In-depth analysis of embryonic sterilizations in surrogate mothers: a scientific perspective from mechanism to management

　 In the fertility journey of surrogate mothers, embryonic abruption is like an unexpected barrier. Statistics show that globally, about 15-20% of clinical pregnancies end in embryonic arrest, with the risk being as high as 50% in women over 40 years of age. This phenomenon not only involves biological mechanisms, but also is closely related to lifestyle, environmental exposure and medical interventions. This article will systematically dismantle the complex causes of embryonic arrest and provide coping strategies guided by evidence-based medicine.
　　I. Biological nature of embryonic arrest in surrogate mothers
　　Embryonic arrest in surrogate mothers is medically referred to as an “induced abortion”, meaning that the embryo or fetus stops developing in the uterus but is not expelled naturally. Diagnosis is made by continuous ultrasound monitoring:
　　Stagnation of the gestational sac: absence of yolk sac structure even though the sac is more than 25 millimeters in diameter.
　　Absence of fetal buds/heart: absence of fetal heartbeat in the presence of a bud ≥ 7 mm in length or disappearance of the previously detected fetal heart.
　　Time window verification: at least 7 days between retests to confirm developmental arrest
　　This process is often accompanied by the sudden resolution of pregnancy symptoms (e.g., nausea, breast tenderness), but about 30% of patients do not have any obvious physical sensation, highlighting the importance of regular obstetric examination.
　　Three-dimensional analysis of the causes of infertility cessation
　　1. Genetic defects: fundamental errors in the blueprint of life
　　About 60% of embryonic sterilizations are caused by chromosomal abnormalities. Among them:
　　Autosomal trisomies predominate, such as trisomy 16 (leading to 22% of early miscarriages)
　　Monosomy X syndrome (Turner syndrome) accounts for 15% of cases, with embryos mostly surviving until about 9 weeks
　　The risk of chromosomal abnormalities in the offspring spikes to 30% when parents carry a balanced translocation in a recessive manner
　　Sperm DNA Fragmentation Index (DFI) above 30% or mitochondrial dysfunction in oocytes significantly reduces embryonic developmental potential. Next-generation sequencing (NGS) can accurately identify embryonic chromosome microdeletions/microduplications.
　　2. Imbalance of the maternal internal environment: the crisis of the breeding soil
　　Coagulation-immune storm: antiphospholipid antibodies activate the complement system, triggering microthrombosis in the metaphase blood vessels; natural killer cells (NK cells) are overactive and attack the embryo directly.
　　Metabolic disorders: Vitamin D level below 20ng/mL leads to Th1/Th2 immune imbalance, homocysteine above 15μmol/L triggers placental vasculopathy.
　　Anatomical anomalies: unicornuate uterus reduces the space for embryo attachment by 50%, and uterine adhesions cut off the nutrient supply pathway.
　　3. Invisible attack of environmental toxins
　　Endocrine disruptors: Bisphenol A (BPA) interferes with embryo implantation through estrogen receptor signaling.
　　Air Pollution: When the average daily concentration of PM2.5 exceeds 35μg/m³, the rate of mitochondrial DNA damage in the placenta rises 2-fold.
　　Nicotine metabolites: Decrease the partial pressure of oxygen in the intervillous space of the chorionic villi by 40%, which is equivalent to the embryo being in a state of chronic asphyxia.

III. Precision pathways for clinical interventions
　　1. Optimized solutions for pregnancy termination
　　Medication abortion: Mifepristone combined with misoprostol regimen has a 92% complete abortion rate in patients within 9 weeks of gestation, with preserved tissues sent for genetic analysis
　　Microscopic hysteroscopic surgery: cold knife technology with real-time ultrasound navigation, endometrial damage rate is controlled at less than 3%, and the risk of uterine adhesion is significantly reduced.
　　2. embryo genetic diagnosis
　　Chromosome microarray analysis (CMA) of aborted fetuses detects 95% of aneuploidies, and whole-exome sequencing (WES) identifies 15% of single-gene etiologies. These data provide key guidelines for re-pregnancy strategies.
　　Golden preparation period for re-pregnancy
　　1. Time window for physiologic repair
　　Endometrium requires 3 menstrual cycles to complete regeneration: endometrial volume ≥2.5mL and pulsatility index (PI) <2.0 by transvaginal ultrasound assessment
　　Ovarian reserve rebuilding: AMH ≥1.1 ng/mL and ≥5 basal sinus follicles suggesting restoration of fertility
　　2. Targeted pretreatment program
　　Anticoagulation: low molecular heparin (e.g. enoxaparin 40mg/d) combined with aspirin to improve uterine perfusion.
　　Immunomodulation: intravenous immunoglobulin (IVIG) to correct Th17/Treg cell imbalance, fat emulsion to inhibit NK cell toxicity
　　Metabolic optimization: methylfolate (for MTHFR gene mutation) combined with vitamin D3 (2000IU/d) to remodel the immune microenvironment.
　　3. Preconception screening upgrade
　　Extended Carrier Screening (ECS) covers more than 500 monogenic diseases
　　Endometrial tolerance assay (ERA) precisely locates the individualized window for implantation.
　　V. Psychological reconstruction and support system
　　40% of couples experiencing miscarriage develop anxiety-depression co-morbidity. Stepped interventions include:
　　Post-traumatic stress relief: 8-week course of positive stress reduction training (MBSR) to reduce anxiety scores by 40%.
　　Relationship Repair: rebuild trust through “emotional banking” exercises and develop a joint birth plan.
　　Community Support Network: Join the RPL Alliance for the latest research advances.
　　What the Science Tells Us About Restarting Life
　　The nature of embryo termination is the mechanism of natural selection at work. For single pregnancy loss, 70% of couples can have another successful pregnancy within 1 year. In recurrent cases (≥2), the live birth rate can be increased from 45% to 78% by systematic etiologic screening (e.g., antiphospholipid syndrome, easy embolism, abnormal uterine anatomy). Modern reproductive medicine has made the leap from “passive waiting” to “active intervention” – through multi-omics analysis (genomic, proteomic, metabolomic) of the embryo-maternal interface. The development of precise prevention and treatment strategies. The conception of life is full of unknowns, but the power of science is transforming the unknown into the controllable.