Evolving perspectives on blood transfusion in obstetric hemorrhage: a narrative review

Abstract

Globally, postpartum hemorrhage is still among the most significant factors in preventable maternal morbidity and mortality. Although early recognition and intervention have improved with advances in obstetric care, transfusion practices are often based on fixed thresholds that may not accurately reflect the unique physiological changes that occur during pregnancy or in the clinical context of acute bleeding. In this narrative review, we propose a phase-specific, patient-centered transfusion strategy for the preoperative, intraoperative, and postpartum periods. Key components of this strategy include proactive anemia correction during pregnancy, timely administration of uterotonic agents, early implementation of antifibrinolytic therapy, such as tranexamic acid within 3 hours of bleeding onset, and appropriate activation of massive transfusion protocols when severe hemorrhage is ongoing. Clinical decision-making should be based on continuous assessment of maternal status, rather than on static hemoglobin values. Point-of-care coagulation monitoring, including thromboelastography and rotational thromboelastometry, can allow rapid identification of coagulopathy and support goal-directed transfusion. For high-risk populations, such as those with placenta accreta spectrum or those who decline allogeneic transfusion, strategies can include intraoperative cell salvage and non-blood interventions. Balanced transfusion approaches, using equal ratios of red blood cells, plasma, and platelets, at an early stage have demonstrated improved outcomes. Standardized protocols, multidisciplinary collaboration, and the integration of emerging technologies may further improve safety, minimize unnecessary transfusions, and promote consistency of care in the management of obstetric hemorrhage.

Introduction

Globally, obstetric hemorrhage remains a leading cause of maternal mortality. It often results in hypovolemic shock, coagulopathy, multi-organ failure, or emergency hysterectomy [1]. Postpartum hemorrhage (PPH) can cause rapid hemodynamic collapse; thus, immediate recognition and a coordinated multidisciplinary response is requisite [1,2]. PPH is particularly concerning because it affects physiologically vulnerable young women who are otherwise healthy, highlighting the potential for severe outcomes even in low-risk individuals. Even short delays in intervention may lead to death, infertility, or psychological trauma [3,4]. Pregnancy-induced cardiovascular changes can mask early signs of hypoperfusion, rendering standard vital signs unreliable [4–7]. Objective tools, such as the Obstetric Shock Index (OSI) and quantitative blood loss (QBL) measurement, are essential for timely diagnosis of and intervention for PPH [1,2,4–6].

Effective management of PPH includes targeted hemostatic resuscitation with early administration of uterotonics, tranexamic acid (TXA), and blood component therapy, guided by laboratory or viscoelastic testing [7,8]. Rapid implementation of massive transfusion protocols (MTPs), with attention to fibrinogen and coagulopathy, is critical [7,9].

In this review, we present a transfusion framework for obstetric hemorrhage that is structured across clinical phases and is aligned with maternal physiology to promote evidence-based and individualized patient care.

Definition and etiology of PPH

PPH is among the most common obstetric complications and is a major contributor to maternal morbidity and mortality worldwide [10]. Primary PPH is defined as blood loss exceeding 500 ml within 24 hours [11]. Severe PPH is defined as ongoing blood loss exceeding 1000 ml or any blood loss accompanied by clinical signs of hypovolemia [11]. Massive life-threatening PPH is defined as ongoing blood loss exceeding 2500 ml or the presence of hypovolemic shock [11]. PPH affects approximately 1%–10% of all deliveries globally, although reported rates vary significantly depending on the population studied, clinical definitions used, and methods of blood loss surveillance [10]. Delay of intervention for PPH can result in adverse outcomes, such as unplanned hysterectomy, intensive care unit admission, and maternal death [7,12].

Multiple factors contribute to the risk of PPH development, including uterine atony; abnormal placental implantation, such as placenta previa or placenta accreta spectrum (PAS); uterine rupture; retained placenta; and coagulopathies [1,7,13,14]. Additional maternal and obstetric factors, such as advanced maternal age, obesity, prior cesarean delivery, multifetal pregnancy, and induction of labor, have also been identified as significant contributors to PPH risk [15–17]. Early recognition and stratification of these risk factors are essential for the prevention of PPH and tailoring of hemorrhage response protocols to the institutional capabilities and patient-specific needs [15].

Physiological changes in pregnancy and their impact on transfusion strategy

Hemodynamic and hematologic adaptations during pregnancy

Pregnancy involves significant hemodynamic and hematologic adaptations to support fetal development and to prepare for delivery. These adaptations directly influence transfusion strategies in cases of obstetric hemorrhage (Table 1). During pregnancy, plasma volume increases by approximately 40%–50%, outpacing the increase in red blood cell (RBC) mass by 20%–30% and resulting in physiological dilutional anemia [7,18,19]. This adaptation promotes uteroplacental perfusion by reducing blood viscosity but also delays the clinical recognition of blood loss. Moreover, cardiac output increases by 30%–50% due to elevated stroke volume and increased maternal heart rate [18,19]. This physiological enhancement may obscure the early signs of hypovolemia, as the maternal heart rate and blood pressure can remain within normal ranges even in the presence of significant blood loss. Furthermore, systemic vascular resistance decreases by 20%–30%, contributing to a lower baseline blood pressure during pregnancy, which further complicates the early detection of volume depletion [18].

Table 1.

Physiological Adaptations during Pregnancy Relevant to Transfusion Management in Obstetric Hemorrhage

Physiological parameter	Change during pregnancy	Transfusion-related clinical implications	Recommended management strategy
Plasma volume	↑ 40%–50%	Dilutional anemia; delayed detection of blood loss	Avoid fixed hemoglobin thresholds; individualized assessment
RBC mass	↑ 20%–30%	Physiological anemia despite increased RBC mass	Preoperative anemia screening; optimize RBC mass (iron therapy, erythropoietin)
Coagulation factors	↑ Fibrinogen (50%–100%), factors VII, VIII, X, vWF	Hypercoagulable state; rapid factor depletion during severe bleeding	Early fibrinogen replacement; consider ROTEM/TEG-guided protocols
Platelets	Slight decrease (gestational thrombocytopenia)	Early platelet dysfunction; impaired coagulation in severe hemorrhage	Platelet function monitoring; early platelet transfusion when indicated
Cardiac output	↑ 30%–50% (stroke volume, heart rate)	Compensated initial response; masking of early hemorrhage symptoms	Use advanced monitoring (shock index, lactate); avoid reliance on HR and BP alone
SVR	↓ 20%–30%	Lower baseline BP; masking early hypovolemic signs	Monitor closely; recognize subtle changes promptly
Uterine blood flow	~20% of cardiac output	High sensitivity to blood loss; rapid fetal compromise	Early recognition of maternal hypovolemia; prompt transfusion and resuscitation

RBC: red blood cell, vWF: von Willebrand factor, ROTEM: rotational thromboelastometry, TEG: thromboelastography, HR: heart rate, BP: blood pressure, SVR: systemic vascular resistance.

Hematologic adaptations during pregnancy include marked elevation in coagulation factors, most notably fibrinogen levels, which can increase by 50%–100%, as well as higher concentrations of von Willebrand factor and factors VII, VIII, and X, establishing a physiological hypercoagulable state [18,19]. Although this is protective during normal pregnancy, these factors can be rapidly depleted during hemorrhage, which necessitates timely and targeted replacement therapy that is guided by viscoelastic assays, such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM) [20–22]. In parallel, the modest decline in platelet count leads to gestational thrombocytopenia, which can compromise effective hemostasis in severe bleeding [19,23].

With advancing pregnancy, approximately 20% of the maternal cardiac output is directed to the uterus; thus, the uteroplacental circulation is highly susceptible to volume loss [24]. Even moderate hemorrhage can quickly compromise fetal oxygenation and maternal stability [18,24]. These physiological changes underscore the need for dynamic transfusion strategies that are based on vigilant monitoring and individualized thresholds, rather than on static laboratory values.

Limitations of conventional indicators and role of viscoelastic testing

Standard clinical indicators, such as maternal blood pressure, heart rate, and hemoglobin (Hb) concentration, may remain within normal ranges during the early phases of obstetric hemorrhage. This masking is due to physiological compensatory mechanisms and fluid redistribution, which can potentially delay the detection of tissue hypoperfusion [18,21]. Conventional coagulation tests, such as prothrombin time (PT), activated partial thromboplasmin time (aPTT), and international normalized ratio (INR), are also limited in the setting of acute obstetric bleeding. These tests are plasma-based, time-consuming, and cannot evaluate the dynamic interaction between platelets and fibrin, often resulting in delayed or insufficient hemostatic interventions [21,25,26].

These limitations are increasingly addressed by viscoelastic assays. These assays provide rapid, dynamic evaluation of whole-blood clot formation and strength and have been incorporated into obstetric hemorrhage management protocols in many institutions (The ROTEM/TEG parameters and interpretation are discussed later in this review). Moreover, to address the abovementioned limitations, additional markers, such as elevated serum lactate levels and altered mental status, are increasingly included to assess perfusion adequacy in clinical practice [27].

Preoperative phase: transfusion planning and anemia management

Effective preoperative transfusion planning is essential for obstetric patients who are at increased risk of massive hemorrhage, particularly those with conditions such as placenta previa, multiple prior cesarean deliveries, PAS, or pre-existing hematological disorders. In these patients, optimal outcomes depend on timely risk identification; early coordination among obstetricians, anesthesiologists, and transfusion medicine specialists; and proactive logistical planning [17]. Such planning includes type and screen testing, antibody identification, and early communication with blood banks to ensure the availability of compatible blood products. In cases where high-volume blood loss or surgical complexity is anticipated, MTP implementation should be arranged in advance to facilitate a rapid and effective hemostatic response [17,28,29]. In Table 2, a comprehensive overview of preoperative management strategies for both obstetric and non-obstetric patients, including transfusion protocols and non-blood interventions, such as anemia correction, risk stratification, and logistical planning for anticipated blood loss is presented.

Table 2.

Preoperative Blood and Non-blood Strategies in Obstetric vs Non-obstetric Patients

Management strategy	Obstetric	Non-obstetric
Anemia correction	IV iron (ferric carboxymaltose 1000 mg IV) if Hb 8–10.5 g/dl at 28–32 weeks; ESA if no response after 2–3 weeks.	Oral iron for Hb 8–10 g/dl; IV iron if Hb < 8 g/dl or if surgery is planned within 2 weeks; ESA for refractory cases.
Preoperative transfusion	RBC transfusion if Hb < 8 g/dl or in case of hemodynamic instability; prioritize before high-risk deliveries (PAS, previa).	RBC transfusion if Hb < 8 g/dl or in case of symptomatic anemia before major surgery.
Risk stratification	Mandatory hemorrhage risk assessment (PAS, previa); crossmatch if EBL > 1000 ml anticipated.	Bleeding risk assessed by surgery type; crossmatch if EBL > 500 ml anticipated.
Blood product preparation	Crossmatch 2–4 RBC units; arrange cell salvage in case of high hemorrhage risk.	Routine crossmatch if EBL > 500 ml; arrange MTP readiness for high-risk surgeries.

IV: intravenous, Hb: hemoglobin, ESA: erythropoiesis-stimulating agent, RBC: red blood cell, PAS: placenta accreta spectrum, EBL: estimated blood loss, MTP: massive transfusion protocol.

Risk stratification and institutional tools

Although no universally accepted risk stratification model exists, institution-specific scoring systems can facilitate allocation of transfusion resources and can guide clinical decisions [30]. Examples include the California Maternal Quality Care Collaborative toolkit and the Association of Women’s Health, Obstetric, and Neonatal Nurses risk assessment tool, both of which stratify patients based on surgical history, placental abnormalities, and coagulation disorders [30–32]. These tools facilitate anemia correction, early blood product preparation, and customized transfusion planning.

International guidelines for preoperative anemia management

International guidelines, including those of the World Health Organization (WHO), National Institute for Health and Care Excellence (NICE), American College of Obstetricians and Gynecologists (ACOG), and Network for the Advancement of Patient Blood Management, Hemostasis, and Thrombosis (NATA) consensus, advocate timely screening and appropriate management of maternal anemia during the third trimester [11,33–35].

When Hb levels fall below 10 g/dl, particularly in patients for whom blood loss exceeding 1000 ml is anticipated, intravenous (IV) iron supplementation is recommended [33–35]. Although the WHO recommends oral iron as the first-line therapy for pregnant women with anemia, IV iron is considered more appropriate in situations where rapid anemia correction is needed, oral iron cannot be tolerated or absorbed, or delivery is imminent [33]. In preoperative settings, particularly among high-risk obstetric patients, IV iron is frequently preferred over oral formulations given its faster efficacy and greater reliability [33–35]. The NICE guidelines also recommend IV iron when oral therapy is unsuitable or when time constraints require a prompt hematological response [34].

Additionally, the ACOG supports early anemia correction by means of IV iron or erythropoiesis-stimulating agents (ESAs) in high-risk women, such as those with PAS or multiple prior cesarean deliveries [35]. ESAs may be selectively used when the response to iron, typically initiated 2–3 weeks prior to delivery, is inadequate. However, the use of ESAs requires careful consideration because of their high cost and the potential for thromboembolic complications [11,36]. Therefore, the employment of ESAs is not routinely recommended and should be reserved for selected cases under close monitoring [11,36].

Transfusion thresholds

Transfusion thresholds must be established to enable individualized care and informed, shared decision-making between clinicians and patients [30,37]. In general, RBC transfusion is only applied in patient in whom Hb levels fall below 7 g/dl, particularly in individuals with cardiovascular comorbidities or those with an elevated risk of bleeding complications [38].

Iron therapy, ESAs, and antifibrinolytics

For asymptomatic patients, IV iron therapy is preferred over oral formulations because of the more rapid hematological response and superior tolerability profile [39]. Among the available IV preparations, ferric carboxymaltose and iron sucrose are considered safe and effective when administered after the 28th week of gestation in cases with Hb <10 g/dl (Table 3) [40].

Table 3.

Safety and Use of Tranexamic Acid, Iron, and Erythropoiesis-stimulating Agents in Obstetric Patients

Agent	Phase	Safety in Obstetric Patients	Usage and Considerations
Intravenous iron	Preoperative	Safe. Preferred over oral iron.	Administer ferric carboxymaltose or iron sucrose 2–3 weeks before delivery in anemic patients.
	Intraoperative	Not applicable.	Not used due to delayed hematologic effect.
	Postoperative	Safe. Preferred for postpartum anemia treatment.	Induces faster hemoglobin recovery than does oral iron.
			Monitor for hypersensitivity.
ESA	Preoperative	Recommended.	Initiate 2–3 weeks before delivery with IV iron; monitor Hb and thrombosis.
		Generally safe but increased thrombotic risk.
	Intraoperative	Not recommended.	No immediate effect; focus on non-pharmacologic blood conservation
	Postoperative	Selective use.	Use in stable patients unable to receive transfusion; combine with IV iron.
		Safe with appropriate monitoring.
TXA	Preoperative	Safe in high-risk patients; routine use not universal.	Prophylactic use requires caution; consider in patients at high risk of hemorrhage.
	Intraoperative	Safe; no increase in thromboembolic risk.	Give 1 g IV at hemorrhage onset, ideally within 3 h; repeat if bleeding persists.
	Postoperative	Safe and effective for PPH control.	Early use improves outcomes; monitor for thrombotic complications.

ESA: erythropoiesis-stimulating agents, IV: intravenous, Hb: hemoglobin, TXA: tranexamic acid, PPH: postpartum hemorrhage.

ESA therapy can improve pre-delivery Hb levels, reduce transfusion requirements, and enhance maternal recovery [11,41]. ESA therapy can effectively optimize Hb levels in patients at risk of obstetric hemorrhage and in those who decline transfusion, such as Jehovah’s Witnesses (Table 3) [41–44]. When initiated 2–3 weeks before delivery, ESA use is generally safe but requires close monitoring because of the associated thrombotic risk [45]. Concurrent administration of IV iron is recommended to maximize erythropoietic response and to minimize the need for transfusion [11,39].

TXA is considered safe for prophylactic use in high-risk obstetric patients and can effectively reduce intraoperative blood loss and transfusion requirements [46,47]. Prophylactic use of TXA during cesarean delivery in high-risk patients has been shown to reduce intraoperative blood loss and transfusion requirements [11,46–48]. Nevertheless, routine administration is not universally recommended; instead, its use should be guided by individualized risk assessments (Table 3).

Intraoperative phase: transfusion and hemorrhage control

QBL determination is a direct method of estimating the amount of blood lost during obstetric procedures and typically involves gravimetric (weighing surgical materials) or volumetric (measuring suction canister volume) techniques. QBL provides a more accurate estimate than does visual assessment and allows the timely recognition of bleeding, particularly during cesarean delivery [49]. However, contamination with amniotic or irrigation fluid can compromise its accuracy, potentially leading to blood loss overestimation [50]. Considering these limitations, additional physiological markers are required to guide appropriate and timely clinical decisions.

The OSI, defined as the ratio of the heart rate to systolic blood pressure, is a dynamic indicator of hemodynamic instability [51,52]. The normal range of the OSI within 1-h postpartum ranges between 0.52 and 0.89 [53]. An OSI ≥ 0.9 is associated with an increased risk of adverse maternal outcomes, while an OSI ≥ 1.7 strongly predicts severe complications, including the need for massive transfusion (≥ 4 units; odds ratio: 4.24) [54]. Conversely, an OSI < 0.9 has a high negative predictive value for maternal death, making it a valuable tool for ruling out significant hypovolemia [54]. Furthermore, the OSI has been shown to outperform conventional vital signs in detecting clinical deterioration in cases of PPH, providing a sensitive and continuous monitoring parameter. In clinical practice, QBL and the OSI are not mutually exclusive but rather complementary. While QBL provides an objective quantification of external blood loss, the OSI reflects the internal physiological impact of that loss.

Nevertheless, transfusion decisions must incorporate multiple clinical factors other than hemodynamic indices. The decision to initiate transfusion therapy is generally guided by the estimated blood loss and ongoing hemorrhage. In PPH, Hb levels and vital signs often fail to reflect early blood loss, thus delaying recognition [35]. When bleeding exceeds 1500 ml or if the vital signs become unstable (persistent hypotension, mental status changes, and low urine output), transfusion should be initiated promptly. By this stage, coagulation factors are typically depleted, increasing the risk of disseminated intravascular coagulation and requiring treatment with platelets and clotting factors, in addition to RBCs [35,55–57].

Rather than relying solely on fixed Hb thresholds, current recommendations support a more individualized approach that integrates physiological parameters, such as hemodynamic status, perfusion markers (e.g., lactate levels and shock index), and ongoing bleeding trends [55,58]. This approach is particularly important in PPH, where standard indicators may not reflect the severity of hypoperfusion, and early signs of disseminated intravascular coagulation require massive transfusion strategies, including platelet and plasma components.

Transfusion

RBC transfusion

A restrictive RBC transfusion strategy, defined as an Hb concentration < 7–8 g/dl, has traditionally been recommended for most hospitalized patients, including those with stable cardiovascular disease (Table 4) [59]. A randomized controlled trial comparing restrictive and liberal transfusion strategies in cases of PPH demonstrated no significant differences in maternal fatigue or recovery, supporting the safety of the restrictive approach in hemodynamically stable patients who do not have ongoing bleeding [60]. Furthermore, while this strategy may reduce unnecessary transfusions, it may result in moderate-to-severe postpartum anemia once the bleeding is controlled; this, in itself, has also been associated with increased maternal morbidity [11]. However, women with pre-existing cardiovascular disease may have reduced physiological tolerance to anemia and have a higher risk of myocardial ischemia and circulatory decompensation. In such patients, a higher transfusion threshold, typically 8–10 g/dl, may be needed to maintain adequate oxygen delivery and prevent hemodynamic deterioration [11,61,62].

Table 4.

Intraoperative Transfusion Strategies in Obstetric Hemorrhage

Component	Indication	Dose/Strategy	Clinical Notes
RBC	Hb < 7–8 g/dl (or < 8–10 g/dl with cardiovascular comorbidity); clinical signs of hypoperfusion	1 unit initially, reassess; individualized thresholds	Restrictive strategy generally safe
FFP	Coagulopathy suspected; > 4 units RBC transfused	15–20 ml/kg; or at minimum 1:2 FFP:RBC ratio	Empiric use if laboratory results are unavailable and bleeding is ongoing
Platelets	Platelet < 75 × 103/µl	5–10 ml/kg; maintain > 50 × 103/µl	Assess function with ROTEM/TEG if available
Fibrinogen	Fibrinogen < 200 mg/dl	Cryoprecipitate (10 units) → raises ~100 mg/dl	Goal: ≥ 200 mg/dl in PPH; early replacement critical
TXA	At onset of PPH (preferably within 3 h of bleeding)	1 g IV over 10 min; repeat 1 g IV if bleeding persists after 30 min or restarts within 24 h	Reduces mortality if given early; safe with uterotonics
MTP	EBL > 1500–2000 ml or > 4 RBC units in < 1 h or hemodynamic collapse	1:1:1 ratio (RBC:FFP:Platelet); early activation	Associated with improved maternal outcomes; delay increases ICU-admission risk
Cell salvage	High-risk cases (e.g., PAS, cesarean hysterectomy, transfusion refusal)	Autologous transfusion with leukocyte-depletion filters	Safe with precautions; useful for Jehovah’s Witness patients

RBC: red blood cell, Hb: hemoglobin, FFP: fresh frozen plasma, ROTEM: rotational thromboelastometry, TEG: thromboelastography, TXA: tranexamic acid, PPH: postpartum hemorrhage, IV: intravenous, MTP: massive transfusion protocol, EBL: estimated blood loss, ICU: intensive care unit, PAS: placenta accreta spectrum.

Therefore, in obstetric patients, transfusion thresholds should be individualized based on a comprehensive physiological assessment, with consideration of cardiovascular status, degree and persistence of hemorrhage, and physiological markers of inadequate perfusion, such as hypotension, tachycardia, oliguria, and altered mental status. Close hemodynamic monitoring is essential to guide timely intervention, to avoid both under- and over-transfusion, and ultimately, to reduce maternal morbidity [11,59].

Fresh frozen plasma transfusion

Transfusion of fresh frozen plasma (FFP) should be considered in cases of clinical suspicion of coagulopathy and abnormal coagulation test results, such as prolonged PT, INR, aPTT, or abnormal viscoelastic parameters [11]. If laboratory results are unavailable and bleeding continues after transfusion of 4 units of RBCs, empirical FFP transfusion, at a minimum FFP:RBC ratio of 1:2 is advised in the interim until test results become available (Table 4). The standard FFP dose for severe ongoing PPH is 15–20 ml/kg [11].

Platelet transfusion

Platelet transfusion is also a key element in MTPs for massive PPH, although evidence for its use in severe but nonmassive cases is limited [11]. In women with underlying conditions, such as preeclampsia, gestational thrombocytopenia, or placental abruption, thrombocytopenia may develop and may worsen with ongoing bleeding or with large-volume resuscitation [11]. Platelet transfusion (5–10 ml/kg) should be initiated when platelet counts fall below 75 × 10³/µl, or when point-of-care testing (e.g., TEG or ROTEM) indicates impaired platelet function, striving to maintain platelet counts above 50 × 10⁹/µl during active hemorrhage (Table 4) [11].

Fibrinogen replacement

During PPH, fibrinogen is the first clotting factor to decrease, and its replacement is recommended when fibrinogen levels fall below 200 mg/dl [48]. The target level of fibrinogen during massive transfusion is at least 150–200 mg/dl. Although FFP can be used, cryoprecipitate is preferred, given that its fibrinogen content is higher than that in FFP. Each unit of cryoprecipitate is approximately 100 ml and contains approximately 2 g of fibrinogen, which increases serum fibrinogen levels by approximately 10 mg/dl [48]. A typical dose of 10 units (1000 ml in total) increases fibrinogen levels by approximately 100 mg/dl. Further dosing should be based on follow-up laboratory results (Table 4) [48].

Increasingly, fibrinogen concentrate is recognized as an effective alternative to FFP or cryoprecipitate, particularly when rapid correction of hypofibrinogenemia is required or when volume overload is a concern [63]. Fibrinogen concentrate provides a standardized dose, does not require ABO compatibility, and can be prepared and administered more rapidly [63].

Recent studies have explored the efficacy of fibrinogen concentrate in managing PPH, but yielded inconclusive findings. In two studies involving 674 women, no significant reduction in intensive care unit admissions was observed (risk ratio: 1.09), and no consistent evidence of a benefit in terms of reducing the risk of hysterectomy or thromboembolic events was found [64,65]. Additionally, a multicenter randomized controlled trial revealed that, as compared to a placebo, early administration of fibrinogen concentrate did not reduce RBC transfusion requirements [66].

Viscoelastic testing allows for rapid functional assessment of fibrinogen levels during PPH (ROTEM/TEG-based fibrinogen monitoring, including FIBTEM A5 thresholds and transfusion triggers, are discussed later in the review) [11,67].

Early implementation of MTPs

In cases of massive PPH, a shift to an MTP is crucial [11]. Massive transfusion is generally defined as the transfusion of 10 or more units of packed RBCs (PRBCs) within 24 hours, transfusion of 4 or more units within 1 hours, with ongoing blood loss, or replacement of the patient's total blood volume [35]. In cases of major hemorrhage, a balanced 1:1:1 ratio of PRBCs, FFP, and platelets is recommended to restore hemostasis and maintain perfusion (Table 4) [35,48,55,68,69]. The Pragmatic, Randomized Optimal Platelet and Plasma Ratios (PROPPR) trial demonstrated that this strategy could improve hemostasis and reduce exsanguination-related mortality in patients with trauma, without increasing complications [70].

Although randomized obstetric data are lacking, retrospective studies have shown that deviations from balanced transfusion protocols correlated with worse maternal outcomes in cases of PPH [71]. Consequently, many institutions have adopted a trauma-based 1:1:1 transfusion protocol in PPH, based on institutional experience and observational data, with improved maternal outcomes [72,73]. Importantly, while these protocols are widely applied, they have primarily been derived from trauma and general surgical populations and may not fully reflect the unique physiological and hemostatic adaptations of pregnancy. Therefore, their use in obstetrics requires clinical adaptation and judgment.

In high-risk situations, such as PAS, uterine rupture, or hemodynamic collapse, early MTP implementation is essential. Delayed RBC transfusion in patients with PPH is associated with worse maternal outcomes [74]. When transfusions were delayed for over 30 minutes, intensive care unit admissions increased, whereas early MTP implementation significantly improved outcomes in patients with blood loss exceeding 1500 ml [75,76]. These findings emphasize the need for rapid transfusion response in obstetric emergencies. Furthermore, transfusion decisions must be guided by clinical evaluation and point-of-care diagnostics rather than by static thresholds, to enable timely and individualized management of cases of PPH [77].

Viscoelastic testing for coagulation

The most effective tools for assessing coagulation are viscoelastic hemostatic assays, including ROTEM and TEG, which offer real-time visualization of the initiation of clotting, clot strength, and clot stability [21,22,27,78]. Recent studies have demonstrated that ROTEM-guided transfusion protocols can reduce RBC utilization and improve clinical outcomes in patients with PPH [22,79]. These assays allow early identification of fibrinogen depletion and platelet dysfunction in patients with PPH, conditions that are often missed by standard coagulation tests during pregnancy-related bleeding [21,22].

In recognition of this clinical utility, the 2025 multidisciplinary consensus statement formally endorsed the routine integration of TEG and ROTEM into obstetric transfusion protocols, to support the use of goal-directed, individualized hemostatic management strategies [20]. However, the widespread adoption of viscoelastic testing is hindered by the high equipment and reagent costs, as well as the need for trained personnel, which limits its availability in low-resource or rural settings [8,22,78]. This underscores the urgent need for resource-appropriate hemostatic strategies in maternal health systems globally.

Viscoelastic hemostatic assays, such as TEG and ROTEM, are essential tools for managing obstetric hemorrhage, facilitating real-time transfusion-related decision-making based on dynamic clot function analysis [21,22,27]. Unlike conventional coagulation tests that offer static assessments, TEG and ROTEM provide comprehensive insights into clot initiation, propagation, strength, and fibrinolysis [21,22,27].

By analyzing key parameters, these assays facilitate the early detection of specific coagulopathies. Reaction time (R-time, TEG) and Clotting Time (CT, ROTEM) are used to assess clotting factor activity. Kinetics time (K-time, TEG), Clot Formation Time (CFT, ROTEM), and the α-angle reflect fibrin polymerization.

Maximum Amplitude (MA, TEG) and Maximum Clot Firmness (MCF, ROTEM) evaluate overall clot strength, which is influenced by platelet count and fibrinogen levels.

Lysis at 30 minutes (LY30, TEG) and Maximum Lysis (ML, ROTEM) reflect fibrinolytic activity [21,22,27,78].

Interpretation of these parameters facilitates targeted transfusion therapy. Table 5 summarizes the interpretation of the TEG and ROTEM parameters, pregnancy-specific reference ranges, abnormal findings, and corresponding therapeutic interventions, providing a concise, quick-reference guide for real-time transfusion decision-making in obstetric hemorrhage.

Table 5.

Interpretation of TEG/ROTEM Parameters and Clinical Implications in Obstetric Hemorrhage

Parameter (T/R)	Interpretation	Pregnancy-specific reference range*	Abnormal finding	Recommended intervention/blood product
R-time/CT	Time until initial clot formation; reflects coagulation factor activity	T: ~6 min	Prolonged	FFP, PCC, or specific factor replacement
		R: 37–60 s (pre-delivery); 34–66 s ≤ 1 h postpartum
K-time/CFT	Time to reach defined clot strength; fibrin build-up	T: 1–3 min	Prolonged	Cryoprecipitate or fibrinogen concentrate
		R: 41–103 s pre-delivery; 44–154 s postpartum
α-angle	Rate of clot strengthening (fibrin cross-linking and thrombin generation)	T: ~ 60°	Decreased	Fibrinogen concentrate (preferred) or cryoprecipitate
		R: 72–83° pre-delivery; 63–81° postpartum
MA/MCF	Maximum clot strength (platelet + fibrin contribution)	T: ~60 mm	Low	Platelets ± fibrinogen replacement
		R: 66–79 mm pre-delivery; 55–78 mm postpartum
LY30/ML	Degree of clot lysis at 30 min (fibrinolysis)	T: ~6%	Increased	TXA
		R: < 15%
FIBTEM A5/T-FF MA	Fibrinogen contribution to clot strength (platelet-independent)	R: ≥ 12 mm	Low	Fibrinogen concentrate (preferred) or cryoprecipitate
		T: > 12.7 mm

TEG: thromboelastography, ROTEM: rotational thromboelastometry, T: TEG, R: ROTEM, CT: clotting time, FFP: fresh frozen plasma, PCC: prothrombin complex concentrate, R-time: reaction time, K-time: kinetic time, CFT: clot formation time, α-angle: alpha angle, MA: maximum amplitude, MCF: maximum clot firmness, LY30: lysis at 30 min, ML: maximum lysis, TXA: tranexamic acid, FIBTEM: fibrin-based thromboelastometry assay, A5: amplitude at 5 min, T-FF: TEG functional fibrinogen assay, EXTEM: extrinsic thromboelastometry assay.

Among these methods, the FIBTEM A5 is the key viscoelastic parameter obtained from the FIBTEM assay during ROTEM testing [11,67]. This parameter reflects the clot amplitude measured at 5 minutes after coagulation initiation and provides an early estimate of fibrin-based clot strength, independent of platelet function. The FIBTEM A5 serves as a rapid indicator of functional fibrinogen activity, can be obtained at the bedside, and is particularly useful in patients with active bleeding. Recent reports recommend using the FIBTEM A5 to guide fibrinogen administration in cases of severe hemorrhage (> 2500 ml with ongoing bleeding). If the FIBTEM A5 < 7 mm, immediate fibrinogen concentrate is advised, replacing the traditional FFP + platelet “shock pack.” In cases with massive bleeding, fibrinogen may be considered when the FIBTEM A5 is < 12 mm [11,67].

Clinical evidence for viscoelastic testing

Clinical evidence supports the integration of viscoelastic hemostatic assays into obstetric hemorrhage protocols. As described earlier, fibrinogen is typically the first clotting factor to decline during massive bleeding, and early replacement is critical [21,22]. TEG and ROTEM enable rapid and individualized transfusion decision-making related to correcting fibrinogen deficiency and other coagulopathies [21,22,27]. Although viscoelastic testing allows rapid and dynamic assessment of coagulation, it should be used as a complement to, rather than a replacement for conventional coagulation assays, particularly in complex clinical scenarios.

Viscoelastic-guided strategies reduce RBC and FFP use, lower hysterectomy rates, and improve maternal outcomes, as compared to conventional laboratory tests [78,80]. The former tools are more sensitive in detecting hypofibrinogenemia and support earlier administration of fibrinogen products, such as fibrinogen concentrate or cryoprecipitate [79,81].

Nevertheless, in the field of obstetrics, the absence of large-scale randomized controlled trials limits the strength of the current evidence, and further studies are needed to establish definitive outcome benefits. The point-of-care use of TEG and ROTEM has been linked to faster detection of coagulopathy and improved clinical response during hemorrhage [82]. Their adoption enhances clinical decision-making, supports individualized care, and reduces maternal morbidity and mortality. The 2025 international consensus of the interdisciplinary working group has endorsed the use of these tools for real-time patient-specific transfusion management [20].

Pharmacologic management of active hemorrhage

Uterotonics

In active obstetric hemorrhage cases, along with blood products, uterotonic agents should be administered without delay to promote effective uterine contractions, particularly in cases of uterine atony, which accounts for up to 80% of primary PPH [7,13,20,35,36]. Uterotonics, such as oxytocin, methylergonovine, carboprost, and misoprostol, are crucial for restoring uterine tone and limiting further blood loss [35]. No single agent has been proven to be superior; therefore, unless an agent is contraindicated, selection is at the clinician’s discretion. As first-line uterotonic treatment for PPH, we recommend the use of 5–10 IU oxytocin administered intravenously or intramuscularly as a slow infusion or by injection, because it is the most effective and well-tolerated initial therapy [11,35,48]. If oxytocin is unavailable or if its quality cannot be guaranteed, the use of other uterotonics, such as ergometrine/methylergometrine or misoprostol, is recommended [48].

Iron and ESAs

In contrast, IV iron and ESAs are not appropriate for use intraoperatively because their hematological effects are delayed, and thus they are not effective for hemodynamic stabilization during acute bleeding. As these agents require days to weeks to exert measurable effects, they are more appropriate for antenatal anemia correction or postoperative recovery than for emergent resuscitation scenarios (Table 3) [11,39,41,45].

TXA

TXA is essential for managing PPH, because it stabilizes fibrin clots by inhibiting the excessive fibrinolysis that commonly occurs after placental delivery, due to increased levels of plasminogen activators and reduced levels of inhibitors [7,83]. TXA should be considered when medical therapy fails, and is more effective when administered early [35]. The greatest benefit is observed when TXA is administered within 3 hours of bleeding onset or delivery (Tables 3 and 4) [7,35,84,85]. In a major clinical trial, TXA given within 3 hours of delivery reduced bleeding-related mortality by 31% as compared to a placebo [85]. The benefit of TXA decreases by approximately 10% with every 15-min delay in administration, with no demonstrable benefit observed when it is administered beyond 3 hours postpartum [11,48].

When administered together with uterotonic drugs, TXA can reduce PPH risk [48]. At standard doses, TXA has shown a good safety profile for obstetric use, with no significant increase in thromboembolic complications [85–87]. Accordingly, guidelines recommend an initial 1 g IV TXA dose when PPH is diagnosed, followed by a second 1-g dose if bleeding continues for 30 minutes or recurs within 24 hours (Table 3) [11,48,84,86]. Additionally, prophylactic use has demonstrated a modest reduction in blood loss and no increased risk of thrombosis [35]. Although it is not currently recommended for routine prophylactic use outside research settings, TXA has been widely incorporated into hemorrhage management protocols because of its proven efficacy and safety and is considered a first-line pharmacological option for PPH management [11,35,48].

Cell salvage and transfusion refusal considerations

Intraoperative cell salvage

Intraoperative cell salvage (ICS) has been performed successfully during both cesarean and vaginal deliveries. ICS is particularly beneficial for obstetric patients with a high hemorrhage risk, such as those with PAS, multiple prior cesarean deliveries, or those who decline allogeneic transfusion for religious reasons [88–90]. ICS may be considered when Hb drops below 8–10 g/dl or when blood loss exceeds 800–1000 ml [11]. In obstetrics, autologous transfusion rates with ICS range from 36% to 100%, with 6%–97% of patients successfully avoiding allogeneic transfusion [91]. In high-risk cases, such as those with planned cesarean hysterectomy for PAS, up to 75% of patients received autologous transfusion, and allogeneic transfusion could be avoided completely in 87% [92].

Although ICS has historically been avoided because of concerns about amniotic fluid embolism (AFE) and maternal alloimmunization, recent evidence has supported its safe use in cesarean sections and high-risk deliveries when appropriate safeguards are applied [68,88–90]. Safety measures, such as leukocyte-depletion filters and dual-suction techniques, which separate amniotic fluid from salvageable blood, are critical to minimize the abovementioned risks [11,35,55,68]. The SALVO trial, which included > 3000 women undergoing cesarean section, reported no cases of AFE in the ICS group, confirming its safety. Nevertheless, the incidence of fetomaternal hemorrhage was significantly higher in the ICS group (25.6% vs. 10.5%), indicating the need for careful risk-benefit evaluation [93].

Ethical and clinical management of transfusion refusal

Patients who refuse blood transfusions, such as Jehovah’s Witnesses, require distinct clinical and ethical considerations. For these individuals, preoperative optimization with IV iron and ESAs is essential to increase Hb levels before delivery [41,42]. Intraoperative strategies, such as ICS with leukocyte-depletion filters, normovolemic hemodilution, and volume expanders can also help to reduce the need for allogeneic transfusions [41]. When these safeguards are appropriately applied, complications, such as AFE, do not increase significantly [41,42]. Effective care of these cases requires thorough preoperative planning, with individualized informed consent specifying acceptable interventions to ensure clear guidance for urgent clinical decision-making in emergency situations. Moreover, close coordination within a multidisciplinary team is crucial, and should include ethical consultations when necessary. To minimize the risk of legal or ethical disputes, the ethics consultation process, including involvement of the patient’s family, the institutional ethics committee, and, when appropriate, the hospital’s administrative or legal support services, should be carefully documented.

Postpartum phase: evaluation and management of anemia

Postpartum anemia is usually defined as an Hb level < 10 g/dl within 24–48 hours after delivery. It is considered severe when Hb < 7 g/dl [11]. The prevalence of postpartum anemia (PPA) at 48-h postpartum is estimated to be approximately 50% in Europe and 50%–80% in developing countries [11,58,94]. PPA is associated with postpartum depression, fatigue, impaired cognition, and disrupted maternal–infant bonding [94]. Table 6 summarizes the diagnostic thresholds and management options for PPA.

Table 6.

Postpartum Anemia: Assessment, Diagnosis, and Management Overview

Category	Clinical Focus	Recommendations
Screening	Hemoglobin reassessment within 24–48 h after delivery.	Especially in women with significant blood loss greater than 1000 ml, clinical signs of anemia, high-risk conditions, such as advanced maternal age or multiple gestations.
Diagnosis	Hemoglobin level less than 10 g/dl suggests postpartum anemia.	Evaluate symptoms including fatigue, dizziness, and breathlessness.
	Hemoglobin level less than 7 g/dl or presence of symptoms indicates need for transfusion.
Treatment options	Intravenous iron, preferably ferric carboxymaltose.	More rapid hemoglobin restoration, fewer gastrointestinal side effects compared to oral iron.
Transfusion considerations	Hemoglobin < 7 g/dl, ongoing bleeding, cardiovascular disease, or persistent anemia-related symptoms despite higher hemoglobin levels.	Reserved for unstable patients or severe anemia cases.
Follow-up and support	Oral iron supplementation for mild anemia, patient education regarding anemia symptoms, scheduled follow-up reassessment of hemoglobin levels and clinical status.	Routine follow-up recommended within 2–6 weeks postpartum.

Transfusion

Once active hemorrhage is controlled and hemodynamic stability is restored, transfusion management should shift toward addressing persistent PPA. This should involve considering both Hb levels and clinical indicators of tissue hypoxia. Hb should be reassessed in the first 48-h postpartum in women with blood loss exceeding 1000 ml or who have clinical signs of anemia [58]. Guidelines recommend RBC transfusion in women with Hb levels < 7 g/dl or who have moderate anemia with persistent symptoms, such as fatigue or tachycardia [35,58]. In obstetric patients, a lower transfusion threshold of 6.0 g/dl is generally accepted, with a slightly higher threshold of 6.5 g/dl applied in cases with cardiovascular instability [58,94]. For asymptomatic, hemodynamically stable women with low Hb levels, individualized management, including transfusion, oral iron, and IV iron therapy, is advised [35]. In cases of PPA due to massive bleeding, postpartum transfusion management should follow intraoperative transfusion strategies until the patient is clinically stable. Historically, transfusion involved 2 units of PRBCs, but is now recommended to start with 1 unit, followed by reassessment, particularly in patients who are stable [35,94]. However, whether a restrictive approach applies fully to the obstetric population remains unclear, and decisions should be individualized based on the clinical status of the patient [58,94].

Iron and ESAs

The first-line treatment for mild PPA is oral iron, whereas IV iron is preferred for stable patients with moderate-to-severe PPA (Hb 6–9 g/dl) or those without active bleeding [11,58,94]. Compared to oral iron, IV iron provides faster Hb recovery and has fewer gastrointestinal side effects (Table 3) [11,58,95]. Clinical studies have confirmed the effectiveness of IV iron in reducing transfusion needs and improving fatigue and quality of life [95,96].

ESAs may be considered after hematology consultation in women with severe anemia and a poor response to IV iron or in those who refuse blood transfusion (Table 3) [11,41]. ESAs have been explored as an adjunct to iron therapy for PPA; it may allow faster anemia correction and is safe for postpartum use [41]. When combined with IV iron, ESA therapy can accelerate recovery and reduce late transfusion needs [97]. However, ESAs have no significant advantage over IV iron alone in terms of improving Hb levels [41]. Therefore, ESA use requires careful consideration and should be individualized [41]. In addition, careful risk assessment is needed prior to ESA use, particularly regarding potential thrombotic complications and their implications during lactation [41,42].

Future directions in obstetric transfusion strategies

Transfusion practices in obstetric anesthesiology are evolving toward individualized approaches that emphasize clinical assessment over relying on fixed Hb thresholds. Patient blood management strategies, including antenatal anemia correction, restrictive transfusion criteria, and postpartum Hb optimization, have been adopted by many institutions and have suggested favorable outcomes, although robust evidence is still emerging [7,11,59].

To enhance precision in transfusion decision-making, point-of-care coagulation monitoring using viscoelastic assays, such as TEG and ROTEM, is increasingly being utilized, particularly in high-risk deliveries. These tools allow rapid detection of coagulopathies, support targeted administration of blood components, minimize unnecessary transfusion, and can improve safety [21,22,78].

Emerging technologies, including artificial intelligence and predictive analytics, are expected to provide further support for clinicians by identifying patients at high risk of hemorrhage, optimizing the timing of interventions, and integrating real-time hemodynamic and laboratory data to guide decisions about transfusions [16,98,99].

To ensure consistent and high-quality care, clinical protocols should continue to align with established international standards, with an emphasis on evidence-based transfusion thresholds, pharmacological interventions, and structured hemorrhage management. Standardization of practices across institutions will help to reduce variability and could support equitable maternal outcomes [11,34–36,48].

Ongoing progress in this field will require expansion of multidisciplinary education, strengthening of institutional infrastructure, and promotion of collaborative research to refine transfusion strategies and improve maternal safety in obstetric anesthesiology.

Conclusion

Optimal management of obstetric hemorrhage requires a transfusion approach that is individualized for each patient and is guided by continuous monitoring of the patient’s clinical status. This approach considers the unique cardiovascular and hematologic adaptations that occur during pregnancy. Effective treatment includes the timely use of uterotonic agents and TXA, rapid implementation of MTPs, and goal-directed transfusion guided by point-of-care viscoelastic assays, such as TEG and ROTEM. These tools allow real-time evaluation and targeted correction of coagulopathy, while minimizing the unnecessary use of blood products. Balanced transfusion strategies, particularly the early use of equal proportions of RBCs, plasma, and platelets, have demonstrated benefits in the management of severe bleeding. The consistent application of clinical guidelines, collaboration among multidisciplinary teams, and future use of advanced technologies, such as artificial intelligence and predictive models, are expected to improve maternal outcomes in both well-resourced and resource-limited settings.