CHAPTER 51 Alexandria J. Hill1,2,3, Karin Fox4,5, and Stephanie R. Martin6 1High Risk Pregnancy Center, Las Vegas, NV, USA 2Texas A&M College of Medicine, College Station, TX, USA 3University of Arizona, Phoenix, AZ, USA 4Maternal‐Fetal Medicine, Baylor College of Medicine, Houston, TX, USA 5Texas Children’s Hospital, Pavilion for Women, Houston, TX, USA 6Clinical Concepts in Obstetrics, Scottsdale, AZ, USA This chapter will focus specifically on the obstetrical patient experiencing a postpartum hemorrhage (PPH). The goal is to identify the emergency, explain the etiology, and understand general management tools to assist in decision‐making during such emergencies. We introduce two clinical scenarios and lead you through management decisions for the event based on best available evidence. Table 51.1 Acute causes of postpartum hemorrhage PPH remains a leading cause of maternal morbidity and mortality worldwide [1, 2], and the immediate postpartum period is the most common time for complications from hemorrhage [2]. The most frequent cause of PPH is uterine atony. Table 51.1 lists causes of PPH [1]. In industrialized nations, the prevalence of obesity, advancing maternal age, multiple gestations, rates of induction, cesarean delivery, and subsequent trials of labor after cesarean are on the rise, thereby increasing the overall potential for PPH. Definitions of PPH (also described as massive obstetrical hemorrhage, MOH) vary widely. In general, accepted definitions include estimated blood loss >500 ml following a vaginal delivery or >1000 ml following a cesarean delivery. It has been proposed that a drop in hematocrit by 10% or need for blood transfusion should also be criteria for the diagnosis of PPH [1, 3]. Other studies have defined PPH as a blood loss exceeding 1, 2.5 l, or need for at least 5 units of packed red blood cells (PRBCs) [4]. Management of acute PPH focuses initially on identifying and addressing underlying etiology (i.e. treatment of uterine atony or repair of a laceration). Maternal mortality in the United States declined dramatically over the last century, but reached a nadir in the late‐1980s, but has had a small, but steady increase over the last 2 decades [5]. Although a majority of maternal deaths have been deemed unpreventable, hemorrhage is one of the identified preventable causes of maternal death, and thus the Joint Commission has recommended that protocols for rapid identification and response should be in place in the hospital setting [6]. In this chapter, the focus will be on identifying causes of hemorrhage as well as treatments and outcomes of various interventions. Addressing the topic of PPH can be guided by first identifying the cause of the hemorrhage. One might begin with a broad search of PPH in common electronic databases such as MEDLINE and OVID, specifically searching for prospective studies, systematic reviews, and randomized trials regarding this subject. The Cochrane Library can assist in finding systematic reviews of treatment strategies in the various causes of PPH. These three search engines were used throughout this chapter for data retrieval. Acute PPH is often defined as estimated blood loss of >500 ml after a vaginal delivery and > 1000 ml after a cesarean delivery. Quantification of PPH is often subjective and visual. Data indicate that blood loss in the obstetric patient is commonly underestimated by medical professionals including midwifes, nurses, and physicians [7–12]. Objective measures of blood loss including weighing of sponges, measurement of volume in premarked drapes and assessment of hemoglobin can assist in estimation of blood loss [13]. When a collection drape is used, studies have shown a reduction in maternal morbidity and mortality [13] yet no significant decrease in PPH severity [14]. Prevention of hemorrhage is an important component of the management of patients at the time of delivery. Active management of the third stage of labor (AMTSL) has proven to reduce the risk of PPH [15]. AMTSL includes: (i) use of prophylactic uterotonics; (ii) early cord clamping; and (iii) cord traction for delivery of the placenta. The uterotonic agent of choice has been oxytocin, which has proven more effective than prostaglandins [16]. Although AMTSL is easy to perform, many institutions worldwide perform only one or two of the necessary three components of AMTSL [17]. Continuing education and training for providers to consistently utilize AMTSL are necessary to reduce the incidence of highly morbid complications of PPH. The World Health Organization recommends inclusion of the three criteria for AMTSL to prevent PPH, yet recent findings indicate that the most protective measure of the three is immediate administration of oxytocin after delivery of the fetus (or the anterior shoulder) [18]. A recent double‐blind, randomized controlled trial compared oxytocin alone to ergometrine (Syntometrine) plus oxytocin, finding that blood loss was less with the administration of both uterotonics, yet side effects of ergometrine were significant (nausea, vomiting, elevated blood pressures) [19]. Studies have been done on women with identifiable risk factors for PPH, such as a distended uterus (e.g.: polyhydramnios, multiple gestation, fetal macrosomia) or abnormal placentation (placenta previa, placenta accreta) and found that patients who received Hemabate and oxytocin (over either drug alone) prophylactically had significantly less bleeding than controls [20]. When PPH is identified, a general, stepwise approach is used. After vaginal delivery, the cervix and vagina should be well visualized and any bleeding lesions should be repaired. The uterus should also be examined for any retained products of conception and bimanually compressed to decrease immediate bleeding due to atony. If atony is felt to be the cause of hemorrhage, first line therapy is the administration of uterotonic medications and repletion of intravenous fluids and blood products as necessary. If hemorrhage persists, the decision is then made to either proceed with uterine packing or balloon tamponade, uterine artery embolization (UAE), or exploratory laparotomy to ligate vessels, place compression sutures, or a combination of these methods. Hysterectomy may be required should the other interventions fail, and if done in a timely manner, may be life‐saving. Commonly recommended uterotonics include: oxytocin (Pitocin®), methylergonovine (Methergine®), misoprostol (Cytotec®), and prostaglandin formulations such as F2α (Hemabate®) and E2 (Dinoprostone). Examples of uterotonic drugs, dosing, and route of administration can be found on Table 51.2 [1]. All uterotonics may cause nausea and/or vomiting. The physician must also be aware of the contraindications of specific uterotonic medications. For example, Methergine should be avoided in patients who are hypertensive or with a history of hypertension and Hemabate should be avoided in patients with active cardiac, pulmonary, renal, or hepatic disease [1]. Some uterotonic drugs have the advantage to be administered via more than one route, like misoprostol (Cytotec®), which can be given rectally, buccally or orally, and oxytocin, which may be given intravenously or intramuscularly. This is potentially advantageous for patients who do not have IV access or are unable to tolerate oral medications. Table 51.2 Uterotonic medications IV, intravenous; IM, intramuscular; IU, intrauterine; PR, per rectum; PO, per oral; *1st line; N/V, nausea and vomiting. Misoprostol (Cytotec®) is a shelf‐stable medication in tablet form that does not require refrigeration. This affords it the potential benefit of use in remote, low‐resource settings. A notable trend toward reduction in postpartum blood loss, drop in hemoglobin, and need for additional interventions was seen in patients that received misoprostol (600 mcg sublingually) versus placebo when they had an estimated blood loss >500 ml after a normal spontaneous vaginal delivery [21]. Misoprostol can also be administered rectally, up to 1000 mcg, and has been shown to decrease need for further intervention for PPH [22]. Although a randomized control trial comparing interventions for treatment of PPH showed insufficient evidence for misoprostol to be added to the current combination of oxytocin/ergometrine (Syntometrine), misoprostol showed a better clinical response when administered rectally than did IV Syntometrine. Misoprostol, however, is associated with a significant increase in maternal pyrexia and shivering [23]. Oxytocin, the most commonly used uterotonic, has a rapid onset of action and a short half‐life. It can be administered intravenously or intramuscularly. When administered too rapidly, it can cause maternal hypotension [24]. Studies have shown that oxytocin administered in an immediate bolus (5 units over one minute) after cesarean delivery can be as effective in preventing PPH as a bolus plus an additional IV infusion (40 units in 500 ml saline over four hours). However, a decreased need for other uterotonics is seen when a continued IV infusion of oxytocin is administered after cesarean delivery [25]. Oxytocin agonists, such as Carbetocin, have been studied for their effectiveness in preventing PPH. A large Cochrane Database search revealed that Carbetocin reduced the need for other uterotonics (after cesarean delivery), need for uterine massage (after cesarean or vaginal delivery), and overall risk of PPH when compared to oxytocin [26]. Another medication that has been proposed to assist with management of PPH is estradiol. When compared to routine management of PPH (uterine massage and uterotonics), women experiencing acute PPH who received 4 mg estradiol benzoate intramuscularly had less blood loss and did not require hysterectomy as often [27], however this is not currently widely used. Tranexamic acid acts as an antifibrinolytic agent, preventing breakdown of fibrin by plasmin [28], and has been used in trauma patients and gynecologic patients with significant menorrhagia to stop further bleeding. A recent randomized controlled trial confirmed data from prior studies [29–32] indicating that tranexamic acid administration can decrease intra‐ and post‐operative blood loss in patients undergoing a cesarean delivery [28]. The WOMAN (World Maternal Antifibrinolytic) trial was designed to enroll patients with a PPH following the delivery of an infant via cesarean or vaginal delivery and randomized them to either tranexamic acid (1 g IV) or placebo (sodium chloride 0.9%), an analysis based on intent to treat. Enrollment is aimed at 15 000 women, with the aim to reduce mortality or need for hysterectomy in this patient population [2]. Recombinant factor VIIa (rFVIIa) has been administered in the setting of PPH, to improve coagulopathy, and may contribute to an improvement in predicted maternal mortality [33], however its use remains controversial. A notable decrease in prothrombin time (PT), to nearly a normal level, can be seen in patients who receive rFVIIa in the setting of massive hemorrhage and need for blood transfusion [34]. However, this medication may be ineffective in the setting of hypofibrinogenemia, due to the role of FVII in the coagulation cascade, such that factor VII cleaves fibrinogen to fibrin, which is then available for clot formation. Therefore, transfusion of cryoprecipitate must often precede administration of rFVIIa. Whether or not rFVIIa decreases the need for blood products is also questionable [33, 35]. Moreover, the dosing range of rFVIIa is very broad (16–128 mμg kg−1) [36], and optimal dosing remains unknown. The disadvantages of rFVIIa are the possible complication of arterial thromboembolism due to activation of the clotting cascade and high cost per dose [37]. Its use has been limited in the obstetric context. In the face of MOH, it is imperative to replete blood products appropriately and in a timely manner. Timely transfusion and resuscitation must be initiated during PPH and may be given concomitantly during both conservative and surgical methods to identify and stop hemorrhage. Continual assessment of bleeding activity, patient vital signs and symptoms is imperative, as obstetrical hemorrhage can rapidly deteriorate toward hypovolemic shock or disseminated intravascular coagulopathy. Blood products should be transfused as needed, and without unnecessary delay [38]. Trauma patients transfused at a ratio of 1 : 1 of fresh frozen plasma (FFP) to PRBC when compared to more traditional ratios of 1 : 4 or 1 : 5 showed increased survival [39]. Quantification of PPH is often subjective and visual. Data indicate that blood loss in the obstetric patient is commonly underestimated by medical professionals including midwifes, nurses, and physicians [7–12]. Objective measures of blood loss including weighing of sponges, measurement of volume in premarked drapes and assessment of hemoglobin can assist in estimation of blood loss [13]. When a collection drape is used, studies have shown a reduction in maternal morbidity and mortality [13] yet no significant decrease in PPH severity [14]. If collection tools are not utilized, training medical providers in assessment of blood loss has been shown to improve accuracy of blood loss estimation [40]. Although medical therapy can often slow hemorrhage due to uterine atony, surgical intervention, including hysterectomy, should be anticipated, particularly in patients with severe blood loss requiring blood transfusion. A three‐year study of 117 major obstetrical hemorrhage patients in Dublin, Ireland found that in patients who received at least 5 units of PRBC (majority due to uterine atony) only 15% were managed successfully with medical therapy (oxytocin, misoprostol, Hemabate, ergometrine, or rarely, rFVIIa) alone [4]. Given that PPH is an unfortunately common morbidity in obstetrics, various protocols for management of PPH have been designed that decrease the need for blood products, prevent development of disseminated intravascular coagulation (DIC), and allow earlier resolution of maternal bleeding [41]. For example, investigators from the United Kingdom reviewed the use of the algorithm “HEMOSTASIS” (Help, Establish etiology, Massage the uterus, Oxytocin infusion and prostaglandins, Shift to operating room, Tamponade test, Apply compression sutures, Systemic pelvic devascularization, Interventional radiology, Subtotal/total abdominal hysterectomy) for women with >1500 ml blood loss. Use of this algorithm facilitated proper management as well as a decreased need for blood transfusions, hysterectomies, ICU admissions, and maternal mortality [42]. For institutions that do not routinely manage patients with uterotonics, protocols such as this are suggested to guide management of the PPH patient prior to moving toward operative techniques [43]. A patient experiencing PPH, especially after a vaginal delivery, will often be managed first with uterotonic medications, manual compression of the uterus, and repair of any bleeding lacerations. Invasive procedures are often second‐line therapy if the aforementioned methods are not successful. Invasive procedures reviewed will include uterine packing and tamponade, use of compression sutures, systemic devascularization (arterial ligation), and UAE. Current data will be reviewed regarding effectiveness of these methods in controlling bleeding and preventing the need for hysterectomy in an acute PPH patient. Bleeding from uterine atony can be controlled not only with uterotonic medications, but also with manual compression of the uterus. Classically, a single‐handed Crede maneuver was described, whereby the uterine fundus is grasped through the abdominal wall between the provider’s fingers and thumbs. While still a useful technique, it is difficult in overweight or obese patients and does not provide compression of the lower uterine segment. Bimanual compression can be performed by placing one hand placed intravaginally, just posterior to the cervix, and by placing other hand on the patient’s abdomen, at the fundus, and “sandwiching” the uterus between the hands. This technique also allows the provider to pull the uterus slightly anteriorly, toward the symphysis pubis, providing further compression. This bimanual technique compresses the lower segment, places the uterine arteries on stretch, and applies pressure to the fundus. While effective, manual compression is only a temporizing measure to treat immediate PPH. Intrauterine tamponade is another method to apply pressure to aid with hemostasis. Two main methods have been described in the literature, including uterine packing, using rolled gauze or balloon tamponade. Not only has intrauterine tamponade been used for atony, but also for bleeding due to uterine inversion, with the added benefit of providing structural support to prevent early recurrent uterine inversion [44, 45]. Use of gauze packing is a readily available, inexpensive and older technique that was endorsed in numerous textbooks in the 1930s and 1940s [46]. Gauze is placed manually or with long forceps at the fundus and layered within the uterine cavity until filled, and a “tail” of gauze is allowed to remain visible outside the introitus to monitor bleeding and allow for easy removal. Traditionally, laparotomy sponges tied together or rolled gauze has been used, to ensure that no packing material is retained. More recently, studies have evaluated the feasibility of use of specially saturated gauze, such as gauze saturated in chitosan to better achieve hemostasis, with promising results [47]. In this series of 19 cases of PPH, the need for hysterectomy was reduced by 75% compared to the rate prior to the introduction of chitosan‐soaked gauze. Additionally, the authors concluded that as this gauze was easy to use, and inexpensive, it may prove useful in low‐resource settings. Uterine packing has been shown via angiography not only to halt bleeding by placing pressure within the uterine cavity, but also to reduce the perfusion pressure and flow within the uterine arteries [48]. Balloon tamponade for uterine bleeding was introduced by Bakri et al. in 1992 [49]. In addition to the use of the Bakri® balloon, use of various types of easily accessible balloons has been described, including the use of a water or saline‐filled condom tied to a straight catheter, a Sengstaken‐Blakemore gastrointestinal balloon [50, 51], large Foley catheter, and Ebb® balloon [52]. In multiple retrospective and prospective studies, the use of uterine balloon tamponade was associated with a decrease in the need for invasive surgical interventions between 85% and 100%, and is also very useful for resource poor settings [53]. Various vessels can be ligated in an attempt to stop PPH. In the face of PPH at time of cesarean delivery, the vessel most easily assessable, visualized, and palpable for ligation is the uterine artery. This vessel can be seen entering the inferior lateral borders of the lower uterine segment, adjacent to the internal cervical os. Ligation of the internal iliac artery, or hypogastric artery, may also be performed. The anterior division of this vessel feeds the uterus and vagina. This artery is retroperitoneal and thus dissection and ligation requires extensive experience and knowledge of this anatomical region, which can take time in the face of a rapid and life threatening obstetric hemorrhage. A long‐term study reviewed cases of early PPH that required laparotomy in a 3‐year time span in the 1980s and again in the 2000s. A significant decrease in need for hysterectomy has been described during this time frame (87.5% in the 1980s vs. 22.2% in the 2000s). The authors concluded that use of uterine or hypogastric artery ligation, is associated with successful control of PPH and the ability to avoid hysterectomy [54]. It should be noted that hypogastric artery ligation is a technically complex procedure, with which few obstetrical and gynecologic surgeons have extensive experience, and its utility may thereby be limited. Approximately 40% of patients with attempt at internal iliac artery ligation ultimately required hysterectomy overall, but this varies by etiology of hemorrhage. Internal iliac artery ligation was successful in salvaging the uterus in 63.8% with uterine atony, 85.7% with placenta previa, and 21% of those who experienced uterine rupture [55]. Other studies have found that internal iliac artery ligation controlled PPH, thus preventing need for hysterectomy, in 75–82% of patients [56, 57]. A major limitation to performing this ligation is the technical expertise and experience operating in the retroperitoneal space, especially in the setting of hemorrhage. MRI has shown that the vast majority of patients show complete repermeation of the arteries even after bilateral internal iliac artery ligation [57]. Another method to control hemorrhage in the postpartum patient is to use uterine compression sutures. The B‐Lynch suture is the most well‐known uterine compression suture. To perform this procedure, one should use a large absorbable suture and, in a running fashion, pass the suture through one corner of the hysterotomy, run the suture over the fundus, pass the suture transversely through the posterior lower uterine segment, back over the fundus to the anterior uterus, and then pass through the other corner of the hysterectomy allowing for the suture to then be tied in the anterior lower uterine segment region inferior to the hysterotomy. Proper step‐by‐step placement of this suture can be seen in Figure 51.1 [58]. Multiple studies looking at outcomes in patients who had compression sutures placed due to PPH found that 77–82% of women avoided hysterectomy [58–60]. Moreover, hysterectomy can be avoided in patients with B‐Lynch sutures following unsuccessful vessel ligation; of 15 patients who underwent compression sutures for this purpose only 3 (20%) required hysterectomy [36]. Figure 51.1 B‐Lynch uterine compression suture. A modification of the B‐Lynch suture was proposed by Hayman in 2002, and is illustrated in Figure 51.2 [58]. The surgeon places two separate sutures through the lower uterine segment and each are tied separately at the fundus. This procedure does not require that a hysterotomy be made for evacuation of uterine contents and there is no need for excessive passes through the lower uterine segment. This technique was performed on 11 patients in an Italian study, who also received a protocol of uterotonics for PPH, and only one patient required hysterectomy [61]. There is little data to guide patient counseling regarding future childbearing or intrauterine scar formation after placement of compression sutures. Women have had imaging of the uterus or direct visualization of the uterus (hysterosalpingogram or hysteroscopy) after compression sutures with a uterine synechiae formation rate ranging from 26.7% to 53.8% [62, 63]. Asherman syndrome has been noted in these patients at time of follow up, but successful subsequent pregnancies have also been reported [63]. Figure 51.2 Hayman suture – Modified B‐Lynch suture. Conservative surgical techniques have been reported to control excessive bleeding caused by uterine atony, cervical scar pregnancy, and uterine‐cervical‐vaginal tears, and in selected placenta previa and accreta cases at 12 institutions in Buenos Aires, Argentina [64]. In this series, hysterectomy was required in only 7.4% of women. The various surgical techniques evaluated were selective arterial ligation (bilateral uterine artery ligation, selective pelvic subperitoneal pedicle ligation) and compression procedures (B‐Lynch, Hayman’s, Pereira’s, Cho’s). Furthermore, patients were followed up with hysteroscopy and MRI, and of the 499 women who retained their uterus, 116 successful pregnancies were reported [64]. UAE has been integrated in many institutions as an intervention to prevent further bleeding in the event of PPH. This procedure has the advantage of being minimally invasive, but requires the expertise of Interventional Radiology (IR). This can be a limitation for those institutions that do not have immediate access to an IR department, or when a patient must be moved long distances to a remote IR unit. UAE has been found to have a 90–95% [65–67] success rate overall with a 98% success rate with acute (or primary) PPH and a 94% success rate with PPH after cesarean deliveries [66]. Other studies have found an 82% success rate of UAE to prevent hysterectomy [68]. UAE also has proven successful in managing PPH patients when other methods such as uterine packing, compression sutures, balloon tamponade, or even hysterectomy have failed. It was found that 94% of patients who failed these methods were made hemostatic with UAE, and no immediate complications were associated with embolization [69]. Even in patients who experience PPH from placenta accreta, UAE has been successful. In 17 patients who underwent UAE to control hemorrhage from a placenta accreta, 14 (82.4%) ceased bleeding, whereas the remaining 3 required hysterectomy [70]. Complications following UAE are uncommon but include thrombus formation and ischemia. This includes emboli in the femoral artery (1 of 11 subjects), likely from particle migration [68] and lower extremity thrombus formation (1 of 26 subjects) [71]. For patients who failed arterial ligation and were treated with UAE (successful in 11 of 12 subjects), two complications were noted: lower extremity ischemia and nerve ischemia. Both resolved without residual complications [72]. An observational retrospective study reviewed deliveries that required blood transfusion for PPH that also underwent UAE or hysterectomy for treatment. Patients who underwent hysterectomy required double the amount of blood products than those who had an UAE. They also found that some patients treated with hysterectomy subsequently underwent UAE to reach hemostasis, where the reverse was true 1/10 of the time [73]. These data are not randomized and therefore may reflect selection bias. Questions also arise regarding fertility after UAE. A 10‐year review at a single institution found that all women who underwent UAE for PPH had return of regular menses. Moreover, of the women who desired future childbearing, all were successful [74]. Resumption of menses after UAE ranges from 91% to 100% [67, 75]. The efficacy of invasive second‐line treatment to stop PPH in women who failed first‐line uterotonic or intrauterine tamponade were as follows (in descending order): UAE 86%, uterine compression sutures 75%, pelvic vessel ligation (internal iliac, uterine, or ovarian) 36% [76]. Some patients received more than one second‐line treatment, and were more clinically complex. One fourth of the patients ultimately required hysterectomy [76]. Interestingly, in a 2007 study from the United Kingdom (UK), women often underwent surgical treatment for PPH without universally being treated with uterotonics, suggesting an opportunity for improved enforcement of a protocol of uterotonics prior to proceeding with operative techniques [43]. In conclusion, the treatment of PPH must be guided first by early recognition and treatment of the underlying etiology. Multiple medical and/or surgical treatment modalities may be required to attain sufficient control and to stabilize the patient. Hemorrhage with vessel ligation and salvaging of the uterus [55]. Compression sutures have been found to have a high success rate in preventing the need for hysterectomy [58–60], but the long‐term effect they have on the uterine cavity is yet to be completely understood [62, 63]. Studies have shown that UAE is an effective adjunct that may not always negatively impact menstruation and fertility [67, 74, 75]. The patient in our scenario likely experienced an acute PPH from uterine atony. The patient can be managed medically with oxytocin IV as well as administration of uterotonics. Identification and repair of any vaginal or cervical lacerations is imperative. Since there is no direct visualization of the uterus after vaginal delivery, balloon tamponade or UAE may be considered. Early transfusion of blood and blood products to prevent hypovolemic shock and coagulopathy is essential. If compression techniques are ineffective, laparotomy should be considered. Compression sutures can be placed and uterine and/or ovarian vessels can be ligated. Finally, attempt at hypogastric artery ligation can be performed if the physician is able to visualize and adequately dissect the retroperitoneum. Finally, the physician can proceed with hysterectomy.
Postpartum hemorrhage
Introduction
Uterine atony
Lower genital tract lacerations (perineal, vaginal, cervical, periclitoral, labial, periurethral, rectal)
Upper genital tract lacerations (broad ligament)
Lower urinary tract lacerations (bladder, urethra)
Retained products of conception (placenta, membranes)
Invasive placentation (placenta accreta/increate/percreta)
Uterine rupture
Uterine inversion
Coagulopathy (hereditary, acquired)
Background
Clinical questions
General search strategy
Critical appraisal of the literature
Agent
Dose
Route
Dosing frequency
Side effects
Contraindications
Oxytocin (Pitocin)
10–80 U in 1000 ml of crystalloid
*IV
IM or IU
Continuous
N/V, emesis, water intoxication
None
Misoprostol (Cytotec)
600–1000 μg
*PR
PO
Single dose
N/V, diarrhea, fever, chills
None
Methylergonovine (Methergine)
0.2 mg
*IM
IU
Every 2–4 h
Hypertension, hypotension, N/V
Hypertension, preeclampsia
Prostaglandin F2α (Hemabate)
0.25 mg
*IM
IU
Every 15–90 min (8 dose max)
N/V, diarrhea, flushing, chills
Active cardiac, pulmonary, renal, or hepatic disease
Prostaglandin E2 (Dinoprostone)
20 mg
PR
Every 2 h
N/V, diarrhea, fever, chills, headache
Hypotension
Bimanual uterine compression and uterine tamponade
Systemic devascularization (arterial ligation)
Compression sutures
Uterine artery embolization (UAE)
Conclusions
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