Obstetric bleeding

Obstetric hemorrhages are bleedings in the second half of pregnancy, during and after childbirth. Early postpartum hemorrhages are bleedings that occur in the first 2 hours, late hemorrhages are bleedings that occur more than 2 hours after childbirth.

ICD-10 code

• O44.1 Placenta previa with hemorrhage
• O45.0 Premature placental abruption with bleeding disorder
  • O45.8 Other premature separation of placenta
  • O45.9 Premature separation of placenta, unspecified
• O46.0 Antepartum hemorrhage with coagulation disorder
  • O46.8 Other antepartum haemorrhage
  • O46.9 Antepartum haemorrhage, unspecified
• O67.0 Intrapartum hemorrhage with coagulation disorder
  • O67.8 Other intrapartum hemorrhage
  • O67.9 Haemorrhage during childbirth, unspecified
• O69.4 Childbirth complicated by vasa praevia
  • O71.0 Uterine rupture before onset of labor
  • O71.1 Uterine rupture during labor
  • O71.2 Postpartum eversion of the uterus
  • O71.3 Obstetric rupture of the cervix
  • O71.4 Obstetric rupture of upper vagina only
  • O71.7 Obstetric pelvic hematoma
• O72.0 Bleeding in the third stage of labor
  • O72.1 Other bleeding in the early postpartum period
  • O72.2 Late or secondary postpartum hemorrhage
• O75.1 Shock during or after labor and delivery

Causes obstetric bleeding

The causes of bleeding during pregnancy and childbirth are considered to be premature detachment of a normally and low-lying placenta, placenta previa, uterine rupture, and velamentous attachment of the umbilical cord. The causes of bleeding in the third period of labor and the early postpartum period are hypotension and atony of the uterus, placental defects, tight attachment and rotation of the placenta, trauma to the birth canal, eversion of the uterus, and blood clotting disorders. It is proposed to define the causes of postpartum hemorrhage as 4 "T":

• tone,
• textile,
• injury,
• thrombin.

Every year, approximately 125,000 women die from childbirth-related bleeding worldwide. Maternal mortality from obstetric bleeding in the Russian Federation for 2001-2005 ranged from 63 to 107 per 100,000 live births, or 15.8-23.1% of the maternal mortality structure.

Physiological blood loss is considered to be blood loss during childbirth within 300-500 ml or 0.5% of body weight. Blood loss during a cesarean section is 750-1000 ml, during a planned cesarean section with hysterectomy - 1500 ml, during an emergency hysterectomy - up to 3500 ml.

Massive obstetric hemorrhage is defined as a loss of more than 1000 ml of blood, or more than 15% of the BCC, or more than 1.5% of body weight. Severe, life-threatening bleeding is considered:

• loss of 100% of the BCC within 24 hours, or 50% of the BCC within 3 hours,
• blood loss at a rate of 150 ml/min, or 1.5 ml/(kg x min) (for a period of more than 20 minutes),
• one-time blood loss of more than 1500-2000 ml, or 25-35% of the BCC.

[ 1 ], [ 2 ]

Pathogenesis

Blood loss of more than 15% of the BCC leads to a number of compensatory reactions, including stimulation of the sympathetic nervous system due to reflexes from the baroreceptors of the carotid sinus area, large intrathoracic arteries, activation of the hypothalamic-pituitary-adrenal system with the release of catecholamines, angiotensin, vasopressin, and ADH. This leads to spasm of arterioles, increased tone of venous vessels (increased venous return and preload), increased heart rate and force, decreased excretion of sodium and water in the kidneys. Due to the fact that hydrostatic pressure in the capillaries is reduced to a greater extent than in the interstitium, starting from the first hour and up to 40 hours after blood loss, a slow movement of intercellular fluid into the vascular bed (transcapillary replenishment) occurs. Reduced blood flow in organs and tissues leads to changes in the acid-base balance of arterial blood - an increase in lactate concentration and an increase in base deficit (BE). In order to maintain normal pH, when acidemia affects the chemoreceptors of the respiratory center in the brainstem, minute ventilation increases, leading to a decrease in paCO2.

With blood loss of more than 30% of the BCC, decompensation occurs, expressed in arterial hypotension, i.e. a decrease in systolic blood pressure to less than 90 mm Hg. At the same time, with previous hypertension, this level can be 100 mm Hg, and with severe gestosis - even normal systolic blood pressure figures. Further release of stress hormones causes glycogenolysis, lipolysis with moderate hyperglycemia and hypokalemia. Hyperventilation no longer provides normal pH of arterial blood, as a result of which acidosis develops. Further reduction in tissue blood flow leads to increased anaerobic metabolism with increased secretion of lactic acid. As a result of progressive metabolic lactic acidosis, pH in tissues decreases and vasoconstriction is blocked. Arterioles dilate, and blood fills the microcirculatory bed. There is a deterioration in cardiac output, and damage to endothelial cells may develop, followed by DIC syndrome.

With blood loss of more than 40% of the BCC and a decrease in systolic blood pressure to less than 50 mm Hg due to CNS ischemia, additional stimulation of the sympathetic nervous system occurs with the formation of the so-called second plateau of blood pressure for some time. Without vigorous intensive therapy, shock passes into an irreversible stage characterized by widespread cell damage, multiple myocardial infarction, deterioration of myocardial contractility up to cardiac arrest. It is believed that after an increase in blood pressure and restoration of blood flow, more pronounced organ damage is observed than during the period of hypotension. Due to the activation of neutrophils, their release of oxygen radicals, and the release of inflammatory mediators from ischemic tissues, damage to cell membranes, an increase in the permeability of the pulmonary endothelium with the possible development of ARDS, mosaic intralobular liver damage with an immediate increase in the level of transaminases in the plasma occur. Spasm of the afferent arterioles of the renal glomeruli with the development of acute tubular necrosis and acute renal failure is possible. The supply of energy substrates to the heart and brain may be disrupted due to a decrease in the secretion of glucose by the liver, disruption of hepatic ketone production and inhibition of peripheral lipolysis.

Physiological changes in late pregnancy

Compensatory changes in hemodynamics, the respiratory system, and gas exchange that occur at the end of pregnancy affect the diagnosis and implementation of intensive therapy in case of massive bleeding.

During pregnancy, the BCC increases by 30-50%. The plasma volume and the number of erythrocytes increase disproportionately, creating physiological hemodilution. CO increases by 30-50%, mainly in the first and second trimesters due to the stroke volume and to a lesser extent in the third trimester due to an increase in heart rate by 15-20%. CVP and PCWP do not change significantly, despite a significant increase in intravascular volume. This occurs as a result of a decrease in total peripheral and pulmonary vascular resistance. To the greatest extent, there is a decrease in vascular resistance and an increase in blood flow in the vessels of the uterus and kidneys.

Oncotic pressure decreases to 18 mm Hg on average (by 14%). The risk of OL during infusion therapy increases due to a decrease in the oncotic pressure/PCWP gradient.

During pregnancy, all four chambers of the heart enlarge, and the wall of the left ventricle thickens. There is a predisposition to the development of ventricular and supraventricular rhythm disturbances. More than 90% of healthy pregnant women have signs of tricuspid regurgitation, and a third have minor mitral regurgitation. The sizes of the chambers of the left atrium and ventricle gradually return to normal values 2 weeks after delivery, and the thickness of the left ventricle wall - 24 weeks.

Changes also occur in the respiratory system. An increase in oxygen consumption by 20% is the result of increased metabolic needs of the mother and fetus. An increase in minute ventilation and tidal volume by 40% leads to compensated respiratory alkalosis with a decrease in paCO2 to 27-32 mm Hg. There is no significant change in pH due to a decrease in plasma bicarbonate concentration by the kidneys to 18-21 mmol/l. A decrease in plasma bicarbonate concentration may limit buffering capacity during pregnancy. These changes should be taken into account when interpreting blood acid-base balance data in a patient with shock. It is assumed that physiological hyperventilation during pregnancy is due to an increase in blood progesterone levels, the concentration of which rapidly decreases after delivery.

Symptoms obstetric bleeding

Signs of hypovolemic shock outside pregnancy appear with blood loss of 15-20% of the BCC. Practical application of the hypovolemic shock severity scheme during pregnancy and in the early postpartum period can be difficult, since patients, due to an increase in BCC and CO, young age and good physical condition, are able to tolerate significant blood loss with minimal changes in hemodynamics until a very late stage. Therefore, in addition to taking into account the blood loss, indirect signs of hypovolemia are of particular importance.

The main sign of decreased peripheral blood flow is the capillary filling test, or the "white spot" symptom. It is performed by pressing the nail bed, the elevation of the thumb, or another part of the body for 3 seconds until a white color appears, indicating the cessation of capillary blood flow. After the pressure is stopped, the pink color should be restored in less than 2 seconds. An increase in the time it takes to restore the pink color of the nail bed by more than 2 seconds is noted in cases of impaired microcirculation.

A decrease in pulse pressure is an earlier sign of hypovolemia than systolic and diastolic blood pressure, assessed separately.

Shock index is the ratio of heart rate to systolic blood pressure. Normal values are 0.5-0.7.

Hemoglobin and hematocrit concentrations are often used to determine the amount of blood loss. A significant decrease in hemoglobin and hematocrit concentrations indicates major blood loss and requires immediate action to find the source and stop the bleeding. After bleeding of 1000 ml, or 15% of the CBV, or 1.5% of body weight, there is no significant change in these values for at least 4 hours. Changes in hemoglobin and hematocrit concentrations that occur after this time require up to 48 hours. Intravenous infusion may result in an earlier decrease in hemoglobin and hematocrit concentrations.

A decrease in diuresis with hypovolemia often precedes other signs of circulatory disorders. Adequate diuresis in a patient not receiving diuretics indicates sufficient blood flow in the internal organs. To measure the rate of diuresis, 30 minutes is enough.

• Insufficient diuresis (oliguria) - less than 0.5 ml/(kg h).
• Decreased diuresis - 0.5-1 ml/(kg h).
• Normal diuresis is more than 1 ml/(kg h).

Obstetric hemorrhages are usually divided into 4 classes depending on the amount of blood loss. It is necessary to be guided by the clinical signs corresponding to blood loss in order to roughly assess it and determine the volume of necessary infusion.

Patients with grade 1 hemorrhage rarely have a volume deficit. Grade 2 hemorrhage often presents with complaints of unexplained restlessness, a feeling of coldness, shortness of breath, or malaise. The earliest symptoms are mild tachycardia and/or tachypnea.

Increased respiratory rate is a non-specific response to decreased circulating blood volume and a relatively early sign of its mild deficit, often remaining unnoticed. Patients with grade 2 hemorrhage may have orthostatic changes in blood pressure, peripheral circulation disorders in the form of a positive capillary refill test. Another sign of grade 2 hemorrhage is a decrease in pulse pressure to 30 mm Hg or less.

Grade 3 bleeding is characterized by signs of hypovolemic shock: severe hypotension, tachycardia, and tachypnea. Peripheral circulatory disorders are more pronounced. The skin may be cold and moist.

In case of grade 4 bleeding, patients are in deep shock, there may be no pulsation in the peripheral arteries, undetectable blood pressure, oliguria or anuria. In the absence of adequate volume-replacing infusion therapy, circulatory collapse and cardiac arrest can be expected.

Diagnostics obstetric bleeding

Various methods are used to estimate the amount of blood loss. The widely used visual assessment is subjective and leads to an underestimation of the average, frequently encountered blood loss by 30-50%. At the same time, a volume less than average is overestimated, and a large volume of blood loss is significantly underestimated. Quantitative methods are more advanced, but they are not free from shortcomings. The use of a measuring container makes it possible to take into account the blood that has spilled, but does not allow one to measure the blood remaining in the placenta (approximately 153 ml). Inaccuracy is possible when mixing blood with amniotic fluid and urine.

Gravimetric method - determining the difference in weight of the material before and after use. Napkins, balls and diapers should be of standard size. The method is not free from error in the presence of amniotic fluid.

The most accurate is the acid-hematin method - determination of plasma volume using radioactive isotopes, using labeled erythrocytes, but it is more complex and requires additional equipment.

[ 3 ], [ 4 ], [ 5 ], [ 6 ]

Treatment obstetric bleeding

Massive obstetric hemorrhage is a complex problem that requires coordinated actions that should be rapid and, if possible, simultaneous. Intensive care (resuscitation assistance) is carried out according to the ABC scheme: airway, breathing and circulation.

After assessing the patient's breathing and starting oxygen inhalation, notification and mobilization for the upcoming joint work of obstetricians-gynecologists, midwives, surgical nurses, anesthesiologists-resuscitators, nurse anesthetists, emergency laboratory, blood transfusion service are carried out. If necessary, a vascular surgeon and angiography specialists are called.

The most important step is to ensure reliable venous access. It is preferable to use two peripheral catheters - 14G (315 ml/min) or 16G (210 ml/min). However, even a functioning 20G catheter (65 ml/min) allows for further assistance. If peripheral veins have collapsed, venesection or central vein catheterization are indicated.

When installing a venous catheter, it is necessary to take a sufficient amount of blood to determine the initial parameters of the coagulogram, hemoglobin concentration, hematocrit, platelet count, and to conduct compatibility tests for possible blood transfusion.

Catheterization of the bladder should be performed and minimal hemodynamic monitoring (EKG, pulse oximetry, noninvasive blood pressure measurement) should be provided. All changes should be documented. Blood loss should be taken into account.

Methods of stopping obstetric bleeding

When bleeding stops during pregnancy, emergency delivery and the use of drugs that increase the tone of the myometrium are indicated. If ineffective, proceed to the following measures:

• selective embolization of uterine arteries (if possible),
• hemostatic suture according to B-Lynch, or hemostatic “square” suture according to Cho, and/or ligation of the uterine arteries,
• ligation of the main vessels (a hypogastnca),
• hysterectomy.

To stop bleeding after childbirth, the following should be used in the order listed:

• external massage of the uterus,
• uterotonics,
• manual examination of the uterus,
• suturing of ruptures of the birth canal.

After manual examination, intrauterine balloon tamponade (tamponade test) may be used. If there is no effect, all the above-mentioned surgical (including angiographic) methods of stopping bleeding are indicated.

Artificial ventilation of the lungs

The indication for artificial ventilation is usually the beginning of general anesthesia when stopping bleeding surgically. In a critical situation - with symptoms of ARF, impaired consciousness, artificial ventilation is indicated.

• Use of artificial ventilation:
• prevents aspiration in cases of decreased consciousness,
• improves oxygenation,
• is a therapeutic measure for acute respiratory failure,
• helps correct metabolic acidosis,
• reduces the work of breathing, increasing oxygen consumption by 50-100% and reducing cerebral blood flow by 50%.

General anesthesia includes antacid prophylaxis (omeprazole 20 mg and metoclopramide 10 mg intravenously), preoxygenation, rapid sequence induction with cricoid pressure, and tracheal intubation. Anesthesia is provided with ketamine in a reduced dose of 0.5-1 mg/kg or etomidate 0.3 mg/kg, relaxation is provided with suxamethonium chloride 1-1.5 mg/kg followed by the use of non-depolarizing muscle relaxants. In patients in a state of severe shock, with maximum stimulation of the sympathetic nervous system, ketamine can have a depressor effect on the myocardium. In this situation, the drug of choice is etomidate, which ensures hemodynamic stability. Until sufficient BCC is restored, drugs that cause peripheral vasodilation should be avoided. The course of anesthesia is usually maintained by fractional administration of small doses of ketamine and narcotic analgesics.

When performing mechanical ventilation in a patient with shock, PEEP setting is necessary to prevent alveolar collapse leading to ventilation-perfusion disorders and hypoxemia.

If regional anesthesia is started before massive bleeding, it can be continued until successful stopping of bleeding and hemodynamic stability. In unstable situations, early transition to general anesthesia is indicated.

[ 7 ], [ 8 ], [ 9 ], [ 10 ]

Features of infusion therapy

During infusion therapy, priority is given to restoration and maintenance of:

• BCC,
• sufficient oxygen transport and tissue oxygenation,
• hemostasis systems,
• body temperature, acid-base and electrolyte balance.

In volume replenishment, the advantage of colloids or crystalloids is not determined. Crystalloids, compared with colloids, more effectively replace extracellular water, while 80% moves into the interstitial space. Colloidal solutions preserve intravascular volume and microcirculation more effectively, increase CO, oxygen delivery and blood pressure at approximately 3 times smaller infusion volumes than crystalloids. All synthetic colloids in in vitro studies, confirmed clinically, affect hemostasis, causing a tendency to hypocoagulation in decreasing order: dextrans, hydroxyethyl starch 200/0.5, hydroxyethyl starch 130/0.42, 4% modified gelatin. Dextrans are currently not recommended for use. In volume replenishment against the background of bleeding, hydroxyethyl starch 130/0.42 and 4% modified gelatin are preferable.

Albumin has limited use in hemorrhagic shock and is indicated:

• as an additional means when reaching the maximum dose of synthetic colloids,
• with hypoalbuminemia less than 20-25 g/l.

A rational approach is a balanced therapy with crystalloids and colloids. With blood loss of up to 30% of the BCC (bleeding class 1 or 2) and stopped bleeding, replacement with crystalloids in a volume three times the blood loss will be adequate. If bleeding continues or blood loss is 30% of the BCC or more (bleeding class 3 or 4), a combination of crystalloids and colloids with minimal effect on hemostasis is necessary. A possible option for initial BCC replacement in case of bleeding class 3-4 with blood loss of 30-40% of the BCC may be an infusion of 2 liters of crystalloids and 1-2 liters of colloids. Special devices may be needed to speed up the infusion.

Initial replenishment of the circulating blood volume is carried out at a rate of 3 l for 5-15 min under the control of ECG, blood pressure, saturation, capillary filling test, blood acid-base balance and diuresis. It is necessary to strive for systolic blood pressure values of more than 90 mm Hg or, in case of previous hypertension, more than 100 mm Hg. In conditions of reduced peripheral blood flow and hypotension, noninvasive blood pressure measurement may be inaccurate or erroneous (up to 25% of observations). The most accurate method is invasive blood pressure measurement, which also allows for the study of arterial blood gases and acid-base balance. Heart rate and blood pressure do not reflect the state of tissue blood flow, the restoration of which is the ultimate goal of infusion therapy. Normal values for pulse oximetry, capillary filling test and diuresis indicate the adequacy of the infusion therapy. Base deficit less than 5 mmol/l, lactate concentration less than 4 mmol/l are signs of shock, their normalization indicates restoration of tissue perfusion. Hourly diuresis value less than 0.5 ml/(kg x h) or less than 30 ml/h after initial replenishment of circulating blood volume may indicate insufficient tissue blood flow. Urine sodium concentration less than 20 mmol/l, urine/plasma osmolarity ratio more than 2, urine osmolality more than 500 mOsm/kg indicate decreased renal blood flow and prerenal renal failure. But restoration of diuresis rate may be slow in relation to restoration of blood pressure and tissue perfusion in severe gestosis, development of acute renal failure. Diuresis is a relative reflection of tissue blood flow, the assessment of the state of which must be confirmed by other signs (capillary filling test, pulse oximetry, blood acid-base balance).

In case of hemorrhagic shock or blood loss of more than 40% of the circulating blood volume, central vein catheterization is indicated, which ensures:

• additional intravenous access for infusion,
• control of central hemodynamics during infusion therapy A catheter (preferably multi-lumen) can be inserted into one of the central veins

The method of choice is catheterization of the internal jugular vein, but in hypovolemia its identification may be difficult. In conditions of impaired blood coagulation, access through the cubital vein is preferable.

Negative CVP values indicate hypovolemia. The latter is also possible with positive CVP values, so the response to volume loading is more informative, which is carried out by infusion at a rate of 10-20 ml/min for 10-15 minutes. An increase in CVP over 5 cm H2O or PCWP over 7 mm Hg indicates heart failure or hypervolemia, a slight increase in CVP, PCWP or its absence indicates hypovolemia.

In hemorrhagic shock, venous tone is increased and venous capacity is decreased, so replacing the loss of circulating blood volume can be a difficult task. Rapid intravenous infusion of the first 2-3 liters (over 5-10 minutes) is considered safe. Further therapy can be carried out either discretely by 250-500 ml over 10-20 minutes with an assessment of hemodynamic parameters, or with continuous monitoring of CVP. Quite high CVP values (10 cm H2O and higher) may be required to obtain sufficient filling pressure of the left heart chambers to restore tissue perfusion. In rare cases, when low tissue blood flow persists with positive CVP values, the contractility of the left ventricle should be assessed. In other areas of medicine, pulmonary artery catheterization, which is extremely rarely used in obstetrics and has a number of serious complications, is used as a standard technique for this purpose. Alternatives include pulse contour analysis during radial artery catheterization, assessment of central hemodynamic parameters and intrathoracic volume indices during transpulmonary thermodilution (RICCO method), and transesophageal echocardiography.

Lactate clearance and mixed venous blood saturation are used to assess tissue perfusion. Lactate clearance requires determination of blood acid-base balance two or more times. If lactate concentration does not decrease by 50% within the first hour of intensive therapy, additional efforts should be made to improve systemic blood flow. Intensive therapy should be continued until lactate decreases to less than 2 mmol/L. If lactate concentration does not normalize within 24 hours, the prognosis is questionable.

Mixed venous oxygen saturation reflects the balance between oxygen delivery and consumption and correlates with the cardiac index. Mixed venous oxygen saturation (central venous oxygen saturation) values of 70% or more should be aimed for.

[ 11 ], [ 12 ], [ 13 ], [ 14 ], [ 15 ], [ 16 ], [ 17 ]

Features of therapy of loss of blood in severe gestosis

In patients with severe gestosis, protective increase in circulating blood volume often does not occur during pregnancy. Antihypertensive drugs used for treatment may affect the ability to compensatory vascular spasm in case of bleeding. There is also a higher probability of developing OL during infusion therapy due to increased capillary permeability, hypoalbuminemia and left ventricular dysfunction.

Restoration of oxygen transport function of blood

Oxygen transport is the product of CO and the oxygen content in arterial blood. Normally, oxygen transport exceeds VO2 at rest by 3-4 times. There is a critical level of oxygen transport, below which VO2 is not provided and tissue hypoxia occurs. The oxygen content in arterial blood consists of oxygen bound to hemoglobin and dissolved in plasma. Therefore, the oxygen content in arterial blood and its transport can be increased:

• increase in SV,
• increasing the saturation of hemoglobin with oxygen,
• by increasing the concentration of hemoglobin.

Red blood cell transfusion can significantly increase the oxygen content of arterial blood and is usually performed when the hemoglobin concentration is less than 60-70 g/L. Red blood cell transfusion is also indicated when blood loss exceeds 40% of the CBV or hemodynamic instability persists despite ongoing bleeding and the infusion of 2 L of crystalloids and 1-2 L of colloids. In these situations, a decrease in hemoglobin concentration to less than 60 g/L or lower can be expected.

In a patient weighing 70 kg, one dose of red blood cell mass increases the hemoglobin concentration by approximately 10 g/l, and the hematocrit by 3%. To determine the required number of doses of red blood cell mass (p) with ongoing bleeding and a hemoglobin concentration of less than 60-70 g/l, an approximate calculation using the formula is convenient:

P = (100- [Hb])/15,

Where n is the required number of red blood cell doses, [Hb] is the hemoglobin concentration.

For transfusion, it is advisable to use a system with a leukocyte filter, which helps to reduce the likelihood of immune reactions caused by leukocyte transfusion.

Alternatives to red blood cell transfusion. The following methods have been proposed as alternatives to red blood cell transfusion: autodonation, acute normo- and hypervolemic hemodilution.

Another option is intraoperative hardware blood reinfusion, which consists of collecting blood during surgery, washing the red blood cells, and then transfusing the autologous red blood cell suspension. A relative contraindication for its use is the presence of amniotic fluid. To remove it, a separate surgical suction device is used to remove the fluid, wash the red blood cells with a double volume of solution, and use a leukocyte filter when returning the red blood cells. Unlike amniotic fluid, fetal red blood cells can enter the autologous red blood cell suspension. Therefore, if a newborn is Rh-positive, an Rh-negative mother must be given an increased dose of human immunoglobulin anti-Rho [D].

Maintenance of the blood coagulation system

During treatment of a patient with bleeding, the functions of the hemostasis system can most often be disrupted due to:

• influence of infusion drugs,
• dilutional coagulopathy,
• DIC syndrome.

Dilution coagulopathy is clinically significant when more than 100% of the circulating blood volume is replaced and is primarily manifested by a decrease in the concentration of plasma coagulation factors. In practice, it is difficult to distinguish it from DIC syndrome, the development of which is possible:

• in case of placental abruption, especially in combination with intrauterine fetal death,
• amniotic fluid embolism,
• hemorrhagic shock with acidosis, hypothermia.

The hypocoagulation phase of DIC syndrome is manifested by a rapid decrease in the concentration of coagulation factors and the number of platelets (coagulation factors are less than 30% of the norm, prothrombin time and APTT are increased by more than one and a half times from the initial level). Clinically, the diagnosis is confirmed by the absence of clots in the spilled blood with ongoing bleeding.

Initially, the state of hemostasis can be assessed using the Lee-White clotting time, in which 1 ml of venous blood is placed in a small test tube with a diameter of 8-10 mm. Every 30 seconds, the test tube should be tilted by 50°.

The moment when the blood level ceases to occupy a horizontal position is determined. The test is best performed at 37 °C. The norm is 4-10 minutes. After the clot has formed, its retraction or lysis can be observed. Subsequently, the diagnosis and treatment of DIC syndrome should be carried out with laboratory monitoring of coagulogram parameters and determination of the activity of coagulation factors, including antithrombin III, thromboelastogram, concentration and aggregation of platelets.

Fresh frozen plasma (FFP)

The indication for transfusion of FFP is replacement of plasma coagulation factors in the following situations:

• prothrombin time and APTT increased more than one and a half times from the baseline level with ongoing bleeding,
• In case of grade 3-4 bleeding, it may be necessary to begin transfusion of FFP before obtaining coagulogram values.

It is necessary to take into account that defrosting takes about 20 minutes. The initial dose is 12-15 ml/kg, or 4 packages of FFP (approximately 1000 ml), repeat doses are 5-10 ml/kg. There is data that in the hypocoagulation phase of DIC syndrome, FFP doses of more than 30 ml/kg are effective. The rate of FFP transfusion should be at least 1000-1500 ml/h, with stabilization of coagulation parameters, the rate is reduced to 300-500 ml/h. The purpose of using FFP is to normalize prothrombin time and APTT. It is advisable to use FFP that has undergone leukoreduction.

Cryoprecipitate containing fibrinogen and coagulation factor VIII is indicated as an adjunctive treatment for hemostasis disorders with fibrinogen levels greater than 1 g/L. The usual dose is 1-1.5 units per 10 kg of body weight (8-10 packets). The goal is to increase fibrinogen concentrations to greater than 1 g/L.

Thromboconcentrate

The possibility of platelet transfusion should be considered if clinical manifestations of thrombocytopenia/thrombocytopathy (petechial rash) are present, as well as the platelet count:

• less than 50x10 ⁹ /l against the background of bleeding,
• less than 20-30x10 ⁹ /l without bleeding.

One dose of platelet concentrate increases the platelet count by approximately 5x10 ⁹ /l. Typically 1 unit per 10 kilograms of body weight is used (5-8 packets).

Antifibrinolytics

Tranexamic acid and aprotinin inhibit plasminogen activation and plasmin activity. The indication for the use of antifibrinolytics is pathological primary activation of fibrinolysis. To diagnose this condition, a euglobulin clot lysis test with streptokinase activation or a 30-minute lysis test with thromboelastography are used.

[ 18 ], [ 19 ], [ 20 ], [ 21 ], [ 22 ]

Antithrombin III concentrate

If the activity of antithrombin III decreases to less than 70%, restoration of the anticoagulant system is indicated by transfusion of FFP or antithrombin III concentrate. Its activity must be maintained at a level of 80-100%.

Recombinant factor VIla was developed for the treatment of bleeding in patients with hemophilia A and B. However, as an empirical hemostatic, the drug began to be effectively used in various conditions associated with severe, uncontrolled bleeding. Due to an insufficient number of observations, the role of recombinant factor VIla in the treatment of obstetric hemorrhage has not been definitively determined. The drug can be used after standard surgical and medical means of stopping bleeding. Conditions of use:

• hemoglobin concentration - more than 70 g/l, fibrinogen - more than 1 g/l, platelet count - more than 50x10 ⁹ /l,
• pH - more than 7.2 (correction of acidosis),
• warming the patient (desirable, but not necessary).

Possible protocol of application:

• initial dose - 40-60 mcg/kg intravenously,
• if bleeding continues, repeat doses of 40-60 mcg/kg 3-4 times every 15-30 minutes,
• if the dose reaches 200 mcg/kg and there is no effect, check the conditions for use and make adjustments if necessary,
• Only after correction can the next dose (100 mcg/kg) be administered.

[ 23 ], [ 24 ], [ 25 ]

Maintaining temperature, acid-base and electrolyte balance

Each patient with hemorrhagic shock should have their core temperature measured using an esophageal or pharyngeal sensor. At a core temperature of 34°C, atrial arrhythmia, including atrial fibrillation, may develop, and at a temperature of 32°C, VF is likely. Hypothermia impairs platelet function and reduces the rate of blood coagulation cascade reactions by 10% for every 1°C decrease in body temperature. In addition, the cardiovascular system, oxygen transport (shift in the oxyhemoglobin dissociation curve to the left), and liver drug elimination deteriorate. Therefore, it is extremely important to warm both the intravenous solutions and the patient. The core temperature should be maintained at a level greater than 35°C.

Extracellular potassium may be introduced with red blood cell transfusion. Also, the low pH of preserved red blood cells may worsen metabolic acidosis. The consequences of acidemia include a rightward shift in the oxyhemoglobin dissociation curve, decreased sensitivity of adrenergic receptors, and additional impairment of blood coagulation. Acidosis usually corrects with improved organ and tissue perfusion. However, severe acidosis with a pH of less than 7.2 can be corrected with sodium bicarbonate.

During massive transfusion, a significant amount of citrate enters with plasma and erythrocyte mass, which absorbs ionized calcium. Prevention of transient hypocalcemia should be carried out by intravenous administration of 5 ml of calcium gluconate after each package of FFP or erythrocyte mass.

In intensive care, hypercapnia, hypokalemia, fluid overload and excessive correction of acidosis with sodium bicarbonate should be avoided.

Position of the operating table

In hemorrhagic shock, the horizontal position of the table is optimal. The reverse Trendelenburg position is dangerous due to the possibility of an orthostatic reaction and a decrease in MC, and in the Trendelenburg position, the increase in CO is short-lived and is replaced by a decrease due to an increase in afterload.

Adrenergic agonists

Adrenergic agonists are used in shock, in case of bleeding during regional anesthesia and sympathetic blockade, when time is needed to establish additional intravenous lines, in case of hypodynamic hypovolemic shock.

Humoral factors released during tissue ischemia may have a negative inotropic effect in severe shock. The condition for the use of adrenomimetics in hypodynamic shock is adequate replacement of the BCC.

In parallel with the replenishment of the BCC, intravenous administration of ephedrine 5-50 mg may be indicated, repeated if necessary. It is also possible to use 50-200 mcg of phenylephrine, 10-100 mcg of adrenaline. It is better to titrate the effect of adrenomimetics by intravenous infusion of dopamine - 2-10 mcg / (kg x min) or more, dobutamine - 2-10 mcg / (kg x min), phenylephrine - 1-5 mcg / (kg x min), adrenaline - 1-8 mcg / (kg x min). The use of drugs carries a risk of worsening vascular spasm and organ ischemia, but may be justified in a critical situation.

[ 26 ]

Diuretics

Loop or osmotic diuretics should not be used in the acute phase during intensive care. The increased urine output caused by their use will reduce the value of monitoring diuresis during volume repletion. Moreover, stimulation of diuresis increases the likelihood of developing acute renal failure. For the same reason, the use of glucose-containing solutions is undesirable, since significant hyperglycemia may subsequently cause osmotic diuresis. Furosemide (5-10 mg intravenously) is indicated only to accelerate the onset of fluid mobilization from the interstitial space, which should occur approximately 24 hours after bleeding and surgery.

Postoperative therapy of obstetric hemorrhage

After stopping the bleeding, intensive therapy is continued until adequate tissue perfusion is restored. The goals of the therapy are:

• maintaining systolic blood pressure over 100 mm Hg (with previous hypertension over 110 mm Hg),
• maintaining hemoglobin and hematocrit concentrations at levels sufficient for oxygen transport,
• normalization of hemostasis, electrolyte balance, body temperature (more than 36 °C),
• diuresis more than 1 ml/(kg h),
• increase in SV,
• reversal of acidosis, reduction of lactate concentration to normal.

They carry out prevention, diagnosis and treatment of possible manifestations of PON.

Criteria for stopping mechanical ventilation and transferring the patient to independent breathing:

• the problem that caused the artificial ventilation has been resolved (bleeding has been stopped and blood flow to tissues and organs has been restored),
• oxygenation is adequate (pO2 over 300 with PEEP 5 cm H2O and FiO2 0.3-0.4),
• hemodynamics are stable, i.e. there is no arterial hypotension, the infusion of adrenergic agents has been discontinued,
• the patient is conscious, follows commands, administration of sedatives has been discontinued,
• muscle tone has been restored,
• there is an attempt to inhale.

Tracheal extubation is performed after monitoring the adequacy of the patient's independent breathing for 30-120 minutes.

With further improvement of the condition to moderate severity, the adequacy of the BCC replenishment can be checked using the orthostatic test. The patient lies quietly for 2-3 minutes, then the blood pressure and heart rate are noted. The patient is asked to stand up (the option with standing up is more accurate than with sitting up on the bed). If symptoms of cerebral hypoperfusion appear, i.e. dizziness or pre-syncope, the test should be stopped and the patient should be laid down. If there are no such symptoms, the blood pressure and heart rate are noted after a minute. The test is considered positive if the heart rate increases by more than 30 or there are symptoms of cerebral hypoperfusion. Due to significant variability, changes in blood pressure are not taken into account. The orthostatic test can detect a BCC deficit of 15-20%. It is unnecessary and dangerous to perform in case of hypotension in a horizontal position or signs of shock.