Infants from diabetic mothers usually have several blastogenic malformations. Diabetic embryopathy is therefore an etiological subgroup of defects of blastogenesis that present different monotopic and polytopic developmental defects. Abortion and perinatal deaths
Diabetic embryopathy may result in early or late spontaneous abortion and stillbirth. In maternal diabetes, 90% of pregnancy losses happen in the first trimester due to oxidative stress. Diabetic embryopathy abortions in the second-trimester are most likely due to severe birth defect, maternal metabolic derangement, placental insufficiency and fetal hypoxia due to membrane rupture. Pathogenesis
The development of birth defects associated with maternal hyperglycemia is multi-factorial. Environmental factors and genetic predisposition (paternal, maternal and offspring genome) are important in diabetic embryopathy. The diets of diabetic mothers impacts the rate at which malformations form in their offspring. Furthermore, there is evidence that resistance to certain malformations caused by diabetes is genetic. Epigenetics and its relationship with various environmental factors such as metabolism and diet play a significant role in teratogenesis. Hyperglycemia and associated teratogenic mediators influence DNA methylation, non-coding RNA expression, histone modifications and other epigenetic regulation mechanisms. Research is focused on exploring the impact of diabetic embryopathy on methylation signatures, which could potentially serve as a diagnostic biomarker for the condition. Prevention
Preconception
The probability of major birth defects in offspring of mothers with diabetes is 0.7-4.4% for glycohemoglobin levels <7%. For glycohemoglobin levels >10% the probability of major birth defects is 16.1-100% with an average of 26.6%.
Uterine inversion is when the uterus turns inside out, usually following childbirth. Symptoms include postpartum bleeding, abdominal pain, a mass in the vagina, and low blood pressure. Rarely inversion may occur not in association with pregnancy.Risk factors include pulling on the umbilical cord or pushing on the top of the uterus before the placenta has detached. Other risk factors include uterine atony, placenta previa, and connective tissue disorders. Diagnosis is by seeing the inside of the uterus either in or coming out of the vagina.Treatment involves standard resuscitation together with replacing the uterus as rapidly as possible. If efforts at manual replacement are not successful surgery is required. After the uterus is replaced oxytocin and antibiotics are typically recommended. The placenta can then be removed if it is still attached.Uterine inversion occurs in about 1 in 2,000 to 1 in 10,000 deliveries. Rates are higher in the developing world. The risk of death of the mother is about 15% while historically it has been as high as 80%. The condition has been described since at least 300 BC by Hippocrates. Signs and symptoms
Uterine inversion is often associated with significant postpartum bleeding. Traditionally it was thought that it presented with haemodynamic shock "out of proportion" with blood loss, however blood loss has often been underestimated. The parasympathetic effect of traction on the uterine ligaments may cause bradycardia.