Pregnancy with thrombotic disease

Introduction to pregnancy with thrombotic diseases Vascular disease is more likely to occur during pregnancy because of the favorable conditions for embolization during pregnancy, such as a 2-fold increase in fibrinogen, the number of platelets increases during pregnancy compared with non-pregnancy, with an average of 210 × 109 / L in the early pregnancy and 203 in the middle ×109/L, the late stage is 184×109/L, and the concentrations of coagulation factors V, VII, VIII, IX, X and XII are also increased. If the pregnant woman is less moving, the blood flow is slow, and the vein during pregnancy is thicker than the original. Thickening is the ovarian blood vessels, which is 6 times larger than the original, and the blood is prone to stagnation, so thrombosis and embolism increase during pregnancy. basic knowledge Sickness ratio: 0.5% Susceptible population: pregnant women Mode of infection: non-infectious Complications: multiple organ dysfunction syndrome

Pregnancy with thrombotic disease

(1) Causes of the disease

Coagulation during pregnancy, physiological changes in the fibrinolytic system create protective conditions for preventive hemostasis in the future exfoliation of the placenta, and also provide an opportunity for venous thrombosis. During pregnancy, the risk of venous thrombosis in women during puerperium is higher than that of non-pregnant women. The significant increase was five times that of non-pregnant women of the same age. Thrombosis was caused by imbalance between blood clotting and anticoagulation, thrombosis and antithrombotic.

(two) pathogenesis

The thrombus is mainly from the deep veins of the lower extremities. The thrombosis mechanism was as early as 1856. The German pathologist Virehow pointed out that blood changes, blood vessel wall damage and blood composition changes are the three major factors of thrombosis.

Blood changes

(1) The average blood volume increased by about 45% during pregnancy, and the cardiac output increased by 30% to 50%. The venous dilatation of pregnant women increased significantly, which slowed down the blood flow. The enlarged uterus pressed the abdominal pelvic vein and the lower extremity vein. The increase in pressure causes blood stasis in the pelvic and lower extremity veins.

(2) Increased fibrinogen in the late pregnancy, promote red blood cell aggregation, increase hematocrit, and increase blood viscosity. In the blood during pregnancy, the resistance of red blood cells through capillaries and small blood vessels increases, and the increased uterus in the third trimester increases the pressure on the abdominal cavity. After the child enters the basin, the iliac vein is compressed. The above conditions may cause the venous blood in the pelvic cavity and the lower extremities to slowly stagnant, the reflux is blocked, and the blood viscosity is increased and the blood vessel wall is involved, so thrombosis is easily caused.

2. Changes in blood composition

From the gestation period, plasma fibrinogen increased by 2 times, up to 6g / L, vitamin K-dependent factor (II, VII, IV, X) increased by 1.2 to 1.8 times, clotting factor increased by 1.5 times, so that the blood is in a hypercoagulable state Accelerated erythrocyte sedimentation during pregnancy, it is easy to increase the adhesion and aggregation of red blood cells in the blood vessels, reaching the highest peak within 24 hours after delivery, and the fibrinolytic activity is decreased in the late pregnancy, which makes the platelet adhesion increase, especially after childbirth or surgery, especially when blood loss is excessive. A large number of new platelets are released from the bone marrow, and the viscosity is extremely high, so that a woman who is in a hypercoagulable state is more likely to form a thrombus.

3. Changes in the blood vessel wall

Vascular endothelium damage and vasculitis caused by various causes can cause thrombosis factors, such as huge fetuses, polyhydramnios, twins, etc., for any mechanical or chemical reasons. Abdominal pelvic arteriovenous injury of the endothelium, such as direct compression of blood vessels during surgery, infection, postpartum sepsis, etc., can lead to vascular endothelial cell damage.

4. Other

Coagulation inhibition or protein deficiency in the fibrinolytic system, some women have these defects, leading to hypercoagulable and repeated venous thromboembolism, Hellgren et al (1989) and Trauscht Van Hon et al (1992) reported that there is hereditary antithrombin Complications, women with protein C deficiency can develop thromboembolism in 1/3 of pregnancy, and Hellgren et al (1995) found that 60% of pregnant women with thromboembolism had a factor V gene defect that caused activation of protein C resistance.

Pregnancy with thrombotic disease prevention

When there are three factors of thrombosis, you can take small doses of aspirin 40 ~ 80mg / d and clomiphene 150 ~ 200mg / d, combined with anti-thrombosis, compound Danshen solution 10 ~ 20ml plus low molecular dextran 500ml intravenously, continued 7 ~10 days.

Pregnancy with complications of thrombotic disease Complications, multiple organ dysfunction syndrome

Can be complicated by skin and mucous membrane embolic necrosis, microcirculation failure and organ dysfunction.

Symptoms of pregnancy complicated with thrombotic diseases Common symptoms Venous thrombosis, edema, low fever

Superficial vein thrombosis

Shallow thrombophlebitis, systemic reaction is light, local symptoms are obvious, there is obvious pain and tenderness, and pain is relieved or disappeared within 2 to 4 weeks.

2. Deep vein thrombosis

The signs and symptoms of deep vein thrombosis involving the lower extremities vary, depending on the degree of occlusion and the intensity of the inflammatory response. In the early stage of deep vein thrombosis, the symptoms are not obvious. After 1 week of the lesion, low fever and rapid pulse rate begin. Leukocytes are slightly elevated, and about 55% of deep vein thrombosis occurs within 3 weeks after delivery or surgery. The general incidence is 7 to 10 days after delivery, and the earliest on the 2nd day, within 6 weeks, there is a certain Risk, if the pregnant woman has a tendency to thrombosis before pregnancy or has a history of previous thromboembolism, thrombosis occurs more than 3 months after pregnancy, the disease occurs in the lower limbs and pelvic cavity, the left side of the lower limb is more than the right side, the reason Is the left common iliac vein under the common iliac artery, due to local compression, blood flow resistance from the left lower limb and pelvic vein is greater than the right side.

(1) swelling of the limbs: venous thrombosis, causing blood flow back obstacles, due to large, small veins and capillary hypoxia, resulting in hypoxia, endothelial cells, inflammation, capillary wall permeability, tissue edema, Limb edema, and arteries are often accompanied by paralysis, lymphatic stasis and reflux disorders, limb swelling is aggravated, thrombosis in the patellofemoral or femoral vein upper end, acute onset, severe pain, typical thrombosis phlebitis involving the lower limbs The thrombus involves the deep venous system from the foot to the patellofemoral region. Reflex arterial spasm can cause pale limbs, coldness and weakened pulse. It is likely that there are already a considerable number of clots, calf muscles, armpits, and medial groin. Waiting for tenderness, Homan sign positive.

(2) Pain: After venous thrombosis, inflammation around the wall and its surrounding area leads to pain around the thrombus. Superficial venous thrombosis is mainly caused by local inflammatory pain and tenderness in the upper part. Deep iliac vein and femoral vein thrombosis Mostly, it is painful, pain in the inner thigh, tenderness, and tenderness in the deep leg.

Examination of pregnancy with thrombotic disease

Thrombotic superficial phlebitis generally does not require special laboratory tests. The following tests can be performed during deep venous thrombosis:

Hematological examination: There is no uniform understanding of the laboratory diagnosis of thrombosis. At present, there seems to be a lack of laboratory-specific diagnostic indicators, and the results found in the laboratory during thrombus formation vary greatly, and the method of detection is not sensitive enough, especially In the early stage of thrombosis, there are still many difficulties in accurately determining the pre-thrombotic or hypercoagulable state. The following blood tests can confirm or predict thrombosis.

1. Endothelin-1 detection Endothelin-1 (ET-1) is the only endothelin synthesized and secreted by vascular endothelium. ET-1 has strong vasoconstrictive activity and stimulates endothelial cells to release t-PA. In the population distribution, the plasma level of ET-1 in the elderly is higher than that in the population, which may be one of the factors that are susceptible to thrombosis in the elderly.

2. Thrombin regulatory protein increases thrombin regulatory protein (thrombumudulin, TM) is a receptor for thrombin, a single-chain anticoagulant protein present on the surface of endothelial cells, TM and thrombin in the endothelium The cell surface binds to form a complex that specifically converts protein C into activated protein C (APC), a sensitive and specific molecular marker that reflects endothelial cell damage, and increased plasma or endothelial cell surface TM. Indicates hypercoagulable state and thrombosis.

3. Platelet examination includes platelet adhesion, increased aggregation; increased platelet emission in plasma, especially the increase of specific protein thromboglobulin (-TG) and platelet factor 4 (PF4) in alpha particles and platelet alpha granule membrane The protein GMP-140 is increased, the release of serotonin in the plasma of -platelet dense particles is increased and the intraplatelet concentration is decreased; the TXB2 metabolite of plasma TXA2 is increased and/or the product of prostacyclin (6-keto-PGF1) Decrease; both respond to platelet activation.

4. Coagulation factor activation increases the levels of human coagulation factors (F:A) and antigenicity (F:Ag) are generally 100%. In thrombotic diseases, F:A and F:Ag can be significantly increased, coagulation The levels of zymogen fragments 1 2 (F1 2) and 2 (F2) are elevated, F1 2 is the activity reflecting thrombin, F1 and F2 are activities reflecting endogenous thrombin, and clotting time and APTT are shortened.

5. Plasma anticoagulant factor reduces antithrombin-III, protein C, protein S, HC-II, APC sensitivity and CL-inhibitor determination of thrombosis, especially for hereditary, familial thrombosis The diagnosis has certain clinical significance.

6. Fibrinolytic activity decreased fibrin (original) degradation products (FDP) determination of fibrinolytic activity, increased D-dimer in FDP is a marker of cross-linked fibrin degradation, increased fibrin peptide A content suggests that there is coagulation Enzyme formation is an early indicator of the conversion of fibrinogen to fibrin. Positive serum co-coagulation test indicates an increase in soluble fibrin monomer complex, suggesting an increase in thrombin and plasmin production, in addition to plasminogen activity. Measurement, t-PA and PAI measurement can also be used as an indicator of fibrinolytic observation.

7. Changes in Hemorheology Changes in blood rheology usually use hematocrit (HCT), whole blood viscosity, whole blood reduction viscosity, plasma viscosity, erythrocyte electrophoresis time, fibrinogen quantification, erythrocyte thixotropy and viscoelasticity. Such indicators reflect changes in blood rheology in patients with thrombotic diseases. In thromboembolic diseases, whole blood or plasma viscosity increases, erythrocyte thixotropy, and viscoelasticity tend to decrease.

Other auxiliary inspections:

Interventional examination

(1) venography: due to the shortcomings of pregnant women and radiation exposure to the fetus, and the intervention itself can induce and aggravate thrombophlebitis and thrombosis, so generally do not advocate prenatal application, if necessary, can be used after the birth of veins The angiography was clearly diagnosed, and the main imaging feature was a venous filling defect.

(2) Determination of radioactive fibrinogen: 125I-labeled fibrinogen was injected intravenously, and then scanned at various parts of the lower limbs to determine the location and count of fibrinogen deposition. This test can only detect the formation of calf vein thrombosis. A value increase of more than 20% indicates that there is thrombosis in the deep vein. In addition, the labeled fibrinogen must be administered before thrombosis, whereas fibrinogen is no longer deposited in the lesion, and this test is negative.

2. Non-invasive examinations include impedance plethysmography (IPG), color Doppler ultrasound, and MRI.

(1) Impedance phlebography (IPG): The principle is to use blood to have electrical conductivity. When the amount of blood changes, it can cause changes in resistance (impedance) and affect voltage. The resistance is measured according to the result of voltage measurement. Changes, thereby indirectly understanding changes in blood volume, when the vein is empty, IPG decline, and vice versa, such as venous return obstruction, venous volume and maximum venous return flow are significantly reduced, the advantage of IPG is a non-invasive examination method It has a diagnostic value of 65% for deep venous thrombosis of the lower extremity, but the sensitivity to distal DVT is only 30%.

(2) Doppler ultrasound vascular examination: When DVT is suspected, color Doppler ultrasonography is an ideal method. When the examination is performed, the ultrasound probe is pressed against the dilated vein of the affected area, and the compressibility is detected. The presence of thrombus, when the DVT occurs, the sound of blood flow in the vein disappears. This kind of sound can be detected by Doppler ultrasound, so it can help the diagnosis of DVT. The sensitivity of this method to detect the proximal DVT of the affected area is 93%. The sex is 99%.

(3) MRI: Ultrasound diagnosis is suspicious or negative for ultrasound examination, but MRI examination is feasible when clinically highly suspected. It can be clearly seen from the anatomy that the phase scan of the inguinal ligament can diagnose the pelvic venous blood flow and can be scanned. Sagittal and coronal planes have been reported to have a sensitivity of 100% and a specificity of 90% for MRI diagnosis of DVT.

Diagnosis and diagnosis of pregnancy complicated with thrombotic diseases

According to the clinical manifestations, most DVT can be diagnosed, especially in the late pregnancy and puerperium. The above symptoms and signs should be highly suspected of DVT. If necessary, the diagnosis can be obtained by auxiliary examination.

It must be differentiated from acute calf myositis, calf cellulitis, acute arterial occlusion and lymphedema.

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