Diseases information. Disorders. Treatment.

Management
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Antenatal management should include attention to nutrition, avoidance of strenuous physical activity, frequent prenatal visits, and counseling on symptoms of preterm labor, PROM, and hypertensive disorders of pregnancy. Ultrasound assessment of fetal growth and amniotic fluid volume should be performed every 4 weeks unless evidence of an abnormality suggests that this be done more frequently. Discordant fetal growth may be due to constitutional differences in otherwise normal twins, growth restriction of one fetus, a chromosomal or anatomic abnormality of one fetus, or the twin-twin transfusion syndrome. In situations of threatened or imminent delivery before 34 weeks, maternal antenatal steroid administration is recommended for acceleration of fetal lung maturity and prevention of intraventricular hemorrhage. If preterm labor occurs, controversy exists over the safety and efficacy of the various tocolytic drugs currently available. As indicated, fetal surveillance with an NST or BPP is recommended.
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Vaginal delivery is the preferred approach when both twins are in a vertex presentation. After delivery of twin A, and with continuous surveillance of twin B with real-time ultrasonography or electronic monitoring, it is believed that the interval between delivery of the twins is not important in the presence of a reassuring FHR.

Embryo Reduction

The higher-order multiple gestations resulting from assisted reproductive technologies has resulted in an increased risk of preterm delivery, which is directly proportional to the number of fetuses developing in utero. Multifetal pregnancy reduction is a procedure designed to increase the chances of delivering closer to term by decreasing the number of fetuses in the uterus.
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Multifetal pregnancy reduction is usually performed via the transabdominal or transvaginal route. A needle is guided under direct ultrasonic visualization into the fetal heart or thorax, and potassium chloride solution is injected to accomplish asystole. The procedure is usually performed late in the first trimester rather than earlier because this allows for 1) the possibility of spontaneous loss of one or more fetuses before the procedure, 2) easier accessibility to the fetuses given their increased size, and 3) greater opportunity to detect disturbances in growth or morphology.

The incidence of preterm delivery increases with increasing numbers of fetuses; the mean gestational age of delivery for singletons, twins, triplets, and quadruplets is 39, 35, 33, and 31 weeks, respectively. Multifetal pregnancy reduction increases gestational age at delivery. This clearly has had a beneficial impact on the outcome of pregnancies that begin with four or more fetuses.
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The data regarding triplets, however, are not as definitive. Some studies have suggested that multifetal pregnancy reduction reduces the spontaneous loss rate in these gestations, and the rates of intraventricular hemorrhage and respiratory distress syndrome are increased in unreduced triplets compared with twins. It is not clear, however, whether these differences during the neonatal period have a meaningful impact on later cognitive, physical, and psychologic ability. Although fetal benefit can be debated, maternal advantages are obvious. Women with triplets have an increased risk of preterm labor, prolonged hospitalization, PIH, anemia, and postpartum hemorrhage compared with those carrying twins.

The antenatal care of post-multifetal pregnancy reduction twins is no different from that of spontaneous twins, except for one screening tool. Maternal serum alpha-fetoprotein levels after a reduction are consistently higher than those for non-reduced twins at comparable ages because of the retained dead fetus(es). Therefore, maternal serum alpha-fetoprotein cannot be used to screen for NTDs or other anomalies in these patients. Studies comparing the morbidity and mortality of reduced versus unreduced twins show comparable results.

Multifetal pregnancy reduction optimizes the chances of a woman successfully maintaining her pregnancy by decreasing the risks of preterm delivery. For many women, this is not a light decision. Multifetal pregnancy reduction is associated with mourning for the lost fetus(es), guilt, and sadness, but overall, it is well tolerated. One study revealed that 93% of the women who underwent multifetal pregnancy reduction did not regret their decision. Until the multifetal gestations created by modern infertility therapy can be limited to twins, multifetal pregnancy reduction will remain an option available to help couples maximize their potential for delivering healthy infants at low risk for developing the devastating sequelae that can accompany severe prematurity.
Multiple Gestation

Multiple gestation occurs in about 1.5% of all births. Multiple pregnancies of greater than three constitute a relatively small component of the total; however, these numbers are increasing as a result of the widespread use of assisted reproductive technologies.

Twins may result either from the splitting of a single fertilized ovum into two genetically identical individuals (monozygotic) or when two separate ova are each fertilized by a sperm, leading to genetically distinct siblings (dizygotic). Start taking cialis professional to regain your sexual vigor and potential virility. Although the incidence of monozygotic twinning is fairly constant throughout the world at a rate of approximately 1 per 250 births, there is evidence that the use of ovulation induction drugs may almost double this figure. The frequency of dizygotic twinning is increased with African-American race, increasing maternal age up to 40 years, increasing parity, family history of twins, and, especially, use of assisted reproductive techniques.

Multiple gestation should be suspected when there is a history of use of a fertility agent, a discrepancy between the estimated gestational age and uterine size, or abnormally elevated laboratory screening tests such as maternal serum alpha-fetoprotein or triple screens. A careful ultrasound examination will not only confirm the diagnosis, but also should determine zygosity and detect significant abnormalities of fetal anatomy or placental position.
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Perinatal morbidity and mortality increase in direct proportion to fetal number. Complications related to preterm birth, such as respiratory distress syndrome, intracerebral hemorrhage, sepsis, and necrotizing enterocolitis, account for most of these adverse outcomes. Congenital malformations, fetal growth restriction, and umbilical cord prolapse also occur more frequently in multifetal pregnancies. In twin pregnancies, perinatal morbidity is increased twofold, infant mortality is increased sixfold, and severe neurologic handicap is increased twofold over that seen in singletons. Perinatal morbidity and mortality of monozygotic twins is two to three times that of dizygotic twins, with much of the increase being due to problems resulting from vascular anastomoses in monochorionic placentas between the two fetal circulations.
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The shunting of blood from one placental circulation to the other through placental vascular anastomoses can lead to the twin-twin transfusion syndrome. This can cause marked discrepancies in fetal size and circulating blood volume, massive differences in amniotic fluid volume, and altered hemodynamics in either or both circulations that results in hypoxia or death in utero. The use of serial amniocentesis and newer techniques such as laser ablation of the communicating vessels has considerably improved the outcome for fetuses with this syndrome. Monozygotic twins also have a 1-2% incidence of monoamniotic sacs, which can be associated with sudden death in utero due to cord entanglement. In triplet pregnancies, perinatal mortality is increased 3-fold, infant mortality is increased 19-fold, and severe neurologic handicap is increased 3-fold over that seen in singleton pregnancies. Multifetal pregnancy reduction has been shown to improve perinatal outcome in higher-order pregnancies by significantly reducing the incidence of early preterm delivery.

Multiple gestations increase the maternal risk of hyperemesis gravidarum, spontaneous abortion, PIH, anemia, abnormal placentation, hydramnios, PROM, and postpartum hemorrhage. There is also an increased risk of operative delivery with all of its associated complications.

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The diagnosis; a lot is written both in diagnosis and treatment and it always changes, but I think with syphilis you have to have some common sense and know your patient and know what the future is and whether you are going to see them again, and things like that. The mother without adequate history of therapy and positive VDRL or FTA, that is somebody where the baby is likely to be infected. You would think an IgM test would be helpful but there are no commercial IgM tests that are accurate, because in previous tests they have been falsely positive very frequently. You can do serial VDRL’s in infants without symptoms when the mother has only a positive VDRL, and again you should have significant drop over a short period of time. Dark-field examination of the lesions in babies and also the cord, the cut cord, and obviously examine the CSF.
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The treatment; again, there has been a lot written about treatment and I think finally some people have become smart and tried to give the minimal therapy. I think today that you should treat every infant as if they have syphilis and if they also have neurologic involvement, which is 150,000 units per kilo per day, given q.8 or q.12, and most recommendations say 10-14 days. The aqueous procaine penicillin is also recommended, but I think if there is neurologic involvement it may not be as good.
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So just to finish up, for congenital infection workup in general you should have a high index of suspicion. Any small-for-dates baby should be studied. Babies with congenital heart disease and other problems, congenital malformations, congenital infections, should be considered. Babies with high risk maternal history. Looking for a safe and reliable means of treating ED? Buy Viagra oral jelly. And rather than doing TORCH titers, you want to do some titers but for CMV and rubella. The main thing is virus isolation using the specimens, IgM and IgG antibodies studies, but you want to be sure. You don’t necessarily want to believe the results you get if they aren’t in keeping with what you think is happening. I should have said this with toxoplasmosis, there are many IgM many commercial tests are notoriously falsely negative for IgM, if the IgG antibody is high. So these serologic tests should be sent to a very special laboratory, such as the laboratory in Palo Alto, California. So there can be both false negative and false positive IgM tests. The last thing is a very simple test doing a quantitative IgM. Just total IgM on babies who have some congenital defect or small-for-dates-for-age. If on them, if you have an elevated IgM, then you can go ahead with a further workup. So I think that takes care of congenital infections.

Next is parvovirus B19. The infection in pregnant women results in infection of the fetus and the timing of that depends a bit on what happens. But in the first half of pregnancy you get red cell aplasia and it may lead to fetal hydrops and abortion. The risk of abortion in maternal infection is about 5-8%. An important thing is that in babies that survive there has been no evidence of congenital malformations. So you don’t want to do what some obstetricians do, and that is perform an abortion to prevent an abortion. The important thing to realize in outbreaks to begin with, about 50% of adult women of child-bearing age already have antibody and they are at no risk. So there is not much you can do, but the big concern is with school teachers who are pregnant. One of the things you can do is antibody studies on them and if they are positive they have no risk.
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The next is toxoplasmosis. Toxoplasmosis gets missed. The congenital infection that anywhere between 70-90% are asymptomatic at birth, so this leads to sort of a lower estimate of the risk of this problem because many of these babies who are asymptomatic at birth go on to have problems later on in childhood, or to have evidence of retinitis later on in life. The actual infection rate is somewhere between 1:1000 births to 1:10,000 births. The manifestations; the list looks sort of like that that I showed you for rubella. The findings that you see here. The outcomes are retardation in 85% of diagnosed cases, convulsions 80%, spasticity 65%, impaired vision 60%, hydrocephalus and microcephalus 20%, deafness 15%. Of recognized cases at birth, only 10% are normal. Those staggering statistics bothered people for a long time. Now about ten years ago a national study was undertaken to look at treatment. I think that many of these babies look pretty bad and yet the amazing thing with treatment and a standardized protocol, or several protocols, that the treated babies had actually rather marked responses to treatment. So any baby today should be treated and treatment is complicated. So in general, if in doubt you should get help from somebody else and at least refer to a center where treatment can be done under controlled conditions. Pyrimethamine is difficult to administer, particularly in young babies because you suppress the blood count – both white cells and red cells – and the treatment is for a prolonged period; up to a year. But the results are very clear and it does lessen morbidity and prevents mortality.
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Okay, last congenital infection is syphilis. Risk of transmission, major risk after 16 weeks but there is evidence of some transmission before 16 weeks. In primary syphilis 70-100% chance of transmission, secondary syphilis 90% and latent syphilis there is still a 30% chance of transmission. The manifestations here again are those of active infection of fair duration with hepatomegaly, skeletal abnormalities similar to those of rubella, low birth weight, bullous lesions of the skin – which are teeming with spirochetes and a lot of people don’t recognize that but are highly contagious – hyperbilirubinemia, a severe pneumonia and splenomegaly. Anemia, hydrops, nasal discharge, painful limbs. They have meningitis and meningoencephalitis, nephritis and failure to thrive. This is a picture of the hand of a baby, and this is a very large lesion but these are loaded with organisms.
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As far as treatment … I should go back. I realize I didn’t say anything about treatment with CMV and the babies with congenital CMV; you would like to treat them and with recent successes with toxoplasmosis it makes this more likely. A better idea. However a national study using ganciclovir failed to show benefit. Having said that, any severe baby with CMV I would treat with ganciclovir.
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Coming back to varicella infection; there is no data on treatment if they have any evidence of activity, which you don’t usually see, that I would treat these babies with acyclovir.
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The second aspect is infection near term and the risk period is very clear and it’s at a time when the mother is infected and the baby gets infected in utero but gets no antibody. This period is five days or less before delivery, or two days after delivery. These babies will have a congenital infection and will have an illness that looks like smallpox. That is the lesions come all at once, and the mortality, untreated, is very high; 30%. So any babies with these criteria should receive varicella zoster immune globulin at birth. They shouldn’t get prophylactic acyclovir, but as soon as any symptoms develop, they should be treated with acyclovir.
The next are enteroviruses and again enterovirus infections are exceedingly common in pregnant women in the summer. Fortunately, even though infection probably gets to the fetus, the majority of these are not a problem. However, infections in the last two weeks percentage-wise, most are mild but can lead at birth to severe meningoencephalitis and myocarditis and sepsis-like illness, with hepatitis and disseminated intravascular coagulation. The diagnosis again for enteroviruses is culture and now PCR of CSF and actually now PCR can be done on stool, throat and urine specimens as well.
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Treatment; there is no specific treatment. In nursery outbreaks that end in severe disease, giving IVIG makes sense, although there is little evidence of benefit. Lastly there is a new drug, not licensed yet, called proconerol which is in trial for neonatal infection but has been shown to be effective in older patients with meningitis.

Next is herpes and this is a newspaper from right after acyclovir was first licensed. The main situation with herpes is that the congenital infection is only a small part. The major problem with herpes is acquisition of virus infection during the birth process. So the congenital infection is actually rare but it is virtually always severe and almost never without residual. The important thing is a vesicular rash at birth and I’ve seen some real tragedies, because the vesicles here people look and think they are going see a vesicle like you see in a cold sore or what you see in older people with herpes. These vesicles are very thin-walled and they break very easily, and I’ve seen a tragedy where these vesicles were looked at and they said, “Well, they are not herpes.” So they can be very thin and not looking at all like what you would expect to find. Low birth weight, chorioretinitis, brain damage, small for gestational age, microcephaly, intracranial calcifications, microphthalmia and cataracts. This is a baby with congenital varicella who right at birth had vesicular lesions right here.
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The diagnosis again is culture. Herpes should grow out. Culture of lesions, if you have lesions, also culture from many sites; throat, blood buffy coat, urine, CSF and also direct antigen tests which are quicker and also PCR from CSF. One thing about PCR from CSF in newborns; it is the percent positive in only about 75% whereas older people with herpes encephalitis, it’s close to 95%. Lastly, specific IgM antibody. Treatment of course is acyclovir and in general, one of the mistakes that’s made is not to treat long enough and also to use too low a dose. The dose that’s indicated in most of the literature is 10 mg/kg per dose three times a day. But regularly, particularly in congenital infections, you should push this to 45 mg/kg per day and give it for at least three weeks and then evaluation because some of these should go on long term therapy.
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Next is congenital infection with varicella and there are two events. Early infection in pregnancy and then infection right before birth, maternal infection right before birth. The infections of the mother early in pregnancy, first of all is not too common and transmission to the baby is relatively rare. In fact the earlier epidemiologic literature said there was no risk. But then people noted a very specific syndrome, particularly with limb atrophy. More recent studies suggest the risk is somewhere around 2-3% of mothers infected in the first 20 weeks. Your findings are scars and hypopigmentation, hypoplasia of limbs, encephalitis and cortical atrophy. Most of these babies do very poorly. Low birth weight, immune defects, are the findings that you have here. Sometimes we’ve seen several babies with just chorioretinitis, no other findings. Frequently that plus some scars like they have apparently had some chicken pox-like lesions in utero and now they are scabbed over.
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