Resuscitation in Obstetric Hemorrhage: “Less Is More”

Abstract

Obstetric hemorrhage accounts for one-third of maternal deaths worldwide. Risk factors have been identified, being common in developing countries. Mortality due to this complication has increased in recent years in countries like United States. Therefore, intensivists should be aware of the clinical tools and technology available for diagnosing and treating patients with severe hemorrhage. The main goal of resuscitation is to restore tissue oxygen delivery and perform initial management with crystalloids, while evaluating perfusion windows, which has been a long-time study, followed by transfusion of blood products (if initially not available) with the aim of restoring circulating volume. In recent years, complications of a large volume of fluids during resuscitation have proved harmful, as fluid accumulation in different organs such as the brain, heart, lung, and kidneys may cause edema, decreased lactate clearance, oxygen diffusion, weaning failure, increased hospital stay, and coagulopathy. The “less is more” approach is a strategy based on optimizing resources such as time to evaluation, treatment with fluids and blood products, clinical and laboratory data to assess severity to provide stabilization, and avoiding common complications in the ICU due to severe hemorrhage.

1. Introduction

Throughout the world, obstetric hemorrhage is one of the main causes of maternal death. However, there may be a great disparity between the prevalence of obstetric hemorrhage and its mortality in different countries due to individual implementation of preventive and preplanning measures in high-risk patients. The World Health Organization (WHO) has defined maternal death as the death of a woman during pregnancy or childbirth, or within 42 days of pregnancy termination, due to any cause related to or aggravated by pregnancy or its management.

A fourth of all maternal deaths in the world result from obstetric hemorrhage, accounting for approximately 140,000 deaths per year; the incidence of potentially deadly bleeding is 5–15% and is defined by the Royal College of Obstetrics and Gynecology (RCOG) as an estimated loss of blood of >2.5 liters or the required administration of >5 blood product units, or treatment of coagulopathy, all warranted in 3.7 of every 1000 pregnancies. Despite an observed decrease in the incidence of maternal deaths in the past few years, over half of them are still due to obstetric hemorrhage, whereby their incidence increased from 2.7 to 4.3% between 2000 and 2019 [1, 2]. As a result of this higher incidence, we analyzed the current therapeutic efforts used to improve the in-hospital response and thus decrease the hemorrhage-dependent mortality rate.

2. Definition

As of 2014, the American College of Obstetricians and Gynecologists (ACOG) published the reVITALize initiative and classically defined obstetric hemorrhage in the immediate postpartum period as blood loss above 1000 mL during vaginal delivery and/or secondary to a cesarean section. Bleeding quantification must be standardized although the exact measurement of blood loss in these procedures, and in general, is difficult to determine and usually underestimated, leading to inconsistent values; thus, a few medical centers have standardized the gravimetric method for its precise quantification in the operating room [3, 4]. Due to the frequent imprecision in blood loss calculation, the early intervention of a critical medicine specialist in the operating room is a recommended strategy, particularly if the patient shows signs of hypoperfusion and acute hemodynamic abnormalities that could lead to organ compromise.

The obstacles faced by low-income countries are clearly predictable. The lack of continuous medical education, insufficient resources, suboptimal infrastructure, and the paucity of qualified and certified personnel who can appropriately respond to an obstetric emergency are further complicated by the fact that many institutions are not supported by an immediate response team capable of following established care guidelines. In previously healthy women, severe hemorrhage may lead to a broad range of comorbidities: hemorrhagic shock, acute kidney failure, acute respiratory distress syndrome (ARDS), endocrine dysfunction, reperfusion injury, endotheliopathy secondary to massive resuscitation, coagulopathy, etc. This is further compounded by the secondary abnormalities resulting from massive transfusion of blood products (Figure 1) [5, 6].

Figure 1.

Rate of severe maternal morbidity. Source: CDC.

According to its temporality, obstetric hemorrhage is classified as primary if it occurs in the first 24 hours postpartum or cesarean section, and the most frequent etiology (70%) is uterine atony; less frequently, it results from placenta accreta, increta, or percreta that cause potentially deadly hemorrhages. Different studies have reported a median blood loss between 2000 and 7800 mL in placenta accreta cases (Figure 2). In these scenarios, resuscitation must be conservative in terms of the use of blood products, albumin, and balanced crystalloid solutions.

Figure 2.

Hysterectomy due to placenta percreta; hemorrhage: 7500 ml. Source: Hospital General Victoria. Tamaulipas, Mexico. 2023.

There are severity staging systems such as the one established by the California Department of Health that describes several stages organized according to the patient’s clinical characteristics and the blood loss volume (Figure 3).

Figure 3.

The California pregnancy-associated mortality review. Report from 2002-2017 maternal death reviews. Source; Sacramento: California Department of Public Health, Maternal, Child and Adolescent Health Division, 2017.

3. Evaluation of hemorrhagic shock by the ICU team

First, one must acknowledge the available tools that can identify hemorrhage risk factors, and these have been slowly incorporated into clinical care and applied immediately before the development of hemorrhagic events (Table 1); identify promptly those patients at risk of warranting medical care progression if excessive hemorrhaging is observed, and obtain immediate care in the intensive care unit [8].

Intermediate risk	High risk
Blood loss: 500–1000 mL	Accumulated blood loss >1000 ml
Vaginal deliveries: > 4	Placental abruption and/or active bleeding
Platelets: 50,000–100,000	Platelets: < 50,000
Hematocrit: < 30% (Hb < 10gr/dL)	Hematocrit: < 24% (< 8gr/dL)
Genital laceration (3rd–4th degree)	Known associated coagulopathy
Multiple gestations	Placenta accreta
Chorioamnionitis	HELLP

Table 1.

Risk factors for obstetric hemorrhage.

Table 1 Adapted and used with permission from Lagrew et al., and originally adapted from the “Improving Health Care Response to Obstetric Hemorrhage: A California Quality Improvement Toolkit”, funded by the California Department of Public Health, 2015; supported by Title V funds. Adaptations are also works protected by copyright. To publish this adaptation, authorization must be obtained both from the owner of the copyright of the original work and from the owner of the translation or adaptation copyright [7].

The early systematic evaluation of the patient in the recuperation area will reveal an obstetric patient with severe hemorrhagic shock and clinically recognizable macro- and microcirculatory findings that lead to the generation of free oxygen radicals and subsequent cell death. The patient will be at risk of multiorgan dysfunction compounded by the effects of resuscitation in the operating room resulting in ischemia-reperfusion injury and the initial phases of multiple organ dysfunction [9, 10].

Among patients at high risk of obstetric bleeding, the following parameters should be gauged before the delivery or cesarean section: metabolic status, renal function, cystatin-C, lactate, C reactive protein (CRP), coagulation profile, and acid-base status. The well-known hemodynamic changes of pregnancy include a 30–40% increase in cardiac output (CO), systolic volume (SV) (30–40%), left ventricular ejection fraction (LVEF) (5%), and a 20–30% decrease in peripheral vascular resistance (PVR), all to increase oxygen availability (O₂A) during gestation and satisfy the additional oxygen consumption (VO₂) of the obstetric patient.

3.1 Hemorrhage ≥1000 ml in the perioperative period

Hemorrhagic shock-induced endotheliopathy (SHINE) is fostered by an effective hypovolemic state followed by adrenal activation and a secondary massive release of catecholamines leading to dysregulated endothelial activation as well as of its glycocalyx, which in turn, activate a series of different biochemical markers such as E-selectin, intracellular adhesion molecule-1 (ICAM-1), the family of four heparan sulfate proteoglycans (Syn1–Syn4) (HSPGs), and angiopoietin (Agpt-1 and Agpt-2). Simultaneously, fibrinolysis signaling is triggered, altering the coagulation pathway, particularly the phase of “coagulation amplification,” which can in turn lead to the development of uncontrolled disseminated intravascular coagulation, further complicating the baseline state of hypovolemic shock [11].

During active bleeding caused in 70% of cases by uterine atony, we must not waste time making decisions, because “less is more.” We must optimize the timing of every therapeutic decision and implement efforts based on guidelines with a strong grade of clinical evidence quality (GRADE). When pharmacologic interventions do not control the bleeding rate, a surgical approach should be rapidly implemented (strong recommendation, high); compression sutures, the ligation of the uterine, iliac, or internal iliac arteries, and uterine artery embolization are effective interventions to consider; however, hysterectomy should not be delayed in patients that remain unstable due to active bleeding (strong recommendation, high) [12].

During active hemorrhage, all the initial measures implemented in the operating room by the multidisciplinary team must be reinforced, whereby two peripheral, permeable intravenous accesses must be available, an electrocardiogram should be obtained or electrocardiographic monitoring should be initiated for the timely detection of myocardial ischemia secondary to the decreased availability of oxygen, and venous and/or arterial blood gases should be obtained to determine the patient’s acid-base status, as well as hematocrit and lactate levels; blood gases should be closely monitored [13].

Hemostatic resuscitation is a new concept referring to the prompt replacement of the intravascular volume with blood products and further reflects the idea of “less is more”: this was concluded from the results of a systematic review of various trials that compared the administration of fresh frozen plasma (FFP), platelets, and red blood cells in 1:1:1 ratio with the practice of laboratory-guided transfusion (n = 69), early cryoprecipitate transfusion following standard practice (n = 41), and early administration of fibrinogen concentrate, in comparison with placebo (n = 45); one trial compared the effect of a 1:1:1 proportion of FFP, platelets, and red blood cells with 1:1:2 proportion in terms of mortality at 24 hours and at 30 days [n = 680]; another compared treatment with [whole blood with 24-hour blood [n = 107]; another compared the administration of FFP with red blood cells at 1:1 ratio with 1:4 ratio [n = 16]; all protocols were based on limited available evidence and did not reach a conclusion on the best approach in terms of mortality or morbidity [14].

Other authors are also investigating the predictive performance of the shock index in women with bleeding ≥1000 mL, but no significant correlation has been found, with an AUC ROC of 0.54 (95% CI: 0,47–0,61), a similar value to other vital signs [15].

If available, the coagulation model must be evaluated by thromboelastography prior to admission to the intensive care unit, to consider the early administration of tranexamic acid (TXA) or another directed pharmacologic measure. Several clinical trials, two large meta-analyses, and a randomized controlled trial revealed that 1 g TXA administered intravenously in the context of early obstetric bleeding can decrease blood loss, rate of hysterectomies, and most probably, mortality [16, 17]. A recent placebo-controlled trial revealed that the prophylactic administration of tranexamic acid during cesarean section did not decrease the risk of maternal death or the need for blood transfusions [18].

3.2 Transfer and admission to the intensive care unit (ICU)

The transfer of patients with obstetric hemorrhage must be as timely as possible once the intensive care team has evaluated the patient’s status and analyzed the potential risks implicit in the transfer. In patients who are hemodynamically unstable and mechanically ventilated, in terms of timelines, again, “less is more,” whereby the transfer should be prompt as the patient will require early interventions by the ICU team, such as the placement of monitoring equipment, precise and personalized adjustments to mechanical ventilation to prevent ventilator-induced lung injury (VILI), and set up an alveolar protection ventilation model [18, 19].

During the transfer to the ICU, the patient must be continuously monitored electrocardiographically as well as via pulse oximetry, her blood pressure must be periodically measured non-invasively, and the heart and respiratory rates should be easily visualized on the monitor; some selected patients may benefit from capnography. All drugs initiated before the transfer such as vasoactive, inodilator, antiarrhythmic, and/or sedating drugs must still be administered with continuous infusion pumps powered with portable batteries. All patients who require intubation and mechanical ventilation due to hemodynamic instability should be transferred with a transport ventilator, and initial ventilatory parameters should be maintained unless the ICU team decides to increase or activate the 100% oxygen in the first 2-minute function and then make further necessary adjustments [20, 21, 22].

3.3 Resuscitation in the ICU

In the presence of a massive hemorrhage that could potentially lead to hemodynamic instability and clear signs of hypoperfusion, crystalloid solutions must be combined with albumin and blood products, while still individualizing every case to prevent hemodilution, coagulopathy, and mainly, fluid retention with positive balances in the first 24 hours.

Three physiological concepts are key in a hemorrhagic shock scenario in obstetric patients: the evaluation of response to fluid administration, circulatory reserve, and microcirculation. One way to test these variables is with a fluid challenge, administering initially a balanced crystalloid solution (Ringer Lactate, Ringer Acetate, Plasma-Lyte), the most similar solution to plasma. The underlying physiological principle of this maneuver is an attempt to increase the mean systemic filling pressure (Pmsf) to increase the systemic venous return per the central venous pressure (CVP) and hence increase the cardiac output by increasing the compartment volume: the “stressed volume.”

In septic shock with borderline bleeding volume, and in which hypovolemia is greater, the state of hypoperfusion and shock is secondary to a vasodilated state with relative hypovolemia; the Frank-Starling mechanism is tested and allows to determine the benefit of fluid administration for resuscitation purposes. In severe hemorrhage scenarios, the test aims to evaluate the Frank-Starling mechanism and establish whether blood loss has been physiologically stanched, whether the arteriolar system is functional or if we are faced with an uncontrollable hemorrhage.

If blood loss is severe or if consumption coagulopathy develops during the active hemorrhage, platelets must be transfused and maintained at a value >50 × 10⁹/L. The main purpose of fresh plasma administration is to maintain an INR <1.8; fibrinogen should always be maintained above 2 g/L, and if necessary, several cryoprecipitate units should be administered to increase its value by 150–200 mg/dL. Another option is the use of fibrinogen concentrates (RiaSTAP) at a dose of 60–70 mg/kg weight or a standard dose of 4 g, which may increase serum fibrinogen up to 100 mg/dL [23].

In animal hemorrhagic shock models, systemic endothelial inflammation is induced and increases the risk of multiple organ dysfunction. Shedding of the endothelial glycocalyx may be secondary to the activation of cell signaling; however, the therapeutic use of unbalanced crystalloid solutions may also cause this injury. Crystalloids have been one of the most studied interventions in resuscitation scenarios; the administration of this treatment modality must be thought through since sooner or later, we must face their secondary effects; their use, however, is indispensable in the initial stages of hypovolemic shock. In a hemorrhagic shock canine model, Smart et al. observed that the administration of up to 80 ml/kg of crystalloids led to a considerable increase in endothelial inflammatory markers such as interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), and hyaluronan in comparison with colloids and blood products [24].

Xavier Monnet et al. referred that resuscitation with a rapidly administered load of crystalloid fluids (250–500 ml in 10–15 minutes) in hemorrhagic shock does not increase cardiac output (CO) but rather improves tissue oxygenation albeit not constantly, even in patients who respond well to fluid administration; hence, the response tends to be dynamic and inconsistently harmful, so treatment must be personalized [25].

Despite the development of shock, and the appropriate medical management of bleeding as well as the correction of macrohemodynamic parameters with transfusions, the microvasculature frequently remains altered: a concept known as hemodynamic coherence [26].

Functional capillary density refers to the capillary segments in which a red blood cell transits in an interval of 15 seconds and, that with the venular exit, allows the performance of two relevant physiological phenomena: optimization of O₂ transport to cells by convection and diffusion, important markers of microvascular perfusion that are key to maintain the integrity of endothelial glycocalyx [27]. In other words, fluid therapy seeks to improve convection, and real hypovolemia states in the territory of functional microcirculatory hemodynamics (FMH), thus ameliorating the volume quantity transported per second in the microcirculation. Diffusion refers to the maintenance of the functional capillary density (FCD) by not excessively increasing interstitial edema due to liberal resuscitation measures and decreasing oxygen diffusion from the capillaries to the mitochondria (Figure 4).

Figure 4.

Non-liberal resuscitation balance vs. early deresuscitation/de-escalation. U-shape relationship between hypovolemia/fluid overload and mortality (Adapted from Bellamy’s theoretical framework) [28].

3.4 Focusing on resuscitation in obstetric hemorrhage

The first “resuscitation” insult refers to the initial 59 minutes in which there is an imminent risk of death if the primary disorder is not corrected, such as in severe hypovolemia due to the hemorrhage. This initial phase may last 3 to 6 hours in septic shock but is much shorter in continuous obstetric hemorrhages, which is why prompt therapeutic management is mandatory. This is the time point in which bolus fluid administration is most relevant, although this strategy should be temporary until blood products are available, so we can avoid hemodilution in a patient with an already limited circulating blood volume. It is not necessary to wait for the hemoglobin result to initiate resuscitation with intravenous fluids as it only informs us of its baseline value. The purpose of this phase is to restore the circulating volume, preserve tissue oxygenation, revert or prevent the development of coagulopathy, and eliminate/treat the underlying obstetric hemorrhage source.

“Optimization,” the second phase, refers to the second insult: ischemia-reperfusion. The critical decision on when to stop fluid therapy becomes key. In the case of obstetric hemorrhages, this will occur once bleeding is under control, macro- and microcirculatory perfusion indices are adequate, and laboratory test results have been obtained (coagulogram, coagulation profile, bleeding time, viscoelastic tests, etc.).

The third phase, “stabilization,” refers to the success of the previously administered therapies, and this is the point at which intravenous fluids, including solutions, and drug diluents should be strictly controlled.

Finally, the “evacuation” phase represents the evaluation of fluid accumulation due to its deleterious effects on organs such as the heart, lungs, liver, and kidneys. At this point, the intensive care physician must ask him/herself two questions: when to begin removing fluid and when to stop removing it [29, 30, 31].

As previously mentioned, the endothelial glycocalyx is the main target responding to a state of shock, in response to changes in blood flow, perfusion pressure, and blood viscosity. This is relevant because the injury caused by inflammatory mediators leads to endotheliopathy or SHINE (shock-induced endotheliopathy) that has been linked with hemostatic abnormalities, either pro or antithrombotic. Viscoelastic hemostatic tests or assays have required decades of study in coagulation disorders, particularly when applied to liver transplants and heart surgery [32]. It is not infrequent for coagulation disorders to develop in association with obstetric hemorrhage, and they are reflected in prolonged coagulation times, hypofibrinogenemia, and/or thrombocytopenia, especially in catastrophic scenarios [33].

Therefore, a disadvantage to the use of crystalloids during resuscitation is the referred endothelial glycocalyx injury, despite their low cost and availability. In hemorrhagic shock, resuscitation with fresh frozen plasma has been shown to decrease pulmonary capillary hyperpermeability and syndecan-1 levels when compared with crystalloids such as Ringer’s lactate; less volume is also needed to ensure macrohemodynamic perfusion [34]. Patients in hemorrhagic shock have high levels of syndecan-1 that invariably decrease after resuscitation unlike crystalloids such as saline solution that increase endothelial permeability; hence, early administration of fresh frozen plasma is recommended [35, 36].

3.5 Coagulopathy and blood-derived products

Hemostatic viscoelastic tests were introduced as a research tool in 1948, and have been useful for several decades as a reference to the appropriate reanimation when the use of blood products is warranted. Table 2 shows the proposed values of the various results obtained with the commercial tests, rTEG® 5000 and ROTEM® [37]. Figure 5 presents the components of TEG®.

rTEG® trigger value	ROTEM® trigger value	Intervention
ACT >128 s	EXTEM CT < 80 s	CCP/FFP
α angle <65°; MAff/CFF < 11 mm	EXTEM α angle <63°; FIBTEM CA 10 < 7 mm	Fibrinogen/cryoprecipitate
MA < 55 mm	MCF < 45 mm	Fibrinogen/cryoprecipitate/platelets
LY30/60 > 7.5%	EXTEM; CLI30/60 < 82%; ML < 15%	TXA/Aminocaproic acid

Table 2.

Proposed trigger values for rTEG® 5000 and ROTEM®.

Abbreviations: Activated coagulation time (ACT); clot amplitude at 10 min (CA10); clot lysis index at 60 minutes after CT (CLI60); coagulation time (CT); extrinsic thromboelastometry activator (EXTEM); fresh frozen plasma (FFP); fibrinogen-based thromboelastometry (FIBTEM); lysis at 30 min (LY30); maximal amplitude (MA); functional fibrinogen, TEG (MAff/CFF); maximum clot firmness (MCF); prothrombin complex concentrate (PCC); maximum lysis after 30/60 min (ML30/60); rotational thromboelastometry (ROTEM®); Rapid TEG (rTEG®); Thromboelastography (TEG®); tranexamic acid (TXA) [37].

Figure 5.

TEG® of a cardiac surgery patient. Superior image shows low α-angle and maximum amplitude during active bleeding. Inferior image resulted after fresh frozen plasma and cryoprecipitate administration. Source: High Specialty Regional Hospital, Victoria, Tamaulipas, Mexico, 2023.

The use of these assays in obstetrics has been evaluated in several clinical trials and systematic reviews, particularly to predict the development of coagulopathy in patients with pre-eclampsia. Two therapeutic approaches have been evaluated in the management of obstetric hemorrhage: one in which the patient is hemodiluted (due to the use of crystalloid fluids), and the other when using blood product transfusions with viscoelastic test guidance. Despite the advantages offered by these tests such as a decreased need for blood transfusions or specific blood products if deficient, standard tests such as the prothrombin time and activated thromboplastin time remain very useful when detecting coagulation abnormalities and correlate well with blood loss. A clear disadvantage of this reanimation strategy is its complexity and the added cost of viscoelastic assays. Undeniably, viscoelastic tests are an area of opportunity in massive obstetric hemorrhage, decreasing the frequency of multiple transfusions and their known consequences [38, 39].

The management of hemorrhagic coagulopathy will depend on its phenotype or clinical presentation, manifested as either hypocoagulable or hyperfibrinolytic state, and the patient’s status may worsen due to uncontrollable bleeding, hemodilution, and/or hypocalcemia due to products with citrate. Therefore, there are different phenotypes upon which management with blood products or anticoagulant drugs will depend [40]. Viscoelastic assays are helpful in damage control management, whereby transfusions are administered to fulfill a physiological objective. A study conducted in 2015 analyzed reanimated patients treated with cryoprecipitates to correct the fibrinogen levels before the routine availability of ROTEM in the hospital (57 patients), and after (28 patients), and showed a decreased need for transfused blood products (p < 0.001), less warranted hysterectomies, admissions to the ICU, and shorter hospitalization, perhaps the result of rapid correction of the coagulopathy [41]. Current evidence supports the use of transfusions based on physiological parameters in patients with massive hemorrhage [42].

The use of blood components is a complex process that requires fine tuning the risk-benefit ratio, and timely decisions decrease morbidity and mortality. The current recommendation when transfusing packed red blood cells hinges on a hemoglobin level < 7 g/dL or in the case of symptomatic active hemorrhage, 8–10 g/dL (hematocrit 21–24%), with changing values over a six-hour period. The presence of thrombocytopenia is established with platelet values below 100,000/μL; platelet administration, either concentrates or by apheresis, must be considered when values are below 50,000/μL, and bleeding is active. In vaginal deliveries, platelets should be transfused if their value is under 1000/μL. Concentrations below 10,000/μL may lead to spontaneous bleeding. The prothrombin time and the international normalized ratio (TP/INR) are used to evaluate the extrinsic pathway, and clinically, they assess fibrinogen and factor II, V, VII, and X deficiencies. The aim is to maintain the INR between 1.5 and 2. Evaluation of the intrinsic pathway is based on the activated thromboplastin time (aPTT). If the aPTT is 1.5 times above the upper normal limit, transfusion of fresh frozen plasma (FFP) should be considered. The use of fibrinogen is also important in patients in whom it has decreased 1 g/dl as they have a 2.6-fold greater risk of severe bleeding. Fibrinogen should be administered to maintain its value between 150 and 200 mg/dl [43].

The use of blood products entails risks such as transfusion reactions or the transmission of pathogens. Most reactions are considered minor and include nonhemolytic febrile reactions, hemolytic reactions, anaphylaxis, and TRALI (transfusion-related acute lung injury) or TACO (transfusion-associated circulatory overload). A clear understanding of these events and their therapeutic approach is most relevant because although transfusions are the main treatment in the reanimation of patients with obstetric hemorrhage, they may also increase the rate of complications and the duration of the in-hospital stay [44].

3.6 Deresuscitation and de-escalation

The final step in resuscitation is to deal with the consequences of the employed therapy in case large blood product and solution volumes were administered, a process known as deresuscitation. This concept describes the active removal of fluid by ultrafiltration (UF) in patients with fluid overload. As soon as resuscitation is successful, the de-escalation phase must begin, decreasing the volume of the administered solutions, be they crystalloids, blood products, or drugs, and promoting the early use of diuretics to maintain an overall balance of zero.

When the fluid balance negatively impacts an organ as in patients with difficult extubation, deresuscitation must be initiated; because of deleterious effects on organs such as the heart, lung, gastrointestinal tract, kidney, abdominal cavity, and central nervous system, several therapeutic strategies must be implemented, including the use of diuretics – loop diuretics, aldosterone antagonists, or thiazides are highly recommended [45].

In cases of resistance to diuretics, Chawla et al. have suggested using the furosemide stress test when acute kidney injury (KDIGO I-II) is suspected early in the patient’s course; a dose of 1–1.5 mg/kg is administered, the response is evaluated whereby diuresis should be apparent within the following 2 hours, and the use of ultrafiltration is recommended [46].

4. Complications

The mortality resulting from continuous massive hemorrhage is the result of metabolic complications and a general state of hypoperfusion that throughout the first 24 hours may trigger irreversible coagulopathy, prolonged bleeding, and in the worst-case scenario, multiple organ dysfunction and early death. Damage-control conservative resuscitation attempts to revert organ dysfunction and avoid the trauma-lethal prognosis triad (hypothermia, acidosis, and coagulopathy) which could in turn partially or completely control hemorrhaging and preclude the development of a vicious circle in which the patient continues bleeding [47].

In obstetric hemorrhage, hypothermia is usually due to hampered cellular heat kinetics secondary to severe tissue hypoperfusion. It is usually worsened and exacerbated by intraoperative heat loss resulting from inadequate preventive maneuvers such as the lack of intraoperative heated blankets, reanimation with cold crystalloid fluids, and perhaps most importantly, prolonged exposure of the open abdominal cavity during surgery. In this setting, aside from the significant bleeding, the patient’s course may be complicated by hypothermia-induced cardiac arrhythmias, a decrease in cardiac output, and an abnormal hemoglobin-oxygen dissociation curve that increases erythrocyte oxygen affinity and decreases its release into cells [48].

Metabolic acidosis, mostly resulting from anaerobic metabolism, and secondarily from increased blood lactate concentrations during obstetric bleeding, leads to a drop in intracellular and extracellular pH, which in turn causes hemodynamic failure and progressive organ and system shutdown. A pH < 7.2 worsens the cardiovascular function by increasing the amplitude of the systolic calcium transient, thus altering calcium binding to troponin C and decreasing its systolic properties [49].

Any specialist’s patients may require transfusions, but obstetric hemorrhage is one of the complications that most frequently warrants massive transfusions defined as the administration of 10 units or more of whole blood or packed red blood cells over 24 hours. On rare occasions, ultramassive transfusions are needed and are defined as the need for more than 20 units of packed red blood cells over a 24–48-hour period. The main objective of a massive transfusion is to prevent the deadly results of critical complications relating to hypoperfusion while we attempt to achieve hemostasis. In the final phases, coagulopathy develops due to coagulation factor consumption and activation due to the hemorrhage per se and the administration of multiple transfusions; dilution, prolonged shock, hypoxia-induced acidosis, and hypothermia decrease the activity of coagulation factors. Another process resulting from multiple transfusions is metabolic alkalosis due to sodium citrate and citric acid in blood products. Hypocalcemia also develops as the metabolism of citrate generates 23 mEq of bicarbonate per blood unit and compromises oxygen delivery to cells. Hypocalcemia may also promote the development of arrhythmias with QT interval alterations that combined may lead to fatal outcomes [50].

Transfusion-related acute lung injury (TRALI), transfusion-related circulatory overload (TACO), and acute respiratory distress syndrome (ARDS) are characterized by pulmonary injury with accumulation of fluids in the interstitium, reflected as low- or high-pressure pulmonary edema depending on its origin. It is manifested as progressive respiratory failure with a high possibility of associated cardiopulmonary dysfunction and deadly cardiovascular outcomes. Despite the different conditions that can generate these complications, it is important to distinguish them as their etiology-directed management will lead to better results [51].

5. Conclusions

Obstetric hemorrhage is common in developing countries, accounting for less than 3% of ICU admissions. However, its social impact implies that the resources available in the critical care area are used for correct resuscitation from shock to avoid fatality. The initial approach involves clinical skills to identify signs of tissue hypoperfusion, restore cardiac output by initially administering volume, and quick and secure transport to ICU.

Detecting coagulation alterations is important because it involves identifying the blood component indicated to correct said alteration. In this way, the use of viscoelastic tests arises as an aid to limit the amount of blood products transfused, without leaving aside the usefulness of classic tests that evaluate intrinsic and extrinsic pathways. The “less is more” care strategy is aimed at optimizing the use of time and therapeutic resources and thus limiting the complications of the use of large resuscitation volumes. All these are aimed at restoring DO2, microvascular perfusion, limiting endothelial damage, and preventing and reversing coagulopathy.

It is preferable to avoid fluid accumulation due to aggressive resuscitation, although not uncommon that it occurs. Deresuscitation implies the active elimination of fluid accumulation that causes alteration in organ perfusion, increased hydrostatic capillary pressure, impaired lactate clearance, and weaning failure, mainly with drugs and ultrafiltration. This last part of critical care has an impact in improving prognosis in obstetric patients.

“Less is more” implies the knowledge of available resources to identify, resuscitate, transport, assess, and treat hemorrhagic shock in obstetric patients.

Conflict of interest

The authors declare no conflict of interest.