**7. Other hemostatic agents**

#### **7.1 Prothrombin complex concentrate**

PCCs or prothrombin complex concentrates are plasma-derived compounds containing highly purified vitamin K-dependent coagulation factors (II, VII, IX, and X) with hemostatic activity [21].

Originally, the main indication for PCC was the reversal of the effect of vitamin K antagonists; however, they are now also used to treat congenital or acquired conditions such as factor II or factor X deficiencies and are useful in the treatment of massive traumatic bleeding [22].

Systematic reviews have identified little scientific evidence on the use of PCC in adult patients with major bleeding; although the use of PCC is safe and recommended for urgent cases of reversal of the effect of vitamin K antagonists, there is currently limited evidence to support its use in the management of major bleeding unrelated to vitamin K antagonists [20].

In addition to a Cochrane review published on PCC for patients with vitamin K antagonists undergoing emergency surgery, PCCs appear to have a very safe profil with a minimal thromboembolic risk in these cases. One report has described the beneficial use of PCC in PPH in one patient with a non-hereditary coagulation deficiency [19].

In a retrospective study of 14 obstetric cases with disseminated intravascular coagulation (DIC), the use of PCCs failed to alter the outcome, which is why the use of PCCs cannot be considered a part of standard clinical practice for obstetric hemorrhage [20].

Efficacy in INR correction is also an advantage of prothrombin complex concentrates over fresh frozen plasma [21]. A retrospective study compared both treatments in patients with intracranial hemorrhage associated with anticoagulation and demonstrated that subjects treated with prothrombin complex concentrates had an average decrease in INR from 2.83 to 1.22 in 4.8 hours vs. a decrease from 2.97 to 1.74 in 7.3 hours in those who received fresh frozen plasma, that is, 4 to 5 times longer and less effective, with a statistically significant difference (p ≤ 0.001) [21].

A single 40 mL (1000 IU) dose of PCC is functionally equivalent to the adult FFP dose of 10 to 15 mL/kg, or four to five plasma quantity units or 1000 mL volume, all classes of PCC include factors II, IX, and X, whereas the four-factor PCC also contains clinically relevant factor VII.

*Patient Blood Management in Cesarean Section DOI: http://dx.doi.org/10.5772/intechopen.110331*

Some authors suggest a dose of 25–30 IU/kg, supported by the results of an open clinical study, without random distribution, carried out in patients with high INR (between 8.9 and 18 and greater than 20) [21].

In Canada, the approved PCC indications include rapid reversal of vitamin K deficiency in patients with severe bleeding or need for emergency surgery within 6 hours, but it is not recommended for surgery that may get delayed 6 to 12 hours, since in PCC anticoagulant reversal, its effect is temporary due to the short half - life of factor VII factor, which falls after 6 hours [23].

Consequently, intravenous administration with 10 mg of vitamin K with PCC is recommended to activate existing coagulation factors and maintain the reversal effect, as vitamin K1 reaches clinical effect within 6 hours by which PCC effects begin to weaken [23].

The administration of higher doses of prothrombin complex concentrates has been described in relation to the degree of INR prolongation.

It is not recommended to pass a maximum dose of PCC of 3000 IU (120 mL).

#### **7.2 Fibrinogen concentrate**

Fibrinogen, also called Factor I, is a blood plasma protein produced by the liver that plays a key role in hemostasis. It is the coagulation factor with the highest plasma concentration, between 150 and 400 mg/dl [24].

In its mechanism of action we have, it acts in both primary and secondary hemostasis; its soluble form serves to bind to activated platelets, forming bridges between them after binding to the glycoprotein IIb -IIIa receptor on its surface, contributing to the platelet aggregation and platelet plug formation during primary hemostasis; subsequently, fibrinogen is converted to fibrin monomers, which are polymerized, with the help of factor XIIIa, to an insoluble form (fibrin) that stabilizes the platelet plug and provides a firm mesh for clot propagation during secondary hemostasis [24].

Hypofibrinogenemia as a result of blood loss, factor consumption, or hemodilu-


tion is associated with poor patient outcomes and increased mortality in trauma patients [25]. The fibrinogen concentration upon arrival at the hospital may vary depending on the individual, patient factors; for example, low fibrinogen levels have been associated with young age, male gender, long time since injury, low base excess, and high injury severity score [25].

There are several techniques available to determine the fibrinogen concentration; the Clauss technique is recommended for diagnostic purposes or when decisions regarding the clinical management of patients with hemorrhage must be made [18]. The determination of FIBTEM with ROTEM or Functional Fibrinogen in TEG allows rapid detection of changes in fibrinogen levels in trauma patients. In this regard, it has been confirmed that the determination of fibrinogen using the FIBTEM test in ROTEM® is closely related to the values obtained with the Clauss method [18].

Fresh frozen plasma or FFP, cryoprecipitate, and human fibrinogen concentrate are available options for fibrinogen replacement. They contain approximately 2.5, 15, and 20 g/L of fibrinogen, respectively. Both FFP and cryoprecipitate require thawing and crossmatching prior to infusion, with known potential transfusion-related complications and risks. Cryoprecipitate is still not available in many European countries [22].

FIBTEM amplitude at 10 min from onset of clot formation (FIBTEMA10) correlates with fibrinogen concentration and thus allows early identification of fibrinogen deficiency. FIBTEMA10 < 7 mm has been suggested as a trigger for fibrinogen replacement with the aim of raising FIBTEMA10 to at least 10 mm during ongoing bleeding [18].

In maternity patients, fibrinogen levels rise to an average of 5–6 g/L at term (compared to nonpregnant levels of 2.0–4.5 g/L). Low fibrinogen levels are an independent risk factor for the development of severe PPH, with a study that showed levels below 2 g/L with a 100% positive predictive value for the development of severe PPH [14].

In Australia, the most common way to increase plasma fibrinogen levels is to transfuse cryoprecipitate. This plasma-derived blood product contains high levels of fibrinogen, factor VIII, von Willebrand factor, factor XIII, and fibronectin. To provide a 3 to 4 g dose of fibrinogen, about 8 to 10 bags (typically 30 to 40 mL), which require thawing [14].

Fibrinogen concentrate is available as a lyophilized powder in 1- or 2-gram vials, and the protein is reconstituted with 50 or 100 mL, respectively, of sterile water. The final concentration, therefore, is 2 g/100 ml. It can be kept at room temperature, with a durability of 5 years [24].

Pharmacokinetic studies in patients with congenital afibrinogenemia show that substitution of 1 mg/kg of fibrinogen increases the plasma concentration by around 1.38– 1.5 mg/dl, with a volume of distribution of 90–100 ml/kg [24]. The infusion rate should not exceed 5 ml/min (1 g/10 min), although cases have been described with a much higher transfusion rate without thrombus formation being observed in the vessel [24].

Fibrinogen concentrate prevents adverse effects associated with allogeneic blood products, including transfusion-related acute lung injury and incompatibility [20].

The administration of CCP together with factor XIII and fibrinogen (guided by the results of TEM) more effectively reversed the associated coagulopathy and the need for massive transfusion than conventional plasma therapy, without observable differences in the development of multi-organ failure, in hospital stay or mortality [14].

#### **7.3 Clot stability and FXIII (Fibrin Stabilizer)**

FXIII is known to be an essential contributor to clot strength through its ability to cross-link and stabilize fibrin; however, most bleeding management guidelines currently do not include measurement and subsequent supplementation of FXIII [25].

Clot instability due to FXIII deficiency has been identified in some cases by ROTEM; in the neurosurgical setting, a postoperative FXIII level < 60% was found to be an independent risk factor for postoperative ICH [14].

In cases of bleeding and low FXIII activity (e.g., <30%), the administration of FXIII concentrate (30 IU/kg) is suggested, [25] although other studies recommend its use at a dose of 20 IU/kg of ideal weight, either by cryoprecipitates or plasma [26].

#### **7.4 Activated recombinant human factor VII (rhFVIIa)**

Recombinant human factor VIIa (rhFVIIa) is a tissue factor, activated prohemostatic agent, the efficacy of rhVIIa has been demonstrated in nonrandomized studies *Patient Blood Management in Cesarean Section DOI: http://dx.doi.org/10.5772/intechopen.110331*

in severe postpartum hemorrhage. The risk of thromboembolic complications has not been systematically investigated; it requires correction of hypothermia, acidosis, fibrinogen levels, and anemia; therefore, if bleeding could not be controlled by other measures, rhFVIIa could reduce the need for second-line therapies [13].

In a prospective cohort study with 22 patients with severe PPH, rhVIIa contributed to PPH control, and hysterectomy was avoided, and in life-threatening PPH, rFVIIa administration could be used; however, this should not replace or postpone vital interventions, but it should be noted that patients should be monitored for thromboembolism, especially if rhVIIa is administered in combination with tranexamic acid [13].

### **8. Administration of blood products**

#### **8.1 Packed red blood cells**

There is a lack of evidence to support the benefit of blood transfusions, specifically in the case of hemodynamically stable patients undergoing elective surgery. Furthermore, it is an independent risk factor for adverse effects [18].

It is recommended to base its administration on clinical (blood pressure, heart rate) and biological (lactate, base excess) parameters, with a hemoglobin target of 8 g/dl, considering figures >9 g/dl for risk patients (heart disease). ischemic, cardiac surgery, etc.) considering the transfusion of red blood cells in most patients only when the Hb concentration is less than 7 g/ dL [26].

The Transfusion Requirements in Septic Shock (TRISS) trial showed that severely ill patients with septic shock could safely benefit from an Hb threshold of 7 g/dL132. Furthermore, an RCT of upper gastrointestinal bleeding in 921 patients, of whom a third were admitted with signs of hypovolemic shock (systolic BP <100 mmHg), demonstrated that an Hb threshold of 7 g/dl was safe and increased survival at 45 days when applied from the earliest phase [19].

The indication for blood transfusion should be more restrictive without fixed criteria for red blood cell transfusions; Hb below 6 g/dl generally requires a transfusion of 1 RGC, while this is rarely the case in a hemodynamically stable situation with an Hb of 8 g/dL or higher. Between 6 and 8 g/ dL, the indication for transfusion should be more restrictive, depending on the clinical situation and the patient's symptoms, since the best recommendation is to avoid the transfusion of packed red blood cells [13].

#### **8.2 Fresh frozen plasma**

Fresh frozen plasma (FFP) has limited clotting capacity and is inferior to fibrinogen concentrate for the treatment of hypofibrinogenemia. As a colloidal infusion, FFP is given for volume resuscitation in situations with severe hypovolemia and concomitant coagulopathy [13]**.**

We suggest transfusing a standard dose of plasma (15–20 mL/kg) in ongoing severe PPH guided by abnormal coagulation tests (e.g., prolonged TEG time) [19].

From an empirical point of view, the administration of fresh plasma should be started after the loss of 1–1.5 blood volumes. During massive hemorrhage, early administration of fresh plasma is recommended to prevent or treat coagulopathy, taking into account that thawing of FFP requires a long time, and therefore, timely organization of FFP is recommended [26].

The use of large volumes of fresh plasma can lead to transfusion-associated circulatory overload (TACO), probably the most common complication today, while others, such as acute respiratory distress syndrome (ARDS), lung injury related to transfusion (TRALI), and hemolytic reactions, are exceptional. PFC should not be used prior to a procedure to correct mild to moderate elevated INR (less than 2.0) [26].

#### **8.3 Platelet concentrate**

Platelets play a key role in hemostasis and clot formation. Although very few trauma patients have low platelet counts on admission, it is very likely that platelet deficiency will develop over time depending on treatment [13]. The insufficient number of platelets is characterized by EXTEMCA10 < 40 mm (but normal FIBTEM amplitude) and low platelets (<50,000/L), which will indicate the need for administration of platelet concentrate [25].

Platelet transfusions have been considered a safe and potentially effective intervention in major bleeding; the results of the PATCH trial demonstrated that platelet transfusion increased the risk of death in patients receiving antiplatelet therapy (mainly aspirin) and presenting with acute spontaneous intracerebral hemorrhage (stroke), although methodological limitations have been described [20].

There are no solid data on the number of platelets necessary to guarantee primary hemostasis in different clinical situations, so its administration is also based on the severity of the bleeding and the particular circumstances that caused the massive bleeding. It is recommended to maintain a platelet count >50 × 109/l in patients with active bleeding, and it is suggested to increase it to 75–100 × 109/l in situations of uncontrolled massive bleeding or head trauma [26].

Long-term prophylactic platelet transfusions should be avoided due to the risk of complications (including alloimmunization and platelet refractoriness) [18].

#### **8.4 Improvement of platelet function: desmopressin**

Desmopressin, 1-desamino-8-D-arginine vasopressin (DDAVP) is a synthetic analog of the antidiuretic pituitary hormone arginine vasopressin. In vivo, it causes an increase in factor VIII levels and stimulates the release of von Willebrand factor from endothelial cells, which promotes platelet adhesion to wound sites. DDAVP can be used to correct the anti-hemostatic effect of aspirin and clopidogrel and can also be applied as part of the treatment for platelet dysfunction or von Willebrand's disease and also as an alternative use for enhancement of platelet increase [22].

#### **8.5 Cryoprecipitates**

Cryoprecipitate is a high molecular weight protein concentrate containing coagulation factors VIII and XIII and von Willebrand, together with fibronectin and platelet microparticles. It is obtained in blood banks from a PFC unit by thawing it at low temperature (1–6°C). The precipitated proteins are separated by centrifugation, and the supernatant is removed, leaving the insoluble precipitate, which is later resuspended in 5–20 ml of plasma that is then frozen again and stored at −18°C. Each unit of cryoprecipitate is generally collected in bags *(pool)* of five units [24].

Mortality and the number of RGC units transfused in 24 h are higher in patients who receive cryoprecipitate transfusions compared to those who do not. Mortality at 30 days was higher in patients who received cryoprecipitate transfusions compared with those who did not [12].

The number of cryoprecipitates transfused was higher in those who received cryoprecipitate transfusions compared to those who did not receive cryoprecipitate. No evidence was found for the critical impact parameters [18].

Consider transfusing cryoprecipitates in patients without major bleeding who have the following:

clinically significant bleeding

Fibrinogen levels below 2 g/l

## **9. Third Pillar:optimizing postoperative/postpartum treatment of anemia**

Apart from the identification and appropriate action in each phase of obstetric hemorrhage, another fundamental pillar in the management of severe primary obstetric hemorrhage is the assessment with laboratory tests that include: blood biometrics, fibrinogen, coagulation studies, and lactate and base deficit (arterial blood gases) as they are tools to evaluate systemic tissue perfusion and are called **"optimal laboratory,"** since hemoglobin and hematocrit do not accurately reflect the amount of blood lost acutely [27].

Within coagulation studies should be requested fibrinogen concentration, prothrombin time, and activated partial thromboplastin time; this coagulation panel should be repeated every 30 to 60 minutes to observe trends until bleeding is controlled; coagulation studies are usually normal in the early stages of bleeding, but they can be abnormal when comorbidities exist, such as placental abruption, liver disease, stillbirth, sepsis, or amniotic fluid embolism. Eventually, significant bleeding without replacement of clotting factors will result in clotting abnormalities [27].

Fibrinogen is a cable point in the assessment of hemostasis since it falls to critically low levels before other clotting factors during a hemorrhage, so the level of fibrinogen is the most sensitive indicator of a significant loss of blood in progress, since its fall is related to the loss of fibrinogen through bleeding, increased fibrinolytic activity, and hemodilution secondary to fluids administered to maintain blood pressure during initial resuscitation, so it can be used to guide the aggressiveness of treatment [28, 29]. The normal level of fibrinogen in a full-term pregnancy is 350 to 650 mg/dl, which is almost twice that of a non-pregnant woman (200 to 400 mg/ dl); a low level of fibrinogen (less than 200 mg/dL) is a predictor of major bleeding that is associated with the need for transfusion of multiple units of blood and blood products, the need for surgical treatment of bleeding, and increased maternal morbidity and mortality [30, 31].

Another pillar of the assessment is viscoelastic tests such as thromboelastography (TEG) and rotational thromboelastometry (ROTEM), which are very useful when available, as they are useful to guide the administration therapy of plasma and other coagulation products. These tests provide a global assessment of complete hemostasis (time to clot development, clot stabilization/resistance, and clot dissolution) and can be performed at the bedside, so results are available within minutes. The results are useful for choosing only the transfusion-specific blood components that a patient requires and evaluating the efficacy of the interventions performed [32, 33]. The use of viscoelastic testing has led to fibrinogen replacement much earlier than with standard coagulation tests, and this early and aggressive fibrinogen replacement is thought to prevent severe coagulopathy and reduce maternal morbidity and mortality [33].

Once the initial treatment was established, bleeding control was achieved, and optimal laboratory tests were run; the objectives in the patient after obstetric hemorrhage are: [26].


The first objective is to obtain a hemoglobin of 7.5 g/dl; to make the corrections, we must remember that most guides recommend continuing to transfuse patients with hemoglobin values lower than 7.5 to 8 g/dl; however, our recommendation is to maintain a hemoglobin level of at least 8 g/dl after transfusion, since values below this level may be associated with hemostasis altered by lower platelet adhesion and high blood velocity, as well as an increased likelihood of myocardial ischemia; however, a common practice is to maintain blood transfusion in any patient with hemoglobin less than 7 g/dl, regardless of whether it is symptomatic or not, and to transfuse symptomatic patients with a hemoglobin value <8 g/dL [33].

Iron supplements are also recommended because the amount of iron lost is not completely replaced with transfused blood. Oral supplements are an option, and single-dose parenteral iron therapy is another option. The advantages of parenteral iron are that hemoglobin levels increase faster, anemia symptoms improve earlier, and less gastric discomfort occurs compared to oral therapy. However, most women with mild to moderate anemia resolve anemia quickly enough with oral iron, and this measure is inexpensive and convenient [33].

Erythropoietin may increase the rate of recovery to normal hemoglobin levels; however, it does not have an immediate effect and has not been shown to reduce transfusion requirements after bleeding, is also no more effective than iron therapy in this setting, and is expensive, so its use is not advised. However, for the few women with severe anemia who do not respond to iron therapy due to dull erythropoiesis due to infection and/or inflammation, some hematologists consider recombinant human erythropoietin to be an alternative to transfusion.

Regarding the second objective, there are no universally accepted guidelines for the replacement of blood components in patients with obstetric bleeding; recommendations are usually based on expert opinion, as there is no strong evidence from randomized trials, and these opinions are often extrapolated from data from studies in trauma patients, that is, a 1:1:1 replacement; in this case, our suggestion is to administer a packet of platelet apheresis only if the platelet count is less than 50,000/ mm3 [34, 35].

To achieve the objectives of hemostasis and prevention of coagulopathy, it is recommended that you try to raise the level of fibrinogen to a value >300 mg/dl in those situations in which there is active bleeding and in which resuscitation is still being performed, given the highest level of normal basal fibrinogen in pregnancy; however, if we face a controlled bleeding, a fibrinogen value greater than 200 mg/ dl will be the objective; the correction of fibrinogen deficiency can be done by using

#### *Patient Blood Management in Cesarean Section DOI: http://dx.doi.org/10.5772/intechopen.110331*

fresh frozen plasma, cryoprecipitate, and fibrinogen concentrates. It is important to emphasize that critically low levels of fibrinogen cannot return to normal using only fresh frozen plasma, without the use of cryoprecipitate or fibrinogen concentrates, since their irrational use only increases the risk of fluid overload and transfusion complications because they only contain a small concentration of fibrinogen in a large volume [35].

Cryoprecipitate is an option for correcting fibrinogen deficiency, but it also contains other clotting factors (VIII, XIII, von Willebrand). The dose depends on the measured and target fibrinogen levels. A reasonable approach is 30 units for fibrinogen <50, 20 units for fibrinogen <100, and 10 units for fibrinogen from 100 to 200. The advantages of cryoprecipitate are that large amounts of fibrinogen can be administered in a low-volume and that it is a low-cost product, and its disadvantages are that it takes time to thaw and prepare for transfusion and that it carries a risk of transmissible infections, since it is a pooled blood product that has not undergone any pathogen inactivation procedure [29, 30].

Another option for correction is fibrinogen concentrate containing approximately 1000 mg of fibrinogen. Usually given alone, it can be used in combination with cryoprecipitate; it is especially useful when fibrinogen levels are critically low (i.e., <100 mg/dl) [36].

Three-factor (II, IX, X) and four-factor (II, VII, IX, X) prothrombin complex concentrates (II, IX, X) are available and have been suggested as an alternative to fresh frozen plasma. The perceived advantages are a reduced risk of volume overload, without the need for thawing or blood typing, and a reduced risk of transfusionrelated acute lung injury and allergic reactions. The disadvantages include a very high cost and an increased risk of thrombosis [37].

Recombinant human activated factor VII has been successfully used to control intractable bleeding associated with uterine atony, placenta acreta, or uterine rupture; although this therapy appears to show promise for patients with bleeding refractory to standard therapy, medication is very expensive, and some studies have reported failure in 50% of patients and a possible increase in thrombotic events. Doses range from 16.7 to 120 mcg/kg in a single bolus injection for a few minutes, and repeat the dose every two hours until hemostasis is achieved, usually controlling bleeding within 10 to 40 minutes of the first dose [38].

We additionally recommend:

**Maintain oxygenation**: Oxygen saturation should be maintained at >95% by administering oxygen (10 to 15 l/minute) through a face mask; if the objective is not achieved, the need for tracheal intubation and mechanical ventilation should be assessed [26, 39].

Avoid hypothermia and **acidosis:** Blood fluids and components must be normothermic to avoid hypothermia, which has been linked to coagulopathy in traumatized patients.

Warming devices (blankets, devices to heat all intravenous fluids, insulating water mattresses, and/or upper and lower body forced-air heating devices) should be used to maintain normothermia (temperature ≥ 35.5°C), since hypothermia results in sympathetic stimulation with increased myocardial oxygen consumption, particularly if chills occur, which can lead to myocardial ischemia. Other adverse consequences of hypothermia include sepsis, coagulopathy, decreased platelet function, and increased mortality [40].

The combination of hypothermia and acidosis increases the risk of clinically significant bleeding despite adequate replacement of blood, plasma, and platelets [26, 40].

In addition, in any mass transfusion situation in which multiple units of blood are rapidly transfused, calcium and potassium should be monitored, with timely treatment of abnormalities. The most common electrolyte abnormalities are low levels of ionized calcium and hyperkalemia. Both disorders, if severe, can lead to cardiac arrest or significantly depressed heart function that prevents optimal resuscitation.

Ionized calcium: Ionized calcium should be measured at baseline and then every 15 to 30 minutes during a massive transfusion and then every hour for the next few hours after transfusions have stopped due to possible hypercalcemia and rebound hypokalemia.

An ionized calcium level < 1 mmol/L (normal 1.1 to 1.3 mmol/L) disrupts clotting and puts the patient at risk of cardiac arrest. Emergency replacement can be achieved by infusion of 1 gram of calcium chloride over two to five minutes through a central line; alternatively, 1 to 2 grams of calcium gluconate can be empirically infused intravenously for two to three minutes for every four units of red blood cells transfused. Hypocalcemia has a linear relationship, a low concentration correlates with a lower concentration of fibrinogen, and a higher likelihood of developing severe acidosis and a lower platelet count.

Potassium: Hyperkalemia can result from rapid transfusion of multiple red blood cell units, especially if they are older units and if they were transfused at a high infusion rate. When an urgent reduction in K+ is needed, a commonly used regimen for delivering insulin and glucose is 10 to 20 units of regular insulin in 500 mL of 10% dextrose, administered intravenously over 60 minutes.

## **10. Conclusions**

Worldwide, every minute, a woman dies due to complications during pregnancy, obstetric hemorrhage being the leading cause; however, most of these deaths are preventable. Hypovolemic shock is the main consequence of obstetric hemorrhage [2, 3].

Patient blood management (PBM) consists of the timely application of evidencebased medical and surgical procedures aimed at maintaining hemoglobin concentration, optimizing hemostasis, and minimizing blood loss to improve patient outcome, considering various strategies to reach the main goal, including transfusional, nontransfusional, and surgical measures.

Despite of the hemodilution, the rheological changes ensure enough oxygen delivery, better placental perfusion, and less risk for thrombosis, despite the bleeding that occurs with childbirth, to improve these objectives being the main outcome of the first pillar [5, 6]. Anemia treatment has the potential to improve outcomes for affected women and their fetuses and neonates and minimize the illness burden and cost due to this common disease [9].

After optimizing the volume of bleeding, the second pillar of management consists of minimizing blood loss, for which its necessary to identify the forecast of surgical bleeding; adequate management of antiplatelet agents and anticoagulants; optimal anesthetic techniques to minimize bleeding; monitoring of the bleeding and coagulopathy; and devising an anesthetic plan.

Apart from the identification and appropriate action in each phase of obstetric hemorrhage, another fundamental pillar in the management of severe primary obstetric hemorrhage is the assessment with laboratory tests that include: blood

biometrics, fibrinogen, coagulation studies, and lactate and base deficit (arterial blood gases) as they are tools to evaluate systemic tissue perfusion and are called **"optimal laboratory."**

The objectives in the patient after obstetric hemorrhage are: [26].

