D-dimer: normal during pregnancy

A study of the blood coagulation system is one of the important diagnostic factors for monitoring pregnancy. For this, there is a special package of laboratory indicators - a coagulogram. But in some cases, for example, with IVF, problems with pregnancy or conception, the doctor prescribes additional examination. The list of such tests includes D-dimer - determination of fibrin breakdown products in the blood, leading to an increased risk of thrombosis.

You can take a D-dimer test in our clinic or at home from 9 to 13.00 on weekdays.

What is D-dimer

D-dimers are small protein fragments. They are formed during the breakdown of fibrin, a substance whose synthesis occurs in the liver during the breakdown of a blood clot.

Why do you need a D-dimer test?

During pregnancy, a number of hormonal changes occur in a woman’s body, which affect many organs and systems, including the hemostasis (blood clotting) system. Therefore, an elevated level of D-dimer is a physiological norm. Nevertheless, it is advisable to constantly monitor its level and, if it increases significantly, take immediate measures to prevent thrombosis. With varicose veins (and this is observed in at least a third of pregnant women), blood clotting disorders can lead to serious, sometimes life-threatening consequences for the mother and child.

Currently, treatment of pregnant women with drugs that affect the hemostasis system is widespread. It is difficult to find a patient who would not be prescribed dipyridamole during the 40th week of pregnancy. The practice of “correcting” some hemostasiogram parameters with anticoagulants is spreading. The duration of treatment and the combination of drugs used are determined differently, often completely arbitrarily; there are no laboratory methods for monitoring treatment that prove the effectiveness and safety of anticoagulant dosages. Last but not least is the cost of treatment. The physiological response of the body to pregnancy is hypercoagulation in the procoagulant part of the hemostasis system, probably with an adequate response of the anticoagulant part, which is difficult to assess due to the limited capabilities of modern clinical biology. It is important that the levels of hypercoagulability markers do not correlate with the level of clinical risk of thrombosis in pregnant women at high risk of developing venous thromboembolism (VTE) [7].

Rational anticoagulant therapy for pregnant women seems to us to be a treatment system for specific indications with appropriate laboratory monitoring to correct homeostasis indicators in a pregnant woman and prevent obstetric complications, thrombosis and bleeding. It is intended to use dosages of drugs whose pharmacological action is well known for the period necessary to realize the therapeutic effect.

Over the past 3 decades, there has been a consistent upward trend in maternal mortality from VTE. In addition, in most industrialized countries, the age of women giving birth is increasing, and the proportion of pregnant women suffering from severe extragenital pathology is growing. The successes of modern medicine lead to an increase in the life expectancy of patients and promote pregnancy in women with systemic connective tissue diseases, cancer, pathologies of the cardiovascular system, respiratory organs, endocrine pathology, diseases of the blood system, antiphospholipid syndrome, etc. Correct diagnosis and treatment can improve perinatal outcomes in such severe complications of pregnancy as recurrent miscarriage, intrauterine growth restriction syndrome, and gestosis. All of the above situations are associated with the intensification of intravascular thrombus formation both in the vascular bed of the pregnant woman and in the uteroplacental-fetal blood flow system, therefore the use of coagulologically active substances is pathogenetically justified. When prescribing anticoagulants, it should be remembered that the mechanisms of thrombus formation are different in the arterial and venous parts of the vascular bed, in macrovessels and the microcirculatory system (distal to the level of the precapillary sphincter).

The group of pregnant women for whom anticoagulant therapy is indicated include patients with:

1) deep vein thrombosis and pulmonary embolism during real pregnancy,

2) mechanical heart valves,

3) antiphospholipid syndrome (with a correct diagnosis),

4) with thrombophilia: antithrombin-III defect, a combination of hereditary thrombophilias, such as deficiency of proteins S and C, resistance to activated protein C due to the Leiden mutation FV, hyperprothrombinemia due to the prothrombin G20210A mutation, hyperhomocysteinemia, mutation in plasminogen activator inhibitor I like,

5) manifestation of arterial thrombosis,

6) non-developing pregnancy and a decrease in the number of platelets and/or fibrinogen in their preparation for emptying the uterine cavity,

7) fetoplacental insufficiency, confirmed by the results of fetometry, Doppler studies and/or hormonal studies and/or using cardiotocography.

The purpose of anticoagulant treatment is to prevent thromboembolic complications, bleeding, improve blood circulation in the mother-placenta-fetus system, and ensure an uncomplicated course and prolongation of pregnancy.

In our opinion, a necessary and sufficient technique for the prevention of thromboembolic disease (TED) is the use of a risk assessment scale and the prescription of anticoagulant prophylaxis, as is practiced in general surgical practice [9].

A score of 1 point is given if you are over 40 years old, have a body weight of more than 80 kg, have a history of abdominal surgery less than 6 months after, significant varicose veins of the lower extremities, or recent immobilization. 2 points are assessed for compliance with bed rest for more than 3 days, severe chronic obstructive pulmonary disease, inflammation of the intestinal tract, severe infection (pneumonia), condition after delivery (within 1 month), use of oral contraceptives or hormone replacement therapy. The presence of cancer, heart failure, myocardial infarction less than 3 months ago, and a history of an episode of pulmonary embolism are assessed as 3 points. If the score is 5 points or more, enoxaparin is prescribed prophylactically at a dose of 40 mg once subcutaneously until the patient is completely mobilized, the duration of treatment is up to 2 weeks.

Risk factors for VTE in pregnant women comprise two groups [14]. Group 1 includes factors related to the patient herself: age over 35 years, obesity (body mass index more than 29 kg/m2) in early pregnancy, thrombophilia, history of venous thromboembolism, severe varicose veins of the lower extremities, serious extragenital diseases , for example, nephrotic syndrome, the presence of infection or inflammation, immobilization, paraplegia, physical inactivity during long travel, dehydration, intravenous drug use, ovarian hyperstimulation syndrome. The 2nd group includes factors that make up complications of pregnancy: cesarean section, especially emergency in a woman in labor, operative vaginal delivery, massive obstetric hemorrhage, vomiting of pregnant women, gestosis.

More than 12 years ago, work [23] appeared on significantly greater perinatal losses in patients with such types of thrombophilia as deficiency of antithrombin-III, protein S, protein C, and the FV Leiden mutation.

M. de Swiet [29] draws attention to the age of pregnant women and the increase in the incidence of THA in pregnant women over 40 years of age (100 times compared to the group aged 20-25 years). Additional risk factors are excess body weight and a history of more than 3 pregnancies, surgical delivery (caesarean section), suppression of lactation by estrogen. Antenatal risk factors for TEB include in vitro fertilization, gestational diabetes, multiple pregnancies and maternal age over 35 years, and postnatal risk factors include gestosis, eclampsia, placenta previa, placental abruption and cesarean section [17] .

The method for confirming the diagnosis of deep vein thrombosis of the lower extremity in pregnant women is compression ultrasonography, and pulmonary embolism is ventilation-perfusion scanning of the lungs [13]. The low specificity of D-dimer does not allow the use of this laboratory indicator in pregnant women as a laboratory test for confirming TEB [11, 13, 22].

When determining a treatment regimen, the following conditions must be met: firstly, the safety of the drug for the fetus and mother; secondly, the effectiveness of the applied treatment and/or prevention regimen; thirdly, the dosage for the initial course of treatment and maintenance therapy during pregnancy, childbirth and the postpartum period [13].

Let's consider the most commonly used anticoagulant drugs used in obstetric practice.

Unfractionated heparin (UFH).

UFH is obtained from the intestinal mucosa of pigs or from the lungs of cattle. Drugs from different companies have their own pharmacodynamic characteristics, which, however, is offset by the fact that the dosage of the drug is selected depending on the reaction of the patient’s hemocoagulation system.

A. Continuous intravenous administration.

The success of UFH treatment depends on a sufficient initial dose, which should be at least 30,000-35,000 units/day [13]. This treatment regimen is used in acute cases with mandatory monitoring of the effectiveness and safety of treatment using a laboratory test - the activated partial thromboplastin time (aPTT) [29].

B. Subcutaneous intermittent administration

[13]:

a) mini-doses of UFH: 5000 units every 12 hours without laboratory control;

b) moderate doses of UFH: subcutaneously every 12 hours, monitoring changes in the antifactor Xa content to 0.1-0.3 U/ml 6 hours after injection;

c) adapted doses of UFH: subcutaneously every 12 hours, monitoring changes in APTT to values ​​1.5-2 times higher than normal, 6 hours after injection.

B. Inhalation

[1].

Indications for heparin inhalation:

1) prevention of obstetric complications: gestosis, fetoplacental insufficiency;

2) the presence of mild or moderate gestosis;

3) decompensation of diabetes mellitus;

4) treatment of fetoplacental insufficiency.

Inhalations are carried out using an ultrasonic inhaler, diluting heparin with distilled water 1:4, inhalations are carried out 2 times a day with an interval of 12 hours. For the prevention of gestosis, the daily dose is 300 IU/kg, course duration is 7 days, 2-3 courses are required, interval there are 2 days between courses, it is necessary to stop treatment 10 days before delivery; for other indications, the daily dose is 500 units/kg, course duration is 21 days, number of courses is 1-2, interval between courses is 2 weeks, treatment must be stopped 14 days before delivery.

Low molecular weight heparins (LMWH).

LMWH (Table 1)


are obtained by depolymerization of UFH with nitrous acid, or by induction of the benzyl ring and alkaline hydrolysis, or by depolymerization from amyl nitrate, or by peroxidation and, finally, cleavage by heparinase [26].
In general, rational therapy with heparins is presented in Table. 2.

Like UFH, LMWHs do not cross the placental barrier into milk, are safe for the fetus, and are considered the treatment of choice for the treatment of VTE in pregnant women [10, 13].

A prophylactic dose of the LMWH tinzaparin, according to K. Khasia et al. [18], should be 4500 IU/day if the patient’s body weight is less than 100 kg and 5000 IU/kg if she weighs more than 100 kg. The authors suggest that the final dose of LMWH should be based on antifactor Xa activity.

In 2001-2005 the main LMWH in Denmark used during pregnancy was tinzaparin - 95.2% of cases, and dalteparin sodium accounted for 4.8% [4]. According to A. Andersen et al. [4], indications for treatment of pregnant women with low molecular weight heparins in Denmark were an episode of thromboembolism with/or without thrombophilia - 37.3%, perinatal losses and congenital thrombophilia - 35%, recurrent miscarriage and congenital thrombophilia - 7.2%, other causes - 20 ,5%.

Taking into account the poor perinatal outcomes for mother and fetus in patients with antithrombin III deficiency, S. Schulman [27], in order to prevent thrombotic complications, recommends prescribing UFH in a dosage that can increase the aPTT to 1.3-1.5 reference values ​​after 5 days. 6 hours after injection with three subcutaneous injections or the use of LMWH with an antifactor Xa activity level of 0.1-0.2 U/ml.

Antivitamins K (warfarin).

The use of antivitamins K in pregnant women is limited by doctors' fear of the possible teratogenic effects of the drugs and the risk of bleeding in both the mother and the fetus. Disadvantages of drugs should also be considered a delayed onset of action and aftereffect of the drug, an unpredictable clinical effect depending on the dose, which requires laboratory monitoring, a narrow “therapeutic corridor”, multiple interactions with drugs and food products that change the effect of the drug [5]. Antivitamins K are used in pregnant women with artificial heart valves, with allergic reactions to heparin, and in the presence of a high titer of antiphospholipid antibodies [29]. Antivitamins K are not secreted into breast milk and can be used in nursing women [16].

When comparing anticoagulant therapy regimens in pregnant women with an artificial heart valve, the smallest number of thromboembolic and hemorrhagic complications were noted when using heparin in early pregnancy and during the period of organogenesis up to 12 weeks, then when pregnant women were transferred to taking indirect anticoagulants with a return to heparin therapy before childbirth [24 ].

Many drugs affect the effectiveness of antivitamins K; The effect is enhanced by drugs such as erythromycin, co-trimoxazole, fluconazole, isoniazid, metronidazole, amiodarone, clofibrate, propafenone, propranolol, sulfinperazone, phenylbutazone, piroxicam, ethyl alcohol, cimetidine, omeprazole. The effect of antivitamins K is weakened by griseofulvin, nafcillin, rifampin, cholestyramine, barbiturates, carbamazepine, chlordiazepoxide, and sucralfate [15].

Aspirin.

Aspirin acts by irreversibly inhibiting cyclooxygenase, which impairs thromboxane A2 synthesis and prostaglandin metabolism. At the same time, platelet aggregation induced by collagen, adenosine diphosphate, thrombin and thromboxane A2 is reduced [6].

Treatment with aspirin is usually given in conjunction with heparin therapy. The effectiveness of using 75 mg of aspirin with subcutaneous administration of 5000 units of heparin at an interval of 12 hours or in combination with the use of LMWH parnaparin at a dose of 0.3 ml subcutaneously in patients with the presence of antiphospholipid antibodies and recurrent miscarriage has been proven to improve perinatal parameters [25].

Japanese researchers, in 20 confirmed cases of VTE in pregnant women (up to 30 weeks), used UFH with aPTT monitoring to select an adequate dose, followed by switching to low doses of aspirin after the disappearance of the thrombus; However, not a single patient had a filter installed in the inferior vena cava. The need to continue anticoagulant treatment after the disappearance of thrombosis is absent in the Japanese population due to the lack of resistance to activated protein C [21].

A significant issue in clinical practice is the tactics of using anticoagulants during and after childbirth. Most researchers recommend discontinuation of heparin 24 hours before induction of labor during programmed labor, and in a group at very high risk of developing thromboembolic complications, intravenous administration of UFH is canceled 4-6 hours before induction of labor; with an excessive dosage of heparin, it is possible to use a solution of protamine sulfate; resumption of anticoagulant therapy is possible 12 hours after birth [13]. In high-risk groups (for example, the first episode of THA during pregnancy, a mechanical heart valve with thrombosis, multiple congenital thrombophilia with venous thrombosis), heparin therapy during labor is acceptable, for example, 7500 units subcutaneously 2 times a day [29]. If labor is prolonged for more than 18 hours and if labor does not occur within the next 3 hours, a prophylactic dose of LMWH may be used [16]. An original system has been developed [19], which provides anticoagulation during labor in high-risk patients receiving LMWH in a therapeutic dose, without the risk of hemorrhagic complications.

On the eve of a programmed birth or planned cesarean section, an infusion of an UFH solution of 15,000 units/24 hours - 625 units/hour begins with an infusion pump, and in the evening the subcutaneous injection of the drug is canceled.

4 hours before delivery (with the onset of the active phase of labor) or epidural analgesia during abdominal delivery, the infusion is stopped and resumed 2-4 hours after delivery.

Laboratory monitoring of anticoagulant treatment.

Use of APTT.

When monitoring the continuous intravenous administration of heparin, the aPTT should be increased by 1.5-2 times normal after 6 hours from the start of therapy.

Determination of antifactor Xa activity index.

The difficulty of using LMWHs in clinical practice is due to the fact that these drugs can have significant antithrombotic activity in vivo without demonstrating an anticoagulant effect in laboratory tests in vitro [26].

Monitoring of LMWH treatment is carried out monthly, while the level of antifactor Xa should be 0.5-1.2 U/ml (maximum value - 3-4 hours after injection) with a double dose of the drug and 1.0-2.0 U/ml ml if the drug is prescribed once a day [13, 16]. If the level of antifactor Xa activity is less than 0.4 U/ml, the patient will not have bleeding caused by taking heparin [29].

In the presence of artificial mechanical heart valves in pregnant women, with double subcutaneous administration of LMWH, peak concentrations of antifactor Xa should be 0.7-0.8 U/ml and echocardiography should be performed in parallel [2].

The prophylactic dose of tinzaparin should be 0.5-0.8 U/ml within 2 hours after injection, and with a small dose, the dose is adjusted according to the above-mentioned indicator [18].

There is an opinion [28] about the low predictive value of determining the activity of antifactor Xa in relation to the progression of thrombosis and the risk of bleeding.

Monitoring treatment with indirect anticoagulants-antivitamins K.


international normalized ratio
is currently used . INR is the ratio of the patient's prothrombin time to the control prothrombin time, raised to the power of the international sensitivity index of the thromboplastin used. These complexities are needed to standardize the laboratory reagent thromboplastin, which allows comparison of INR values ​​obtained anywhere in the world. To prevent thrombosis, the INR should be 2-3, with the exception of patients with mechanical heart valves and with antiphospholipid syndrome, in whom this indicator should be 3-4 [20].

Complications of anticoagulant therapy.

Complications of heparin treatment include bleeding, heparin-induced thrombocytopenia, and osteoporosis [13]. M. Damodaran et al. [10] reported greater blood loss during childbirth and a significantly higher number of congenital malformations in fetuses of pregnant women receiving LMWH, therefore, according to the authors, treatment with LMWH should be based on clear clinical indications.

In 166 observations of long-term use of LMWH, there were no cases of thromboembolic episodes or significant hematomas, as well as fractures due to osteoporosis with good perinatal indicators, although in 9.6% of observations there was increased blood loss after childbirth [4].

Until now, the question of preventive treatment with anticoagulants remains open. They are increasingly used to improve perinatal pregnancy outcomes in cases of vascular placental complications [8]. To address the issue of prophylactic use of anticoagulants in pregnant women, they are divided into high- and low-risk groups. In the absence of other risk factors, a repeated episode of thrombosis or thromboembolism in pregnant women has a probability of occurrence of 12%, therefore they are either limited to observation or prescribed aspirin in low (up to 100 mg/day) doses. High-risk patients have more than one episode of VTE during pregnancy, thrombophilia, and a family history of VTE. Such patients receive subcutaneous injections of UFH or LMWH from the moment pregnancy is confirmed [29]. The prophylactic use of LMWH and its effectiveness was assessed by M. Aldea et al. [3] in 14,624 pregnant women. Risk factors were obesity, the presence of varicose veins, uterine fibroids, arterial hypertension, cardiopathy, and a history of episodes of venous thrombosis. 22% of patients received prophylactic treatment with LMWH; anticoagulant treatment was discontinued 12 hours before and resumed 12 hours after delivery. The authors attribute the ineffectiveness of heparin prophylaxis (4 cases of venous thrombosis due to the use of drugs) to the use of a small dose of the drug (once a day) and draw attention to the use of LMWH according to indications - with existing risk factors, so as not to excessively increase the cost of treatment. The question of the dosage of heparin for its prophylactic use in patients with congenital antithrombin deficiency is raised in the publication of I. Dubedal et al. [12]: total doses of LMWH were 2500-17,500 U/day; at a daily dose of less than 7500 units/day, more than 50% of pregnant women developed thromboembolic complications, at a higher dose - in 15% (the difference is significant).

Contraindications to heparin therapy:

1) thrombocytopenia - platelet count less than 100 · 109/l;

2) arterial hypertension - systolic blood pressure above 160 mm Hg. Art.;

3) vascular or parenchymal bleeding;

4) acidosis - a decrease in the expected anticoagulant effect;

5) liver and kidney failure.

Thus, the prescription of anticoagulant drugs in pregnant women should be carried out according to clinical indications in groups of patients at high risk of developing VTE or to improve perinatal outcomes during current pregnancy. Monitoring of treatment with anticoagulants is not carried out in the case of inhaled heparin therapy, the use of mini-doses of UFH with subcutaneous administration up to 15,000 units/day, intravenous administration up to 20,000 units/day, and preventive treatment with LMWH with one dose per day. Control is carried out using a certain laboratory test at a certain time with subcutaneous administration of UFH - monitoring the change in aPTT to a level exceeding the norm by 1.5-2 times after 4-6 hours from the moment of injection of the drug; with subcutaneous administration of LMWH, the activity of antifactor Xa is monitored through 4-6 hours after injection to a level of 0.3-0.6 or 0.6-1.2 U/ml depending on the treatment regimen, treatment with warfarin is carried out under the control of INR to levels of 1.5-2.5 depending on groups of patients. A promising, reliable and convenient method of treating pregnant women is the use of warfarin, with the exception of periods from 5 to 15 weeks of pregnancy (the period of organogenesis) and the period before childbirth, taking into account the long half-life of the drug. Treatment with aspirin or chimes when there is a threat of developing VTE is not pathogenetically justified and should not be used. Anticoagulant therapy should be used as indicated and for a long time, sometimes throughout pregnancy. The problem of the future is the development of heparin therapy for amniotic fluid embolism.

Preparing for the study

To obtain the most accurate result, you must adhere to certain rules for preparing for the study. The day before taking blood, you should follow a special diet, which involves excluding a number of foods from your diet:

  • fried foods;
  • foods high in fat (butter, lard, cream, full-fat yogurt and sour cream);
  • dishes containing spices and vinegar (in particular canned food).

It is not recommended to eat chips, crackers and other snacks with a lot of irritating seasonings and flavorings - these products should be completely avoided during pregnancy. You should also try to avoid rooms with people who smoke.

Blood for D-dimer analysis is taken from a vein strictly on an empty stomach. Ideally, 12 hours should pass from the last meal to the blood draw, but during pregnancy this period of time is quite difficult to maintain, so it can be reduced to 8 hours. In the morning, on the day of the study, you are allowed to drink clean still water (last time - 30 minutes before blood sampling).

Also, the accuracy of test results can be affected by the psycho-emotional state of a pregnant woman. Therefore, on the eve of the study, you should avoid meeting with unpleasant and conflict-ridden people and watching “heavy” dramatic films.

You should arrive at the clinic a little early to rest a little before taking blood.

Important! Be sure to tell the technician and your doctor if you are taking any medications. If possible, medication should be stopped, but this can only be decided by the doctor who ordered the study.

In the presence of acute infectious diseases, the examination is postponed until complete recovery.

Causes of increased D-dimer

One of the reasons for the increase in the level of D-dimer and the activation of the coagulation system is the preparation of the body for childbirth, which in any case is accompanied by blood loss of varying degrees of intensity. Therefore, the maximum level of D-dimer will be observed precisely in late pregnancy. In general, its level increases approximately threefold compared to non-pregnant healthy women.

An increase in D-dimer is often observed along with other signs of late toxicosis of pregnancy (preeclampsia). These include:

  • persistent increase in blood pressure, which is difficult to treat with antihypertensive drugs;
  • the appearance of protein in the urine;
  • swelling of the upper and lower extremities, face and neck.

Reference! Preeclampsia is a condition that is dangerous due to its complications - eclampsia and preeclampsia. These pathologies are characterized by cerebral circulation disorders and, if left untreated, pose a serious threat to the life of the mother and child.

If D-dimer is slightly elevated

A slight excess of D-dimer levels can be observed in the following cases:

  • during multiple pregnancy;
  • after operations (even if they were performed a year or two before the study);
  • for influenza, acute respiratory infections and acute respiratory viral infections;
  • for injuries and burns.

In these cases, D-dimer increases temporarily, its level returns to normal values ​​after stabilization.

Pathological causes of increased D-dimer

In some cases, an increase in D-dimer levels can be observed in certain chronic diseases, often asymptomatic. These include:

  • regular and gestational diabetes mellitus (the latter is typical only during pregnancy and goes away after childbirth);
  • liver and gallbladder diseases;
  • various kidney diseases that impair their function;
  • cardiovascular pathologies (including those of inflammatory origin - myocarditis, pericarditis);
  • constant exposure to allergens.

Important! An increase in D-dimer can sometimes be one of the first signs of incipient placental abruption. Symptoms: nagging pain in the abdominal area of ​​varying degrees of intensity, discharge mixed with blood, nausea and dizziness. The appearance of these signs requires immediate medical attention!

What to do if D-dimer is elevated

If the level is slightly exceeded and the patient is feeling normal, treatment can be carried out in a day hospital. Therapy includes injections and drips of blood thinning drugs.

The following recommendations will also help reduce D-dimer (but they will not replace the main treatment):

  • Drink more pure still water;
  • Do physical exercise (special classes for pregnant women and water aerobics are especially useful);
  • Walk more in the fresh air;
  • Don't overwork yourself;
  • Pay attention to proper nutrition.

Important! If any of your relatives suffered from blood clotting disorders during pregnancy, you are at increased risk of thrombotic complications. In this case, consultation with a geneticist is recommended, since in some cases these pathologies are inherited. It is advisable to do this at the stage of pregnancy planning.

What is fibrinogen?

Fibrinogen is a protein that is one of the main blood clotting factors. It is necessary for the formation of blood clots and stopping bleeding, helps in the healing of damaged tissues and restoration of their blood supply. When the walls of blood vessels of any size are damaged, a cascade of biochemical reactions is triggered in the blood, the final result of which is the conversion of fibrinogen into fibrin. A blood clot forms. Almost immediately after this, another cascade of reactions is launched - the anticoagulation system of the blood.

Fibrinogen is synthesized by liver cells and is constantly present in the blood in a certain concentration. When the vascular wall is damaged, it is converted into fibrin, with the help of the enzyme thrombin, which forms polymers in the form of white threads - they are part of the blood clot. Changes in the concentration of fibrinogen in the blood threaten bleeding or thrombosis.

During pregnancy, about 600 ml of blood passes through the vessels of the placenta every minute. After the placenta separates and is delivered during labor, the lining of the uterus is left with a bleeding surface. During childbirth, a woman loses about 500 ml of blood (during a caesarean section, twice as much - an average of 1000 ml). But then the uterus contracts, the blood vessels contract, and the bleeding stops. It is very important that there is a balance in the functioning of the blood coagulation and anticoagulation systems.

During pregnancy, under the influence of hormones, the blood coagulation system is activated. The body is, as it were, “preparing” to cope with physiological blood loss at a crucial moment.

The level of fibrinogen in the blood of the expectant mother gradually increases and in the third trimester increases 2-3 times compared to normal values. This happens under the influence of hormones.

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