Thrombosis in pregnant women is a pathological condition characterized by the formation of blood clots in the lumen of blood vessels, which are called thrombi. They do not allow blood to circulate freely through the circulatory system, seriously impeding blood flow and causing a number of serious complications. Vein thrombosis in pregnant women is not uncommon. It appears against the backdrop of a number of changes occurring in a woman’s body during this period, and requires special attention both from the woman herself and from doctors.
Prevention of thrombosis in pregnant women and its treatment is one of the areas of work of the CELT Phlebology Department. Our clinic has been operating since 1993 and is multidisciplinary, so phlebologists work closely with gynecologists, achieving the best results. They have at their disposal a powerful diagnostic and treatment base, as well as modern gentle techniques that allow them to maintain the patient’s health and give birth to a healthy baby.
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How does blood clotting occur?
The actual clot is formed by creating a fibrin network that strengthens and stabilizes it. This is due to the activation of the coagulation cascade - inactive blood coagulation factors circulating in the blood plasma begin to activate each other.
Under the influence of mechanical damage, platelets secrete thrombokinase, which triggers a number of processes leading to the formation of the corresponding factor that initiates blood clotting - calcium ions and plasma protein factors are important in this process.
Blood coagulation diagram
As a result of the blood clotting cascade, factor X together with factor Va forms a complex called prothrombinase, which converts prothrombin into thrombin. Thrombin, in turn, converts fibrinogen (a plasma protein that circulates in the blood) into fibrin (a water-insoluble protein), which forms a network of fibers that form the backbone of the clot.
Causes of blood clots
Thrombosis is promoted, in particular:
- surgical intervention;
- extensive injuries;
- respiratory failure;
- heart failure;
- oral contraceptives;
- use of certain hormonal drugs;
- phlebeurysm;
- obesity;
- stroke;
- age > 40 years.
The risk of thrombosis increases significantly during pregnancy and the postpartum period.
The risk of developing thrombosis during pregnancy is many times higher in people with congenital or acquired thrombophilia. It is estimated that 20-30% of cases of thromboembolic disease are associated with a genetic predisposition to its development.
The main genetic causes of the disease are the carrier of the Leiden variant of the factor V gene of the blood coagulation system (F5 gene, mutation p.Arg534Gln) or a mutation of the prothrombin gene (F2 gene, mutation c. * 97G>A). Other known predispositions are hereditary deficiencies of blood clotting inhibitors (antithrombin, protein C or protein S) and hereditary hyperhomocysteinemia (associated, for example, with mutations in the MTHFR gene). In families with thrombosis, factor V Leiden mutation and prothrombin gene mutation are detected in approximately 60% of cases.
Diagram of blood clot formation
Why is a blood clot dangerous?
Thrombosis is life-threatening when a blood clot breaks away from the wall of a vein. A clot that travels through the bloodstream may travel into the atrium or ventricle or into the pulmonary artery, causing shock, cardiac arrest, and respiratory arrest due to a heart attack or pulmonary embolism. These conditions pose a direct threat to the life of a pregnant woman and can cause her sudden death.
Other consequences of thrombosis include: post-thrombotic syndrome, which manifests itself as changes in skin color, pulmonary hypertension and leg ulcers. In pregnant women, thrombosis can cause miscarriage, and pregnancy and the postpartum period significantly increase the risk of its occurrence.
The risk of thrombosis during pregnancy is associated with pressure on the iliac veins, which increases as the baby grows. In this case, embolism most often develops in the iliofemoral region of the deep veins, and in 90% of women, symptoms appear only on the left leg.
Deep vein thrombosis (DVT) and resulting pulmonary embolism (PE) are the most dangerous complications of pregnancy and the postpartum period. The incidence of venous thromboembolic complications (VTEC) in pregnant women is up to 5 cases per 1000 women, which is several times higher than in non-pregnant women. This indicator tends to increase [1-3].
Pregnancy is a thrombotic condition due to an increase in the amount of certain blood coagulation factors (VII, VIII, IX and fibrinogen) and a weakening of the fibrinolysis system, dilation, decreased tone of the venous wall due to the increasing effect of progesterone, as well as impaired venous outflow from the lower extremities [1 , 4, 5]. Such changes prepare the pregnant woman’s body for childbirth and reduce possible blood loss. However, quite often the activation of the coagulation component of hemostasis becomes pathological. Pregnancy itself does not cause the development of thromboembolic complications. The basis for the development of phlebothrombosis is physiological hypercoagulation, increased blood viscosity, the formation of blood stasis in the veins of the pelvis and lower extremities against the background of changes in hormonal status and topographic-anatomical relationships of vessels and pelvic organs [4, 6].
Management of pregnant women with VTEC is a complex task, which is due to the special social and medical status of the woman, as well as serious restrictions that the need to eliminate or minimize the negative impact of diagnostic and therapeutic manipulations on the fetus imposes on the actions of doctors.
The purpose of this study is to analyze the experience accumulated by the clinic in treating pregnant women with DVT and PE, and to optimize surgical tactics in this group of patients.
Material and methods
From 1996 to 2006, 100 pregnant women with DVT were treated in the Faculty Surgery Clinic. 15 women were admitted with symptoms of pulmonary embolism. The age of the patients ranged from 15 years to 41 years (average age 28.5 years), gestational age - from 5 to 40 weeks (average 28 weeks). There were 19 women in the first trimester of pregnancy, 18 in the second trimester, and 63 in the third trimester.
The main objective of the instrumental examination was to determine the embolic danger of the thrombus. In 98 cases, the first stage of examination was ultrasound angioscanning. In 16 cases, additional retrograde iliocavography was required. In 2 pregnant women, using this method, a primary examination of the condition of the proximal venous bed was carried out. Pulmonary angiography was performed in 8 women with pulmonary embolism.
Results and discussion
In 87 cases, DVT was proximal, in 13 cases it was distal. VTEC in the majority of pregnant women under our supervision (63%) developed in the third trimester. This allows us to characterize this period as the most thrombotic. In the third trimester, blood flow in the inferior vena cava (IVC) system significantly slows down as a result of a decrease in venous tone (hormonal influences) and compression of the main veins by the growing uterus, and the procoagulant potential of the blood increases.
The choice of surgical treatment tactics for VTEC in a pregnant woman depended not only on the pathological process (localization and embolic danger of thrombosis), but also on the gestational age, since the degree of maturity of the fetus and the size of the uterus most limit the surgeon’s actions. It is advisable to correlate the trimester of pregnancy with possible surgical interventions during this period.
In 4 out of 56 pregnant women with pulmonary embolism, instrumental examination revealed non-embolic (occlusive and parietal)
thrombosis. In 8 cases it complicated the course of the first trimester, in 11 - the second trimester and in 37 - the third trimester of pregnancy. In this subgroup, direct anticoagulants and elastic compression of the lower extremities were prescribed. One pregnant woman with a massive pulmonary embolism underwent thrombolytic therapy; in the remaining patients, given the nature of the damage to the vascular bed of the lungs, it was decided to refrain from thrombolysis. On average, inpatient treatment lasted up to 2 weeks. An increase in the level of thrombosis, the formation of its embolic variants, and pulmonary embolism by the time of discharge from the hospital was not recorded in these patients.
An unfavorable pregnancy outcome was noted in one woman admitted to the surgical hospital with massive pulmonary embolism. According to vital indications, thrombolytic therapy was started, against the background of which a spontaneous miscarriage occurred.
In the long-term period, the course of pregnancy was monitored in 27 women. In 21 patients, pregnancy proceeded without complications, in 6 the complications (preeclampsia, polyhydramnios, chronic intrauterine fetal hypoxia) with which they were admitted to the surgical hospital persisted. We did not observe any complications of pregnancy caused by antithrombotic therapy and long-term anticoagulant prophylaxis. 17 women gave birth on their own; in 10 cases, delivery due to the peculiarities of the obstetric situation (in particular, due to gestosis) was performed by caesarean section.
In 44 cases, the proximal part of the thrombus had an embolic
nature, there was a threat of pulmonary embolism, which required surgical interventions to prevent it. In women who were in the first trimester of pregnancy, ultrasound examination revealed embolic thrombosis of the iliocaval segment in 6 and femoropopliteal segment in 3. In 2 cases, ultrasound angioscanning failed to visualize the apex of the thrombus in the IVC, and therefore retrograde iliocavography was performed, the data of which confirmed the embolic nature of the thrombotic lesion.
In the first trimester of pregnancy, the choice of surgical method for preventing pulmonary embolism is significantly limited due to the fact that the fetus during this period is most sensitive to external influences, and their consequences lead to embryogenesis disorders. We consider plication of the IVC to be the safest for the fetus when the iliocaval segment is affected. Implantation of a vena cava filter, accompanied by X-ray irradiation, is possible when termination of pregnancy is planned at the request of the patient or in case of pathology of the pregnancy itself (indications for termination are determined by an obstetrician-gynecologist). In such cases, a vena cava filter (preferably removable) should be implanted, and then the pregnancy should be terminated (see diagram).
Scheme 1. Selection of tactics for diagnosis and treatment of DVT of the lower extremities during pregnancy. Note. COF - common femoral vein; SPV—superficial femoral vein; RICG—retrograde iliocavography; USAS - ultrasound angioscanning.
All 11 patients with embolic DVT at this stage of gestation underwent surgical interventions: in 8 cases IVC plication, in 1 case thrombectomy from the common femoral vein, in 2 patients a removable vena cava filter was implanted.
The postoperative period in all patients was without complications. There were no IVC thrombosis, pulmonary embolism, or deaths. In one case, an embolism occurred in the area of IVC plication. Both removable vena cava filters were removed within 2 months. Pregnancy was preserved in 5 women, another 5 underwent termination of pregnancy (in 3 cases for medical reasons, in 2 at the woman’s request), 1 patient had a spontaneous abortion during thrombolytic therapy (the same patient was planned to terminate her pregnancy due to angiopulmonography ).
In the second trimester of pregnancy, 7 patients were operated on for floating thrombosis of the iliocaval and/or femoropopliteal segment.
During this period, the choice of treatment tactics is most difficult: on the one hand, it is possible to use any method of preventing pulmonary embolism, since there are no absolute contraindications to the use of x-ray diagnostic methods and endovasal interventions, on the other hand, the size of the pregnant uterus, which compresses the vessels, can create technical difficulties during implantation vena cava filter and when performing thrombectomy from the iliocaval segment.
In all cases, IVC plication was performed. In one of the patients with the spread of a floating thrombus to the suprarenal section of the IVC, the first stage was thrombectomy from the suprarenal, renal and infrarenal sections of the IVC, and then its plication with a mechanical suture immediately distal to the renal veins.
In one case, an embolism occurred in the area of pulmonary embolism plication in the postoperative period. There were no deaths. Pregnancy was maintained in all women.
In the third trimester of pregnancy, the choice of method of surgical prevention of pulmonary embolism depends not only on the size of the uterus, but also on the course of pregnancy and the degree of fetal maturity. Enlargement of the uterus does not always allow a reliable assessment of the proximal border and the nature of the apex of the thrombus, which significantly complicates the choice of optimal treatment tactics. Our attitude towards the choice of treatment method in such cases has changed with the accumulation of experience. Until 2004, we regarded all thrombi whose embolic danger was not clearly established during instrumental examination as potentially embolic and performed IVC plication. Subsequently, we drew attention to the results of ultrasound studies performed in the early postpartum period, which indicated that the upper limit of post-thrombotic changes in the iliocaval segment, as a rule, coincided with the boundary of the thrombus identified by ultrasound angioscanning during pregnancy. Probably, the enlarged uterus not only compresses the iliac veins, but also prevents the proximal growth of thrombosis. In this regard, after 2004, in the absence of the ability to visualize the proximal part of the thrombus, we performed surgical intervention only in women with full-term pregnancy, combining it with cesarean section. Similar tactics were also used in cases where, during a shorter pregnancy, women with iliocaval thrombosis needed premature surgical delivery due to complications of the pregnancy itself (for example, due to premature placental abruption).
As for other surgical interventions aimed at preventing pulmonary embolism, a significant increase in the size of the uterus and compression of the IVC and iliac veins makes it almost impossible to reliably implant a vena cava filter and thrombectomy from the iliocaval segment.
Performing thrombectomy from the initial section of the external iliac vein is technically possible, but severe venous hypertension and blood stasis against the background of compression of the iliac veins by the uterus causes a high risk of rethrombosis in the postoperative period. IVC plication remains the method of choice (see diagram).
Moreover, in the case of a full-term pregnancy (corresponding to the maturity of the fetus), it is possible to perform it simultaneously with surgical delivery, the choice of which method in this group of women is determined by the surgical situation. The presence of an embolic thrombus in a case where labor can begin at any moment requires surgical prevention of pulmonary embolism on an emergency basis, before the development of the pushing period. The need for laparotomy to perform plication of the IVC, the maturity of the fetus and the possible development of labor in the immediate postoperative period dictate the need for cesarean section (see diagram).
In the third trimester of pregnancy and in the prenatal period, surgical interventions were performed in 26 patients with embolic iliocaval thrombosis (complicated by pulmonary embolism in 7 cases). The patients were divided into two subgroups depending on the possibility of delivery as soon as possible after admission to the hospital. The possibility or need for an early delivery was determined by the obstetrician-gynecologist after examining the woman and ultrasound examination of the fetus.
In 12 cases, the fetus was recognized as immature, the pregnancy was premature, but the course of pregnancy itself was not disturbed. These patients underwent IVC plication (9 cases), thrombectomy from the external iliac and common femoral vein (1), and implantation of a permanent vena cava filter (2). Implantation of a vena cava filter was carried out in cases where the gestational age was 26 and 28 weeks, the enlargement of the uterus was considered insignificant, but in the future we abandoned this approach.
In 9 women, pregnancy was recognized as full-term and delivery was possible. All these women were delivered by cesarean section simultaneously with IVC plication.
Premature surgical delivery was required in 5 women: in 2 due to the development of fetal complications (intrauterine infection, intrauterine growth retardation syndrome), in 2 due to premature placental abruption during thrombolytic therapy for massive pulmonary embolism. Another patient had antepartum rupture of water. In all these cases, simultaneous IVC plication and surgical delivery were also performed.
In the postoperative period, 2 patients developed thrombosis of the IVC up to the plication zone; in both cases it was preceded by metroendometritis after cesarean section. After thrombectomy, the patient developed rethrombosis from the external iliac and common femoral vein (the thrombus was of a parietal nature). We did not observe any cases of pulmonary embolism. One patient died in the early postoperative period. The cause of the unfavorable outcome was atonic uterine bleeding with the development of DIC syndrome.
Of the women who did not undergo delivery, 1 at 26 weeks with recurrent miscarriage and antiphospholipid syndrome had a miscarriage on the next day after IVC plication. Since the miscarriage occurred with a living fetus, it was considered a premature birth. In the remaining patients, subsequent pregnancies proceeded without complications.
Thus, mortality after surgical interventions in pregnant women with VTEC was 2.3% (1 case out of 44). Pregnancy after surgery was preserved in 73.3% of cases (22 out of 30 women with premature pregnancy). In 14 cases, cesarean section was performed simultaneously with IVC plication. In 5 patients, pregnancy had to be terminated due to early X-ray contrast studies or at the request of the patient. In one case, a miscarriage occurred during thrombolytic therapy, in another, intrauterine fetal death was diagnosed, and another patient developed premature birth in the early postoperative period.
Conclusion
The choice of treatment tactics in pregnant women with DVT is one of the most difficult problems arising in surgical practice. There are two main reasons that make it difficult to conduct research in this direction. The first is the difficulty in accumulating sufficiently extensive material. Even in our clinic, which traditionally specializes in the diagnosis and treatment of VTE, only 100 pregnant women were hospitalized over 10 years. The second is that it is almost impossible to plan and conduct clinical studies using the principles of evidence-based medicine due to the need to make a decision on treatment tactics for the mother and fetus as soon as possible. There is not and, apparently, there cannot be a single rigid scheme for all possible cases. It is possible that when choosing a method of treating venous thromboembolic complications during pregnancy, it is necessary to take into account not only the type of thrombosis and gestational age, but also the individual characteristics of the course of this pregnancy.
Our results indicate that in most cases the situation can be resolved successfully. We hope that the experience of our clinic will be useful to all surgeons who have to treat pregnant women with DVT, and we invite all interested colleagues who have their own views on the problem to share their data.
Causes of thrombosis during pregnancy
During pregnancy and the perinatal period, the cause of thrombosis can be:
- hormonal changes necessary to maintain pregnancy (hormones cause vasodilation and stagnation of blood in the veins, increase blood viscosity, which contributes to the formation of blood clots);
- difficult outflow of blood from the legs due to pressure on the veins by the enlarging uterus;
- C-section;
- prolonged immobilization after childbirth, contributing to venous stagnation.
Stagnation of blood in the veins
The above risk factors, coexisting with an individual genetically determined predisposition to thrombosis, significantly increase the risk of thrombosis during pregnancy and its dangerous consequences.
Treatment
Treatment consists of taking small doses of anticoagulants with periodic laboratory and ultrasound monitoring. The day before the planned CS, medications are stopped. If the birth is natural, then the expectant mother should inform the doctor about the onset of contractions immediately.
Compression bandages or stockings are used during childbirth. They should be worn during the day for a month after birth for any type of delivery.
The Medical Center on Bratislavskaya provides diagnosis and treatment of vein diseases. For inquiries and appointments with specialists at a convenient time, please call.
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Symptoms of thrombosis in pregnant women
Thrombosis in pregnant women is often asymptomatic. The symptoms that may appear with thrombosis during pregnancy can be ambiguous and can occur with other diseases, and when they do occur, they are often underestimated and considered typical pregnancy symptoms.
The most common symptoms that appear several days after a clot forms include:
- swelling, usually in one leg, around the ankle, then swelling in the calf or the whole leg (usually one leg is affected);
- pain in the legs, aggravated by walking, with increased pain and tenderness when touched, disappearing when the limb is immobilized;
- redness and increased warmth of the skin of the painful limb.
Dangerous symptoms of thrombosis appear when a blood clot breaks off and migrates along with the bloodstream. During complications of thrombosis (pulmonary embolism), difficulty breathing occurs with shortness of breath and chest pain. Difficulty in breathing progresses rapidly and can kill the patient within seconds.
Diagnosis of thrombosis
Diagnostic tests for thrombosis include blood chemistry tests (especially D-dimer levels) and duplex Doppler ultrasound of the venous vessels, which will determine the correct venous blood flow in the extremities and the presence of blood clots. These tests can confirm the occurrence of thrombosis only when symptoms first appear.
Ultrasound examination of venous vessels
A test to determine the risk of thrombosis is to perform DNA tests that look for abnormal gene mutations, and most often mutations that predispose to congenital thrombophilia, especially during pregnancy and the puerperium.
Determining the risk of the disease in women during the precontraceptive period will allow the doctor to begin appropriate prevention and treatment of thrombosis during pregnancy. To determine whether you are at risk of developing thrombosis, it is necessary to carry out thrombophilia tests, that is, tests that detect mutations in the genes encoding: factor V Leiden (Leiden-FVL mutation), prothrombin, methylenetetrahydrofolate reductase (MTHFR), factor PAI-I. / SERPINE1 Factor V R2.
In pregnant women, thrombosis most often occurs in the form of FVL mutation (2-10%), mutation of the methylenetetrahydrofolate reductase gene MTHFR (8-16%), mutation of the prothrombin gene (2-6%), deficiency of proteins C and S (0.2-1% ) and the presence of anticardiolipin antibodies (1-7%).
Both congenital (hereditary) thrombosis and acquired thrombosis increase the risk of pregnancy loss. An estimated 15% of pregnancies end in miscarriage, and this affects 0.4–2% of couples. The results of a clinical study conducted by the Nimes Obstetrics and Hematology Department (NOHA) showed a strong correlation between unexplained pregnancy loss and the presence of prothrombin and factor V mutations in the heterozygous system.
The Leiden mutation is a genetic defect that affects approximately 5% of white people, is associated with a 3- to 7-fold increased risk of venous thrombosis, and is predominantly inherited.
This means that a person who has a mutation in one copy of the gene (known as a heterozygote) has an increased risk of thrombophilia. The risk is even higher for people who are homozygous, i.e. have a mutation in both copies of the F5 gene. Heterozygotes for the Leiden mutation have a 2-3 times increased risk of pregnancy loss and other complications during pregnancy (for example, eclampsia, fetal malnutrition, premature placental abruption).
Thrombophilia associated with factor V Leiden mutation and thrombophilia associated with resistance to active protein C are inherited in an autosomal dominant manner. The resistance of factor V to activated protein C accelerates the blood clotting process and does not inhibit the growth of a blood clot.
Activated coagulation factor V is a component of the factor X enzyme complex that converts prothrombin to thrombin during blood clotting. Factor V deficiency is inherited in an autosomal recessive manner and promotes a slower blood clotting process due to decreased amounts of factor V.
Factor II of the prothrombin F2 gene (G20210A) causes thrombophilia associated with thrombin deficiency. The mutation increases the concentration of prothrombin in the blood and is inherited in an autosomal dominant manner. Prothrombin is activated to thrombin during blood clotting, which allows fibrinogen to be converted into fibrin; the presence of mutations disrupts this process.
The MTHFR gene encodes the enzyme methylenetetrahydrofolate reductase, which catalyzes the formation of 5-methyltetrahydrofolate, which is necessary for the conversion of the potentially toxic amino acid homocysteine to methionine by methionine synthase. This mutation is manifested by an increase in the concentration of homocysteine in the blood serum. Excess homocysteine in the body can damage the endothelium of blood vessels and, as a result, lead to atherosclerosis and venous and arterial thrombosis.
Thrombophilia associated with prothrombin is predominantly inherited and is characterized by symptoms of venous thromboembolism, in adults mainly deep vein thrombosis or pulmonary embolism. Thrombophilia associated with the presence of the c.20210G>A variant of the F2 gene has been shown to increase the risk of pregnancy loss.
Deep vein thrombosis
The risk of thrombosis during pregnancy and pulmonary embolism is reduced by any measures to improve blood flow and prevent its stagnation. In pregnant women with a genetically confirmed predisposition to the disease, prophylactic anticoagulants (low molecular weight heparins) are used under strict medical supervision. These women should wear special tights, maintain a healthy body weight, eat a healthy low-fat diet, hydrate regularly, be physically active and avoid prolonged sitting.
By performing genetic tests for thrombophilia and gene mutations that cause thrombosis, a pregnant woman can prevent serious complications (mainly pulmonary embolism and miscarriage) by administering prophylactic or anticoagulant treatment in close collaboration with her doctor. Only this procedure guarantees the correct course of pregnancy, childbirth and the postpartum period for both mother and child.
Once performed, genetic testing will provide lifelong information and enable you to make better decisions, including preventative measures and reducing symptoms of thrombosis during pregnancy and throughout the fertile period.
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