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Obstentrics_Williams. Vigil-De Gracia P, Solis V, Ortega N: Ibuprofen versus acetaminophen as a postpartum analgesic for women with severe preeclampsia: randomized clinical study.] Matern Fetal Neonatal Med 30(11): 1279,n2017 Vigil-De Gracia P, Tejada OR, Minaca AC, et al: Expectant management of severe preeclampsia remote from term: the MEXPRE Latin Study, a randomized multicenter clinical trial. Am] Obstet Gynecol 209:425.el, 2013 Vikse BE, Irgens LM, Leivestad T, et al: Preeclampsia and the risk of end-stage renal disease. N Engl ] Med 359:800, 2008 Villa PM, Kajantie E, Raikkonen K, et al: Aspirin in the prevention of preeclampsia in high-risk women: a randomized placebo-controlled PREDO Trial and a meta-analysis of randomized trials. B]OG 120(1):64,n2013


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Obstentrics_Williams. Villar], Purwar M, Merialdi M, et al: World Health Organisation multicentre randomised trial of supplementation with vitamins C and E among pregnant women at high risk for pre-eclampsia in populations oflow nutritional status from developing countries. B]OG 116(6):780,n2009 Viteri OA, England ]A, Lash A, et al: Should non-steroidal anti-inlammatory drugs be avoided in puerperal hypertensive women? Abstract No. 49, Am] Obstet GynecoIn216:S34, 2017 Volhard F: Die doppelseitigen haematogenen Nierenerkrankungen. Berlin, Springer, 1918 von Dadelszen P, Firoz T, Donnay F, et al: Preeclampsia in low and middle income countries-health services lessons learned from the PRE-EMPT (PRE-eclampsia monitoring, prevention, and treatment) Project. ] Obstet Gynaecol Can 34(10):917,n2012 Wagner 5], Craici 1M, Grande ]P, et al: From placenta to podocyte: vascular and podocyte pathophysiology in preeclampsia. Clin Nephrol 78(3):241, 2012 Wallace DH, Leveno K], Cunningham FG, et al: Randomized comparison


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Obstentrics_Williams. 1M, Grande ]P, et al: From placenta to podocyte: vascular and podocyte pathophysiology in preeclampsia. Clin Nephrol 78(3):241, 2012 Wallace DH, Leveno K], Cunningham FG, et al: Randomized comparison of general and regional anesthesia for cesarean delivery in pregnancies complicated by severe preeclampsia. Obstet Gynecol 86:1n93, 1995 Wallenburg He, Makovitz ]W, Dekker GA, et al: Low-dose aspirin prevents pregnancy-induced hypertension and preeclampsia in angiotensin-sensitive primigravidae. Lancet 327: 1, 1986 Walsh SW: Plasma from preeclamptic women stimulates transendothelial migration of neutrophils. Reprod Sci 16(3):320, 2009 Wang Le, Huang CY, Want HK, et al: Magnesium sulfate and nimesulide have synergistic efects on rescuing brain damage after transient focal ischemia.] Neurotrauma 29(7):1518,n2012 Wang Y, Gu Y, Granger ON, et al: Endothelial junctional protein redistribution and increased monolayer permeability in human umbilical vein endothelial cells isolated during


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Obstentrics_Williams. 29(7):1518,n2012 Wang Y, Gu Y, Granger ON, et al: Endothelial junctional protein redistribution and increased monolayer permeability in human umbilical vein endothelial cells isolated during preeclampsia. Am ] Obstet Gynecol 186:214, 2002 Ward K, Taylor RN: Genetic factors in the etiology of preeclampsia. In Taylor RN, Roberts ]M, Cunningham FG (eds): Chesley's Hypertensive Disorders in Pregnancy, 4th ed. Amsterdam, Academic Press, 2015 Wardhana MP, Dachlan EG, Dekker G: Pulmonary edema in preeclampsia: an Indonesian case-control study. ] Matern Fetal Neonatal Med March 1, 2017 [Epub ahead of printJ Watt-Morse ML, Caritis SN, Kridgen PL: Magnesium sulfate is a poor inhibitor of oxytocin-induced contractility in pregnant sheep. ] Matern Fetal Med 4:139, 1995 Weiner CP, hompson LP, Liu Z, et al: Endothelium derived relaxing factor and indomethacin-sensitive contracting factor alter arterial contractile responses to thromboxane during pregnancy. Am ] Obstet Gynecol 166: 1171,n1992


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Obstentrics_Williams. Z, et al: Endothelium derived relaxing factor and indomethacin-sensitive contracting factor alter arterial contractile responses to thromboxane during pregnancy. Am ] Obstet Gynecol 166: 1171,n1992 Weinstein L: Syndrome of hemolysis, elevated liver enzymes and low platelet count: a severe consequence of hypertension in pregnancy. Am ] Obstet GynecoIn142:159,n1982 White WM, Garrett AT, Craici 1M, et al: Persistent urinaty podocyte loss following preeclampsia may reflect subclinical renal injury. PLoS One 9(3):e92693,n2014 White M, Mielke MM, Araoz PA, et al: A history of preeclampsia is associated with a risk for coronary artery calcification 3 decades later. Amn] Obstet GynecoIn214(4)519.e1,n2016 Wicke C, Pereira PL, Neeser E, et al: Subcapsular liver hematoma in HELLP syndrome: evaluation of diagnostic and therapeutic options-a unicenter study. Am ] Obstet Gynecol 190: 1 06, 2004


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Obstentrics_Williams. Wide-Swensson DH, Ingemarsson I, Lunell NO, et al: Calcium channel blockade (isradipine) in treatment of hypertension in pregnancy: a randomized placebo-controlled study. Am] Obstet GynecoI173(1):872, 1995 Widmer M, Villar], Benigni A, et al: Mapping the theories of preeclampsia and the role of angiogenic factors. Obstet Gynecol' 109: 168, 2007 Wiegman M], de Groot]e, ]ansonius NM, et al: Long-term visual functioning after eclampsia. Obstet Gynecol 119(5):959,2012 Wikstrom AK, Stephansson 0, Cnattingius 5: Previous preeclampsia and risks of adverse outcomes in subsequent non preeclamptic pregnancies. Am ] Obstet GynecoI204(2):148.e1, 2011 Widin AG, Friedman SA, Sibai BA: The efect of magnesium sulfate therapy on the duration of labor in women with mild preeclampsia at term: a randomized, double-blind, placebo-controlled trial. Am] Obstet Gynecol 176:623, 1997


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Obstentrics_Williams. Worley LC, Hnat MD, Cunningham FG: Advanced extrauterine pregnancy: diagnostic and therapeutic challenges. Am] Obstet GynecoIn198(3):297.el, 2008 Yamada T, Obata-Yasuoka M, Hamadea H, et al: Isolated gestational proteinuria preceding the diagnosis of preeclampsia-an observational study. Acta Obstet Gynecol Scand 95(9):1048, 2016 Yang], Pearl M, DeLorenze GN, et al: Racial-ethnic diferences in midtrimester maternal serum levels of angiogenic and anti angiogenic factors. Am ] Obstet GynecoIn215:359.el, 2016 Yangn], Shangn], Zhang 5, et al: he role of renin-angiotensin-aldosterone system in preeclampsia: genetic polymorph isms and micro RNA. ] Mol Endocrinol 50(2):R53, 2013


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Obstentrics_Williams. Yangn], Shangn], Zhang 5, et al: he role of renin-angiotensin-aldosterone system in preeclampsia: genetic polymorph isms and micro RNA. ] Mol Endocrinol 50(2):R53, 2013 Ye W, Shen L, Xiong Y, et al: Preeclampsia is associated with decreased methylation of the GNA12 promoter. Ann Hum Genet 80(1):7, 2016 Yefet E, Braester Y, Suleiman A, et al: he efect of magnesium sulfate at 1 gram versus 2 grams maintenance doses on serum magnesium concentrations and adverse efects profile in women with severe preeclampsia. [Abstract No. 884J Am] Obstet Cynecol 216:5504, 201


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Obstentrics_Williams. Yoshihara M, Mayama M, Ukai M, et al: Fulminant liver failure resulting from massive hepatic infarction associated with hemolysis, elevated liver enzymes, and low platelets syndrome.] Obstet Gynaecol Res 42(10):1375,n2016 Zachary 5, Rubeo ZS, ]ortani SA: The association of N-terminal pro-brain natriuretic peptide with severe preeclampsia, HELLP syndrome, and eclampsia Abstract No. 990, Am] Obstet Gynecol 216:5557,n201 Zeeman G, Alexander ]M, Vollaard E, et al: "Delta eclampsia"-a hypertensive encephalopathy of pregnancy in "normotensive" women. Abstract No. 479, Am] Obstet Gynecoln197(6 Suppl):S140, 2007 Zeeman GG, Alexander ]M, McIntire DO, et al: Homocysteine plasma concentration levels for the prediction of preeclampsia in women with chronic hypertension. Am] Obstet Gynecol 189:574,n2003


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Obstentrics_Williams. Zeeman GG, Alexander ]M, McIntire DO, et al: Homocysteine plasma concentration levels for the prediction of preeclampsia in women with chronic hypertension. Am] Obstet Gynecol 189:574,n2003 Zeeman GG, Cunningham FG, Pritchard ]A: he magnitude of hemoconcentration with eclampsia. Hypertens Pregnancy 28(2): 127, 2009 Zeeman GG, Fleckenstein ]L, Twickler OM, et al: Cerebral infarction in eclampsia. Am] Obstet Gynecol 190:714, 2004a Zeeman GG, Hatab M, Twickler OM: Increased cerebral blood flow in preeclampsia with magnetic resonance imaging. Am ] Obstet Gynecol 191(4):1425,n2004b Zeisler H, L1urba E, Chantraine F, et al: Predictive value of the sFlt-1:PIGF ration in women with suspected preeclampsia. N Engl] Med 374:l3, 2016a Zeisler H, L1urba E, Chantraine F, et al: Soluble fms-like tyrosine kinase-1-toplacental growth factor ratio and time to delivery in women with suspected preeclampsia. Obstet Gynecol 128(2):261, 2016b


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Obstentrics_Williams. Zhou 5], Yelland L, McPhee A], et al: Fish-oil supplementation in pregnancy does not reduce the risk of gestational diabetes or preeclampsia. Am ] Clin Nutr 95(6):l378, 2012 Zhou Y, Damsky CH, Fisher 5]: Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype. ] C1in Invest 99(9):2152, 1997 Zinaman M, Rubin ], Lindheimer MD: Serial plasma oncotic pressure levels and echoencephalography during and after delivery in severe preeclampsia. Lancet 1:1245,n1985 Zondervan HA, Oosting ], Smorenberg-Schoorl ME, et al: Maternal whole blood viscosity in pregnancy hypertension. Gynecol Obstet Invest 25:83, 1988 Zwart J], Richters A, Ory F, et al: Eclampsia in he Netherlands. Obstet Gynecol 112:820, 2008 GENERAL CONSIDERATIONS ......................755 UTERINE ATONY.................................758 UTERINE INVERSION.............................761


Obstentrics_Williams

Obstentrics_Williams. GENERAL CONSIDERATIONS ......................755 UTERINE ATONY.................................758 UTERINE INVERSION.............................761 INJURIES TO THE BIRTH CANAL....................763 PUERPERAL HEMATOMAS........................764 UTERINE RUPTURE.............................. 765 PLACENTAL ABRUPTION..........................767 PLACENTA PREVIA. . . .. . . . . . . . . . . . . . . . . . . . . . .... 773 MORBIDLY ADHERENT PLACENTA..................777 OBSTETRICAL COAGULOPATHIES..................782 MANAGEMENT OF HEMORRHAGE..................787 ADJUNCTIVE SURGICAL PROCEDURES.............. 792 A profuse hemorrhage occurring prior to or shorty ater the birth of the child is always dangerous and not inrequenty a atal complication. -J. Whitridge Williams (1903)


Obstentrics_Williams

Obstentrics_Williams. As in Williams' time, obstetrical hemorrhage continues along with hypertension and infection to be one part of the infamous "triad" of maternal death causes. It also is a leading reason for admission of pregnant women to intensive care units (Chantry, 2015; Crozier, 2011; De Greve, 2016; Guntupalli, 2015). Hemorrhage was a direct cause of 11r.4 percent of 5367 pregnancy-related maternal deaths from 2006 to 2013 in the United States (Creanga, 2015, 2017). Similarly, 16 percent of1102 maternal deaths recorded in the Nationwide Inpatient Sample were caused by hemorrhage (Kuriya, 2016). In developing countries, hemorrhage's contribution is even more striking, and it is the single most important cause of maternal death worldwide (Gofman, 2016; Oladapo, 2016; Thomas, 2016). Despite these numbers, a declining maternal mortality rate from hemorrhage in the United States has been a seminal achievement. But, as discussed in Chapter 1 (p. 5), it seems unlikely that deaths from hemorrhage have


Obstentrics_Williams

Obstentrics_Williams. a declining maternal mortality rate from hemorrhage in the United States has been a seminal achievement. But, as discussed in Chapter 1 (p. 5), it seems unlikely that deaths from hemorrhage have reached an irreducible minimum.


Obstentrics_Williams

Obstentrics_Williams. • Mechanisms of Normal Hemostasis A major concept in understanding the pathophysiology and management of obstetrical hemorrhage is the mechanism by which hemostasis is achieved after normal delivery. Recall that near term an incredible amount of blood-at least 600 mLi min-flows through the intervillous space (Pates, 2010). his prodigious flow circulates through the spiral arteries, which average 120 in number. Also, recall that these vessels have no muscular layer because of their remodeling by trophoblasts, which creates a low-pressure system. With placental separation, these vessels at the implantation site are avulsed, and hemostasis is achieved first by myometrial contraction, which compresses this formidable number of large vessels. Compression is followed by clotting and obliteration of vessel lumens. If, after delivery, the myometrium contracts vigorously, fatal hemorrhage from the placental implantation site is unlikely.


Obstentrics_Williams

Obstentrics_Williams. If, after delivery, the myometrium contracts vigorously, fatal hemorrhage from the placental implantation site is unlikely. Importanty, an intact coagulation system is not necessary or postpartum hemostasis unless there are lacerations in the uterus, birth cana, or perineum. At the same time, however, fatal postpartum hemorrhage can result from uterine atony despite normal coagulation. 70 he blood volume of a pregnant D < 500 mL woman with normal pregnancy-induced hypervolemia usually rises by half, but individual increases range from 30 to 60 D 1000-1e500 mL percent, that is, 1500 ) • > 2500 mL average-sized woman (Pritchard, 1965).


Obstentrics_Williams

Obstentrics_Williams. D 1000-1e500 mL percent, that is, 1500 ) • > 2500 mL average-sized woman (Pritchard, 1965). ) 40 The equation to calculate blood volume is shown in Table It is axiomatic ) ates, without any decrease in postpartum ..e hematocrit, blood loss at delivery that approaches the volume of blood that she added during pregnancy. Thus, if blood loss is less than the pregnancy-added vol ume, the hematocrit remains the same acutely and during the irst several days delivery delivery with hysterectomy postpartum. It then rises as nonpregnant FIGURE 41-1 Blood loss associated with vaginal delivery, repeat cesarean delivery, and plasma volume normalizes during the repeat cesarean delivery plus hysterectomy. (Data from Pritchard, 1962.)


Obstentrics_Williams

Obstentrics_Williams. Traditionally, postpartum hemorrhage is defined as the loss of ::500 mL of blood after completion of the third stage of labor. This is problematic because almost half of all women delivered vaginally shed that amount of blood or more when losses are carefully measured (Pritchard, 1962). These results are depicted in Figure 41-1 and show further that approximately 5 percent of women delivering vaginally lose more than 1000 mL of blood. According to the American College of Obstetricians and Gynecologists (2017d), postpartum hemorrhage is deined as cumulative blood lossr> 1000 mL accompanied by signs and symptoms ofhypovolemia. And, almost a third of women undergoing cesarean delivery have blood loss that exceeds 1000 mL. These studies show that estimated blood loss is commony ony approximatey hafthe actual loss. Because of this, estimated blood loss in excess of "average" should alert the obstetrician to possible excessive bleeding. Whether quantiication of blood loss improves accuracy


Obstentrics_Williams

Obstentrics_Williams. hafthe actual loss. Because of this, estimated blood loss in excess of "average" should alert the obstetrician to possible excessive bleeding. Whether quantiication of blood loss improves accuracy is controversial (Hamm, 2017; Toledo, 2007).


Obstentrics_Williams

Obstentrics_Williams. TABLE 41 -1. Calculation of Maternal Total Blood Volume next week or so. Whenever thepospartum hematocrit is lower than one obtained on admission or deivery, blood loss can be estimated as the sum of the calculated pregnancy-added volume plus 500 mL or each 3 volume percent decline ofthe hematocrit. Excessive blood loss has been estimated by several methods. Sosa and colleagues (2009) used specially constructed drapes and reported that 10.8 percent of women had hemorrhage in excess of 500 mL with vaginal delivery, whereas 1.9 percent lost > 1000 mL. Compared with the indings of Figure 41-1, these estimates likely are too low. Tita and associates (2012) used a 6-volume percent drop in the postpartum hematocrit to define clinically signiicant blood loss with vaginal delivery. This decline easily signifies a > 1000-mL blood loss in the averaged-sized woman. hey documented this amount in a fourth ofwomen, which agrees with Figure 41-1.


Obstentrics_Williams

Obstentrics_Williams. Another marker used to estimate hemorrhage incidence is the transfusion rate. In the study by Tita just cited, more than 6 percent of women who delivered vaginally underwent blood transfusions. In a study of more than 66,000 women delivered at Parkland Hospital, 2.3 percent overall were given Nonpregnant blood volumea: [Height (inches) x 50J + [Weight (pounds) x 25J = Blood volume (mL) Pregnancy blood volume: Average increase is 30 to 60 percent of calculated nonpregnant Increases across gestational age and plateaus at approximately 34 weeks Usually larger with low normal-range hematocrit (-30) and smaller with high normal-range hematocrit (-40) Average increase is 40 to 80 percent with multifetal gestation Average increase is less with preeclampsia-volumes vary inversely with severity Postpartum blood volume with serious hemorrhage:


Obstentrics_Williams

Obstentrics_Williams. Average increase is less with preeclampsia-volumes vary inversely with severity Postpartum blood volume with serious hemorrhage: Assume acute return to nonpregnant total volume after fluid resuscitation Pregnancy hypervolemia cannot be restored postpartum aFormula arrived at by measuring blood volume and blood loss in more than 100 women using 51Cr-labeled erythrocytes. Data from Hernandez, 201n2. blood transfusions for hypovolemia (Hernandez, 2012). Half 25 of these women had undergone cesarean delivery. Importantly, for those transfused, these investigators calculated blood loss to E average approximately 3500 mLl Finally, Green and coworkers (2016) reported that the incidence of massive tranfusion for From the foregoing, it is apparent that significant blood loss � t postpartum hemorrhage was 23 per 100,000 births.


Obstentrics_Williams

Obstentrics_Williams. From the foregoing, it is apparent that significant blood loss � t postpartum hemorrhage was 23 per 100,000 births. accompanies up to a fourth of vaginal deliveries. The amounts and proportions for cesarean delivery are much greater. And, � £ hemorrhage is underreported. For example, data from the O. postpartum hemorrhage incidences of only 2.0 and 2.6 per cent for two epochs in the United States (Berg, 2009). Similar incidences have been reported by others (Kramer, 2013; Mehrabadi, 2013; Patterson, 2014). Numerous clinical circumstances raise the risks for obstetrical hemorrhage. he imposing list shown in Table 41-2 illustrates that hemorrhage can manifest at any time throughout pregnancy, delivery, and the puerperium. Thus, any description TABLE 41 -2. Obstetrical Hemorrhage: Causes, Predisposing Factors, and Vulnerable Patients Anesthesia or analgesia Halogenated agents Conduction analgesia with Previous uterine atony Parity: primiparity, high parity


Obstentrics_Williams

Obstentrics_Williams. Anesthesia or analgesia Halogenated agents Conduction analgesia with Previous uterine atony Parity: primiparity, high parity Acute fatty liver Anticoagulant treatment Congenital coagulopathies Amnionic fluid embolism Prolonged retention of Cause of hemorrhage FIGURE 41-2 Contributions to maternal death from various causes of obstetrical hemorrhage. Percentages are approximations because of different classification schemata used. DIC = nated intravascular coagulopathy. (Data from AI-Zirqi, 2008; Berg, 201o0; Creanga, 201o5; Zwart, 2008.) of obstetrical hemorrhage should include gestational age. Contributions to maternal death from some of these causes of are shown in Figure 41-2.


Obstentrics_Williams

Obstentrics_Williams. Obstetrical hemorrhage is traditionally classified as antepartumsuch as with placenta previa or placental abruption, or as pospartum-commonly caused by uterine atony or genital tract lacerations. In individual women, however, these terms are nonspeciic, and it is reasonable to speciy the cause and gestational age as descriptors. to its cause. Many aspects of bleeding during the first half of pregnancy from abortion or ectopic pregnancy are covered in Chapters 18 and 19. Discussions that follow concern pregnan cies with a viable-size fetus. In these cases, rapid assessment should always consider the deleterious etal fects ofmaternal hemorrhage.


Obstentrics_Williams

Obstentrics_Williams. Chapters 18 and 19. Discussions that follow concern pregnan cies with a viable-size fetus. In these cases, rapid assessment should always consider the deleterious etal fects ofmaternal hemorrhage. During active labor, slight vaginal bleeding is common. This "bloody show" is the consequence of efacement and dilation of the cervix, with tearing of small vessels. Uterine bleeding above the cervix, however, is concerning. It may follow some separation of a placenta previa implanted in the immediate vicinity of the cervical canal, or it may be from a placental abruption or uterine tear. In some women, especially with a placenta previa, cervical varicosities may bleed (O'Brien, 2013). Rarely, there may be velamentous insertion of the umbilical cord, and the involved placental vessels may overlie the cevix-vasa previa. In this case, serious fetal hemorrhage follows laceration of these vessels at the time of membrane rupture (Swank, 2016).


Obstentrics_Williams

Obstentrics_Williams. N ear term in many women, the source of uterine bleeding is not identified, bleeding ceases, and no apparent anatomical cause is found at delivery. In most of these cases, bleeding likely originated from 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 sonographicaly. Injuries to the Birth Canal


Obstentrics_Williams

Obstentrics_Williams. Injuries to the Birth Canal Bleeding after midpregnancy is associated with several adverse outcomes. he 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 frequent causes identified. In a third, no cause was found. Of all women, 44 percent were delivered before 29 weeks' gestation. In more than 68,000 women in Scotland, the incidence of antepartum hemorrhage after the irst trimester was 11 percent (Bhandari, 2014). hese women were at signiicantly higher risk for preterm birth, labor induction, and postpartum hemorrhage.


Obstentrics_Williams

Obstentrics_Williams. In most cases, the source of postpartum hemorrhage 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 exceptions are unrecognized intrauterine and intravaginal blood accumulation and uterine rupture with intraperitoneal or retroperitoneal bleeding. Another consideration is an expanding vulvar or vaginal hematoma (p. 764). Initial evaluation attempts to diferentiate uterine atony from genital tract lacerations. For this, risk factors are sought, the lower genital tract is examined, and uterine tone is assessed. Atony is identiied by a boggy, soft uterus during bimanual examination and by expression of clots and hemorrhage during uterine massage.


Obstentrics_Williams

Obstentrics_Williams. Persistent bleeding despite a firm, well-contracted uterus suggests that hemorrhage most likely is from lacerations. Bright red blood further suggests arterial bleeding. To conirm that lacerations are a source of bleeding, carful inspection of the vagina, cervix, and uterus is essential. Sometimes bleeding may be caused by both atony and trauma, especially after forceps or vacuum-assisted vaginal delivery. Examination is easier if conduction analgesia was given. If there are no lower genital tract lacerations and the uterus is contracted, yet supracervical bleeding persists, then manual exploration of the uterus is done to exclude a uterine tear (Kaplanoglu, 2016). his also is completed routinely after internal podalic version, breech extraction, or successful vaginal birth after cesarean.


Obstentrics_Williams

Obstentrics_Williams. Late pospartum hemorrhage describes bleeding after the irst 24 hours. Found in up to 1 percent of women, it may be serious and is discussed in Chapter 37 (American College of Obstetricians and Gynecologists, 2017 d). As noted, visual estimates are notoriously inaccurate, especially with excessive bleeding. Instead of sudden massive hemorrhage, postpartum bleeding is frequently steady. If atony persists, bleeding may appear to be only moderate at any given instant but may continue until serious hypovolemia develops. Bleeding from an episiotomy or a vaginal laceration can also appear to be only minimal to moderate. But, constant seepage can lead to enormous blood loss relatively quickl)r . 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 of blood. In others, postpartum uterine massage is applied to a roll of abdominal fat mistaken for the uterus.


Obstentrics_Williams

Obstentrics_Williams. All of these factors can lead to an underappreciation of the magnitude of hemorrhage over time. he efects of hemorrhage depend to a considerable degree on the maternal nonpregnant blood volume and the corresponding degree of pregnancyinduced hypervolemia. For this and other reasons, hypovolemia may not be recognized until very late. A treacherous eature of pospartum hemorrhage is the ailure of the pulse and blood pressure to undergo more than moderate alterations until large amounts of blood have been lost. The normotensive woman initially may actually become somewhat hypertensive from catecholamine release in response to hemorrhage. And importantly, women with preeclampsia may become "normotensive" despite remarkable hypovolemia.


Obstentrics_Williams

Obstentrics_Williams. Some gravidas may be particularly susceptible to hemorrhage because their blood volume expansion is less than expected. This situation is most commonly encountered in small womeneven those with normal pregnancy-induced hypervolemia. Women with severe preeclampsia or eclampsia are also more vulnerable to hemorrhage because they frequently do not have a normal blood volume accrual. Specifically, Zeeman and associates (2009) documented a mean increase above nonpregnant volume of only 10 percent in eclamptic women (Chap. 40, p. 718). A third example is the moderate-to-severe curtailing of pregnancy-induced volume expansion in women with chronic renal insuiciency (Chap. 53, p. 1034). When excessive hemorrhage is suspected in these high-risk women, cystalloid and blood are prompty administered or suspected hypovolemia.


Obstentrics_Williams

Obstentrics_Williams. The most frequent cause of obstetrical hemorrhage is failure of the uterus to contract suiciently after delivery and to arrest bleeding from vessels at the placental implantation site (p. 755). That said, some bleeding is inevitable during thirdstage labor as the placenta begins to separate. Blood from the implantation site may escape into the vagina immediately-the Duncan mechanism of placental separation, or it remains concealed behind the placenta and membranes until the placenta is delivered-the Schultze mechanism. After signs of placental separation, the uterus should be massaged if it is not contracted irmly, and placental descent is indicated by a slack umbilical cord. Importanty, separation and delivey of the placenta by cord traction, especialy when the uterus is atonic, may cause uterine inversion.


Obstentrics_Williams

Obstentrics_Williams. If heavy bleeding persists after delivery of the newborn and 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 should be used. As illustrated in Figure 41-3, the fingertips of one hand, with fingers approxi mated, are insinuated between the uterine wall and placenta. A sweeping forward motion in this plane will peel the placenta of its uterine attachmenc. After its removal, trailing membranes are carefully teased free from the decidua using ring forceps as needed. Another method to clear membranes is to wipe out the uterine cavity with a gauze-wrapped hand. Most recommend FIGURE 41 -3 Manual removal of placenta. A. One hand grasps the fundus. The other hand is inserted into the uterine cavity, and the fingers are swept from side to side as they are advanced. B. When the placenta has become detached, it is grasped and removed.


Obstentrics_Williams

Obstentrics_Williams. removal (World Health Organization, 2015). he fundus is always palpated following placental delivery to conirm that the uterus is well contracted. If it is not irm, hemorrhage from atony (Hofmeyr, 2013). Simultaneously, 20 units of oxytocin in 1000 mL of crystalloid solution will of 200 m U / min. Higher concentrations are minimally more efective (Tita, 2012). Oxytocin is never given as an undiluted bolus dose because serious hypotension or cardiac arrhythmias can develop.


Obstentrics_Williams

Obstentrics_Williams. In many women with known risks, uterine atony can at least be anticipated well in advance of delivery. In one study, however, up to half of women with atony after cesarean deliveY had no risk factors (Rouse, 2006). The magnitude of risk for atony imposed by each of the factors shown in Table 41-2 varies considerably between reports. Primiparity and high parity are risk factors (Driessen, 2011). In one study, the incidence of postpartum hemorrhage rose from 0.3 percent in women of low parity to 1.9 percent with parity of four or greater. It was 2.7 percent with parity of seven or greater (Babinszki, 1999). The overdistended uterus is prone to hypotonia after delivery, and thus women with a large fetus, multiple fetuses, or hydramnios are at greater risk. 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 followed by atony (Driessen, 2011). he frequency of


Obstentrics_Williams

Obstentrics_Williams. atony and include hyper-or hypotonic labor. Similarly, labor induction or augmentation with either prostaglandins or oxytocin is more likely to be followed by atony (Driessen, 2011). he frequency of hemorrhage increases with prolongation of the third stage (Frolova, 2016). Finally, the woman who has had aprior postpartum hemorrhage is at risk for recurrence.


Obstentrics_Williams

Obstentrics_Williams. With immediate postpartum hemorrhage, careful inspection is done to exclude birth canal laceration. Because bleeding can be caused by retained placental fragments, inspection of the placenta after delivery should be routine. If a defect is seen, the uterus should be manually explored and the fragment removed. Occasionally, retention of a succenturiate lobe may cause postpartum hemorrhage (Chap. 6, p. 112). During examination for lacerations and causes of atony, the uterus is massaged and uterotonic agents are administered.


Obstentrics_Williams

Obstentrics_Williams. Several compounds can prompt the postpartum uterus to contract (Chap. 27, p. 527). One of these is routinely selected and given to prevent postpartum bleeding by ensuring uterine contractions. Nfost of these same agents are also used to treat uterine atony with bleeding. Moreover, because many trials combine results from atony prophylaxis and treatment, their evaluation is problematic. For example, oxytocin has been used for more than 70 years, and in most cases, it is infused intravenously or given intramuscularly after placental delivery. Neither route has been shown to be superior (Dagdeviren, 2016). his or other utero tonics given prophylactically will prevent most cases of uterine atony.


Obstentrics_Williams

Obstentrics_Williams. To treat uterine atony, ergot alkaloids have been used for centuries. If atony persists despite oxytocin and other preventive measures, ergot derivatives can be used for secondline treatment. Ergot preparations include methylergonovine (Methergine) and ergonovine, however, only methylergonovine is currently manufactured in the United States. Given parenterally, these drugs rapidly stimulate tetanic uterine contractions and act for approximately 45 minutes (Schimmer, 2011). A common regimen is 0.2 mg of either drug given intramuscularly. Methergine can be repeated at 2-to 4-hour intervals as needed. A caveat is that ergot agents, especialy given intravenousy, may cause dangerous hypertension, especialy in women with preeclampsia. Severe hypertension is also seen with concomitant use of protease inhibitors given for human immunodeiciency viral (HIV) infection. These adverse efects notwithstanding, it is speculative whether ergot derivatives ofer superior therapeutic efects compared with


Obstentrics_Williams

Obstentrics_Williams. inhibitors given for human immunodeiciency viral (HIV) infection. These adverse efects notwithstanding, it is speculative whether ergot derivatives ofer superior therapeutic efects compared with oxytocin.


Obstentrics_Williams

Obstentrics_Williams. In cases of atony refractory to one agent, an agent from a diferent group can be added. At least two randomized studies have addressed combined ergot-oxytocin regimens. In one, ergometrine plus oxytocin was compared with ergometrine alone to prevent postpartum hemorrhage (Koen, 2016). The overall need for transfusion was signiicantly lower with the combination regimen. Another comparable study reairmed these indings (�enti.irk, 2016).


Obstentrics_Williams

Obstentrics_Williams. During the past 40 years, other second-line agents for atony have included the E-and F-series prostaglandins. Carboprost tromethamine (Hemabate) is the 15-methyl derivative of prostaglandin F2a• It is approved for uterine atony treatment in a dose of 250 Lg (0.25 mg) given intramuscularly. This dose can be repeated if necessary at 15-to 90-minute intervals up to a maximum of eight doses. Observational data indicate an 88-percent success rate (Oleen, 1990). Carboprost causes side efects in approximately 20 percent of women. These include, in descending order of frequency, diarrhea, hypertension, vomiting, fever, flushing, and tachycardia. Another pharmacological efect is pulmonary airway and vascular constriction. hus, carboprost should not be used for asthmatic women and those with suspected amnionic fluid embolism (p. 785). We have occasionally encountered severe hypertension with carboprost given to women with preeclampsia. It has also been reported to cause arterial oxygen


Obstentrics_Williams

Obstentrics_Williams. suspected amnionic fluid embolism (p. 785). We have occasionally encountered severe hypertension with carboprost given to women with preeclampsia. It has also been reported to cause arterial oxygen desaturation that averaged 10 percent (Hanins, 1988). Relative contraindications to carboprost include renal, liver, and cardiac disease (American College of Obstetricians and Gynecologists, 2017 d).


Obstentrics_Williams

Obstentrics_Williams. E-series prostaglandins can also prevent or treat atony. Dinoprostone-prostaglandin E2-may be used of label and is given as a 20-mg suppository per rectum or per vaginum every 2 hours. It typically causes diarrhea, which is problematic for the rectal route, whereas vigorous vaginal bleeding may preclude its use per vaginum. Hypotension, which is commonly encountered with hemorrhage, is considered a contraindication by some. Intravenous prostaglandin E2-suprostone-is used in Europe, but it is not available in the United States (Schmitz, 2011).


Obstentrics_Williams

Obstentrics_Williams. Misoprostol-Cytotec-is a synthetic prostaglandin Ej analogue that is used for prevention and treatment of atony (AbdelAleem, 2001; Ugwu, 2016). Most studies have addressed prevention and have conflicting conclusions. In a Cochrane review, Mousa and associates (2014) reported no added benefits for misoprostol use compared with oxytocin or ergonovine for treatment. Derman and coworkers (2006) compared a 600-l-Lg oral dose given preventively at delivery against placebo. They found that the drug lowered the incidence of hemorrhage from 12 to 6 percent and that of severe hemorrhage from 1.2 to 0.2 percent. In another study, Gerstenfeld and Wing (2001) concluded that 400 ILg misoprostol administered rectally was not superior to intravenous oxytocin given to prevent postpartum hemorrhage. From a systematic review, Villar (2002) found that oxytocin and ergot preparations administered after delivery were more efective than misoprostol for prevention of postpartum hemorrhage (Chap. 27, p. 527).


Obstentrics_Williams

Obstentrics_Williams. systematic review, Villar (2002) found that oxytocin and ergot preparations administered after delivery were more efective than misoprostol for prevention of postpartum hemorrhage (Chap. 27, p. 527). If misoprostol is used to treat atony, the American College of Obstetricians and Gynecologists (2017 d) recommends a dose of 600 to 1000 ILg rectally, orally, or sublingually.


Obstentrics_Williams

Obstentrics_Williams. Bleeding Unresponsive to Uterotonic Agents If bleeding persists after initial measures for atony have been implemented, then the following management steps are performed immediately and simultaneously: 1. Begin bimanual uterine compression, which is easily done and controls most cases of continuing hemorrhage (Fig. 41-4). This technique is not simply fundal massage. The posterior uterine wall is massaged by one hand on the abdomen, while the other hand is made into a fist and placed into the vagina. his fist kneads the anterior uterine wall through the anterior vaginal wall and the uterus is also compressed between the two hands. 2. Immediately mobilize the emergent-care obstetrical team to the delivery room and call for whole blood or packed red cells. 3. Request urgent help from the anesthesia team. 4.


Obstentrics_Williams

Obstentrics_Williams. 2. Immediately mobilize the emergent-care obstetrical team to the delivery room and call for whole blood or packed red cells. 3. Request urgent help from the anesthesia team. 4. Secure at least two large-bore intravenous catheters so that crystalloid with oxytocin can be continued simultaneously with blood products. Insert an indwelling Foley catheter for continuous urine output monitoring. 5. Begin volume resuscitation with rapid intravenous infusion of crystalloid (p. 788). 6. With sedation, analgesia, or anesthesia established and now with optimal exposure, once again manually explore the uterine cavity for retained placental fragments and for uterine abnormalities, including lacerations or rupture. FIGURE 41-4 Bimanual compression for uterine atony. The uterus is positioned with the fist of one hand in the anterior fornix pushing against the anterior wall, which is held in place by the other hand on the abdomen. The abdominal hand is also used for uterine massage. 7.


Obstentrics_Williams

Obstentrics_Williams. 7. Thoroughly inspect the cervix and vagina again for lacerations that may have escaped attention. 8. If the woman is still unstable or if there is persistent hemorrhage, then blood transfusions are given (p. 788). At this juncture, after causes other than atony have been excluded and after hypovolemia is reversed, several other measures are considered if bleeding continues. Their use depends on several factors such as parity, desire for sterilization, and experience with each method.


Obstentrics_Williams

Obstentrics_Williams. Balloon Tamponade. Uterine packing to treat refractory uterine atony fell from favor because of concerns regarding concealed bleeding and infection (Gilstrap, 2017). Newer techniques of balloon tamponade help alleviate some of these concerns (Sentilhes, 2016; Zelop, 201l). In one technique, the tip of a 24F to 30F Foley catheter with a 30-mL balloon is guided into the uterine cavity and illed with 60 to 80 mL of saline. The open tip permits continuous drainage of blood from 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. If bleeding subsides, the catheter is typically removed ater 12 to 24 hours. Similar devices for tamponade include SegstakenBlakemore, Rusch, and ebb balloons and condom catheters (Antony, 2017; Georgiou, 2009).


Obstentrics_Williams

Obstentrics_Williams. Enthusiasm has developed for specially constructed intrauterine balloons to treat hemorrhage from uterine atony and other causes. A Bakri Pospartum Baloon or BT-Cath may be inserted and inlated to tamponade the endometrial cavity and stop bleeding (Fig. 41-5). Insertion requires two or three team members. he irst performs abdominal sonography during the procedure. The second places the delated balloon into the uterus and stabilizes it. The third member instills luid to inlate the balloon, rapidly infusing at least 150 mL followed by further instillation over a few minutes for a total of 300 to 500 mL to arrest hemorrhage. It is reasonable to remove the balloon after approximately 12 hours (Einerson, 2017). In prospective studies, nearly 150 women have been managed for postpartum hemorrhage with these uterine balloons FIGURE 41 -5 Intrauterine Bakri balloon for postpartum hemorrhage.


Obstentrics_Williams

Obstentrics_Williams. In prospective studies, nearly 150 women have been managed for postpartum hemorrhage with these uterine balloons FIGURE 41 -5 Intrauterine Bakri balloon for postpartum hemorrhage. (Gronvall, 2013; Kaya, 2016; Vintejoux, 2015). Perhaps a fourth of cases were caused by uterine atony. For all causes, the success rate was noted to be approximately 85 percent. Combinations of balloon tamponade and uterine compression sutures have also been described (Diemert, 2012; Yoong, 2012). Failures for all of these require various surgical methods including hysterectomy. These include uterine compression sutures, pelvic vessel ligation, angiographic embolization, and hysterectomy. hese are discussed on page 792.


Obstentrics_Williams

Obstentrics_Williams. These include uterine compression sutures, pelvic vessel ligation, angiographic embolization, and hysterectomy. hese are discussed on page 792. Puerperal inversion of the uterus is one of the classic hemorrhagic disasters encountered in obstetrics. Unless promptly recognized and managed appropriately, associated bleeding often is massive. Risk factors include alone or in combination: (1) fundal placental implantation, (2) uterine atony, (3) cord traction applied bore placental separation, and (4) abnormally adhered placentation such as with the accrete syndromes (p. 777). Depending on which of these factors are contributory, the incidence and severity of uterine inversion varies. There is progressive severity of inversion as shown in Figure 41-6. The worst scenario is complete inversion with the uterus protruding from the birth canal (Fig. 41-7).