الفهرس 
Fetal Growth and MacrosomiaOnly 14 pages are availabe for public view
 |  | from | 32 |  |  |
| | | from | 32 | | |
Abstract
M
acrosomic infants as well as their mothers are at increased risk for intrapartum injury. Perinatal mortality is more common among these fetuses.
The most commonly accepted definition for macrosomia is that of birth weight equal to or exceeding 4000g. According to ACOG (2000), it is reasonable to consider all newborn infants weighing 4500g or more as macrosomic. The most recent studies reported an incidence of 8.9% for fetuses with macrosomia (>4000g).
Enlargement of the size of the fetus may be generalized or confined to certain parts: head, neck, thorax, abdomen or pelvis. Enlargement of the size of the fetus as a whole may be symmetrical or asymmetrical.
The etiology of fetal macrosomia is believed to be multifactorial. Etiologic factors include gestational age, diabetes mellitus, male sex, multiparity, maternal weight gain during pregnancy, birth weight of a prior macrosomic infant, ethnicity as well as genetic and congenital disorders.
Many studies have largely defined the essential role of insulin, insulin like growth factors (IGF-I & IGF-II), and their receptors in embryonic and fetal growth. Other potential mechanisms of fetal somatic overgrowth include genetic factors, utero-placental constraints, thyroid and growth hormones, and leptin.
Since its recognition, macrosomia has been one of the corner stones of diabetic fetopathy. Hyperglycemia exists in women with poorly controlled diabetes, glucose crosses the placenta by facilitated diffusion and the fetus maintains a level of about 70-80% of the maternal glucose concentration. This results in a carbohydrate surplus to the fetus with subsequent hyperinsulinemia. Fetal hyperinsulinemia causes direct growth stimulation, increased cellular glucose utilization, increased deposition and decreased mobilization of fat and increased protein production, this leads to overgrowth and the birth of a neonate with macrosomia.
Fetal macrosomia has an important effect on maternal and fetal morbidity and mortality. Maternal complications include arrest disorders, protraction disorders, instrumental delivery with more obstetric lacerations, post partum hemorrhage and puerperal infection, cesarean delivery and shoulder dystocia. Fetal complications include birth injuries, asphyxial injuries, neonatal hypoglycemia, and childhood and adolescent obesity.
Birth injuries include mainly brachial plexus injury and fracture clavicle. Brachial plexus injury results from downward traction on the brachial plexus during delivery of the anterior shoulder. Erb’s palsy from injury to the spinal nerves C5-6.
Accurate prenatal diagnosis of macrosomia is important for planning and timing of the method of delivery.
There are three major strategies used to predict macrosomia which are risk assessment, clinical estimation of fetal weight and ultrasonography. The strongest risk factor is maternal diabetes, which results in a two-fold increase in the incidence of macrosomia. Other risk factors include prolonged gestation, obesity and multiparity. However, 34% of macrosomic infants are born to mothers with no identifiable risk factor.
Clinical estimation of fetal weight includes fundal level, measurement of the girth circumference at the level of the umbilicus as well as the measurement of symphysial- fundal height. When clinical estimates were compared with sonographic estimates of fetal weight, the results were comparable and clinical estimates performed favorably.
Sonographic methods for diagnosis of macrosomia were developed in hopes of improving clinical estimates. Measured parameters include: head circumference (HC), abdominal circumference (AC), thigh circumference (ThC), femur diaphysis length (FDL), weight estimate (WE) and body proportionality (HC/AC and FDL/HC). The true value of Ultrasonography in the management of fetal macrosomia may be its ability to rule out the diagnosis. Ultrasound-derived fetal weight estimates alone are not sufficient grounds for deciding the route of delivery.
Doppler indices in the middle cerebral arteries,the cerebroplacental Doppler ratio and umblical artery Doppler indices are not significant parameters in diagnosis of macrosomia.
Preventive factors of fetal macrosomia include reduction of pre-pregnancy weight and weight gain during pregnancy, limitation of post term pregnancy and control of diabetes.
The management of patients with suspected fetal macrosomia is controversial. Elective cesarean delivery and labor induction have been proposed as interventions to prevent maternal and perinatal complications.
Labor should not be induced in non-diabetic pregnancies. The best policy is to await spontaneous birth or to induce labor after 42 weeks completion.
A great number of cesarean sections have to be performed to avoid a single case of brachial plexus paresis resulting from a difficult shoulder delivery.
Reasons for inducing labor at term in pregnancies complicated by diabetes include the avoidance of fetal loss and the prevention of excessive fetal growth and its concomitant conditions, shoulder dystocia and cesarean delivery.
Objectively evaluating the risks and benefits of labor induction is potentially confound by the status of the cervix at the time of initiation of induction, early determination of an arrest disorder and physician bias toward cesarean delivery for women who have diabetes.
Some authors recommend performing a prophylactic cesarean section in cases of macrosomia. This aims at preventing maternal and fetal complications of macrosomia. However, this recommendation is controversial and some studies revealed that this is not the ideal management for cases of macrosomia.