SCCM Resource Library-Special Delivery: Critical Care of the Obstetric Patient

Video Transcription

Hello, my name is Richard Pino. Many of you have expressed interest in critical care of the obstetrics patients.  And whether you're in a community hospital or a tertiary medical center, often obstetric calamities can occur very acutely.  And critical care practitioners need the understanding to deal with this. So today's session is special delivery, critical care of the obstetric patient.  That will present three subjects of interest. The first is acute neurologic issues in pregnancy and in the postpartum period.  The second is either too much or too little clotting, because as we know that obstetric patients can have derangements of the clotting system.  And finally, organization of resources for the complex pregnant patient. Thank you. Thank you for the opportunity to talk to you today.  My name is Taylor Kimberly and I'm Chief of the Division of Neurocritical Care at Massachusetts General Hospital.  And I'm going to talk to you about acute neurologic issues in the obstetrical patient with a focus on preeclampsia and postpartum angiopathy.  Here are my disclosures, none of which are related to the topic of this talk. And I also want to acknowledge Dr. Scott Shankar of Maternal Fetal Medicine at Harvard Medical  School and the Beth Israel Deaconess Medical Center, who provided some of the slides that I'm going to share with you today.  So first, a little bit of background about intensive care unit admissions in the obstetrical patient.  The overall incidence of ICU admissions is about 2.7 admissions per 1,000 deliveries. In contrast to ICU admissions in the non-obstetrical patient, the most common diagnoses for ICU  admissions include hypertensive disorders, such as preeclampsia, accounting for about a third. And slightly less common than that is postpartum hemorrhage.  Conditions like sepsis and respiratory failure are less common in this patient population. And today I'm going to focus on the hypertensive disorders, such as preeclampsia.  I'm going to go through the evaluation and management of these types of patients through two case examples.  The first case is an 18-year-old G1 P0 woman who's 29 weeks gestation and presented to the labor and delivery emergency room with a headache and is found to have a blood pressure  of 175 over 115. Her laboratory workup reveals a urinalysis with 2 plus protein, a white count of 7, a  hemoglobin level of 11, low platelets at 90,000, an elevated liver function test at an AST of 250 and an ALT of 190. Her LDH is also elevated with an undetectable haptoglobin.  So in terms of thinking about this patient, how would you classify this patient's disorder and how would you manage her?  The options include A, she has preeclampsia and the appropriate treatment is an oral calcium channel blocker.  B, she has preeclampsia with severe features that should be treated with IV labetalol and urgent delivery. C, she has preeclampsia that should be treated with IV labetalol.  Or D, she has preeclampsia with severe features that should be treated with IV labetalol. And we'll return to the answer to this question after the following slides.  So it's important to recognize that preeclampsia is a spectrum disorder. At the milder end, it's characterized by gestational hypertension that emerges about halfway through  pregnancy and this is defined as a blood pressure of 140 over 90 without other evidence of end organ injuries such as proteinuria.  Preeclampsia is defined as having elevated blood pressure and in addition there's evidence of proteinuria.  Typically this is defined as a spot protein to creatinine ratio of 0.3 or more or a 24 hour urine protein level of 300 milligrams or greater.  Often this is screened through a urinalysis dipstick which shows proteinuria. At the more severe end of this spectrum disorder is preeclampsia with severe features and this  is characterized by an elevated blood pressure of greater than 160 to 110, evidence of proteinuria  and in some variants such as preeclampsia with help there can be low platelets, less than 100,000, elevated LFTs greater than two times the upper limit of normal, evidence  of renal failure with a creatinine of 1.1 or greater or pulmonary edema. When eclampsia or HELP emerges, this can occur even in the absence of an elevated blood pressure  and of course eclampsia is defined as the presence of seizure activity and HELP which is also known as hemolysis, elevated liver enzymes and low platelet count, can also present  without the elevated blood pressure abnormality. There are a wide variety of signs and symptoms that are associated with the preeclampsia spectrum disease.  There are a series of symptoms, most commonly is headache but it can also be associated with epigastric pain, shortness of breath, bleeding, hyperreflexia and as mentioned earlier  in severe forms seizures. Elevated blood pressure is characteristic of preeclampsia and the two key thresholds  to keep in mind are a blood pressure of 140 over 90 or in severe forms a blood pressure of 160 over 110.  Capillary leak can lead to abnormalities in a variety of organs including proteinuria from kidney, a capillary leakage, pulmonary edema in the lungs or pleural effusions and  then the abdomen ascites. Finally there can be abnormalities in the coagulation cascade and in liver function  causing a fibrinolysis, hemolysis and presenting with DIC, hypofibrinogenemia, elevated LFTs or low platelets.  In terms of treatment there are three main areas of focus in treatment. The first is and this is the only curative therapy for preeclampsia spectrum disorder  and that's delivery of the fetus. The timing and rapidity in which this occurs is at the discretion of the obstetrician  balancing both the severity of the mother's condition as well as the age of the fetus. The second area of treatment focus is seizure risk and the third is treating hypertension.  So let's talk about seizure risk. Over the years many different antiepileptics have been evaluated for the treatment of seizure  disorders in women with preeclampsia but the evidence basis for this was somewhat limited. This led to the MAGPIE trial which was a randomized placebo controlled trial evaluating  the treatment of women with preeclampsia randomized to either IV magnesium or placebo controlled. The trial enrolled over 10,000 women.  About one quarter had severe preeclampsia, the remainder had preeclampsia and about 10% had the postpartum variant which we'll talk about in just a moment.  The women who were randomized to magnesium received a bolus dose typically about 4 grams  and then this was followed by administration that approximated about 1 to 2 grams of magnesium per hour.  Although in this trial there was no target magnesium therapy, it's common now to target treatment of a magnesium level of between 4 and 7 milliequivalents per liter.  The primary outcome of the trial was prevention and reduction of eclampsia defined by seizure  onset and as shown here in this table there was a greater than 50% reduction in the rate of eclampsia in women who were treated with magnesium sulfate.  Although it wasn't the primary endpoint in the MAGPIE trial, there was also a significant reduction in maternal death, almost 50%.  What's interesting here is that the cause of death were related to systemic injuries. So in summary, the MAGPIE trial, which was designed to reduce seizure risk, successfully  reduced the risk of eclampsia by more than 50% and also reduced the risk of maternal death without any substantive harmful effects to either the mother or baby in the short-term.  So what about the treatment of hypertension? It is a little bit different in the setting of pregnancy where the definition of severe  hypertension is lower as compared to the non-obstetrical patient, 160 over 110 relative to 180 over 120, and it's not necessary to have evidence of symptoms or end-organ damage.  In terms of the management goals of the obstetrical patient with severe hypertension, it's of  course important to lower the blood pressure quickly, but it's important to keep in mind  that the placenta does not have the auto-regulatory capability and so it's important to avoid placental hypoperfusion.  A variety of medications are used in the setting of hypertension. The most common are vasodilators and adrenergic blockers, and of this list, the most commonly  used are labetalol, hydralazine, and nifedipine, with nifedipine being the first-line treatment  due to its evidence that shows it reduces the risk of long-term hypertension afterwards.  It's also important to recognize that the obstetrical patient with preeclampsia carries a future risk of cardiovascular disease, and in fact, in 2011, the American Heart Association  added preeclampsia as a list to the risk factors for cardiovascular disease, and a woman with preeclampsia in preterm delivery has the same risk for future cardiovascular disease as  a patient with diabetes, and a woman with recurrent preeclampsia has a risk for future CVD equivalent to a patient with obesity and smoking.  So returning to our 18-year-old woman who presented at 29 weeks gestation, she had severe  hypertension greater than 160 over 110, a urinalysis revealed proteinuria, she had thrombocytopenia  as well as elevated liver enzymes, and evidence of hemolysis with an elevated LDH and an undetectable haptoglobin.  So she had the HELP syndrome, and she was managed with IV labetalol, IV magnesium, and the fetus was urgently delivered.  Let's move on to a second case which illustrates the postpartum variant. This is a 36-year-old G2P3 female who was five days postpartum, and she too presented with headaches.  Also found to have an elevated blood pressure of 190 over 80, and she had a witness seizure in the ED.  The UA revealed proteinuria, she did not have low platelets, her LFTs were normal, and a lumbar puncture was also normal. So how would you classify her disorder?  A, does she have preeclampsia that should be treated with an oral calcium channel blocker? Does she have B, eclampsia treated with IV labetalol, IV levotiracetamine, and magnesium?  C, does she have postpartum angiopathy treated with hydralazine, levotiracetamine, and magnesium?  Or D, does she have postpartum angiopathy and eclampsia treated with hydralazine, levotiracetamine, and magnesium?  Well, it's important to recognize that there are many potential causes of headache in the  postpartum woman, and these include primary headache disorders such as migraine, tension-type headaches, and primary thunderclap headache.  And these types of headaches, particularly migraine, typically improve during the period of pregnancy but then recur after delivery.  And then there are a variety of secondary headache disorders that can be quite serious and include subarachnoid hemorrhage, stroke, venous sinus thrombosis, or DBT of the brain,  pituitary apoplexy, infections such as meningitis and encephalitis, postdural puncture headaches, as well as the postpartum preeclampsia and eclampsia, and postpartum angiopathy.  The incidence of postpartum eclampsia is slightly more than 5% of all deliveries, and the symptom  onset typically occurs within the first two days in about half of patients, but can occur several days later in the other half.  There are a lot of similarities between postpartum and antepartum eclampsia with similar signs, symptoms, and brain imaging abnormalities.  This slide shows the overlap as well as the differences between the antepartum and postpartum  eclampsia variants, where headache, hypertension, seizure, and visual changes are in common. But in the antepartum eclampsia, of course the placenta is present, the HELP syndrome  is typically restricted to the antepartum variant, and cerebral vasospasm is not that common.  In contrast, the postpartum eclampsia version is characterized by thunderclap headache and severe cerebral vasospasm.  And as shown here in our case number two, the woman was admitted to the hospital and on a CT angiogram of the head one day after admission, it shows diffuse, widespread cerebral  vasospasm characterized by a softsygenous string, vasodilation, and vasoconstriction throughout all of her cerebral arteries.  She was admitted to the intensive care unit, treated with vasodilators, and the cerebral vasospasm improved on a follow-up CTA four days later.  So in this case, this 36-year-old woman had elevated blood pressure, she had a seizure in the ED as well as in her UA, and her head CTA showed cerebral vasospasm.  So she had the condition of postpartum eclampsia as well as postpartum cerebral angiopathy, and she was treated with IV magnesium, an oral calcium channel blocker specific to the  cerebral blood vessels called nemodipine, as well as IV leptoracetam. So in summary, hypertensive disorders and preeclampsia are the most common reason for  hospital ICU admission in the obstetrical patient. Delivery, antihypertensive therapy, as well as magnesium are the mainstays of treatment,  and the postpartum eclampsia and angiopathy variant is usually benign and self-resolves, but in rare cases can lead to neurological deficits or strokes, which often are successfully  treated with cerebral vasodilators. Thank you for your attention. Greetings. Thank you so much for joining me today, and thank you to the Society for this opportunity to speak.  I do not have any conflicts of interest or financial relationships, but I will be discussing the use of off-label medications throughout the talk.  Today we'll review the changes to the coagulation system that occur in pregnancy, describe who  should get VTE prophylaxis on the whole, and how to manage acute VTE in pregnant populations, and the bulk of our talk will evaluate obstetric-specific approaches to hemorrhage.  Common changes throughout pregnancy induce a procoagulant state that is associated with increased rates of VTE.  Alternately, obstetric hemorrhage is a life-threatening disorder that requires prompt and aggressive treatment.  Throughout pregnancy, plasma volume increases about 40%, and red cell volume also increases, but only at about 25%, which results in a net reduction in hemoglobin concentration,  which is known as the physiologic anemia of pregnancy. Pregnancy counts decrease as well from dilutional effects as well as due to consumption by the  uteroplacental unit, but this is rarely enough to impact bleeding. The most impactful changes will be seen at term, and normal values are listed here.  Normal changes in hemostatic balance shifts towards hypercoagulability to avoid postpartum hemorrhage in patients.  This is mostly seen through increases in coagulation factors, von Willebrand factor, and large increases in fibrinogen.  The normal increases in fibrinogen throughout pregnancy are listed here, but it's not uncommon for fibrinogen levels to up to triple by term. So VTE prophylaxis, who should get it?  Well, chances are if they're admitted to your ICU, they'll likely need DVT prophylaxis, and so I bolded here the most common reasons for ICU admission, and these can broadly be  broken down into bleeding, preeclampsia complications, and infection. Either one major risk factor or two minor risk factors will require DVT prophylaxis,  and you have two major options, either low molecular weight heparin or unfractionated heparin. Acute VTE treatment is honestly not that much different from other populations.  It needs to be treated, and in order to reduce mortality and recurrent VTE, the big differences are in which agents we choose.  So here, low molecular weight heparin in the long term is preferred over infractionated heparin, but either agent is reasonable short term.  Dinaporoid is also available internationally, but not within the United States, and that's a fine choice as well. Fondoparanox can be used in heparin-induced thrombocytopenia.  The only thing to note is that a small fraction of that anti-tinnate activity is detectable within the newborn.  Agents that should be avoided include warfarin and the oral anticoagulants that are now available.  Dabigatran, especially in the first term, first trimester, are associated with teratogenicity and developmental side effects.  They also cross the placenta, which is associated with an anticoagulated newborn and increases in fetal bleeding.  And dabigatran and the oral factor tinnate inhibitors likely cross the placenta, and the reproductive effects are unknown, so they're contraindicated in this population.  While fully switching gears towards obstetric hemorrhage, it is known that rapid recognition and early aggressive treatment saves lives.  Protocols should be followed whenever possible, and whether this is a protocol guiding your uterotonic agent use or your transfusion principles, if available, it should be utilized.  Of note, coagulopathy is also an early feature of postpartum hemorrhage and should be addressed early on.  Typical first-line approaches to obstetric hemorrhage always approach uterine atony and the treatment thereof.  There should also be an assessment for other causes of bleeding that can be easily treated early on.  And second-line agents, either you're going to move on to an alternate uterotonic, consider tranexamic acid or more mechanical or surgical measures to control bleeding, and this is  all in an effort to avoid hysterectomy or other invasive procedures that would limit the reproductive capacity of the woman in the future.  Obstetric hemorrhage can be broken down into four main causes. So uterine atony, where we'll spend a lot of our time, I'll briefly discuss what placental  problems can occur, genital trauma, and then again go into depth over coagulation defects. So uterine atony, atony is responsible for approximately 80% of postpartum hemorrhage.  Outflow to the uterus at term is approximately 700 mLs per minute, and therefore a perfusion of an unoccupied placental bed can cause significant quick postpartum blood loss.  Uterine atony can occur due to myriad reasons, including the four listed here of note. Uterine distension can be caused by high parity or multiple gestations.  Desensitization can be caused due to induced or prolonged labor.  Uterine involution typically occurs with either a retained placenta or a placenta accreta. Decreased myometrial tone is often due to pharmaceutical agents such as anesthetics,  magnesium, or prior topolytic agent administration. Again myometrial contraction is essential to stop bleeding and therefore we utilize  these agents to produce sustained prolonged contractions of the uterus. Oxytocin is typically first line and may be used in combination with these other products.  Oxytocin again, first line in most algorithms and the standard dosing is listed here. Alternate agents are typically chosen according to patient condition or past medical history.  For example methyl argonavine should be avoided in hypertension, carbaprost is contraindicated  in most major organ failure, it also causes bronchoconstriction which is therefore contraindicated  in patients with asthma, and mesoprostol is well, has a large safety profile but is likely not as effective as oxytocin or methyl argonavine.  And of note there's increasing concern about the safety of standard oxytocin regimens. Oxytocin causes peripheral vasodilation with high doses in rapid administration which causes  hypotension and cardiovascular complications. Interestingly oxytocin also causes coronary vasoconstriction and is thought to explain  why higher doses such as the 10 unit boluses have been linked to ST depression even in healthy women.  Because of these safety concerns the British National Formulary advised a reduction in their dose from 10 units down to 5 due to maternal deaths after cardiovascular instability  with the higher doses, but it's been shown that even 5 units injected rapidly results in clinically significant hypotension in up to 20% of patients.  Particularly as a result of structural similarities with vasopressin, large doses of oxytocin can cause water retention, hyponatremia, and result in seizures or coma, that's pretty  rare. So if I argue that traditional doses are too high what should we use instead? Well there's a body of evidence that shows that much lower doses might be effective.  Carvalho showed that only .35 units is needed to achieve effective uterine contraction. This was an elective cesarean procedure so these patients hadn't seen exogenous oxytocin  before but that is way lower than 10 units. This was followed up by a study by Balki and colleagues in non-elective cesarean deliveries  in which patients were receiving oxytocin augmentation. This group showed that 10 times the amount was needed, so about 3 units was required for adequate uterine contraction.  So this seems to confirm a couple of things, that one, that receptor desensitization or tachyphylaxis does indeed occur and that maybe it suggests we need to move on to another  uterotonic agent in these scenarios. Surprisingly few studies have assessed the dose of continuous infusions of oxytocin but  it appears that lower doses, such as 1 unit per minute or less, are comparably effective to larger doses and with fewer side effects. These studies are few and they are limited.  They are limited due to heterogeneous populations, lack of controls for confounding obstetric or anesthetic factors, and they're really lacking in actively hemorrhaging patients.  But I believe this data on the whole points to the efficacy of lower doses and the need to use extreme care in dosing oxytocin in hemodynamically unstable patients.  Abnormal abnormalities account for fewer causes of postpartum hemorrhage as compared to uterine atony but are of great clinical significance.  So placenta accreta occurs when there's abnormal implantation of the placenta to the uterine  wall, placenta previa occurs when the placenta overlies the endocervical odds, and abruption occurs when there is separation of the placenta from the uterine wall.  Uterine rupture should also likely be mentioned on this slide as a cause for ongoing postpartum hemorrhage.  Abnormal tract trauma is associated with every vaginal delivery but is typically of minimal  hematologic consequences, but if ongoing postpartum hemorrhage is recognized it is likely appropriate  to assess for further trauma that could be amenable to mechanical or surgical interventions. And then finally coagulation defects, and this is again where we'll dive deeper.  So first we know that early evaluation of coagulation is necessary in postpartum hemorrhage as these defects are common, so we'll start and discuss how we're going to assess these  patients, the role of fibrinogen maintenance and the potential administration of tranexamic acid, transfusional principles within these populations, the appropriate use of empiric  procoagulant agents, and briefly discuss the management of heritable coagulation disorders. So first off with assessment, TAG and Rotem are advised, they measure clock kinetics and  strength from formation through fibrinolysis and allow for targeted interventions based on the results obtained.  These are guideline-recommended tests and should likely be obtained every 30 to 45 minutes along with complete blood counts and fibrinogen levels during ongoing resuscitation.  Standard tests of coagulation are mostly ineffective in this scenario, they take too long to come back and they're really just not designed for this purpose, so those can be avoided  most likely. Obtaining an adequate fibrinogen level is essential for hemostasis, the optimal level  is likely greater than 200 mg per deciliter and you have two main ways to supplement that level if it falls below 200, so you either have cryoprecipitate or fibrinogen concentrates.  Cryoprecipitate has a higher fibrinogen concentrate than plasma, it's widely available and easy to dose.  Fibrinogen concentrations are also available, they do allow for more precise dosing and avoid the necessity to thaw a product, but they can be prohibitive in that they cost  greater than $1,000 per gram typically and this is an off-label indication here. Tranexamic acid is an antifibrinolytic agent that has been used in a wide variety of trauma  and surgical applications to control bleeding. It's inexpensive, widely available and the WHO added it to their guidelines in 2012 and  this was for administration after initial uterotonics had failed and at the time this was extrapolated from trauma and surgical data, but the WOMEN trial has really cemented  its place in therapy. The WOMEN trial assessed the efficacy of tranexamic acid on death, hysterectomy and other outcomes in postpartum hemorrhage.  It was an international multicenter randomized placebo-controlled trial primarily in under-resourced settings throughout Africa and Asia.  All participants received either 1 gram of tranexamic acid or placebo and this dose could be repeated at 30 minutes of bleeding continued.  Patients that were included were 16 years and older undergoing either vaginal or section birth experiencing postpartum hemorrhage with hemodynamic instability.  The exclusion criteria really mirrored the CREST-2 trials in that the certainty that tranexamic acid would or would not help was only the true exclusion.  The primary outcome was death from all causes or hysterectomy within 42 days and secondary outcomes included death due to hemorrhage specifically, thromboembolic events, surgical  interventions and complications, and other functional outcomes. Of note, it was initially calculated that a sample size of 15,000 would be needed to  power that primary outcome, but early on it was noticed that the decision to randomize and the decision to perform a hysterectomy were effectively made at the same time.  Therefore, to adequately power that secondary outcome of death due to hemorrhage specifically,  the sample size was increased from 15,000 to 20,000 and they did meet that recruitment goal. These two groups were very well balanced.  On average, the patient was 16 to 33 years old. The baby was delivered at the randomized hospital via vaginal delivery and these patients were  also balanced in terms of uterotonic agent use and blood product administration and this study found that there was no difference in their primary outcome of death from all causes  of hysterectomy, but if you look specifically at death from bleeding, there was a significant decrease from 1.9% down to 1.5%.  That calculates to a number needed to treat of 250 patients to save one life. There were no differences in rates of VTE or other complications and while it should  be noted that this is an exceedingly high death rate in well-resourced countries, of note, like the United States, as of January 2018, put our death due to bleeding at 0.0174%.  So these high rates of maternal death due to bleeding in the study may be why it hasn't caught on in well-resourced countries, but with such a safe side effect profile and low  cost transamic acid should be considered, I believe, whenever first or second line uterotonic agents have failed and postpartum hemorrhage is ongoing.  Imaging principles in the obstetric patient are not wildly different than other populations. A protocol should be followed whenever possible.  It's essential to maintain adequate fibrinogen and platelet levels and cell salvage should be pursued whenever possible.  It was initially thought that amniotic fluid embolism or the risk of induction of maternal alloimmunization was inappropriate, but modern filters really negate these.  It's likely going to be more cost effective in patients with predictably high rates of transfusion such as placenta accreta or previa, but this should and can be utilized whenever  possible. Empiric administration of either prothrombin complex concentrates or recombinant factor 7A should really be reserved from when all else has failed.  There's minimal data supporting its use or effectively noted in PCC administration and really should be used as a last resort scenario.  Of note, there are significant risks of life-threatening thrombosis in recombinant factor 7A use up to 12%.  And then last but not least, inherited coagulation disorders, and so I can't think of honestly of a scarier patient hitting the unit other than this, but luckily it's a team sport,  so you should always call in any and all colleagues that you have available whether this is your  OB-GYN team, trauma surgery, hematology, anesthesia, any and all available support staff. Hopefully this patient has been hooked in with her hematologist throughout pregnancy  and factor levels have been monitored whenever indicated. Also I hope that this patient has created a delivery plan with that hematologist that  is available or can be taken with her that allows for the appropriate dosing of prophylactic factor or therapeutic administration in the event of postpartum hemorrhage.  If you do need to give factor, recombinant proteins are preferred whenever possible and you should always consider other adjuncts whenever appropriate, either DDAVP or tranexamic  acid, and also note that these can be contraindicated in some inherited disorders. And last but not least, don't forget about that second patient in the room.  Pediatric hematologists and neonatologists need to be informed of any deliveries of neonates with these same potential bleeding disorders. Thank you very much.  I appreciate your time. Hi. My name is Sherry Berg. I am one of the anesthesiologists and ICU physicians at Massachusetts General Hospital.  I also am the medical director of the post-anesthesia care units. I'm the director of anesthesia for our ECT service and also the director of anesthesia for our ketamine clinic.  So I want to thank you for joining us today. I am the last part of our special delivery for critical care of the obstetric patient.  The title of my talk is Organization of Resources for the Complex Patient. So I have no disclosures today to let you guys know about, and today we're actually  going to discuss the elements that help define what teamwork is actually made of and how to communicate within your team, what types of communication are paramount in establishing  the we in team. And I know there is no we in team, but there's also no I in team, so I prefer a we.  We're going to look at how this leads to basically your patient receiving the safest and best care.  And then we're going to go through two cases where hopefully you'll see how teamwork and communication demonstrated to the fullest basically with regarding the mobilization  of resources that were acquired or are acquired to take care of our patients. So we do have so many resources, so little time, so you want to always remember that  obstetric critical care is a team activity. Teamwork and communication are key to minimizing adverse events.  Teamwork skills and effective communication are imperative given the complexity, acuity, and often unexpected nature of this and these intricately complicated medical specialties.  So basically, is the baby ready to be delivered now? Okay, what do we need to do? Oh no, mom is hemorrhaging. Okay, who do we need to call? What resources do we need to get?  And then wait, what? Mom's PA pressures are how high? So again, we need to realize that we have so many things and people and technology available  to us and we need to know exactly what we can get and when we can get it. So again, so many resources, so little time.  There are a multitude of resources that are available to care for the special patient population that often becomes plural, right?  We have a mom who's your patient and then we're going to have a baby who is going to be either your patient or somebody else's patient for the most part by the end of this  event that we're going to have. There often can feel that there are resources available, but there is not enough time to realize, to mobilize everyone and everything that we need.  So planning, teamwork and communication are key words here and we're going to kind of go with that theme for the rest of the talk.  So communication and teamwork training, whether it's in person, if it's, you know, a simulation,  any kind of communication and teamwork training basically leads to better outcomes for mom and for the baby. You always need to focus on what is important.  So you have the mom who is your patient, you have the baby, you have your entire team, and then you have all the logistics, which will definitely vary between each situation.  So communication issues are among the leading contributor to patient harm. So again, we want to avoid that.  And effective communication is essential for effective teamwork by establishing and maintaining a shared mental model by the members of your team.  So with teamwork concepts and behavioral skills, we basically have SBAR, which is like a very good acronym for situation, background, assessment and response.  So it can help to efficiently communicate essential clinical information quickly, which is obviously what you need.  You always want transparent thinking, so you want to state out loud to your team what is going on in your head. They can't read your mind.  So if you don't say it out loud, they're never going to know what you're thinking. Directed and closed-loop communication, so you want to basically speak directly to an  individual using their name. And in a lot of simulations, we usually will go, you know, hi, I'm so-and-so from anesthesia,  and just so you directly state your name and then what part of the team you actually are. And then we repeat back.  So with regards to closed-loop communication, you repeat back what someone asked of you. They said, can you go get me two units of red cells?  You said, yes, Sherry is going to go get you two units of red cells. And therefore, you demonstrate that you heard what they said and then that you actually  understood and you're going to reiterate it back to them. So an example of SBAR, using SBAR, so situation, background, assessment and response.  So the situation, you realize you need to mobilize resources because you have a postpartum patient who is acutely hemorrhaging and now she's in shock.  So the background, you're talking to the triage nurse. You need to get the patient moved. So you tell them on the phone, I have called the ICU triage team and in the meantime, we're  rapidly transfusing four units of red cells and four units of FFP. The assessment, clearly I'm concerned that she's continuing to hemorrhage and becoming increasingly unstable.  And then the response that I'm looking for is please come evaluate her immediately. So basically role of assertions.  So assertions are a critical language and basically a feeling that you can speak up if something is going on and doesn't feel 100% like okay to you, whether or not you're  uncomfortable in the situation or anything like that, but you definitely need to speak up. It can be difficult basically though, secondary to entrained hierarchical structures.  So whether or not the nurse feels uncomfortable telling the doctor what they think or the resident feels uncomfortable telling their attending.  And then again, some people do have inherent personality traits and characteristics that we will never be able to change.  But basically by the role of assertions, it kind of hopefully will overcome the fear of speaking up.  You want to use words like I'm concerned, I'm uncomfortable, I'm unsafe, or even I'm scared because if you don't communicate your feelings, no one's ever going to know them.  There are leadership styles that reduce hierarchy and promote assertions and they've actually been associated with improved patient care, right? Seems like a no brainer.  So we clearly should be doing this. So with situational awareness and resource management, we need to know human and technical resources.  We need to know how to access them quickly and then how to mobilize them. If you deem a situation as an emergency, call it. I need some help in here. We need help in here.  You need to be vigilant. You need to monitor the surroundings. We can have team meetings about previously discussed plans that will promote a common  situational awareness amongst your team members, again, leading to really great teamwork. You want to distribute the workload resource management. One person can't do everything.  You want to help team members complete their tasks and you want to have a shared sense of purpose because that allows each team member to conquer the situation at hand.  So there has to be a leader and followers and then basically definition of role clarity.  So leaders who flatten the hierarchy to promote universal exchange of information are actually  more effective leaders and their team members actually feel it's a safer place to speak up. So even though the care team is likely to be diverse and multidisciplinary, there needs  to be one basically efficacious leader. There should be a team event manager. So basically that's been used and it's an individual who is not really responsible for  making medical decisions but in turn is responsible for managing the people and then the resources that we have at hand. So now we're going to discuss our two cases.  So our complex patient one, she is a 32-year-old G4P2 female who presents to her OB for her  24-week checkup, looks okay, no major issues. She is a little obese so you talk to her about the importance of a healthy diet and basically  that she should be, you know, not gaining too much weight. And then she also tells you she has a history of a blood clot in her lungs.  She continues to tell you she's been following the diet and she does try to exercise but she has been short of breath. And then you want to think this is exercise-induced asthma.  However, you get a CT scan and a TTE and then unfortunately you realize she has severe pulmonary hypertension.  So you're looking at your patient and you know you need to start mobilizing resources now. So who do I need to consult for peripartum management? How about for delivery?  And we have so many resources available. You do set up a multidisciplinary team. You have your MFM colleagues, an OB anesthesiologist, the ICU staff, social work, and the patient  and her family, all going to work together, follow her closely for the pregnancy. You all decide together that you're going to induce her in the ICU at 36 weeks.  She'll arrive a week early. You're going to give her Flolan and Heparin. So she comes in, you titrate the Flolan to the side effects.  The day before she's scheduled to be induced, she's going to go to the cath lab. So again, mobilizing more resources that we didn't need at first, our cath lab constituents,  our cardiology colleagues, and we did have an art line placed by one of the ICU physicians. So clearly the goals during labor, we're going to prevent pain, hypoxia, and hypercarbia,  anything that's going to worsen her pulmonary hypertension. She gets oxygen. She's a well-functioning epidural. We keep her euvolemic.  And basically we're following her systemic and pulmonary pressures with the PA line that was placed. So she's being monitored. Everything looks great.  And then you're called urgently, stat, because basically the baby has a non-reassuring fetal heart rate. Her epidural is working great.  So this is an emergency and we need to mobilize our resources. So who do you need to call? Well, we need an event manager.  We need to get our OB anesthesiologist, our MFM colleagues. We need to get pediatrics and neonatology on board right now because we are going to have this baby.  They did a forceps mediated delivery and her EBL was about one and a half liters. You're thinking everything's fine, but she's becoming noticeably hypovolemic with a lot  of tachycardia and hypotension. So we need help now and teamwork and communication are key. So what should we do? What medications? And then who do we need to help us?  We have our pharmacist, our OB colleagues, and we're all working simultaneously on our dedicated tasks that were designated to us by our event manager while working as a coherent  team to ensure the best care of the patient and the baby. We start low dose oxytocin to minimize side effects. We also start some levophed to maintain her pressure.  And thankfully she appears to stabilize and we do not transfuse her. So we had some really great teamwork here.  So clearly we're all concerned because we know that pulmonary hypertension is very detrimental in pregnancy and also for the mom and the baby.  So you can clear why we need a multidisciplinary team and why teamwork and effective communication were key here to ensure a safe delivery.  So the normal drugs that we could give basically can be a problem. We stuck here with oxytocin just because it was the safest and it was the easiest to titrate.  Now we have our second complex patient. She is a 32 year old G4P3 female at 35 weeks. Her first child was a vaginal delivery, vacuum extraction that resulted in laceration.  And then her subsequent deliveries were all C-section. We know she has an anterior placenta previa and placenta accreta, and we're ready to deliver baby today.  So we clearly need to mobilize all the resources and the care team that we previously discussed in our multidisciplinary meetings. So who do we have here?  We have anesthesia, OB, high-risk OFM. We have vascular surgery, urology, vascular and OB nurses, as well as pediatrics and neonatology.  So our plan, we have an epidural, we're going to have the vascular surgeons put up some bilateral ILEAP balloons, the urologists are going to do bilateral ureteral stem placements,  a repeat C-section by OB-MFN, and then we're going to do a gravid hysterectomy under general anesthesia and CICU post-op.  So everything looks great, C-section, uterine incision, the baby is out. Anesthesia intubates her. She looks fine.  She's maintained on general anesthesia with a low dose phenylephrine drip going in the background. So we have an emergency anesthesia to-do list. We have to secure the airway.  We have large IV access, hemodynamic monitoring, hemodynamic support. OB has their emergency checklist. And basically, what is our plan going forward?  So clearly, we need effective and active communication. We use our SBAR and transparent thinking, as well as directed and closed-loop communication.  So thankfully, the vascular surgeons did inflate the balloon, so we minimize the fear, complication of postpartum hemorrhage.  Things seem to be going fine, but then the anesthesiologist notes a drop in oxygen saturation followed by difficult-to-control hypotension and increasing hips.  So yes, we have another emergency. So we need transparent communication between the team members. What are we thinking? What could be happening?  And we need our event manager who needs to direct tasks and call for more resources. So basically, an amniotic fluid embolism is very scary. It's very detrimental.  It was proposed in 1996, the pathophysiology is not 100% clear. But unfortunately, there are two phases that all lead to basically mom's body shutting down in complete shock.  So how do you know? Well, an amniotic fluid embolism is a clinical presentation. So you'll see respiratory distress, drop in oxygen saturation, hemorrhage from DIC, and death.  So what are we going to do now? Well, we're all going to work together to keep mom alive. We're going to provide supportive therapy and kind of go from there.  We have to correct all her coagulation abnormalities as well. So she has shock. What are we going to do? So we're resuscitating her. We have her on pressers.  And one of the nurses calls out, should we get a SAT ECMO consult? So we do. There is VB ECMO and VA ECMO. Luckily, she only required VB ECMO at this time.  We were able to catch her early. So you want to initiate therapy now, and you can save a life.  And again, just shows to show you that communication and teamwork here were key to successfully saving this patient. Some references.  And I wanted to thank you all for joining us today from this talk. I hope you learned something. Have a good day.

Video Summary

The video transcript discusses the critical care of obstetric patients and the need for understanding and resources in managing obstetric calamities. It focuses on three subjects of interest: acute neurologic issues in pregnancy and postpartum, clotting disorders in obstetric patients, and organization of resources for complex pregnant patients.<br /><br />The first subject discussed is acute neurologic issues in obstetric patients, particularly preeclampsia and postpartum angiopathy. The speaker highlights the symptoms and management of these conditions, including the use of magnesium sulfate for seizure prevention.<br /><br />The second subject is clotting disorders in obstetric patients, such as preeclampsia, and the importance of evaluating and managing coagulation abnormalities in these patients.<br /><br />The third subject is the organization of resources for complex pregnant patients. The speaker emphasizes the importance of teamwork and effective communication in managing these patients and mobilizing the necessary resources. Two case examples are presented to illustrate the importance of teamwork and communication in managing complex obstetric patients.<br /><br />Overall, the video transcript emphasizes the need for critical care practitioners to have the understanding and resources to manage obstetric calamities. Effective communication and teamwork are crucial in providing the best care for these patients.

Asset Subtitle

Obstetrics, 2021

Asset Caption

The Society of Critical Care Medicine's Critical Care Congress features internationally renowned faculty and content sessions highlighting the most up-to-date, evidence-based developments in critical care medicine. This is a presentation from the 2021 Critical Care Congress held virtually from January 31-February 12, 2021.

Learning Objectives

Recognize neurologic issues of pregnancy that require critical care in the ICU
Assess alterations of coagulation and treatment options during pregnancy and the postpartum period
Identify the complexities of organizing scheduled delivery and emergent care of the pregnant patient in the ICU

Acute Neurologic Issues in Pregnancy and the Postpartum Period
W. Taylor Kimberly

Either Too Much or Too Little Clotting
Cassie Barton

Organization of Resources for the Complex Patient
Sheri Berg

Meta Tag

Content Type Presentation

Knowledge Area Obstetrics

Knowledge Level Advanced

Membership Level Select

Tag Pregnancy

Tag Coagulation

Year 2021

Keywords

critical care

obstetric patients

acute neurologic issues

preeclampsia

postpartum angiopathy

clotting disorders

coagulation abnormalities

organization of resources

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