Prenatal Diagnosis

Prenatal diagnosis employs a variety of techniques to determine the health and condition of an unborn fetus. Without knowledge gained by prenatal diagnosis, there could be an untoward outcome for the fetus or the mother or both. Congenital anomalies account for 20 to 25% of perinatal deaths. Specifically, prenatal diagnosis is helpful for:

Managing the remaining weeks of the pregnancy
Determining the outcome of the pregnancy
Planning for possible complications with the birth process
Planning for problems that may occur in the newborn infant
Deciding whether to continue the pregnancy
Finding conditions that may affect future pregnancies
There are a variety of non-invasive and invasive techniques available for prenatal diagnosis. Each of them can be applied only during specific time periods during the pregnancy for greatest utility. The techniques employed for prenatal diagnosis include:

Ultrasonography
Amniocentesis
Chorionic villus sampling
Fetal blood cells in maternal blood
Maternal serum alpha-fetoprotein
Maternal serum beta-HCG
Maternal serum estriol
Ultrasonography
This is a non-invasive procedure that is harmless to both the fetus and the mother. High frequency sound waves are utilized to produce visible images from the pattern of the echos made by different tissues and organs, including the baby in the amniotic cavity. The developing embryo can first be visualized at about 6 weeks gestation. Recognition of the major internal organs and extremities to determine if any are abnormal can best be accomplished between 16 to 20 weeks gestation.

Although an ultrasound examination can be quite useful to determine the size and position of the fetus, the size and position of the placenta, the amount of amniotic fluid, and the appearance of fetal anatomy, there are limitations to this procedure. Subtle abnormalities may not be detected until later in pregnancy, or may not be detected at all. A good example of this is Down syndrome (trisomy 21) where the morphologic abnormalities are often not marked, but only subtle, such as nuchal thickening.

Amniocentesis
This is an invasive procedure in which a needle is passed through the mother's lower abdomen into the amniotic cavity inside the uterus. Enough amniotic fluid is present for this to be accomplished starting about 14 weeks gestation. For prenatal diagnosis, most amniocenteses are performed between 14 and 20 weeks gestation. However, an ultrasound examination always proceeds amniocentesis in order to determine gestational age, the position of the fetus and placenta, and determine if enough amniotic fluid is present. Within the amniotic fluid are fetal cells (mostly derived from fetal skin) which can be grown in culture for chromosome analysis, biochemical analysis, and molecular biologic analysis.

In the third trimester of pregnancy, the amniotic fluid can be analyzed for determination of fetal lung maturity. This is important when the fetus is below 35 to 36 weeks gestation, because the lungs may not be mature enough to sustain life. This is because the lungs are not producing enough surfactant. After birth, the infant will develop respiratory distress syndrome from hyaline membrane disease. The amniotic fluid can be analyzed by fluorescence polarization (fpol), for lecithin:sphingomyelin (LS) ration, and/or for phosphatidyl glycerol (PG).

Risks with amniocentesis are uncommon, but include fetal loss and maternal Rh sensitization. The increased risk for fetal mortality following amniocentesis is about 0.5% above what would normally be expected. Rh negative mothers can be treated with RhoGam. Contamination of fluid from amniocentesis by maternal cells is highly unlikely. If oligohydramnios is present, then amniotic fluid cannot be obtained. It is sometimes possible to instill saline into the amniotic cavity and then remove fluid for analysis.

Chorionic Villus Sampling (CVS)
In this procedure, a catheter is passed via the vagina through the cervix and into the uterus to the developing placenta under ultrasound guidance. Alternative approaches are transvaginal and transabdominal. The introduction of the catheter allows sampling of cells from the placental chorionic villi. These cells can then be analyzed by a variety of techniques. The most common test employed on cells obtained by CVS is chromosome analysis to determine the karyotype of the fetus. The cells can also be grown in culture for biochemical or molecular biologic analysis. CVS can be safely performed between 9.5 and 12.5 weeks gestation.

CVS has the disadvantage of being an invasive procedure, and it has a small but significant rate of morbidity for the fetus; this loss rate is about 0.5 to 1% higher than for women undergoing amniocentesis. Rarely, CVS can be associated with limb defects in the fetus. The possibility of maternal Rh sensitization is present. There is also the possibility that maternal blood cells in the developing placenta will be sampled instead of fetal cells and confound chromosome analysis.

Maternal blood sampling for fetal blood cells
This is a new technique that makes use of the phenomenon of fetal blood cells gaining access to maternal circulation through the placental villi. Ordinarily, only a very small number of fetal cells enter the maternal circulation in this fashion (not enough to produce a positive Kleihauer-Betke test for fetal-maternal hemorrhage). The fetal cells can be sorted out and analyzed by a variety of techniques to look for particular DNA sequences, but without the risks that these latter two invasive procedures inherently have. Fluorescence in-situ hybridization (FISH) is one technique that can be applied to identify particular chromosomes of the fetal cells recovered from maternal blood and diagnose aneuploid conditions such as the trisomies and monosomy X.

The problem with this technique is that it is difficult to get many fetal blood cells. There may not be enough to reliably determine anomalies of the fetal karyotype or assay for other abnormalities.

Maternal serum alpha-fetoprotein (MSAFP)
The developing fetus has two major blood proteins--albumin and alpha-fetoprotein (AFP). Since adults typically have only albumin in their blood, the MSAFP test can be utilized to determine the levels of AFP from the fetus. Ordinarily, only a small amount of AFP gains access to the amniotic fluid and crosses the placenta to mother's blood. However, when there is a neural tube defect in the fetus, from failure of part of the embryologic neural tube to close, then there is a means for escape of more AFP into the amniotic fluid. Neural tube defects include anencephaly (failure of closure at the cranial end of the neural tube) and spina bifida (failure of closure at the caudal end of the neural tube). The incidence of such defects is abbout 1 to 2 births per 1000 in the United States. Also, if there is an omphalocele or gastroschisis (both are defects in the fetal abdominal wall), the AFP from the fetus will end up in maternal blood in higher amounts.

In order for the MSAFP test to have the greates utility, the gestational age must be known with certainty. This is because the amount of MSAFP increasses with gestational age (as the fetus and the amount of AFP produced increase in size). Also, the race of the mother and presence of gestational diabetes are important to know, because the MSAFP can be affected by these factors. The MSAFP is typically reported as multiples of the mean (MoM). The greater the MoM, the more likely a defect is present. The MSAFP has the greatest sensitivity between 16 and 18 weeks gestation, but can still be useful between 15 and 22 weeks gestation.

However, the MSAFP can be elevated for a variety of reasons which are not related to fetal neural tube or abdominal wall defects, so this test is not 100% specific. The most common cause for an elevated MSAFP is a wrong estimation of the gestational age of the fetus.

Using a combination of MSAFP screening and ultrasonography, almost all cases of anencephaly can be found and most cases of spina bifida. Neural tube defects can be distinguished from other fetal defects (such as abdominal wall defects) by use of the acetylcholinesterase test performed on amniotic fluid obtained by amniocentesis--if the acetylcholinesterase is elevated along with MSAFP then a neural tube defect is likely. If the acetylcholinesterase is not detectable, then some other fetal defect is suggested.

NOTE: The genetic polymorphisms due to mutations in the methylene tetrahydrofolate reductase gene may increase the risk for NTDs. Folate is a cofactor for this enzyme, which is part of the pathway of homocysteine metabolism in cells. The C677T and the A1298C mutations are associated with elevated maternal homocysteine concentrations and an increased risk for NTDs in fetuses. Prevention of many neural tube defects can be accomplished by supplementation of the maternal diet with only 4 mg of folic acid per day, but this vitamin supplement must be taken a month before conception and through the first trimester.

The MSAFP can also be useful in screening for Down syndrome and other trisomies. The MSAFP tends to be lower when Down syndrome or other chromosomal abnormalities is present.

Maternal serum beta-HCG
This test is most commonly used as a test for pregnancy. Beginning at about a week following conception and implantation of the developing embryo into the uterus, the trophoblast will produce enough detectable beta-HCG (the beta subunit of human chorionic gonadotropin) to diagnose pregnancy. Thus, by the time the first menstrual period is missed, the beta-HCG will virtually always be elevated enough to provide a positive pregnancy test. The beta-HCG can also be quantified in serum from maternal blood, and this can be useful early in pregnancy when threatened abortion or ectopic pregnancy is suspected, because the amount of beta-HCG will be lower than expected.

Later in pregnancy, in the middle to late second trimester, the beta-HCG can be used in conjunction with the MSAFP to screen for chromosomal abnormalities, and Down syndrome in particular. An elevated beta-HCG coupled with a decreased MSAFP suggests Down syndrome.

Very high levels of HCG suggest trophoblastic disease (molar pregnancy). The absence of a fetus on ultrasonography along with an elevated HCG suggests a hydatidiform mole. The HCG level can be used to follow up treatment for molar pregnancy to make sure that no trophoblastic disease, such as a choriocarcinoma, persists.

Maternal serum estriol
The amount of estriol in maternal serum is dependent upon a viable fetus, a properly functioning placenta, and maternal well-being. The substrate for estriol begins as dehydroepiandrosterone (DHEA) made by the fetal adrenal glands. This is further metabolized in the placenta to estriol. The estriol crosses to the maternal circulation and is excreted by the maternal kidney in urine or by the maternal liver in the bile. The measurement of serial estriol levels in the third trimester will give an indication of general well-being of the fetus. If the estriol level drops, then the fetus is threatened and delivery may be necessary emergently. Estriol tends to be lower when Down syndrome is present and when there is adrenal hypoplasia with anencephaly.


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Listed below are some of the more common chromosomal abnormalities that can occur. The descriptions are for the completely abnormal condition in which all fetal cells contain the abnormal karyotype. Bear in mind that "mosaicism" can occur. A "mosaic" is a person with a combination of two cell lines with different karyotypes (normal and abnormal). When karyotyping is performed, multiple cells are analyzed to rule out this possibility. An example would be a Turner's mosaic, with a 45,X/46,XX karyotype, with some cells having the abnormal karyotype and some cells having a normal karyotype. The mosaic condition is not as severe as the completely abnormal karyotype, and the features may not be as marked, and livebirths may be possible. Sometimes the mosaicism is confined to the placenta ("confined placental mosaicism"). A placenta with an abnormal karyotype may lead to stillbirth, even though the fetus has a normal karyotype; conversely, a placenta with a normal karyotype may allow longer survival for a fetus with a chromosomal abnormality. Rarely, a translocation of part of one chromosome to another in the parent will be passed on to the child as a partial trisomy (such as 6p+ or 16p+) which may not be as severe as a complete trisomy.

Trisomy 21: Down syndrome; incidence based upon maternal age, though translocation type is familial; features include epicanthal folds, simian crease, brachycephaly, cardiac defects.

Trisomy 21 (47, XY, +21) karyotype, diagram
Down syndrome, facial features, gross
Down syndrome, cystic Hassall's corpuscles in thymus, medium power microscopic
Trisomy 18: Features include micrognathia, overlapping fingers, horseshoe kidney, rocker bottom feet, cardiac defects, diapragmatic hernia, omphalocele.

Trisomy 18 (47, XY, +18) karyotype, diagram
Clenched hand with trisomy 18, gross
Diaphragmatic hernia, gross
Trisomy 13: Features include microcephaly, cleft lip and/or palate, polydactyly, cardiac defects, holoprosencephaly.

Trisomy 13 (47, XX, +13) karyotype, diagram
Cleft lip with trisomy 13, gross
Polydactyly, hands, with trisomy 13, gross
Cyclopia with proboscis, trisomy 13, gross
Trisomy 16: Seen in abortuses from first trimester. Never liveborn.

Trisomy 16 karyotype, diagram
Monosomy X: Turner's syndrome; can survive to adulthood; features include short stature, cystic hygroma of neck (leading to webbing), infertility, coarctation.

Monosomy X, or Turner's syndrome (45, X) karyotype, diagram
Monosomy X, or Turner's syndrome, streak ovaries in adult, gross
Massive fetal hydrops with monosomy X, or Turner's syndrome, gross
Cystic hygroma with monosomy X, or Turner's syndrome, gross
XXY: Klinefelter's syndrome; features include elongated lower body, gynecomastia, testicular atrophy (incidence: 1/500 males)

Klinefelters' syndrome karyotype, diagram
Triploidy: There is often a partial hydatidiform mole of placenta. Fetal features include 3-4 syndactyly, indented nasal bridge, small size.

Triploidy karyotype, diagram
Partial hydatidiform mole, gross
3-4 syndactyly with triploidy, gross
A host of other chromosomal abnormalites are possible. In general, fetal loss earlier in gestation, and multiple fetal losses, more strongly suggests a possible chromosomal abnormality.
Neural Tube Defects
The maternal serum alpha-fetoprotein (MSAFP) is useful for screening for neural tube defects, but the gestational age must be known for proper interpretation. The frequency of neural tube defects has been shown to be reduced if women supplement their diet with folic acid (before and during pregnancy).

Anencephaly: There is absence of the fetal cranial vault, so no cerebral hemispheres develop. Anencephaly is the most common congenital malformation--about 0.5 to 2/1000 live births. Other neural tube defects are as frequent, but the incidence varies with geography.

Anencephaly, gross
Anencephaly, gross
Iniencephaly: Imperfect formation of the base of the skull, with rachischisis and exaggerated lordosis of the spine.

Iniencephaly, gross
Iniencephaly, gross
Exencephaly: Incomplete cranial vault, but the brain is present.

Exencephaly, gross
Meningomyelocele: Defect in the vertebral column allowing herniation of meniges and spinal cord; location and size determine severity.

Meningomyelocele, gross
Meningomyelocele, gross
Encephalocele: Herniation of brain through a skull defect.

Occipital encephalocele, radiograph
Occipital encephalocele with iniencephaly, gross
Spina bifida: A defective closure of the posterior vertebral column. It may not be open (spina bifida occulta).

Hydrops Fetalis
There are many causes for fetal hydrops, and in about 25 to 30% of cases, no specific cause for hydrops can be identified. Multiple congenital anomalies can also be associated with hydrops, though the mechanism is obscure for everything except cardiac anomalies that produce heart failure.


Hydrops can be classified as immune and non-immune. Immune causes such as Rh incompatibility between mother and fetus are now uncommon. Non-immune causes can include:

Congenital infections
Cardiac anomalies
Chromosomal abnormalities
Fetal neoplasms
Twin pregnancy
Fetal anemia
Other anomalies (pulmonary, renal, gastrointestinal)
Congenital Infections
The hallmark of congenital infections is fetal hydrops along with organomegaly. Diagnosis can depend upon:

TORCH titers

Tissue culture

Histologic examination

Disruptions
It is becoming increasingly recognized that many fetal abnormalities result from problems with embryogenesis early on. Some of these abnormalities may involve problems with vascular supply. The result is abnormal formation of a body region or regions. Such disruptions are generally asymmetric. Examples may include:

Limb-Body Wall Complex (amnionic band syndrome)

Omphalocele, gross
Gastroschisis, gross
Amnionic bands, gross
Limb-body wall (LBW) complex, gross
Limb-body wall (LBW) complex, gross
Sirenomelia

Sirenomelia, gross
Sirenomelia, gross
Hydranencephaly

Hydranencephaly, gross
Renal Cystic Disease
For examples of these diseases, go to the tutorial on renal cystic disease.

Recessive Polycystic Kidney Disease (RPKD)

This condition is inherited in an autosomal recessive pattern, giving a 25% recurrence risk for parents having subsequent children. The kidneys are affected bilaterally, so that in utero, there is typically oligohydramnios because of poor renal function and failure to form significant amounts of fetal urine. The most significant result from oligohydramnios is pulmonary hypoplasia, so that newborns do not have sufficient lung capacity to survive, irrespective of any attempt to treat renal failure. RPKD may be termed "Type I" cystic disease in the Potter's classification. A helpful finding at autopsy is the presence of congenital hepatic fibrosis, which accompanies RPKD.

Multicystic Renal Dysplasia

This condition has a sporadic inheritance pattern. It is perhaps the most common form of inherited cystic renal disease. It results from abnormal differentiation of the metanephric parenchyma during embryologic development of the kidney. However, in many cases it can be unilateral, so the affected person survives, because one kidney is more than sufficient to sustain life. In fact, with absence of one functional kidney from birth, the other kidney undergoes compensatory hyperplasia.

Multicystic renal dysplasia is often the only finding, but it may occur in combination with other anomalies and be part of a syndrome (e.g., Meckel-Gruber syndrome), in which case the recurrence risk will be defined by the syndrome. If this disease is bilateral, the problems associated with oligohydramnios are present.

Multicystic renal dysplasia was termed "Type II" in the Potter classification. There are two main subgroups. If the affected kidney is large, then it is termed "Type IIa". If the affected kidney is quite small, it can be termed "hypodysplasia" or "Type IIb". Different combinations are possible, so that only one kidney or part of one kidney can be affected and be either larger or small; both affected kidneys can be large or both can be small, or one can be larger and the other small. It is quite common for asymmetry to be present.

Dominant Polycystic Kidney Disease (DPKD)

This condition is inherited in an autosomal dominant pattern, so the recurrence risk in affected families is 50%. However, this disease rarely manifests itself before middle age. It may begin in middle aged to older adults to cause progressive renal failure as the cysts become larger and the functioning renal parencyma smaller in volume. This is the "Type III" cystic disease in the Potter classification, but it is rarely manifested prenatally or in children.

Cystic Change with Obstruction

In the fetus and newborn with urinary tract obstruction, it is possible for cystic change to occur in the kidneys, in addition to hydroureter, hydronephrosis, and bladder dilation. Depending upon the point of obstruction, either or both kidneys may be involved. For example, posterior urethral valves in a male fetus, or urethral atresia in a male or female fetus, will cause bladder outlet obstruction so that both kidneys are involved. With bladder outlet obstruction, there will be oligohydramnios and the appearance of pulmonary hypoplasia.

Grossly, this form of cystic disease may not be apparent. The cysts may be no more than 1 mm in size. Microscopically, the cysts form in association with the more sensitive developing glomeruli in the nephrogenic zone so that the cysts tend to be in a cortical location. Thus, "cortical microcysts" are the hallmark of this form of cystic disease, which is "Type IV" in the Potter's classification. There are no accompanying cystic changes in other organs in association with this disease.

Congenital Neoplasms
Such tumors are uncommon, but those that are seen most frequently include:

Teratoma. These tumors occur in midline regions (sacrococcygeal, cerebral, nasopharyngeal).

Nasopharyngeal teratoma, gross
Teratoma, low power microscopic
Immature teratoma, medium power microscopic
Hemangioma. About 1/3 of all soft tissue neoplasms in the first year of life are hemangiomas or lymphangiomas. Fibromatoses are also common.

Hemangioma, gross
Hemangioma, microscopic
Neuroblastoma. The incidence of congenital neuroblastoma is 1:8000

Neuroblastoma, gross
Neuroblastoma, microscopic
Size and location are important, for even histologically benign neoplasms can obliterate normal tissues, be difficult to resect, or recur with incomplete resection. Malignant neoplasms have the capacity for invasion and metastases.

Skeletal Abnormalities
Ultrasound may reveal long bones that are shortened. There are several possibilities, including short-limbed dwarfism, osteogenesis imperfecta, and short rib-polydactyly syndrome. The various forms of short-limbed dwarfism, which can be lethal, are more difficult to diagnose specifically. The features of these various conditions may not be well-developed at 20 weeks gestation or less, making diagnosis more difficult. Limitation of survival is often due to pulmonary hypoplasia because the chest cavity is too small.

Achondroplasia is a form of short-limbed dwarfism that is inherited in an autosomal dominant fashion, though in most cases there is no affected parent and the disease is due to a new mutation. The homozygous form of the disease is lethal. The heterozygous form is not lethal, and affected persons can live a normal life. They have short extremities, but a relatively normal sized thorax and normal sized head.

Thanatophoric dysplasia (TD) is a lethal condition. The long bones are short and curved, with femora that have a "telephone receiver" appearance on radiograph because of the curvature. The vertebrae have marked platyspondyly with widened disc spaces. There are two forms, TD 1 and TD 2, with the latter distinguished by the appearance of a "cloverleaf" pattern to the skull.

Osteogenesis imperfecta occurs in several forms. There is a lethal perinatal form in which fractures appear in long bones even in utero. This condition is due to an abnormal synthesis of type 1 collagen that forms connective tissues, including bone matrix.

Thanatophoric dysplasia, radiograph
Osteogenesis imperfecta, radiograph
Placental Abnormalities
Abruptio placenta: Premature separation of the placenta near term, with retroplacental blood clot.

Abruptio placenta, gross
Placenta previa: Low-lying implantation site can lead to hemorrhage during delivery.

Velamenous insertion: Cord vessels splay out in the membranes before reaching the placental disk and predispose to traumatic rupture.

Velamentous insertion, gross
Long - short cord: Umbilical cord length is determined by the amount of fetal movement. More movement increases cord length. A long cord can become entangled with the baby or more easily prolapse.

Nuchal cord, gross
True knot of umbilical cord, gross
Twin placenta: Monozygous twinning is associated with increased risk for both abnormalities and accidents. A twin-twin transfusion syndrome can occur when a vascular anastomosis is present

Vascular anastomosis in placenta, gross
Vascular anastomosis in placenta, gross
Hypertension: Vascular changes can be associated with pregnancy-induced hypertension (PIH) and the more severe complications of eclampsia and pre-eclampsia.

Decidual arteriopathy, microscopic

When 'Labor Day' Comes Early



July 23, 2001 -- From cancer to diabetes to heart disease, medical advances have been impressive over the past few decades. But there is one area where doctors have not made as much progress -- preventing preterm labor.


For many reasons -- increasing maternal age, rising rates of multiple births thanks to advances in fertility -- the rate of early deliveries has risen sharply in the U.S., with an increase of 23% in the past 20 years.


"The national controversy is what to do about it," says Fung Lam, MD, chief of gynecology and vice chairman of obstetrics and gynecology at California Pacific Medical Center in San Francisco. "The pendulum is swinging back and forth, and currently the national view that's holding sway is that interventions are not successful."


But Lam and others on the frontlines of neonatal care say this is not true. There are many medications and tactics doctors can employ to extend a pregnancy if preterm labor is diagnosed.


'A Major, Major Problem'


Each day in the United States, 1,239 babies are born preterm -- that is, less than 37 weeks into the pregnancy. A normal pregnancy lasts 40 weeks after the first day of the last menstrual period. Infants born early are more likely to be low weight and suffer complicated health problems including underdeveloped lungs. They are 13 times more likely to die in their first year of life than other newborns.


"It is still a major, major problem," says James Martin Jr., MD, president of the Society for Maternal Fetal Medicine and director of maternal-fetal medicine at the University of Mississippi Medical Center in Jackson.


"The thrust of a lot of research is to better diagnose the patient at risk and to intervene effectively ... so baby can safely remain in utero for a longer amount of time," Martin tells WebMD.


But premature labor can be difficult to diagnose. Symptoms can include contractions, backache, a feeling of pelvic pressure, abdominal cramps, gas, and/or diarrhea.


And it's expensive. Consider that neonatal intensive care units cost at least ,000 per day, and preterm infants who survive spend many weeks or months there.


Exactly why it occurs is not fully understood, but women are more likely to experience preterm labor or deliver prematurely if they have done so in the past, are carrying multiple babies, and/or have certain medical conditions that can complicate pregnancy.


"Doctors get a failing grade at how well we understand the process, and we are not much better at treatment," says Stephen Chasen, MD, director of high-risk obstetrics at New York Weill-Cornell Center.


The Pharmaceutical Approach


If a women comes in with uterine contractions before 34 weeks, doctors typically assess the cervix to document contractions and/or other changes to the cervix.


"For practical purposes, the cut-off most people use is 34 weeks for treating preterm labor," Chasen says. Between 34 and 37 weeks, complications of prematurity are rare, so doctors don't necessarily employ aggressive treatment, he says.


"The most important thing is to give steroids to accelerate the maturity of the baby should he or she be born," he says. "Giving steroids can decrease lung complications or brain complication and decrease mortality."


A type of medications called tocolytic agents may be used to stop the whole labor process and let the pregnancy progress. They include terbutaline, which relaxes the uterus and decreases contractions, but this drug has not been officially approved for preterm labor. Another drug, ritodrine, was pulled from the market when the FDA required further testing and the company declined to bear the cost of further studies.


Magnesium sulfate may also be used to disrupt the communication that allows muscles to contract. It is usually given through an intravenous infusion into the arm. The heart drug Procardia may also be used to decrease contractions by blocking the muscle's communication system.


"These medications can delay delivery long enough for steroids to have beneficial effects," Chasen says. Another drug, Antocin, is in the FDA pipeline.


The Home-Monitoring Approach


Sometimes women at high risk of preterm labor will choose home uterine monitoring, which is basically a belt they strap on twice a day for an hour each time. While the pregnant woman is wearing the belt, she will push a button on it every time she thinks she feels a contraction. The information is then transmitted to her doctor.


The emergence of these home-monitoring devices rubs many professionals the wrong way.


"The bottom line is that no one has demonstrated that it leads to healthier pregnancies or delivery at a later gestational age," Chasen says.


Lam, however, says they're a fine way to keep tabs on things and to alert the woman if she needs medical attention.


"You use a thermometer to take someone's temperature to see if they have a fever, and if they do, you have to treat them because the thermometer won't cure the fever," he says. "The same is true with home uterine monitoring. It's a diagnostic tool, not a therapeutic tool."


Janet Bleyl is an advocate of home uterine activity monitoring. "We have thousands of women who have known early on they're having preterm labor because of home monitoring," says Bleyl, founder and president of the Triplet Connection, a Stockton, Calif.-based nonprofit group for families who have had or who are expecting triplets or more.


"We have seen lots of patients in preterm labor who, due to drugs and aggressive treatment, have prolonged their pregnancy from weeks to months," she tells WebMD.


Because of the insidious nature of premature labor, "women who find themselves in it are unable to detect it themselves, which is why home monitoring can be so important and useful," she says.


What to Watch For


Women should be on the lookout for:

Mild uterine contractions
Low back pain or pelvic heaviness
Increased pink or brown vaginal discharge or vaginal discharge with foul odor

"Realize that preterm labor is not painful," Bleyl says. "Most are watching for painful contractions, but if they are in a high-risk situation even minor contractions are big news and need to be checked out. Most often it can be stopped or helped if doctors intervene early enough.