INTRODUCTION — Postpartum hemorrhage (PPH) is an obstetric emergency. It is one of the top five causes of maternal mortality in both resource-abundant and resource-limited countries, although the absolute risk of death from PPH is much lower in the former. Timely recognition, availability of appropriate resources, and appropriate response are critical for preventing death and severe maternal morbidity. To ensure an appropriate response, provider and institutional planning and preparation are essential.
This topic will present an overview of major issues relating to PPH. Clinical use of specific medical and minimally invasive interventions, and surgical interventions at laparotomy, for management of PPH are discussed separately. (See "Postpartum hemorrhage: Medical and minimally invasive management" and "Postpartum hemorrhage: Management approaches requiring laparotomy".)
TERMINOLOGY
●Primary or early PPH refers to PPH occurring in the first 24 hours after delivery and is the subject of this topic.
●Secondary, late, or delayed PPH refers to PPH occurring from 24 hours to 12 weeks after delivery, and is discussed separately. (See "Secondary (late) postpartum hemorrhage".)
CRITERIA FOR DIAGNOSIS
Our approach — We make the diagnosis of PPH in postpartum patients with bleeding that is greater than expected and results in signs and/or symptoms of hypovolemia (table 1). The diagnosis may be delayed when bleeding is not observed, such as intraabdominal bleeding after a vaginal birth or after closure of the abdomen in a cesarean birth.
Excessive blood loss at birth can be inferred from large studies evaluating uterotonic drugs for prevention of PPH. In such studies, at vaginal birth, less than 10 percent of parturients receiving routine prophylaxis against postpartum hemorrhage had blood loss ≥500 mLs and less than 2 percent had blood loss ≥1000 mL [1]; at cesarean birth, 63 percent had blood loss >500 mL and 30 percent had blood loss >1000 mLs [2].
Other criteria — Various criteria for diagnosis of PPH are in use worldwide, as shown in the table (table 2).
Although some guidelines utilize the classic definition of PPH for diagnosis (ie, estimated blood loss ≥500 mL after vaginal birth or ≥1000 mL after cesarean birth), this is problematic because bleeding may not be visible externally, blood in collection devices may be mixed with amniotic fluid, and postpartum morbidity is relatively infrequent among patients with blood loss 500 to 999 mL [3].
In acknowledgement of the limitations of the classic definition, the American College of Obstetricians and Gynecologists (ACOG) revised their definition of PPH in 2017 from the classic one described above to the following [4]:
●Cumulative blood loss ≥1000 mL, or
●Bleeding associated with signs/symptoms of hypovolemia within 24 hours of the birth process, and
●Regardless of route of birth
This definition should reduce the number of patients inappropriately labeled with PPH. However, ACOG went on to state that despite this new definition, a blood loss greater than 500 mL in a vaginal birth should be considered abnormal and should serve as an indication for the health care provider to investigate the increased blood deficit.
Classification of severity
California Maternal Quality Care Collaborative staging system — The California Maternal Quality Care Collaborative (CMQCC) obstetric hemorrhage toolkit describes the following stages of PPH [5]:
●Stage 0 – Every patient in labor/giving birth
●Stage 1 – Blood loss ≥500 mL vaginal birth or ≥1000 mL cesarean birth with continued bleeding or signs of concealed hemorrhage: vital signs abnormal or trending (heart rate ≥110 bpm, blood pressure ≤85/45 mmHg, O2 saturation <95%, shock index 0.9) or confusion
●Stage 2 – Continued bleeding or vital sign instability, and <1500 mL cumulative blood loss
●Stage 3 – Continued bleeding with cumulative blood loss >1500mL or >2 units transfusion of packed red blood cells or abnormal vital signs or suspicion of disseminated intravascular coagulation
Advanced trauma life support classification — The Advanced Trauma Life Support manual describes four classes of hemorrhage to emphasize the progressive signs and symptoms leading to the shock state [6]. The following classes were derived from nonpregnant populations and thus may be somewhat different in postpartum patients, but remain useful:
●Class I hemorrhage involves a blood volume loss of up to 15 percent. The heart rate is minimally elevated or normal, and there is no change in blood pressure, pulse pressure, or respiratory rate.
●Class II hemorrhage occurs when there is a 15 to 30 percent blood volume loss and is manifested clinically as tachycardia (heart rate of 100 to 120 bpm), tachypnea (respiratory rate of 20 to 24 breaths per minute), and a decreased pulse pressure, although systolic blood pressure changes minimally if at all. The skin may be cool and clammy, and capillary refill may be delayed. An increasing maternal heart rate and tachypnea with stable systolic blood pressure should be regarded as evidence of compensated shock and should prompt investigation and institution of a PPH protocol, even if only light vaginal bleeding is observed.
●Class III hemorrhage involves a 30 to 40 percent blood volume loss, resulting in a significant drop in blood pressure and changes in mental status. Any hypotension (systolic blood pressure less than 90 mmHg) or drop in blood pressure greater than 20 to 30 percent of the measurement at presentation is cause for concern. While diminished anxiety or pain may contribute to such a drop, the clinician must assume it is due to hemorrhage until proven otherwise. Heart rate (≥120 bpm and "thready") and respiratory rate are markedly elevated, while urine output is diminished. Capillary refill is delayed.
●Class IV hemorrhage involves more than 40 percent blood volume loss leading to significant depression in blood pressure and mental status. Most patients in class IV shock are hypotensive (systolic blood pressure less than 90 mmHg). Pulse pressure is narrowed (≤25 mmHg), and tachycardia is marked (>120 bpm). Urine output is minimal or absent. The skin is cold and pale, and capillary refill is delayed.
INCIDENCE — PPH is generally reported to occur in 1 to 3 percent of births [7-9]. In an analysis of population-based data from the United States National Inpatient Sample, the rate of postpartum hemorrhage increased from 2.7 percent in 2009 to 4.3 percent in 2019 [9]. However, many reports are based on subjective estimates of blood loss; when blood loss is measured quantitatively, prospective studies have reported PPH rates as high as 10 percent [10]. Variations in criteria for PPH (eg, >500 versus >1000 mLs, presence/absence of symptoms) also contribute to variations in reported incidence.
PHYSIOLOGIC MECHANISMS THAT LIMIT POSTPARTUM BLOOD LOSS — Normally, hemostasis occurs upon placental separation because uterine bleeding is controlled by a combination of two mechanisms:
●Mechanical hemostasis, whereby contraction of the myometrium compresses the blood vessels supplying the placental bed, resulting in severely reduced blood flow.
●Local thrombosis, whereby the presence or release of local decidual hemostatic factors (tissue factor [11,12] and type-1 plasminogen activator inhibitor, respectively [13,14]) and systemic coagulation factors (eg, platelets, circulating clotting factors) lead to thrombosis of damaged blood vessels supplying the placental bed, resulting in severely reduced blood flow.
The potential for massive hemorrhage from pathology in these normal physiologic mechanisms is high because, in late pregnancy, uterine artery blood flow is 500 to 700 mL/min and accounts for approximately 15 percent of cardiac output.
RISK FACTORS FOR PPH — Many risk factors for PPH have been reported and are often interdependent. Although there are many known risk factors for PPH, knowledge of these risk factors is of limited usefulness because of low-positive and negative predictive value. (See 'PPH risk assessment tools and risk-based preparation' below.)
The types and frequencies of risk factors are illustrated by the following large series:
●In a study of over 154,000 births comparing 666 cases of PPH with controls without hemorrhage, factors significantly associated with hemorrhage were, in decreasing order of frequency [15]:
•Retained placenta/membranes (odds ratio [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 spectrum (PAS; OR 3.3, 95% CI 1.7-6.4)
•Lacerations (OR 2.4, 95% CI 2.0-2.8)
•Forceps- or vacuum-assisted vaginal birth (OR 2.3, 95% CI 1.6-3.4)
•Large for gestational age newborn (eg, >4000 g) (OR 1.9, 95% CI 1.6-2.4)
•Hypertensive disorders (preeclampsia, eclampsia, HELLP [Hemolysis, Elevated Liver enzymes, Low Platelets]) (OR 1.7, 95% CI 1.2-2.1)
•Induction of labor (OR 1.4, 95% CI 1.1-1.7)
•Prolonged first or second stage of labor (OR 1.4, 95% CI 1.2-1.7)
●In a study of over 690,000 births, the four risk factors associated with the highest odds for predicting the need for massive transfusion (406 cases) during hospitalization for delivery were [16]:
•Abnormal placentation (placenta accreta or previa) (1.6 in 10,000 births, adjusted OR [aOR] 18.5, 95% CI 14.7-23.3)
•Placental abruption (1.0 in 10,000 births, aOR 14.6, 95% CI 11.2-19.0)
•Severe preeclampsia (0.8 in 10,000 births, aOR 10.4, 95% CI 7.7-14.2)
•Intrauterine fetal demise (0.7 in 10,000 births, aOR 5.5, 95% CI 3.9-7.8)
Other risk factors include: previous PPH (see 'Recurrence' below), family history of PPH in the maternal line (eg, mother, sister), obesity, high parity, precipitous labor, uterine overdistention, chorioamnionitis, uterine inversion, leiomyoma, Couvelaire uterus, assisted reproductive technology, anemia, postterm pregnancy, and use of some drugs (uterine relaxants, antithrombotic medications, antidepressants [particularly selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors]) [17-32].
CAUSES OF POSTPARTUM HEMORRHAGE — The most common causes of PPH can be considered using the Four Ts mnemonic [33]:
●Tone: uterine atony
●Trauma: laceration, hematoma, rupture
●Tissue: retained tissue or placenta accreta spectrum
●Thrombin: coagulopathy
Focal or diffuse atony — Uterine atony (ie, a lack of effective uterine contraction after birth) prevents mechanical hemostasis from occurring and is responsible for at least 80 percent of cases of PPH; it complicates approximately 1 in 40 births in the United States [34]. Although diffuse uterine atony is the most common cause of PPH, it is often responsive to administration of additional uterotonic medications; thus, it is not the most common reason for massive transfusion at the time of birth [17]. Nevertheless, atony-related PPH is the indication for 27 percent of peripartum hysterectomies [35].
●Diagnosis – The diagnosis is made when the uterus does not become firm to palpation after expulsion of the placenta. Prophylactic administration of a uterotonic drug after birth is a routine practice worldwide to prevent atony. (See "Management of the third stage of labor: Prophylactic pharmacotherapy to minimize hemorrhage".)
With diffuse atony, the flaccid, dilated uterus may contain a significant amount of blood so blood loss can be much greater than observed. With focal localized atony, the fundal region may be well contracted while the lower uterine segment is dilated (ballooning) and atonic, which is difficult to appreciate on abdominal examination, but may be detected on vaginal examination.
●Risk factors for atony – Prior PPH and prolonged labor are the most well-established risk factors for atony-related PPH [36]. Uterine inversion can be associated with fundal atony, even though there is constriction of the lower uterine segment/cervix.
Trauma — Trauma-related bleeding can be due to lacerations (including complete or partial myometrial rupture [37]) or surgical incisions. Cervical and vaginal lacerations may occur as a result of the provider interventions or natural processes during birth. Trauma (genital or surgical) was the most common cause of massive PPH (ie, >2500 mLs) in a series of 349 such cases, accounting for 55 percent of cases compared with 23 percent for atony alone [38].
●Diagnosis – Tissue trauma after a vaginal birth is diagnosed on physical examination but may not be noted until excessive postpartum vaginal bleeding prompts careful examination of the lower genital tract beyond the perineum, including examination for vaginal and vulvar hematomas and cervical lacerations.
At cesarean birth, hemorrhage from the uterine incision is generally caused by lateral extension of the incision, which can result from spontaneous tearing of an edematous lower uterine segment during an otherwise uneventful cesarean after prolonged labor, from an incision made too low or not sufficiently curved on the lower segment, or from delivery of the fetus through an incision that is too small. Bleeding from lateral extension of the uterine incision is readily ascertained by inspection of the incision, lateral pelvic sidewalls, and broad ligament. Retroperitoneal enlargement and bulging of the broad ligament at cesarean birth can be signs of retroperitoneal hemorrhage.
Bleeding can also occur as a result of uterine rupture, which may be anterior, lateral, or posterior. (See "Uterine rupture: Unscarred uterus" and "Uterine rupture: After previous cesarean birth".)
●Risk factors for trauma – Risk factors for severe perineal trauma during vaginal birth include instrument-assisted vaginal birth, midline episiotomy, and persistent occiput posterior position [39]. In cesarean births, delivery after full dilation is a risk factor for unintended uterine incision extension, particularly in the setting of past cesarean birth or failed vacuum attempt [40].
Placental disorders — Placental disorders, such as placenta accreta spectrum (PAS), placenta previa, abruption, and retained placenta, cause PPH because effective uterine contraction and hemostasis of decidual vessels is inhibited, either focally or diffusely. In addition, abruption can trigger disseminated intravascular coagulation.
●Diagnosis – PAS and placenta previa are typically diagnosed prenatally by ultrasound. The diagnosis of abruption is primarily clinical, but findings from laboratory studies can support the clinical diagnosis. Retained placenta is diagnosed when the placenta has not been expelled within 30 minutes of birth.
●Risk factors – There are multiple risk factors for occurrence of a placental disorder. For example, prior cesarean birth is a common risk factor for placenta previa and PAS. Hypertension is a risk factor for abruption. Uterine anomalies are a risk factor for retained placenta.
•(See "Placenta accreta spectrum: Clinical features, diagnosis, and potential consequences".)
•(See "Placenta previa: Epidemiology, clinical features, diagnosis, morbidity and mortality".)
•(See "Retained placenta after vaginal birth".)
•(See "Acute placental abruption: Pathophysiology, clinical features, diagnosis, and consequences".)
Coagulopathy or other bleeding diathesis — Coagulopathy complicates approximately 1 in 500 births in the United States and is responsible for less than 7 percent of cases of PPH [34].
Coagulopathy or platelet dysfunction can contribute to PPH in patients with an inherited or acquired bleeding diathesis.
Coagulopathy can also be a result of PPH when there is a severe reduction of clotting factors due to consumption and hemodilution of the remaining clotting factors (eg, PAS). However, coagulopathy is a late finding in these cases. In a study including >18,000 patients with ≥1500 mL blood loss at birth, the median prothrombin time (PT) was 12.3 seconds, the longest activated partial thromboplastin time (aPTT) was 30.4 seconds, and the lowest fibrinogen was 360 mg/dL; all of these values are within the normal range for pregnancy.
●Diagnosis – In acute PPH, coagulopathy should be suspected in patients with one or more of the following: low fibrinogen level (<300 mg/dL); thrombocytopenia (<100,000/microL); prolonged PT, international normalized ratio (INR >1.5), and/or aPTT.
Thromboelastography (TEG)/Rotational Thromboelastometry (ROTEM), where available, provides a global assessment of hemostasis in whole blood that includes contributions of platelets, fibrinogen, fibrinolysis, and coagulation factors. It can be particularly useful in diagnosing dilutional coagulopathy.
After the acute event, an evaluation for von Willebrand disease (VWD) factor and platelet function may be warranted. An acquired factor VIII inhibitor may be suspected in an individual with no prior bleeding history and a prolonged aPTT. (See "Approach to the adult with a suspected bleeding disorder".)
●Risk factors for coagulopathy – Acute acquired coagulopathies can be caused by amniotic fluid embolism, placental abruption, preeclampsia with severe features, HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets), sepsis, or fetal demise. Patients with von Willebrand disease are at risk for PPH because VWD factor levels, which typically increase during pregnancy, decline rapidly after birth.
INSTITUTIONAL PLANNING AND PREPARATION
PPH risk assessment tools and risk-based preparation — Patients identified prenatally as high risk for PPH (eg, placenta previa, placenta accreta spectrum) should plan to give birth at a facility that has an appropriate level of care for their needs.
In the United States, The Joint Commission requires use of an evidence-based tool for determining maternal hemorrhage risk both on admission to labor and delivery and on admission to postpartum [41]. Specific tools for risk assessment and management were not provided. However, knowledge of risk factors for PPH and risk assessment tools have limited utility because many patients without risk factors experience severe PPH (40 percent in one study [17]) [26,42] and most high-risk patients do not experience significant hemorrhage (risk of severe hemorrhage ranges from 2 to 7 percent [42,43]). A systematic review of 14 prognostic models for PPH found that none were sufficiently validated in the general obstetric population, and three were potentially useful in high-risk populations (patients undergoing cesarean birth, patients with placenta previa, and patients with placenta accreta) [44].
Despite the low predictive value of current risk assessment tools, use of a tool is likely better than no risk assessment as the risk stratification process may raise consciousness and preparation. Several tools for risk assessment and risk-based management have been developed. One example is the California Maternal Quality Care Collaborative (CMQCC) toolkit version 3.0 and another example is the tool used at the author's institution (table 3). A tool created by the American College of Obstetricians and Gynecologists (ACOG) Safe Motherhood initiative is available online and others are available on the UpToDate society guidelines links page for obstetric hemorrhage (see "Society guideline links: Obstetric hemorrhage"). The CMQCC risk classification scheme is used for patients admitted to the labor unit [5]. Although it classifies patients as low, medium, or high risk for PPH, in a validation study of an earlier version (version 1.0 in 2010), the incidence of severe PPH (ie, necessitating transfusion) in the three groups was 0.8, 2.0, and 7.3 percent, respectively, and only 22 percent of severe PPH cases occurred in the high-risk group [42].
Planning for selected groups of high-risk patients
●Patients who decline to accept blood transfusion (see "The approach to the patient who declines blood transfusion")
●Patients with placenta accreta spectrum (PAS) (see "Placenta accreta spectrum: Clinical features, diagnosis, and potential consequences" and "Placenta accreta spectrum: Management")
●Patients with placenta previa (see "Placenta previa: Epidemiology, clinical features, diagnosis, morbidity and mortality" and "Placenta previa: Management")
●Patients with bleeding disorders (eg, Von Willebrand disease, hemophilia, congenital factor XIII deficiency, unclassified bleeding disorder or bleeding disorder of unknown cause) (see "Perioperative blood management: Strategies to minimize transfusions")
●Patients with anemia (see "Anemia in pregnancy", section on 'Management')
Patient education — All patients should receive verbal and printed educational material about PPH, including signs and symptoms, since most PPHs occur in low-risk patients and PPH may occur after hospital discharge [41].
PPH management protocols — Each hospital labor and delivery unit should have a PPH protocol and provide ongoing training to their staff regarding its use [41,45-47]. The protocol should provide a standardized approach to evaluating and monitoring the patient with PPH, notifying a multidisciplinary team, and treatment. Development and consistent application of a comprehensive protocol for management of PPH appears to result in improved outcomes for these patients [48-50]. In an observational study, initiating a PPH protocol was associated with resolution of maternal bleeding at an earlier stage, a 26 percent reduction per 1000 births in use of blood products, a 15 percent reduction per 1000 births in the number of patients with PPH who underwent peripartum hysterectomy, and a 64 percent reduction in the rate of disseminated intravascular coagulation [49,51].
In the United States, The Joint Commission requires obstetric units to have written evidence-based procedures (developed by a multidisciplinary team) for stage-based management of pregnant and postpartum patients who experience maternal hemorrhage, including [41]:
●Use of an evidence-based tool that includes an algorithm for identification and treatment of hemorrhage
●Use of an evidence-based set of emergency response medication(s) that are immediately available on the obstetric unit
●Required response team members and their roles in the event of severe hemorrhage
●How the response team and procedures are activated
●Blood bank plan and response for emergency release of blood products and how to initiate the organization's massive transfusion procedures
●Guidance on when to consult additional experts and consider transfer to a higher level of care
●Guidance on how to communicate with patients and families during and after the event
●Criteria for when a team debrief is required immediately after a case of severe hemorrhage
The author's institution uses a checklist system that addresses some of these requirements (figure 1).
Resources for developing a PPH protocol include:
●The California Maternal Quality Care Collaborative, which provides comprehensive information in several formats for management of PPH [5].
●Medical society and government-sponsored guidelines, which can be found on the UpToDate society guidelines links page for obstetric hemorrhage (see "Society guideline links: Obstetric hemorrhage"). There is large variation in obstetric and hematologic management of severe PPH across resource-abundant countries worldwide [52].
Massive transfusion algorithm — Massive transfusion (MT) is often required with severe PPH and can be facilitated by use of an algorithm (algorithm 1) specific to the hospital. All providers should be well versed in the application of such a protocol. In addition, regular simulation of PPH and MT protocol activation will improve compliance and facilitate the performance of the team in low-frequency/high-complexity/high-risk events [53,54]. (See 'Training and simulation' below.)
MT protocols should include specific recommendations for empiric calcium replacement, potassium monitoring (hyperkalemia), and core body temperature management. Calcium is often necessary in severe PPH due to the citrate used for anticoagulation in blood products [55]. During an MT, the obstetric anesthesiologist will often check ionized calcium in arterial blood gas specimens and will replete as necessary. In practice, calcium infusion may occur after two to three units of blood transfusion.
Rapid infusion of blood and other fluids is important to manage hypovolemia, but rapid infusion of cold fluids can lead to substantial heat loss [56]; therefore, direct warming of fluids should occur during resuscitation.
Equipment
PPH carts — Planning for PPH involves ensuring availability of resources that might be needed, including personnel, uterotonic and other medications, equipment for control of bleeding, adequate intravenous access, topical hemostatic agents, and blood products. One way to achieve this is to assemble carts that contain medications, devices, and instruments that may be needed to manage PPH so that these resources are readily available when needed (similar to a "code cart") (table 4) [5,54]. In the United States, The Joint Commission requires obstetric units to have a standardized, secured, dedicated hemorrhage supply kit stocked per the organization's defined process and, at a minimum, emergency hemorrhage supplies as determined by the organization and the organization's approved procedures for severe hemorrhage response [41].
Cell salvage — Use of a cell saver (blood salvage) is an option for patients undergoing cesarean birth and at increased risk of PPH. It is not cost-effective as a routine in all cesarean deliveries [57]. (See "Postpartum hemorrhage: Management approaches requiring laparotomy", section on 'Role of intraoperative cell salvage'.)
Cell salvage has been used successfully in patients with PPH after a vaginal birth, but data are sparse and the procedure should be considered investigational [58]. The potential presence of blood contaminants, including stool, urine, cleansing agents (eg, betadine, chlorhexidine), and vasoactive medications (eg, misoprostol) is a contraindication, thus severely limiting use.
Teamwork — In the author's opinion, it is critical to appreciate that clinical training programs that encourage a team approach for early recognition of PPH can improve outcomes by engaging the necessary providers before hypovolemia and uncompensated shock occur.
Obstetricians, midwives, nurses, anesthesiologists, hematologists, blood bank personnel, laboratory medicine, surgical subspecialists (eg, vascular, urology), and interventional radiologists may be involved in managing PPH. These individuals are often summoned and required to work together under conditions of great stress and time pressures. Coordination is essential and can be facilitated by protocols and flow diagrams that anticipate how the team will communicate and function together [5].
Training and simulation — In the United States, The Joint Commission recommends that obstetric staff [41]:
●Undergo team training to teach staff to work together and communicate more effectively when PPH occurs
●Conduct clinical drills to help staff prepare for PPH, and
●Conduct debriefings after PPH to evaluate team performance and identify areas for improvement
Simulation team training can help to identify areas that need practice, and regular unannounced simulated PPH scenarios in a real-life setting, such as the labor and delivery unit or post-anesthesia care unit, may also increase comfort with the protocols and teamwork required in such emergencies [59]. (See "Reducing adverse obstetric outcomes through safety sciences", section on 'Postpartum hemorrhage'.)
Review — PPH cases that meet severity criteria established by the hospital should be reviewed to evaluate the effectiveness of the care, treatment, and services provided during the event [41].
EARLY IDENTIFICATION OF PATIENTS WITH PPH
Quantify blood loss — We recommend quantification of blood loss (QBL) with standardized processes for all births because delay in the recognition of excessive blood loss delays timely initiation of life-saving interventions and is a common finding in cases of maternal morbidity and mortality from hemorrhage [60-62]. Standardization of as many procedures as possible is an important principle for improving quality and safety, thus, if QBL is reserved only for cases of significant bleeding, staff may be unfamiliar with the process/procedures and less likely to obtain accurate data. With practice and routine adoption, QBL requires only minutes to perform in the majority of births [5].
QBL options include:
●Volumetric measurement – Collect blood in graduated measurement containers, such as V-drapes with calibrated pockets and calibrated suction canisters.
●Gravimetry – Measure the total weight of bloody materials and subtract the known weight of the same materials when dry. The difference in weight between wet and dry in grams approximates the volume of blood in milliliters.
●Colorimetry – Colorimetry addresses some of the limitations of other methods. A smartphone application calculates blood loss by taking photographs of used surgical gauze and canisters and then filtering out the effects of nonblood components mixed into each sponge and canister. The hemoglobin mass present in the gauze or canister is then calculated from the image and subtracted from the preoperative hemoglobin level. A meta-analysis found this method correlated well with a validated reference, but more data are needed before it can be recommended for clinical use [63].
●Visual aids – Use visual aids (eg, posters) that correlate the size and appearance of blood on specific surfaces (eg, maternity pad, bed sheet, lap sponge) with the volume of blood absorbed by that surface (picture 1). Regularly scheduling standardized training in the use of these charts can be helpful for this assessment.
For each of the above methods, the clinician should attempt to account for fluids other than blood (eg, amniotic fluid, irrigation fluid, urine) that are collected or absorbed. A systematic review of two trials found insufficient evidence to support the use of two objective methods of QBL (volumetric measurement, gravimetry) over visual estimation (quantitative or semiquantitative) of blood loss after vaginal birth or to support use of volumetric measurement over gravimetry [64]. Although objective methods of QBL are more accurate (visual estimation is more likely to underestimate the actual blood loss when volumes are excessive and overestimate when volumes are normal), use of objective methods or a specific objective method of QBL did not clearly improve maternal and neonatal clinical outcomes. Additional appropriately powered, randomized trials that correlate method of estimating blood loss with relevant clinical outcomes are needed.
Recognize alarm findings and intervene early — Timeliness in recognition of PPH followed by rapid determination of the cause and initiation of appropriate treatment is critical, as almost 90 percent of deaths due to PPH occur within four hours of giving birth [65,66].
Alarm findings include:
●Early warning vital sign criteria – Standardized maternal early warning systems (MEWS) that target specific vital sign criteria (table 5) and mandate an immediate response at these thresholds can reduce maternal morbidity [67,68]. Several maternal mortality review committees have found that delayed response to abnormal vital signs is a common factor in preventable mortality [69,70]. In some cases, the delay may be related to alarm fatigue because the trigger values used in the system have low specificity. However, a large reduction in blood pressure is a late sign of severe PPH as it is generally not manifested until substantial bleeding has occurred, and up to 25 percent of a patient's blood volume (≥1500 mL in pregnancy) can be lost before blood pressure falls and heart rate rises [71]. The possibility of concealed hemorrhage must always be considered, especially in symptomatic patients without excessive external bleeding.
From a pragmatic perspective, it is wise to always assume, and rule out, PPH as the cause of symptoms of hypovolemia before assigning a less concerning diagnosis. Although vasodilatation due to neuraxial anesthesia and vasovagal reactions may result in lightheadedness/syncope, tachycardia, and hypotension, these entities are less likely postpartum than PPH, and they are readily reversible and generally not dangerous. Lightheadedness, tachycardia, or hypotension is unlikely to be due to neuraxial anesthesia if the patient was hemodynamically stable prior to birth, the level of the block did not become significantly higher immediately following birth, and symptoms did not abruptly follow systemic administration of a drug known to cause hypotension. (See "Adverse effects of neuraxial analgesia and anesthesia for obstetrics", section on 'Hypotension'.)
●Low fibrinogen – A low fibrinogen level (less than 200 mg/dL) is an excellent predictor of severe PPH, defined as need for transfusion of multiple units of blood and blood products, need for angiographic embolization or surgical management of hemorrhage, or maternal death. It was the most frequently observed coagulation deficit in a cohort of patients with massive PPH, occurring in 17 percent of cases [38]. For this reason, this author recommends measuring the fibrinogen level as soon as PPH is suspected and keeping the level above 300 mg/dL in patients at high risk for, or experiencing, PPH, given the higher normal baseline fibrinogen level in pregnancy and the desire to maintain the fibrinogen level well-above the danger zone in these patients.
Hemoglobin and hematocrit values are poor indicators of acute blood loss since they may not decline immediately after an acute bleed. It can take four hours for changes in laboratory values to be seen, and the nadir may not be seen for 48 to 72 hours [5]. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Laboratory evaluation'.)
It is important to not allow the patient to become moribund before initiating life-saving measures. Early intervention may prevent shock (inadequate perfusion and oxygenation of tissues) and the development of the potentially lethal triad of hypothermia, acidosis, and coagulopathy.
The types and choices of intervention depend, in part, on whether the birth was vaginal or cesarean (with the abdomen still open), and are described in detail separately. (See "Postpartum hemorrhage: Medical and minimally invasive management" and "Postpartum hemorrhage: Management approaches requiring laparotomy".)
Identify the cause of bleeding — After a vaginal birth with quantitative cumulative blood loss of 500 mL, continued bleeding can be a sign of PPH and requires increased surveillance [5]. Physical examination includes assessment for vaginal and cervical lacerations, abdominal examination, and possibly bimanual examination of the uterus. Ultrasound can be useful if there is suspicion of retained placental fragments or membranes or concealed hemorrhage (eg, lower uterine genital tract hematoma with extension, uterine rupture, broad ligament laceration, or another source of internal bleeding).
Monitor bleeding, vital signs, and laboratory results and perform an examination — Close maternal monitoring is critical to assess the best approach to and aggressiveness of intervention, and requires bedside evaluation by the provider.
Laboratory evaluation includes complete blood count, coagulation studies, potassium and ionized calcium levels. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Routine'.)
Point-of-care viscoelastic testing provides nearly real-time data for guiding transfusion of blood products. Its use leads to better hemorrhage control, in part because of rapid detection and targeted treatment of hypofibrinogenemia and thrombocytopenia. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Viscoelastic testing'.)
TREATMENT — Many potential interventions for treatment of PPH are available and listed in the table (table 6). Treatment goals and our approach achieving these goals are described in the following sections.
Goals — The goals of treatment are to:
●Restore or maintain adequate circulatory volume to prevent hypoperfusion of vital organs
●Restore or maintain adequate tissue oxygenation
●Reverse or prevent coagulopathy
●Eliminate the obstetric cause of PPH
Initial approach — The initial treatment approach is based on a combination of factors, including the cause and severity of bleeding and whether the abdomen is already open because of cesarean birth. The obstetric provider should initiate a sequence of nonoperative and operative interventions for control of bleeding based on the cause of PPH and promptly assess the success or failure of each measure. If an intervention fails, the next treatment in the sequence must be swiftly instituted. Indecisiveness delays therapy and results in excessive hemorrhage, which eventually causes dilutional coagulopathy and severe hypovolemia, tissue hypoxia, hypothermia, and acidosis. This will make control of hemorrhage much more difficult and will increase the likelihood of hysterectomy, major morbidity from hemorrhagic shock, and death.
Regardless of the cause of PPH, all patients should receive initial circulatory support with crystalloid. In those with severe bleeding, switching to blood transfusion when blood is available and early administration of tranexamic acid (an antifibrinolytic drug) can reduce the risk of death due to bleeding. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Resuscitate with crystalloid and blood' and "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Transfuse red blood cells, platelets, plasma' and "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Administer tranexamic acid'.)
●Atony – Treatment of atony, the most common cause of PPH, is influenced by both the route of birth and severity of bleeding. After a vaginal birth, treatment of atony begins with uterotonic drugs and minimally invasive procedures (eg, intrauterine balloon tamponade, vacuum-induced uterine tamponade) and progresses to more invasive procedures (eg, uterine artery embolization) until hemorrhage is controlled. It is usually possible and desirable to avoid laparotomy and its associated morbidity. Treatment of atony after vaginal birth (eg, choice of drugs, dosing) is discussed in detail separately. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Manage atony'.)
Uterotonic drugs are also used to treat atony at cesarean birth, but since the abdomen is already open, surgical procedures to control bleeding requiring laparotomy (eg, uterine artery and utero-ovarian artery ligation, uterine compression sutures) are employed much sooner than after a vaginal birth, and uterine artery embolization is considered if these procedures fail. Hysterectomy is the definitive therapy when bleeding cannot be controlled by other measures within a timeframe appropriate for the clinical scenario. These procedures are described separately. (See "Postpartum hemorrhage: Management approaches requiring laparotomy".)
●Trauma – Traumatic, hemorrhaging lacerations are controlled surgically, either via a transvaginal or transabdominal approach, as appropriate for the site of bleeding. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Repair genital tract lacerations' and "Postpartum hemorrhage: Management approaches requiring laparotomy", section on 'Myometrial lacerations' and "Postpartum hemorrhage: Management approaches requiring laparotomy", section on 'Laceration of the uterine artery or utero-ovarian artery branches'.)
●Retained placental tissue – Retained placental tissue must be identified intraoperatively at cesarean or by palpation after vaginal birth. It can be removed manually or by instruments (eg, hemostat, Kelly, or curette). In cases of delayed hemorrhage, it is usually detected by ultrasound and removed by curettage. Placenta accreta spectrum (PAS) generally requires hysterectomy. (See "Retained placenta after vaginal birth" and "Placenta accreta spectrum: Management".)
●Coagulopathy – Coagulopathy is treated medically with transfusion of blood products and/or clotting factors to correct clotting factor deficiencies. Treatment of coagulopathy is reviewed in detail separately. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Correct clotting factor deficiencies'.)
Additional considerations for hemodynamically unstable patients — In addition to the initial approach to treatment described above, the following considerations apply to patients who are hemodynamically unstable.
●Move patients to or keep them in an appropriate area – Unstable patients in a coagulopathic state with active bleeding should be managed in the most appropriate area for resuscitation and emergency surgery. Under most circumstances, this is a warm operating room with a full multidisciplinary team in attendance.
●Transfuse as soon as possible – When hemorrhage is the cause of hemodynamic instability, initial (and expedited) management with blood and blood products is advised (as opposed to large volume crystalloid infusion). Hypovolemic hemorrhagic shock is treated with aggressive volume resuscitation with packed red cells and other appropriate blood products. Transfusion should keep up with blood loss, with early activation of a protocol for large volume transfusion in those patients with heavy bleeding. Development of a standardized institutional approach to massive transfusion improves outcome (algorithm 1). There are no data from clinical trials of PPH to help guide management of transfusion specifically in PPH [72]; our approach is described separately. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Transfuse red blood cells, platelets, plasma'.).
●Correct severe hypofibrinogenemia with high-concentration fibrinogen products – If the patient is severely coagulopathic with an extremely low fibrinogen level (50 to 100 mg/dL), cryoprecipitate and/or other high-concentration fibrinogen products (eg, fibrinogen concentrate, prothrombin complex concentrate) are indicated since fresh frozen plasma alone will not increase the fibrinogen level to the normal range (ideally greater than 300 mg/dL) without requiring excessive volume infusion. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Correct clotting factor deficiencies' and "Plasma derivatives and recombinant DNA-produced coagulation factors" and "Postpartum hemorrhage: Management approaches requiring laparotomy", section on 'Evaluation of the abdomen'.)
●Begin temporizing measures – Temporizing measures allow resuscitation to a point where general anesthesia and surgery, if necessary, are better tolerated. These interventions include bimanual uterine compression, intrauterine balloon tamponade, and aortic compression. The author believes early recourse to intrauterine balloon tamponade can be useful to decrease ongoing uterine blood loss following vaginal birth or after the abdomen is closed following cesarean birth, and that this measure will allow additional time for assessment and evaluation, stabilization, and institution of resuscitative procedures. In some cases, intrauterine balloon tamponade may avoid the need for surgical management of PPH [73]. (See "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Perform uterine tamponade in patients with atony or lower segment bleeding' and "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Perform uterine massage and compression' and "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Consider external aortic compression'.)
In patients who continue to bleed at the time of cesarean and where the abdominal incision is still open, compression sutures and devascularization are more easily accomplished than placing a tamponade balloon. (See "Postpartum hemorrhage: Management approaches requiring laparotomy", section on 'Temporary measures for stabilizing hemodynamically unstable patients'.)
●Role of hysterectomy – Early resort to hysterectomy is appropriate in patients with severe bleeding due to diffuse PAS or a large uterine rupture. In contrast, hysterectomy is generally a last resort in patients with atony, as these patients can often be managed successfully with medical therapy and less aggressive surgical interventions.
Unless absolutely necessary, emergency hysterectomy should be avoided in a coagulopathic patient with inadequate intravenous access for massive transfusion/correction of electrolyte imbalances, as major surgery in this setting may cause further deterioration in maternal status as a result of uncontrolled retroperitoneal hemorrhage and myocardial depression. However, once hemodynamic and hemostatic resuscitation have been initiated, hysterectomy should not be delayed in those who require prompt control of uterine hemorrhage to prevent death. (See "Postpartum hemorrhage: Management approaches requiring laparotomy", section on 'Role of hysterectomy'.)
●Keep unstable patients with persistent bleeding in the operating room – If the abdomen was opened for management of PPH but bleeding was not completely controlled, temporarily closing the abdomen with towel clips enables the surgical team direct access to the pelvis to repack or readdress ongoing bleeding. The aorta can also be directly visualized if necessary, and direct pressure or temporary clamping can be undertaken.
The author is aware of situations where unstable, actively bleeding patients in a coagulopathic state have had their abdomen packed and then were transported to an intensive care unit (ICU), where they expired. In the author's opinion, in these desperate situations, having the patient under anesthesia on a surgical table in a warm environment while acid-base resuscitation and volume, electrolyte, and blood product replacement are carried out gives the team the most options. Keeping the hemodynamically unstable patient in the operating room for a few hours after surgery while gaining control of the situation may be logistically difficult but should be encouraged as opposed to taking the patient to an ICU. ICU consultants can be summoned to the operating room for assistance.
Teams should remember that even in the direst situations, as long as transfusion of appropriate blood products can be continued and the volume of such products exceeds the volume of the ongoing loss, blood pressure can be maintained, and efforts to reverse the coagulopathy, acidosis, and hypothermia may ultimately be successful and should be continued.
Hemodynamically stable patients with persistent bleeding after initial therapy — Arterial embolization is an effective treatment for hemodynamically stable patients with persistent bleeding in whom the capacity for blood replacement exceeds that of the ongoing hemorrhage. In a systematic review of 20 observational studies (1739 patients), a single procedure completely arrested bleeding in 89 percent of cases, re-embolization was necessary in 4 percent, and hysterectomy was required in 7 percent, primarily after embolization failure [74]. Sixty-two percent of the patients in these studies were post cesarean birth.
Generally, arterial embolization should not be attempted in unstable patients who have to be transferred to a radiology suite for the procedure and should not be considered an emergency procedure for managing uncontrolled PPH of indeterminate cause. (See "Postpartum hemorrhage: Management approaches requiring laparotomy" and "Postpartum hemorrhage: Medical and minimally invasive management", section on 'Consider uterine or hypogastric artery embolization'.)
Role of nonpneumatic anti-shock garments — In ambulances and facilities where definitive treatment of PPH is not possible or will be delayed because of lack of resources, use of a nonpneumatic anti-shock garment (NASG) may reduce bleeding, stabilize patients until they are transferred to an appropriate referral/tertiary facility, and decrease mortality from hypovolemic shock [75-79].
NASG consists of nine articulated segments that are wrapped tightly and sequentially around the legs, pelvis, and abdomen and then closed with Velcro. It is thought to work by applying circumferential counterpressure, thus decreasing blood flow to the compressed area (abdominal aorta, pelvis, and lower extremities) and increasing blood flow to the heart, lungs, and brain [80]. The addition of a small foam ball provides some degree of aortic as well as uterine compression and blood flow to the pelvis is reduced [80,81]. Intrauterine balloon tamponade can also be employed. With minimal training, NASG can be applied within two minutes and is reusable. In an analysis of five observational studies, NASG use was associated with a ≥50 percent reduction in median blood loss in three of four studies and a smaller reduction in one study [75]. The analysis also found a 38 percent reduction in mortality overall across the five studies, although one study reported increased mortality.
Thromboprophylaxis after transfusion — In trauma patients, transfusion is an independent risk factor for development of venous thromboembolism (VTE) [82]. The postpartum state is also a risk factor for VTE. For these reasons, in all patients who have been transfused for PPH:
●Initiate mechanical thromboprophylaxis (graduated compression stockings or pneumatic compression device) as soon as feasible and continue thromboprophylaxis until discharge [83].
●Add pharmacologic thromboprophylaxis 12 to 24 hours after bleeding has been controlled and coagulation tests are normal or close to normal. (See "Use of anticoagulants during pregnancy and postpartum".)
OUTCOME
Mortality — Maternal mortality after PPH has wide variations worldwide depending on both the overall health of the pregnant population and the resources for treatment of PPH [84]. Death rates vary from 0.01 percent of patients with PPH in the United Kingdom to 20 percent of patients with PPH in parts of Africa, and from 1 in 100,000 births in the United Kingdom to 1 in 1000 births in resource-limited regions. Patients with anemia at birth due to poor nutrition or malaria are particularly vulnerable to severe sequelae of PPH.
Short-term morbidity — In the WOMAN trial, which included over 20,000 patients worldwide with PPH, the following morbidities were reported [85]:
●Transfusion – 54 percent. By comparison, in the United States the frequency of transfusion in births with PPH has been reported to be 16 percent [34] and the frequency of transfusion in the overall obstetric population has been reported to be 4 to 7 per 1000 births [86]. Risks of transfusion include infection, electrolyte abnormalities, allergic reactions, alloimmunization, and volume overload. (See "Indications and hemoglobin thresholds for red blood cell transfusion in the adult", section on 'Risks and complications of transfusion'.)
●Organ failure related to hemodynamic instability – 60 percent of patients with PPH had clinical signs of hemodynamic instability at diagnosis of PPH and almost 4 percent developed renal failure, heart failure, respiratory failure, or hepatic failure. Treatment of hemodynamic instability with fluids and blood can lead to volume overload, resulting in pulmonary edema and dilutional coagulopathy.
●Hysterectomy – 3.5 percent. By comparison, in the United States, 2.1 percent of patients with PPH underwent hysterectomy in 2014, and atony accounted for almost 60 percent of these cases [34].
●Thromboembolism – 0.3 percent (deep vein thrombosis, pulmonary embolus, stroke, myocardial infarction) within 42 days of birth
Postpartum anemia — Postpartum anemia is common and usually defined as a hemoglobin level <11 g/dL at one week postpartum and <12 g/dL at eight weeks postpartum [87]. Patients with PPH often have a 10-point decline in postpartum hematocrit from antepartum levels. The type of treatment depends on severity of anemia.
●Role of transfusion – Severe anemia due to PPH may require one or more red cell transfusions, depending on the severity of anemia and the degree of symptomatology attributable to anemia. A common practice is to offer a transfusion to symptomatic patients with a hemoglobin value <7 g/dL [4]. (See "Indications and hemoglobin thresholds for red blood cell transfusion in the adult".)
●Iron supplementation – In most cases of PPH, iron supplementation is required because the amount of iron lost is not fully replaced by any transfused blood. Oral supplements are one option and single-dose parenteral iron therapy is another option. Advantages of parenteral iron are that hemoglobin levels rise faster, symptoms of anemia improve sooner, and less gastric upset occurs compared with oral therapy [88,89]. Nevertheless, most patients with mild to moderate anemia resolve the anemia sufficiently rapidly with oral iron, and it is inexpensive and convenient [90-92]. Assessment and treatment of iron deficiency anemia is discussed in detail separately. (See "Treatment of iron deficiency anemia in adults".)
●Role of recombinant human erythropoietin – Although erythropoietin can increase the rate of recovery to normal hemoglobin levels, it does not have an immediate effect and has not been proven to reduce transfusion requirements after PPH [93]. It is no more effective than iron therapy in this setting [94], and it is expensive. However, for the few women with severe anemia who do not respond to iron therapy because of blunted erythropoiesis due to infection and/or inflammation, some hematologists consider recombinant human erythropoietin an alternative to transfusion [87].
Abdominal compartment syndrome — Abdominal compartment syndrome (organ dysfunction caused by intraabdominal hypertension) is a rare but life-threatening complication of PPH with intraabdominal bleeding. The diagnosis should be considered in patients with a tensely distended abdomen and progressive oliguria who are developing multiorgan failure. Of note, the normal postpartum patient after cesarean birth has been reported to have an intraabdominal pressure that approaches that seen in abdominal compartment syndrome in nonpregnant individuals [95].
Clinical presentation, diagnosis, and management are discussed in detail separately. (See "Abdominal compartment syndrome in adults".)
Long-term morbidity
Sheehan syndrome — Sheehan syndrome (ie, postpartum hypopituitarism) is a rare but potentially life-threatening complication. The pituitary gland is enlarged in pregnancy and prone to infarction from hypovolemic shock. Damage to the pituitary can be mild or severe, and can affect the secretion of one, several, or all of its hormones. A common presentation is a combination of failure to lactate postpartum and amenorrhea or oligomenorrhea, but any of the manifestations of hypopituitarism (eg, hypotension, hyponatremia, hypothyroidism) can occur any time from the immediate postpartum period to years after birth.
Patients who remain hypotensive after control of PPH and volume replacement should be evaluated and treated for adrenal insufficiency in the immediate postpartum period; evaluation of other hormonal deficiencies can be deferred until four to six weeks postpartum. This evaluation is described in detail separately. (See "Clinical manifestations of hypopituitarism" and "Diagnostic testing for hypopituitarism".)
Treatment is also reviewed separately. (See "Treatment of hypopituitarism".)
Asherman syndrome — Development of intrauterine adhesions (termed Asherman syndrome) can lead to menstrual abnormalities and infertility. Approximately 90 percent of cases of severe intrauterine adhesive disease are related to uterine curettage for pregnancy complications, such as PPH [96,97]. Uterine compression sutures used to treat PPH have also been associated with the development of intrauterine adhesions [98-101].
Diagnosis and treatment are discussed separately. (See "Intrauterine adhesions: Clinical manifestation and diagnosis" and "Intrauterine adhesions: Treatment and prevention".)
RECURRENCE — Patients with a prior PPH have as much as an 18 percent risk of recurrence in the subsequent pregnancy and 27 percent after two consecutive pregnancies with PPH [102-104]. The risk of recurrence likely depends, at least in part, on the underlying cause. In a study of patients with PPH from atony, lacerations, or retained placenta, the risks of atony and retained placenta remained increased in the next two pregnancies with vaginal births, whereas the risk of lacerations went down [102]. Although the risk of recurrence was greatest for a PPH of the same subtype, the risk was also increased for PPH from other causes.
PREVENTION — Active management of the third stage of labor, primarily by routine prophylactic use of uterotonic drugs such as oxytocin, substantially reduces the incidence of PPH due to atony. While evidence is lacking regarding the optimal approach specifically in patients who have experienced PPH, it seems reasonable to prolong the duration of postpartum oxytocin administration when the cause was atony. Drug choice, dosing, and efficacy are described separately. (See "Management of the third stage of labor: Prophylactic pharmacotherapy to minimize hemorrhage".)
Specific interventions are available for managing risk in patients when certain specific disorders are identified antenatally. (See 'Planning for selected groups of high-risk patients' above.)
A prior PPH alone is not a strong indication for screening for inherited bleeding diatheses, given that undiagnosed bleeding disorders are a rare cause of PPH [105]. However, unexplained PPH that does not respond to general measures should alert clinicians to the possibility of a bleeding disorder as a causative factor [106], especially in patients with a history of heavy menstrual bleeding, excessive bleeding after minor trauma, or a family history of a bleeding disorder. (See "Clinical manifestations and diagnosis of hemophilia", section on 'Obstetric considerations' and "Use of anticoagulants during pregnancy and postpartum", section on 'Labor and delivery' and "Thrombocytopenia in pregnancy", section on 'Management decisions' and "von Willebrand disease (VWD): Gynecologic and obstetric considerations", section on 'Obstetric considerations'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Obstetric hemorrhage".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Postpartum hemorrhage (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Terminology and incidence – Primary or early postpartum hemorrhage (PPH) is reported to occur in 1 to 3 percent of patients in the first 24 hours after birth; however, when blood loss is measured quantitatively, prospective studies have reported rates as high as 10 percent. PPH in the 24 hours to 12 weeks after birth is called secondary, late, or delayed PPH. (See 'Terminology' above and 'Incidence' above.)
●Diagnosis and assessment of severity – We make the diagnosis of PPH in postpartum patients with:
•Bleeding that is greater than expected using a quantitative method to estimate blood loss, and
•Results in signs and/or symptoms of hypovolemia (table 1)
Other definitions are shown in the table (table 2). (See 'Criteria for diagnosis' above and 'Quantify blood loss' above.)
Maternal early warning systems (MEWS) target specific vital sign criteria and mandate an immediate response at these thresholds (table 5) to reduce maternal morbidity. A low fibrinogen level (less than 200 mg/dL) is predictive of severe PPH, defined as the need for transfusion of multiple units of blood and blood products, the need for angiographic embolization or surgical management of hemorrhage, or maternal death. (See 'Recognize alarm findings and intervene early' above and 'Monitor bleeding, vital signs, and laboratory results and perform an examination' above.)
●Causes – The most common causes of PPH are atony, trauma, placental disorders, and coagulopathy/bleeding diatheses. (See 'Causes of postpartum hemorrhage' above.)
●Planning
•Risk assessment – Patients with risk factors for PPH should be identified (table 3), when possible, and counseled as appropriate for their level of risk. However, only a small proportion of at-risk patients develop PPH (abnormal placentation is an exception), and many patients without risk factors experience PPH. (See 'Risk factors for PPH' above and 'PPH risk assessment tools and risk-based preparation' above.)
-PPH alone is not a strong indication for screening for inherited bleeding diatheses, given that undiagnosed bleeding disorders are rarely the cause of PPH. However, unexplained PPH that does not respond to general measures should alert clinicians to the possibility of a bleeding disorder as a causative factor, especially in patients with a history of heavy menstrual bleeding, excessive bleeding after minor trauma, or a family history of a bleeding disorder. (See 'Recurrence' above.)
-Patients with a prior PPH have as much as an 18 percent risk of recurrence in a subsequent pregnancy. (See 'Recurrence' above.)
•Preparation – Planning for PPH involves quantifying blood loss in all deliveries (eg, visual estimation, volumetric/gravimetric methods) and ensuring availability of resources that might be needed, including personnel, medications, equipment (eg, intrauterine balloon tamponade, cell salvage), adequate intravenous access, and blood products. Hospitals with obstetric services should have PPH carts available (table 4) and protocols to manage PPH, including a massive transfusion protocol (algorithm 1); providers should be made aware of and be familiar with these protocols. Coordination is essential and can be facilitated by regular training and simulation drills, which should be instituted to ensure compliance, emergency stage-based response, and unit preparedness. (See 'Institutional planning and preparation' above.)
●Treatment
•All patients – The initial treatment approach is based on a combination of factors, including the cause and severity of bleeding and whether the abdomen is already open because of cesarean birth. Treatment of traumatic, hemorrhaging lesions is surgical and treatment of coagulopathy is medical, with infusion of blood products and/or concentrates to replace depleted coagulation factors. Uterotonic drugs are required for treatment of atony; second-line treatment depends on the route of birth, as there is less concern about the morbidity of open operative interventions when the patient's abdomen is already open. (See 'Initial approach' above.)
Regardless of the cause of PPH, initial circulatory support with crystalloid is required in all patients. In those with severe bleeding, switching to blood transfusion when blood is available and early administration of tranexamic acid (an antifibrinolytic drug) reduces the risk of death due to bleeding. (See 'Initial approach' above.)
•Hemodynamically unstable patients – Additional considerations that apply to patients who are hemodynamically unstable include management in the most appropriate area for resuscitation and emergency surgery; transfusion as soon as possible; correction of severe hypofibrinogenemia (50 to 100 mg/dL) with cryoprecipitate and/or other high-concentration fibrinogen products (eg, fibrinogen concentrate, prothrombin complex concentrate); use of temporizing measures to allow resuscitation to a point where general anesthesia and surgery, if necessary, are better tolerated; early resort to hysterectomy; and keeping unstable patients with persistent bleeding in the operating room. (See 'Additional considerations for hemodynamically unstable patients' above.)
●Outcome – PPH is associated with potentially serious short-term morbidities from hemorrhage and hypotension and may be lethal. Potential long-term morbidities include Sheehan syndrome (in patients with hypotension) and Asherman syndrome (in patients who were curetted). (See 'Outcome' above.)
●Prevention – Active management of the third stage of labor reduces the incidence of PPH due to atony. Specific interventions are available for managing risk in patients with abnormal placentation or bleeding diatheses. (See 'Prevention' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Allan J Jacobs, MD, who contributed to earlier versions of this topic review.
