retained placental fragments pathophysiology of diabetes
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Retained placental fragments pathophysiology of diabetes how do you fork ethereum

Retained placental fragments pathophysiology of diabetes

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Some research suggests that women may be predisposed to retained placenta. Retained placenta in a prior delivery appears to be an important risk factor for recurrence. Of arguably greatest significance is the risk of postpartum hemorrhage, with retained placenta the second leading cause of significant and even fatal hemorrhage in the obstetric population.

The authors found that both manual removal of the placenta and PPH decreased with increasing gestational age, and that the two were related. However, causal association could not be determined. These can include delayed postpartum hemorrhage or endomyometritis.

Evidence of infection risk, particularly endometritis, following manual or surgical removal of retained placenta has been inconsistently demonstrated. Diagnosis Retained placenta is clinically diagnosed when the placenta fails to spontaneously separate during the third stage of labor, with or without active management, or in the setting of severe bleeding in the absence of placental delivery. Selection of a clinical time definition can be based either on a population curve of observed spontaneous placental delivery times or on a time at which morbidity significantly increases.

Thirty minutes have been used as a loose guideline, which comes from a study by Combs et al. This timing has been supported by other studies as well. Because PPH incidence did not increase until after 30 minutes, Combs et al recommended this timing for initiation of manual removal of the placenta. However, this guidance is not uniformly supported.

In a subsequent study by Deneux-Tharaux, surveys from 14 European countries exhibited wide variations in wait time prior to manual placental removal, largely by country but also by the hospital. On the opposite end of the spectrum, overnutrition in the womb—such as can occur in GDM—can result in fetal overgrowth.

Consequences of Gestational Diabetes The importance of aiming to understand and effectively treat or prevent GDM is illustrated by the wide-ranging consequences of GDM for both the mother and the fetus. Mother—GDM increases the risk of a number of short-term and long-term maternal health issues.

In addition to the stress of normal pregnancy, GDM is associated with antenatal depression [ 56 ]. There is also an increased risk of additional pregnancy complications, including preterm birth and preeclampsia, and, in many cases, surgical delivery of the baby is required [ 57 ]. Emerging evidence also suggests that the vasculature of women with a prior case of GDM is permanently altered, predisposing them to cardiovascular disease CVD. This is of major concern, as CVD is the number one cause of death in the world [ 60 ].

Child—GDM also poses short- and long-term consequences for the infant. Together, these can cause fetal overgrowth, often resulting in macrosomia at birth [ 61 ]. Macrosomia is also a risk factor for shoulder dystocia—a form of obstructed labor. Thus, babies of GDM pregnancies are usually delivered by caesarean section [ 63 , 64 ].

Once delivered, these babies are at increased risk of hypoglycemia, which is likely due to formed dependence on maternal hyperglycemia fetal hyperinsulinemia , which can contribute to brain injury if not properly managed [ 65 ]. There is also evidence that GDM increases the risk of stillbirth [ 66 ]. Children born to mothers with GDM have almost double the risk of developing childhood obesity when compared with nondiabetic mothers, even after adjusting for confounders such as maternal BMI [ 67 , 68 ], and impaired glucose tolerance can be detected as young as five years old [ 69 ].

Females are therefore more likely to experience GDM in their own pregnancies, contributing to a vicious intergenerational cycle of GDM [ 70 ]. Pathophysiology of Gestational Diabetes The remainder of this review will discuss molecular processes underlying the pathophysiology of GDM. In most cases, these impairments exist prior to pregnancy and can be progressive—representing an increased risk of T2DM post-pregnancy [ 71 ].

A number of additional organs and systems contribute to, or are affected by, GDM. These include the brain, adipose tissue, liver, muscle, and placenta. Defects can occur at any stage of the process: pro-insulin synthesis, post-translational modifications, granule storage, sensing of blood glucose concentrations, or the complex machinery underlying exocytosis of granules. Chronic Insulin Resistance Insulin resistance occurs when cells no longer adequately respond to insulin.