Hi, this is Dr. Marie Baldessari. Today's lecture will be about obstetric emergencies. I'm a professor of critical care, neurocritical care at the University of Pittsburgh. I actually began my career in high-risk obstetrics and have continued that interest for some time now, literally all throughout my career. So I'm delighted to be talking to you about this today because this is certainly an important part of our practice in critical care medicine, and certainly in the board review, as well as the examinations. You will have a significant amount of information and testing that will be done in obstetrical critical care. So let's talk about the first question, which are the following increases of pregnancy? SVR, transaminases, blood pressure, and cardiac output. So this should be intuitive that cardiac output is dramatically increased in pregnancy, up to about 50%, as a result primarily of the stroke volume, although the heart rate does increase, albeit not as dramatically as the stroke volume. So it's not unusual to see patients at term with heart rates up to about 100, but anything higher than that should be a little bit alarming and put in a clinical scenario of what's happening with that patient, unless they're in labor and obviously the heart rate would be higher. Systemic vascular resistance, sort of similar to the sepsis profile. If you put a pulmonary artery catheter in these patients, we have significant vasodilatation as a result of the progesterone. This is dramatically different in hypertensive states, including preeclampsia, where the SVR is increased. Liver function tests are decreased, except in liver disease, the various liver diseases in pregnancy, primarily the HELP syndrome, which is probably the most common as a part of the severe preeclamptic syndrome. Blood pressure is in fact decreased during pregnancy, not surprisingly because the SVR is decreased, primarily in the diastolic pressure, but it's not surprising to see normal pregnant patients present, particularly in that second trimester with systemic or systolic blood pressure as low as 85. It really becomes a matter of your clinical acumen and judgment as to whether this blood pressure is a decrease because of sepsis or volume depletion, et cetera, versus the normal pregnant homeostasis. As I alluded to, blood volume is dramatically increased up to almost 50%, as is the cardiac output. Blood pressure is decreased, the stem and vascular resistance decreased, although the filling pressures per se are relatively unchanged if you did a cardiac catheterization or put a swan gance catheter into these patients. So we're talking about the filling pressures in the right and left side of the heart. Respiratory, we have an increase in metaventilation, both as a result of tidal volume and respiratory rate. So for us, that is pregnant women, we have a compensatory respiratory alkalosis with a PCO2 of about 28 to 32, with a relatively normal to high pH of 7, 4, or 5. If you see a patient come in with a normal PCO2 of 40, that usually signifies someone who's actually in extremis if they're pregnant. We have a tendency to bleed. We have a lot of mucosal edema and a tendency to bleed, particularly during intubations. We have a decrease in chest wall compliance, not surprisingly because of the size of the abdomen and the chest, but really no significant change in a gradient. I think what's most important and one of the biggest take home messages I would like you to have is this increase in hypoxic risk as a result of a decrease in the functional residual capacity, as well as an increase in oxygen delivery and consumption. So the oxygen consumption as a result of placental consumption, maternal consumption, and fetal consumption as well. And these make us a significant risk for hypoxia and anoxia, particularly during the intubation attempts of a pregnant woman. So gastrointestinal, unfortunately, we have a risk of aspiration due to the increase in abdominal pressure, as well as a decrease in the esophageal sphincter pressure, bilirubin, and transaminases, as I mentioned before, usually decrease. Because of the increase in blood volume and cardiac output, stroke volume, we have a tremendous increase in our GFR, which means that we do not have normal BUN and creatinines. In fact, we have quite low BUN and creatinines, normal creatinine, about 0.2 to 0.3 milligrams per deciliter, as opposed to the normal values of up to 0.7 to 1 in the non-pregnant patient. Because of the increase in blood volume, as well as the plasma volume, we have a dilutional anemia. We do have an increase in red blood cell mass, but this is disproportionate to the increase in blood volume. So our hemoglobins are about 9 to 11 grams per deciliter. We do have an increase in the white blood cell count, and this leukocyte increase can sometimes be problematic in terms of differential diagnosis, because particularly when those patients present with suspected sepsis, the question is, you know, is this patient infected versus is this the normal physiologic response to pregnancy? The hematologic system is really quite convoluted in pregnancy. There's both an increase and a decrease in the clotting factors. So we certainly have a tendency to clot, as you know. We have an increase in pulmonary embolism, DVTs, arterial occlusions. But unfortunately, depending upon the balance of the clotting factors, we also have a tendency to bleed as well. So let's talk about some of the hypertensive disorders of pregnancy, such as pregnancy-induced hypertension, which has previously been called gestational hypertension. We have many women who are older now who are presenting with chronic essential hypertension. Preeclampsia is a very common entity, unfortunately, probably the most common entity among pregnant women in terms of severe disease. It is secondary to placental dysfunction. It is related to pro-inflammatory angiogenic factors. So you have a decrease in VEGF and placental growth factor as well with a decrease in nitric oxide. It's basically a generalized vasospastic disease with endothelial dysfunction and predilection, particularly for the renal and cerebral vasculature. So very common to see renal symptomatology as well as neurologic symptoms. Eclampsia, the sine qua non of eclampsia, is generalized tonic-clonic seizures. So this is defined as severe preeclampsia with end-organ dysfunction, particularly of the cerebral vasculature. So severe preeclampsia, and that's the type of preeclampsia that you and I will see in our ICUs. We're not going to see the mild or moderate. We're going to see the severe preeclampsia with end-organ dysfunction. So they can present with hypertension and significant end-organ dysfunction, and not necessarily proteinuria. So there are really two types, the hypertension and proteinuria, and those that present with elevated blood pressures and significant end-organ dysfunction. So preeclampsia is defined as those patients usually greater than 20 weeks. You can have earlier onset preeclampsia, less than 20 weeks, albeit it is somewhat rare, but they certainly have a worse prognosis in terms of end-organ damage. Severe preeclampsia, the blood pressure is certainly higher than mild to moderate, 160 over 110, and as I've mentioned several times, there is significant end-organ dysfunction. Eclampsia presents with generalized tonic-clonic seizures. Usually there are very few seizures, only one, two, or three seizures. And keep in mind that eclampsia, similar to severe preeclampsia, can occur up to one to two weeks post-delivery. For those patients who have recurrent or refractory generalized tonic-clonic seizures, those are the patients that you really need to do a full neurologic workup, you know, continuous EEG, CT scan, MRI, et cetera, looking for a different etiology. Because the seizures of eclampsia are usually easily treated, very easily treated with magnesium. Magnesium is used both prophylactically as well as the end-organ damage. So severe preeclampsia, as we mentioned, can have significant proteinuria, significant blood pressure elevation, 160 over 110. Because of the renal vasculature being affected, usually oliguria, they tend to be hyperuricemic. And end-organ dysfunction can present as pulmonary edema, cerebral disturbances, visual disturbances because of edema in the occipital lobes, hepatic dysfunction, including the HELP syndrome, thrombocytopenia, as well as cardiac insufficiency with myopathy. So what is the treatment? Certainly if the patient is close to term, that is greater than 34 weeks, you want to deliver this patient because really the fetus and the placenta are the nidus of why this is occurring. So delivering the fetus and the placenta will usually resolve this syndrome. Although as I mentioned, there is a certain proportion of patients, about a third of patients, who actually present postpartum. That is after the fetus and placenta have been delivered. Certainly maternal and fetal monitoring for any patient with a gestational age of greater than 20 to 24 weeks. Remember, be very careful about decreasing blood pressure. We certainly have learned this from our stroke population, as well as many other populations in the world of neurology and neurosurgery, that you want to really decrease their blood pressure slowly, not precipitously. So decreasing the mean arterial pressure by about 25% within the first hour or two is probably judicious. As I alluded to before, seizure prophylaxis and therapy with intravenous magnesium. For those patients with severe preeclampsia who present in the prepartum, that is a pre-delivery, we will usually continue the magnesium infusion for 24 hours postpartum. Keep in mind that most of your patients will be oligarchic. So whereas, for the typical ICU patient, we're happy with 0.5 to 1 milliliters per kilogram per cc on a daily basis. Our patients here, we're lucky if they have 25 to 50% of that. So you really need to be extremely cautious, aggressively volume resuscitating these patients because their cholera and oncotic pressure is dramatically increased because of the loss of protein that happens in the preeclamptic process. They have a significant tendency towards pulmonary edema. So you really need to volume resuscitate them judiciously and cautiously. Blood pressure control, I alluded to before, you want to be careful, not go too quickly, at least get the diastolic blood pressure over time down to about 90 to 100. Most of us, at least in the U.S. and some of the other countries throughout the world, use libidolol. Libidolol is a sort of kind and gentle drug, doesn't cause these big precipitous drops in the blood pressure, which is what you want. Hydralazine has been the standard of care for years and years and decades. And there are many countries that don't have libidolol and use hydralazine. The only cautionary note that I would have about hydralazine is it works so incredibly well and is a vasodilator and can really precipitously drop the blood pressure, particularly those patients who are volume depleted. And keep in mind, the preeclamptic, unlike the average pregnant patient who has an increase in blood volume, the preeclamptic patient, because of this generalized vasospastic phenomenon, is relatively volume depleted. Other agents that are available to us, nifedipine, nicardipine, there are certain things that we very much avoid during pregnancy, ACE inhibitors, ARBs, nitroprusside, diuretics. For various reasons, both maternal and fetal, these drugs are usually not used while the patient is pregnant, but certainly can be used in the postpartum state. Also mentioned before, seizure prophylaxis, obstetricians clearly have documented and proven to us beyond a shadow of a doubt that magnesium is the superior agent. There have been many studies comparing phenytoin, benzodiazepines, other agents, and magnesium seems to be the preferred agent as an anti-epileptic. Benzodiazepine also certainly calms the nerves as an anti-epileptic. It works as a diuretic as well. And so it just is a very, very effective drug. It's good for the heart. It's good for the brain. We usually give intravenously, although it can be giving intramuscularly. The loading dose is about four to six grams with an infusion of one to two grams. And as I mentioned before, 24 hours postpartum is the usual duration of therapy. If per chance there is any risk of magnesium toxicity, particularly with those patients who have very, very low urine outputs and have an accumulation of magnesium and you suspect magnesium toxicity with a change in their respiratory pattern or an absence of deep tendon reflexes, then calcium gluconate or calcium chloride is usually given. The HELP syndrome is a variant of severe preeclampsia. There are sort of different variants, the HELL syndrome, the ELP syndrome, but the classic severe preeclamptic HELP syndrome is hemolysis, elevated liver function tests, and low platelet count. Similar to preeclampsia per se, most of them happen intrapartum, but about a third of these can happen postpartum. And unfortunately, a pretty high percentage of these syndromes are associated with acute kidney injury. It occurs a little later as opposed to the severe preeclamptic syndrome, which usually happens up to 20 weeks. This can happen as far out as 27 to 36 weeks and up to seven days postpartum as well. Hypertension plus minus may or may not be present. Once again, the treatment of choice if the patient is intrapartum is delivery, treat them with magnesium, antihypertensive therapy as well. Plasma pheresis has been recommended, has been tried, has been shown to be quite effective, particularly if there's a suspicion that there may be TTP and it persists greater than 72 hours postpartum. There's been some talk about giving steroids, particularly dexamethasone, but it really hasn't panned out in terms of the randomized controlled trials. And there are significant complications associated with the HELP syndrome. Probably the most significant complication is the subcapsular hematoma plus minus hepatic rupture and renal failure. This is a patient as you see here with the CT showing a very, very significant capsular hematoma here. So TTP in pregnancy is very similar to the HELP syndrome. Some variants or some differences, and I've listed them here, higher LDHs, certainly neurologic changes predominate with mental status changes, the treatment of choice, steroids, plasma exchange. And most people now believe, and it's very interesting that all of these syndromes here are probably a spectrum of a disease. So you have the HELP syndrome, acute fatty liver pregnancy, hemolytic uremic syndrome, where you have predominantly renal symptoms and TTP where you have predominantly neurologic symptoms. Usually when preeclampsia lasts for greater than, you know, more than a week or two after pregnancy, the diagnosis of exclusion is usually TTP. So hemorrhagic shock, the most common cause of maternal death worldwide, often due to placental problems such as previa, such as abruption, ectopic pregnancy, trauma, etc. It's defined as at least a liter blood loss coinciding with signs and symptoms of hypovolemia within 24 hours after delivery of the fetus or abortion or any intrapartum loss. The most common cause, as you know, is uterine acne, but there may be other causes including retained placenta, inversion, uterine rupture, which is very, very rare. Resuscitation, TXA can be given, obviously removal of the placenta, manual compression of the uterus, oxytocin, prostaglandin. Obviously you want to correct any medical or surgical coagulopathy. And really we have come so far in how we treat this, balloon tamponade, arterial embolization, hysterectomy. Certainly arterial embolization is only done at the largest centers, but an extremely high success rate. Hysterectomies we really try and deserve for those patients who have failed all other treatments. But those patients obviously with uterine rupture are usually candidates for hysterectomy. So peripartum cardiomyopathy, one of the most fascinating entities. It's a dilated cardiomyopathy epidemiologically, it's similar to idiopathic dilated cardiomyopathy in the non-pregnant patient, but happens in young, healthy women. Happens in the last month of pregnancy to five months postpartum. Many patients present in that last month of pregnancy, but it's often missed simply because most patients in their last month of pregnancy tend to be a little short of breath, have pedal edema, may have an extra heart sound, may have some palpitations. So very difficult to distinguish between those patients with so-called cardiomyopathy and just sort of the classic symptoms of being very advanced in their pregnancy. Certainly the treatment of choice is very much what we do for all of our patients, diuretics, vasodilators, inotopes. Certainly as I mentioned before, if the patient is still interpartum, we avoid the use of ACEs and ARBs. Most of these patients have to be anticoagulated for a significant period of time, and that could be six months to six years, depending upon their symptomatology and their presentation. Because as I mentioned, we have a tendency to clot, and particularly in patients with peripartum cardiomyopathy, they have a high incidence of both systemic and pulmonary thrombosis. About a quarter of cases, so keep in mind, these are young, relatively healthy women who went into pregnancy, and about a quarter of these cases will end up on ECMO and subsequent cardiac transplantation. So let's go to our second question. Pregnant woman, she's 34 weeks, she was involved in an MVA, blood pressure is 70 over 40, she's a little tacky at 110, respirators are 20. Which of the following is the most appropriate intervention? Rh negative blood, operative delivery, intubation, mechanical ventilation, elevation of the right hip, or two liters of ringers lactated? Well, the easy thing about pregnancy, when they ask you a question, if you ever see this in the answer, elevation of the right hip, it's pretty much always the right answer. Because the problem is, when you have your patient supine, and you're compressing the inferior vena cava, as well as the aorta, you immediately decrease cardiac output, you decrease blood pressure, because of a decrease in venous return to the right side of the heart. So regardless of the situation, elevation of the right hip is always the right answer. All right, so as I mentioned, left lateral decubitus position, either with a wedge or have someone displace the uterus, Rh blood is always, Rh negative blood is given. You know, keep in mind that even simple or minor motor vehicle accidents, you know, somebody rear ends them. The mantra is that we have to monitor these patients for at least four hours in the ED. And the reason for that is because the vital signs of a woman can be somewhat misleading, lower blood pressure, slightly higher respiratory rate, slightly higher heart rate, we can get fooled into thinking maybe this is more, maybe this is less. So these, these vital signs can be misleading, because our blood volume is increased, and the heart rate and blood pressure changes the slower to occur. So we need to follow them just for a few hours. Keep in mind, obviously, abdominal shielding, if you have to do any radiography, but whatever needs to be done in terms of radiographic tests, whether it's a chest x ray, CT, CT of the chest, CT of the abdomen, MRI, all of these, if they need to be done need to be done to make a diagnosis, we can try and shield the abdomen as much as possible. But delaying a diagnosis or not making a diagnosis because you're afraid of the radiographic insult to the fetus is the wrong answer. Don't forget about immune globulin within the first 72 hours. So mechanical ventilation, because we have so much edema in the mucosal area of the trachea and the larynx, we tend to use smaller endotacheal tubes, usually less than 7.6 or 6.5. We try and keep the SATs a little bit higher, just give that a little bit extra to the fetus. Remember, we have a compensatory respiratory alkalosis. So keeping the PCO2 28 to 32 is appropriate. Higher airway pressure should be expected. Our plateau pressures are usually higher than 30, particularly as we advance in pregnancy. We have restrictive chest wall motion. This becomes dramatically emphasized and underscored when we have ARDS patients. We try and keep those plateau pressures under 30, but it's extremely difficult with patients who are very close to term because our abdominal pressure is high. Non-invasive ventilation used to be discouraged because of the risk of aspiration, but it has now been shown to be a very effective mode of ventilation prior to intubation and for stalling intubation at times. But you need to be very careful with these because we do have a higher risk of aspiration. And clearly, monitoring the fetus is always important at any moment, particularly for those who are greater than 24 weeks gestation. The fetus is oftentimes the first vital sign that shows us that something is wrong with the mom. All right. Some of you may have heard tocolytic-associated pulmonary edema. We're well aware of this now. We try not to use these agents or keep them to a minimum in terms of causing tocolysis to butylene, ritidine, albuterol. But clearly, the treatment is plus-minus diuretics. It's rarely noted that we have to ventilate these people and obviously discontinuing the tocolytics. Asthma in pregnancy is an interesting phenomenon. It's probably the most common respiratory disorder in pregnancy. About a third get better, a third worsen, and a third have no change. But we certainly know that there are more maternal and fetal complications with asthma in pregnancy. There tend to be more exacerbations in the second trimester. The treatment of choice is exactly the same as it is in our non-pregnant patients, bronchodilators and inhaled and systemic steroids. Acute respiratory failure, I think I would be remiss if I don't mention a little bit about COVID-19, and we'll talk about a few of these. Pregnancy and COVID, certainly the hormonal cardiovascular physiology and immunomodulatory changes during pregnancy increase our susceptibility to respiratory infections. This has been well known for all type of respiratory infections in pregnancy, including simple pneumonia, and certainly now applies to COVID as well, that pregnant women have a greater risk of contracting COVID. If you look here from January 2020 to 2021 of July, you can see this is based on race, ethnicity, certainly whites, Hispanics, Latinos have a higher incidence. This is the number of total cases that we had and the number of deaths as well. Mechanical ventilation and ECMO, unfortunately, well, this one in 2020, this was from January to October of 2020 and did show an increase in ICU admissions. If you look at the adjusted risk ratio, which I've circled here, certainly ICU admissions higher for pregnant patients, higher mechanical and ventilation, higher ECMO, and overall death, albeit not as high as the other categories. These are the hospitalized cases from 2020 to July admitted to the ICU, maybe about maybe a fourth of these required mechanical ventilation and certainly a certain number required ECMO as well. Now let's talk a little bit about advanced life support. Remember, always get your patient off of that right, get them off of the right hip. You do not want them supine. So doing cardiac arrest maneuvers such as CPR can be very difficult when you have a patient in the left lateral decubitus position. So most of the time we just have someone move the uterus, literally just take the uterus between one hand or two hand and move it to the other side. In terms of defibrillation energy, ACLS dosing, standard compressions, where to compress defibrillation energy, everything is exactly the same as you would in a non-pregnant patient. Ideally we prefer that you place IV access above the diaphragm. The one caveat to ACLS, which is clearly different than the non-pregnant patient, is the perimortem cesarean delivery, which should be considered within five minutes of the arrest. If the fetal age is greater than 24 weeks, this is not done for the sake of the fetus. This is done for the sake of the mom to improve CPR. But certainly what we have found is that we have improved fetal survivability. So question three, which of the following suggests the diagnosis of AFE, that is amniotic fluid embolism rather than venous air embolism, cardiovascular collapse, occurrence during labor, diffused bilateral infiltrates and DIC. So DIC is really sort of the sine qua non of amniotic fluid embolism. Certainly in any of the embolic events, including pulmonary embolism, you can have sudden cardiovascular collapse. Obviously anything can happen during labor, including air embolism, pulmonary embolism. Pulmonary infiltrates are very suggestive of venous air embolism as well as AFE. But it's really the DIC presence which makes it a part of the AFE syndrome. So as I mentioned, cardiovascular collapse, DIC, hemorrhage, ARDS, the treatment of choice is really to treat everything. So there is no specific treatment of AFE. It's to treat everything that happens, whether it's DIC, whether it's hemorrhage, whether it's ARDS, whether it's CHF. And these are some of the differences between the two here listed between AFE and venous embolism. So question four, 32 weeks, she has a PE, she has no leg symptoms, chest radiograph is normal. What would you do? D-dimer, VQ scan, CT, angio or MR. And I think this is an important slide because there's always so much concern about what is the risk to the fetus. And I think I've mentioned this before, CTA is certainly the best test to diagnose pulmonary embolism. VQ scans, as you know, can be somewhat difficult to interpret, particularly based on habitus as well as if the patient has any underlying chest radiographic signs. D-dimer can be elevated in pregnancy. So this is not the treatment of choice or the therapeutic diagnostic modality of choice. So thromboembolic disease, keep in mind, pregnancy is a hypercoagulable state. We have increased thrombin activity as well as fibroinolysis. So we do have a tendency to bleed. Our incidence of DVT and pulmonary embolism, unfortunately, is higher. I alluded to the fact that D-dimer levels were increased, particularly after 16 weeks. We can do VQ scanning, particularly if the chest X-ray is normal, but really the best diagnostic modality is the CTA. All right. DVT, I mentioned this before, primarily happens in the left leg, but can be seen in the pelvic, iliofemoral, and popliteal clots as well. All right. So adjusted dose, low molecular weight, heparin is preferred, but we can use adjusted dose and fractionated heparin during pregnancy. Warfarin, Coumadin, is contraindicated during pregnancy, particularly in that first trimester, although there have been people who have used it in the second and third trimester. But the problem is pregnancy, that is delivery in particular, can be very unpredictable. So not having to reverse the warfarin is probably better if we don't have to do that. So most of us would use the unfractionated heparin or the low molecular weight heparin. We don't have a lot of information about DOACs, but we certainly avoid them simply because we don't have a lot of information. TPA can be given, particularly for hemodynamic unstable or life-threatening pulmonary embolism. And usually if a patient has a significant DVT or PE, they're treated for at least a minimum of six weeks postpartum. All right. Maternal sepsis is a life-threatening condition defined as organ dysfunction resulting from infection during the entire pregnancy spectrum up until the postpartum period. It's the third most common cause of maternal mortality globally. Certainly has been associated with poor maternal and fetal outcomes. 23% of all maternal deaths were sepsis related. Half of them occurred in the hospital and half of them outside the hospital. This was based on a study in JAMA published in 2019. Often times maternal sepsis is a polymicrobial, but you can have gram negatives. We worry very much about group A, group B, streptococcus. And most of our respiratory infections actually tend to be very typical, such as the pneumococcal. Influenza varicella can be very deadly in a pregnant woman. So unfortunately we seem to be more susceptible to infections and our morbidity and mortality is higher once we get infected. Imaging, I mentioned this before. Certainly you don't want to delay any important diagnosis by not doing the appropriate test. Shielding the abdomen is most important. CT of the abdomen or pelvis actually is quite within the normal range and should not cause the fetus any harm. MRI, we're a little more careful about because the fetus doesn't particularly like to get selenium, but we can use lower doses. Drugs in pregnancy, this is best discussed with your pharmacy. Because our blood volume, our plasma volume is so dramatically increased. Many antibiotics, et cetera, other drugs that we use have to be increased. We don't have a lot of data on this, but certainly whenever I'm taking care of a pregnant patient, I will consult my pharmacist. As I mentioned before, there are some drugs that we're very much nervous about during pregnancy such as ACEs and ARBs, barbiturates, warfarin, quinolones, all of those can affect the fetus. All right. Thank you so much for your attention and I've enjoyed talking to you and I hope it was a good lecture for you. Thank you.

obstetric emergencies

physiological changes during pregnancy

hypertensive disorders of pregnancy

monitoring pregnant women

respiratory infections in pregnant women

acute pulmonary embolism

medication for pregnant women