The reasons for this are varied and complex, and some of them are unknown. The reason for fetal stoppage 1, endocrine disorders: embryo bed and continue to develop depends on the complex endocrine system coordinated with each other, any one link is out of order, can cause miscarriage. In the early development of the embryo, three important hormone levels are needed: estrogen, progesterone and human chorionic gonadotropin. As the mother, her own endogenous hormones are insufficient to meet the needs of the embryo, which may cause embryonic abortion and miscarriage. Luteal insufficiency can cause delayed endometrial development and short luteal phase, which can affect the implantation of fertilized eggs or early pregnancy miscarriage. Luteal insufficiency is often accompanied by other glandular abnormalities, such as hyper- or hypothyroidism, diabetes, androgenism and hyperprolactinemia, etc. These factors are not conducive to embryonic development and are closely related to miscarriage. 2. Uterus abnormalities: The internal environment in the uterus and the overall environment of the uterus may have an impact on the embryo. The internal environment is the endometrium, if it is too thin or too thick, it will affect the implantation. Miscarriages due to uterine defects account for about 10% to 15%, and the common ones are (a) abnormalities of congenital Mullerian ducts including unicornuate, bicornuate and bicornuate uterus resulting in narrow uterine cavity and restricted blood supply. Abnormal development of the uterine arteries can lead to asynchronous müllerianization and abnormal implantation. (b) Uterine adhesions, mainly caused by uterine cavity adhesions and fibrosis after trauma, infection or residual placental tissue. This prevents normal molting and placental implantation. (c) Pregnancy failure can also be caused by reduced blood supply due to fibroids and endometriosis leading to ischemia and venous dilatation, asynchronous metaplasia, abnormal implantation, and hormonal changes caused by fibroids. (d) Congenital or injurious endocervical relaxation and abnormal cervical development due to intrauterine treatment with ethylene estradiol often lead to miscarriage in midterm pregnancies. Chromosomal abnormalities can cause early miscarriage if the embryo does not develop. Chromosomal abnormalities include quantitative and structural abnormalities. quantitative abnormalities can be divided into aneuploidy and polyploidy, the most common abnormal karyotype is triploidy, and trisomy 16 accounts for 1/3, which is often lethal. 25-67% of trisomy 21, 4-50% of trisomy 13, and 6-33% of trisomy 18 are bound to miscarriage. Others are haploid (4SX), tetraploid due to abnormal oogenesis resulting in embryonic failure. Structural abnormalities include deletions, balanced translocations, inversions, and overlaps. Balanced translocations are the most common chromosomal abnormalities. Current research on chromosomal issues suggests that chromosomes pair, interchange and separate to form gametes, and gametes combine to form conjoins. If there is an abnormality in one of the congeners, it results in failure to develop normally and can lead to miscarriage, stillbirth, stillbirth, and malformed children; therefore, prenatal diagnosis is required to prevent the birth of chromosomally affected children. There is no effective treatment for miscarriage and fetal abortion caused by carrying chromosomal abnormalities in Western medicine, and only prenatal genetic counseling and diagnosis can be performed. For chromosomal abnormalities, theoretically there is a chance of delivering normal karyotype and carrier babies, and prenatal diagnosis is done for these couples to ensure the birth of normal babies. Of course, current research has also shown that both couples have normal chromosomes, but chromosomal abnormalities occur during gamete formation and embryo development. For example, if a woman is older than 35 years old and her eggs are aging, she is prone to chromosomal non-separation, resulting in chromosomal abnormalities; abnormal semen, such as large-headed malformed sperm that are mostly diploid and form polyploid embryos after fertilization leading to miscarriage. The influence of adverse environment such as toxic chemicals, radiation, high temperature, etc. can also cause chromosomal abnormalities in embryos. Therefore, the key to prevent chromosomal abnormalities that lead to fetal abortion is to regulate the health of both spouses, so that the function of the internal organs is normal and coordinated, the balance of yin and yang, choose the best pregnancy, and away from the bad environment. 4, reproductive tract infection: In addition to the above factors, infection caused by early pregnancy miscarriage has been increasingly important to scholars at home and abroad. Severe TORCH infection in early pregnancy can cause embryonic death or miscarriage, while milder infections can also cause embryonic malformation. Studies have shown that cytomegalovirus can cause premature abortion and intrauterine fetal death. After maternal infection, the pathogens can travel to the placenta through the bloodstream, causing damage to the chorionic villus and capillary endothelium, and destroying the placental barrier, resulting in miscarriage, embryonic arrest and fetal malformation. In recent years, many studies have shown that mycoplasma infection is associated with embryonic arrest, and the positive rate of cervical secretion mycoplasma infection in women with embryonic arrest is significantly higher than that in normal women, and there is a highly significant difference. 5, environmental factors: changes in the physiological state of pregnancy, so that the mother’s absorption, distribution and excretion of therapeutic drugs and various environmentally harmful substances have changed significantly, in the early stages of development, the embryo is extremely sensitive to the impact of therapeutic drugs and environmental factors, at this time, various harmful factors can lead to damage to the embryo, or even loss. Many drugs and environmental factors are important factors in causing early embryonic death or fetal malformations. Environmental hormones can act directly on the central neuroendocrine regulatory system, causing disruption of reproductive hormone secretion, decreased fertility and abnormal embryonic development. There are various environmental factors that cause miscarriage, including physical factors such as X-rays, microwaves, noise, ultrasound, high temperature, and heavy metals such as aluminum, lead, mercury, and zinc that affect the fertilized egg’s implantation or directly damage the embryo and cause miscarriage. Various chemical drugs such as dichlorohydrin, carbon disulfide, anesthetic gas, oral anti-diabetic drugs, etc. can interfere with and damage reproductive function, causing embryo miscarriage, stillbirth, malformation, developmental delay and dysfunction, as well as bad habits such as smoking, alcohol, coffee, drugs, certain drugs, etc. all affect early embryo development. Second, comprehensive examination: Immunity, thrombotic factors and examination 1, antiphospholipid syndrome and thrombosis items: antiphospholipid antibodies (including IgM, IgA and IgG type anti-cardiolipin antibodies and anti-β2 glycoprotein I antibodies and lupus anticoagulant), easy embolism combination (containing lupus anticoagulant and protein S and protein C, etc.), antithrombin III, coagulation III (containing D-dimer and fibrinogen, etc.), and platelet aggregation rate. Antiphospholipid antibodies are a group of specific autoantibodies produced against phospholipid components of self-glycerol. In the physiological state, negatively charged phospholipids are not exposed to the exterior of the cell membrane, while in the pathological state, negatively charged phospholipids are distributed to the exterior surface of the cell, and binding to the phospholipids of the endothelial cell membrane can change the stability of the cell membrane; binding to the platelets can increase the adhesion and aggregation ability of platelets, thus promoting thrombosis, and with the aggravation of placental vascular thrombosis, causing placental infarction, resulting in miscarriage. 2, thyroid function project: many women have hypothyroidism or hyperthyroidism, which can also lead to recurrent miscarriage due to abnormal thyroid function. 3.Blood group and blood group antibodies check: the couple’s blood group does not match, especially O blood group mothers are prone to recurrent spontaneous abortion (because O mothers can produce IgG antibodies to AB antigens and can pass the placental barrier). The abnormally increased blood group antibodies act on the trophoblast cells or enter the fetus through the placenta, leading to damage to the fetal-placental unit multi-organ tissue cells, and miscarriage. 4, HLA genetic examination: large HLA similarity between husband and wife (large common antigen similarity) may be one of the causes of recurrent spontaneous miscarriage. Under normal circumstances, the HLA antigen of the father can stimulate the mother to produce the corresponding HLA antibodies to protect the fetus from the maternal immune system. If the HLA compatibility between the couple is too high and the maternal immune recognition of the paternal antigen of the embryo is incomplete, the mother cannot be effectively stimulated to produce protective antibodies and the fetus is exposed to the surveillance of the maternal immune system, causing the mother to have a rejection reaction, leading to miscarriage and The fetus is exposed to the surveillance of the maternal immune system, resulting in rejection by the mother, leading to miscarriage and stillbirth. The frequency of HLA-DR, HLA-A and HLA-B in couples with recurrent spontaneous abortions is significantly higher than in couples with normal births. 5, closed antibody: the lack of closed antibody is also one of the important causes of recurrent spontaneous abortion. The fetal placental unit is not rejected by the mother and relies on maternal production of confinement antibodies and other immunosuppressive substances, thus preventing harmful maternal reactions. Containment antibodies are produced mainly against embryonic HLA-II antigens and lymphocyte cross-reacting antigens and help to maintain pregnancy by binding to fetal placental trophoblast antigens or maternal lymphocytes to prevent embryonic paternal antigens from being recognized and killed by the maternal immune system and to prevent immune attack on the embryonic trophoblast. Currently, the following are detected: (1) anti-warm B-cell antibodies (anti-HLA-DR antibodies); (2) anti-lymphocyte cross-reactive antigen antibodies; (3) anti-FC (i.e. antibody FC segment) receptor antibodies; (4) microlymphotoxic antibodies; (5) anti-cold B-cell antibodies (non-HLA cold B-cell antibodies); (6) anti-father complement-dependent antibodies, etc. Anti-HLA-DR antibodies and anti-lymphocyte cross-reacting antigen antibodies can bind to local trophoblast-related antigens at the maternal-fetal interface, blocking fetal antigens and blocking the attack of maternal immune cells; anti-FC receptor antibodies can prevent certain IgG antibodies that are harmful to the fetus from passing through the placental barrier, which plays a protective role for the fetus. In addition, the mother also produces anti-closing antibody unique type antibodies, which can not only localize at the mother-fetal immune interface, but also interact with harmful immune active cells (such as killer T cells, natural killer cells, etc.) and related factors such as IL-2 in the body circulation, blocking harmful immune responses and forming an important immune protection network with closing antibodies. 6. Anti-reproductive immune antibodies include anti-sperm antibodies, anti-endometrial antibodies, anti-ovarian antibodies, anti-chorionic gonadotropin antibodies, anti-nuclear antibody profile (including ANA, ENA and ds-DNA, etc.) and anti-hyaluronic antibodies. Anti-sperm antibodies not only interfere with sperm metabolism and energy acquisition, but also affect fertilization, fertilized egg implantation and embryonic development, eventually leading to miscarriage. The serum and cervical mucus of normal women of childbearing age do not contain anti-sperm antibodies, and the seropositivity rate of women with recurrent spontaneous abortion is 36.4%. The endometrium of women of childbearing age is regulated by ovarian hormones and exfoliates periodically, and the exfoliated endometrium flows out of the body with menstrual blood, which generally does not induce an autoimmune response. Due to endometrial injury and inflammation, the endometrial tissues stimulate the body to produce anti-endometrial antibodies as self-antigens, which can bind with the target antigens in the endometrium and activate the complement reaction, destroying the structure of the endometrium, causing endometrial dysplasia and reducing the acceptability of the pregnant egg, which is not conducive to the implantation of the pregnant egg, leading to infertility and miscarriage. 7. T and B lymphocyte subsets and natural killer (NK) cells, immunoglobulins and complement, interleukin 2, interferon γ and tumor necrosis factor: Th1/Th2 cytokine imbalance is associated with recurrent spontaneous abortions. CD4+ helper T cells can be divided into subsets with two different functions according to the cytokines they secrete, namely Th1 (T helper 1) and Th1 cells mainly secrete interleukin 2, interferon γ and tumor necrosis factor; Th2 cells mainly produce interleukin 4, 5, 6 and 10. th1 cytokines mainly mediate cellular immunity and local inflammatory response, participate in immune response and are associated with immune damage. th2 cytokines mainly promote B cell proliferation and antibody production, mediate humoral immunity and participate in immune response. Th2 cytokines mainly promote B-cell proliferation and antibody production, mediate humoral immunity, and are involved in mediating immune tolerance formation. Pregnancy is a physiological phenomenon dominated by Th2-type cytokines. In women with recurrent spontaneous abortion, the meconium immune cells produce excess embryotoxic cytokines and the Th1/Th2 balance is biased toward Th1, while Th2 is suppressed. 8. Hysteroscopy to assess the morphology and environment of the uterine cavity, whether there are adhesions, polyps, mediastinum, inflammatory lesions. 9.Karyotype examination of both spouses. If available, fetal villi are retained for chromosomal examination at the time of miscarriage. In conclusion: among them, thrombotic factors and immune factors should be the focus of miscarriage causes and examination, and also the focus of treatment when anti-thrombotic treatment, heparin and immunotherapy interventions are used to preserve fetus.