delivery and the timing of delivery kind of has to do with the length of resuscitation. Just as a reminder, for pregnant patients, compression rates are at 100, 2-inch depth, minimizing the interruptions, max 10 seconds, the hand position is the same. The addition here is the addition of continuous left uterine displacement. So for pregnant patients that suffer cardiopulmonary arrest or cardiopulmonary collapse, manual left uterine displacement is a key piece of the basic support system or basic life support for these patients. They have significant fetal aorta cable compression, increasing afterload can significantly decreasing preload significantly. And so left uterine displacement will hopefully help improve afterload, reduce afterload and will increase preload and hope to improve cardiac output to some extent. And as you can see on the slide, there's a couple of different, there's a one-handed method and a two-handed method. Left uterine displacement is typically initiated in someone who has peri-umbilical presentation despite the weeks of gestation. If you're unsure of the weeks of gestation, you're going to use left uterine displacement. And left uterine displacement is going to be maintained until delivery. Once delivery has been completed by OBGYN or maternal fetal medicine, then left uterine displacement can stop at that point. This is an, I'm hope to improve the cardiac output. There's already a significant amount of cardiac output that's going to the uterus and to the fetus. And so improving cardiac output is the overall goal here. So when we're thinking about these patients as a part of the management strategy for amniotic fluid embolism is these resuscitative measures. And one of the significant pieces of doing a resuscitative hysterectomy is the location. Where should we do it? What is the timing? How should this work out? And what needs to happen is perform a rapid assessment and estimation of gestational age. The Society of Maternal Fetal Medicine recommends delivery of any fetus at a minimum of 23 weeks gestation or greater. There are reports and there are information within the literature that says that this can take place with improvement at 20 weeks, although there's no statistically significant evidence that supports using 23 weeks. Delivery should be performed as soon as possible. If return of spontaneous circulation hasn't occurred within just a few moments of onset. Typically, what will happen here is that you will interface with these patients. They will be in a PEA or they may be in a VTAC, V-fib. You will have done initial resuscitative measures and the patient is not responsive to those initial resuscitative measures. And that's the kind of the what I think about as the clue or the trigger to moving forward with your resuscitative hysterectomy. When you look at data related to emergency resuscitative hysterectomies in the setting of cardiac arrest and maternal outcome, and you look at moms that survive and moms that don't survive, and you look at the timing from arrest to that C-section, data reveals statistically the faster that we can do it, the higher the opportunity or the chances we are to have return of spontaneous circulation for mom, and the better chances we are to have optimal fetal outcomes. For this reason, there has been adopted this kind of four to five minute rule for delivery. And the reason that that kind of four minute rule, and from a critical care perspective, what I like to think about is you've done one round of CPR and resuscitation, and you have no improvement. You're at your two minute mark. You're starting to move forward, and you're no improvement. You're at your two minute mark. You're starting your second round. Things you don't believe are going to turn around quickly. At this point, you have to start to pull your obstetrical and your maternal fetal medicine colleagues in and have them prepared to start for delivery. And we do that at the place of delivery. We do not delay delivery. We do not transfer. We know by transferring a patient that's in full cardiac arrest for a C-section in the labor and delivery OR is a significant amount of delay of time. And what we have seen, and Littman et al, and Rose et al found in a couple of different studies, was the goal here is to optimize fetal outcomes. And then 74%, 23 out of 38 women that underwent a perimortem C-section resulted in a viable newborn. Goals for maternal hemodynamics were optimized, and 55% of patients that had a resuscitative hysterotomy resulted in substantial improvements in maternal hemodynamics, with a third of those patients having a benefit of survival of maternal survival with no instances of detrimental effects. So a third of these patients went home with no significant morbidity or neurologic dysfunction. 60% proved to have an increase in cardiac output following delivery, and 67% had a return of spontaneous circulation. So in the obstetrical and gynecologic world, and maternal fetal medicine, this paradigm shift has been going on for a little while. And if you work in a critical care unit where you see a lot of obstetrical patients, this kind of perimortem cesarean delivery is kind of moving itself to a resuscitative hysterotomy or an emergency delivery perspective, with this focus on that four to five-minute mark, making that delivery, and really hoping to optimize the outcome for both fetus or baby and mom. Again, here is an additional set of data. This was a study that was done, a randomized control trial. Participants, this was a simulation. This is not something that you can randomize control trial very easily. So participants knew they would be involved in a simulation that would require a resuscitative hysterotomy, and they knew the location at the bedside or in the OR. There were 14 cases that were evaluated, and you can see the difference here. The resuscitative hysterotomy in the labor room or the site of code was an average of four minutes and 25 seconds compared to transfer to the OR, which was almost eight minutes. So delaying the resuscitative hysterotomy until transfer can significantly delay the abdominal incision and other tasks that are focused on optimizing return of spontaneous circulation and improving fetal outcomes. Inva and Kaufman noted in a review of 94 published cases of maternal cardiac arrest, only 7% of these patients were delivered within five minutes. And so this look, and this was data is a little bit historic at 2012, and there's been a lot of strides to have this resuscitative hysterotomy happen at the site of arrest. And I think that's a big key piece when we tie it back to amniotic fluid embolism is that you want to make sure that you are resuscitating the patient, that you're delivering the baby, that you're managing the cardiopulmonary arrest as a part of amniotic fluid embolism with the forward thinking that RV failure is going to be a significant piece, that LV failure is going to be a significant piece, and coagulopathy are going to be a significant piece. And so despite being focused on the resuscitation piece, we also have to be thinking about the anticipated next steps about how to manage the sequela of the RV failure, the subsequent LV failure, and the DIC. Briefly, post resuscitation care for amniotic fluid embolism patients matches any other post resuscitation care, including targeted temperature management. There have been very few case reports of antepartum or peripartum targeted temperature management. And the thought here and the literature reveals that really we're going to cool patients, we're going to avoid fever, because we know fever causes some significant neurologic dysfunction, with the focus on monitoring for this coagulopathy, especially in the setting of the emergency section, the risk for coagulopathy with being very hypothermic, compounded with the risk for coagulopathy with amniotic fluid embolism. So in these cases, it may be better to focus on a temperature of 36 degrees Celsius compared to going down to the lower degree Celsius of 34. Moving away from resuscitation and the cardiopulmonary collapse with amniotic fluid embolism into kind of this early phase and second or late phase of cardiovascular management. In this early phase, these patients are going to have elevated right ventricular pressures. ECHO is going to be your friend at this point to get an evaluation of the RV, looking for things like McConnell sign or left ventricular or interventricular septum impingement into the LV, worsening cardiac output. This right ventricular elevated pressure, secondary to this endothelium activation and microobstruction can cause severe RV dilation, severe RV pressure overload and acute RV failure. Followed in the second phase, which we'll talk about, about LV failure leading to cardiogenic pulmonary edema, complicating hypoxemia in these patients. Right ventricular failure is acute with amniotic fluid embolism. You have a severely dilated hypokinetic RV with acute corpulmonal. You'll get Boeing or that McConnell sign of the interventricular septum into the left ventricle, worsening cardiac output for the patient, worsening hemodynamics, making the patient more hypotensive. You want to avoid the following things, things that are going to worsen RV failure, hypoxia, acidosis and hypercarbia, which are going to worsen pulmonary vascular resistance and worsen this RV failure. One of the suggested treatment strategies through the Society of Maternal Fetal Medicine and their guidelines on the management of amniotic fluid embolism is to kind of focus initially on managing this RV failure with the forward look of the fact that you know that there may be significant LV failure and cardiogenic pulmonary edema. So we have to start to think about fluid management here. And there's a lot of discussion about fluid management and figuring out the appropriate amount of fluid and how much fluid into little fluid. And so with amniotic fluid embolism, you're clearly going to volume resuscitate these patients. There is this component of DIC where they may need massive transfusion, but you're going to want to keep in mind about your fluid volume assessment and reassessment and management for these patients because the excessive fluid will cause worsening RV failure, worsening bowing, worsening cardiac output throughout the left ventricle. So fluid management in these patients can be a little bit tricky. So some therapies that are helpful for RV failure, kind of improving that RV output is inotropes. You can try dibutamine or milrinone. I will say about dibutamine, it's at lower doses. It's a two and a half to five mic per kilo per minute. Higher doses may compromise the RV filling time because of the excessive tachycardia that happens with the dibutamine. Milrinone at 0.25 to 0.75 mics per kilo per minute. It's a common side effect of systemic hypotension. There are other additional agents that can aid in pulmonary vasodilatation. Inhaled prostacyclines and intravenous prostacyclines are here. Again, both of these can cause systemic hypotension, some nausea, vomiting, jaw pain, and diarrhea. Sildenafil has been used 20 milligrams enterally, whether that's oral, if the patient's awake, versus enteral. My experience with these patients has told me that most of these patients are intubated and are extremely hemodynamically unstable and require some type of enteral access. And then inhaled nitric oxide between five and 40 parts per million, again, with the focus of monitoring the methemoglobin levels to not become too terribly toxic. And an important thing about nitric oxide is you want to wean and taper it off. You don't want aggressive disruption of it because it will cause some rebound pulmonary vascular, increased pulmonary vascular resistance and worsening the function of the RV. And for patients that have hypotension, the preferred vasoconstrictors of choice are going to be norepinephrine and vasopressin. And that's even true outside of RV failure. Norepinephrine and vasopressin are going to be beneficial to you for managing hypotension and hemodynamic compromise secondary to amniotic fluid embolism. Subsequent to the RV failure, which sometimes can resolve, I've seen as quickly as 15 to 20 minutes. Sometimes it takes several hours to resolve. But there will be this very intense hypoxemia. There'll be this very intense RV failure. And you'll be managing those things with those RV failure tactics. And then the patient will have this LV failure that develops. And so, again, that fluid assessment and watching out for that intravascular excessive fluid replacement, watching out for that development of the LV failure, things like cardiogenic pulmonary edema, which becomes a very principal finding in amniotic fluid embolism, specifically after the RV resolves, is they've had all this fluid during the code. They've had all this fluid during massive transfusion. And now your RV starts to wake up and work again. And you mobilize this fluid forward. And it winds up in the lungs with this significant cardiogenic pulmonary edema. LV failure treatment strategies obviously include optimization of cardiac preload, vasopressor use for hypotension. Again, norepinephrine and vasopressin are the vasoconstrictors of choice, reaching for your inotropic support, utilization of your echo, serial echoes, other ways to manage and look at hemodynamics. Diuretic therapy for pulmonary edema is a commonstay for amniotic fluid embolism treatment. And dialysis may actually be needed for diuretic-resistant or diuretic-failed patients. Kind of the third piece of amniotic fluid embolism is this coagulopathy. It can be immediate or delayed. My experience, I've seen it most of the time in the immediate perspective. Most of my experience has given rise to massive transfusion requirements and then the treatment of uterine acne. DSC is present in up to 83% of the cases. It can occur in conjunction with cardiopulmonary arrest or after resuscitation is complete. And it's generally manifested very classically with hemorrhagic complications of surgical site bleeding, GI bleeding, vaginal bleeding, hematuria, and very classic DIC consumptive coagulopathy findings on labs. Low platelets, elevated INR, and depending upon the significant amount of blood loss, anemia as well. The treatment for DIC can be seen immediately instituted during cardiovascular collapse or even in the later phases of amniotic fluid embolism as a syndrome. There'll be need for early rapid assessment of clotting factors, including CBCs and DIC panels inclusive of PT, PTT, INR, and fibrinogen levels. This may require simultaneous medical and surgical intervention. Medical therapy in relation to massive transfusion and replacement of clotting factors and surgical intervention if necessary to control bleeding. And so there is a work here, again, from a multidisciplinary perspective to combat this DIC from both angles. General speaking goals, hemoglobin is greater than seven or if there's significant hemodynamic compromise or tissue dysoxia may indicate for a higher level of hemoglobin. Platelet count goals greater than 50,000 and a goal towards a normalization of a PTT, INR levels and normalization of fibrinogen as well. My experience tells me that most of these patients will need massive transfusion. These patients will need a traditional kind of one to one to one ratio of transfusions, that kind of classic kind of trauma, massive transfusion. The problem here is that the patients are going to need these transfusions and maybe even need massive transfusions, and that's going to impact that whole kind of fluid balance that we talked about a little bit earlier. So that kind of cognizant, like looking at all of these things together and then being aware of transfusion related syndromes that are associated with this as secondary complications from managing it. The big focus here with the DIC with amniotic fluid embolism is that during these cases there's a lot of emotion, there's a lot of anxiety, there's a lot of moving parts, and the part of the treatment strategy specifically from a critical care perspective is to kind of keep in mind that you have these three buckets. You have the code of the cardiovascular collapse piece, you have the kind of the RV failure, respiratory failure piece that's usually transient, and then you have this DIC component that's immediate or delayed. And to kind of manage all of these things together requires that multidisciplinary team approach. Here are references utilized in the development of this presentation for amniotic fluid embolism, additional resources. In summation, amniotic fluid embolism is something that happens infrequently, even rarely, and some providers may never encounter amniotic fluid embolism. Some may only once or twice in their career. Some, depending upon delivery numbers, may see it more often. It's been my experience in the last 10 years, I've seen about four to five cases I've managed and facilitated and assisted with resuscitation in these patients, and they are very complex. And so again, to summarize, cardiovascular collapse is managing the cardiopulmonary resuscitation, having that focused on the RV failure, the hypoxemia, which again is transient, sometimes as quick as 15 minutes, up to 30 minutes that will resolve itself, and then the subsequent LV failure and cardiogenic pulmonary edema, and then managing the septic shock. Thank you for your time. Thank you for your attention.

Amniotic fluid embolism

childbirth complication

cardiorespiratory collapse

pulmonary vascular resistance

disseminated intravascular coagulation

maternal-fetal interface disruption