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Kim LaMar, ND, RNC, CNNP; Cheryl Hamernik, MSN, RNC, CNNP

NBIN 3(4):136-142, 2003. © 2003 W.B. Saunders

Posted 01/29/2004

Abstract

The education of nurses working with newborns and infants does not typically include a lengthy discussion on the fetal environment, yet existence in the womb has a significant impact on the long-term outcome. This article is a review of the specific aspects of the fetal environment, including the cervix, uterus, placenta, chorion, amnion, amniotic fluid, and maternal aspects, and the potential meaning of these facets to the newborn and infant.

Introduction

In nursing school, nurses are taught pathophysiology, growth and development, and assessment of the infant and family, to plan the care of the neonate. This article provides a basic review of the different aspects of the fetal environment and the impact on the emerging newborn. This article is not intended to cover every aspect (indeed an entire professional specialty is dedicated to that task), but to heighten the awareness of the newborn and infant nurse about intrauterine life. The focus of this review is on the embryology, anatomy and physiology of seven distinct entities of the fetal environment: the cervix, uterus, placenta, fetal membranes– chorion and amnion, amniotic fluid, and maternal influences on fetal development.

The cervix plays a crucial role in maintaining pregnancy by keeping the fetus from passing through the birth canal prematurely. The cervix consists of three structures: the endocervical canal; the internal os, found at the cephalic end of the cervix; and the external os, found caudal to the endocervical canal. The cervix consists mostly of connective tissue (85 to 90%) covered by a thin layer of smooth muscle (10 to 15%). Although many authors disagree about the importance of this layer of smooth muscle, Pajntar^[1] feels that the smooth muscle of the cervix contracts or constricts independently of the uterus. It is theorized that this constriction allows the cervix to remain rigid during pregnancy and helps to allow the uterus to retain the fetus. During labor, however, as the uterus contracts more, the cervix also contracts, but with less intensity, allowing for softening and dilation to permit passage of the fetus through the birth canal. The components of the extracellular matrix of the cervix, namely water and collagen, also play an important role in maintaining pregnancy and cervical ripening.Although pressure from the presenting part of the fetus plays a role in cervical dilation, the mechanism by which the cervix softens, effaces, and dilates is very complex and not well understood. It represents an area of research that is still needed. The composition of the components of the cervix must change to allow the cervix to soften from the rigid structure that it is during pregnancy. In the first trimester, under the influence of estrogen and progesterone, the collagen content of the cervix increases, making the cervix a rigid structure. The collagen content of the cervix then slowly decreases by 30 to 50% throughout the remaining two trimesters.^[2] As cervical ripening begins late in pregnancy, enzymes are released that rearrange the collagen content of the cervix. Failure of this process to occur may result in an unripe cervix. Hormones including estradiol, progesterone, relaxin, Prostaglandin E2, and Prostaglandin F2 exert a localized influence on the cervix and are also responsible for softening the cervix. The mechanisms by which this is accomplished are unknown. Prostaglandin gel is commonly used topically to induce cervical ripening. After the cervix has undergone these changes and softens, dilation begins. The main force behind cervical dilation is uterine contractions. As contractions increase in intensity, the presenting fetal part exerts constant tension against the cervix and begins stretching and passively dilating the lumen. This continues until the cervix dilates to a point at which the fetus can pass through and be expelled.

Cervical incompetence (CI) has been thought to be responsible for approximately 20% of second-trimester deliveries.^[3] CI can be the result of many factors, including cervical trauma, maternal diethylstilbestrol (DES) exposure, congenital anomalies associated with or without uterine anomalies, muscular cervix, or multiple gestation. Cervical trauma can be the result of lacerations from previous deliveries, therapeutic abortion, or cone biopsy. Maternal DES exposure can result in cervical muscular abnormalities as well as uterine abnormalities such as a T-shaped uterus. A muscular cervix is one that contains a decreased amount of connective tissue that is important in maintaining a pregnancy. CI associated with multiple-gestation pregnancies does not have a high rate of reoccurrence.^[4] Treatment of CI can consist of a variety of surgical procedures in the nonpregnant woman or cerclage placement for fetal salvage in the pregnant woman.

Many studies have been done to identify markers for premature cervical ripening and dilation. Cook and Ellwood^[5] found an increase in preterm delivery with cervical length reduction at 24 to 28 weeks' gestation. Fetal fibronectin, a protein synthesized by the choriodecidual cells, has also been associated with the onset of cervical ripening in term infants. Therefore, the presence of fetal fibronectin in the cervicovaginal canal may identify women at risk for preterm labor. Maternal salivary estriol has also been useful as a predictor for preterm delivery.^[6]

The uterus plays an essential role in pregnancy by protecting and supporting the fetus. The uterus is composed of three layers: the endometrium, the myometrium, and an external serous epithelial layer. Recently, some authors discovered through magnetic resonance imaging that the myometrium can further be divided into three layers: an endometrial stripe, an outer myometrium, and a subendometrial myometrium, also referred to as the junctional zone.^[7] In early pregnancy, the junctional zone is responsible for allowing trophoblast invasion while blocking continued invasion throughout the layers of the uterus. To accommodate implantation, the uterine blood supply must undergo a series of complex changes. The blood supply of the basal layer of the endometrium remains relatively unchanged, while the functional layer of the endometrium is constantly changing in response to hormonal levels. It is believed that estradiol increases uterine blood flow while progesterone has the inverse effect on blood flow. Changes in microvascular permeability also make the uterus receptive for implantation. Once implantation begins, an avascular zone is created around the embryo that is believed to weaken maternal tissues and further promote the process. At this point, the embryo becomes reliant on anaerobic metabolism for growth and development since it is now isolated from maternal sources of nutrition. With this avascular zone, the control of proliferation of endometrial cells shifts from the mother to the embryo.

The myometrium has two unique properties: contractility and elasticity. Elasticity allows the uterus to grow and stretch to accommodate the growing fetus. Contractility is the major force behind delivery of the fetus during labor. Smooth muscle cells in the myometrium transmit tension to other smooth muscle cells that result in synchronous uterine contractions that occur during labor. Toward the end of gestation, contractions increase in intensity as a result of many factors. Stretch of uterine muscles at the end of gestation help to stimulate contractions of increased frequency and intensity. Distention of the uterus is reached earlier in multiple gestations and it is theorized this contributes to the onset of labor and the shortening of gestation. Other changes include change in action potentials, hypertrophy and hyperplasia of the myometrial cells, formation of closer gap junctions and increased number of mitochondria and ATP. The result is the onset of regular, intense contractions that are able to help to expel the fetus from the uterus.^[8]

Congenital uterine anomalies can result in recurrent pregnancy loss, abnormal fetal presentation, premature labor, and premature birth. Premature labor in these women usually is the result of altered endometrial blood supply, early loss of the protective function of the cervix, and overdistention and stretching of a smaller uterine cavity. Congenital uterine malformations can be found in as many as 27% of women with a history of recurrent pregnancy loss.^[9] Most uterine anomalies are a result of defects in muellerian embryogenesis. In the female fetus at approximately weeks 10 to 11 of gestation, the mesonephric ducts regress and the paramesonephric or muellerian ducts continue to develop. The caudal portions of these structures eventually fuse and form the uterus, vagina, and cervix.

The most common uterine defects include septate, bicornate, and didelphic uteri. Another less common anomaly is the unicornate uterus. A septate uterus results from failure of reabsorption of the medial portions of the paramesonephric ducts. Although numbers vary among researchers, a decreased percentage of live births have been reported among women with septate uterus. Alterations in blood supply and structure of the uterine cavity as well as other associated cervical and hormonal abnormalities have been thought to be the cause of pregnancy loss. Partial or complete failure of muellerian duct fusion results in a bicornate uterus. Two separate, communicating endometrial cavities with a single cervix characterize this anomaly. Premature birth and spontaneous abortion rates are higher in women with complete bicornate uterus. Uterus didelphys also results from failure of fusion of the muellerian ducts. This defect consists of two endometrial cavities, each with its own cervix. Improved fetal survival with this defect is thought to be the result of better uterine blood supply. Lastly, unicornate uterus results from unilateral muellerian duct agenesis. Reduced uterine capacity and vascular anomalies can lead to prematurity, breech presentation, and fetal growth restriction.^[9]

The placenta is an amazing structure in design and function. This section deals with the placenta in a broad, generalized form and is not by any means all inclusive. Placental pathology is an important diagnostic technique for the clinician caring for a sick newborn or infant. Placentas should be unfixed and refrigerated. Freezing should be avoided as it blurs the histology. Conditions that should have a placental examination include history of prematurity, suspicion of perinatal infection, diabetes, erythroblastosis, multiple births, dysmorphism, hydrops, multiple births, and meconium staining.^[10]

The placental beginning is found in the human blastocyst before implantation. The blastocyst is surrounded with trophoblasts that will contact and invade the endometrium to form the placenta around the seventh day after ovulation. During this invasion, the cytotrophoblasts break down the uterine spiral arterial walls and replace them with tissue that has no muscle or elastic components. This change makes the vessels permanently distended and unable to respond to maternal constriction as her other vessels would. Rarely, this burrowing in of the placenta may go out of control and cause a placental accreta that can lead to postpartum hemorrhage or uterine rupture and its concomitant fetal distress.^[11]

The maternal circulation has high pressure and resistance and the intervillous space has low pressure and resistance. There has been considerable attention paid to uteroplacental blood flow, but it remains logistically difficult to accurately measure. Uteroplacental blood flow may be affected by increases in maternal vascular resistance or medication aimed at affecting maternal vascular resistance, such as hydralazine or captopril. As the trophoblast continues its invasion through maternal endometrial veins and arteries, cavities are formed with chorionic villi extending into them. Maternal and fetal cells intermingle in the maternal side of these spaces and the umbilical cord is formed on the fetal side of this intervillous space. Maternal blood enters the intervillous space, contacts the villous surface, and leaves through the uterine veins. Fetal blood travels from the umbilical arteries to fetal capillaries that contact this space and return through the umbilical vein. It is important to note that fetal and maternal blood is never mixed. The fetal capillaries are made of trophoblasts, thereby allowing substances to directly enter maternal blood pooling in these intervillous spaces and maternal substances must cross this trophoblast membrane before they will reach fetal blood. Fetal villous flow rate is about 400 ml/min and maternal flow is about 500 ml/ min.^[11] These villous masses are grouped together into cotyledons. Each placenta has about 7 to 10 cotyledons that are responsible for placental function.

The placenta is a transporter of oxygen, nutrients, waste material, and carbon dioxide between mother and fetus. Whether a substance may pass through the placenta between mother and fetus depends on its molecular size, shape, and charge.^[12] The substances not likely to pass in significant amounts include bacteria, heparin, sIgA, and IgM. Most antigens are small whereas IgM is a large molecule. This makes IgM a useful test in the neonate when searching for infection, as the most likely way the neonate will have a level greater than 20 mg/dL is if it was produced in response to a specific antigen that did pass through the placenta. IgG on the other hand is a small molecule that will readily pass through the placenta making it less useful as a diagnostic marker for infection in the neonate. Maternal IgG has four subclasses that transfer across the placenta as early as 16 weeks' gestation. The third subclass of IgG does not cross the placenta until 32 weeks' gestation, with the majority of the transfer occurring in the last trimester. Small-for-gestation infants or postdate infants have a lower level of IgG than appropriate for gestation infants, leading to the hypothesis that placental function impacts the transfer of antibodies. The IgG antibodies are instrumental in fetal passive immunity to infection, although they may also be harmful, as in cases of maternal Graves disease, antiplatelet antibody, maternal systemic lupus erythmatosus, or Rho (D) isoimmunization. Other substances that pass through the placenta include red blood cell antigens, carbon dioxide, oxygen, some viruses, and nutrients.

The placental size increases throughout the pregnancy, but not in constant proportion. The placenta comprises 85% of the combined fetal/placental weight at 8 weeks' gestation, but only 12% at 38 weeks.^[13] Late growth restriction will not affect placental weight as much as early growth restriction. Low-weight placentas may be seen with pregnancy-induced hypertension or congenital anomalies; high-weight placentas may be seen with maternal diabetes mellitus, severe maternal anemia, or hydrops fetalis.^[14] This makes it important for the neonatal team attending deliveries to communicate with the obstetrical staff about the condition of the placenta as part of their history taking. Outcome-related placental diseases include infarction, retroplacental hematoma, septal cysts, calcification, thrombosis, tumors, villous edema, acute and chronic villitis, and umbilical cord abnormalities.^[14] These may have an effect on uteroplacental blood flow and cause problems for the fetus. Specifically, infarction of 5 to 10% may be associated with poor outcomes and can lead to stillbirth. Hematoma may lead to preterm delivery and its associated complications. Cysts usually are insignificant for the fetus, as are calcifications. Fetal artery thrombosis may affect the fetus, but only if it involves more than half of the placenta. The only placental tumor of fetal significance is chorioangioma. Chorioangioma is associated with fetal hydrops, fetal congestive heart failure, neonatal anemia, and thromobcytopenia.^[14] Villous edema may be present in maternal diabetes mellitus, preeclampsia, and placental infections and may be an ominous sign for the fetus. The affect on the fetus of acute and chronic villitis is related directly to the degree of fetal infection. Umbilical cord abnormalities include short cords (less than 32 cm), resulting in cord rupture; long cords (greater than 72 cm), increasing risk of entanglement and prolapse; hematoma, resulting in fetal death; and true knots in the cord, accounting for up to 11% of perinatal mortality. Cord insertion usually is not remarkable to the fetus unless it is velamentous, a paper-thin, widespread insertion into the membranes rather than the placenta itself. The umbilical cord usually is attached near the center of the placenta but may be inserted toward the margins of the placenta without fetal compromise. If inserted near the margin, the placenta is referred to as a "battledore" placenta in reference to a bat used in a medieval game that this form of a placenta resembles. Much attention has been given to two vessel cords with a single vein and artery. It is reported that up to 50% have an associated congenital anomaly, often affecting the urogenital system.^[12,14]

Multiple gestations impact placental health as well. The pathologist examining the placenta may determine placental anastomoses. The anastomoses of concern are when the arterial tree of one fetus drains to the venous tree of another fetus. One should remember that, even in groups of three fetuses and higher, "twin-to-twin" transfusions may occur among the group in different combinations. Twin-to-twin transfusions may be associated with fetal mortality as high as 70%.^[14] Zygosity may also be determined by a thorough examination of the placenta by a pathologist.

An elaborate discussion on the endocrine function of the placenta is beyond the purpose of this paper. Briefly, the placenta has a variety of endocrine functions with the ability to produce proteins and steroid hormones being the most notable. Some of the significant hormones produced by the human placenta are human chorionic gonadotrophin (hCG), decidual prolactin and chorionic somatomammotrophin (hCS), prolactin, and human placental growth hormone. Indeed, hCG is the hormone tested to diagnose pregnancy. These substances all have effects on mother, fetus, or both. They may play a role in preparing the maternal breast for lactation and determining fetal growth rates or placental nutrient transfer. Much more information is needed to decipher the biologic purpose of many of these placental hormones.^[15]

Substance abuse in pregnancy is a concern for fetal health.^[16] The majority of drugs, prescriptive, nonprescriptive, or illicit are transferred across the placenta by passive diffusion owing to their small lipid-soluble molecules.^[16] The placenta has enzyme systems that assist in the metabolism of certain drugs, however, these systems are easily defeated with the fetal liver carrying the work of metabolizing drugs. Alcohol freely crosses the placenta and will have a direct toxic effect on the fetus as opposed to an indirect effect through uteroplacental blood flow. Consumption of alcohol may give rise to fetal alcohol syndrome with its associated dire effects. Unfortunately, the amount of alcohol consumption that results in fetal alcohol syndrome continues to remains elusive. Tobacco's effect on the placenta will result in a reduction of fetal capillary volume, thereby affecting the transport function of the placenta. Abnormal lung morphology and decreased cerebral perfusion have been noted in fetuses exposed to nicotine.^[17] The net result of this decreased function is small-for-gestation babies.^[18]

Illicit drugs, such as opiates, readily cross the placenta and have been associated with growth restriction and prematurity. Marijuana also crosses the placenta and may affect placental blood flow. The most pressing concern in maternal marijuana use is an association with shortened gestation.

Maternal cocaine use has a vasoconstrictive effect on the uterus, and thus the placenta, with an increase in placental abruption. Animal studies have shown enzymes in the placenta that metabolize cocaine and offer some protection to the fetus.^[16] Further, one of the metabolites of cocaine, benzoylecgonine, does not cross the placenta very readily. Unfortunately, the placenta is a direct target for cocaine and placental transfer systems are adversely affected for essential nutrients as well. Placental perfusion can be compromised by as much as 50% in mothers who ingest cocaine. Decreased fetal oxygen levels have also been noted with maternal cocaine exposure.^[16] In animal studies, a decreased level of oxygenation was not seen with direct administration of cocaine to the fetus.^[16] This problem suggests decreased oxygenation results from poor placental perfusion. Other fetal effects from cocaine include prematurity, intrauterine growth restriction, limb defects, cerebral infarctions or hemorrhages, cardiac and renal defects, and behavioral abnormalities.

Amphetamines also affect uteroplacental blood flow, but do not cross the placenta readily for direct fetal effect.^[19] When faced with a mother with a history for use of these substances, it is important to remember that they may occur simultaneously and can be associated with other lifestyle effects to the baby, such as sexually transmitted infections. Many units are utilizing a meconium drug screen test to detect fetal exposure to maternal substance use for the last 3 months before delivery.

The fetal membranes consist of the chorion, amnion, yolk sac, and allantois. The chorion has three layers: cytotrophoblastic, chorionic connective tissue, and basement membrane. The chorion lies closest to the placenta. The chorionic sac encompasses the fetus and the amnion and is covered with chorionic villi until the 8th week. After the 8th week, these villi are constricted due to a decreased blood supply until a smooth chorion is formed in the portion of the sac that is not forming the placenta.^[12] The chorion is thicker than the amnion.

The amnion has five distinct layers: amniotic epithelium, basement membrane, compact layer, fibroblast layer, and intermediate layer. There are no blood vessels or nerves in the amnion. This membrane lies closest to the fetus and the amnion is supplied with nutrients by the amniotic fluid.^[20] In the 3rd and 4th weeks' gestation, the amnion will somewhat fold over and engulf the yolk sac and body stalk that attaches the conceptus to the uterus. The amnion eventually forms an epithelial covering of the umbilical cord, which is further assisted by its own formation of Wharton's jelly as a protective substance for the precious umbilical vessels within. As the amnion expands, it moves into the chorionic sac until it completely fills the chorionic sac at around 10 weeks' gestation.^[11]

The yolk sac is a primitive structure that usually disappears after 20 weeks' gestation. A remnant of the yolk sac merges in the forming embryo into the primitive gut. The role of the yolk sac in early gestation is to supply the embryo with oxygen and nutrients until the formation of the placenta is accomplished. The yolk sac is also the first site of hematopoeisis, with embryonic red blood cells and macrophages visible in the yolk sac as early as 2 weeks' gestation. Neutrophils, platelets, and lymphocytes are not produced in the yolk sac.^[21] The allantois develops into a fibrous cord, the urachus, which runs from the fetal bladder to the umbilicus. This urachus can remain patent in the neonate with urine secreted from the umbilicus. The yolk sac and allantois are the only portions of the fetal membranes that develop to form a part of the fetus itself. The chorion and amnion are discarded after birth when their usefulness has ended.

The purposes of the fetal membranes include protection of the fetus from ascending infection by forming a physical barrier, containment of the amniotic fluid, and secretion of substances into the amniotic fluid.^[20]

Fetal membranes may develop abnormally into amniotic sheets or bands occurring in 0.8% of all pregnancies. Previous scars of the uterus either from cesarean section or dilation and curettage (D&C) can result in amniotic sheets forming around the scar tissue and may have an association with early labor. Amniotic bands are less common than amniotic sheets, occurring in 0.08% of all pregnancies. Amniotic bands are fibrous strands that stretch through the amniotic cavity as a result of rupture to the amnion without compromise of the chorion. Amniotic bands usually occur spontaneously. The danger to the fetus occurs when the bands compromise limb development but they have been known to entrap the fetal trunk and head as well. Up to 70% of all amniotic bands seen on prenatal ultrasound disappear upon repeat ultrasound. If the ultrasound demonstrates amniotic bands with free fetal movement and lack of fetal attachment to the band, they are termed innocent amniotic bands and pose little risk to the fetus.^[22]

Amniotic fluid surrounds the growing fetus and provides a ballotable environment that is protective for the fetus. Amniotic fluid also assists in pulmonary development and the avoidance of compression defects, especially of the limbs. Its normal state is sterile and it should be free of meconium, blood, or pus.

Amniotic fluid is isotonic with fetal and maternal blood in the first trimester and, as fetal skin matures around 23 to 25 weeks' gestation, movement of water across fetal skin is reduced. As fetal kidneys excrete urine and contribute to the amniotic fluid, the fluid changes to a more hypotonic solution.^[23] As fetal kidneys mature, fetal urine is more diluted and amniotic fluid osmolality decreases. The major solutes in amniotic fluid are sodium, chloride, potassium, urea, bicarbonate, and lactate. The impact of solutes in regulating amniotic fluid volume is unclear.

Amniotic fluid production begins during the first trimester. The blastocyst divides into two layers, with the inner layer forming the embryo and the outer layer forming the placenta and amniotic cavity. In the beginning, water and electrolytes are transferred across the fetal skin. After about 11 weeks' gestation, most amniotic fluid production is by the fetal kidneys as fetal urine, although the fetal lungs contribute through the net movement of fetal lung fluid out of the lungs into the amniotic cavity.^[23]

Amniotic fluid removal is largely done through fetal swallowing, through the amniochorion to maternal circulation, and/or into the fetal blood to the placenta. Amniotic fluid volume changes often correlate with neonatal diseases secondary to the inability of the fetus to remove amniotic fluid or contribute to the volume of amniotic fluid. Examples of this relationship include some fetal kidney diseases and upper gastrointestinal (GI) disorders. Potter association, a disease characterized by aplastic kidneys, results in oligohydramnios from the lack of renal contribution to the amniotic fluid volume. With upper GI disorders, such as esophageal atresia, the fetus' inability to swallow amniotic fluid and pass it through the gastrointestinal tract results in polyhydramnios.

There are a variety of maternal disease states that affect the fetus. This paper is limited to a brief overview of some of the more common maternal disease states that newborn and infant nurses will encounter: maternal hypertension, diabetes mellitus, autoimmune disorders, thyroid disorders, hemoglobinopathies, and cardiac and renal disease.

Hypertension in pregnancy can be classified into four different disease states: chronic hypertension, preeclampsia, preeclampsia with superimposed hypertension, and transient hypertension. Preeclampsia is defined by hypertension with proteinuria and/or liver involvement or coagulopathies. Preeclampsia may rapidly progress to eclampsia, resulting in convulsions of the mother and lack of blood flow or oxygen to the fetus. The only curative treatment for preeclampsia/eclampsia is delivery of the fetus, although supportive treatments may be employed in the interest of continuing the pregnancy, if deemed safe for both mother and fetus. Maternal hypertension occurs in 10 to 20% of pregnancies and can result in placental insufficiency and decreased oxygen delivery. The fetus can initially adapt to chronic oxygen deficiency by decreasing growth rate and oxygen consumption. This process can continue until the decrease in placental flow exceeds 50% of fetal requirements.^[24] Accelerated maturation occurs in the lungs and brain as an adaptive process in intrauterine growth restriction. Other risks to the fetus from maternal hypertension include prematurity, fetal death, and placental abruption. Risks to the mother include placental abruption, disseminated intravascular coagulation, cerebral hemorrhage, hepatic failure, and acute renal failure. Maternal hypertension is responsible for 20 to 33% of all maternal mortality. The risk of placental abruption is very low in women with chronic hypertension versus those with preeclampsia.

Maternal diabetes mellitus can be a preexisting condition or can occur only with the pregnancy as gestational diabetes. The fetal effects can vary depending on the onset of diabetes. For mothers with preexisting diabetes, fetal growth may actually be retarded due to uterine vascular compromise in advanced disease. Otherwise, increased maternal levels of glucose result in increased fetal insulin levels. Insulin is the fetal growth hormone and increased levels result in large-for-gestational age infants with possible macrosomia and its inherent risk for birth trauma. Infants of diabetic mothers are also at increased risk of fetal anomalies such as caudal regression syndrome, neural tube defects, left microcolon syndrome, and cardiac defects. These defects usually occur around the 7th to 8th week of gestation. There are also risks to the infant of the diabetic mother for polycythemia, hyperbilirubinemia, respiratory distress syndrome, hypomagnesemia, and hy-pocalcemia.^[25]

Autoimmune disorders that impact pregnancy can include systemic lupus erythematosus (SLE), scleroderma, and rheumatoid arthritis.^[26] These diseases can cause an increased incidence of intrauterine growth restriction, stillbirth, prematurity, and perinatal death, mostly through placental compromise. The risk of these complications is very low in rheumatoid arthritis compared with SLE and scleroderma. Hemoglobinopathies such as sickle cell anemia and thalasemia can result in fetal polycythemia as the fetus tries to compensate for chronic oxygen deficiency.^[27]

Hypothyroidism rarely compromises the fetus, while hyperthyroidism can result in maternal preeclampsia and congestive heart failure.^[28] Maternal renal and heart disease can result in increased perinatal mortality and morbidity. There are a variety of fetal genetic disorders that occur during gestation. These can be the result of single gene abnormalities, multifactorial disorders, familial influence, or teratogen exposure. Pregnancy loss is increased with fetal genetic disorders and it is thought that half of spontaneous abortions are due to the influence of genetic abnormalities.^[13,29]

The uterine environment plays a crucial role for the developing fetus by several mechanisms, some of which are outlined in this article. Nurses attending deliveries and caring for the infant must be aware of any potential for neonatal compromise. Anticipatory guidance is imperative for positive outcomes for the infant and its family. By being cognizant of the potential for neonatal depression through one or more of these antenatal situations, the neonatal nurse can assemble a team skilled in the resuscitation and management of these infants. Newborn and infant nurses are also responsible for assuring an appropriate bed space with equipment and personnel to manage the admission of an infant with acute problems. Ancillary departments then can be alerted to a situation that may require their assistance, including respiratory therapy, laboratory, pharmacy, and radiology as well as the extracorporeal membrane oxygenation team, if needed. Further, delivery may be planned at a tertiary center with full transport capabilities if a quaternary center is required.

This article has explored the cervix, uterus, placenta, fetal membranes–chorion and amnion, amniotic fluid, and maternal influences on fetal development. This information may give the newborn/infant nurse some insight into the complications experienced by newborns after they leave the delivery room. Consideration of these factors may help the nurse to anticipate and prevent some post-birth complications, influence further research, and help to improve newborn and infant care.

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Reprint Address

Address reprint requests to Kimberly LaMar, ND, RNC, CNNP, 12126 E. Paradise Dr., Scottsdale, AZ 85259.

Kim LaMar, ND, RNC, CNNP, and Cheryl Hamernik, MSN, RNC, CNNP, Neonatal Experts Organization (NEO), University of Michigan Hospitals, Ann Arbor, MI