Postpartum Hemorrhage

1. Ahamed Mubin

2. Rysbaeva Aiganysh Zhoomartovna

(1. Student, International Medical Faculty, Osh State University, Osh, Kyrgyzstan.

2. Teacher, Department of Obstetrics, Gynecology and Surgical Disciplines, International Medical Faculty, Osh State University, Osh, Kyrgyzstan.)

Abstract

Postpartum hemorrhage (PPH) remains a leading cause of maternal morbidity and mortality worldwide. Definitions vary, but modern guidance emphasizes both objective blood loss and the presence of hemodynamic compromise. Objectives: To provide a concise, evidence-based review of PPH including definitions, epidemiology, etiology, pathophysiology, risk factors, clinical presentation, diagnostics, acute and definitive management (medical, interventional, surgical), transfusion strategies, prevention, postpartum care and prognosis. Methods: Narrative synthesis of international guidelines and contemporary reviews (WHO, ACOG, RCOG, FIGO, NCBI/StatPearls). Conclusions: Rapid recognition, standardized protocols (bleeding bundles), early uterotonic use, prompt resuscitation, use of tranexamic acid (TXA) when indicated, and escalation to minimally invasive or surgical bleeding control are central to reducing morbidity and mortality. Simulation training, preparation (emic kits and blood-availability planning), and clear escalation pathways markedly improve outcomes.

Introduction

Postpartum hemorrhage (PPH) is one of the most important obstetric emergencies. Historically defined by a quantitative blood-loss threshold (≥500 mL after vaginal birth; ≥1,000 mL after cesarean), contemporary practice recognizes that these thresholds alone under-estimate clinically important hemorrhage and that PPH should also be defined by hemodynamic instability or the need for transfusion or operative intervention. PPH may be classified as primary (within 24 hours of birth) or secondary (from 24 hours to 6–12 weeks postpartum) and has multiple etiologies. Despite improvements in obstetric care, PPH remains a major cause of maternal death worldwide, particularly in low- and middle-income countries.

Definitions and Classification

Traditional quantitative definitions

Primary Postpartum Hemorrhage (PPH): defined as blood loss ≥500 mL after a vaginal delivery or ≥1,000 mL after a cesarean section, occurring within the first 24 hours postpartum. This traditional quantitative definition is widely cited in obstetric literature and clinical references including NCBI/StatPearls.

Severe Postpartum Hemorrhage: Commonly defined as blood loss exceeding 1,000 mL, regardless of delivery mode, or any amount of bleeding that results in signs of hemodynamic instability (hypotension, tachycardia, altered mental status, poor perfusion). This functional definition aligns with modern NCBI guidance, emphasizing clinical impact over volume alone.

Contemporary clinical definitions

ACOG defines PPH as cumulative blood loss ≥1,000 mL or blood loss with signs/symptoms of hypovolemia within 24 hours after birth (this definition emphasizes clinical impact rather than an arbitrary volume alone).

Timing: Primary (Immediate) PPH: Occurs within the first 24 hours after delivery and represents the most common form of postpartum hemorrhage. It is often associated with causes such as uterine atony, trauma, or retained placental tissue. Secondary (Late) PPH: Occurs from 24 hours up to 6–12 weeks postpartum. Common etiologies include retained products of conception, uterine infection (endometritis), and subinvolution of the placental site.

Etiologic classification (the “Four T’s”)

1.    Tone — uterine atony (most common).

2.    Tissue — retained placenta, clots, invasive placenta.

3.    Trauma — genital tract lacerations, uterine rupture.

4.    Thrombin — coagulopathy (pre-existing or acquired).

Epidemiology and Significance

PPH accounts for a substantial proportion of maternal deaths globally; exact figures vary by region and health system. Mortality is highest where access to emergency obstetric care and blood transfusion is limited. Improvements in recognition and management (transfusion, hysterectomy when needed) have reduced mortality in high-resource settings, but PPH remains a leading cause of maternal morbidity and mortality worldwide.

Pathophysiology

Postpartum hemorrhage arises from one or more of the classic “4 T’s”: Tone, Tissue, Trauma, and Thrombin. These mechanisms collectively represent the vast majority of PPH cases, with uterine atony being the predominant cause.

1.Uterine Atony (Tone): Uterine atony—defined as the failure of the uterus to effectively contract following delivery—is the most common cause of primary PPH.
Inadequate myometrial contraction results in persistent bleeding from the low-resistance uteroplacental vessels. Risk factors include overdistended uterus (multiple gestation, polyhydramnios, macrosomia), prolonged or rapid labor, chorioamnionitis, and use of uterine relaxants. Without timely intervention, atony can progress rapidly to severe hemorrhagic shock.

2. Retained Products of Conception (Tissue): Retained placental fragments, membranes, or blood clots mechanically impair myometrial contraction and prevent proper involution of the placental bed. Retained tissue is a major contributor to secondary (late) PPH, occurring days to weeks after delivery, and may also predispose to infection and subinvolution of the uterus.

3. Genital Tract Trauma (Trauma): Trauma to the cervix, vagina, perineum, or uterine structures can produce significant hemorrhage even when the uterus is well contracted. Lacerations may result from instrumental delivery, precipitous labor, macrosomic fetuses, or episiotomy. Uterine rupture or inversion, though less common, can result in catastrophic bleeding requiring immediate surgical management.

4. Coagulopathies (Thrombin): PPH may arise from congenital or acquired coagulation disorders. Congenital causes: von Willebrand disease, factor deficiencies. Acquired coagulopathies: disseminated intravascular coagulation (DIC) associated with placental abruption, severe preeclampsia/HELLP syndrome, amniotic fluid embolism, sepsis, and massive transfusion leading to dilutional coagulopathy. Coagulopathies impair the formation of stable clots and complicate hemorrhage control.

5. Placenta Accreta Spectrum and Placenta Previa: Placenta accreta spectrum (accreta, increta, percreta) involves abnormal adherence of the placenta to or through the myometrium, preventing normal separation at delivery. Attempts at placental removal can trigger massive, life-threatening hemorrhage. Similarly, placenta previa—where the placenta overlies the cervical os—presents high bleeding risk due to disruption of the highly vascular lower uterine segment. Physiologically, pregnancy produces hypervolemia and hypercoagulability; however, massive bleeding can rapidly overwhelm compensatory mechanisms leading to shock, DIC, organ hypoperfusion and death if not controlled.

Risk Factors

Maternal history and labor factors: Previous PPH, uterine overdistension (multiple gestation, polyhydramnios, macrosomia), prolonged/augmented labor (oxytocin use), chorioamnionitis, high parity, retained placenta, preeclampsia, coagulation disorders, cesarean delivery, placenta previa, placenta accreta/increta/percreta, instrumental delivery and large lacerations.

Clinical Presentation

• Early signs: excessive vaginal bleeding, failure of uterus to firm up after delivery, tachycardia, hypotension, pallor, oliguria, altered mental status.

• Quantification challenges: visual estimation notoriously underestimates blood loss. Use calibrated collection drapes and weigh soaked materials when possible; monitor hemodynamics and trends (pulse, blood pressure, urine output, mental status). 

Diagnosis and Assessment

1.    Immediate evaluation: ABCs (airway, breathing, circulation), call for help, assign roles, activate hemorrhage protocol/obstetric emergency team.

2.    Measure blood loss objectively where possible (calibrated drapes, weighing sponges).

3.    Rapid assessment for causes (the 4 T’s) — inspect uterus, examine for lacerations, assess placenta completeness, review labor events.

4.    Baseline investigations: CBC, coagulation profile (PT/INR, aPTT), fibrinogen, blood type and crossmatch (or type & screen), serum electrolytes, arterial blood gas if concern for lactic acidosis.

5.    Point-of-care tests: bedside hemoglobin, thromboelastography (TEG)/ROTEM when available to guide blood component therapy.

Immediate Management Principles (Resuscitation First)

• Simultaneous resuscitation and attempts to control bleeding (do not delay one for the other).

• Call for help — senior obstetrician, anesthesiologist, blood bank, theatre team.

• Airway/Breathing: oxygen, support as needed.

• Circulation: large-bore IV access (two 14–16G if possible), rapid infusion of warmed isotonic crystalloids, consider early blood product activation. Isotonic crystalloids are recommended over colloids for initial resuscitation.

• Uterine massage and manual removal of retained products if indicated.

• Uterotonics: oxytocin (IV bolus followed by infusion) as first line; if inadequate, add ergometrine (unless hypertensive), carboprost (prostaglandin F2α) if not asthmatic, and misoprostol where other agents are unavailable. Timely uterotonic use is crucial. 

Medical Management

Uterotonics (first-line and adjuncts)

• Oxytocin: first line (IV bolus/infusion).

• Ergometrine/ergonovine: effective but contraindicated in severe hypertension/coronary disease.

• Carboprost tromethamine (PGF2α): for refractory atony (avoid in asthma).

• Misoprostol (PGE1): useful where refrigeration/other agents limited — variable routes (sublingual, rectal).

Tranexamic acid (TXA)

• TXA is an antifibrinolytic shown to reduce death due to bleeding if given early (within 3 hours) in PPH and is recommended in treatment bundles for PPH (but not universally for prevention). Dose commonly used: 1 g IV over 10 minutes; a second 1 g may be given if bleeding continues after 30 minutes or reoccurs. Early administration is emphasized in WHO/FIGO guidance.

Mechanical and Interventional Measures

1.    Uterine balloon tamponade (UBT): a uterine balloon (commercial or condom-catheter) can control atonic PPH when uterotonics insufficient, and is recommended in appropriate settings as a temporizing or definitive measure. Success depends on cause and setting.

2.    Compression sutures (e.g., B-Lynch): surgical uterine compression for atony when less invasive measures fail.

3.    Uterine artery ligation or internal iliac (hypogastric) artery ligation: surgical bleeding control preserving uterus where possible.

4.    Angiographic embolization: arterial embolization to control bleeding in centers with interventional radiology. Suitable when patient is stable enough for transfer or procedure and resources are available.

5.    Peripartum hysterectomy: definitive life-saving procedure for uncontrolled hemorrhage (placenta accreta spectrum, uterine rupture, severe uncontrolled bleeding).

Transfusion and Hemostatic Management

• Massive transfusion protocols (MTPs) adapted for obstetrics should be available. Early blood product transfusion is associated with reduced morbidity. Use balanced resuscitation with RBCs, plasma and platelets guided by labs and point-of-care coagulation tests where possible.

• Fibrinogen is crucial — low fibrinogen predicts severe PPH; consider cryoprecipitate or fibrinogen concentrate when fibrinogen is low.

• Blood bank coordination: O-negative emergency units may be used while crossmatch is arranged; communicate anticipated needs early.

Prevention Strategies

Active management of the third stage of labor (AMTSL): includes prophylactic uterotonic (oxytocin), controlled cord traction, and uterine massage as per guidelines — shown to reduce PPH incidence. WHO and national guidelines recommend uterotonic prophylaxis for all women. Risk assessment and preparedness for higher-risk deliveries (placenta previa/accreta, prior uterine surgery) — plan for delivery in higher-level facilities with blood access and multidisciplinary teams.

• Avoidance of unnecessary interventions that increase risk (unindicated induction/augmentation) and careful management of the third stage.

• Simulation training and protocols (PPH bundles, checklists) improve team performance and outcomes and are recommended by major bodies. 

Postpartum Care and Monitoring

• Monitor vitals, bleeding, uterine tone, uterine size, lochia, urine output and hemoglobin trends. Provide iron therapy and consider additional follow-up for anemia. Provide counseling on signs of delayed bleeding and ensure timely access to care. 

Complications and Prognosis

Postpartum hemorrhage is associated with a wide spectrum of short-term and long-term complications, many of which carry significant morbidity and mortality, particularly in resource-limited settings. The severity of complications is influenced by the rapidity of blood loss, timeliness of intervention, and availability of transfusion and surgical services.

Short-Term Complications

1. Hypovolemic Shock: Uncontrolled hemorrhage rapidly leads to decreased circulating blood volume, reduced organ perfusion, and hemodynamic instability. Severe hypovolemia may progress to multi-organ dysfunction if not promptly corrected.

2. Disseminated Intravascular Coagulation (DIC): Massive bleeding, placental abruption, or amniotic fluid embolism can precipitate consumptive coagulopathy. DIC results in widespread clot formation followed by depletion of platelets and coagulation factors, exacerbating hemorrhage and complicating management.

3. Acute Kidney Injury (AKI): Renal ischemia due to prolonged hypotension may lead to acute tubular necrosis. Severe cases require dialysis and can contribute to extended hospitalization.

4. Need for Hysterectomy: Life-saving peripartum hysterectomy may be required when bleeding is refractory to uterine-sparing interventions, particularly in placenta accreta spectrum or uncontrolled atony. This results in immediate loss of fertility.

5. Transfusion-Related Complications: Massive transfusion protocols carry risks including hemolytic reactions, transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), and electrolyte disturbances such as hypocalcemia or hyperkalemia.

6. Acute Respiratory Distress Syndrome (ARDS): Severe hemorrhage, massive transfusion, or sepsis may trigger ARDS, characterized by non-cardiogenic pulmonary edema and respiratory failure requiring ventilatory support.

7. Intensive Care Unit (ICU) Admission: women with severe PPH often require ICU monitoring for hemodynamic stabilization, ventilatory support, correction of coagulopathy, and close observation for further complications.

Long-Term Complications

1. Anemia: Chronic iron-deficiency anemia is common after significant blood loss and may persist for weeks to months postpartum. This can lead to fatigue, decreased functional capacity, and impaired maternal-infant bonding.

2. Psychological Impact: PPH is a traumatic obstetric emergency and may result in postpartum depression, anxiety, or post-traumatic stress disorder (PTSD). Psychological support and counseling are essential components of post-event care.

3. Reproductive Consequences: Women who undergo hysterectomy lose future reproductive potential. Even when fertility is preserved, intrauterine adhesions from surgical or manual interventions may affect subsequent pregnancy outcomes.

Prognosis

Prognosis in postpartum hemorrhage is directly correlated with early recognition and timely intervention. Access to skilled birth attendants, rapid uterotonic administration, availability of blood products, and the capacity for operative management (e.g., uterine artery ligation, hysterectomy) significantly reduce maternal mortality. In well-resourced settings, mortality is rare; however, in low-resource environments where delays in transportation, transfusion, and surgical care are common, PPH remains a leading cause of maternal death.

Special Situations

• Placenta accreta spectrum: anticipate massive hemorrhage; delivery in a tertiary center with planned cesarean hysterectomy and blood resources is recommended.

• Coagulopathy (e.g., abruption, amniotic fluid embolism, severe preeclampsia): requires parallel management of the hemostatic disorder and bleeding control, often with aggressive transfusion and critical care support.

• Low-resource settings: focus on AMTSL, uterotonics availability (including misoprostol), UBT with low-cost devices, rapid referral, training and blood-supply strengthening. WHO consolidated guidance provides tailored recommendations. 

Algorithms and Bundles (Summary of Recommended Approach)

1.    Immediate recognition → call for help → resuscitate (ABCs) + uterine massage + uterotonic(s).

2.    Simultaneously identify cause (4 T’s).

3.    If bleeding persists: escalate to second-line uterotonics, uterine balloon tamponade, transfusion activation, prepare for theatre.

4.    If still uncontrolled: compression sutures, arterial ligation or interventional radiology embolization where available. Proceed to hysterectomy if life-threatening and uncontrollable.

5.    Use TXA early (within 3 hours) for treatment of PPH.

6.    Follow MTP and use goal-directed blood component therapy guided by labs/TEG.

 Case Vignette (Illustrative)

Case: A 29-year-old primipara delivers vaginally after augmentation for slow labour. Immediately postpartum, the uterus is boggy, and heavy bleeding continues despite uterine massage. Estimated blood loss in 10 minutes exceeds 600 mL, patient becomes tachycardic (HR 125) and systolic BP falls to 85 mmHg.

Management steps:

1.    Call for help (obstetric senior, anesthesiology, blood bank).

2.    Two large-bore IV lines, begin crystalloids, oxygen.

3.    Continue uterine massage; start oxytocin infusion and give additional uterotonic.

4.    Activate hemorrhage protocol, send labs (CBC, coag. panel, fibrinogen), type & crossmatch, consider immediate crossmatch-negative units if required.

5.    If bleeding persists despite uterotonics and uterus remains atonic, insert uterine balloon tamponade and give TXA 1 g IV.

6.    Escalate to theatre for compression sutures or uterine artery ligation if tamponade unsuccessful; prepare for hysterectomy if uncontrolled.

7.    Use MTP with balanced transfusion guided by labs/TEG.

Research Gaps & Future Directions

• Optimization of prediction models for PPH risk and individualized prophylaxis.

• Refinement of algorithms for TXA use in prevention vs treatment subgroups.

• Improved access to blood and interventional radiology in low-resource settings.

• Trials comparing low-cost uterine tamponade devices and implementation research on system approaches (bundles, team training).

Conclusion

PPH is a common, potentially life-threatening obstetric emergency. Early recognition, immediate resuscitation, prompt uterotonic therapy, timely use of tranexamic acid, activation of hemorrhage protocols and escalation to mechanical, interventional or surgical measures when needed form the backbone of effective management. Systems-level preparedness — standardized protocols, simulation, and access to blood and higher care — is as important as individual clinician actions in reducing PPH-related morbidity and mortality.

Practical Recommendations (Short Checklist)

• Active management of third stage (oxytocin prophylaxis). (World Health Organization)

• Have a clear, practiced hemorrhage protocol and hemorrhage cart. (PMC)

• Use objective blood-loss measurement where possible. (World Health Organization)

• Administer TXA early for treatment of significant PPH (within 3 hours). (NCBI)

• Consider uterine balloon tamponade and surgical/interventional options early if bleeding persists. (sogvzla.org)

References (key guidance and reviews)

1.    ACOG Practice Bulletin No. 183, Postpartum Hemorrhage. Obstet Gynecol. 2017. (ACOG)

2.    WHO — Recommendations for the prevention and treatment of postpartum hemorrhage; consolidated PPH guidance. (2012–2021 updates). (World Health Organization)

3.    FIGO Working Group. FIGO recommendations on the management of postpartum hemorrhage (2022). (PMC)

4.    RCOG Green-top Guideline No. 52: Prevention and Management of Postpartum Haemorrhage. (2016). (RCOG)

5.    StatPearls / NCBI Bookshelf — Postpartum Hemorrhage (2024 review). (NCBI)