nursing journal articles on postpartum hemorrhage

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Postpartum Hemorrhage: A Comprehensive Review of Guidelines

Affiliations.

1 Resident.
2 Clinical Fellow in Maternal-Fetal Medicine.
3 Associate Professor.
4 Professor.
5 Consultant in Obstetrics and Gynecology.
6 Assistant Professor, Third Department of Obstetrics and Gynaecology, School of Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, Thessaloniki, Greece.
PMID: 36345105
DOI: 10.1097/OGX.0000000000001061

Importance: Postpartum hemorrhage (PPH) is a common complication of childbirth and the leading cause of maternal deaths worldwide, also associated with important secondary sequelae.

Objective: The aim of this study was to review and compare the most recently published influential guidelines on evaluation, management, and prevention of this severe, life-threatening obstetric complication.

Evidence acquisition: A descriptive review of guidelines from the American College of Obstetricians and Gynecologists, the Royal College of Obstetricians and Gynecologists, the Royal Australian and New Zealand College of Obstetricians and Gynecologists, the Society of Obstetricians and Gynecologists of Canada, the Network for the Advancement of Patient Blood Management, Hemostasis and Thrombosis in collaboration with the International Federation of Gynecology and Obstetrics, the European Board and College of Obstetrics and Gynecology and the European Society of Anaesthesiology, and the World Health Organization on PPH was carried out.

Results: There is a consensus among the reviewed guidelines that once PPH occurs, it is important to identify the underlying cause (4 T's), estimate the blood loss, and immediately initiate a resuscitation protocol with fluid replacement, blood transfusion, and close monitoring of the woman. In case of uterine atony, all the reviewed medical societies recommend uterine massage, bimanual uterine compression, and administration of uterotonics, although minor discrepancies are observed regarding the optimal regimens. If these measures fail, the use of intrauterine balloon tamponade or other surgical interventions is unanimously recommended. There is also agreement regarding the management of PPH due to retained placenta, placenta accreta, obstetric trauma, uterine rupture or inversion, and acute coagulopathy. Massive transfusion protocols are not consistent in the reviewed guidelines. Finally, all guidelines highlight the importance of the active management of the third stage of labor for the prevention of PPH, suggesting several interventions, with the administration of oxytocin being the criterion standard.

Conclusions: Postpartum hemorrhage is a significant contributor of maternal morbidity and mortality. Thus, the development of consistent international practice protocols for the effective management and prevention of this major complication seems of paramount importance and will hopefully improve obstetric outcomes and especially maternal mortality rate.

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Comments on the case, correspondence, prevention and treatment of postpartum hemorrhage: focus on hematological aspects of management.

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Claire McLintock; Prevention and treatment of postpartum hemorrhage: focus on hematological aspects of management. Hematology Am Soc Hematol Educ Program 2020; 2020 (1): 542–546. doi: https://doi.org/10.1182/hematology.2020000139

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Postpartum hemorrhage (PPH) is the leading cause of global maternal mortality and accounts for approximately one-quarter of all maternal deaths worldwide. Prevention of excess maternal deaths requires a coordinated approach to prevention, early recognition, and intervention by a multidisciplinary team. Although some women have risk factors for PPH that can be identified during pregnancy or during labor or birth, most women with severe PPH do not have any risk factors. Therefore, all pregnant women must be considered to be at risk of PPH. Common causes include uterine atony, retained placenta, trauma to the genital tract or uterus, and coagulopathy. The pivotal role of fibrinogen and hyperfibrinolysis in the evolution and as a treatment target for PPH is increasingly recognized. Coagulopathy can be an early feature in PPH that may be unrecognized, as it can be present before massive transfusion has occurred. Identification of coagulopathy by viscoelastic point-of-care testing or conventional laboratory assays can be helpful in guiding management of PPH and preventing severe maternal outcomes.

Recognize the importance of risk assessment of pregnant women to identify PPH risk factors in the antenatal period and during labor and birth

Recognize the importance of coagulation tests in women with PPH, to enable early identification and treatment of coagulopathy and hyperfibrinolysis

The patient was a 29-year-old Black woman in her first pregnancy. Her body mass index was 33 kg/m 2 . She had no other medical history of note, and antenatal care had been uncomplicated, apart from iron deficiency treated with oral iron supplements from 28 weeks’ gestation. At the 38-week scan, the fetus was well developed (estimated weight, 4100 g).

The patient had spontaneous onset of labor at 39 +5 weeks’ gestation. Her admission observations were normal: afebrile, pulse 88 per minute, blood pressure (BP) 110/68 mm Hg, and respiratory rate 14 per minute. A complete blood count on admission showed hemoglobin (Hb) 10.4 × 10 9 /L, platelets 152, white blood cell count 7.8 × 10 9 /L. She made slow progress in the first stage of labor, requiring augmentation with IV oxytocin. At 11 hours, an epidural was placed after the IV oxytocin was started. The first stage of labor was complete at 17 hours, and initial effective pushing occurred in the second stage, with the head on the perineum at 65 minutes with no further advancement. A successful vacuum extraction (ventouse) was performed after episiotomy by the senior resident, with birth of the infant after 80 minutes in the second stage. Active management of the third stage of labor appeared complete, with controlled cord traction, intramuscular oxytocin, and delivery of the placenta. Immediate postpartum blood loss was estimated at 1200 mL. The pediatric team was called to review the infant, who had a 3990-g birth weight and some initial floppiness but responded rapidly to basic resuscitation.

Ongoing vaginal blood loss continued in the postpartum period. The patient’s uterus remained atonic but responded well to “rubbing up,” and IV oxytocin infusion was started. The team agreed to move her to an operating room (OR) for examination under anesthesia to determine whether there were any retained products of conception or any genital tract trauma that would explain the ongoing blood loss. Maternal observations were pulse, 106 per minute; BP, 98/60 mm Hg; and respiratory rate, 18 per minute.

On arrival in the OR, the observations were pulse, 114 per minute; BP, 94/60 mm Hg; and respiratory rate, 20 per minute. Vaginal blood loss continued, with estimated blood loss of 400 mL on new drapes and swabs in the OR.

Blood taken in the OR and tested on the blood gas analyzer showed Hb of 8.2 g/dL. Two units of packed red cells were ordered from the blood bank. The uterus remained atonic, and there were some abrasions of the vaginal wall and bleeding from the episiotomy; no other cause was identified. Ongoing vaginal blood loss was noted, with loss estimated at 1600 mL. Uterine atony persisted and further uterotonics were given, after which the maternal observations were pulse, 118 per minute; BP, 90/58 mm Hg; and respiratory rate, 22 per minute.

A senior obstetrician and anesthesiologist were called for support.

Obstetric hemorrhage is the leading cause of maternal mortality and bleeding after childbirth. Postpartum hemorrhage (PPH) accounts for two-thirds of cases of obstetric hemorrhage and for approximately one-quarter of all maternal deaths worldwide. There is no universally accepted definition of PPH, with some suggesting that blood loss volume >500 or 1000 mL represents standard or severe PPH. 1 Most otherwise fit and healthy pregnant women will have minimal physiological response to this degree of blood loss, leading some clinicians to suggest more relevant clinical definitions, such as persistent PPH: ongoing active bleeding >1000 mL occurring within 24 hours after birth that continues despite the use of measures such as first-line uterotonic therapy and uterine massage. 2

Maternal deaths represent only the tip of the iceberg in terms of the overall impact of major bleeding on maternal health. Women who have life-threatening hemorrhage but do not die of PPH can face long-term health complications including loss of fertility and psychological trauma. Although nearly all women with severe PPH live in countries with limited economic resources, PPH and its complications can affect women living in any resource setting. Data from the United States show that rates of severe PPH are increasing. 3 Well-resourced health care settings with access to skilled practitioners, drugs, and blood banks offer the best opportunity to provide optimal care for women. In any care setting, early recognition of abnormal postpartum bleeding and mobilization of appropriate staff and resources is essential to stop the bleeding promptly and minimize morbidity and mortality.

Postpartum hemorrhage should not be viewed as a diagnosis but rather a clinical manifestation of an underlying condition or conditions that require identification and treatment. The differential diagnosis is not wide and includes one or more of the following: uterine atony, retained placenta, and placental malimplantation (previa, accreta, increta, or percreta), and genital tract trauma or coagulopathy, often referred to as the “4 T’s” (tone, tissue, trauma, and thrombin). Some women enter pregnancy with risk factors for PPH or develop these risk factors during the course of pregnancy or labor and birth ( Table 1 ). Women with risk factors identified antenatally should be managed in the appropriate setting with access to skilled staff and a blood bank and with precautionary steps taken during labor and childbirth to minimize the risk of PPH and respond early if it occurs ( Figure 1 ). However, it is critical that all staff caring for women in labor and childbirth be aware that most women who have severe PPH have no identifiable antenatal risk factors and that a high level of awareness be maintained. Risk factors should be reassessed frequently during labor and birth.

Risk factors for PPH


Previous PPH	Retained placenta
Labor >12 h	Placental abruption
Induction of labor	Placenta previa
Prolonged third stage of labor	Placenta accreta
Baby >4 kg
Multiple pregnancies	Amniotic fluid embolism
Increased body mass index	Acute fatty liver of pregnancy
Infection	Maternal sepsis
	Massive transfusion
Instrumental delivery
CS	Inherited
Uterine rupture	Acquired (receiving anticoagulant therapy)


Previous PPH	Retained placenta
Labor >12 h	Placental abruption
Induction of labor	Placenta previa
Prolonged third stage of labor	Placenta accreta
Baby >4 kg
Multiple pregnancies	Amniotic fluid embolism
Increased body mass index	Acute fatty liver of pregnancy
Infection	Maternal sepsis
	Massive transfusion
Instrumental delivery
CS	Inherited
Uterine rupture	Acquired (receiving anticoagulant therapy)

How urgently is red cell transfusion needed?

Setting the scene for the “PPH perfect storm”

Most women with PPH respond to initial measures of uterine massage and therapeutic uterotonics. However, if bleeding continues despite these interventions, the situation can rapidly escalate with more severe blood loss, maternal morbidity, and even mortality. Failure to recognize and respond to an evolving situation of severe PPH is frequently described in reviews of adverse outcomes caused by hemorrhage. This delay in response can be explained by several factors that create the “perfect storm” where the clinical team fails to recognize the severity of the blood loss and to take the appropriate steps.

Potential for rapid loss of a large volume of blood

In pregnancy, the total blood volume is ∼5 to 7 L (70-80 mL/kg lean body mass). By term, the blood supply to the uterine arteries is ∼500 to 600 mL per minute, increased from its normal level of 10 to 15 mL per minute outside of pregnancy. 4 After delivery of the placenta, the uterine muscles contract, effectively staunching blood flow from the uteroplacental bed. Uterine atony, retained placental tissue, and abnormal placental implantation impede the normal action of the uterus in completing this critical mechanical hemostatic process. Given the high blood flow to the uterine arteries, it is easy to appreciate how rapidly a large volume of blood can be lost in a short time.

Underestimation of the degree of blood volume loss

In many clinical settings the volume of blood loss is estimated by using visual assessment rather than objective measurement, which significantly underestimates the actual blood volume, especially at higher volumes. 5 Accurate measurements of blood volume using graduated containers and gravimetric measurement of blood-soaked pads and swabs reported to the clinicians in real time can help alert them to the development of severe continued bleeding. Providing a cumulative total of blood volume loss is especially important when women are moved during the process of PPH management (for example, from the delivery room to the OR) if required for an examination while the patient is under anesthesia, to assess for retained products of conception or genital tract trauma.

Most pregnant women are healthy and physiologically robust

Healthy pregnant women show minimal physiological response to blood loss of 1000 to 1500 mL, perhaps only becoming slightly tachycardic with a minor decline in systolic BP. By the time women have significant hypotension or tachycardia or an increased respiratory rate or become distracted or agitated, they usually have lost in excess of 2000 to 2500 mL. Careful and repeated clinical assessments and documentation of vital signs, such as pulse rate, BP, temperature, and respiratory rate is essential for identifying a trend indicating physiological decompensation in response to hypovolemia. The use of maternity early warning scoring to improve early detection of clinically deteriorating patients and escalation of the clinical response is increasing. 6,7 These systems assign a score to a range of clinical vital signs to form a total maternity early warning score. An increasing score suggests a deviation from a normal physiological state and indicates clinical deterioration, which should prompt an escalation in response by clinicians who have the appropriate level of skill to care for the patient.

Lack of anticipation of the presence of early coagulopathy with PPH, before a massive transfusion is needed

Dilutional coagulopathy is common in patients with hemorrhage after multiple transfusions. Urgent red cell transfusion is preferred to infusion of significant volumes of crystalloid, but in an unstable patient, volume replacement with up to 2 to 3 L of crystalloid may be necessary prevent severe hypotension. 2 Coagulopathy resulting from conditions, such as amniotic fluid embolism, placental abruption, and sepsis, can be present early, before administration of IV fluids or blood products. Early identification of coagulopathy by testing basic hemostatic function, with either laboratory-based assays or point of care (POC) testing, can help identify coagulopathy early and enable directed transfusion of the appropriate blood products.

Standard thrombin-based functional clotting assays for fibrinogen, such as the Clauss fibrinogen assay, measure the time it takes for a fibrin clot to form. In most clinical settings the final result will not be available for at least 45 to 60 minutes. Viscoelastic point of care (VE-POC) tests, such as rotational thromboelastometry (ROTEM) and thromboelastography, are increasingly used to assess global hemostasis, determining the activity of the coagulation factors and the amount of fibrinogen available to form a fibrin clot, as well the resistance of the clot to fibrinolysis. 8 In the setting of PPH, hyperfibrinolysis is not uncommon, especially in more severe PPH. The results of POC tests are usually available within 15 to 20 minutes, especially if the instrument is available in the OR.

Fibrinogen and fibrinolysis in PPH

The importance of fibrinogen and fibrinolysis in major postpartum bleeding has been brought into focus in recent years. Fibrinogen levels in pregnant women at term are increased at ∼4 to 6 g/L, compared with levels of 2 to 4 g/L in nonpregnant patients. In 2007, Charbit et al showed that fibrinogen levels were lower in women who developed severe PPH than in women with nonsevere PPH (median levels, 3.3 and 4.4 g/L, respectively). 9 Importantly, this difference was evident early in the evolution of PPH and before any blood or blood products had been administered. Other studies have confirmed this finding 10,11

Although these studies suggested that a low level of fibrinogen is predictive of development of severe PPH, they did not ascertain whether early fibrinogen replacement could modify the degree of blood loss. A controlled study of women with moderate PPH (blood loss >1000 mL after Cesarean section [CS], >500 mL in women who required manual removal of placenta, and >1000 mL in women who required exploration of the uterus) randomized women to 2 g of fibrinogen or placebo. 12 Transfusion rates were the same in women (n = 25 of 123; 20%) given fibrinogen as in those who received placebo (n = 26 of 121; 22%). Of note, the mean fibrinogen level in each group was normal (4.5 g/L) and the median blood loss was <1500 mL, indicating that perhaps fibrinogen would not be a key factor in this population.

A second multicenter, double-blind, randomized, placebo-controlled trial of early fibrinogen replacement in women with severe PPH (>1000-1500 mL measured blood loss, with ongoing bleeding and reduced fibrinogen on ROTEM: FIBTEM A5 <15 mm, equivalent to ∼3 g/L fibrinogen). 13 Of 606 women eligible for inclusion, only 57 (9.4%) were randomized, with 55 women analyzed for the primary outcome (the number of allogeneic units transfused: red blood cells and plasma products). There was no difference in blood products transfused or in any of the secondary outcomes, such as invasive procedures for control of blood loss or transfer to intensive care. Analysis of prespecified subgroups showed that, in women with fibrinogen >2 g/L (n = 22), there was no difference in blood loss or blood transfusion after administration of the study medication, whereas the median blood loss was lower in the fibrinogen arm than in the placebo arm in women with fibrinogen <2 g/L. The researchers concluded that a fibrinogen level of >2 g/L appeared sufficient for hemostasis in the setting of PPH. Too few women in the cohort had very low fibrinogen (<2 g/L) for them to determine whether early administration of fibrinogen would modify outcomes in that patient group.

Although Collins et al 13 did not demonstrate an improvement in outcomes in women who were given fibrinogen concentrate, they observed that, over the course of the clinical trial, their approach of routine risk assessment for PPH, objective measurement of cumulative blood loss, and early involvement of senior staff enabled early recognition and intervention in the course of the PPH to take steps to respond to and control blood loss. The prompt recognition allowed for timely and appropriate escalation of care and involvement of senior staff at an early stage. Also, the study led to the practice of early assessment of hemostasis, Hb, and lactate by using POC tests. The clinicians used the study protocol to inform the development of a nationwide interventional program for standardized management of PPH, “OBS Cymru,” which has been effectively implemented across all obstetric units in Wales. 14

Approach to transfusion of blood and plasma products in management of PPH

Using empiric fixed ratios of red blood cells, fresh frozen plasma (FFP), and platelets in women with PPH >1500 mL has been shown to reduce progression to severe PPH. Most women with PPH <2000 mL do not have low levels of fibrinogen or other clotting factors, and fibrinogen does not appear to decrease to <2 g/L until blood volumes of >4000 mL are lost, although early coagulopathy is a feature of placental abruption and amniotic fluid embolism. Empiric transfusion in the absence of hemostatic testing may lead to overtransfusion of blood and plasma products increased risk of complications, such as transfusion-associated circulatory overload and transfusion-associated lung injury. Collins et al advocate using targeted transfusion protocols with viscoelastic-POC (VE-POC) testing. 15 They reported that fibrinogen levels decrease sooner than other coagulation factors, so that correction of low fibrinogen levels may be a more important therapeutic target.

The International Society on Thrombosis and Haemostasis (ISTH) recommends using either cryoprecipitate (∼15 g/1000 mL) or fibrinogen concentrate (20 g/1000 mL) to maintain fibrinogen >2 g/L when managing PPH. 16 The fibrinogen concentration of FFP is much lower (2 g/1000 mL), and its use for fibrinogen replacement could lead to hemodilution.

Deficiencies of other clotting factors tend to occur at a later stage in PPH, suggesting that there is a more limited requirement for FFP. When VE-POC testing is not available, conventional laboratory testing may be helpful and the ISTH Scientific and Standardization Committee recommends targeting using 15 mL/kg FFP to maintain activated partial thromboplastin time/prothrombin time >1.5 × normal. 16

Severe thrombocytopenia is uncommon in most women with PPH, leading to a recommendation (ISTH) to limit platelet transfusions, unless platelet count is <75 × 10 9 /L. 16

Inhibition of fibrinolysis

Over the past 20 years or so, the impact of hyperfibrinolysis in major bleeding has been recognized. The CRASH-2 study demonstrated tranexamic acid, a potent inhibitor of fibrinolysis, reduction in death related to bleeding by 21% (risk ratio [RR], 0.79; 95% confidence interval [CI], 0.64-0.97) in trauma patients who received it within 3 hours and by 32% (RR, 0.68; 95% CI, 0.57-0.82) in patients who received it within 1 hour. 17

The WOMAN study is a placebo-controlled trial conducted in 21 countries that assessed the impact of tranexamic acid in 20 021 women with PPH >500 mL after vaginal birth or >1000 mL after CS. 18 The maternal mortality rate was 2.4% (n = 483) with 72% (n = 346) of deaths caused by hemorrhage. Administration of 1 g of tranexamic acid (with a second dose given for ongoing bleeding) resulted in an overall reduction in death related to bleeding of 19% (RR, 0.81; 95% CI, 0.65-1.00) when given within 3 hours.

As a result of this study, the World Health Organization now strongly recommends early use of IV tranexamic acid (within 3 hours of birth) in addition to standard care for women with clinically diagnosed PPH after vaginal birth or CS. 19

Recognition and response to major PPH also requires rapid response with transfusion of red blood cells to maximize oxygen delivery and prevent tissue hypoxia, development of acidosis, organ failure, and worsening of shock. The urgency of red cell transfusion depends on the degree of maternal clinical instability and rapidity of blood loss. Transfusion of O − red blood cells may be required in women who are clinically unstable or who are losing blood rapidly when cross-matched blood is not available.

Antenatal risk factors

In the clinical case, the only identifiable antenatal risk factors for PPH were increased body mass index and fetal macrosomia. Although the patient was iron deficient, she was not anemic. However, during labor she needed augmentation with oxytocin and had prolonged first and second stages of labor, with an assisted delivery. The immediate estimated postpartum blood loss was high, confirming a PPH, and importantly, the bleeding did not stop after initial interventions of uterine massage and therapeutic uterotonics.

An opportunity for escalation of intervention and a call for backup was missed at the time the patient was transferred to the OR. The degree of tachycardia and the increase in the respiratory rate were signs that this otherwise healthy, physiologically robust woman had lost a significant amount of blood. As a rule of thumb, a pulse rate higher than the systolic BP indicates a problem.

Estimated rather than measured blood loss

It is likely given the drop in the Hb that the woman had lost >1600 mL blood. Accurate cumulative measurement of blood loss would have alerted the clinicians to the severity of blood loss and the potential for progression.

Failure to perform an early coagulation test

A test of coagulation is helpful in identifying unanticipated coagulopathy. If available, a VE-POC test (ROTEM or thromboelastography) can provide a result within 15 minutes. Even though a conventional laboratory-based fibrinogen assay may be delayed by 60 minutes, it could still provide additional help if the PPH is not being controlled by initial maneuvers.

Ongoing significant postpartum bleeding in a woman with a well-contracted uterus with no evidence of genital tract trauma or retained placenta should alert the clinicians to the possible presence of coagulopathy.

Claire McLintock, Auckland City Hospital, Grafton Road, Auckland 1143, New Zealand; e-mail: e-mail [email protected] .

Competing Interests

Conflict-of-interest disclosure: The author declares no competing financial interests.

Author notes

Off-label drug use: None disclosed.

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Published: 10 September 2024

Incidence of postpartum depression among women with postpartum haemorrhage in Kano, northern Nigeria

Fatimah Isma’il Tsiga-Ahmed 1 , 2 ,
Musa Usman Umar 3 , 4 ,
Aishatu Lawal Adamu 1 , 2 ,
Sahabi Kabir Sulaiman 5 ,
Amole Taiwo Gboluwaga 1 , 2 , 6 ,
Rabiu Ibrahim Jalo 1 , 2 ,
Usman Muhammad Ibrahim 7 ,
Aminatu Kwaku Ayaba 2 ,
Zainab Datti Ahmed 8 ,
Surayya Murtala Sunusi 2 ,
Nafisat Tijjjani Abdullahi 2 ,
Hajara Shehu Kabir 4 ,
Stephen Mohammed Abu 5 &
Hadiza Shehu Galadanci 6

npj Women's Health volume 2 , Article number: 32 ( 2024 ) Cite this article

Metrics details

Health care

The burden of postpartum depression (PPD), an important but largely neglected cause of maternal morbidity, is often increased by the presence of common co-morbidities, such as postpartum haemorrhage (PPH). Additionally, stress and the absence of social support can amplify PPD risk. Understanding the relationship between these conditions will help identify at-risk women and allow prompt intervention. Using a prospective cohort design, we recruited 72 women who had experienced PPH and another 72 women who had not within 24 h of delivery to assess the risk of PPD among them. The cumulative incidence of PPD among all participants was 15.3% (19/124). There was insufficient evidence to suggest that women with PPH have a higher risk of PPH than women without PPH (OR: 1.32; 95% CI: 0.55–3.13). Poor social support and high perceived stress increased the risk of PPD. We recommend screening for PPD among women with high perceived stress and low social support.

Mapping global prevalence of depression among postpartum women

nursing journal articles on postpartum hemorrhage

Perinatal depression and anxiety of primipara is higher than that of multipara in Japanese women

Perinatal depression and mental health uptake referral rate in an obstetric service

Introduction.

Postpartum depression (PPD) is a mood disorder that manifests as a feeling of melancholy and disinterest, which occurs within the first four weeks of delivery and may last up to a year after childbirth 1 , 2 . PPD affects approximately 1 in 7 new mothers globally, with an estimated prevalence of 17.7% in the first year following delivery 1 , 3 . The frequency of PPD varies between African countries, albeit higher than values found in high-income settings. In Nigeria, rates ranging from 10.7% to 44.39% have been documented in various sub-geographical regions 2 . PPD has been linked to suicide in the mother, impaired mother-infant bonding, as well as a negative influence on the child’s emotional and cognitive development 4 , 5 . Akin to PPD, postpartum haemorrhage (PPH) is a worldwide public health priority, resulting in over 70,000 annual maternal deaths globally 6 , 7 . Globally, about 14 million people experience PPH annually 6 , and it is the leading preventable cause of maternal mortality and morbidity, globally. In sub-Saharan Africa, PPH is responsible for between 30% and 50% of maternal deaths 8 , and in Nigeria, PPH is estimated to account for nearly a quarter (23%) of maternal deaths 9 .

In addition to the potentially fatal outcomes, PPH has also been linked with increased maternal morbidity, particularly due to improved survival associated with improving maternal health services. Notably among these PPH-related consequences are mental illnesses, including anxiety, post-traumatic stress disorder and postpartum depression (PPD) 10 . A recent review and metanalysis involving nine studies reported that PPH was strongly linked to a higher risk of developing postpartum depression. More specifically, compared to women without PPH, the risk of PPD was raised by 27% in women with PPH 5 . Similarly, a population-based longitudinal study from the United Kingdom found a substantial correlation between PPH and a higher incidence of postnatal depression and posttraumatic stress disorder (PTSD) in the first year after delivery. The prevalence of PND was 5.34%, and that of PTSD was 0.20% among women who had PPH 11 . Several other studies have documented a similar relationship between PPH and PPD 12 , 13 , 14 , 15 , 16 .

The development of PPD is linked to the physiological changes of the postpartum period, characterised by profound changes in placental and maternal hypothalamic hormones, a decline in circulating blood volume, and alterations in metabolism 17 , 18 . PPH is a pathologically stressful event that can in addition to reducing blood volume, also lead to endocrine imbalance, a documented aetiologic factor for PPD 18 . The most common consequences of PPH are anaemia and trauma. Furthermore, clinical symptoms of PPH, such as fatigue, reduced cognitive abilities, and emotional instability, can lead to increased stress levels that alter the hypothalamic–pituitary–adrenal (HPA) axis function, leading to increased vulnerability to mood disorders 18 . Consistent with a role for HPA axis dysfunction in PPD, levels of the stress hormones are altered in patients with PPD.

Postpartum haemorrhage and postpartum depression are common and serious public health problems associated with maternal and child distress 5 . Although PPD is the most common psychiatric disorder during the 5 years after delivery 19 , the relationship between this disorder and the traumatic experience of postpartum haemorrhage is under-studied, in developing countries like Nigeria. Most studies exploring the relationship between PPH and PPD are from high-income settings. Given the prevalence of PPH and over 7 million births occurring in Nigeria annually 20 , over a million women will experience PPH, and many will suffer its health sequelae. Therefore, there is a need to investigate this relationship further. This study aimed to recruit women with and without PPH within 24 h of delivery and follow them up to estimate the incidence of PPD at 6, 10 and 14 weeks postpartum and to evaluate the effect of social support and perceived stress on the risk of PPD.

At the end of the study period, complete data on 124 women was analysed, giving a response rate of 82.7%. Eleven women from the PPH group and thirteen from the comparative group were excluded because they either did not fulfil the inclusion criteria or had incomplete data. There were 63 women who had PPH and 61 women without PPH, the majority of whom were from Gwale LGA (26.2% non-PPH and 28.6% PPH respondents). The respondent’s ages ranged from 18 to 44 years, with a mean and standard deviation (SD) of 27 ± 5 years. All but two women (98.39%, n = 122) were married, 76.61% ( n = 95) were from a monogamous setting, and 30.65% ( n = 38) had post-secondary education. The husbands’ mean age ± SD was 39 ± 7 years, and 52.83% ( n = 65) were educated up to tertiary level.

Among respondents who had PPH, the quantity of blood loss ranged from 500 to 1500 mls (IQR 500,1000 mls). Approximately a third of the respondents (31.75% < n = 20) were transfused after PPH, and only one woman (1.59% < n = 1) had a hysterectomy secondary to PPH. Among all respondents, a sizeable number had strong social support (62.90%, n = 78), and the majority of the respondents reported experiencing moderate levels of perceived stress (59.68%, n = 74). Baseline characteristics are presented in Table 1

At the conclusion of follow-up, the overall cumulative incidence of postpartum depression among all respondents was 15.32% ( n = 19); 17.46% ( n = 11) among women who had PPH and 13.11% ( n = 8) among women who did not have PPH. The incidence was highest in both groups on the first visit, despite insufficient evidence to support a difference between the groups (Table 2 ).

The distribution of PPD by baseline characteristics and risk factors for PPD is presented in Table 3 . Among all respondents, the incidence of PPD was higher among respondents who were less than 25 years (84.21%) and from monogamous households (78.95%). There was insufficient evidence of a difference in the incidence of PPD between women who had PPH and those who did not, and this relationship was maintained even after adjusting for the effects of age, parity, perceived stress and social support. Nonetheless, perceived stress and social support were found to be independent risk factors for PPD after adjusting for these variables. Compared to women who had low perceived stress, the odds of PPD were approximately three times in those who had moderate stress [AOR: 2.60, 95% CI: 1.10–13.20] and 4 times among those with high perceived stress [AOR: 4.20, 95% CI: 1.04–18.55]. Similarly, respondents with strong [AOR: 11.68, 95% CI: 4.03–18.74] and moderate social support [AOR: 6.20, 95% CI: 1.22–13.60] had higher odds of PPD compared to those with poor support.

On stratified analysis, we did not observe evidence of effect modification of both perceived stress (P = 0.266) and social support (0.601) on the relationship between PPH and PPD ( Table 4 )

This is a prospective cohort study of women with and without PPH who were followed up until 14 weeks postpartum in order to evaluate the incidence of PPD. The findings of our study show that the overall cumulative 14-week incidence of PPD for all respondents was 15.32%(17.46%, and 13.11% for women with PPH and without PPH respectively).

The incidence of PPD was not significantly different between women who had PPH and those who didn’t, and this lack of association persisted even after controlling for age, parity, perceived stress and social support. After controlling for these confounders, the only independent risk factors for PPD were perceived stress and social support. Social support and perceived stress, however, did not modify the relationship between PPH and PPD.

Our findings reveal that approximately 1 in 5 women who had postpartum haemorrhage in Kano develop PPD, a value higher than the 13.11% risk of PPD obtained from women who did not have PPH. The risk of PPD among both groups of women obtained in this study is akin to findings from China, where puerperal women with PPH were more likely to screen positive for postpartum depressive symptoms than those without PPH (16.4% vs 11.7%) 13 . Values from around the world, however differing from ours, also showed higher rates of PPD among women who had PPH as opposed to those who did not; from France (35% vs 15%) 21 , from Sweden (2.0% vs 1.9%) 14 . and from the UK (5.34% as opposed to 4.75%). 11 . Even though these results were consistent, the variances seen could have been caused by different inclusion criteria and methodological variations. For instance, one study defined PPD as having a value of EDPS score of 11 or above 21 , another defined PPH as losing >1000 mls 13 , while the third study limited its study group to term births with a non-anomalous pregnancy 14 . Two recent metanalyses revealed pooled evidence which showed that women with PPH are at increased risk of PPD compared with women without PPH 5 , 22 .

Over a third of the women who experienced PPH in this study reported high perceived stress relative to those who did not. Additionally, having high perceived stress was associated with increased odds of PPD. Epidemiological data has linked the occurrence of traumatic birth events, including PPH to higher stress levels 10 , 23 , 24 , 25 . Our results are in keeping with a review which reported a pooled incidence of PTSD after traumatic childbirth of 19.4% (95% CI 11.9–26.5%) 26 . Postpartum haemorrhage can have a profound psychological impact on mothers leading to feelings of fear, anxiety, helplessness, and loss of control. Witnessing or experiencing a life-threatening event during childbirth can trigger symptoms of post-traumatic stress disorder (PTSD) or contribute to general feelings of distress 12 . These psychological factors are closely linked to the development of postpartum depression. Thus, it is unsurprising that more than half of the PPD cases among women who experienced PPH were those with high perceived stress. The physical consequences of PPH, such as fatigue, weakness, anaemia, and the need for medical interventions like blood transfusions or surgery, can contribute to postpartum physical recovery challenges. This physical trauma and stress can exacerbate feelings of emotional distress and increase the risk of developing postpartum depression, pre-term deliveries and a pre-existing medical condition prior to pregnancy.

Our findings revealed an inverse relationship between social support and PPD. A significant number of our study participants among both groups had strong social support, however, there were more women with poor social support among those who had PPD. In line with our discovery, strong social support has been seen to positively influence the occurrence of PPD in African communities 2 , 27 , 28 . Social support plays a crucial role in promoting individual well-being, resilience, and community cohesion. In Africa, social support encompasses a rich tapestry of familial, communal, religious, and cultural practices that contribute to individual and collective well-being. African communities often exhibit strong bonds of solidarity and reciprocity, where neighbours, friends, and community members come together to support one another. In addition, family is central to social support in Africa, with strong kinship ties serving as the primary source of support. Extended family networks provide emotional, financial, and practical assistance to mothers after childbirth. This may further explain why women from monogamous homes in this study had a higher risk of PPD.

A major strength of this study is its prospective design. The prospective design allowed us to correctly estimate blood loss during delivery, a major flaw identified from previous studies, disentangle the temporal direction of association between PPH and PPD and assess the risk of PPD over time at three follow-up periods postpartum. Our study had some limitations, and the results must therefore be interpreted with caution. While all measures were put in place to reduce bias due to loss of follow-up, a negligible number of respondents could not be located after assessing the baseline information. A major source of potential bias in cohort studies arises from the degree of accuracy with which subjects have been classified with the outcome status. To avoid this, all staff collecting information underwent rigorous training with continuous supportive supervision. We also measured both PPH and PPD objectively using standardised tools.

We investigated the risk of PPD among women with and without PPH. Our findings showed insufficient evidence to suggest that women with PPH have a higher risk of PPH than women without PPH. However, perceived stress and social support were significantly associated with the development of PPD. We recommend the provision of holistic postpartum care that addresses both physical and emotional recovery needs as well as integrating mental health screening and support services into routine postpartum visits, alongside medical assessments.

This study is a multicenter prospective cohort study carried out in two tertiary hospitals (Aminu Kano Teaching Hospital and Murtala Muhammad Specialist Hospital) and one secondary hospital (Sabo Bakin Zuwo Maternity Hospital) within Kano, northern Nigeria. Kano state is one of the most populous states in Nigeria, with an estimated population of >14 million in 2022. Kano State is also among the states with poor maternal and child health indices, with a maternal mortality ratio of 1025 deaths per 100,000 live births (compared to the National figure of 576 per 100,000) 29 , and a high total fertility rate of over 6.5 births per woman 30 .

Aminu Kano Teaching Hospital (AKTH) and Murtala Muhammad Specialist Hospital (MMSH) serve as referral centres serving people from Kano and neighbouring states, while Sabo Bakin Zuwo Maternity Hospital (SBZMH) mainly serves people from within the Kano metropolis. The average number of annual births is 3800, 14,000 and 4000 in AKTH, MMSH and SBZMH, respectively.

The study population included women who gave birth in the three designated hospitals between April 13th 2023, and July 30th 2023, irrespective of parity and age. The study only comprised eligible women who were Kano residents, had a live birth, and received prenatal care in these facilities. In addition, women who had undergone a caesarean section, had a severe illness or had a history of mood disorders were excluded.

Prior data indicate that the incidence of PPD is 16% in Kano 2 . We hypothesise an absolute difference of 20% between our two study groups, based on observed difference of 20% found in a similar study 21 . Thus, a sample size of 75 for each group (total sample of 150), will achieve a power of 80% to observe a difference in incidence risk of 20% between women with and without PPH at 5% level of significance.

Baseline sociodemographic data, medical and obstetric history were obtained using a structured interviewer-administered questionnaire and other clinical data were obtained from the hospital records.

A Hausa-translated version of the Edinburgh postnatal depression scale (EDPS) was used to screen for PPD 31 . The EDPS is a 10-item, widely used, efficient and easy-to-use scale for identifying women at risk of postpartum depression 32 . Responses are scored between 0 and 3 based on the severity of the symptom, and the sum of the points for the 10 elements determines the final score, which can reach a maximum of 30. The EPDS is not a diagnostic tool but rather a means to identify the presence of a depressive symptom. The validity of EDPS has been tested in different settings, including Nigeria 33 , 34 , and has also been translated into several languages, including the Hausa Language 31 , 33 , 35 .

This study employed the Mini International Neuropsychiatric Interview (MINI) version 7.0.2 for DSM-5 to diagnose depressive disorders among the participants 36 . MINI is a short, standardised, structured instrument of choice often used for quick psychiatric evaluation in clinical and research settings. It covers a range of psychiatric disorders, including mood disorders, anxiety disorders, psychotic disorders, substance use disorders, and more. Studies have confirmed the validity and reliability of MINI 37 . Adopted by mental health practitioners and health organisations in over 100 countries, the MINI is the most extensively used psychiatric structured diagnostic interview instrument globally and has been verified and translated into more than 70 languages 36 . The scoring of the MINI entails determining whether or not specific criteria for a range of psychiatric disorders are present. Usually, responses are categorised as “Yes”, denoting the presence of symptoms or “No”, denoting their absence.

Social support was evaluated using the Oslo Social Support Scale (OSSS-3). The OSSS-3 is a brief measure designed to assess perceived social support, especially in population-based surveys and clinical contexts and has been recommended as a tool to assess social support in Nigeria 38 , 39 . Respondents score each of the three items on a Likert scale, which captures various facets of social support. The scores for each item are typically summed, with higher scores indicating greater perceived social support.

Perceived stress was measured using the Perceived Stress Scale. The Perceived Stress Scale (PSS-10) is a 10-item widely used psychological instrument for measuring the perception of stress in individuals over the past month. The PSS-10 covers various aspects of stress, including unpredictability, lack of control, and coping ability. Respondents rate their answers on a Likert scale, typically ranging from 0 (never) to 4 (very often). The PSS can be self-administered, making it appropriate for surveys. The total score can range from 0 to 4, with higher scores on the PSS indicating a higher level of perceived stress 40 .

The primary outcome, postnatal depression, was evaluated at 6, 10 and 14 weeks using the Edinburgh postnatal depression scale and the Mini International Neuropsychiatric Interview version 7.0.2 for DSM-5. Initial screening was conducted using the EDPS, and as recommended, a score of 9 or higher on the EDPS was the threshold for administering the MINI to establish the diagnosis of postpartum depression 31 . Confirmation of a major depressive disorder, as well as categorisation into current, past or recurrent, was made using the elements A1 to A6 on the A module of the MINI version 7.0.2.

The primary exposure, primary postpartum haemorrhage, was defined using the WHO description i.e. excess bleeding from the uterine cavity associated with childbirth in the quantity of 500 mls or more within 24 h of delivery 41 .

Other exposures included were social support classified as poor social support (score of 3–8), moderate social support (9–11) and strong social support (12–14) and perceived stress defined as low perceived stress (scores from 0 to 13), moderate stress (14 to 26), and high stress (scores from 27 to 40).

Explanatory variables were sociodemographic characteristics of the respondents, past medical history, obstetric history, and information regarding the most recent birth, including clinical findings, were also included as explanatory variables.

Selection of exposed group began with midwives in the delivery rooms of the three facilities being trained on how to quantify the volume of blood loss within 24 h of delivery. Under-buttock plastic calibrated drapes were used immediately after a woman delivered to collect blood around delivery time. Subsequently, sanitary towels were collected and weighed and specially formulated charts were used to calculate blood loss based on weight. Two nurses (research assistants) visited the delivery unit daily to identify women who had lost more than 500 mls within 24 h using the blood loss chart. Any woman who met the inclusion criteria was then enrolled as a participant in the exposed group. For each woman recruited into the exposed group, one woman who fulfilled the inclusion criteria but had not lost up to 500 mls of blood within 24 h was selected using a random sampling technique for recruitment into the unexposed group. This was done using randomly generated numbers from a tablet form within the list of the women without PPH who delivered that day.

Upon recruitment, baseline information was collected from participants of both groups. Clinical data and information on perceived stress and social support were also obtained.

All respondents were followed up for 14 weeks and the time for data collection was made to coincide with the second, third and fourth immunisation visits, which are at 6, 10 and 14 weeks. Index date of follow up was the date of the delivery. For participants who did not show up, phone calls were made, and they were visited in their homes.

Two nurses at the well-child clinic where women come for routine childhood immunisation collected data on the outcome (PPD). The EPDS was administered to each participant during the first visit, and those with a score of 9 and above were further evaluated using the MINI. Participants with scores less than 9 had the EPDS re-administered during the next visit, and the procedure was repeated until the last visit (at 14 weeks).

We utilised STATA version 15.0 (StataCorp LLC, College Station, TX, USA) for data analysis. Background characteristics were presented using frequencies and proportions as well as means and their corresponding standard deviations (SD) or median and interquartile range as appropriate. We estimated the cumulative incidence of PPD as the total number of PPD cases at the end of follow-up divided by the number of respondents followed up from the beginning of the study. We fitted logistic regression models to report the crude odds ratio (OR) and 95% confidence interval (CI) for the factors associated with PPD among all respondents and then employed a multivariable logistic regression modelling to report the adjusted odds ratio (aOR) and CI for the independent risk factors for PPD. We adopted a backward selection approach to modelling, beginning with a complete model that included all relevant variables and sequentially removing variables with a p -value > 0.20 and no established theoretical relevance. The likelihood ratio test was used to identify better models. The final model included our primary exposure to PPH status, age, parity, perceived stress and social support. We employed Mantel Haenszel (MH) odds to stratify the effect of PPH on PPD by perceived stress and social support and presented the ORs and CIs for each category.

Ethical approval for this study was obtained from the Health Research Ethics Committees of the Kano State Ministry of Health (SHREC/2022/3366) and Aminu Kano Teaching Hospital (NHREC/28/01/2020/AKTH/EC/3355). Permission to conduct the study was sought from the management of the three hospitals. Every respondent provided signed informed consent, and the provisions of the Helsinki declarations were adhered to.

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Acknowledgements

The project was supported by an institutional-based research grant, TETFund grant TETF/DR&D/CE/UNIV/KANO/INR/2020/V0L1, and the Fogarty International Centre (FIC) and the National Institute on Alcohol Abuse and Alcoholism (NIAAA) of the U.S. National Institutes of Health (NIH) award number 1D43TW011544. The findings and conclusions are those of the authors and do not necessarily represent the official position of the FIC, NIAAA, NIH, the Department of Health and Human Services, or the government of the United States of America.

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Fatimah Isma’il Tsiga-Ahmed, Aishatu Lawal Adamu, Amole Taiwo Gboluwaga & Rabiu Ibrahim Jalo

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Fatimah Isma’il Tsiga-Ahmed, Aishatu Lawal Adamu, Amole Taiwo Gboluwaga, Rabiu Ibrahim Jalo, Aminatu Kwaku Ayaba, Surayya Murtala Sunusi & Nafisat Tijjjani Abdullahi

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F.I.T., U.M.U., A.T.G., Z.D.A. and H.S.G. conceived and designed the study. F.I.T., S.M.A., S.M.S., N.T.A. and H.K.S. collected data. R.I.J., A.A.K., S.M.A. and S.K.S. performed a literature search. F.I.T., A.L.A. and R.I.J. performed the statistical analysis. F.I.T., U.M.I., A.T.G. and A.L.A. drafted the paper. Z.D.A., U.M.U. and S.K.S. assisted with data interpretation and critically reviewed the paper for intellectual content. A.A.K., S.M.S. and N.T.A. revised the paper. All authors contributed to and approved the paper.

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Tsiga-Ahmed, F.I., Umar, M.U., Adamu, A.L. et al. Incidence of postpartum depression among women with postpartum haemorrhage in Kano, northern Nigeria. npj Womens Health 2 , 32 (2024). https://doi.org/10.1038/s44294-024-00031-1

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PMC10181876

Postpartum Hemorrhage

P ostpartum hemorrhage continues to be the leading prevent -able cause of maternal illness and death globally. 1 , 2 Worldwide, postpartum hemorrhage accounts for 8% of maternal deaths in developed regions of the world and 20% of maternal deaths in developing regions. 2 The United States has one of the highest maternal mortality rates among developed countries, with approximately 11% of all maternal deaths associated with postpartum hemorrhage. 3 During the period from 1993 through 2014, the rate of postpartum hemorrhage (which was defined as blood loss >1000 ml after vaginal or cesarean delivery) requiring a blood transfusion 4 increased from approximately 8 cases per 10,000 deliveries to 40 per 10,000 deliveries in the United States. 5

With the increasing prevalence of postpartum hemorrhage, well-designed cohort studies and randomized clinical trials that evaluate interventions that are critical for predicting, preventing, and managing postpartum hemorrhage remain a high priority. 6 However, as a result of challenges in the quantification of blood loss, various definitions of postpartum hemorrhage, and differences in outcome reporting, data from relevant randomized clinical trials are difficult to interpret and compare across studies. 6 In addition, guidelines for preventing and managing postpartum hemorrhage vary substantially among major national obstetrics and gynecology organizations, including the American College of Obstetricians and Gynecologists, 7 the Society of Obstetricians and Gynaecologists of Canada, the French College of Gynecologists and Obstetricians, the Royal College of Obstetricians and Gynaecologists (United Kingdom), and the Royal Australian and New Zealand College of Obstetricians and Gynaecologists. 8 This review discusses the causes, identification, management, prevention, and prediction of postpartum hemorrhage.

DEFINITION, CAUSES, AND RISK FACTORS

The normal rate of blood flow to the uterus at full term is approximately 600 ml per minute, in contrast to approximately 60 ml per minute in the nonpregnant state. 9 The control of postpartum blood loss depends primarily on uterine contractions and, to a lesser degree, on activation of the coagulation cascade.

The traditional definition of postpartum hemorrhage is blood loss of more than 500 ml after a vaginal delivery or more than 1000 ml after a cesarean delivery. 10 More recently, postpartum hemorrhage has been redefined as a cumulative blood loss of 1000 ml or more or blood loss associated with signs or symptoms of hypovolemia, irrespective of the route of delivery. 10 Typical clinical signs and symptoms of hypovolemia (e.g., hypotension and tachycardia) due to postpartum hemorrhage may not appear until blood loss exceeds 25% of total blood volume (>1500 ml during late pregnancy). 11

Postpartum hemorrhage is considered to be primary when it occurs within the first 24 hours after delivery and secondary when it occurs between 24 hours and up to 12 weeks after delivery. 10 , 12 The causes of postpartum hemorrhage can be summarized by the four “T’s”: tone (uterine atony), trauma (lacerations or uterine rupture), tissue (retained placenta or clots), and thrombin (clotting-factor deficiency). 10 The most common cause is uterine atony (accounting for approximately 70% of cases), followed by obstetrical lacerations (approximately 20%), retained placental tissue (approximately 10%), and clotting-factor deficiencies (<1%). 10 Postpartum hemorrhage can lead to severe anemia requiring blood transfusion, disseminated intravascular coagulopathy, hysterectomy, multisystem organ failure, and death. 10

Postpartum hemorrhage due to uterine atony is often preceded by chorioamnionitis, therapeutic use of magnesium sulfate, prolonged labor or precipitous delivery, labor induction or augmentation, uterine fibroids, or uterine overdistention as a result of multiple gestation, fetal macrosomia, or polyhydramnios. Cesarean delivery is associated with a higher risk of postpartum hemorrhage than vaginal delivery. Advanced maternal age and extremes of parity (0 and >4) are additional risk factors.

Other risk factors for postpartum hemorrhage are closely linked to the type of hemorrhage that develops. For example, obstetrical lacerations can be caused by operative vaginal delivery, precipitous delivery, or episiotomy, whereas retained placental tissue can be caused by placenta accreta spectrum (PAS; a spectrum of abnormal placentation disorders, including placenta accreta, placenta increta, and placenta percreta), which is associated with prior uterine surgery. Retained placental tissue can also be the result of incomplete delivery of the placental tissue and membranes. Maternal coagulopathy that leads to postpartum hemorrhage can be a complication of severe preeclampsia and eclampsia, HELLP (hemolysis, elevated liver-enzyme level, and low platelet count) syndrome, intrauterine fetal death, placental abruption, or a coagulation disorder that is acquired (e.g., amniotic fluid embolism) or inherited.

Despite efforts to identify patients who are at increased risk for postpartum hemorrhage, this life-threatening complication often occurs in women who have no identifiable risk factors. 10 Therefore, vigilance is crucial after all deliveries.

MANAGEMENT OF POSTPARTUM HEMORRHAGE

General approach.

Management of postpartum hemorrhage necessitates a coordinated multidisciplinary approach, which involves good communication, accurate assessment of blood loss, monitoring of maternal vital signs and symptoms, fluid replacement, and arrest of the source of hemorrhage, all occurring concurrently ( Fig. 1 ). 10 , 13 Assessment of ongoing blood loss is a critical step in the management of postpartum hemorrhage. Blood loss can be assessed on the basis of visual estimation or weighing of materials, including blood and amniotic fluid–soaked surgical sponges and drapes. 7 Although there is no strong evidence that one method of assessing blood loss is better than the other, quantification provides a more accurate estimation of blood loss, as compared with subjective assessment. 7 , 14 Morbidity among women with severe postpartum hemorrhage may be reduced when quantitative estimation of blood loss is used as a component of maternal safety protocols, 7 but this method has not consistently been found to improve clinical outcomes. A recent Cochrane review and meta-analysis showed no evidence that quantitative estimation of blood loss reduces the need for uterotonic agents, blood transfusion, or volume expanders during postpartum hemorrhage. 15 Despite these limitations, some obstetrics and gynecology societies 7 favor quantification of blood loss by weighing of blood-soaked materials (lap sponges and pads), monitoring of fluid used during irrigation, and use of underbuttock, graduated cylinder drapes during postpartum hemorrhage. More recently, the use of colorimetric techniques, which involve electronic artificial intelligence (e.g., smartphone applications), to estimate blood loss in real time seems encouraging. 16

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The abbreviation aPTT denotes activated partial-thromboplastin time, BMP basic metabolic panel, CBC complete blood count, FFP fresh-frozen plasma, IV intravenous, PT prothrombin time, and T and S type and screen.

Once a woman is admitted for delivery, if there is a high index of suspicion for the development of postpartum hemorrhage (e.g., placenta previa, PAS, or active vaginal bleeding), two large-bore intravenous cannulas should be inserted, a complete blood count should be obtained, and a specimen should be sent to the blood bank. The blood bank should be notified, and at least 2 units of blood should be typed and cross-matched for the patient. Additional maternal monitoring should be tailored to the cause and degree of increased risk of postpartum hemorrhage and can include the use of continuous pulse oximetry, assessment of urine output with the use of an indwelling bladder catheter, continuous cardiac monitoring, assessment of coagulation status (on the basis of prothrombin time, fibrinogen level, and activated thromboplastin time), and a comprehensive metabolic panel. 10 If the patient is at very high risk for postpartum hemorrhage, central venous and arterial catheters should be placed. A heating–cooling circulating water pad or a forced-air warming system may be used to help mitigate the hypothermia that is often associated with massive fluid resuscitation and prolonged surgery. Although both crystalloids and colloids can be used as intravenous fluids, 17 crystalloids are slightly favored over colloids. 18

MANAGEMENT OF RETAINED PLACENTAL TISSUE

Inspection of the placenta after delivery is important to rule out retained placental tissue or a retained succenturiate lobe of the placenta (an abnormality in the placental structure in which one or more accessory lobes is connected to the main part of the placenta by blood vessels). When retained placental tissue is suspected, evacuation with manual exploration or a banjo (blunt) curette under ultrasonographic guidance is recommended; the positive and negative predictive values of ultrasonography in detecting retained placental tissue are approximately 58% and 87%, respectively. 19 Abnormal uterine bleeding that warrants manual removal of the placenta increases the likelihood that the bleeding is due to a PAS disorder. 20

MANAGEMENT OF GENITAL TRACT LACERATIONS

Careful inspection of the lower genital tract for cervical, vaginal, perineal, or rectovaginal lacerations is important. Lacerations should be promptly repaired with absorbable sutures. There is insufficient evidence in support of routine antibiotic prophylaxis after uterine evacuation for postpartum hemorrhage or repair of a perineal laceration. 21

MANAGEMENT OF UTERINE ATONY

Bimanual uterine massage is usually the first step in the management of postpartum hemorrhage due to uterine atony. Massage is performed in an attempt to induce uterine contractions by stimulating endogenous prostaglandins. 10 , 22 Oxytocin (administered intravenously or intramuscularly) is the mainstay of treatment for controlling postpartum hemorrhage due to uterine atony; administration of oxytocin is usually begun simultaneously with uterine massage, if the agent has not already been administered prophylactically. The uterine response after the administration of intravenous oxytocin is usually immediate (oxytocin half-life, 1 to 6 minutes in plasma). 23

Additional agents (e.g., methylergonovine maleate, a semisynthetic ergot alkaloid) and intramuscular prostaglandins (e.g., carboprost tromethamine, a 15-methyl analogue of prostaglandin F 2 α ) can be used as second-line pharmacotherapy to control postpartum hemorrhage. A Cochrane review and meta-analysis have questioned the usefulness of misoprostol, a prostaglandin E 1 analogue. 24 , 25 Although oxytocin causes rhythmic contractions of the uterus, methylergonovine maleate stimulates uterine smooth muscle and uterine vascular α 1 -adrenergic receptors in a sustained manner, causing vasoconstriction and cessation of bleeding. Methylergonovine maleate is often considered the next agent to be administered after oxytocin. 23 The indications and contraindications for pharmacotherapy in postpartum hemorrhage are listed in Table 1 .

Medical Therapy for Postpartum Hemorrhage. *

Medication	Mechanism of Action	Route of Administration and Dose	Concerns and Contraindications	Adverse Effects
First-line therapy: oxytocin	Stimulates oxytocin receptors in the uterus	IV route, 10–40 IU/500–1000 ml of lactated Ringer’s solution; IM or IMM route, 5–10 IU for up to 4 doses	SIADH, hypotension	Rapid bolus administration may cause hyponatremia, hypotension, tachycardia, and arrhythmia
Second-line therapy
Methylergonovine maleate (ergot alkaloid)	Partial agonist or antagonist at serotoninergic, dopaminergic, -adrenergic receptors in the uterus	IM or IMM route, 0.2 mg every 2–4 hr, for a maximum of 5 doses; oral route, 0.2 mg every 6–8 hr for 2–7 days	Hypertension, cardiovascular disease (stroke, Renaud’s disease)	Elevated blood pressure, nausea, vomiting, myocardial infarction
Carboprost tromethamine (PGF )	PGF agonist in uterine myometrium	IM or IMM route, 250 g every 15–90 min for a maximum of 8 doses	Asthma, cardiovascular disease, hepatic disease, renal disease	Nausea, vomiting, and diarrhea
Adjunctive agents
Tranexamic acid	Diminishes the dissolution of hemostatic fibrin by plasmin, stabilizing clot in uterine vessels	IV route, 1 g (100 mg/ml) over a 10-min period; if bleeding persists after 30 min or stops and restarts within 24 hr after the first dose, a second dose may be administered	Contraindicated if known hypersensitivity to tranexamic acid, thromboembolic event during pregnancy, history of hypercoagulopathy	Headache, musculoskeletal pain, nausea, diarrhea
Recombinant factor VIIa	Activates clotting cascade by cleaving factor IX and factor X, which activates these factors and leads to activation of thrombin and fibrin	IV route, 50–100 g/kg (single dose)	Severe anemia, severe thrombocytopenia, hyperfibrinogenemia, allergy to mouse, hamster, or bovine proteins	Thromboembolic events, cerebrovascular infarcts, myocardial infarction
Treatment of uncertain usefulness: misoprostol	PGE agonist in the uterine myometrium	Sublingual, oral, or rectal route (sublingual route preferred), 600–1000 g in single dose; repeat doses not recommended	Sepsis, allergy to misoprostol, concurrent anticoagulant therapy, cardiovascular disease; efficacy is disputed	Nausea, vomiting, fever, diarrhea

If pharmacotherapy fails in the management of uterine atony, mechanical methods, including balloon tamponade ( Fig. 2A ) and uterine compression sutures ( Fig. 2B ), can be lifesaving. Balloon tamponade systems, such as the Bakri balloon, first described in 2001, 26 involve instilling fluid (to a maximum volume of approximately 500 ml) into an intrauterine balloon, with removal of the balloon up to 24 hours after insertion; the tamponade effect of the filled balloon is intended to stop or reduce intrauterine bleeding. 27 A 2020 systematic review and meta-analysis concluded that uterine balloon tamponade systems appear to be safe, 28 with a success rate of more than 85% in the management of postpartum hemorrhage.

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Panel A shows balloon tamponade (with a Bakri balloon), Panel B uterine compression sutures (B-Lynch sutures, placed according to the numbers, from 1 to 6), and Panel C uterine artery ligation.

Uterine compression sutures, also known as “brace sutures,” were first described in 1997 by B-Lynch and colleagues and were shown to be highly effective in controlling postpartum hemorrhage. 29 Since 1997, several other compression suture techniques have been described. 30 - 36 Some techniques involve sutures that enter the uterine cavity 34 and abut the anterior and posterior walls of the uterus, with a potential to increase the risk of uterine synechiae, but other techniques do not. 29 , 36 Several systematic reviews of case series have shown a combined success rate of more than 90% with the use of brace sutures in managing postpartum hemorrhage. 37 , 38 Uterine necrosis and intrauterine synechiae are possible complications of uterine compression procedures. 39 , 40 The frequency of successful pregnancy after management of postpartum hemorrhage with uterine compression sutures has ranged from 11 to 75%. 37

Uterine and vaginal packing has been used successfully in cases of postpartum hemorrhage, but it is not routinely recommended because of the potential for intrauterine infection. 41 Although a positive tamponade test (decreased bleeding with bimanual uterine compression involving a hand on the maternal abdomen to compress the uterine fundus from above and a hand in the vagina to compress from below) has not been rigorously studied in postpartum hemorrhage trials, it is a reasonable pretest to consider using before choosing uterine balloon placement or compression sutures. 42

In severe cases of postpartum hemorrhage, when pharmacologic therapy, uterine compression or tamponade, and other conservative measures have failed to control bleeding, surgical methods can be lifesaving. Bilateral uterine artery ligation ( Fig. 2C ) is an appropriate next step at the time of laparotomy. Described by Waters in 1952 43 and by O’Leary and O’Leary in 1966, 44 this surgical technique involves suture ligation of the uterine vessels on the lateral aspect of the lower uterine segment. If bilateral uterine artery ligation fails, the vessels of the utero-ovarian pedicle can be suture-ligated in a stepwise fashion (bilateral utero-ovarian artery ligation). Internal iliac artery ligation, initially described in 1964 by Burchell et al. for controlling postpartum hemorrhage, 45 is usually a suture ligation procedure of last resort, with a 50 to 60% success rate, but it has largely fallen out of favor because of the extent of surgical dissection that is necessary. 45 Hysterectomy (total or supracervical) for the control of postpartum hemorrhage can be a lifesaving procedure. 10

USE OF BLOOD PRODUCTS

Although there are no strict criteria for initiating blood transfusion in cases of postpartum hemorrhage, transfusion is typically begun when the estimated blood loss exceeds 1500 ml or when hemodynamic changes become apparent. 10 , 46 If the need arises, massive blood transfusion (defined as infusion of ≥10 units of packed red cells in a 24-hour period or ≥4 units of packed red cells within 1 hour) 47 is initiated. No data from randomized clinical trials provide the ratio for transfusing blood products in obstetrics 10 ; the obstetrical protocols for transfusion of packed red cells, fresh-frozen plasma, and platelets in a ratio of 6:4:1, 4:4:1, or 1:1:1 were derived from the trauma literature. 48 , 49 Treatment goals are to maintain the hemoglobin level at more than 8 g per deciliter, the fibrinogen level at more than 2 g per liter, the platelet count at more than 50,000 per microliter, and the activated partial-thromboplastin and prothrombin times at less than 1.5 times the normal values, on the basis of practical guidelines such as those established by the British Committee for Standards in Haematology. 50 In an observational study, thrombo-elastography or rotational thromboelastometry was recommended for maintaining adequate coagulation while managing severe postpartum hemorrhage. 51 Blood-product replacement therapy for the management of postpartum hemorrhage, when to administer it, and dosage recommendations are listed in Table 2 .

Blood-Product Replacement Therapy for Postpartum Hemorrhage.

Blood Product	Component Therapy	Dose	When to Administer
Packed red cells	Red cells	1 Unit is 450 ml in volume and is expected to increase the maternal hemoglobin level by 1 g/dl	If hemoglobin <7 or <8 g/dl (depending on local protocols and coexisting maternal conditions)
Fresh-frozen plasma	Plasma proteins, clotting factors (except platelets), fibrinogen, anticoagulants (proteins C and S)	1 Unit is approximately 250 ml in volume; a dose of 10–20 ml/kg will increase clotting factors by 10–20%	After every 1, 4, or 6 units of packed red cells (depending on local protocols) or if prothrombin time is prolonged (INR or aPTT >1.5 times the normal value)
Platelet concentrate	Platelets	1 Pack of pooled platelets	If platelet count <75,000/ l or after every 1, 4, or 6 units of packed red cells
Cryoprecipitate	Factor VIII, fibrinogen	2 Pools of cryoprecipitate	If fibrinogen <1 or <2 g/liter

PLACENTA ACCRETA SPECTRUM DISORDERS

The frequency of peripartum hysterectomy performed for the management of postpartum hemorrhage due to PAS disorders continues to rise with increased cesarean delivery rates. 52 There is insufficient evidence to determine the optimal time of delivery; however, the American College of Obstetricians and Gynecologists recommends planned cesarean delivery, with or without hysterectomy, at 34 weeks to 35 weeks 6 days of gestation in cases of PAS disorders, whereas the Royal College of Obstetricians and Gynaecologists 53 recommends delivery between 35 weeks and 36 weeks 6 days of gestation.

Cesarean hysterectomy in women with PAS disorders is a complex procedure. When performed by obstetricians and gynecologists with expertise in complex pelvic surgery, working in collaboration with other surgical specialties, such as vascular surgery, interventional radiology, urology, and hematology, cesarean hysterectomy has the potential to reduce maternal morbidity and mortality. 54 Both ureters may be stented before the procedure to facilitate their identification and reduce the risk of injury during the procedure, especially if extensive pelvic dissection is anticipated. 55 In women thought to be at very high risk for placenta percreta, placement of balloon catheters in the internal iliac arteries immediately before the procedure, with inflation immediately after delivery of the fetus, may reduce intraoperative bleeding. 55 Although definitive management of PAS disorders involves immediate hysterectomy with the placenta left in situ, some experts recommend expectant management and delayed hysterectomy in selected cases in order to minimize hemorrhage and the need for massive blood transfusion. 56 In planned cases of cesarean hysterectomy, a midline vertical incision should ideally be used, since it minimizes dissection of tissue planes that may bleed if coagulopathy develops and provides good visualization of the abdomen, uterine pedicles, and pelvis.

MANAGEMENT OF UTERINE INVERSION

Uterine inversion, a protrusion of the uterus through the vaginal orifice at the time of delivery, can cause postpartum hemorrhage and hypotension, which may be disproportionate to blood loss. The first step in management is immediate manual replacement of the uterus (with the placenta still in place). If this attempt is unsuccessful, relaxing the uterus with tocolytic agents (nitroglycerin, terbutaline, magnesium sulfate, or halothane) is an appropriate next step. 57 If replacing the uterus is still unsuccessful, laparotomy can be performed, followed by one of several techniques: reduction of the uterine inversion back into the abdomen by gentle upward traction with Allis clamps placed at both uterine cornua (Huntington’s method) 58 ; posterior longitudinal incision of the cervical ring, followed by gentle upward traction of the uterus with Allis clamps placed at both cornua (Haultain’s method) 59 ; or placement of a Silastic cup of a vacuum extractor on the fundus from above and use of negative pressure to restore the uterus back to its normal position (Antonelli’s method). 60 Once the uterus is replaced, uterotonic agents are administered to aid uterine contraction, and manual extraction of the placenta may be performed.

OTHER MANAGEMENT APPROACHES

A nonpneumatic antishock garment has been used in the treatment of hypovolemic shock from postpartum hemorrhage. The garment is worn to decrease blood flow in the aorta and increase venous return from the inferior vena cava, 61 making it an invaluable device in cases of hypovolemic shock to temporarily maintain blood pressure while awaiting definitive management. 62 If the patient’s condition is stable enough for the patient to be transported to the radiology suite and preservation of fertility is desired, uterine artery embolization (often as a supplement to intrauterine balloon tamponade) can be considered. The uterine artery embolization procedure involves injection of gelatin or polyvinyl alcohol particles into the uterine artery or the anterior division of the internal iliac arteries through the femoral arteries with the use of the Seldinger technique under fluoroscopic and ultrasonographic guidance. 63 Success rates in the control of postpartum hemorrhage range from 75 to 100%, 64 and pregnancy after uterine artery embolization has been reported in 43 to 48% of women. 65 , 66

SECONDARY POSTPARTUM HEMORRHAGE

Secondary postpartum hemorrhage accounts for approximately 1 to 2% of cases. 10 The causes include uterine subinvolution, retained products of conception, endomyometritis, uterine vascular disorders such as arteriovenous malformations, and coagulopathies such as von Willebrand disease. 10 Management of secondary postpartum hemorrhage is directed at correcting the suspected cause of the hemorrhage. 10

COMPLICATIONS OF POSTPARTUM HEMORRHAGE

In the immediate postpartum period, complications of postpartum hemorrhage include hypovolemic shock from massive blood loss, disseminated intravascular coagulopathy, acute renal failure, hepatic failure, and complications of blood transfusion, including transfusion-related acute lung injury, acute respiratory distress syndrome, transfusion-associated circulatory overload, and death. 10 , 67 Late complications such as Sheehan’s syndrome (pituitary necrosis and panhypopituitarism) and infertility may also occur. 10 , 67 It is critical to manage postpartum hemorrhage promptly and adequately in order to minimize the risk of these complications.

PREVENTION OF POSTPARTUM HEMORRHAGE

Preventive measures for postpartum hemorrhage should be undertaken when possible, ideally beginning before conception, with identification of women at high risk and interventions to increase iron stores and hemoglobin levels when necessary. Screening women during pregnancy and labor for risk factors for postpartum hemorrhage can be useful in the preparation for delivery, including identifying an appropriate location for delivery ( Table 3 ). Blood typing and screening are important for women at moderate risk for postpartum hemorrhage, whereas those at high risk should undergo blood typing and cross-matching of at least 2 units of packed red cells in anticipation of possible postpartum hemorrhage.

Classification of Postpartum Hemorrhage Risk and Potential Need for Transfusion.

Risk Level (Preparation for Transfusion)	Defining Factors
Low risk (having blood specimen available in case blood products become needed)	No previous uterine incision Singleton pregnancy ≤4 Previous vaginal deliveries No known bleeding disorders No history of postpartum hemorrhage
Medium risk (blood typing and screening)	Prior cesarean delivery or uterine surgery Multiple gestation <4 Previous vaginal deliveries Chorioamnionitis History of postpartum hemorrhage Large uterine fibroids Fetal death Estimated fetal weight <4000 g Morbid obesity (body-mass index <40)
High risk (blood typing and cross-matching of at least 2 units of packed red cells)	Placenta previa or low-lying placenta Suspected placenta accreta spectrum Hemoglobin >10 mg/dl and other risk factors Platelet count >100,000/ l Active bleeding on admission Known coagulopathy

Active management of the third stage of labor, including prophylactic use of uterotonic agents and controlled umbilical cord traction, has been shown to reduce blood loss during this stage 68 and to reduce the risk of postpartum hemorrhage by approximately 66%, as compared with expectant management. 68 However, controlled umbilical cord traction has limited benefits in cases of severe postpartum hemorrhage and may lead to uterine inversion if the management team is inexperienced. 69 Another method, early cord clamping, can result in decreased neonatal iron stores and an increased risk of infant anemia 70 and therefore is no longer recommended as a component of active management of the third stage. Uterine massage, although a mainstay of management, has not been consistently shown to be beneficial in the prevention of postpartum hemorrhage. 22

PREDICTION OF POSTPARTUM HEMORRHAGE

Identification of patients at risk for postpartum hemorrhage, early intervention with the use of standardized protocols, and a coordinated, team-based approach once hemorrhage occurs have been shown to decrease maternal morbidity and mortality. 7 , 71 Prenatal diagnosis of PAS disorders in women who have undergone prior uterine surgery is invaluable for surgical planning. 72 Although obstetrical ultrasonography (color Doppler or three-dimensional power Doppler) and magnetic resonance imaging (MRI) have similar diagnostic accuracy in detecting PAS disorders (sensitivity of approximately 94% and specificity of approximately 84%), 73 MRI can complement ultrasonography in assessing the depth of uterine muscular and parametrial invasion. 72 Categorization of patients on admission to labor and delivery into risk strata (low, medium, or high risk) ( Table 3 ) may identify up to 85% of pregnant women at risk for postpartum hemorrhage, 74 with negative predictive values of more than 98%. 71 , 75 In a case–control study, Nyfløt et al. showed that prolonged active labor (duration >12 hr) is associated with an increased risk of severe postpartum hemorrhage. 76 Risk stratification can help the multidisciplinary team to be alert to a patient’s risk and make informed choices about the need for and availability of intravenous access, uterotonic medications, blood products, and additional personnel.

CONCLUSIONS

Postpartum hemorrhage remains a clinically significant cause of maternal complications and death; worldwide, one woman dies from postpartum hemorrhage every 7 minutes. Therefore, prompt identification of patients who are at risk for postpartum hemorrhage, routine active management of the third stage of labor, expeditious assessment of blood loss, appropriate patient monitoring, and management of postpartum hemorrhage are important. 77

No potential conflict of interest relevant to this article was reported.

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Postpartum Hemorrhage

Simpson, Kathleen Rice PhD, RNC, FAAN

Kathleen Rice Simpson is a Perinatal Clinical Nurse Specialist, St. John's Mercy Medical Center, St. Louis, MO, and an Editorial Board Member of MCN. Dr. Simpson can be reached via e-mail at [email protected]

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Postpartum Hemorrhage. Simpson, Kathleen Rice PhD, RNC, FAAN. Author Information. Kathleen Rice Simpson is a Perinatal Clinical Nurse Specialist, St. John's Mercy Medical Center, St. Louis, MO, and an Editorial Board Member of MCN. Dr. Simpson can be reached via e-mail at [email protected] MCN, The American Journal of Maternal/Child Nursing 35 ...

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Postpartum Hemorrhage

DEFINITION, CAUSES, AND RISK FACTORS

MANAGEMENT OF POSTPARTUM HEMORRHAGE

MANAGEMENT OF RETAINED PLACENTAL TISSUE

MANAGEMENT OF GENITAL TRACT LACERATIONS

MANAGEMENT OF UTERINE ATONY

USE OF BLOOD PRODUCTS

PLACENTA ACCRETA SPECTRUM DISORDERS

MANAGEMENT OF UTERINE INVERSION

OTHER MANAGEMENT APPROACHES

SECONDARY POSTPARTUM HEMORRHAGE

COMPLICATIONS OF POSTPARTUM HEMORRHAGE

PREVENTION OF POSTPARTUM HEMORRHAGE

PREDICTION OF POSTPARTUM HEMORRHAGE

CONCLUSIONS

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Postpartum Hemorrhage

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