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It is recommended that women with vasa previa should deliver through elective cesarean prior to rupture of the membranes. Given the timing of membrane rupture is difficult to predict, elective cesarean delivery at 35–36 weeks is recommended. This gestational age gives a reasonable balance between the risk of death and that of prematurity. Several authorities have recommended hospital admission about 32 weeks. This is to give the patient proximity to the operating room for emergency delivery should the membranes rupture. Because these patients are at risk for preterm delivery, it is recommended that steroids should be given to promote fetal lung maturation. When bleeding occurs, the patient goes into labor, or if the membranes rupture, immediate treatment with an emergency caesarean delivery is usually indicated.
Although the risk of placental abruption cannot be eliminated, it can be reduced. Avoiding tobacco, alcohol and cocaine during pregnancy decreases the risk. Staying away from activities which have a high risk of physical trauma is also important. Women who have high blood pressure or who have had a previous placental abruption and want to conceive must be closely supervised by a doctor.
The risk of placental abruption can be reduced by maintaining a good diet including taking folic acid, regular sleep patterns and correction of pregnancy-induced hypertension.
It is crucial for women to be made aware of the signs of placental abruption, such as vaginal bleeding, and that if they experience such symptoms they must get into contact with their health care provider/the hospital "without any delay".
The first step in management of uterine atony is uterine massage. The next step is pharmacological therapies, the first of which is oxytocin, used because it initiates rhythmic contractions of the uterus, compressing the spiral arteries which should reduce bleeding. The next step in the pharmacological management is the use of methylergometrine, which is an ergot derivative, much like that use in the abortive treatment of migraines. Its side effect of hypertension means its use should not be used in those with hypertension or pre-eclampsia. In those with hypertension, the use of prostaglandin F is indicated (but beware of its use in patients with asthma).
Another option Carbetocin and Carboprost where Oxytocin and ergometrin is inappropriate.
Preventive measures against pre-eclampsia have been heavily studied. Because the pathogenesis of pre-eclampsia is not completely understood, prevention remains a complex issue. Below are some of the currently accepted recommendations.
Supplementation with a balanced protein and energy diet does not appear to reduce the risk of pre-eclampsia. Further, there is no evidence that changing salt intake has an effect.
Supplementation with antioxidants such as vitamin C, D and E has no effect on pre-eclampsia incidence; therefore, supplementation with vitamins C, E, and D is not recommended for reducing the risk of pre-eclampsia.
Calcium supplementation of at least 1 gram per day is recommended during pregnancy as it prevents preeclampsia where dietary calcium intake is low, especially for those at high risk. Low selenium status is associated with higher incidence of pre-eclampsia.
Circumvallate placenta is a placental morphological abnormalitiy, a subtype of placenta extrachorialis in which the fetal membranes (chorion and amnion) "double back" on the fetal side around the edge of the placenta. After delivery, a circumvallate placenta has a thick ring of membranes on its fetal surface.
The fetal surface is divided into a central depressed zone surrounded by a thickened white ring which is incomplete the ring is situated at varying distance from the margin of the placenta. The ring is composed of a double fold of amnion and chorion with degenerated decidua vera and fibrin in between. Vessels radiate from the cord insertion as far as the ring and then disappear from the view.
Complete circumvallate placenta occurs in approximately 1% of pregnancies. It is diagnosed prenatally by medical ultrasonography, although one 1997 study of prenatal ultrasounds found that "of the normal placentas, 35% were graded as probably or definitely circumvallate by at least one sonologist," and "all sonologists misgraded the case of complete circumvallation as normal." The condition is associated with perinatal complications such as placental abruption, oligohydramnios, abnormal cardiotocography, preterm birth, and miscarriage.
It is associated with gestational diabetes, smoking and high altitude.
Some doctors recommend complete bed-rest for the mother coupled with massive intakes of protein as a therapy to try to counteract the syndrome. Research completed shows these nutritional supplements do work. Diet supplementation was associated with lower overall incidence of TTTS (20/52 versus 8/51, P = 0.02) and with lower prevalence of TTTS at delivery (18/52 versus 6/51, P = 0.012) when compared with no supplementation. Nutritional intervention also significantly prolonged the time between the diagnosis of TTTS and delivery (9.4 ± 3.7 weeks versus 4.6 ± 6.5 weeks; P = 0.014). The earlier nutritional regimen was introduced, the lesser chance of detecting TTTS ( P = 0.001). Although not statistically significant, dietary intervention was also associated with lower Quintero stage, fewer invasive treatments, and lower twin birth weight discordance. Diet supplementation appears to counter maternal metabolic abnormalities in monochorionic twin pregnancies and improve perinatal outcomes in TTTS when combined with the standard therapeutic options. Nutritional therapy appears to be most effective in mitigating cases that are caught in Quintero Stage I, little effect has been observed in those that are beyond Stage I.
Small chorangiomas are not treated. Large chorangioma can be treated several ways, including chemical ablation and laser coagulation.
The prognosis of this complication depends on whether treatment is received by the patient, on the quality of treatment, and on the severity of the abruption. Outcomes for the baby also depend on the gestational age.
In the Western world, maternal deaths due to placental abruption are rare. The fetal prognosis is worse than the maternal prognosis; approximately 12% of fetuses affected by placental abruption die. 77% of fetuses that die from placental abruption die before birth; the remainder die due to complications of preterm birth.
Without any form of medical intervention, as often happens in many parts of the world, placental abruption has a high maternal mortality rate.
This procedure involves the ligation or otherwise occlusion of the umbilical cord to interrupt the exchange of blood between the fetuses. The procedure is typically offered in cases where one of the fetuses is presumed moribund and endangering the life or health of the other twin through resultant hypotension. Use of this treatment has decreased as TTTS is identified and treated in earlier stages and with better outcomes. When used, it is associated with an 85% survival rate of the remaining fetus(es) with 5% risk of cerebral palsy and a 33–39 weeks of gestation at delivery.
There is no effective pharmacological treatment for retained placenta. It is useful ensuring the bladder is empty. However, ergometrine should not be given as it causes tonic uterine contractions which may delay placental expulsion. Controlled cord traction has been recommended as a second alternative after more than 30 minutes have passed after stimulation of uterine contractions, provided the uterus is contracted. Manual extraction may be required if cord traction also fails, or if heavy ongoing bleeding occurs. Very rarely a curettage is necessary to ensure that no remnants of the placenta remain (in rare conditions with very adherent placenta such as a placenta accreta).
However, in birth centers and attended home birth environments, it is common for licensed care providers to wait for the placenta's birth up to 2 hours in some instances.
Most women with GTD can become pregnant again and can have children again. The risk of a further molar pregnancy is low. More than 98% of women who become pregnant following a molar pregnancy will not have a further hydatidiform mole or be at increased risk of complications.
In the past, it was seen as important not to get pregnant straight away after a GTD. Specialists recommended a waiting period of 6 months after the hCG levels become normal. Recently, this standpoint has been questioned. New medical data suggest that a significantly shorter waiting period after the hCG levels become normal is reasonable for approximately 97% of the patients with hydatidiform mole.
In some very rare cases, a GTD can coexist with a normal fetus. This is called a "twin pregnancy". These cases should be managed only by experienced clinics, after extensive consultation with the patient. Because successful term delivery might be possible, the pregnancy should be allowed to proceed if the mother wishes, following appropriate counselling. The probability of achieving a healthy baby is approximately 40%, but there is a risk of complications, e.g. pulmonary embolism and pre-eclampsia. Compared with women who simply had a GTD in the past, there is no increased risk of developing persistent GTD after such a twin pregnancy.
In few cases, a GTD had coexisted with a normal pregnancy, but this was discovered only incidentally after a normal birth.
A Cochrane review concluded that "simple maternal hydration appears to increase amniotic fluid volume and may be beneficial in the management of oligohydramnios and prevention of oligohydramnios during labour or prior to external cephalic version."
In severe cases oligohydramnios may be treated with amnioinfusion during labor to prevent umbilical cord compression. There is uncertainty about the procedure's safety and efficacy, and it is recommended that it should only be performed in centres specialising in invasive fetal medicine and in the context of a multidisciplinary team.
In case of congenital lower urinary tract obstruction, fetal surgery seems to improve survival, according to a randomized yet small study.
Vasa praevia, also spelled vasa previa, is a condition in which babies' blood vessels cross or run near the internal opening of the uterus. These vessels are at risk of rupture when the supporting membranes rupture, as they are unsupported by the umbilical cord or placental tissue.
Risk factors include in vitro fertilization.
Vasa praevia occurs in about 0.6 per 1000 pregnancies. The term "vasa previa" is derived from the Latin; "vasa" means vessels and "previa" comes from "pre" meaning "before" and "via" meaning "way". In other words, vessels lie before the baby in the birth canal and in the way.
Chorangiosis is a placental pathology characterized by an abundance of blood vessels within the chorionic villi.
In places where a Caesarean section could not be performed due to the lack of a surgeon or equipment, infant could be delivered vaginally. There were two ways of doing this with a placenta previa:
- The baby's head can be brought down to the placental site (if necessary with Willet's forceps or a vulsellum) and a weight attached to its scalp
- A leg can be brought down and the baby's buttocks used to compress the placental site
Breus' mole (Ova tuberculosa, massive mole) is a massive, subchorionic, tuberous hematoma, formed out of maternal blood in the uterus in pregnancy. It was first described by Karl Breus in 1892.
It is a rare disease, with an incidence of 1 in 1200 placentas. Women with cardiac problems, disorders of circulation, monosomy, hypertension and diabetes are predisposed to Breus' mole. The mole is formed as a sub-chorionic hematoma, formed out of the intervillous blood, causing progressive accumulation of the clotting substance called fibrin with increasing gestational age. Evidence from Southern blot test reveals that 85 percent of the clotted material is maternal blood. Breus mole is reported to be found in the placetae of macerated stillborn foetuses, indicating that massive subchorionic hematoma could have been the cause of their demise. A massive Breus' mole can cause disturbances in blood flow in the spiral arteries and might result in intrauterine growth restriction of the foetus.
Exact cause of placenta previa is unknown. It is hypothesized to be related to abnormal vascularisation of the endometrium caused by scarring or atrophy from previous trauma, surgery, or infection. These factors may reduce differential growth of lower segment, resulting in less upward shift in placental position as pregnancy advances.
A chorangioma is a non-neoplastic, hamartoma-like growth in the placenta consisting of blood vessels.
A placental disease is any disease, disorder, or pathology of the placenta. The article also covers placentation abnormalities, which is often used synonymously for placental disease.
of fetal membranes (afterbirth) is observed more frequently in cattle than in other animals. In a normal condition, a cow’s placenta is expelled within a 12-hour period after calving.
Confined placental mosaicism (CPM) represents a discrepancy between the chromosomal makeup of the cells in the placenta and the cells in the baby. CPM was first described by Kalousek and Dill in 1983. CPM is diagnosed when some trisomic cells are detected on chorionic villus sampling and only normal cells are found on a subsequent prenatal test, such as amniocentesis or fetal blood sampling. In theory, CPM is when the trisomic cells are found only in the placenta. CPM is detected in approximately 1-2% of ongoing pregnancies that are studied by chorionic villus sampling (CVS) at 10 to 12 weeks of pregnancy. Chorionic villus sampling is a prenatal procedure which involves a placental biopsy. Most commonly when CPM is found it represents a trisomic cell line in the placenta and a normal diploid chromosome complement in the baby. However, the fetus is involved in about 10% of cases.