KEY POINTS
l Thoughclinical and sonographic estimated fetal weight (EFW)can identify newborns with weight4000 g, both methodsare poor at detecting neonates who will weigh 4500 g.
l Prevention of macrosomia is obtained, in women with gestational diabetes (GDM), with the following:
m Diet and glucose monitoring with insulin if needed, compared to no treatment or diet only.
m Postprandial blood glucose monitoring, compared to preprandial, in GDM requiring insulin therapy.
m Strict glucose control, with fasting blood sugar <90 and two hours postprandial<120.
l Among uncomplicated pregnancies, induction for sus- pected macrosomia is not indicated, as it has not been shown to reduce the risk of cesarean section, instrumental delivery, or shoulder dystocia.
l There is insufficient evidence to recommend best man- agement of suspected macrosomia among pregnancies complicated by diabetes mellitus, prior cesarean delivery, or shoulder dystocia, because of the lack of randomized trials and the inaccuracy of predicting birth weight. The American College of Obstetricians and Gynecologists (ACOG) suggests a planned cesarean for women with no diabetes and an EFW of >5000 g, and for those with diabetes and an EFW of 4500 g, but these suggestions are not based on level 1 evidence.
DEFINITION
A fetus with EFW4000 gcan be presumed to be macrosomic.
Macrosomic newborns can be classified as grades I (birth weight 4000–4499 g), II (4500–4999 g), and III (5000 g) (1).
This classification is clinically relevant because the grades are associated with different types of complications.
EPIDEMIOLOGY/INCIDENCE
The prevalence of macrosomia has decreased significantly in the United States (2), though it is increasing in other coun- tries, like Denmark. The rate of neonates in the United States weighing4000 g was 10.2% in 1996, 9.2% in 2002, and 7.6%
in 2008, continuing to decrease over 12 years. For newborns weighing 5000 g, the decrease in the prevalence has been notable as well (from 0.16% in 1996 to 0.13% in 2002 and 0.10% in 2008) (2,3). In some countries, such as Denmark, however, macrosomia is increasing. From 1998 to 2008, that country’s rate of macrosomia (live births weighing>4000 g) has increased from 5.2% to 5.8% (4). The rate of macrosomia in other countries has ranged from 1% in Thailand (5) to 5%
in Antigua and Barbuda (6) and 20% in the Republic of Croatia (7).
RISK FACTORS
Hispanic women, maternal obesity, maternal birth weight>8 lb, grand multiparity (5 deliveries), prior macrosomic fetus, abnormal 50-g glucose screen but normal three-hour glucose test, diabetes (pre- or gestational diabetes), gestational age40 weeks, excessive weight gain during pregnancy are well- known risk factors (8). Intrapartum hydramnios (9) and second stage of labor >120 minutes (10) are other risk factors for macrosomia. The majority of newborns with birth weights 4500 g do not have any known risk factors (8).
COMPLICATIONS
Thematernalcomplications with macrosomic fetuses include prolonged labor, operative vaginal delivery, cesarean deliv- ery, postpartum hemorrhage, and vaginal lacerations(8).
Compared to newborns with birth weights of 3000 to 3999 g,neonatal complications for grade I macrosomia include breech presentation, induction, meconium staining, dysfunc- tional/prolonged labor, cephalopelvic disproportion, and cesar- ean delivery. For grade II macrosomia, the complications arealso Apgar scores3 at 5 minutes, assisted ventilation>30 minutes, birth injuries, meconium aspiration, and hyaline membrane disease. For grade III macrosomia, there is also a significantly higher likelihood ofneonatal and infant mortality(1).
MANAGEMENT
Prevention of Macrosomia
A significant decrease in the rate of macrosomia can be obtained in women with GDM with the following:
l Diet and glucose monitoring with insulin if needed compared to no treatment or diet only (11).
l Postprandialversus preprandialblood glucose monitor- ing in GDM requiring insulin therapy(12).
l Continuous glucose monitoring compared to standard antenatal care with intermittent self-monitoring (13).
l Management of GDM with fasting blood sugar<90 and 2 hour postprandial<120,versus modified blood sugar goal based on whether the abdominal circumference is
<75% versus75% for gestational age (if abdominal cir-
cumference 75% the fasting blood sugar should have been in this study<80 and 2 hour postprandial<100) (14).
l Treatment, including nutrition instruction, diet, glucose testing, and insulin if necessary, of mild or borderline GDM, defined by abnormal one-hour glucose challenge test but normal two-hour glucose tolerance test (15,16).
The rate of macrosomia wasnotsignificantly decreased with
l pre- and gestational diabetes, administering insulin twice daily versus four times daily (17);
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l use of insulin or glyburide in the management of GDM not controlled adequately on diet (18);
l use of glyburide or metformin as alternatives to insulin therapy (19);
l induction of labor versus expectant management for preg- nancy at>41 weeks (20).
Screening
During labor, the detection of neonates weighing at least 4000 g is similar with clinical or sonographic EFWs, though the likeli- hood ratio with clinicians’ estimate was 15, while with measure- ments of biometric parameters it was 42 (i.e., better) (21).
Neither clinical nor sonographic EFW can accurately identify neonates that weigh 4500 g or more (22,23). The posttest probability of detecting macrosomia ranges from 15% to 79% by ultrasound and 40% to 52% with clinical estimates (2).
Management of Suspected Macrosomia
Whenever macrosomia is suspected, the pregnancy should be classified into one of the following groups: (i) uncomplicated, (ii) pre- or gestational diabetes, (iii) prior cesarean delivery, or (iv) history of shoulder dystocia.
Uncomplicated
Induction of labor for suspected fetal macrosomia in non- diabetic women has not been shown to alter the risk of maternal or neonatal morbidity, but the power of the included studies to show a difference in rare neonatal morbidity is limited. Compared to expectant management, induction of labor for suspected macrosomia has not been shown to reduce the risk of cesarean section (RR 0.96, 95% CI 0.67–
1.38) or instrumental delivery (RR 1.02, 95% CI 0.60–1.74).
Shoulder dystocia is not statistically different between groups(RR 1.06, 95% CI 0.44–2.56); one trial reported, how- ever, two cases of brachial plexus injury and four cases of fracture in the expectant management group (24). Labor induc- tion for suspected macrosomia results in an increased rate of cesarean delivery without an improved outcome (25). Thus, there is no indication for induction for suspected macrosomia among uncomplicated pregnancies.
While the ACOG practice bulletin on fetal macrosomia (8) suggests that planned cesarean delivery should be consid- ered if the EFW is at least 5000 g, there is insufficient evidence to assess this intervention, and there are insufficient reports on the peripartum outcomes when the fetus is suspected to have grade III macrosomia (2).
Diabetes
In insulin requiring diabetic pregnancies, induction at 38 weeks, compared to expectant management until 42 weeks, is associated with a significant decrease in the rate of macrosomic fetuses, but the limited sample size does not permit drawing “firm conclusions” (26,27).
A retrospective study concluded that a protocol involving induction for EFW90% but<4250 g and cesarean delivery for sonographic weight 4250 g decreases the rate of shoulder dystocia by 50% but increases the rate of cesarean delivery by 16% (28). While the ACOG practice bulletin on fetal macrosomia (8) suggests that cesarean delivery among diabetics is indicated if the EFW is4500 g, others have set the threshold at4000 g (26,28) or at4250 g (28) (see also chap. 4).
Prior Cesarean Delivery
The majority of patients attempting vaginal birth after cesar- ean delivery (VBAC) can successfully deliver a macrosomic fetus (29–31). The rate of uterine rupture may be higher (3.6%) for a macrosomic trial of labor with prior cesarean delivery, if the patient has not delivered vaginally before (32).
Thus, obstetric factors (prior deliveries, need for induction, etc.) should be considered when attempting VBAC with suspected macrosomia (see chap. 14,Obstetric Evidence Based Guidelines).
Prior Shoulder Dystocia
Women with prior shoulder dystocia are at much higher risk (about 12%) of recurrence (33,34) (see chap. 23,Obstetric Evi- dence Based Guidelines). In the general obstetric population, the likelihood of brachial plexus injury is 1.4/1000 births, but among women who had prior shoulder dystocia and deliver vaginally, it is 13/1000 if there is no recurrent dystocia. If there is recurrent shoulder dystocia, the likelihood of brachial plexus injury is 45/1000 (34).
There are no randomized trials (2) on how to manage these pregnancies, but it is reasonable to discuss cesarean delivery at term when managing a patient with a prior shoul- der dystocia because the likelihood of recurrent shoulder dystocia is quite high (12% vs. 1% in general population) as is the risk of neurologic injury (see chap. 23,Obstetric Evidence Based Guidelines).
REFERENCES
1. Boulet SL, Alexander GR, Salihu H, et al. Macrosomic birth in the United States: determinant, outcomes, and proposed grades of risk. Am J Obstet Gynecol 2003; 188:1372–1378. [Level II-1]
2. Chauhan SP, Grobman WA, Gherman RA, et al. Suspicion and treatment of the macrosomic fetus: a review. Am J Obstet Gynecol 2005; 193:332–346. [Level III]
3. Martin JA, Hamilton BE, Sutton PD, et al. Births: Final Data for 2008. Natl Vital Stat Rep 2010; 59. [Epidemiologic data]
4. Statistics Denmark. Live births and stillbirths by weight of birth.
1998 and 2008 data. Available at: http://www.statbank.dk. [Epi- demiologic data]
5. Serirat S, Deerochanawong C, Sunthornthepvarakul T, et al.
Gestational diabetes mellitus. J Med Assoc Thai 1992; 75:315–
319. [Level II-3]
6. Martin TC, Clarke A. A case control study of the prevalence of perinatal complications associated with fetal macrosomia in Anti- gua and Barbuda. West Indian Med J 2003; 52:231–234. [Level II-3]
7. Mikulandra F, Stojnic E, Perisa M, et al. Fetal macrosomia—
pregnancy and delivery. Zentralbl Gynakol 1993; 115:553–561.
[Level II-3]
8. American College of Obstetricians and Gynecologists: Fetal mac- rosomia. ACOG Practice Bulletin No. 22. Washington DC: ACOG, 2000. [Level III]
9. Chauhan SP, Martin RW, Morrison JC. Intrapartum hydramnios at term and perinatal outcome. J Perinatol 1993; 13:186–189. [Level II-2]
10. Myles TD, Santolaya J. Maternal and neonatal outcomes in patients with a prolonged second stage of labor. Obstet Gynecol 2003; 102:52–58. [Level II-2]
11. Crowther CA, Hiller JE, Moss JR, et al. Effect of treatment of gestational diabetes mellitus on pregnancy outcomes. N Engl J Med 2005; 352:2477–2486. [RCT, n = 1000. Impaired glucose tolerance (defined following 75-g OGTT as fasting<7.0 mmol/
L, 2 hour between 7.8 mmol/L and 11.0 mmol/L). Diet, glucose monitoring, and insulin as needed vs. routine care]
12. de Veciana M, Major CA, Morgan MA, et al. Postprandial versus preprandial blood glucose monitoring in women with gestational diabetes mellitus requiring insulin therapy. N Engl J Med 1995;
333:1237–1241. [RCT,n= 66]
346 MATERNAL-FETAL EVIDENCE BASED GUIDELINES
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978-1-8418-4822-8_CH0045_O.3d] [11/10/011/22:49:48] [345–347]
13. Murphy H, Rayman G, Lewis K, et al. Effectiveness of continuous glucose monitoring in pregnant women with diabetes: rando- mised clinical trial. Br Med J 2008; 337:a1680. [RCT,n= 71]
14. Bonomo M, Cetin I, Pisoni MP, et al. Flexible treatment of gesta- tional diabetes modulated on ultrasound evaluation of intrauter- ine growth: a controlled randomized clinical trial. Diabetes Metab 2004; 30:237–244. [RCT,n= 229]
15. Bonomo M, Corica D, Mion E, et al. Evaluating the therapeutic approach in pregnancies complicated by borderline glucose intol- erance: a randomized clinical trial. Diabet Med 2005; 1536–1541.
[RCT,n= 300]
16. Landon M, Sponge C, Thom E, et al. A multicenter, randomized trial of treatment for mild gestational diabetes. N Engl J Med 2009; 361:1339–1348. [RCT,n= 958]
17. Nachum Z, Ben-Shlomo I, Weiner E, et al. Twice daily versus four times daily insulin dose regimens for diabetes in pregnancy:
randomised controlled trial. Br Med J 1999; 319:1223–1227.
[RCT,n= 392]
18. Langer O, Conway DL, Berkus MD, et al. A comparison of glyburide and insulin in women with gestational diabetes melli- tus. N Engl J Med 2000; 343:1134–1138. [RCT,n= 404]
19. Nicholson W, Bolen S, Witkop CT, et al. Benefits and risks of oral diabetes agents compared with insulin in women with gesta- tional diabetes: a systematic review. Obstet Gynecol 2009;
113:193–205. [Meta-analysis; 9 studies of which 4 RCTs,n= 1229]
20. No authors. A clinical trial of induction of labor versus expectant management in postterm pregnancy. The National Institute of Child Health and Human Development Network of Maternal- Fetal Medicine Units. Am J Obstet Gynecol 1994; 170:716–723.
[RCT,n= 440]
21. Hendrix NW, Grady CS, Chauhan SP. Clinical vs sonographic estimate of birth weight in term parturients: a randomized clin- ical trial. J Reprod Med 2000; 45:317–322. [RCT,n= 758]
22. Gonen R, Spiegel D, Abend M. Is macrosomia predictable, and are shoulder dystocia and birth trauma preventable? Obstet Gynecol 1996; 88:526–529. [Level II-1]
23. Gonen R, Bader D, Ajami M. Effects of a policy of elective cesarean delivery in cases of suspected fetal macrosomia on the
incidence of brachial plexus injury and the rate of cesarean delivery. Am J Obstet Gynecol 2000; 183:1296–1300. [Level II-1]
24. Irion O, Boulvain M. Induction of labour for suspected fetal macrosomia. Cochrane Database Syst Rev 2005; 4. [Meta-analysis;
3 RCTs,n= 372—includes ref. 19]
25. Sanchez-Ramos L, Bernstein S, Kaunitz AM. Expectant manage- ment versus labor induction for suspected fetal macrosomia: a systematic review. Obstet Gynecol 2002; 100:997–1002. [Meta- analysis; 11 studies, of which 2 RCTs;n= 3751]
26. Boulvain M, Stan C, Irion O. Elective delivery in diabetic preg- nant women. Cochrane Database Syst Rev 2001; (2):CD001997.
[Meta-analysis,n= 200]
27. Witkop C, Neale D, Wilson LM, et al. Active compared with expectant delivery management in women with gestational dia- betes: a systematic review. Obstet Gynecol 2009; 113(1):206–217.
[Meta-analysis; 5 studies of which 1 RCT,n= 200]
28. Conway DL, Langer O. Elective delivery of infants with macro- somia in diabetic women: reduced shoulder dystocia versus increased cesarean deliveries. Am J Obstet Gynecol 1998;
178:922–925. [Level II-1]
29. Phelan JP, Eglinton GS, Horenstein JM, et al. Previous cesarean birth. Trial of labor in women with macrosomic infants. J Reprod Med 1984; 29:36–40. [Level II-1]
30. Flamm BL, Goings JR. Vaginal birth after cesarean section: Is suspected fetal macrosomia a contraindication? Obstet Gynecol 1989; 74:694–697. [Level II-1]
31. Zelop CM, Shipp TD, Repke JT, et al. Outcomes of trial of labor following previous cesarean delivery among women with fetuses weighing > 4000 g. Am J Obstet Gynecol 2001; 185:903–905. [Level II-1]
32. Elkousy MA, Sammel M, Stevens E, et al. The effect of birth weight on vaginal birth after cesarean delivery success rates. Am J Obstet Gynecol 2003; 188:824–830. [Level II-1]
33. Lewis DF, Raymond RC, Perkins MB, et al. Recurrence rate of shoulder dystocia. Am J Obstet Gynecol 1995; 172:1369–1371.
[Level II-2]
34. Bingham J, Chauhan SP, Hayes E, et al. Recurrent shoulder dysto- cia: a review. Obstet Gynecol Surv 2010; 65:183–188. [Level II-2]
FETAL MACROSOMIA 347
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46
Cytomegalovirus
Timothy J. Rafael
KEY POINTS
l Cytomegalovirus (CMV) is the most common cause of viral intrauterine infection, affecting 0.5% to 2.5% of all neo- nates.
l In most of the cases, pregnant women acquire CMV by exposure to children in their home or from occupational exposure to children.
l Approximately 2% of immunoglobulin G (IgG)-negative women acquire CMV infection during pregnancy.
Approximately 1/3 (range 30–75%) of pregnant women with a primary infection transmit CMV infection to their fetus.The rate of transmission increases with increase in gestational age (highest in the third trimester), but the severity of disease is instead inversely proportional to gestational age (the infant is most affected when maternal infection is in first trimester). Overall, about15% to 20% of infected infants develop sequelae (so about 5–8% of infants of infected mothers have sequelae).
l Complications of affected infants with congenital CMV infection include jaundice, petechiae (“blueberry muffin baby”), thrombocytopenia, hepatosplenomegaly, growth restriction, microcephaly, intracranial calcifications, non- immune hydrops, and preterm birth, as well as late com- plications such as hearing loss, mental retardation, delay in psychomotor development, chorioretinitis, optic atrophy, seizures, expressive language delays, and learning disabil- ities. Long-term mortality is about 10% to 30%.
l Prevention (including avoiding intimate contact with children, frequent handwashing, and glove use) is asso- ciated with an 84% decrease in CMV seroconversion during pregnancy.
l CMV screening in pregnancy is not routinely recom- mended in most countries, until an appropriate fetal inter- vention is proven to decrease neonatal disease in cases of maternal CMV infection.
l Maternal diagnosis of CMV infection is by serum IgM+.
l Fetal diagnosis of CMV infection is by detection of virus in amniotic fluid (AF) by polymerase chain reaction (PCR) testing.
l Presence or absence offetal abnormalities on ultrasoundcan help counseling (Table 46.1), but ultrasound is very insensitive and poorly predictive of an affected (symptomatic) child.
l There are no trials to assess the effectiveness of any inter- vention aimed at preventing congenital CMV. Gancyclovir and CMV-specific hyperimmune globulin are not sup- ported by sufficient evidence for recommendation, but are the most promising interventions reported so far.
PATHOGEN
CMV is a double-stranded DNA virus of the herpes family (1).
INCIDENCE/EPIDEMIOLOGY
CMV is the most common cause of viral intrauterine infection, affecting0.5% to 2.5% of all neonatesin different parts of the world (2). The birth prevalence of symptomatic congenital CMV is about 1 in 1000 (3). The prevalence of CMV infection varies according to socioeconomic background. Overall in the United States, the seropositivity rate is approximately 50%; by background, it is 40% to 50% for women of middle and high, and 60% to more than 80% for women of lower socioeconomic background. The overall age-adjusted seroprevalence of CMV did not change significantly from 1988–1994 to 1999–
2004 (4).
TRANSMISSION/RISK FACTORS/ASSOCIATIONS Transmission usually occurs from close contact, with contam- ination from urine, saliva, blood, semen, and cervical secre- tions (3). Risk factors are low socioeconomic status, exposure to infective individuals, multiple partners, extremes of age, multiparity, and blood transfusion. Only cellular blood products that contain leukocytes are capable of transmitting CMV, and the risk factor is 0.1% to 0.4% per unit in immunocompetent recipients (5). The incidence of cases with congenital disease following maternal recurrent infection has been shown to be increased with immunodeficiency, hormonal exposure, nutri- tional deficiency, and genital tract infections (6). Although sex- ual transmission of CMV can occur,in most cases pregnant women acquire CMV by exposure to children in their home or from occupational exposure to children. Data extrapolated to the U.S. population estimate that every two years between 31,000 and 168,000 susceptible pregnant women will be exposed to CMV by an infected child (7).
SYMPTOMS
CMV is usually asymptomatic or with symptoms so mild that it goes undiagnosed. The symptoms might include a mononu- cleosis-like or flu-like syndrome, malaise, fatigue, lymphaden- opathy, or persistent fever, and abnormal laboratory values (lymphocytosis, or increased aminotransferase levels). Rarely, hepatosplenomegaly, cough, headache, rash, and gastrointestinal symptoms can occur (8). The presence of symptoms or laboratory abnormalities is highly suggestive of primary infection (9).
PATHOPHYSIOLOGY/CLASSIFICATION General
The CMV virus leads to infected large cells with intranuclear inclusions. It has a 4- to 8-week period of incubation, and 3- to 12-month-long viremia (infants can shed virus for up to 6 years). Serious disease occurs only in immunocompromised adults, or fetuses. The transmission of the virus to the fetus can Downloaded from informahealthcare.com by Yale School of Medicine on 05/27/12 For personal use only.
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follow either a primary or recurrent infection.Approximately 2% of immunoglobulin G (IgG)-negative women acquire CMV infection during pregnancy. Approximately 1/3 (range 30–75%) of pregnant women with a primary infection trans- mit CMV infection to their fetus (Fig. 46.1) (10). Even peri- conception infection a week before or up to five weeks after the last menstrual period (LMP) is associated with this rate of transmission, although these rates may not be as high as previously thought (11). The rate of transmission increases with increase in gestational age (highest in third trimester) but the severity of disease is instead inversely proportional to gestational age (infant is most affected when maternal infection is in first trimester). In fact, one series reported no affected neonates if fetuses were infected after 26 weeks, if the ultrasound findings are normal (12). The risk of congenital CMV disease at birth is mainly associated with maternal primary infection, but the presence of maternal antibodies before conception does not prevent transmission in all cases, even if it is protective in most cases.
Primary Infection
Fetal infection generally (99.5%) occurs following maternal primary infection, and rarely following recurrent CMV infec- tion (Fig. 46.1). Of the women who are not immune (IgG , IgM ) for CMV at the beginning of pregnancy, about 2%
acquire maternal infection. Transplacental transmission may occur weeks or months after primary maternal CMV infection, and can be isolated from the AF by a PCR DNA technique to positively identify intrauterine transmission of CMV.Overall, about 15% to 20% of infected infants develop sequelae (so about 5–8% of infants of infected mothers have sequelae).
Recurrent Infection
Recurrent infections can occur with immunosuppression and during pregnancy. Recurrent infections during pregnancy
are most often asymptomatic and primarily caused by the reactivation of the endogenous virus, but can also be caused by a low-grade chronic infection or reinfection by a different strain of CMV (13). The risk of vertical transmission with recurrent infection is about 1.4% (range 0.5–2%) (10). Recur- rent infection is responsible for only 0.5% of CMV congenital infections. Neonates infected from recurrent maternal infec- tion have no symptoms at birth, do not have CMV in urine, and have a<10% risk of sequelae (hearing loss and chorior- etinitis) (8).
Clinical Neonatal Findings and Complications Clinical findings of symptomatic congenital CMV infection include jaundice, petechiae (blueberry muffin baby), thrombo- cytopenia, hepatosplenomegaly, growth restriction, microce- phaly, intracranial calcifications, nonimmune hydrops, and preterm birth (1,14). CMV disease has late complications such as hearing loss, mental retardation, delay in psychomotor development, chorioretinitis, optic atrophy, seizures, expres- sive language delays, and learning disabilities (2). CMV is the most common cause of congenital sensorineural hearing loss (15). Long-term mortality is about 10% to 30%.
PREGNANCY MANAGEMENT Counseling/Prognosis
Counseling should include at least the natural history of the disease, the chances of vertical transmission, prognosis, and complications (Fig. 46.1, and Table 46.1). A quantitative PCR count of103genome equivalents/mL of AF is a certain sign of congenital infection, and105genome equivalents/mL can predict symptomatic infection (16) (Fig. 46.2). In cases of severely injured fetuses on ultrasound, there is a high likeli- hood of sequelae, and pregnancy termination can be offered as a management option (17). When no ultrasonographic abnor- malities are detected, the incidence of postnatal neurologic abnormalities is about 15% to 20% (16,18).
Prevention Hygiene
Compared with no prevention, prevention (including avoiding intimate contact with children, frequent hand- washing, and glove use) is associated with an 84% decrease in CMV seroconversion during pregnancy, especially in women in contact with children in day care facilities (19).
Following the administration of oral and written hygienic information to susceptible pregnant women, seroconversion rates during pregnancy have been reported to be as low as 0.26% (20).
Vaccine
A live-attenuated CMV vaccine is available, but may be reactivated, and safety issues have not been resolved. In a trial including CMV-seronegative women of childbearing age, a glycoprotein B vaccine demonstrated a 50% efficacy in preventing CMV infection. One congenital infection occurred in the vaccine group, and three infections occurred in the placebo group, although the sample size was not large enough to test the efficacy in reducing congenital infection (21). While this vaccine may have the potential to decrease incident cases of congenital CMV infection, it is likely that a CMV vaccine will not be available clinically for several years.
Figure 46.1 Natural history of CMV perinatal infection.Abbrevia- tions: CMV, cytomegalovirus; PCR, polymerase chain reaction;
IgM, immunoglobulin M; AF, amniotic fluid.
CYTOMEGALOVIRUS 349
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