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Postpartum Hemorrhage

  • Author: John R Smith, MD; Chief Editor: Ronald M Ramus, MD  more...
Updated: Mar 01, 2016


Postpartum hemorrhage (PPH) is the leading cause of maternal mortality. All women who carry a pregnancy beyond 20 weeks’ gestation are at risk for PPH and its sequelae. Although maternal mortality rates have declined greatly in the developed world, PPH remains a leading cause of maternal mortality elsewhere.

Postpartum hemorrhage. Maternal morbidity by subre Postpartum hemorrhage. Maternal morbidity by subregion, 1995.

The direct pregnancy-related maternal mortality rate in the United States is approximately 7-10 women per 100,000 live births. National statistics suggest that approximately 8% of these deaths are caused by PPH.[1] In industrialized countries, PPH usually ranks in the top 3 causes of maternal mortality, along with embolism and hypertension. In the developing world, several countries have maternal mortality rates in excess of 1000 women per 100,000 live births, and World Health Organization statistics suggest that 25% of maternal deaths are due to PPH, accounting for more than 100,000 maternal deaths per year.[2] The most recent Practice Bulletin from the American College of Obstetricians and Gynecologists places the estimate at 140,000 maternal deaths per year or 1 woman every 4 minutes.[3]

The rate of PPH increased from 1.5% in 1999 to 4.1% in 2009, and the rate of atonic PPH rose from 1% in 1999 to 3.4% in 2009. The risk of total PPH with a morbidly adherent placenta was markedly higher.[4]



The definition of PPH is somewhat arbitrary and problematic. PPH is defined as blood loss of more than 500 mL following vaginal delivery or more than 1000 mL following cesarean delivery.[5, 6] A loss of these amounts within 24 hours of delivery is termed early or primary PPH, whereas such losses are termed late or secondary PPH if they occur 24 hours after delivery. This article focuses on early PPH.

Estimates of blood loss at delivery are subjective and generally inaccurate. Studies have suggested that caregivers consistently underestimate actual blood loss. Another proposal suggests using a 10% fall in hematocrit value to define PPH, but this change is dependent on the timing of the test and the amount of fluid resuscitation given.[7] More importantly, the diagnosis would be retrospective, perhaps useful for research but not so in the clinical setting.

Another consideration is the differing capacities of individual patients to cope with blood loss. A healthy woman has a 30-50% increase in blood volume in a normal singleton pregnancy and is much more tolerant of blood loss than a woman who has preexisting anemia, an underlying cardiac condition, or a volume-contracted condition secondary to dehydration or preeclampsia. For these reasons, various authors have suggested that PPH should be diagnosed with any amount of blood loss that threatens the hemodynamic stability of the woman.

The diagnosis of PPH is usually reserved for pregnancies that have progressed beyond 20 weeks’ gestation. Deliveries at less than 20 weeks’ gestational age are spontaneous abortions. Bleeding related to spontaneous abortion may have etiologies and management in common with those for PPH.




United States and industrialized countries

The frequency of PPH is related to the management of the third stage of labor. This is the period from the completed delivery of the baby until the completed delivery of the placenta. Data from several sources, including several large randomized trials performed in industrialized countries, indicate that the prevalence rate of PPH of more than 500 mL is approximately 5% when active management is used versus 13% when expectant management is used. The prevalence rate of PPH of more than 1000 mL is approximately 1% when active management is used versus 3% when expectant management is used.[8, 9] See Medscape Reference article Management of the Third Stage of Labor.

Developing countries

The increased frequency of PPH in the developing world is more likely reflected by the rates given above for expectant management because of the lack of widespread availability of medications used in the active management of the third stage.[2] A number of factors also contribute to much less favorable outcomes of PPH in developing countries. The first is a lack of experienced caregivers who might be able to successfully manage PPH if it occurred. Additionally, the same drugs used for prophylaxis against PPH in active management of the third stage are also the primary agents in the treatment of PPH. Lack of blood transfusion services, anesthetic services, and operating capabilities also plays a role. Finally, the previously mentioned comorbidities are more commonly observed in developing countries and combine to decrease a woman's tolerance of blood loss.



PPH has many potential causes, but the most common, by a wide margin, is uterine atony, ie, failure of the uterus to contract and retract following delivery of the baby. PPH in a previous pregnancy is a major risk factor and every effort should be made to determine its severity and cause. In a recent randomized trial in the United States, birthweight, labor induction and augmentation, chorioamnionitis, magnesium sulfate use, and previous PPH were all positively associated with increased risk of PPH.[10]

In a large, population-based study, significant risk factors, identified using multivariable analysis, were as follows:

  • Retained placenta (OR 3.5, 95% CI 2.1-5.8)
  • Failure to progress during the second stage of labor (OR 3.4, 95% CI 2.4-4.7)
  • Placenta accreta (OR 3.3, 95% CI 1.7-6.4)
  • Lacerations (OR 2.4, 95% CI 2.0-2.8)
  • Instrumental delivery (OR 2.3, 95% CI 1.6-3.4)
  • Large-for-gestational-age (LGA) newborn (OR 1.9, 95% CI 1.6-2.4)
  • Hypertensive disorders (OR 1.7, 95%CI 1.2-2.1)
  • Induction of labor (OR 1.4, 95%CI 1.1-1.7)
  • Augmentation of labor with oxytocin (OR 1.4, 95% CI 1.2-1.7). [11]

PPH is also associated with obesity. In a study by Blomberg, the risk of atonic uterine hemorrhage rapidly increased with increasing BMI; in women with a BMI over 40, the risk was 5.2% with normal delivery and 13.6% with instrumental delivery.[12]

A study by Hanley et al reported that serotonin-norepinephrine reuptake inhibitor exposure in late pregnancy was associated with a 1.6- to 1.9-fold increased risk of postpartum hemorrhage.[13, 14]

As a way of remembering the causes of PPH, several sources have suggested using the “4 T’ s” as a mnemonic: tone, tissue, trauma, and thrombosis.[15]


Uterine atony and failure of contraction and retraction of myometrial muscle fibers can lead to rapid and severe hemorrhage and hypovolemic shock. Overdistension of the uterus, either absolute or relative, is a major risk factor for atony. Overdistension of the uterus can be caused by multifetal gestation, fetal macrosomia, polyhydramnios, or fetal abnormality (eg, severe hydrocephalus); a uterine structural abnormality; or a failure to deliver the placenta or distension with blood before or after placental delivery.

Poor myometrial contraction can result from fatigue due to prolonged labor or rapid forceful labor, especially if stimulated. It can also result from the inhibition of contractions by drugs such as halogenated anesthetic agents, nitrates, nonsteroidal anti-inflammatory drugs, magnesium sulfate, beta-sympathomimetics, and nifedipine. Other causes include placental implantation site in the lower uterine segment, bacterial toxins (eg, chorioamnionitis, endomyometritis, septicemia), hypoxia due to hypoperfusion or Couvelaire uterus in abruptio placentae, and hypothermia due to massive resuscitation or prolonged uterine exteriorization. Recent data suggest that grand multiparity is not an independent risk factor for PPH.


Uterine contraction and retraction leads to detachment and expulsion of the placenta. Complete detachment and expulsion of the placenta permits continued retraction and optimal occlusion of blood vessels.

Retention of a portion of the placenta is more common if the placenta has developed with a succenturiate or accessory lobe. Following delivery of the placenta and when minimal bleeding is present, the placenta should be inspected for evidence of fetal vessels coursing to the placental edge and abruptly ending at a tear in the membranes. Such a finding suggests a retained succenturiate lobe.

The placenta is more likely to be retained at extreme preterm gestations (especially < 24 wk), and significant bleeding can occur. This should be a consideration in all deliveries at very early gestations, whether they are spontaneous or induced. Recent trials suggest that the use of misoprostol for second trimester termination of pregnancy leads to a marked reduction in the rate of retained placenta when compared to techniques using the intrauterine instillation of prostaglandin or hypertonic saline.[16] One such trial reported rates of retained placenta requiring D&C of 3.4% with oral misoprostol compared to 22.4% using intra-amniotic prostaglandin (p=0.002).[17]

Failure of complete separation of the placenta occurs in placenta accreta and its variants. In this condition, the placenta has invaded beyond the normal cleavage plane and is abnormally adherent. Significant bleeding from the area where normal attachment (and now detachment) has occurred may mark partial accreta. Complete accreta in which the entire surface of the placenta is abnormally attached, or more severe invasion (placenta increta or percreta), may not initially cause severe bleeding, but it may develop as more aggressive efforts are made to remove the placenta. This condition should be considered possible whenever the placenta is implanted over a previous uterine scar, especially if associated with placenta previa.

All patients with placenta previa should be informed of the risk of severe PPH, including the possible need for transfusion and hysterectomy.

Finally, retained blood may cause uterine distension and prevent effective contraction.


Damage to the genital tract may occur spontaneously or through manipulations used to deliver the baby. Cesarean delivery results in twice the average blood loss of vaginal delivery. Incisions in the poorly contractile lower segment heal well but are more reliant on suturing, vasospasm, and clotting for hemostasis.

Uterine rupture is most common in patients with previous cesarean delivery scars. Routine transvaginal palpation of such scars is no longer recommended. Any uterus that has undergone a procedure resulting in a total or thick partial disruption of the uterine wall should be considered at risk for rupture in a future pregnancy. This admonition includes fibroidectomy; uteroplasty for congenital abnormality; cornual or cervical ectopic resection; and perforation of the uterus during dilatation, curettage, biopsy, hysteroscopy, laparoscopy, or intrauterine contraceptive device placement.

Trauma may occur following very prolonged or vigorous labor, especially if the patient has relative or absolute cephalopelvic disproportion and the uterus has been stimulated with oxytocin or prostaglandins. Using intrauterine pressure monitoring may lessen this risk. Trauma also may occur following extrauterine or intrauterine manipulation of the fetus. The highest risk is probably associated with internal version and extraction of a second twin; however, uterine rupture may also occur secondary to external version. Finally, trauma may result secondary to attempts to remove a retained placenta manually or with instrumentation. The uterus should always be controlled with a hand on the abdomen during any such procedure. An intraumbilical vein saline/oxytocin or saline/misoprostol injection may reduce the need for more invasive removal techniques.[8]

Cervical laceration is most commonly associated with forceps delivery, and the cervix should be inspected following all such deliveries. Assisted vaginal delivery (forceps or vacuum) should never be attempted without the cervix being fully dilated. Cervical laceration may occur spontaneously. In these cases, mothers have often been unable to resist bearing down before full cervical dilatation. Rarely, manual exploration or instrumentation of the uterus may result in cervical damage. Very rarely, the cervix is purposefully incised at the 2- and/or 10-o’clock positions to facilitate delivery of an entrapped fetal head during a breech delivery (Dührssen incision).

Vaginal sidewall laceration is also most commonly associated with operative vaginal delivery, but it may occur spontaneously, especially if a fetal hand presents with the head. Lacerations may occur during manipulations to resolve shoulder dystocia. Lacerations often occur in the region overlying the ischial spines. The frequency of sidewall and cervical lacerations has probably decreased in recent years because of the reduction in the use of midpelvic forceps and, especially, midpelvic rotational procedures.

Lower vaginal trauma occurs either spontaneously or because of episiotomy. Spontaneous lacerations usually involve the posterior fourchette; however, trauma to the periurethral and clitoral region may occur and can be problematic.


In the immediate postpartum period, disorders of the coagulation system and platelets do not usually result in excessive bleeding; this emphasizes the efficiency of uterine contraction and retraction for preventing hemorrhage.[5] Fibrin deposition over the placental site and clots within supplying vessels play a significant role in the hours and days following delivery, and abnormalities in these areas can lead to late PPH or exacerbate bleeding from other causes, most notably, trauma.

Abnormalities may be preexistent or acquired. Thrombocytopenia may be related to preexisting disease, such as idiopathic thrombocytopenic purpura, or acquired secondary to HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count), abruptio placentae, disseminated intravascular coagulation (DIC), or sepsis. Rarely, functional abnormalities of platelets may also occur. Most of these are preexisting, although sometimes previously undiagnosed.

Preexisting abnormalities of the clotting system, such as familial hypofibrinogenemia and von Willebrand disease, may occur and should be considered. An expert panel recently issued guidelines to aid in the diagnosis and management of women with such conditions.[18] An underlying bleeding disorder should be considered in a woman with any of the following: menorrhagia since menarche, family history of bleeding disorders, personal history of notable bruising without known injury, bleeding from the oral cavity or GI tract without obvious lesion, or epistaxis of longer than 10 minutes duration (possibly requiring packing or cautery). If a bleeding disorder is suspected, consultation is suggested.

Acquired abnormalities are more commonly problematic. DIC related to abruptio placentae, HELLP syndrome, intrauterine fetal demise, amniotic fluid embolism, and sepsis may occur. Fibrinogen levels are markedly elevated during pregnancy, and a fibrinogen level that would be in the reference range in the nonpregnant state should be viewed with suspicion in the aforementioned clinical scenarios.

Finally, dilutional coagulopathy may occur following massive PPH and resuscitation with crystalloid and packed red blood cells (PRBCs).

Risk factors and associated conditions for PPH are listed above; however, a large number of women experiencing PPH have no risk factors. Different etiologies may have common risk factors, and this is especially true of uterine atony and trauma of the lower genital tract. PPH usually has a single cause, but more than one cause is also possible, most likely following a prolonged labor that ultimately ends in an operative vaginal birth.



High-quality evidence suggests that active management of the third stage of labor reduces the incidence and severity of PPH.[9] Active management is the combination of (1) uterotonic administration (preferably oxytocin) immediately upon delivery of the baby, (2) early cord clamping and cutting, and (3) gentle cord traction with uterine countertraction when the uterus is well contracted (ie, Brandt-Andrews maneuver).

The value of active management in the prevention of PPH cannot be overstated (see Management of the Third Stage of Labor). The use of active versus expectant management in the third stage was the subject of 5 randomized controlled trials (RCTs) and a Cochrane meta-analysis.[19, 8, 9] These trials included more than 6000 women, and the findings are summarized in Table 1.

Table 1. Benefits of Active Management Versus Expectant Management (Open Table in a new window)

Outcome Control Rate, % Relative Risk 95% CI* NNT 95% CI
PPH of 500 mL 14 0.38 0.32-0.46 12 10-14
PPH of 1000 mL 2.6 0.33 0.21-0.51 55 42-91
Hemoglobin < 9 g/dL 6.1 0.4 0.29-0.55 27 20-40
Blood transfusion 2.3 0.44 0.22-0.53 67 48-111
Therapeutic uterotonics 17 0.2 0.17-0.25 7 6-8
*CI: Confidence interval

† NNT: Number needed to treat


The findings show a conclusive benefit for active management, with an approximate 60% reduction in the occurrence of PPH greater than or equal to 500 mL and 1000 mL, hemoglobin concentration of less than 9 g/dL at 24-48 hours after delivery, and the need for blood transfusion. An 80% reduction in the need for therapeutic uterotonic agents was noted. These results were all highly significant as indicated by the 95% confidence interval figures. The results indicate that for every 12 patients receiving active rather than physiological management, one PPH would be prevented. For every 67 patients so treated, one patient would avoid transfusion with blood products.

One concern regarding active management is that retained placenta may occur more frequently. This concern is not supported by the trials. This is especially true if oxytocin is used as the uterotonic.[20, 21] The US RCTs mentioned above compared the use of active management protocols in which the oxytocin was administered either immediately after delivery of the baby or immediately after delivery of the placenta. The authors stated that no statistically significant difference was noted in the PPH rate and that delaying administration until after placental delivery was justified.

Noteworthy is the finding that early administration of oxytocin (before placental delivery) did not increase the rate of retained placenta. Additionally, the trial showed trends toward a benefit for early administration of oxytocin, including a 25% reduction in PPH and a 50% reduction in the need for transfusion.[10] These findings are clearly consistent with the previous RCTs and the early administration of oxytocin with delivery of the baby is strongly recommended.

They also stated that administration with delivery of the baby did not increase the rate of retained placenta, but they did not point out that this finding clearly supports early administration. Additionally, the trial showed trends toward a benefit for early administration of oxytocin, including a 25% reduction in PPH and a 50% reduction in the need for transfusion.[10] These differences may be due to chance, but, given the results of the previous RCTs, the administration of oxytocin with delivery of the baby would seem to be strongly warranted.

Following delivery, administering a uterotonic drug that lasts at least 2-3 hours is reasonable.[3] This could be 10 U of oxytocin in 500 mL of intravenous fluid by continuous drip, 200-250 mcg of ergonovine intramuscularly, or 250 mcg of 15-methyl prostaglandin F2-alpha (carboprost [Hemabate]) intramuscularly. The use of misoprostol and a long-acting oxytocin analogue (carbetocin) is being studied for this use.[22] It has been suggested that distribution of misoprostol ahead of childbirth in communities where home birth is unavoidable can be an effective approach. However, there is insufficient evidence to support this and there are concerns that the drug might be used for starting labor or terminating pregnancy.[23]

The presence of significant antepartum or intrapartum risk factors warrants delivery in maternity units that have readily available resources to deal with massive obstetric hemorrhage. All medical facilities should have protocols for dealing with PPH and obstetric hemorrhage.



Over the course of a pregnancy, maternal blood volume increases by approximately 50% (from 4 L to 6 L). The plasma volume increases somewhat more than the total RBC volume, leading to a fall in the hemoglobin concentration and hematocrit value. The increase in blood volume serves to fulfill the perfusion demands of the low-resistance uteroplacental unit and to provide a reserve for the blood loss that occurs at delivery.[7]

At term, the estimated blood flow to the uterus is 500-800 mL/min, which constitutes 10-15% of cardiac output. Most of this flow traverses the low-resistance placental bed. The uterine blood vessels that supply the placental site traverse a weave of myometrial fibers. As these fibers contract following delivery, myometrial retraction occurs. Retraction is the unique characteristic of the uterine muscle to maintain its shortened length following each successive contraction. The blood vessels are compressed and kinked by this crisscross latticework, and, normally, blood flow is quickly occluded. This arrangement of muscle bundles has been referred to as the "living ligatures" or "physiologic sutures" of the uterus.[5]

Uterine atony is a failure of the uterine myometrial fibers to contract and retract. This is the most important cause of PPH and usually occurs immediately following delivery of the baby, up to 4 hours after the delivery. Trauma to the genital tract (ie, uterus, uterine cervix, vagina, labia, clitoris) in pregnancy results in significantly more bleeding than would occur in the nonpregnant state because of increased blood supply to these tissues. The trauma specifically related to the delivery of the baby, either vaginally in a spontaneous or assisted manner or by cesarean delivery, can also be substantial and can lead to significant disruption of soft tissue and tearing of blood vessels.



Although the presentation of PPH is most often dramatic, bleeding may be slower and seemingly less noteworthy but may still ultimately result in critical loss and shock. This is more likely to be true of bleeding secondary to retained tissue or trauma. Nursing practices for routine care in the postpartum period should include close observation and documentation of maternal vital signs and condition, vaginal blood loss, and uterine tone and size. The uterus should be periodically massaged to express any clots that have accumulated in the uterus or vagina.[24]

The usual presentation of PPH is one of heavy vaginal bleeding that can quickly lead to signs and symptoms of hypovolemic shock. This rapid blood loss reflects the combination of high uterine blood flow and the most common cause of PPH, ie, uterine atony. Blood loss is usually visible at the introitus, and this is especially true if the placenta has delivered. If the placenta remains in situ, then a significant amount of blood can be retained in the uterus behind a partially separated placenta, the membranes, or both.

Even after placental delivery, blood may collect in an atonic uterus. For this reason, the uterine size and tone should be monitored throughout the third stage and in the so-called fourth stage, following delivery of the placenta. This is accomplished by gently palpating the uterine fundus. If the cause of bleeding is not uterine atony, then blood loss may be slower and clinical signs and symptoms of hypovolemia may develop over a longer time frame. Bleeding from trauma may be concealed in the form of hematomas of the retroperitoneum, broad ligament or lower genital tract, or abdominal cavity. The clinical findings in hypovolemia are listed in Table 2.

Table 2. Clinical Findings in Obstetric Hemorrhage[25] (Open Table in a new window)

Blood Volume Loss Blood Pressure (systolic) Symptoms and Signs Degree of Shock
500-1000 mL (10-15%) Normal Palpitations, tachycardia, dizziness Compensated
1000-1500 mL (15-25%) Slight fall (80-100 mm Hg) Weakness, tachycardia, sweating Mild
1500-2000 mL (25-35%) Moderate fall (70-80 mm Hg) Restlessness, pallor, oliguria Moderate
2000-3000 mL (35-50%) Marked fall (50-70 mm Hg) Collapse, air hunger, anuria Severe


Two important facts are worth bearing in mind. The first is that caregivers consistently underestimate visible blood loss by as much as 50%. The volume of any clotted blood represents half of the blood volume required to form the clots. The second is that most women giving birth are healthy and compensate for blood loss very well. This, combined with the fact that the most common birthing position is some variant of semirecumbent with the legs elevated, means that symptoms of hypovolemia may not develop until a large volume of blood has been lost.[26]

Rapid recognition and diagnosis of PPH is essential to successful management. Resuscitative measures and the diagnosis and treatment of the underlying cause must occur quickly before sequelae of severe hypovolemia develop. The major factor in the adverse outcomes associated with severe hemorrhage is a delay in initiating appropriate management.



Other than nonconsent, absence of surgical expertise or allergy to specific agents, the techniques used in the management of PPH have no absolute contraindications. The vast majority of cases (>99%) are handled without what would traditionally be considered surgical intervention. In most cases, surgical intervention is a last resort. An exception is those cases in which uterine rupture or genital tract trauma has occurred and surgical repair is clearly indicated.

Transfusion of packed RBC and other blood products may be necessary in the management of severe PPH. Some women may refuse such an intervention on personal or religious grounds. The most widely known group that does not accept blood transfusion are Jehovah’s Witnesses. The wishes of the patient must be respected in this matter. Significant increased risk of maternal mortality due to obstetric hemorrhage has been noted in the Jehovah’s Witness population. The increased risk of death was found to be 6-fold in a recent national review of 23 years experience in the Netherlands and 44-fold in a much smaller study of 391 deliveries in a US tertiary level center.[27, 28] Discussion regarding the implications of such prohibitions should be undertaken early in the pregnancy whenever possible and subsequently reviewed.

In almost all cases in which surgical management is chosen after medical management has failed, not attempting surgery would lead to maternal death. Even an unstable condition cannot be considered a true contraindication. One type of surgery may be chosen over another, but when medical management has failed, surgery is most likely the only life-saving option.

Contributor Information and Disclosures

John R Smith, MD FRSCS, FACOG, Physician in Maternal-Fetal Medicine, Departments of Obstetrics and Gynecology and Diagnostic Imaging, Credit Valley Hospital, Ontario

John R Smith, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, College of Physicians and Surgeons of Ontario, Royal College of Physicians and Surgeons of Canada, International Society of Obstetric Medicine

Disclosure: Nothing to disclose.


Barbara G Brennan, MD, PhD FRCSC, FACOG, Associate Professor, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University School of Medicine, Canada

Barbara G Brennan, MD, PhD is a member of the following medical societies: American College of Obstetricians and Gynecologists, College of Physicians and Surgeons of Ontario, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, International Society of Obstetric Medicine, Canadian Medical Protective Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Michel E Rivlin, MD Former Professor, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine

Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, Royal College of Surgeons of Edinburgh, Royal College of Obstetricians and Gynaecologists

Disclosure: Nothing to disclose.

Chief Editor

Ronald M Ramus, MD Professor of Obstetrics and Gynecology, Director, Division of Maternal-Fetal Medicine, Virginia Commonwealth University School of Medicine

Ronald M Ramus, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Institute of Ultrasound in Medicine, Medical Society of Virginia, Society for Maternal-Fetal Medicine

Disclosure: Nothing to disclose.

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Postpartum hemorrhage. Maternal morbidity by subregion, 1995.
Table 1. Benefits of Active Management Versus Expectant Management
Outcome Control Rate, % Relative Risk 95% CI* NNT 95% CI
PPH of 500 mL 14 0.38 0.32-0.46 12 10-14
PPH of 1000 mL 2.6 0.33 0.21-0.51 55 42-91
Hemoglobin < 9 g/dL 6.1 0.4 0.29-0.55 27 20-40
Blood transfusion 2.3 0.44 0.22-0.53 67 48-111
Therapeutic uterotonics 17 0.2 0.17-0.25 7 6-8
*CI: Confidence interval

† NNT: Number needed to treat

Table 2. Clinical Findings in Obstetric Hemorrhage [25]
Blood Volume Loss Blood Pressure (systolic) Symptoms and Signs Degree of Shock
500-1000 mL (10-15%) Normal Palpitations, tachycardia, dizziness Compensated
1000-1500 mL (15-25%) Slight fall (80-100 mm Hg) Weakness, tachycardia, sweating Mild
1500-2000 mL (25-35%) Moderate fall (70-80 mm Hg) Restlessness, pallor, oliguria Moderate
2000-3000 mL (35-50%) Marked fall (50-70 mm Hg) Collapse, air hunger, anuria Severe
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