Causes of Obstetrical Hemorrhage
BS. Nguyễn Hồng Anh
In addition to hypertension and inection, obstetrical hemorrhage remains among the inamous triad o maternal death causes. O more than 7000 pregnancy-related maternal deaths in the United States rom 2006 to 2015, hemorrhage was a direct cause in 11 percent (Creanga, 2015, 2017; Petersen, 2019). Hemorrhage is also the single most important cause o maternal death worldwide (Goman, 2016; Oladapo, 2016).
Notably, perhaps a third o severe cases o hemorrhage are likely preventable (Lepine, 2020). Tese statistics have prompted several organizations to develop programs to prevent hemorrhage-related maternal morbidity. In the United States, one example is the Alliance or Innovation on Maternal Health (AIM) (2015), with its intent to standardize recognition, response, and reporting o obstetrical hemorrhage. Te Joint Commission (2019) has also implemented standards under the Provision o Care, reatment, and Services chapter or obstetrical hemorrhage—the R3 Report. Our ollowing three chapters align with these.
GENERAL CONSIDERATIONS
■ Mechanisms of Normal Hemostasis
Near term, an incredible amount o blood—at least 600 mL/ min—ows through the spiral arteries and into the intervillous space (Pates, 2010). Averaging 120 in number, the spiral arteries lack a muscular layer because o their remodeling by trophoblasts and thereby orm a low-pressure system. With placental separation, vessels at the implantation site are avulsed. Hemostasis is achieved rst by myometrial contraction, which directly compresses the arteries. Compression is ollowed by clotting and eventually by obliteration o vessel lumens. I, ater delivery, the myometrium contracts vigorously, substantial hemorrhage rom the placental implantation site is unlikely. Importantly, an intact coagulation system is not necessary or postpartum hemostasis unless there are lacerations in the uterus, birth canal, or perineum. However, atal postpartum hemorrhage can result rom uterine atony despite normal coagulation.
■ Definition and Incidence
Historically, postpartum hemorrhage has been dened as blood losses ≥500 mL ater the third stage o labor. Tis is problematic because almost hal o all women delivered vaginally shed that amount o blood or more when losses are careully measured. Moreover, approximately 5 percent o women delivering vaginally lose >1000 mL o blood (Fig. 42-1) (Pritchard, 1962). Almost a third o women undergoing cesarean delivery have blood loss >1000 mL. Te American College o Obstetricians and Gynecologists (2019a) now denes postpartum hemorrhage as cumulative blood loss >1000 mL or blood loss accompanied by signs and symptoms o hypovolemia.
In a Maternal-Fetal Network Units study o more than
115,000 deliveries, the incidence o hemorrhage with vaginal
delivery was 5.3 percent, and it was 10.5 percent or cesarean
delivery (Yee, 2019). Importantly, hemorrhage is underreported. From the National Hospital Discharge Summary database, the reported postpartum hemorrhage incidence between
2001 and 2005 was only 2.6 percent (Berg, 2009).
■ Blood Loss Assessment
At delivery, visual estimation is oten used as a qualitative measure o blood loss. However, this method is more likely to under estimate the actual blood loss when volumes are high and to over estimate it when volumes are low (Al Kadri, 2011; Natrella, 2018). Tus, estimated blood loss that is considered greater than “average” should alert the provider. Instead, dierent methods can be used as quantitative measures. First, gravimetric measurement weighs blood-soaked items and subtracts pre-use dry weights. Another evolving tool uses a tablet-device camera and colorimetric analysis to calculate blood loss (Spies, 2020; Venkatesh, 2020). Te American College o Obstetricians and Gynecologists (2019b) recognizes the use o quantitative methods to help identiy severe hemorrhage.
Intrapartum, quantitative measurement is more accurate than visual estimation, but the eectiveness o these methods on clinical outcomes has not been demonstrated. A Cochrane Review o three trials ound no dierences between subjective and objective methods when comparing outcomes that included need or transusion, plasma expanders, or uterotonics (Diaz, 2018).
Postpartum, retrospective estimation also can be inormative. Te blood volume o a pregnant woman with normal pregnancy-induced hypervolemia usually rises by 50 percent. However, individual increases range rom 30 to 60 percent, that is, 1500 to 2000 mL or an average-sized woman (Pritchard, 1965). Te equation to calculate blood volume is shown in Table 42-1. It is axiomatic that a normal pregnant woman tolerates, without any decrease in postpartum hematocrit, blood loss at delivery that approaches the volume o blood that was added during pregnancy. Tus, i blood loss is less than the pregnancy-added volume, the hematocrit remains the same acutely and during the rst several days postpartum.
It then rises as nonpregnant plasma volume levels return during the next week or so. Whenever the postpartum hematocrit is lower than one obtained on admission or delivery, blood loss can be estimated as the sum o the calculated pregnancy-added volume plus 500 mL or each 3-volume-percent decline o the hematocrit.
For research and clinical care initiatives, excessive blood loss has been estimated by several methods (Coviello, 2019; Saoud, 2019). ita and colleagues (2012) used a 6-volumepercent drop in the postpartum hematocrit to dene clinically signicant blood loss with vaginal delivery. Tis decline easily signies a >1000-mL blood loss in the average-sized woman. Tey documented this amount in a ourth o women.
Another marker used to estimate hemorrhage incidence is the transusion rate. In the study by ita just cited, more than 6 percent o women who delivered vaginally underwent blood transusion. In a study o more than 66,000 women delivered at Parkland Hospital, 2.3 percent overall were given blood transusions or hypovolemia (Hernandez, 2012). Hal o these women had undergone cesarean delivery. Importantly, or those transused, these investigators calculated blood loss to average approximately 3500 mL!
Te need or blood transusion is now ollowed as a severe maternal morbidity (SMM) indicator. Te heightened awareness o SMM is outlined in Chapter 1 (p. 5). ransusions represent more than 80 percent o total SMM rates. Te incidence o massive transusion or postpartum hemorrhage has been reported to be rom 25 to 65 per 100,000 births (Green, 2016; Ramler, 2019). However, dening healthcare quality using transusion as an SMM metric is problematic. First, this metric is solely derived rom administrative billing codes. Second, transusion rates may be skewed based on the hospital’s case-mix (Bailit, 2013). Tis can distort values or regional reerral centers that care or women at high risk or hemorrhage, such as those with placenta accreta spectrum.
■ Risk Factors
Hemorrhage can maniest at any time during pregnancy, delivery, or the puerperium. Contributions to maternal death rom some o these causes o are shown in Figure 42-2. Te Joint Commission (2019) requires accredited delivery services to employ tools that evaluate maternal hemorrhage risk on admission to labor and delivery and postpartum. Several methods are available, and the American College o Obstetricians and Gynecologists’ (2019b) scoring tool straties risk using several obstetrical actors listed in Table 42-2. Unortunately, these scoring systems only modestly predict hemorrhage (Chu, 2020). Kawakita and colleagues (2019) examined three commonly reerenced tools and ound moderate perormance in identiying women at risk during cesarean delivery. In contrast, the Association o Women’s Health, Obstetric and Neonatal Nurses (AWHONN) risk assessment tool was predictive o those at high risk (Colalillo, 2021)
■ Timing of Hemorrhage
Obstetrical hemorrhage is traditionally classied as antepartum—such as with placenta previa or placental abruption, or as postpartum—commonly caused by uterine atony or genital tract lacerations. In individual women, however, these terms are nonspecic, and it is reasonable to speciy the cause and gestational age as descriptors. With antepartum hemorrhage, timing may give a clue to its cause. Many aspects o bleeding during the rst hal o pregnancy rom abortion or ectopic pregnancy are covered in Chapters 11 and 12. Discussions that ollow concern pregnancies with a viable-size etus. In these cases, rapid assessment should always consider the deleterious etal eects o maternal hemorrhage.
During active labor, slight vaginal bleeding is common. Tis “bloody show” is the consequence o cervical eacement and dilation and concurrent tearing o small vessels. However, with uterine bleeding above the cervix, placental abruption, placenta previa, and vasa previa must be considered. Te rst two are presented in Chapter 43 and vasa previa is discussed in Chapter 6 (p. 115). In some women, especially those with a placenta previa, cervical varicosities may bleed (O’Brien, 2013). Near term in many women, the source o uterine bleeding is not identied, bleeding ceases, and no apparent anatomical cause is ound at delivery. In most o these cases, bleeding likely originated rom a slight marginal placental separation. Despite this, any pregnancy with antepartum bleeding remains at higher risk or an adverse outcome even though bleeding has stopped and placenta previa has been excluded sonographically.
Bleeding ater midpregnancy is associated with several adverse outcomes. Te Canadian Perinatal Network described 806 women with hemorrhage between 22 and 28 weeks’ gestation (Sabourin, 2012). Placental abruption (32 percent), previa (21 percent), and cervical bleeding (6.6 percent) were the most requent causes identied. In a third, no cause was ound. O all women, 44 percent were delivered beore 29 weeks’ gestation. In more than 68,000 women in Scotland, the incidence o antepartum hemorrhage ater the rst trimester was 11 percent (Bhandari, 2014). Tese women were at signicantly higher risk or preterm birth, labor induction, and postpartum hemorrhage.
With postpartum hemorrhage, the source in most cases can and should be determined. Frequent causes are uterine atony with placental site bleeding, genital tract trauma, or both. Postpartum hemorrhage is usually obvious. Important exceptionsare unrecognized intrauterine and intravaginal blood accumulation and uterine rupture with intraperitoneal or retroperitoneal bleeding. Another consideration is an expanding vulvar or vaginal hematoma (p. 740). Initial evaluation includes attempts to dierentiate uterine atony rom genital tract lacerations. For this, risk actors are sought, the lower genital tract is examined, and uterine tone is assessed. Atony is identied by a boggy, sot uterus during bimanual examination and by expression o clots and hemorrhage during uterine massage.
Persistent bleeding despite a rm, well-contracted uterus suggests that hemorrhage most likely is rom lacerations. Bright red blood urther suggests arterial bleeding. To confrm that lacerations are a source o bleeding, careul inspection o the vagina, cervix, and uterus is essential. Examination is easier i regional analgesia is employed. ranser rom a labor and delivery room to an operative suite also may be prudent. I there are no lower genital tract lacerations and the uterus is contracted, yet supracervical bleeding persists, manual exploration o the uterus is done to exclude a uterine tear (Kaplanoglu, 2016). Tis also is completed routinely ater internal podalic version or breech extraction. Some perorm this ater successul vaginal birth ater cesarean, and this is our practice. Late postpartum hemorrhage describes bleeding ater the rst 24 hours. Found in up to 1 percent o women, one risk actor is postpartum hemorrhage at the time o delivery (Fein, 2021). Delayed hemorrhage may be serious and is discussed in Chapter 36 (p. 637).
■ Appreciation of Estimated Blood Loss
As discussed, visual blood loss estimates are oten inaccurate, especially with excessive bleeding. Instead o sudden and massive hemorrhage, postpartum bleeding is requently steady. I bleeding rom atony or laceration persists, it may appear to be only moderate at any given instant but may continue until serious hypovolemia develops. In some cases, ater placental separation, blood may not escape vaginally but instead may collect within the uterine cavity, which can become distended by 1000 mL or more o blood. Moreover, postpartum uterine massage will be ineective i applied to a roll o abdominal at mistaken or the uterus. All o these actors can lead to an underappreciation o the magnitude o hemorrhage over time.
Te eects o hemorrhage depend mainly on the maternal nonpregnant blood volume and the corresponding degree o pregnancy-induced hypervolemia. Small women—even those with appropriate pregnancy-induced hypervolemia—do not tolerate more than seemingly average blood loss. Some gravidas may be particularly susceptible to hemorrhage because their blood volume expansion is less than expected. An example is women with severe preeclampsia or eclampsia, who are more vulnerable to hemorrhage because they requently do not have a normal blood volume accrual. Specically, Zeeman and associates (2009) documented a mean increase above nonpregnant volume o only 10 percent in eclamptic women (Chap. 40, p. 693). Another example is the moderate to severe curtailing o pregnancy-induced volume expansion in women with chronic renal insufciency (Chap. 56, p. 1004). When excessive hemorrhage is suspected in these high-risk women, crystalloid and blood are promptly administered or suspected hypovolemia.
A treacherous eature o postpartum hemorrhage is the ailure o the pulse and blood pressure to undergo more than moderate alterations until large amounts o blood have been lost. Te normotensive woman initially may actually become somewhat hypertensive rom catecholamine release in response to hemorrhage. Importantly, women with preeclampsia may become “normotensive” despite remarkable hypovolemia. Accordingly, hypovolemia may not be recognized until very late.
UTERINE ATONY
■ Thirdstage Labor Management
Te most requent cause o obstetrical hemorrhage is ailure o the uterus ater delivery to contract sufciently and arrest bleeding rom vessels at the placental implantation site (Yee, 2019). Tat said, some bleeding is inevitable during thirdstage labor as the placenta begins to separate. Blood rom the implantation site may escape into the vagina immediately—the
Duncan mechanism o placental separation, or it remains concealed behind the placenta and membranes until the placenta is delivered—the Schultze mechanism. Placental descent is signi- ed by a slack umbilical cord. Ater signs o placental separation, the uterus should be massaged i it is not contracted rmly. Importantly, separation and delivery o the placenta by cord traction, especially when the uterus is atonic, may cause uterine inversion.
Following placental delivery, the undus is always palpated to conrm that the uterus is well contracted. I it is not rm vigorous undal massage usually prevents postpartum hemorrhage rom atony (Homeyr, 2013). Concurrent administration o a uterotonic agent, discussed in the next sections, is another recommended preventive measure.
■ Risk Factors
In many women with known risks, uterine atony can at least be anticipated. However, as discussed earlier (p. 733), risk-based scoring systems have limited value. In one study, up to hal o women with atony ater cesarean delivery had no risk actors (Rouse, 2006). Te magnitude o risk or atony imposed by each o the actors shown in able 42-2 varies considerably between reports. Primiparity and high parity are two actors (Driessen, 2011). In one study, the incidence o postpartum hemorrhage rose rom 0.3 percent in women o low parity to 1.9 percent with parity o our or greater. It was 2.7 percent with parity o seven or greater (Babinszki, 1999). Te overdistended uterus is prone to hypotonia ater delivery, and thus women with a large etus, multiple etuses, or hydramnios carry greater risk (Blitz, 2019). Labor abnormalities predispose to atony and include hyper- or hypotonic labor. Similarly, labor induction or augmentation with either prostaglandins or oxytocin is more likely to be ollowed by atony (Driessen, 2011). Te requency o hemorrhage increases with third-stage labor lasting >20 minutes (Frolova, 2016). Last, the woman who has had a prior postpartum hemorrhage is at risk or recurrence.
■ Evaluation and Management
o improve immediate postpartum care, clinical saety bundles provide a standardized response (Fig. 42-3). In principle, all o these programs suggest notiying unit personnel, activating resources, and standardizing management. With immediate postpartum hemorrhage, careul inspection aims to exclude birth canal laceration. In some cases, bleeding is caused by retained placental ragments, and placental inspection ater delivery should be routine. I a deect is seen, the uterus should be manually explored and the ragment removed. Occasionally, retention o a succenturiate lobe may cause postpartum hemorrhage (Chap. 6, p. 108). During examination or lacerations and causes o atony, the uterus is massaged and uterotonic agents are administered.
Manual Removal of the Placenta
I heavy bleeding persists ater delivery o the newborn but while the placenta remains partially or totally attached, then manual placental removal is indicated (Cummings, 2016; Frolova, 2016). For this, adequate analgesia is mandatory, and aseptic surgical technique is used. As illustrated in Figure 27-8 (p. 508), the ngertips o one hand, with ngers approximated, are insinuated between the uterine wall and placenta. A sweeping orward motion in this plane will peel the placenta o its uterine attachment. Ater its removal, trailing membranes are careully teased ree rom the decidua using ring orceps as needed. Another method to clear membranes is to wipe out the uterine cavity with a gauze-wrapped hand. Bierer orceps guided by ultrasound to remove retained placenta also has been described (Siegel, 2020).
Some administer a single dose o intravenous antibiotics ater manual uterine exploration, however, one systematic review o observational studies ound no benets (Chibueze, 2015). Te American College o Obstetricians and Gynecologists (2020b) concluded that data neither support nor reute this practice. Te World Health Organization (WHO) (2015) recommends ampicillin or ceazolin antimicrobial prophylaxis ater manual placenta removal. At Parkland Hospital, we routinely provide a single dose o ceazolin ater manual exploration.
Uterotonic Agents
Several compounds can be used to prompt the postpartum uterus to contract. One o these is routinely selected and given to prevent postpartum bleeding. Choices or prophylaxis include oxytocin (Pitocin); the ergots, namely ergonovine (Ergotrate) and methylergonovine (Methergine); or misoprostol (Cytotec) (Chap. 27, p. 507). Te WHO (2018) recommends oxytocin or rst-line use or prophylaxis. For administration, 20 units o oxytocin in 1000 mL o crystalloid solution is eective and given intravenously (IV) at 10 mL/min or a dose o 200 mU/min. Higher concentrations are minimally more efcient (ita, 2012). A summary o oxytocin administration regimens is ound in the Practice Brie o the Association o Women’s Health Objective and Neonatal Nurses—AWHONN (2014). In those without IV access, oxytocin may be given intramuscularly (IM). Adnan and colleagues (2018) ound the IV route to more eectively prevent severe hemorrhage compared with IM administration.
Oxytocin is never given as an undiluted bolus dose because serious hypotension or cardiac arrhythmias can develop. Most agents or prevention o atony are also used to treat it. For atony, IV oxytocin is continued or may be initiated i not selected initially. It is considered rst-line treatment by the WHO (2012). I bleeding and atony are reractory, an agent rom a dierent group can be added (American College o Obstetricians and Gynecologists, 2019a).
Ergot alkaloids have been used or centuries to treat uterine atony. I atony persists despite oxytocin and other preventive measures, ergot derivatives can be used or second-line treatment. Given parenterally, these drugs rapidly stimulate tetanic uterine contractions and act or approximately 45 minutes (Schimmer, 2011). A common regimen is 0.2 mg o either drug given IM. Methergine can be repeated at 2- to 4-hour intervals as needed. A caveat is that ergot agents, especially given IV, may cause dangerous hypertension, especially in women with preeclampsia. Severe hypertension is also seen with concomitant use o protease inhibitors given or human immunodeciency viral (HIV) inection. Tese adverse eects notwithstanding, it is speculative whether ergot derivatives oer superior therapeutic eects compared with oxytocin.
Other second-line agents or atony have included the E- and F-series prostaglandins. Carboprost tromethamine (Hemabate) is the 15-methyl derivative o prostaglandin F2α. It is approved or uterine atony treatment in a dose o 250 μg (0.25 mg) given IM. Tis dose can be repeated i necessary, at 15- to 90-minute intervals up to a maximum o eight doses. Observational data indicate an 88-percent success rate (Oleen, 1990).
Carboprost causes side eects in approximately 20 percent o women. Tese include, in descending order o requency, diarrhea, hypertension, vomiting, ever, ushing, and tachycardia. Another pharmacological eect is pulmonary airway and vascular constriction. Tus, carboprost should not be used or asthmatic women or those with pulmonary hypertension, including women those with suspected amnionic uid embolism (p. 745). It has also been reported to cause arterial oxygen desaturation that averaged 10 percent (Hankins, 1988). We have occasionally encountered severe hypertension with carboprost given to women with preeclampsia. Other relative contraindications to carboprost include renal, liver, and cardiac disease (American College o Obstetricians and Gynecologists, 2019a).
Misoprostol is a synthetic prostaglandin E1 analogue. In a Cochrane review, Mousa and associates (2014) reported no added benets or misoprostol use or treatment compared with oxytocin or ergonovine. I misoprostol is used to treat atony, the American College o Obstetricians and Gynecologists (2019a) recommends a dose o 600 to 1000 μg rectally, orally, or sublingually.
Dinoprostone (Cervidil, Prepidil) is prostaglandin E2. It may also be used o label or atony treatment and is given as a 20-mg suppository per rectum or per vagina every 2 hours. It typically causes diarrhea, which is problematic or the rectal route, whereas vigorous vaginal bleeding may preclude its use per vagina. Hypotension, which is commonly encountered with hemorrhage, is considered a contraindication by some. For this reason, this agent is not deployed or hemorrhage management at Parkland Hospital. IV prostaglandin E2—sulprostone—is used in Europe, but it is not available in the United States.
Tranexamic Acid
Tis antibrinolytic agent has been evaluated to treat postpartum hemorrhage. In the randomized WOMAN trial o gravidas with hemorrhage ollowing vaginal birth or during cesarean delivery, mortality rates rom obstetrical hemorrhage were 1.2 percent in those given a 1-g IV tranexamic acid dose plus traditional care or bleeding. Tis rate was signicantly lower than the 1.7-percent death rate in women given traditional care alone (WOMAN rial Collaborators, 2017). Another study o women with hemorrhage ollowing vaginal birth ound that rates o progression to severe PPH, o transusion, and o peripartum hysterectomy were lower in the XA group compared with the traditional-care group (Ducloy-Bouthors, 2011). Use o tranexamic acid in hemorrhage is discussed urther in Chapter 44 (p. 773).
Bleeding Unresponsive to Uterotonic Agents
I bleeding persists ater initial measures or atony, the ollowing management steps are perormed immediately and simultaneously:
1. Begin bimanual uterine compression, which is easily done and controls most cases o continuing hemorrhage (Fig. 42-4). Tis technique is not simply undal massage. Te posterior uterine wall is massaged by one hand on the abdomen, while the other hand is made into a st and placed into the vagina. Tis st kneads the anterior uterine wall through the anterior vaginal wall, and the uterus is compressed between the two hands.
2. Mobilize the emergent-care obstetrical team and call or whole blood or packed red cells.
3. Request urgent help rom the anesthesia team.
4. Secure at least two large-bore IV catheters so that crystalloid with oxytocin can be continued simultaneously with blood products. Insert a Foley catheter or continuous urine output monitoring.
5. Begin volume resuscitation with rapid IV crystalloid inusion (p. 734).
6. With sedation, analgesia, or anesthesia established and now with optimal exposure, once again manually explore the uterine cavity or retained placental ragments and or uterine abnormalities, including lacerations or rupture.
7. Toroughly inspect the cervix and vagina again or lacerations that may have escaped attention.
8. Administer blood transusions i the woman is still unstable or i bleeding persists (Chap. 44, p. 771).
At this juncture, ater causes other than atony have been excluded and ater hypovolemia is reversed, several other measures are considered i bleeding continues (Merriam, 2020). Teir use depends on several actors such as parity, desire or sterilization, and experience with each method.
Balloon Tamponade and Surgical Procedures. For this, the tip o a 24F to 30F Foley catheter with a 30-mL balloon is guided into the uterine cavity and lled with 60 to 80 mL o saline. Te open tip permits continuous drainage o blood rom the uterus. We have experienced balloon rupture when more than 50 mL was instilled into the balloon, thus a 34F Foley with a 60-ml balloon can be used. I bleeding subsides, the catheter is typically removed ater 12 to 24 hours. Similar devices or tamponade include Sengstaken-Blakemore, Rusch, and ebb balloons and condom catheters (Antony, 2017; Kondoh, 2019). Antibiotic prophylaxis using ceazolin, 1 gram every 8 hours until removal, has recently been suggested to reduce risk o postpartum endometritis (Martingano, 2020).
Instead, specially constructed intrauterine balloons are available to treat hemorrhage rom uterine atony and other causes. A Bakri Postpartum Balloon or BT-Cath may be inserted and inated to tamponade the endometrial cavity and stop bleeding (Fig. 42-5). Insertion requires two or three team members.
Te rst perorms abdominal sonography during the procedure. Te second places the deated balloon into the uterus and stabilizes it. Te third member instills uid to inate the balloon, rapidly inusing at least 150 mL ollowed by urther instillation over a ew minutes or a total o 300 to 500 mL to arrest hemorrhage. It is reasonable to remove the balloon ater approximately 12 hours (Einerson, 2017).
In small studies evaluating uterine balloons or all causes, the success rate approximated 85 percent (Kaya, 2016; Said Ali, 2021; Vintejoux, 2015). From their review, Suarez and associates (2020) used balloon tamponade in 4729 women and reported a similar success rate. At least one case o uterine rupture with a balloon has been reported (Ngyuen, 2018). Combinations o balloon tamponade and uterine compression sutures also have been described (Diemert, 2012; Yoong, 2012). Failure o uterotonic agents and tamponade requires more invasive methods. Tese include uterine compression sutures, major pelvic vessel ligation, angiographic embolization, and hysterectomy. Tese are discussed in detail in Chapters 44 (p. 778). Peripartum hysterectomy is illustrated in Chapter 30 (p. 560).
UTERINE INVERSION
Puerperal inversion o the uterus is one o the classic hemorrhagic disasters encountered in obstetrics. Unless promptly recognized and managed appropriately, associated bleeding oten is massive. Risk actors include alone or in combination: (1) placental implantation at the undus, (2) uterine atony, (3) cord traction applied beore placental separation, and (4) abnormally adherent placentation seen with placenta accreta spectrum disorders (Chap. 43, p. 759). Other risk actors are a short cord, uterine wall weakening at the implantation site, uterine tumors, and excessive undal pressure (Wendel, 2018)
FIGURE 42-6 Progressive degrees of uterine inversion.
Depending on which o these actors are contributory, the incidence and severity o uterine inversion varies and can be progressive (Fig. 42-6). Te worst scenario is complete inversion with the uterus protruding rom the birth canal (Fig. 42-7).
Te incidence o uterine inversion ranges rom 1 case in 2000 to 1 in 20,000 vaginal deliveries (Coad, 2017; Witteveen, 2013). Our experiences at Parkland Hospital correspond with the higher 1:2000 incidence. Tis is despite our policy o discouraging placental delivery by cord traction alone, and beore certainty o its separation. It is unknown i active management o third-stage labor with cord traction applied ostensibly ater signs o placental separation raises the likelihood o uterine inversion (Deneux-Taraux, 2013; Prick, 2013).
■ Recognition and Management
Immediate recognition o uterine inversion improves the chances o a quick resolution and good outcome. I initially unrecognized, continued hemorrhage likely will prompt closer examination o the birth canal. Although complete inversion is usually evident, the partially inverted uterus can be mistaken or a uterine myoma, and sonography can aid dierentiation (Pan, 2015; Smulian, 2013). Many cases are associated with immediate lie-threatening hemorrhage, and a ourth require blood replacement (Coad, 2017).
Once any degree o uterine inversion is recognized, several steps must be implemented urgently and simultaneously:
1. Immediate assistance is summoned, including obstetrical and anesthesia personnel.
2. Blood is brought to the delivery suite or potential use.
3. wo large-bore IV inusion systems are secured to begin rapid crystalloid inusion to treat hypovolemia while awaiting arrival o blood products.
4. Te woman is evaluated or emergency general anesthesia.
5. I the recently inverted uterus has not contracted and retracted completely and i the placenta has already separated, the uterus may oten be replaced simply by pushing up on the inverted undus with the palm o the hand and ngers in the direction o the long axis o the vagina (Fig. 42-8). Some use two ngers rigidly extended to push the center o the undus upward. Care is taken not to apply so much pressure as to perorate the uterus with the fngertips.
6. I the placenta is still attached, attempts are made to reposition the uterus with the placenta in situ. In theory, the uterus contracts to a lesser degree and placenta-site blood loss is less with an attached placenta. At this time a trial o an intravenously administered tocolytic drug may aid uterine relaxation and repositioning. O options, a 250-µg subcutaneous dose o terbutaline, a 50- to 100-µg IV dose o nitroglycerin, or a 4-g IV dose o magnesium sulate are suitable (Catanzarite, 1986; Duour, 1997). I these ail to provide sufcient relaxation, then a rapid-acting halogenated inhalational agent is administered by anesthesia sta. Ater the uterus is replaced, the placenta is careully manually removed.
7. I uterine repositioning ails with the placenta attached, it is peeled o, and uterine repositioning is attempted again.
8. Once the uterus is restored to its normal conguration, tocolysis is stopped, oxytocin is then inused, and other uterotonic agents may be given as described or atony (p. 735). Meanwhile, the operator maintains the undus in its normal anatomical position while applying bimanual compression to control urther hemorrhage until the uterus is well contracted (see Fig. 42-4). Te operator continues to monitor the uterus transvaginally or evidence o subsequent inversion. A Bakri balloon has been used by some to maintain the repositioned uterus (Haeri, 2015; Ida, 2015).
FIGURE 42-7 Maternal death during home delivery caused by exsanguination from uterine inversion, which stemmed from a fundally implanted placenta increta
FIGURE 42-8 Incomplete uterine inversion can be repositioned by using the abdominal hand for palpation of the crater-like depression while simultaneously gently pushing the inverted fundus upward.
■ Surgical Intervention
In most cases, the inverted uterus can be restored to its normal position by the just-described techniques. Occasionally, manual replacement ails. One cause is a dense myometrial constriction ring. At this point, laparotomy is imperative. Te anatomical conguration ound at surgery can be conusing as shown in Figure 42-9. During laparotomy and ater tocolysis is given, a combined eort is made to reposition the uterus by concurrently pushing upward rom below and pulling upward rom above. Application o atraumatic clamps to each round ligament and upward traction may be helpul—the Huntington procedure. In some cases, placing a deep traction suture in the inverted undus or grasping it with tissue orceps may help but can be technically difcult. I a constriction ring still prohibits repositioning, a sagittal surgical cut—Haultain incision—is made posteriorly through the muscular ring to release it. Te exposed undus can then be reinverted (Sangwan, 2009).
Ater uterine replacement, tocolytics are stopped, and oxytocin and other uterotonic agents are given. I the Haultain method is used, the uterine incision is repaired. Risks o separation o this posterior hysterotomy incision during subsequent pregnancy, labor, and delivery are unknown (Wendel, 2018).
Further illustration and discussion are ound in Cunningham and Gilstrap’s Operative Obstetrics, 3rd edition (imoeev, 2017). In some cases, the uterus will again invert almost immediately ater repositioning. With this problem, uterine compression sutures can be used to prevent another inversion (Matsubara, 2009; Mondal, 2012). Occasionally, chronic puerperal uterine inversion may become apparent weeks ater delivery.
FIGURE 42-9 Surgical anatomy of a completely inverted uterus viewed from above at laparotomy.
■ Vulvovaginal Lacerations
Childbirth is invariably associated with trauma to the uterus and cervix, vagina, and perineum. Injuries range rom minor mucosal tears to lacerations that create lie-threatening hemorrhage or hematomas. According to the American College o Obstetricians and Gynecologists (2020a), up to 80 percent o women sustain some type o laceration at vaginal birth. Tese may lie proximally or distally along the lower genital tract.
Small tears o the vaginal wall near the urethra are relatively common. Tey are oten supercial with little to no bleeding but occasionally require ne-gauge absorbable sutures or hemostasis. Tose large enough to require extensive repair are typically associated with short-term voiding difculty, and an indwelling bladder catheter will obviate this.
Deeper perineal lacerations are usually accompanied by varying degrees o injury to the outer third o the vagina. Some extend to involve the anal sphincter or varying depths o the vaginal walls. Repair o these perineal lacerations is detailed in Chapter 27 (p. 510).
Lacerations involving the middle or upper third o the vagina usually are comorbid with injuries o the perineum or cervix. Tese sometimes are missed unless inspection is thorough. Tose that extend upward usually are longitudinal. Tey may ollow spontaneous delivery but requently result rom injuries sustained during operative vaginal delivery. Most involve deeper underlying tissues and thus usually cause signicant hemorrhage, which is controlled by suture repair. For this, eective analgesia or anesthesia, clear visualization, capable assistance, and sufcient resuscitation o hypovolemia are mandatory.
Extensive vaginal or cervical tears should prompt a careul search or evidence o retroperitoneal hemorrhage or o peritoneal peroration with hemorrhage. Intrauterine exploration is also considered to exclude uterine tears or rupture (Conrad, 2015). I peritoneal peroration or uterine rupture is strongly suspected, laparotomy is reasonable (Ra, 2010). As discussed later (p. 742), imaging and potential embolization may be suitable or large retroperitoneal hematomas.
■ Cervical Lacerations
Supercial lacerations o the cervix can be seen on close inspection in more than hal o all vaginal deliveries. Most o these measure <0.5 cm and seldom require repair. Deeper lacerations are less requent, but even these may be unnoticed. Such lacerations are more likely to be associated with vacuum- or orceps-assisted vaginal delivery (Fong, 2014). Due to ascertainment bias, variable incidences are described. For example, with close inspection, the incidence o cervical lacerations in the Consortium on Sae Labor database was 1 percent in nulliparas and 0.5 percent in multiparas (Landy, 2011). But, the overall incidence in a study o more than 81,000 Israeli women was only 0.16 percent (Melamed, 2009).
Cervical lacerations are not usually problematic unless they cause hemorrhage or extend to the vagina. Rarely, the cervix may be entirely or partially avulsed rom the vagina in the anterior, posterior, or lateral ornices, an injury termed colporrhexis.
Another rare injury is avulsion o the entire vaginal portion o the cervix—annular or circular detachment. Tese injuries sometimes ollow orceps deliveries perormed through an incompletely dilated cervix and with the blades applied against the cervix. In some women, cervical tears reach into the lower uterine segment and involve the uterine artery and its major branches. Tey occasionally extend into the peritoneal cavity.
More severe lacerations usually maniest as external hemorrhage or as a hematoma, however, they may occasionally be unsuspected. In the Israeli study just cited, almost 11 percent o women with a cervical laceration required blood transusions (Melamed, 2009).
At times, the edematous anterior cervical lip is compressed between the etal head and maternal symphysis pubis. Tis usually is o little consequence and resolves spontaneously. Rarely, this causes severe ischemia, and the anterior lip may undergo necrosis and later separate rom the rest o the cervix.
As with vulvovaginal lacerations, cervical tears can be more ully appreciated with adequate exposure, which may be best attained with transer to an operating room. An assistant applies rm downward pressure on the uterus, while the operator exerts gentle traction on the lips o the cervix with ring orceps. A second assistant can provide even better exposure with right-angle vaginal wall retractors or Breisky vaginal retractors. Yankauer or other suction tips also can aid viewing. In general, cervical lacerations o 1 to 2 cm are not repaired unless they are bleeding. Such tears heal rapidly and ultimately orm an irregular, sometimes stellate-appearing, external cervical os (Fig. 36-1, p. 635).
Deep cervical tears usually require surgical repair. When the laceration is limited to the cervix or even when it extends somewhat into the vaginal ornix, satisactory results are obtained by suturing the cervix ater bringing it into view as depicted in Figure 42-10. While cervical lacerations are repaired, any associated vaginal lacerations or an episiotomy may be tamponaded with gauze packs to arrest their bleeding. Because hemorrhage usually comes rom the upper angle o the wound, the rst suture using 2–0 chromic or polyglactin is placed in
tissue above the angle. Subsequently, either interrupted or continuous locking sutures are serially placed outward toward the operator. I the uterus is involved and hemorrhage persists, some o the surgical and angiographic methods described in Chapter 44 (p. 777) may be necessary to obtain hemostasis. Following cervical lacerations, subsequent pregnancy outcomes include excessive recurrent lacerations, cervical incompetence, preterm labor, cesarean delivery, and severe perineal lacerations (Hamou, 2020).
■ Puerperal Hematomas
Pelvic hematomas can have several anatomical maniestations ollowing childbirth. One classication is anatomical and describes vulvar, vulvovaginal, paravaginal, and retroperitoneal hematomas. Vulvar hematomas may involve the vestibular bulb or branches o the pudendal artery, which are the inerior rectal, perineal, and clitoral arteries (Fig. 42-11). Paravaginal hematomas may involve the descending branch o the uterine artery. In some cases, a torn vessel lies above the pelvic ascia, and a supralevator hematoma develops. Tese can extend into the upper portion o the vaginal canal and may almost occlude its lumen. Continued bleeding may dissect retroperitoneally to orm a mass palpable above the inguinal ligament. In some cases, it may even dissect up behind the ascending colon to the hepatic exure (Ra, 2010).
Risks or puerperal hematomas include vaginal or perineal laceration, episiotomy, or operative vaginal delivery (Iskender, 2016). Any hematoma can also develop ollowing stretch and rupture o a blood vessel without an associated laceration (Alturki, 2018; Lee, 2020). Tis may be especially true with orceps delivery. Occasionally, they are associated with an underlying coagulopathy (Chap. 44, p. 775).
Diagnosis
Perineal, vulvar, and paravaginal hematomas can develop rapidly and requently cause excruciating pain (Fig. 42-12). A tense, tender swelling o varying size rapidly develops, encroaches on the vaginal lumen, and causes overlying skin or epithelium to become ecchymotic. A paravaginal hematoma may escape detection initially. However, symptoms o pelvic pressure, pain, or inability to void should prompt evaluation.
Others may go undetected until other measures o hypovolemia become evident. With a supralevator extension, the hematoma extends upward in the paravaginal space and between the leaves o the broad ligament. Te hematoma may escape detection until it can be elt on abdominal palpation or until hypovolemia develops. Imaging with sonography or computed tomographic scanning may be useul (Cichowski, 2017; Kawamura, 2014).
Management
Small hematomas oten remain contained and show minimal expansion. In others, the tissues overlying an expanding hematoma may rupture rom pressure necrosis. In some, prouse hemorrhage may ollow, but in other cases, the hematoma drains in the orm o large clots and old blood. In those that involve the paravaginal space and extend above the levator sling, retroperitoneal bleeding may be massive and occasionally atal. In rare instances, we encountered hematomas that rebled up to 2 weeks postpartum (Cunningham, 2017)
Vulvovaginal hematomas are managed according to their size, location, duration since delivery, and expansion. I bleeding ceases, then small- to moderate-sized hematomas may be treated expectantly until absorbed. Cool packs and analgesics are supportive care, and an inability to void merits catheter drainage. But, i pain is severe or i the hematoma continues to enlarge, surgical exploration is preerable. Blood loss with large puerperal hematomas is nearly always considerably more than the clinical estimate. Hypovolemia is common, and transusions are requently required when surgical repair is necessary.
For repair, an incision is made at the point o maximal distention, blood and clots are evacuated, and bleeding points ligated. Oten, no distinct bleeding vessels are identied. Te cavity may then be obliterated in layers with absorbable sutures. With this, layered tissue closure acts to tamponade low-pressure bleeding. With vaginal hematomas, the vagina is packed with 1 to 2 gauze roll(s) or 12 to 24 hours, and the number o rolls is recorded. Supralevator hematomas are more difcult to treat. Although some can be evacuated by vulvar or vaginal incisions, laparotomy or angiographic embolization are considerations i bleeding continues.
Embolization has become popular or management o some puerperal hematomas. Tis is especially true or supralevator or retroperitoneal hematomas. Embolization can be used primarily, or more likely secondarily, i surgical attempts at hemostasis have ailed or i the hematoma is difcult to access surgically (Disteano, 2013; Lee, 2012; Poujade, 2012). Te use o a Bakri balloon or a paracervical hematoma also has been described (Gizzo, 2013; Grönvall, 2014). Last, ultrasound-guided drainage o a recurrent supralevator hematoma has been reported (Mukhopadhyay, 2015).
UTERINE RUPTURE
■ Predisposing Factors
Uterine rupture is another event that may lead to potentially catastrophic hemorrhage. Rupture may be primary, dened as occurring in a previously intact or unscarred uterus. More oten, rupture is secondary and associated with a preexisting incision, anomaly, or injury o the myometrium (Table 42-3). Te contribution o each o these underlying causes has evolved during the past 50 years. Beore 1960, when cesarean delivery was inrequent and women o great parity were numerous, primary uterine rupture predominated. As the incidence o cesarean delivery rose, and especially as a subsequent trial o labor in these women became prevalent through the 1990s, uterine rupture through the cesarean hysterotomy scar became the preeminent cause (Chang, 2020; Gibbins, 2015; Mone, 2016).
Concurrent with the diminished enthusiasm or a trial o labor ater cesarean delivery (OLAC), incidence trends or the two types o rupture have again changed. In a study o 3942 cases o uterine rupture in more than 15 million women, only approximately hal were in women with a prior cesarean delivery (Yao, 2017). Te International Network o Obstetric Survey Systems (INOSS) identied 864 complete uterine ruptures in more than 2.6 million deliveries (Vanderberghe, 2019). Te overall prevalence was 3 cases per 10,000 births. In women without a prior cesarean delivery, the prevalence was 0.6 per 10,000 births, and it was 22 per 10,000 in those with a prior cesarean delivery. Tis is similar to the recent overall rate o 5 cases per 10,000 births at Parkland Hospital. During this time, there were 40 cases o uterine rupture, and despite a very conservative OLAC policy, 25 o the 40 events were in women with a prior hysterotomy.
Te current lower incidence o women o great parity also has lowered the primary-rupture rate. In this regard, advancing maternal age may be a greater risk actor (Hochler, 2020). Another risk is excessive or inappropriate uterine stimulation with oxytocin. Tis previously requent cause has mostly disappeared. In an analysis o three trials comparing contemporaneous high- and low-dose oxytocin regimens or labor induction in those with an unscarred uterus, the rate o uterine rupture did not dier between groups (Budden, 2014). Te rate o rupture, however, is increased with sequential induction o labor with prostaglandins and oxytocin in those both with and without prior cesarean delivery (Al-Zirqi, 2017).
Other operations that traumatize the myometrium include uterine curettage or peroration, endometrial ablation, myomectomy, operative hysteroscopy, or prior uterine rupture (Frank, 2018; Zhao, 2019). Uterine rupture is also linked with disorders associated with connective tissue weakness (Cauldwell, 2019a,b; Noh, 2013). Another report described rupture in a woman with prior childhood pelvic radiotherapy (Huarte Cignada, 2020).
Blunt abdominal trauma also can rupture a substantially gravid uterus (Miller, 1996). Tus, pregnant women in the later second- and third trimesters who sustain such trauma are ideally monitored or signs o uterine rupture. Specic monitoring protocols are outlined in Chapter 50 (p. 896). Uncommon causes today are those due to internal podalic version and extraction, difcult orceps delivery, breech extraction, and unusual etal enlargement such as with hydrocephalus. In one unusual case, undal rupture ollowed spontaneous labor in a woman with an abdominal cerclage (Dandapani, 2019). Rupture associated with multietal pregnancy or uterine anomalies also is rare (Bankada, 2015; arney, 2013; ola, 2014). Although rare, rudimentary uterine horns are especially susceptible and described in Chapter 3 (p. 43). Discussed in Chapter 43 (p. 760), placenta percreta may cause ocal myometrial weakness and rupture (Sun, 2016).
■ Pathogenesis
Rupture o the previously intact uterus during labor most oten involves the thinned-out lower uterine segment. When the rent is in the immediate vicinity o the cervix, it requently extends transversely or obliquely. When the rent orms in the portion o the uterus adjacent to the broad ligament, the tear is usually longitudinal (Fig. 42-13). Although these tears develop primarily in the lower uterine segment, they can extend upward into the active segment or downward through the cervix and into the vagina. In some cases, the bladder also may be lacerated. I the rupture is o sufcient size, the uterine contents will usually escape into the peritoneal cavity. I the presenting etal part is rmly engaged, however, then only a portion o the etus may be extruded rom the uterus. Fetal prognosis is largely dependent on the size o the rent, the degree o placental separation, the magnitude o maternal hypovolemia, and the rapidity o diagnosis and response (Al-Zirqi, 2018; Rottenstreich, 2021).
In some cases, the overlying peritoneum remains intact, and this usually is accompanied by hemorrhage that extends into the broad ligament to cause a large retroperitoneal hematoma. Following vaginal delivery in an unscarred uterus, we and others have occasionally encountered cases o an incomplete tear on the inside o the uterus that extends vertically into the active segment to cause prouse hemorrhage (Conrad, 2015).
Tese tears are usually not visible rom below but are ound at the time o hysterectomy or intractable bleeding despite a contracted uterus. Hemorrhage with this type o tear can be torrential, and bleeding is usually not slowed until the uterine artery pedicles are clamped bilaterally.
■ Management and Outcomes
Te varied clinical presentations o uterine rupture and its management are discussed in detail in Chapter 31 (p. 579). In the most recent national maternal mortality statistics, uterine rupture accounted or nearly 10 percent o hemorrhage-associated deaths (Creanga, 2015, 2017). Maternal morbidity includes hysterectomy that may be necessary to control hemorrhage. Rates o perinatal mortality and morbidity, which may include severe neurological impairment, also are high (Al-Zirqi, 2018; Rottenstreich, 2021). Table 42-4 lists some perinatal outcomes in 72 women with uterine rupture. Last, maternal obesity comorbid with uterine rupture is associated with increased rates o adverse neonatal outcomes (Yao, 2017). With prior rupture and a subsequent pregnancy, Fox (2020) recommends cesarean delivery prior to labor or at the onset o preterm labor.
AMNIONIC FLUID EMBOLISM
■ Pathophysiology
Tis syndrome usually is caused by intravenous embolization o meconium-laden amnionic uid. It results in rapid cardiorespiratory collapse and proound consumptive coagulopathy. Te understanding o the mechanism o injury or amnionic uid embolism (AFE) has evolved. Early theories proposed that amnionic uid and debris entered the maternal circulation and obstructed pulmonary artery ow, which led to hypoxia, right heart ailure, and death. However, during normal delivery, amnionic uid commonly enters maternal circulation through venous channels at the placental implantation site or small lacerations. Accordingly, squames, etal cells, and trophoblasts can oten be identied in maternal peripheral blood at delivery (Clark, 1986; Lee, 1986). And, at least in experimental animals, inused clear amnionic uid is generally innocuous, even in large amounts (Adamsons, 1971; Stolte, 1967).
Instead, meconium-laden amnionic uid is likely a potent cause o symptomatic AFE (Hankins, 1993). Disruption o the maternal-etal interace allows material rom the etal compartment to enter maternal circulation. Tis dyad leads to abnormal activation o proinammatory mediator systems, similar to the systemic inammatory response syndrome (SIRS), and causes initial, transient pulmonary vasoconstriction and hypertension (Bernstein, 2019). Pulmonary hypertension causes acute right ventricular ailure, which is ollowed by hemodynamic collapse rom right ventricular inarction, interventricular septum displacement, and decreased let-sided cardiac output (Pacheco, 2020). Tis right and then let ventricular dysunction leads to cardiogenic pulmonary edema and systemic hypotension.
Acute respiratory ailure with severe hypoxemia rom shunting develops. Notably, the resulting multiorgan dysunction is an interrelated process, with both the cardiac and pulmonary systems aecting each other. Women who survive beyond these rst phases invariably develop the third component o the classic triad—a consumptive coagulopathy. Material rom the etal compartment that contains tissue actor then activates actor VII. Tis leads to the development o disseminated intravascular coagulation. Te rapidity o the coagulopathy is amazing (Fig. 42-14). o those who succumb, postmortem histopathological ndings may be obvious. However, detection o squames and keratin may require special stains, and even then, debris may not be seen. In one study, etal elements were detected in 75 percent o autopsies and in 50 percent o specimens prepared rom concentrated buy coat aspirates taken antepartum rom a pulmonary artery catheter (Clark, 1995).
■ Incidence and Risk Factors
Most reports describe an AFE requency o 1 to 2 cases per 100,000 births (Clark, 2014; Fitzpatrick, 2019; Knight, 2010). Te case-atality rate in all o these studies ranges rom 11 to 43 percent. From another perspective, AFE caused 5 to 15 percent o all pregnancy-related deaths in the United States, Canada, and France (Bonnet, 2018; Kramer, 2012; Petersen, 2019). Predisposing conditions are rapid labor, meconium-stained amnionic uid, and tears into uterine and other large pelvic veins that permit an exchange o uids between the maternal and etal compartment (Society o Maternal-Fetal Medicine, 2016). Other commonly cited risks include older maternal age; postterm pregnancy; labor induction or augmentation; eclampsia; cesarean, orceps, or vacuum delivery; placental abruption or previa; and hydramnios (Indraccolo, 2018; Knight, 2012; Kramer, 2012). Te associations o uterine hypertonus appears to be the eect rather than the cause because uterine blood ow ceases when intrauterine pressures exceed 35 to 40 mm Hg.
Tus, a hypertonic contraction would be the least likely circumstance or amnionic uid and other debris to enter uterine veins (Clark, 1985). For this reason, hypertonus rom oxytocin does not seem implicated.
■ Diagnosis
Te classic triad o abrupt hemodynamic and respiratory compromise along with consumptive coagulopathy underpins its diagnosis (Pacheco, 2020). Proposed criteria or AFE diagnosis are shown in Table 42-5. In a French study, only 60 percent o women with autopsy-conrmed AFE had all our criteria (Bonnet, 2018). Te classic example is dramatic, and a woman in the late stages o labor or immediately postpartum begins gasping or air. Seizures or cardiorespiratory arrest rapidly ollow and are accompanied by massive hemorrhage rom consumptive coagulopathy (Bernstein, 2019; anaka, 2017). Clinical mani- estations vary, and we and others have managed several women in whom otherwise uncomplicated vaginal or cesarean delivery was ollowed by severe acute consumptive coagulopathy without overt cardiorespiratory difculties. In these women, consumptive coagulopathy appears to be the orme ruste o AFE (Kramer, 2012; Porter, 1996).
In such cases, other sources o acute cardiac or respiratory ailure should be considered. Tese include myocardial inarction, pulmonary or air embolism, high spinal blockage, eclampsia, and anaphylactic shock (Bernstein, 2019). In some cases, the temporal relationship o events aids diagnosis. Unortunately, no specifc diagnostic laboratory test confrms or reutes the diagnosis o AFE, and it remains a clinical diagnosis. Importantly, women suering rom excessive blood loss and resulting coagulopathy may be misdiagnosed with AFE, when the true culprit is unrecognized or underappreciated hemorrhage (Clark, 2016). In either event, a woman with cardiopulmonary compromise should receive immediate resuscitation (Society or Maternal-Fetal Medicine, 2016).
■ Management
Te initial period o systemic and pulmonary hypertension with AFE is transient. Tus, immediate high-quality cardiopulmonary resuscitation and advanced cardiac lie support must be initiated without delay (Pacheco, 2020; Society or MaternalFetal Medicine, 2016). Tese are discussed in detail in Chapter 50 (p. 897). Coagulopathy is managed as described in Chapter 44 (p. 777). I resuscitation is successul, hemodynamic instability is common in survivors. Both ever and hyperoxia will worsen ischemia-reperusion injury to the brain. A suitable goal or temperature is 36°C and or mean arterial pressure is 65 mm Hg (Society or Maternal-Fetal Medicine, 2016). Additional supportive care measures such as intubation are usually necessary.
During the phase o right ventricular ailure, inotropic agents such as dobutamine may improve right heart output, and later systemic hypotension should be treated with vasopressors such as norepinephrine. Excess uid administration is discouraged because it can worsen dilation o an already engorged right ventricle, which may cause right-sided myocardial inarction and interventricular septum displacement.
Extracorporeal membrane oxygenation (ECMO) has been described in the treatment o AFE (Bernstein, 2019; Webster, 2020). Further discussed in Chapter 50 (p. 886), venovenous ECMO is used or severe hypoxemic respiratory ailure, without right or let ventricular ailure. Venoarterial ECMO is less readily available and used or impending cardiac arrest and ventricular ailure. One recent review o outcomes in 20 women with AFE managed with ECMO reported a maternal mortality rate o only 15 percent. Te authors concluded that publication biases may have overestimated the avorable outcomes (Viau-Lapointe, 2019).
Either immediately ater cardiopulmonary collapse or during the ensuing phases o injury, a coagulopathy develops in most cases rom activation o actor VII and X. Tis may be exacerbated by ongoing hemorrhage, and a common source is uterine atony. Tus, immediate evaluation o coagulation parameters is indicated with concurrent management o bleeding.
■ Clinical Outcomes
Most reports describe signicant maternal and perinatal mortality with AFE. Tis is likely inuenced by underdiagnosis and reporting biases that avor the most severe cases with the highest mortality rates. From a Caliornia database o 1.1 million deliveries, the mortality rate with AFE was 60 percent (Gilbert, 1999). In the INOSS database, maternal mortality rates ranged rom 30 to 41 percent (Fitzpatrick, 2019). Death can be rapid, and in one study, 12 o the 34 women died within 30 minutes (Weiwen, 2000). Te mortality rate is highest in women who present with cardiac arrest—89 percent (Fitzpatrick, 2019).
Survivors commonly have proound neurological impairment. Clark (1995) observed that only 8 percent o women who lived despite cardiac arrest survived without neurological injury. In a report o 20 cases, the maternal mortality rate was 15 percent, and 40 percent o survivors had neurological disability (Skolnik, 2019). Overall, the prognosis appears to be more associated with disease severity and the attendant cardiac arrest than with any specic treatment modality (Clark, 2014; Fitzpatrick, 2019).
As perhaps expected, perinatal outcomes also are poor and are inversely related to the maternal cardiac arrest-to-delivery interval. Even so, the neonatal survival rate is 70 percent, but unortunately, up to hal o survivors suer residual neurological impairment. In a Canadian study, 28 percent o neonates were considered to be asphyxiated at birth (Kramer, 2012).
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