Chapter 43. Hemorrhagic Placental Disorders. Will Obs.

 Hemorrhagic Placental Disorders

BS. Nguyễn Hồng Anh

Hemorrhage ollowing partial or complete separation o the placenta can be torrential. Recall that the amount o bloo owing through the intervillous space at term excees 600 mL/ min (Pates, 2010). In the secon hal o pregnancy, three placental isorers contribute substantially to maternal mortality rates. Tese inclue placental abruption, placenta previa, an placenta accreta spectrum.

Te contributions o hemorrhagic placental isorers to maternal mortality are iscusse in Chapter 1 (p. 7) an Chapter 42 (p. 733). Te management an clinical experience with these isorers span more than a generation. Placental abruption, or example, has been emphasize in this text or more than 50 years beginning with the work o Dr. Jack Pritchar. Now more common than years past, placenta accreta spectrum is another substantial threat to maternal well-being

PLACENTAL ABRUPTION

■ Etiopathogenesis

Separation o the placenta—either partially or totally—rom its implantation site beore elivery is calle placental abruption or abruptio placentae. From Latin, the latter translates as “ren- ing asuner o the placenta,” which enotes a suen accient, which is characteristic o most cases. In the purest sense, the cumbersome—an thus selom use—term premature separation of the normally implanted placenta is most escriptive because it exclues separation o a placenta previa.

Abruption likely begins with rupture o a eciual spiral artery an hemorrhage into the eciual basalis. Te subsequent expaning retroplacental hematoma splits the eciua an leaves a thin layer aherent to the myometrium. Te eci- ual hematoma grows to lit away an compress the ajacent placenta. In some cases that are associate with preeclampsia, impaire trophoblastic invasion with subsequent atherosis is one unerlying preisposition (Brosens, 2011). Inammation or inection also may be contributory (Mhatre, 2016). However, histological nings cannot be use to etermine the timing o the abruption (Chen, 2017).

In the early stages o placental abruption, clinical symptoms may be absent. Even with continue bleeing an placental separation, placental abruption can still be either total or partial (Fig. 43-1). With either, bleeing typically insinuates itsel between the membranes an uterine wall, ultimately escaping through the cervix to cause external hemorrhage. Less oten, the bloo is retaine, leaing to concealed hemorrhage an elaye iagnosis. Te elay translates into greater maternal an etal hazars. With conceale hemorrhage, the likelihoo o consumptive coagulopathy is also increase. Tis is because increase pressure within the intervillous space, cause by the expaning retroplacental clot, orces more placental thromboplastin into the maternal circulation (Chap. 44, p. 775)

Most bloo in the retroplacental hematoma in a nontraumatic placental abruption is maternal. Tis is because hemorrhage erives rom separation within the maternal eciua, an placental villi are usually initially intact. In 78 women at Parklan Hospital with a nontraumatic placental abruption, etalto-maternal hemorrhage was ocumente in only 20 percent. All o these ha <10 mL etal bloo loss (Stettler, 1992). In another series o 68 women with a placental abruption, etal cells were oun in peripheral bloo in only 4 percent (Atkinson, 2015).

Placental abruption can create a visible circumscribe

epression on the maternal surace o a reshly elivere placenta. Tese epressions usually measure a ew centimeters in iameter an are covere by ark, clotte bloo. Because several minutes are require or these anatomical changes to materialize, a very recently separate placenta may appear totally normal at elivery. Our experiences are like those o Benirschke an associates (2012) in that the “age” o the retroplacental clot cannot be etermine exactly. In the example shown in Figure 43-2, a large ark clot is well orme. It has epresse the placental bulk an likely is at least several hours ol.

Dening placental abruption severity is problematic. We consier placental abruption severe when the etus ies. However, maternal an etal complications are requently serious even with a liveborn etus. Ananth an coworkers (2016) have ene severe placental abruption as isplaying one or more o the ollowing: (1) maternal sequelae that inclue isseminate intravascular coagulation (DIC), shock, transusion, hysterectomy, renal ailure, or eath; (2) etal complications such as nonreassuring etal status, growth restriction, or eath; or (3) neonatal outcomes that inclue eath, preterm elivery, or growth restriction.

Traumatic Abruption

External trauma—usually rom motor vehicle crashes or aggravate assault—can cause placental separation. Te requency o abruption originating rom trauma varies. Importantly, abruption can stem rom relatively minor trauma (Huls, 2018). Te clinical presentation an consequences o these abruptions ier somewhat rom spontaneous cases. For example, associate etomaternal hemorrhage, while selom clinically signicant with most spontaneous abruptions, is more common with trauma because o concomitant placental tears or “ractures” (Fig. 50-10, p. 895). In eight women with traumatic placental abruption care or at Parklan Hospital, we oun etal-to-maternal hemorrhage o 80 to 100 mL in three (Stettler, 1992). Importantly, in some cases o trauma, a nonreassuring etal heart rate tracing may not be accompanie by other evi- ence o placental separation. A sinusoial tracing is one example. Following blunt abominal trauma, uterine contractions are the single most important preictor o placental abruption (Greco, 2019). raumatic abruption is consiere in more etail in Chapter 50 (p. 894).

Chronic Abruption

When placental separation is not ollowe by elivery, the placental abruption is terme chronic. Some o these cases begin early in pregnancy. Dugo an coworkers (2004) observe an association between some abnormally elevate maternal serum aneuploiy markers an subsequent abruption. Others have correlate rst- an secon-trimester bleeing with thir- trimester placental abruption (Ananth, 2006; Weiss, 2004). In some cases, chronic abruption an oligohyramnios evelop an are calle the chronic abruption–oligohydramnios sequence (CAOS) (Elliott, 1998). Even later in pregnancy, hemorrhage with retroplacental hematoma ormation is occasionally arreste completely without elivery. Tese women may have abnormally elevate levels o maternal serum alpha-etoprotein (MSAFP) or placenta-specic RNAs as markers o the event (Miura, 2017; Ngai, 2012).

■ Frequency

Te reporte incience o placental abruption varies because o iering criteria use or iagnosis. Its requency averages 0.5 percent or 1 case in 200 eliveries. From one atabase o more than 125 million births rom 1979 through 2010, the incience o placental abruption was nearly 1 percent (Hill, 2020). In more than 250,000 eliveries at Parklan Hospital rom 2000 through 2015, the incience o placental abruption average 1 case in 290 births (Fig. 43-3).

Te requency o placental abruption has risen in this country, an most o this increase is in black women (Ananth, 2005, 2016). Tis isproportion may be explaine in part by the conservative management o early-onset preeclampsia in some institutions (Chap. 41, p. 714). At Parklan Hospital, however, the requency o severe placental abruption has ecline. Specically, with placental abruption so extensive as to kill the etus, the incience was 0.24 percent or 1 case in 420 births rom 1956 through 1967 (Pritchar, 1967). Trough 2020, this same requency roppe to 0.05 percent or 1 case in 2060 births. Tis likely reects a concurrent ecline in the number o high-parity women giving birth an rise in the availability o prenatal care an emergency transportation.

■ Perinatal Morbidity and Mortality

Overall, perinatal outcomes are inuence by gestational age, an the requency o placental abruption rises across the thir trimester. As seen in Figure 43-4, more than hal o the placental abruptions at Parklan Hospital evelope at gestational ages ≥37 weeks’ gestation. Perinatal mortality an morbiity, however, are more common with earlier abruptions an with concomitant preeclampsia (Furukawa, 2015; Han, 2019). O other relate actors, major etal congenital anomalies have greater association with placental abruption (Riihimäki, 2013).

Although the rates o etal eath have ecline, the contribution o abruption as a cause o stillbirth remains prominent because other causes also have ecrease. For example, since the early 1990s, 10 to 12 percent o all thir-trimester stillbirths at Parklan Hospital have been the consequence o placental abruption. In a review o more than 15 million singleton births between 1995 an 1998 in the Unite States, the perinatal mortality rate associate with placental abruption was 119 eath per 1000 births. Tis was higher than the rate o 8 eaths per 1000 births in the general obstetrical population (Salihu, 2005).

Neonatal eaths also are common ollowing placental abruption. At Parklan Hospital, 15 percent o liveborn neonates ie. Perinatal morbiity also is common in this group (Downes, 2017). Moreover, associate chilhoo mortality mainly stems rom birth-relate asphyxia an prematurity (Riihimäki, 2018). In one series, 20 percent o 43 liveborn neonates ha severe etal aciemia ollowing placental abruption, an 20 percent o survivors evelope cerebral palsy (Matsua, 2013). In another stuy o 84 liveborns, 29 (35 percent) ha an umbilical artery pH <7.00 (Onishi, 2019). Ananth an coworkers (2017) attribute some o the averse neuroevelopmental outcomes to preterm elivery.

Predisposing Factors

Demographic Factors

Several preisposing actors raise the placental abruption risk (Table 43-1). Advancing maternal age is one risk, although ata regaring women o great parity are conicting (see Fig. 43-3) (Okby, 2017). Race or ethnicity also appears important (Eubanks, 2021). In an earlier stuy, in almost 366,000 eliveries at Parklan Hospital, abruption severe enough to kill the etus was most common in black an white women—1 case in 200 births; less so in Asian women—1 in 300; an least common in Latinas—1 in 350 (Pritchar, 1991). A familial association was oun rom one Norwegian population-base registry (Rasmussen, 2009). In this stuy, i a woman ha a severe abruption, the risk or her sister was ouble. Caniate genes involve in mitochonrial biogenesis an oxiative phosphorylation pathways, which coner risk or placental abruption, have been escribe (Workalemahu, 2018).

Pregnancy-associated Hypertension

Some orm o hypertension is the most requent conition associate with placental abruption. Tis inclues gestational hypertension, preeclampsia, chronic hypertension, or a combination. Te hemolysis, elevate liver enzyme levels, low platelet count (HELLP) synrome carries an increase risk or placental abruption. Moreover, expectant management o preeclampsia in signicantly preterm pregnancies was complicate by placental abruption in 4 percent (Shoopala, 2019). In a report by Pritchar an colleagues (1991) that escribe 408 women with placental abruption an etal emise, hypertension was apparent in hal once hypovolemia was correcte. Hal o these latter women—a ourth o all 408—ha chronic hypertension. Examine another way, one Maternal-Fetal Meicine Units (MFMU) Network stuy oun that 1.5 percent o pregnant women with chronic hypertension suere placental abruption (Sibai, 1998). At Parklan Hospital, the placental abruption requency in women with treate chronic hypertension an signicant proteinuria was almost 1 percent. Tis incience compare with the 0.3-percent incience in women with treate hypertension without substantial proteinuria (Morgan, 2016).

Chronic hypertension with superimpose preeclampsia or with etal-growth restriction coners an even greater risk (Lueth, 2020). Even so, the severity o hypertension oes not necessarily correlate with abruption incience (Morgan, 2016; Zetterstrom, 2005). However, women with preeclampsia that experience placental abruption have worse maternal, etal, an neonatal outcomes compare with women experiencing abruption alone (Han, 2019). Te long-term eects o these associations are apparent rom the signicantly elevate cariovascular mortality risk in women with prior abruption, with or without chronic hypertension (DeRoo, 2016; Pariente, 2013).

Observations rom the Magpie rial Collaborative Group suggest that women with preeclampsia, with or without chronic hypertension, given magnesium sulate may have a reuce risk or abruption (Altman, 2002). Last, Roberge an colleagues (2018), perorme a metaanalysis an reporte that a 100-mg aily aspirin may ecrease the incience o placental abruption.

Preterm Prelabor Ruptured Membranes

Te placental abruption risk substantially rises when placental membranes rupture beore term. (Hackney, 2016). O 756 women with rupture membranes between 20 an 36 weeks’ gestation, 5 percent evelope an abruption (Major, 1995). Te requency was 17 percent with previable prelabor rupture membranes (Kibel, 2016). Te risk or abruption with preterm membrane rupture is urther elevate with comorbi inection (Ananth, 2004). In one cohort stuy o pregnancies ≥34 weeks’ gestation, the placental abruption rate was eightol higher i hyramnios was comorbi (Aviram, 2015). From a metaanalysis o 10 stuies that inclue term an preterm gestational ages, hyramnios was associate with a twool greater rate o placental abruption (Khazaei, 2019). Abrupt uterine ecompression uring membrane rupture may be an inciting actor.

Prior Abruption

Many o the preisposing actors in women with a history o an abruption are chronic conitions, an in these cases, placental abruption has a high recurrence rate. Women with abruption an etal eath have a recurrence rate o 12 percent, an hal o these abruptions cause another etal eath (Pritchar, 1970). Furuhashi an colleagues (2002) reporte a 22-percent recurrence rate, an hal recurre at a gestational age 1 to 3 weeks earlier than the rst abruption. In one longituinal Dutch stuy, Ruiter an coworkers (2015) cite a recurrence risk o 5.8 percent. In a population-base stuy o 767,000 pregnancies, the authors oun a sevenol higher risk or recurrence o a “mil” abruption an twelveol risk or a “severe” abruption (Rasmussen, 2009). For women who ha two severe abruptions, the risk or a thir was increase 50-ol.

Management o a pregnancy subsequent to an abruption is ifcult because another separation may suenly occur, even remote rom term. In many o these recurrences, evaluation o etal well-being is almost always reassuring beorehan. Tus, antepartum etal testing is usually not preictive. Because term abruptions ten to be recurrent, Ruiter an coworkers (2015) recommen labor inuction at 37 weeks’ gestation. It seems reasonable to inuce labor at 38 complete weeks i other complications o not evelop beorehan.

Other Associations

O these liste in able 43-1, cigarette smoking is linke to an elevate risk or placental abruption (Eubanks, 2021). One metaanalysis o 1.6 million pregnancies in smokers oun a twool risk (Ananth, 1999). Tis risk was ve- to eightol i smokers ha chronic hypertension, severe preeclampsia, or both. Similar nings are reporte by others (Hogberg, 2007; Kaminsky, 2007). Cocaine abuse is linke, an in one series o 50 women who abuse cocaine uring pregnancy, eight ha a stillbirth cause by placental abruption (Bingol, 1987).

Of potential serum markers, MSAFP, inhibin, an pregnancyassociate plasma protein in abnormal levels carry increase risk (Ananth, 2017). Inee, preliminary ata shows that MSAFP levels >280 µg/L in the thir trimester may be preictive (Ngai, 2012). Subclinical hypothyroiism or high levels o antithyroi antiboies have been associate with a two- to threeol higher risk or placental abruption (Abbassi-Ghanavati, 2010; Maraka, 2016). Lupus anticoagulant is associate with maternal oor inarction o the placenta but is less so with typical abruptions. Women aecte by some o the thrombophilias have higher associate rates o thromboembolic events uring pregnancy, however, no convincing evience supports a link between thrombophilias an placental abruption (American College o Obstetricians an Gynecologists, 2019; 2020).

■ Diagnosis

Te signs an symptoms o placental abruption can vary consierably. Classically, aecte women have a suen onset o abominal pain, vaginal bleeing, an uterine tenerness. In an earlier stuy, 78 percent ha vaginal bleeing, 66 percent ha uterine tenerness or back pain, an 60 percent ha a nonreassuring etal status (Hur, 1983). Other nings inclue requent contractions an persistent hypertonus. However, in a th, preterm labor was iagnose, an placental abruption was not suspecte until etal istress or eath ollowe.

In some women, external bleeing can be prouse, yet placental separation may not be so extensive as to compromise the etus. In others, external bleeing is absent, but the placenta is sufciently sheare o to kill the etus—a conceale abruption. In either case, bleeing can be massive an leas to hypovolemic shock. In an earlier report rom Parklan Hospital, Pritchar an Brekken (1967) escribe 141 women with abruption so severe as to kill the etus. Bloo loss in these women oten amounte to at least hal o their pregnant bloo volume.

Consumptive Coagulopathy

With placental abruption, some egree o intravascular coagulation is almost universal. Placental abruption is the most common cause o clinically prooun consumptive coagulopathy in obstetrics an probably in all specialties (Cunningham, 2015). A primary consequence o intravascular coagulation is the activation o plasminogen to plasmin, which then lyses brin microemboli to maintain microcirculatory patency. With placental abruption severe enough to kill the etus, pathological levels o brinogen–brin egraation proucts an d-imers are almost always oun in maternal serum (Erez, 2015). Teir quantication is not clinically useul.

In a thir o women with an abruption severe enough to kill the etus, the plasma brinogen level will be <150 mg/L. Tese levels are epenent on the maternal preabruption brinogen level, an thus higher levels are “protective” (Cunningham, 2015; Wang, 2016). Clinically signicant low levels may cause troublesome surgical bleeing, an measurement o levels assists brinogen-replacement eorts. Levels o several other coagulation actors also are variably ecrease. Tese are not specically measure in DIC, but actors are replace empirically with resh rozen plasma as a part o massive transusion protocols (Chap. 44, p. 772). In aition, thrombocytopenia, sometimes prooun, may accompany severe hypobrinogenemia an can be common ater repeate bloo transusions. Tis “ilutional coagulopathy” is aitive to DIC (Chap. 44, p. 772).

Consumptive coagulopathy is more likely with a conceale abruption because intrauterine pressure is higher. Tis orces more thromboplastin into the large veins raining the implantation site. With a partial abruption an a live etus, severe coagulation eects are less common. Our experience has been that i serious coagulopathy evelops, it is usually evient by the time abruption symptoms appear. In one unusual case, a woman care or at Parklan Hospital presente with a noseblee. She ha no pain or vaginal bleeing, but her etus was ea. Her bloo i not clot, an the plasma brinogen level was 25 mg/L. A total placental abruption was conrme at elivery.

Couvelaire Uterus

At the time o cesarean elivery, it is not uncommon to n wiesprea extravasation o bloo into the uterine musculature an beneath the serosa (Fig. 43-5). Tis phenomenon is name ater Couvelaire, who in the early 1900s terme it uteroplacental apoplexy. Tese myometrial hemorrhages may incite uterine atony, but are not a sole inication or hysterectomy. Eusions o bloo may collect beneath the tubal serosa, between the leaves o the broa ligaments, in the ovaries, or in the peritoneal cavity.

End-organ Injury

Acute kidney injury (AKI) is a general term escribing renal ys- unction rom many causes (Chap. 56, p. 1006). Delaye or incomplete treatment o hypovolemia is one. However, even with placental abruption complicate by severe DIC, prompt an vigorous treatment with bloo an crystalloi solutions usually prevents signicant renal ysunction. Te risk or renal injury with placental abruption rises when preeclampsia coexists (Alexaner, 2015; Drakeley, 2002). Most cases o AKI are reversible, o not require ialysis, an generally have goo long-term outcomes (Arazi, 2015). However, irreversible acute cortical necrosis occasionally stems rom placental abruption (Gopalakrishnan, 2015).

Rarely, pituitary ailure—Sheehan syndrome—ollows severe intrapartum or early postpartum hemorrhage. Describe in Chapter 61 (p. 1104), the exact pathogenesis is not well unerstoo, especially because enocrine abnormalities are inrequent even in women who suer catastrophic hemorrhage (Matsuwaki, 2014).

Differential Diagnosis

Severe placental abruption usually is obvious. However, less severe orms are not always recognize with certainty, an the iagnosis becomes one o exclusion. Unortunately, no laboratory tests or other iagnostic methos accurately conrm lesser egrees o placental separation. Sonography has limite use because the placenta an resh clots may have similar imaging characteristics. In a stuy o 149 women with a suspecte placental abruption, the sensitivity or sonography was only 24 percent (Glantz, 2002). Tus, negative nings with sonographic examination o not exclue placental abruption.

Conversely, magnetic resonance (MR) imaging is highly sensitive or placental abruption an shoul be consiere i the iagnostic inormation woul change management (Masselli, 2011). Last, elevate serum levels o d-imers may be suggestive, but this has not been aequately teste. Tus, in the woman with vaginal bleeing an a live etus, placenta previa an other bleeing causes are sought with clinical an sonographic evaluation. It has long been taught— perhaps with some justication—that painul uterine bleeing signies placental abruption, whereas painless uterine bleeing inicates placenta previa. Te ierential iagnosis is usually not this straightorwar, an labor accompanying previa may cause pain that suggests placental abruption. Conversely, pain rom placental abruption may mimic normal labor, or it may be painless, especially with a posterior placenta. At times, the vaginal bleeing source remains obscure even ater elivery.

■ Management

reatment varies epening on maternoetal clinical conition, gestational age, an amount o associate hemorrhage. With a living viable-age etus an with vaginal elivery not imminent, emergency cesarean elivery is chosen by most. In some women, etal compromise will be evient as shown in Figure 43-6. When evaluating etal status, sonographic conrmation o etal heart activity may be necessary because sometimes an electroe applie irectly to a ea etus will provie misleaing inormation by recoring the maternal heart rate (Chap. 24, p. 447).

I the etus has ie or i it is not consiere sufciently mature to live outsie the uterus, vaginal birth is preerable or the mother. In either case, prompt an intensive resuscitation with bloo proucts an crystallois is begun. Tese measures are liesaving or the mother an hopeully or her etus. I the iagnosis o placental abruption is uncertain an the etus is alive an without evience o compromise, close observation may be warrante provie that immeiate intervention is available. Colón an coworkers (2016) perorme a ranomize trial an oun no benets to magnesium sulate tocolysis given to women with a preterm “nonsevere” abruption at 24 to 34 weeks’ gestation.

Cesarean Delivery

Te compromise etus is usually best serve by cesarean elivery, an the spee o response is an important actor in perinatal outcomes. In one stuy o 33 singleton pregnancies with a clinically overt placental abruption an etal braycaria, 15 o the 22 neurologically intact survivors were elivere within a 20-minute ecision-to-elivery interval (Kayani, 2003). However, eight o 11 inants who ie or evelope cerebral palsy were elivere ater a 20-minute intervals. Onishi an colleagues (2019) also oun a signicant negative correlation between these intervals an cor arterial pH. At Parklan Hospital, placental abruption was one o the most powerul anteceents to boy-cooling treatment or neonatal encephalopathy (Nelson, 2014).

A major hazar to cesarean elivery is impose by clinically signicant consumptive coagulopathy. Preparations inclue two large-bore intravenous catheters an plans or bloo an component replacement. Measures o hemoglobin, platelet, an brinogen levels as well as protime (P) an partial thromboplastin time (P) guie prouct replacement.

Vaginal Delivery

I the etus has ie, vaginal elivery is usually preerre. As reviewe earlier, hemostasis at the placental implantation site epens primarily on myometrial contraction an not bloo coagulability. Tus, ater vaginal elivery, uterotonic agents an uterine massage are use to stimulate myometrial contractions. Uterine muscle bers compress placental site vessels an prompt hemostasis even i coagulation is eective. In some instances, vaginal elivery may not be preerable, even with a ea etus. One example is brisk hemorrhage that cannot be successully manage by vigorous bloo replacement. Others are the myria obstetrical complications that prohibit vaginal elivery in general. In some women with extensive placental abruption, labor tens to be rapi because the uterus is usually persistently hypertonic (see Fig. 43-6). Tis can magniy etal compromise. In some cases, baseline intraamnionic pressures reach 50 mm Hg or higher, an with contractions, pressures may attain levels exceeing 100 mm Hg. Overall, however, rst- an secon-stage labor oes not appear to be shorter than usual (Downes, 2017).

Early amniotomy has long been champione in the management o placental abruption. Tis ostensibly achieves better spiral artery compression to iminish implantation site bleeing an reuce thromboplastin inusion into the maternal vascular system. Although evience supporting this theory is lacking, membrane rupture may hasten elivery. However, i the etus is small, the intact sac may be more efcient in promoting cervical ilation. I rhythmic uterine contractions are not superimpose on baseline hypertonus, oxytocin is given in stanar oses. No ata inicate that oxytocin augments thromboplastin escape into the maternal circulation to worsen coagulopathy. In 1ight o hypertonus associate with placental abruption, misoprostol may be a less avore inuction agent ue to its association with uterine tachysystole.

In the past, some ha set arbitrary time limits to permit vaginal elivery. Instea, experiences illustrate that maternal outcome epens on the iligence with which aequate ui an bloo replacement therapy are pursue rather than on the interval to elivery. Observations rom Parklan Hospital escribe by Pritchar an Brekken (1967) are similar to those rom the University o Virginia reporte by Brame an associates (1968). Specically, women with severe abruption who were transuse uring 18 hours or more beore elivery ha similar outcomes to those in whom elivery was accomplishe sooner.

Expectant Management

I possible, elaying elivery may benet an immature etus. In one series, 43 women with placental abruption beore 35 weeks’ gestation were expectantly manage, an 31 o them were given tocolytic therapy (Bon, 1989). Te mean interval until elivery or all 43 approximate 12 ays. Cesarean elivery was perorme in 75 percent, an there were no stillbirths. As iscusse earlier, women with a very early abruption may evelop chronic abruption–oligohydramnios sequence. In one report, our women with an abruption at a mean gestational age o 20 weeks subsequently evelope oligohyramnios an elivere at an average gestational age o 28 weeks (Elliott, 1998). In another escription o 256 women with an abruption at <28 weeks’ gestation, a mean o 1.6 weeks was gaine (Sabourin, 2012). O the group, 65 percent were elivere beore 29 weeks, an hal o all women unerwent emergent cesarean elivery.

Unortunately, even continuous etal heart rate monitoring oes not guarantee universally goo outcomes. A normal tracing may precee suen urther separation with instant etal compromise. In some o these, i the separation is sufcient, the etus will ie beore it can be elivere. ocolysis is avocate by some or suspecte abruption i the etus oes not isplay compromise. Some investigators have observe that tocolysis improve outcomes in a highly selecte cohort o women with preterm pregnancies (Bon, 1989; Combs, 1992). In another stuy, owers an coworkers (1999) aministere magnesium sulate, terbutaline, or both to 95 o 131 women with abruption iagnose beore 36 weeks’ gestation. Te perinatal mortality rate was 5 percent in both groups with or without tocolysis. Similar results were reporte rom a ranomize trial (Colón, 2016). A clinical consieration to the use o tocolytic agents, such as terbutaline, is that the rug-inuce tachycar- ia may mask maternal compromise. We are o the opinion that suspecte placental abruption contrainicates tocolytic agent use.

PLACENTA PREVIA

Classification

Te Latin previa means going before, an in this sense, the placenta goes beore the etus into the birth canal. Placenta previa escribes a placenta that is implante somewhere in the lower uterine segment, either over or very near the internal cervical os. Because these anatomical relationships cannot always be precisely ene an because they requently change across pregnancy, terminology can sometimes be conusing. erminology or placenta previa has evolve, an the National Institutes o Health (NIH)-sponsore Fetal Imaging Workshop (Rey, 2014) recommens the ollowing classication:

• Placenta previa: the internal os is covered partially or completely by placenta (Figs. 43-7 an 43-8). In the past, these were urther classie as either total or partial previa.

• Low-lying placenta: implantation in the lower uterine segment is such that the placental ege oes not cover the internal os but lies within a 2-cm wie perimeter aroun the os. A previously use term, marginal previa, escribe a placenta that was at the ege o the internal os but i not overlie it. Clearly, the classication o some cases will epen on cervical ilation at the time o assessment. For example, a low-lying placenta at 2-cm ilation may become a partial placenta previa at 4-cm ilation because the cervix has opene to expose the placental ege. Conversely, a placenta previa that appears to be total beore cervical ilation may become partial at 4-cm ilation because the cervical opening now extens beyon the ege o the placenta. Digital palpation in an attempt to ascertain these changing relations between the placental edge and internal os as the cervix dilates usually causes severe hemorrhage! With any egree o placenta previa, a certain amount o spontaneous placental separation is inevitable uring lower uterine segment remoeling an cervical ilation. Although this requently causes bleeing an thus technically constitutes a placental abruption, this term is usually not applie in these instances.

Somewhat but not always relate is vasa previa, in which etal vessels course through membranes an present at the cervical os. Vasa previa has been reviewe by the Society or Maternal–Fetal Meicine (2015) an is iscusse in Chapter 6 (p. 115).

■ Placental Migration

Beginning with the use o sonography in obstetrics, the term placental migration was coine to escribe the apparent movement o the placenta away rom the internal os (King, 1973). Obviously, the placenta oes not actually move, an the mechanism o apparent movement is not completely unerstoo. o begin with, migration is clearly a misnomer, because eciual invasion anchors chorionic villi.

Explanations o placental migration are likely aitive. First, apparent movement o the low-lying placenta relative to the internal os is relate to the imprecision o two-imensional sonography. Secon, as pregnancy progresses, growth o the lower an upper uterine segments iers. With greater bloo ow in the upper uterus, placental growth towar this supply, terme trophotropism, is thus more likely irecte towar the unus. Many o those placentas that “migrate” most likely never were circumerentially implante with true villous invasion that reache the internal cervical os. Importantly, a lowlying placenta or placenta previa is less likely to “migrate” if there is a prior cesarean delivery scar.

Te requency o placental migration has been quantie. In one stuy o 4300 women at mipregnancy, 12 percent ha a low-lying placenta (Sanerson, 1991). O placentas not covering the internal os, previa i not persist, an none subsequently ha placental hemorrhage. Conversely, approximately 40 percent o placentas that covere the os at mipregnancy continue to o so until elivery. Tus, placentas that lie close to but not over the internal os until the early thir trimester are unlikely to persist as a previa by term (Heller, 2014; Parrott, 2015). Te chance that placenta previa persists increases with a hysterotomy scar (Kohari, 2012; Oyelese, 2006).

■ Incidence and Associated Factors

Te incience o placenta previa has risen uring the past 30 years. Reporte inciences average about 0.4 percent or 1 case per 250 to 400 eliveries (Hill, 2020). Te requency at Parklan Hospital rom 1988 through 2003 or nearly 250,000 births was 2.6 cases per 1000. For the 2004 to 2020 epoch, it rose to 3.8 cases per 1000. Similar requencies have been reporte rom Austria, Finlan, an Israel (Kollmann, 2016; Räisänen, 2014; Rosenberg, 2011). Several emographic actors may contribute to this higher rate o placenta previa. First, maternal age increases the requency (Biro, 2012; Roberts, 2012). In the First- an Secon- rimester Evaluation o Risk (FASER) trial, which inclue more than 36,000 women, the requency o previa was 0.5 percent or women <35 years compare with 1.1 percent in those ≥35 years (Cleary–Golman, 2005). At Parklan Hospital, the incience range rom a rate o approximately 0.65 cases per 1000 births or women ≤19 years to almost 10 cases per 1000 births or women oler than 35.

Multiparity also elevates the rate o placenta previa (Räisänen, 2014). Obviously, the eects o avancing maternal age an parity are conouning. Still, Babinszki an colleagues (1999) reporte that the 2.2-percent incience in women with parity o ve or greater was signicantly higher than that o women with lower parity. Te interpregnancy interval oes not aect this rate (Fox, 2015).

Cigarette smoking increases the relative risk o placenta previa at least twool (Usta, 2005). It has been postulate that carbon monoxie hypoxemia causes compensatory placental hypertrophy an greater surace area. Smoking may also be relate to eciual vasculopathy.

Several clinical characteristics also raise placenta previa risks. Foremost, women with one or more prior cesarean deliveries are at greater risk or subsequent placental isorers that inclue placenta previa, placental abruption, or placenta accreta spectrum (PAS) (Gibbins, 2018; Klar, 2014). Te cumulative risks or placenta previa that accrue with the increasing number o cesarean eliveries are extraorinary. In one MFMU Network stuy o 30,132 women unergoing cesarean elivery, the inci- ence was 1.3 percent or those with only one prior cesarean elivery, but it was 3.4 percent i there were six or more prior cesareans (Silver, 2006). In a retrospective cohort o nearly 400,000 women who were elivere o two consecutive singletons, those with a cesarean elivery or the rst pregnancy ha a 1.6-ol greater rate or previa in the secon pregnancy (GurolUrganci, 2011). Tese same investigators reporte a 1.5-ol higher rate rom six similar population-base stuies. Tis risk is increase eightol in women with parity greater than our an who have more than our prior cesarean eliveries (Gilliam, 2002).

Importantly, women with a prior uterine incision an placenta previa have an increase likelihoo that cesarean hysterectomy will be necessary because o associate PAS (p. 761). In one stuy, 6 percent o women with a primary cesarean elivery or placenta previa require a hysterectomy. Tis rate was 25 percent or women with a placenta previa unergoing repeat cesarean elivery (Freeriksen, 1999).

Multifetal gestation raises placenta previa risk (Ananth, 2003a; Luke, 2017a). Compare with monochorionic twins, ichorionic ones show higher rates, which perhaps stems rom having two implantation sites (Weis, 2012). MSAFP levels, i abnormally elevate or otherwise unexplaine reasons uring prenatal screening, raise the risk or placenta previa an a host o other abnormalities. Moreover, women with a placenta previa an comorbi MSAFP level >2.0 multiples o the meian (MoM) at 16 weeks’ gestation were at greater risk or late-pregnancy bleeing an preterm birth (Chap. 17, p. 338).

Assisted reproductive technology (ART) use or conception elevates placenta previa rates. Some o this association may erive rom overlapping eects. First, oler women constitute a signicant portion o patients electing AR (Luke, 2017b). Secon, even ajusting or multietal gestation, AR is still associate with higher previa rates (Karami, 2018). Last, in one systematic review incluing nearly 256,000 births, uterine leiomyomas were associate with higher placenta previa rates (Jenabi, 2019).

■ Clinical Features

Painless bleeing is the most characteristic event with placenta previa. Bleeing usually oes not evelop until near the en o the secon trimester or later, but it can begin even beore mipregnancy. Unoubtely, some late abortions are cause by an abnormally locate placenta. Initial bleeing rom a previa usually begins without warning, an this sentinel bleed is rarely so prouse as to prove atal. Usually it ceases, only to recur.

However, in perhaps 10 percent o women, particularly those with a placenta implante near but not over the cervical os, bleeing is elaye until labor onset. Bleeing at this time varies in egree, an it may mimic placental abruption. In cases in which the placenta is locate over the internal os, a specic sequence o events leas to bleeing. First, the uterine boy remoels to orm the lower uterine segment. With this, the internal os ilates, an some o the implante placenta inevitably separates. Bleeing that ensues is augmente by the inherent inability o myometrial bers in the lower uterine segment to contract an thereby constrict torn vessels. Similarly, bleeing rom this lower-segment implantation site also requently continues ater placental elivery. Last, lacerations in the riable cervix an lower segment will blee. Tese may be especially problematic ollowing manual removal o a somewhat ahere placenta.

Cervical length may alter the clinical course. Staor (2010) but not ruell (2013), both with their associates, oun that a placenta previa an a thir-trimester cervical length <30 mm increase the risks or hemorrhage, uterine activity, an preterm birth. Similarly, Friszer (2013) but not ruell (2013), both with their coworkers, showe that women amitte or bleeing ha a greater chance o elivery in the subsequent 7 ays when the cervical length measure <25 mm sonographically.

Placenta accreta spectrum is a requent an serious complication associate with placenta previa. Tis abnormal placental attachment erives in part rom poorly evelope eciua that lines the lower uterine segment. Biswas an coworkers (1999) perorme placental be biopsies in 50 women with a placenta previa an in 50 control women. Inltration o spiral arterioles by trophoblastic giant cells, rather than by the expecte enovascular trophoblast cells, was oun in hal o specimens. In contrast, only 20 percent o biopsies rom normally implante placentas ha these changes. In another stuy o 514 cases o placenta previa, abnormal placental attachment was ientie in 7 percent (Freeriksen, 1999). As iscusse, placenta previa overlying a prior cesarean incision conveys a particularly high risk or PAS.

Coagulopathy rarely complicate placenta previa, even when implantation site separation is extensive (Cunningham, 2015). Placental thromboplastin, which incites the intravascular coagulation seen with placental abruption, is presume to reaily escape through the cervical canal rather than be orce into the maternal circulation. Te paucity o large myometrial veins in this area also may be protective.

■ Diagnosis

For uterine bleeing ater mipregnancy, placenta previa an placental abruption are always consiere. In one Canaian stuy, placenta previa accounte or 21 percent o women amitte rom 22 to 28 weeks’ gestation with vaginal bleeing (Sabourin, 2012). Previa shoul not be exclue until sonographic evaluation has clearly prove its absence. I sonography is not reaily available, iagnosis by igital cervical examination is one in an operating room an with preparations in place or operative elivery. We call these preparations a double setup technique. Even the gentlest examination can cause torrential hemorrhage.

Using stanar sonographic techniques, quick an accurate placental localization can be accomplishe (American Institute o Ultrasoun in Meicine, 2018). Tis is usually one with transabominal sonography. I the placenta clearly overlies the cervix or i it lies away rom the lower uterine segment, the examination has excellent sensitivity an negative preictive value (Olive, 2006; Quant, 2014). Obese women may hiner clear viewing o the lower uterine segment. A ull blaer may articially elongate the cervix an compress the lower uterine segment to give the impression that the placenta overlies the cervix.

I placental location remains unclear, transvaginal sonography is the most accurate sonographic metho an is sae even with vaginal bleeing (Fig. 43-9). In a comprehensive stuy, the internal os was visualize in all cases with transvaginal sonography but in only 30 percent with transabominal sonography (Farine, 1988). As iscusse, i the placental ege lies <2 cm rom the internal os, but not covering it, the placenta is consiere low lying (Rey, 2014). In the absence o any other inication, sonography nee not be requently repeate simply to ocument placental position. At Parklan Hospital, women with placenta previa ientie at 18 to 22 weeks’ gestation an a prior cesarean elivery are reevaluate sonographically at 28 weeks an again at 32 weeks i it persists. Tose with a placenta previa but without prior cesarean elivery unergo reimaging at 32 weeks. Restriction o activity is not necessary unless a previa persists beyon 28 weeks’ gestation or i clinical nings such as bleeing or contractions evelop beore this time. At 32 weeks’ gestation, i the placental ege is still <2 cm rom the os, transvaginal sonography is repeate at 36 weeks’ gestation. Using MR imaging, several investigators report excellent visualization o placental abnormalities. However, it is unlikely that this moality will replace sonography or routine evaluation anytime soon given availability an cost ierences compare with sonography. However, MR imaging is useul or evaluation o PAS (p. 761).

■ Management

Care with placenta previa is iniviualize, an three prominent actors inclue etal maturity, associate labor, an blee- ing severity. In one stuy o 214 women with a placenta previa, 43 percent ha an emergency elivery, an hal o these were preterm (Ruiter, 2015). Instea, i active bleeing subsies an the etus is immature, close observation in an obstetrical unit is inicate. Data are sparse regaring tocolytic aministration or uterine contractions. Although robust ranomize trials are lacking, Bose an colleagues (2011) recommen that i tocolytics are given, they be limite to 48 hours o aministration.

As note earlier, the physiological cariovascular responses to tocolytic agents that inclue hypotension an tachycaria can mask maternal compromise. We categorically recommen against their use in this setting. Ater bleeing has cease or approximately 2 ays an the etus is juge to be healthy, a woman can usually be ischarge home with instructions or “pelvic rest.” Te Society or Maternal–Fetal Meicine (2018) oes not recommen routine cervical length screening in these women. Importantly, the woman an her amily must appreciate the possibility o recurrent bleeing an be prepare or immeiate transport back to the hospital. In other cases, prolonge hospitalization may be necessary.

Te requency o emergency elivery in women with placenta previa ranges rom 25 to 40 percent (Erani, 2019; Gibbons, 2018). In properly selecte patients, however, long-term inpatient care oes not appear to a benets compare with outpatient management (Neilson, 2003). In one ranomize stuy o 53 women who ha a bleeing previa at 24 to 36 weeks’ gestation, maternal or etal morbiity rates i not ier between management methos (Wing, 1996). O all stuy women, 60 percent ha recurrent bleeing, an hal eventually require expeitious cesarean elivery.

For women who are near term an who are not bleeing, plans are mae or scheule cesarean elivery. A planne elivery in a controlle setting is optimal, an timing balances etal immaturity against antepartum hemorrhage. Te American College o Obstetricians an Gynecologists an Society or Maternal–Fetal Meicine (2021) recommen elivery or otherwise uncomplicate placenta previa between 360/7 an 376/7 weeks. At Parklan Hospital, we usually perorm elective cesarean elivery at 380/7 weeks. Recommenations or elivery o women with PAS are outline in that section.

■ Delivery

Practically all women with placenta previa unergo cesarean elivery. Some recommen a vertical laparotomy incision to provie rapi entry i bleeing is torrential or i generous operating space is require or hysterectomy. As iscusse, cesarean elivery is emergently perorme in more than hal because o hemorrhage, or which about a ourth require bloo transusion (Sabourin, 2012). Although a low transverse hysterotomy is usually possible, this may cause etal bleeing i the placenta is implante anteriorly an the placenta is incise. In such cases, etal elivery shoul be expeitious (Silver, 2015a). Tus, a vertical uterine incision may be preerable in some instances.

In either case, even when the incision extens through the placenta, maternal or etal outcomes are rarely compromise. Following placental removal, the implantation site may blee uncontrollably ue to poorly contracte smooth muscle, which is characteristic o the lower uterine segment. I hemostasis at the placental implantation site cannot be obtaine by uterotonic agent aministration an pressure, it can be oversewn with no. 0 chromic sutures. Cho an associates (1991)

escribe placing interrupte sutures at 1-cm intervals to orm a circle aroun the bleeing portion o the lower segment to control hemorrhage. Others have reporte success with compression sutures that traverse an compress the anterior an posterior uterine wall (Mohame, 2019; Sallam, 2019). O other methos, Bakri or Foley balloon tamponae use alone or couple with compression sutures has been escribe (Albayrak, 2011; Diemert, 2012). Other surgical options are bilateral uterine or internal iliac artery ligation, illustrate in Chapter 44 (p. 779). Pelvic artery embolization also has gaine acceptance. Yu an colleagues (2020) perorme a ranomize trial o perioperative prophylactic internal iliac artery balloon occlusion uring cesarean elivery or placenta previa an oun that eployment i not reuce postpartum hemorrhage or alter maternal or neonatal morbiity.

I these more conservative methos ail an bleeing is brisk, hysterectomy is necessary. Placenta previa—especially with PAS—currently is a common inication or peripartum hysterectomy at Parklan Hospital an other institutions (Jakobsson, 2015; Wong, 2011). In cases without PAS, the reporte incience o hysterectomy with placenta previa is 2 percent (Gibbins, 2018).

Tus, it is not possible to accurately estimate the eect on the hysterectomy rate rom placenta previa alone without consiering the associate PAS. Again, for women whose placenta previa is implanted anteriorly at the site of a prior uterine incision, the likelihood of an associated morbidly adherent placenta and need for hysterectomy is increased. In a stuy o 318 peripartum hysterectomies perorme in the Unite Kingom, 40 percent were one or abnormal placentation (Knight, 2007). At Parklan Hospital, 44 percent o cesarean hysterectomies were one or bleeing placenta previa or or PAS (Wortman, 2015). Te technique or peripartum hysterectomy is escribe in Chapter 30 (p. 560).

■ Maternal and Perinatal Outcomes

Placenta previa an coexistent PAS both contribute substantively to maternal morbiity an mortality rates. Te maternal mortality ratio is increase approximately threeol or women with a placenta previa (Gibbins, 2018). In a report o 5367 maternal eaths in the Unite States rom 2006 to 2013, placenta previa alone accounte or nearly 3 percent o eaths rom hemorrhage (Creanga, 2014, 2017).

Te report rom the Consortium on Sae Labor emphasizes the ongoing perinatal morbiity with placenta previa (Lai, 2012). In these cases, preterm elivery continues to be a major cause o perinatal eath (Balachanar, 2020; Nørgaar, 2012; Salihu, 2003). Ananth an colleagues (2003b) reporte a comparably elevate risk o neonatal eath even or etuses who elivere at term. Tis is at least partially relate to the etal anomaly rate, which is two- to threeol higher in pregnancies with placenta previa (Crane, 1999; Kancherla, 2015).

Te association o etal-growth restriction with placenta previa is likely minimal ater controlling or gestational age. In a population-base cohort o more than 500,000 singleton births, most low-birthweight newborns associate with placenta previa resulte rom preterm birth (Ananth, 2001). From their large metaanalysis, Balayla an coworkers (2019) oun a slightly increase requency o etal-growth restriction. At least two other stuies reporte an elevate risk (Räisänen, 2014; Weiner, 2016). Apparently, etal growth eects are similar with placenta previa an PAS (Jauniaux, 2019).

PLACENTA ACCRETA SPECTRUM

Te term placenta accreta spectrum (PAS) escribes aberrant placentation characterize by abnormally implante, invasive, or ahere placenta. Derivation o accreta comes rom the Latin ac- + crescere—to ahere or become attache to (Benirschke, 2012). It is also reerre to as the morbily aherent placenta, an in Europe it is reerre to as a pernicious placenta previa with accreta an abnormally adherent placenta.

■ Etiopathogenesis

Te major clinical problem is placental ailure to separate normally rom the myometrium ater etal elivery. Tis abnormal aherence stems in part rom partial or total absence o the eciua basalis an imperect evelopment o the brinoi or Nitabuch layer, escribe in Chapter 5 (p. 85). I the eciual spongy layer is lacking either partially or totally, the physiological line o cleavage is absent, an some or all cotyleons are ensely anchore. Microscopically, placental villi attach to smooth muscle bers rather than to eciual cells. Tis eci- ual eciency then prevents normal separation ater elivery.

Te surace area involve at the implantation site an the epth o trophoblast ingrowth vary between women, but all aecte placentas can potentially cause signicant hemorrhage. Data now suggest that PAS is not solely cause by the eci- ua’s anatomical eciency. Inee, the cytotrophoblasts may control eciual invasion through actors such as angiogenesis (Duzyj, 2018; Goh, 2016). Moreover, some tissue specimens show immunologically meiate “hyperinvasiveness” (Harris, 2019). Some genes that coe or remoeling an or aherence may be highly expresse (Matsukawa, 2019; Shainker, 2020).

Myometrial bers attache to the basal plate in an anteceent pregnancy are preictive markers or a subsequent PAS (Linn, 2015; Miller, 2016). Tis implies an anteceent "constitutional enometrial eect” in most cases. Te greater risk conveye by previous surgical uterine trauma may be partially explaine by an enhance vulnerability to trophoblast invasion (Einerson, 2020; Jauniaux, 2018).

Tis association with prior trauma is reinorce by the close relationship between cesarean scar pregnancy (CSP) an later evelopment o PAS in the same pregnancy. Inee, accruing evience suggests that CSP an PAS lie on a spectrum an that CSP is a precursor (Happe, 2020; imor-ritsch, 2019). Describe in Chapter 12 (p. 229), early rupture an hemorrhage with CSP are not uncommon, an women oten elect pregnancy-terminating interventions to avoi these (Society or Maternal–Fetal Meicine, 2020; imor-ritsch, 2019).

Classification

Variants o PAS are classie by the epth o trophoblastic growth (Figs. 43-10 an 43-11). Placenta accreta inicates that villi are attache to the myometrium. With placenta increta, villi actually invae the myometrium, an placenta percreta enes villi that penetrate through the myometrium an to or through the serosa (Silver, 2018). In clinical practice, these three variants are encountere in an approximate ratio o 80:15:5, respectively (Wong, 2008). At a reerral center, however, the istribution was 22, 24, an 54 percent respectively (Birgani, 2020). In all three varieties, abnormal aherence may involve all lobules—total placenta accreta. I all or part o a single lobule is abnormally attache, it is escribe as focal placenta accreta.

Histological iagnosis cannot be mae rom the placenta alone, an myometrial samples are necessary or conrmation (Jauniaux, 2021). erminology or consistent classication has been lacking because o varying clinical criteria an lack o etaile pathological examinations. o alleviate this, the International Feeration o Gynecology an Obstetrics (FIGO) has recently propose a clinical classication system or PAS (Jauniaux, 2019).

■ Incidence and Risk Factors

Decaes ago, the requency o PAS was 1 in 20,000 births (McKeogh, 1951). As late as 1971, Hellman an Pritchar in the 14th eition o Williams Obstetrics escribe PAS as the subject o case reports. Since then, the incience has grown remarkably in irect relationship to the rising cesarean elivery rate. For example, the incience was 1 case in 2500 births in the 1980s, but it was 1 case per 731 births in a report rom the MFMU Network comprising 115,502 women (Bailit, 2015). From the Nationwie Inpatient Sample, the PAS rate was an astouning 1 case in 270 births (Mogos, 2016).

Tis rising requency has mae PAS one o the most ormiable problems in obstetrics. O 5367 pregnancy-relate maternal eaths in the Unite States rom 2006 to 2013, 13 percent were ue to hemorrhage cause by PAS (Creanga, 2015, 2017). In aition, PAS is a leaing cause o hemorrhage an emergency peripartum hysterectomy (Awan, 2011; Eller, 2011; Rossi, 2010). Te American College o Obstetricians an Gynecologists an the Society or Maternal–Fetal Meicine (2018) have outline optimal management. Te International Society or Abnormally Invasive Placenta also has publishe guielines (Collins, 2019).

In subsequent pregnancies ollowing PAS, recurrence risks are high. Women in whom hysterectomy is avoie have an estimate 20-percent incience o recurrence (Cunningham, 2016; Roeca, 2017). Some evience shows that these women also have greater risks or placenta previa, uterine rupture, manual placental removal, preterm elivery, an hysterectomy (Balwin, 2020; Eshkoli, 2013). PAS risk actors are similar to those or placenta previa (p. 756). Shown in Figure 43-12, the two most important elements are an associate placenta previa, a prior cesarean elivery, or more likely both (Klar, 2014; Silver, 2006). A classical hysterotomy incision has a higher risk or subsequent PAS than a lower uterine segment one (Gyam-Bannerman, 2012). O women with a prior cesarean elivery, almost hal ha myometrial bers seen microscopically ahere to the placenta (Hararottir, 1996; Miller, 2016). Dysunctional eciua may also ollow other myometrial trauma such as curettage or enometrial ablation (Balwin, 2018; Gill, 2015). AR is an inepenent risk actor or PAS (Salmanian, 2020).

Other risk markers are prenatal MSAFP an human chorionic gonaotropin (hCG) use to screen or neural-tube eects an aneuploiies. In one stuy o more than 9300 women screene at 14 to 22 weeks’ gestation, the risk or PAS was eightol higher with MSAFP levels >2.5 MoM, an it was increase ourol with maternal serum ree β-hCG levels >2.5 MoM (Hung, 1999).

■ Diagnosis

With rst- an secon-trimester PAS, hemorrhage usually stems rom a coexisting placenta previa. Such bleeing will typically prompt evaluation, an ieally sonography is use (Chantraine, 2013; Jauniaux, 2018). With lesser egrees o bleeing, rst-trimester measurement o the smallest myometrial thickness can help preict the later risk or peripartum hysterectomy with PAS (Happe, 2020). In a screening stuy o more than 22,000 singleton pregnancies at 11 to 13 weeks’ gestation, 6 percent were at high risk or PAS (Panaiotova, 2019). However imaging was less than perect to ientiy all o these placentas early. Subsequently, only 14 ha a suspecte clinical iagnosis, an 13 o these were conrme at elivery.

Five characteristic sonographic nings suggest PAS: (1) placental lacunae; (2) thinning o the retroplacental myometrium; (3) isruption o the blaer-uterine serosal interace; (4) briging vessels rom the placenta to the blaer-serosal interace; an (5) placental bulge that pushes outwar an istorts the contour o the uterus (Fig. 43-13). In a metaanalysis, the sensitivities o these criteria to ientiy placenta accreta, increta, an percreta were 91, 93, an 89 percent, respectively. Corresponing specicities were 97, 98, an 99 percent, respectively (Pagani, 2018).

Tese gures may be overestimate because o clinical bias an consierable interobserver variability (Silver, 2018). Some investigators report ewer spectacular results with sonography (Jauniaux, 2016; Primo, 2014). Bowman an colleagues (2014) escribe the sensitivity o sonography to be 54 percent; speci- city, 88 percent; positive preictive value, 82 percent; negative preictive value, 65 percent; an accuracy, 65 percent. Location aects sonographic accuracy. Posterior placental location is associate with elaye iagnosis an increase surgical complications (Morgan, 2019; inari, 2021). In one stuy, the etection rate was 90 percent or anterior placenta accreta compare with 50 percent or posterior ones (Pilloni, 2016). Nageotte (2014) conclue that ientication o PAS with sonography shoul be interprete with clinical an operative nings.

Better results have been oun by some using three-imensional (3-D) sonography an power Doppler (Collins, 2015). We too have oun that the aition o Doppler color ow mapping ais preiction o myometrial invasion (Fig. 43-14). Invasion is suspecte i the istance between the uterine serosa– blaer wall interace an the retroplacental vessels measures <1 mm an i large intraplacental lacunae are seen (Rac, 2015a; wickler, 2000). In another stuy, hypervascularity o the uterine serosa–blaer wall interace ha the highest positive an negative preictive values or placenta percreta (Cali, 2013). Intracervical lakes also have been reporte with placenta percreta (i Pasquo, 2020). Yule an coworkers (2020) reporte that the placenta accreta index was useul or iagnosis. Tis inex incorporates the number o prior cesarean eliveries, placental location, lacunae, briging vessels, an smallest myometrial istance. Tese investigators are also exploring rst-trimester color mapping to evelop a quantication algorithm (Yule 2021). o urther elineate anatomy, MR imaging can be ae.

We an others use it to ientiy invasion o ajacent structures (Chalubinski, 2013; Rey, 2014). Interobserver variability was reporte to be excellent to iagnose PAS an assess invasion epth. Tere was less agreement in assessing topography o invasion (Finazzo, 2020). Using MR imaging, Mori an colleagues (2020) escribe a high prevalence o pelvic parasitic arteries with PAS. However, not all investigators have oun MR imaging to be benecial (Einerson, 2018). Although gaolinium is usually not ae uring pregnancy, this contrast may enhance images (Millischer, 2017). Lax an coworkers (2007) escribe three MR imaging n- ings that suggest PAS: uterine bulging, ark intraplacental bans on 2-weighte imaging, an heterogeneous signal intensity within the placenta inicative o lacunae. Some recommen MR imaging i sonography results are inconclusive or there is a posterior previa (American College o Obstetricians an Gynecologists, 2018; Silver, 2018).

■ Management

Preoperative assessment ieally begins once a possible PAS is recognize antenatally. A major decision concerns the timing and the ideal facility for delivery. Consierations inclue appropriate surgical, anesthesia, intensive care, an bloo banking capabilities. An obstetrical surgeon or gynecological oncologist an surgical, urological, an interventional raiological consultants shoul be available (Collins, 2019; Shamshirsaz, 2018). Te American College o Obstetricians an Gynecologists (2018) an the Society or Maternal–Fetal Meicine recommen planne elivery in a tertiary-care acility. In some, specially esigne teams have been assemble an are on call (Shamshirsaz, 2018). A metaanalysis escribe the improve maternal outcomes with such management (Bartels, 2018). Silver an colleagues (2015b) have provie requisites or accreta centers o excellence an their criteria to consier trans- er to a higher level-o-care hospital (Table 43-2). I possible, elivery is best scheule or peak availability o all resources an team members. Even so, a thir o cases require unsche- ule elivery, an contingency plans shoul be reay (Pettit, 2019). Women who reuse bloo or its erivatives pose especially ifcult management ilemmas (Barth, 2011).

Delivery Timing

In one stuy, 40 percent o women with PAS ha bleeing manating unplanne elivery prior to 34 weeks’ gestation. iming balances etal immaturity against averse maternal consequences o hemorrhage an emergency cesarean elivery (Perlman, 2017; Pettit, 2019). Te American College o Obstetricians an Gynecologists (2018; 2021) recommens iniviualization an suggests elivery between 340/7 an 356/7 weeks’ gestation. Tey cite a ecision-analysis stuy that justi- es elective elivery without etal lung maturity testing ater 34 complete weeks (Robinson, 2010). Te Society or Maternal– Fetal Meicine (2018) recommens elivery between 34 an 37 weeks. wo earlier surveys oun that most practitioners o not eliver these women until 36 weeks or later (Esako, 2012; Wright, 2013). At Parklan Hospital, we generally scheule these proceures ater 36 complete weeks but are prepare also to manage them in nonelective situations (Rac, 2015b). In some cases, PAS is not recognize until laparotomy. I resources are inaequate to surgically manage the percreta an i the woman is stable an not bleeing, the etus is not elivere. Te abominal incision is close, an she is transerre to a tertiary-care acility.

Preoperative Prophylactic Catheterization

In cases that may involve the ureters, catheterization may ai their issection or ientication. However, these catheters overall o not lower urinary tract injury rates (Crocetto, 2021). Some, but not all, avocate preoperative ureteral catheterization (American College o Obstetricians an Gynecologists, 2018; Eller, 2011). Te role o catheters or ureteral injury repair is outline in Chapter 30 (p. 564). With arterial catheterization, balloon-tippe catheters aim to mitigate bloo loss an thereby enhance surgical visibility. Catheters are avance preoperatively into the internal iliac arteries an are inate ater etal elivery to occlue pelvic bloo ow (Ballas, 2012; Desai, 2012; Zhou, 2021). Some pre- er an inrarenal aortic balloon occlusion catheter (Mei, 2020). Alternatively, the catheters can be use to eliver occluing emboli to bleeing arterial sites (Mei, 2018). Others have conclue that these proceures oer borerline efcacy an have serious risks (Chen, 2020; Makary, 2019; Mohr-Sasson, 2020). Rare complications have inclue thrombosis o the common iliac artery (Bishop, 2011). At this time, the American College o Obstetricians an Gynecologists (2018) conclues that a rm recommenation cannot be mae or or against intraarterial catheter use. Similarly, there are no obvious benets to prophylactic internal iliac artery ligation in this setting (Po, 2012; Yu, 2020).

Cesarean Delivery and Hysterectomy

Beore commencing with elivery, the risk o hysterectomy to prevent exsanguination shoul be estimate. Some o these abnormal placentations, especially i partial, may be amenable to placental elivery with hemostatic suture placement. Con- rmation o a percreta or increta almost always manates hysterectomy. Because the scope o invasion may not be apparent beore elivery o the etus, some complete a number o issection steps early. Tis also minimizes bloo loss uring potentially teious issection ater hysterotomy an i the placenta blees. Tus, an attempt can be mae to create a wie blaer ap beore making the hysterotomy incision (Cunningham, 2017). Te roun ligaments are ivie, an the lateral eges o the peritoneal reection are issecte ownwar. I possible, these incisions are extene to encircle the entire placental implantation site that visibly occupies the prevesical space an posterior blaer wall. Following this, a classical hysterotomy, transverse unal, or high posterior incision is mae to avoi the placenta (Kotsuji, 2013).

After fetal delivery, the extent of placental invasion is assessed without attempts at manual placental removal. In a report rom the Unite Kingom, attempts at partial or total placental removal prior to hysterectomy were associate with twice as much bloo loss (Fitzpatrick, 2014). Generally speaking, with obvious percreta or increta, hysterectomy is usually the best course, an the placenta is let in situ. With more extensive placental ingrowth, bleeing may be minimal until manual placental removal is attempte. Unless there is spontaneous separation with bleeing that manates emergency hysterectomy, the operation begins ater ull assessment is mae. Cesarean hysterectomy is carrie out as escribe in Chapter 30 (p.560). With heavy bleeing, successul treatment epens on imme- iate bloo replacement an other measures that can inclue uterine or internal iliac artery ligation, balloon occlusion, or embolization. In some cases, the operation is mae easier by perormance o a supracervical hysterectomy (Levin, 2020). Kingom an colleagues (2020) have escribe a moie raical hysterectomy or PAS (Table 43-3). Tis technique is also etaile in Cunningham and Gilstrap’s Operative Obstetrics, 3r eition (Cunningham, 2017). Because o a high risk or postoperative venous thromboembolism, consieration is given or thromboprophylaxis (Silver, 2018).

Conservative Management

Occasionally, it may be possible to trim the umbilical cor, repair the hysterotomy incision, leave the placenta in situ, an not pursue hysterectomy (Sentilhes, 2021). Tis option may be use or women in whom abnormal placentation was not suspecte beore cesarean elivery an in whom uterine closure stops bleeing. Ater this, she can be transerre to a higher level-o-care acility or enitive management. Another consieration is the woman with a strong esire or ertility an who has receive extensive counseling. Resection o the aherent placenta an unerlying myometrium has been avocate as a uterine-sparing technique (Palacios-Jaraquemaa, 2020). Conservative management was reviewe by Perez-Delboy (2014) an Fox (2015) an their colleagues. In some o these cases, the placenta spontaneously resorbe between 1 an 12 months with a mean o 6 months. Numerous complications can occur an inclue sepsis, coagulopathy, pulmonary embolism, an arteriovenous malormation (Fox, 2015; Juy, 2015; Roach, 2015).

In other cases, sutures are place through the outsie wall o the uterus overlying the placental be. Shih an associates (2019) escribe this using a Nausicaa proceure. In some o these women, a subsequent hysterectomy— either planne or prompte by bleeing or inection—is per- orme ays to weeks postpartum when bloo loss might be less (Al-Khan, 2014; Sentilhes, 2009, 2021; Zuckerwise, 2020). In some stuies, 20 percent or ewer o women ultimately require hysterectomy (Bretelle, 2007; Kutuk, 2018). In other reports, however, up to 60 percent eventually require emergency hysterectomy (Clausen, 2013; Pather, 2014). Evience that treatment with methotrexate ais resorption is lacking. Last, or women in whom the placenta is let in situ, serial serum β-hCG measurements are not inormative, an serial sonographic or MR imaging is recommene (immermans, 2007; Worley, 2008).

At this time, we agree with the American College o Obstetricians an Gynecologists (2018) that leaving the placenta in situ shoul be consiere investigational. Exceptions permit transer to a higher level o care. Guielines rom the International Society or Abnormally Invasive Placenta are more permissive (Collins, 2019).

■ Pregnancy Outcomes

In sum, PAS can have isastrous outcomes or both mother an etus. Although the epth o placental invasion oes not correspon with perinatal outcome, it is o paramount maternal signicance. Table 43-4 isplays outcomes o women at tertiary-care hospitals an in whom the PAS iagnosis was usually mae preoperatively. Despite these avantages, complications inclue hemorrhage, urinary tract injury, intensive care unit amission, seconary surgical proceures, an maternal eath. Some o these same reports chronicle outcomes in a secon cohort o women in whom care was not given at a tertiary-care acility or in whom the iagnosis o percreta was not mae until elivery, or both. In these cohorts, morbiity an mortality rates were higher (Erani, 2019)

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