Both multiple abortions and medical abortions put women at increased risk of ectopic pregnancy. The occurrence of ectopic pregnancy in abortion patients is related to post-abortion infection, incomplete re-clearing of the uterus or infected abortion. Ectopic pregnancy caused after abortion is mainly due to post-operative complications of inflammation of the reproductive organs, which may be due to prolonged vaginal bleeding during abortion or tissue residue in the uterine cavity, or lax aseptic operation, etc. can cause pelvic inflammatory disease. In addition, abortion can cause endocrine disorders due to dysfunction of the hypothalamus-pituitary-ovarian axis, and the coordinated function of estrogen and progesterone is affected, resulting in abnormal peristalsis of the fallopian tubes. Endometriosis lesions can lead to the destruction of the pelvic anatomy, and adhesions around the fallopian tubes and ovaries can distort the fallopian tubes and make them move abnormally, affecting the egg collection and fertilized egg transport functions. The main cause of ectopic pregnancy after drug abortion is tubal adhesions, and the main cause of tubal incompetence is inflammation. Prolonged bleeding after drug abortion or infection of the uterine cavity caused by tissue residue can cause bacterial upstream infection resulting in tubal adhesions and semi-obstruction of the fallopian tubes. Ectopic pregnancy is mainly associated with factors that cause tubal abnormalities and affect embryo delivery, among which pelvic inflammatory diseases caused by pathogenic microorganisms are the more common causes. Pathogens causing tubal damage include Neisseria gonorrhoeae, Chlamydia trachomatis, and a mixture of aerobic and anaerobic bacteria, unlike aerobic and anaerobic bacteria, the symptoms of Neisseria gonorrhoeae and Chlamydia trachomatis infections are not obvious, and even early management may not prevent tubal adhesions. Even early management may not prevent damage to the fallopian tubes, whereas chlamydia often leads to severe structural and functional disruption of the fallopian tubes, causing extensive adhesions and scar formation, which interferes with the normal functioning of the fertilized egg and leads to an increased risk of ectopic pregnancy. Numerous domestic and international studies have shown increased expression of both PROKR1 and PROKR2 in the fallopian tubes of women with ectopic pregnancy. PROKR1 is a vascular endothelial growth factor 1 receptor protein that alters the microenvironment in the fallopian tubes, contributing to a microenvironment favorable to embryo implantation. Increasing PROKR1 can also lead to disruption of tubal contractile function, which is achieved by affecting muscle regulation, thus decreasing tubal mobility and delaying the entry of the fertilized egg into the uterine cavity. The metabolite of nicotine in cigarettes, cotinine, can increase the transcription of PROKR1, which induces ectopic implantation of the embryo in the fallopian tube and the occurrence of ectopic pregnancy. In women with a history of previous pelvic surgery, such as myomectomy, ruptured tubal pregnancy, and ovarian cyst debridement, the risk of ectopic pregnancy will increase twofold. This is mainly related to the fact that the tissue adhesions formed after surgery can cause the fallopian tubes to lose their normal anatomical structure and affect their normal physiological function. Perforated appendicitis and appendectomy can cause an increased risk of ectopic pregnancy, which is related to the peri-appendiceal abscess caused by perforated appendix due to appendicitis, or the inflammation around the appendix involving the right fallopian tube, causing adhesions, peristaltic disorders, or even narrowing and distortion of the tubal lumen. This prevents the normal functioning of the fertilized egg and its operation is obstructed, thus leading to ectopic implantation. Compound oral contraceptives are protective against pelvic inflammatory disease caused by Chlamydia, which can reduce the severity of pelvic inflammatory disease and can effectively reduce the incidence of ectopic pregnancy. However, the prerequisite must be regular use. If not taken regularly, slight changes in the ratio of estrogen to progesterone in the pill can lead to dysfunction of the fallopian tubes, affecting the peristalsis of the fallopian tubes and delaying the entry of egg cells into the uterus, thus increasing the chance of ectopic pregnancy due to ectopic implantation of the fertilized egg. So, the contraceptive pill must be taken according to the instructions, do not give up, or not only in vain, but also let ectopic pregnancy “rely” on you. The psychological immaturity of adolescents, early sexual life, irregular sexual partners and lack of proper knowledge of sexual life and guidance on contraceptive measures have led to a history of abortion, mid-term pregnancy induction and medical abortion of varying numbers. The history of pelvic infections caused by different degrees and different pathogens make the fallopian tubes pass but not smooth, which makes unmarried ectopic pregnancy possible, plus the excessive tension and anxiety when premarital sex partners, which affects the physiology through psychology, can easily lead to tubal spasm, thus leading to a high incidence of ectopic pregnancy. One study found that menstrual intercourse and >1 sexual partner were risk factors for ectopic pregnancy. the incidence of pelvic inflammatory disease was significantly increased in adolescents who started having sex before the age of 15, resulting in an increased risk of ectopic pregnancy, chronic pelvic pain and tubal infertility. After IUD placement, the foreign body reaction causes a non-bacterial inflammatory response in the uterus and a large accumulation of endometrial leukocytes and macrophages, which alters the intrauterine environment and prevents the implantation of a pregnant egg. At the same time, although leukocytes and macrophages can engulf sperm and reduce the chance of conception, they cannot completely prevent the fertilization and implantation of the egg in the fallopian tube. Therefore, the chance of ectopic pregnancy is relatively higher in IUD wearers once they become pregnant. Some studies have shown that the IUD itself can be an etiologic factor in ectopic pregnancy and can act through inflammation of the fallopian tubes. The close relationship between IUD use and ovarian pregnancy is mainly due to the fact that IUDs can stimulate the endometrium to secrete large amounts of prostaglandins, which cause uterine contractions and thus prevent intrauterine pregnancy without affecting the ovaries. With the continuous development of assisted reproductive technology, the success rate of obtaining pregnancy through it in infertility patients is increasing. Theoretically, the incidence of ectopic pregnancy should be reduced during in vitro fertilization-embryo transfer, where the embryo is implanted directly into the uterine cavity without passing through the fallopian tube, however, the first pregnancy obtained through in vitro fertilization-embryo transfer worldwide is an ectopic pregnancy. Tubal factor infertility is the main risk factor for ectopic pregnancy after in vitro fertilization-embryo transfer. During in vitro fertilization-embryo transfer, the embryo is placed in the uterine cavity, but it takes 3-5 d for implantation, during which time the embryo may drift into the fallopian tube. The possible mechanisms of ectopic pregnancy due to tubal factors are: 1. inflammation of the mucosa of the fallopian tubes may cause adhesion of the mucosal folds, thickening of the lumen, epithelial damage, loss of cilia, scar contracture, stiffening and narrowing of the lumen, and restriction of peristalsis of the wall of the tubes, resulting in obstruction of the embryo swimming into the fallopian tubes and its development in the fallopian tubes; 2. hydrocele may thicken the fallopian tubes and make it easier for the embryo to swim into the fallopian tubes. The fluid may thicken the fallopian tube, making it easier for the embryo to swim into the fallopian tube, and some proteins in the fluid may facilitate the growth and development of the embryo, which may lead to failure of the embryo to implant in the uterus. In addition, the stimulation of the uterus during embryo transfer causes uterine contraction and endometrial peristalsis, which may squeeze the implanted embryos into the fallopian tubes.