Amniotic Fluid - 8 - Evaluation and Management of Polyhydramnios

In the last couple of posts we have reviewed causes and complications related to excessive amniotic fluid, otherwise known as polyhydramnios or, simply hydramnios. Although 50-60% of cases of hydramnios are idiopathic (no identifiable cause) and about 90% of cases are mild to moderate, about 10% are severe and these latter are the more likely to be accompanied by considerable fetal and neonatal morbidity and mortality secondary to an underlying fetal cause of the hydramnios – chromosomal abnormality, congenital anomaly, fetal anemia, inborn error, or congenital infection. Evaluation of the pregnancy with hydramnios, therefore, focuses primarily on these concerns.

The first step in any evaluation of hydramnios is to take a detailed medical, obstetrical, and family history and to review the course, medical complications, and basic laboratory studies performed to date in the current pregnancy. It is not necessary to cover the extent of such a discussion herein but examples of pertinent information include: the current pregnancy being a multiple gestation; a previous pregnancy accompanied by hydramnios, fetal macrosomia, or diabetes (and the outcome of that pregnancy); known maternal diabetes; known Rh- or other isoimmunization; history of blood transfusion; hemorrhage or trauma during the current pregnancy; history of known/suspected exposure to parvovirus B19 (Fifth’s disease) or illness accompanied by fever and/or rash during the current pregnancy; exposure to young children at home or in the workplace; family history of inborn errors of metabolism or congenital birth defects – particularly, cardiac, gastrointestinal, and neural tube, and neuromuscular disorders; past or family history of aneuploidy or recurrent pregnancy loss; advanced maternal age; report of decreased fetal movement; maternal history of medications and nonprescription (licit and illicit) drug use during the pregnancy. It is also important to get some feel for the onset of the hydramnios related to timing in pregnancy (e.g., gestational age when noticed; slow onset vs. rapid onset) and maternal signs and symptoms of disease and cardiorespiratory compromise.

The next step is to perform a thorough, high resolution ultrasound examination. In this, the degree of hydramnios should be documented objectively by a four-quadrant amniotic fluid index (AFI). This will be valuable as a ‘baseline’ for comparison during subsequent ultrasound evaluations of the pregnancy. Fetal growth should be assessed to determine if the baby is abnormally large or growth-restricted for the gestational age of the pregnancy – either of which might help narrow down the differential diagnosis. A detailed anatomical survey of the baby should include: central nervous system and spine; face and facial midline structures; neck; thorax; heart and rhythm; diaphragm; gastrointestinal tract; genitourinary tract; and, extremities. In addition, it is important to document whether or not the baby appears to have normal movement – flexion and extension – of the extremities since, if this is not present, it might suggest an underlying neuromuscular disorder. Evidence of fetal hydrops (indicative of fetal anemia or high-output cardiac failure) should also be sought.

If there is a twin (or higher order multiple) gestation, it is important not only to assess fetal growth and anatomy, but to determine chorionicity of the twins (i.e., dichorionic-diamnionic; monochorionic-diamnionic; or, monochorionic-monoamnionic) and if there is any significant discordance for growth or amniotic fluid surrounding the babies. Twin pregnancies are at higher risk for fetal anomalies, chromosomal abnormalities, abnormalities of placentation, and in monochorionic twins, a condition called ‘twin-to-twin transfusion syndrome (TTTS)’ (a discussion of which will be reserved for another post at another time).

A critical step in the evaluation of the pregnancy complicated by hydramnios (as it was in that complicated by oligohydramnios) is performing Doppler flow velocimetry (DFV) studies. These should be done at least on the fetal umbilical and middle cerebral arteries (MCA) and should be considered for the fetal ductus venosus and umbilical vein and the maternal uterine arteries. The goals of DFV under these circumstances are to ascertain if there is any difficulty perfusing the placenta (increased resistance indices) from either the fetal or maternal side; assess whether there is any evidence of fetal blood flow redistribution (“cranial sparing”) related to relative ‘placental insufficiency’ (decreased resistance to blood flow in the MCA); if there is increased peak systolic velocity (PSV) of blood flow in the MCA which would be suggestive of significant fetal anemia; or if there is evidence of fetal cardiac decompensation (abnormal wave forms – increased resistance or pulsatility - in the fetal ductus venosus or umbilical vein). DFV is a critical evaluation in the monochorionic twin pregnancy, especially if there is discordance for growth and/or amniotic fluid, that might help differentiate simple intrauterine growth restriction, or hydramnios related to aneuploidy or fetal anomalies, from TTTS.

Once a comprehensive ultrasound has been completed, a discussion should be held with the patient about what else can be done at this time, diagnostically and therapeutically, if indicated. Again, a detailed discussion of this is beyond the purpose of our post today, but some examples are as follows depending on the findings: 1) If the baby is growth-restricted and/or has visible abnormalities (major structural or subtle), an amniocentesis should be offered for fetal chromosomal studies and congenital infection, particularly, for cytomegalovirus (CMV). 2) Growth restriction with hydramnios and abnormal resistance to fetal placental-perfusion by umbilical DFV carries about a 50% chance of aneuploidy, even in the absence of visible abnormalities, so fetal karyotype should be encouraged with this combination of findings as well; 3) If there is increased PSV (> 1.5 MoM) in the fetal MCA, even in the absence of hydrops fetalis, then the baby may need to be evaluated for significant anemia – best done by percutaneous umbilical blood sampling (PUBS) with preparations made for coincident transfusion. This becomes even more critical if the baby already has hydrops; 4) If a fetal arrhythmia has been identified, medical therapy should be attempted to correct this condition; 5) If a twin gestation is present and there appears to be TTTS, then the patient should be counseled and offered a referral to one of the few sites in the country with the expertise to handle this condition.

As a routine part of maternal evaluation, especially if no readily apparent cause of the hydramnios is identified by ultrasound, I will frequently recommend the following: blood type and antibody screen; thyroid studies; a full 3-hour glucose tolerance test (unless the patient has already been diagnosed with diabetes); serologic testing for evidence of recent CMV or Parvovirus B19 infection and consider screening for toxoplasmosis and syphilis. If a woman is a known diabetic, I will include a hemoglobin A1C level and make efforts to optimize her diabetic control.

If a correctible cause for the hydramnios, such as fetal anemia, has not been identified and/or there are significant risks to the pregnancy because of the hydramnios itself, especially, if the pregnancy is less than 30 weeks and there is premature labor to contend with, or the mother has developed cardiorespiratory compromise secondary to massive hydramnios, there are limited options for management. Acute management of maternal cardiorespiratory decompensation may require amnioreduction. This is an amniocentesis procedure in which a large bore needle/catheter is inserted into the uterus and the fluid slowly drained until the AFI is in a ‘normal’ range of 10-20 cm. The most common risks to this procedure are rupture of membranes, premature labor, and placental abruption if the fluid is decompressed too rapidly. Unfortunately, since under normal circumstances, amniotic fluid volume is replaced daily, the fluid will often reaccumulate within 48-72 hours, necessitating repetitive procedures. Under these circumstances, the risk of the previously noted complications, as well as of infection, increase further.

As an adjunct to amnioreduction, or if the situation is not so acute, another option is to use potent prostaglandin synthetase inhibitors that have the effect of decreasing fetal urine production (and, hence, amniotic fluid) and may also decrease uterine contractions that usually accompany hydramnios, thereby, decreasing the risk of premature labor. Indomethacin has had the widest experience in this regard and is relatively safe for both mother and baby. After an initial loading dose of 100 mg, I will frequently place the patient on 25-50 mg of indomethacin every 6 hours. It usually takes at least 4 days (sometimes much longer) to get any response to this regimen. Once indomethacin has been started, it is important to monitor both amniotic fluid and the fetal ductus arteriosus which can constrict in response to the drug and is a primary means of maintaining the “fetal circulation” (bypassing the lungs and allowing proper distribution of well-oxygenated blood throughout the body) while the baby is in utero. One must be especially careful about using indomethacin in women who have underlying kidney problems, cardiac disease, long-standing diabetes, hypertensive disorders, pregestational and pregnancy-related preeclampsia, or evidence of infection because if their renal output also drops significantly, they can be pushed into congestive heart failure.

Another prostaglandin inhibitor that has also been tried, and with which I must admit limited experience, is sulindac (usually dosed at 200 mg every 12 hours). Sulindac has greater selectivity for the cyclooxygenase 2 (COX-2) enzyme and appears to be capable of reducing fetal urine output with less of an effect on the ductus arteriosus, although its effect on the fetal kidneys is also less than that of indomethacin. It may be safer to use later in gestation than indomethacin which I will usually stop at 32 weeks (and no later than 34 weeks) gestation. The risk of premature delivery is so high with severe hydramnios requiring amnioreduction and/or prostaglandin inhibitor therapy that I often couple their use with a course of corticosteroids to accelerate fetal lung maturation in the event that delivery occurs or becomes necessary.

In closing, I would like to mention only one other caution about hydramnios that is often over-looked with regard to my last statement in the paragraph above. If hydramnios is present and associated with diabetes and/or fetal macrosomia, fetal lung maturation may be delayed as much as 2-3 weeks as the result of hyperinsulinemia in the baby. Hyperinsulinemia suppresses the development of lung surfactants and one last study that should be considered, and is highly recommended, prior to the elective delivery of baby because of hydramnios, or macrosomia, is an amniocentesis to assess fetal lung maturity, especially if the planned delivery is by cesarean section.

Well, this concludes our series on amniotic fluid. As I said at the outset, evaluation of amniotic fluid is an important part of every pregnancy and understanding the causes, complications, and management of the pregnancy with abnormalities of amniotic fluid is a daily part of my routine. I have tried to make our discussions digestible for the nonclinician as well as a valuable overview for the primary care professional involved in the care of women during pregnancy and hope that we have accomplished that here! Thanks for reading!
Dr T

Labels: CMV, diabetes, Doppler flow velocimetry, fetal macrosomia, polyhydramnios

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Thanks to Prudence, M.D. for GrandRounds 4.10!

Many thanks to Prudence, M.D. for the time and effort placed into putting together this week's Grand Rounds 4.10. And, thank you so much for including my post "Cytomegalovirus (CMV) Reprise" written in response to a reader's query regarding the association of CMV with recurrent pregnancy loss (RPL). CMV probably does not play much of a role in RPL, but it is still the most common comgenital viral infection and the leading cause of chorioretinitis and sensorineural hearing loss in chidren - and most women have never heard of it or even realize that they have the virus and could pass it along to their babies in utero!

Labels: CMV, cytomegalovirus, recurrent pregnancy loss

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Cytomegalovirus (CMV) Reprise

There is not a week that goes by in my practice that I do not have to address questions regarding cytomegalovirus (CMV) infections and pregnancy. Since we have also been discussing recurrent pregnancy loss in various contexts over the past year, I thought her questions were particularly timely and would be of interest to a good number of other readers. This is a good opportunity to reprise some of the information about CMV that we have provided in the past…

Anonymous has left a new comment on your post "Cytomegalovirus (CMV): Common and Confusing":

I have had reoccurring miscarriages and my OB did a TORCH blood test which showed my CMV levels were slightly elevated. I’m supposed to go back in two weeks for another test to recheck the levels. Could this virus have caused my miscarriages? Is there a period of time I should wait before trying to conceive again? If I do become pregnant again am I at risk of having a baby affected by CMV?

To Anonymous: All of your questions are answered at the very end of this post. You can jump to there if you would like or read on for more information…

The TORCH test looks for antibodies in your blood specific for TOxoplasmosis, Rubella (German measles), Cytomegalovirus, and Herpes simplex virus. It is not unusual to include a screen for syphilis and human immunodeficiency virus (HIV) at the same time. All of these can cause infections of a baby during pregnancy (congenital infections) but by far, CMV is the most common. If antibodies to a specific organism(s) are present, this indicates you have been infected with that organism at some time in the past. Let me elaborate on that point a bit so that you have a better understanding of the tests when you discuss them with your doctor.

Usually, when we contract a virus infection like the flu, our immune systems react by first producing specific antibodies of the IgM class. These usually hang around only for no more than 2-4 weeks after the infection has been cleared. Shortly after IgM antibodies begin to be made, our bodies switch to the production of a second class of specific antibodies called IgG. IgG antibodies generally hang around for a long time after the infection is cleared and provide us with a source of 'permanent immunity' to the organism, helping to prevent reinfection, or decrease the severity of a secondary infection, with the same or similar organisms with which the antibodies might 'cross-react.' It is these IgG antibodies that also afford protective immunity to the baby because they can cross the placenta whereas IgM antibodies cannot.

We can use this information to help us to characterize the status of an infection. If neither IgM nor IgG is present, the individual has probably never been exposed to the organism of concern (or is too early in the course of the infection to have mounted any antibody response). If IgM is present and there is no IgG, then the infection is probably a 'primary' infection, indicating first time exposure to the organism, usually very early in its course. If both IgM and IgG are present, this also usually reflects a primary infection, but later in the course of the disease. And, if only IgG is present, then this indicates a state of permanent immunity established from an infection that occurred at some time in the past. In any of the first three circumstances, if an infection with a specific organism is suspected and could be of concern for a pregnancy, it is probably worth repeating the antibody titers in 4-6 weeks.

Things can be a little confusing with CMV infections. CMV grows very slowly and the incubation period from the time of exposure to onset of symptoms, or asymptomatic excretion of the virus, is on the order of 4-12 weeks. IgG antibodies usually can be detected by 1-2 weeks after the onset of symptomatic infections, but because of the long incubation period of CMV, this might be a month or more after actual exposure to the virus. The presence of IgM in the absence of IgG and in the presence of symptomatic disease (or a history of recent exposure to a known carrier) is highly presumptive of a true 'primary infection.' Similarly, the findings of both IgM and IgG with a significant rise (four-fold or more) in IgG titers (with or without a fall in IgM titers) on a follow-up screen 4-6 weeks later, usually (but not always in the case of CMV) indicates a recent primary infection. Also useful, the presence of IgG in the absence of IgM, is highly suggestive of a remote exposure to the virus, often greater than 6 months previously.

The rub with serology in classifying CMV infections comes in most often when IgM is present but IgG titers are relatively stable or mildly fluctuating. Unlike most common viral infections, CMV-specific IgM can sometimes persist 6-9 months following its appearance. And to make things even more confusing, IgM has been found to reappear on occasion with reactivation of latent CMV infections. In other words, except in the circumstances detailed above, we may not be able to use the presence of IgM in our counseling to tell patients that they have had a primary or recurrent infection during the pregnancy or if the infection might have occurred even prior to the current pregnancy.

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CMV is the MOST common congenitally (fetal) and perinatally (newborn) acquired virus disease in humans and the single most important infectious cause of mental retardation and congenital deafness in the U.S. and other industrialized nations. CMV is a member of the herpes family and human CMV is restricted to humans with no known animal reservoir. At least 80-90% of all individuals are infected with CMV during their lives, but infection may occur in the absence of clinical symptoms or without recognizing that an illness is the result of CMV. As with other herpes viruses, once an individual is infected with CMV, 'recurrences' can result from periodic reactivation of virus replication at various sites in which the virus is latently harbored in the body. During periods of reactivation, the virus can be more readily transmitted to individuals who have not been previously infected. Although probably not that common, secondary infections can also occur with other strains of CMV.

Transmission of CMV can occur from exposure to just about any body fluid, most commonly via saliva, respiratory, and venereal routes or by contact with infected urine or breast milk. Exposure tends to occur at earlier ages in lower socioeconomic groups, promiscuous individuals, and children at day care centers. Antibodies to CMV (seropositivity), indicating a history of infection with the virus, in women during the common childbearing years (18-35) can be found in about 50% of those in middle and upper, and 90% in lower, socioeconomic groups. Among previously noninfected (seronegative) women, the chance of becoming infected with the virus (seroconversion) is about 1-3% per year, however, this is as high as 10-20%in women who work in day care settings and 50% in women with infected children under two years of age!

Congenital infections with CMV occur in 1-2% of ALL pregnancies, accounting for 40-50,000 cases per year, indicating the virus can cross the placenta with relative ease compared to other herpes and most other common virus infections. Transmission of CMV to the fetus can occur with both primary and recurrent infections despite maternal immunity and has been documented in consecutive pregnancies. However, congenital infection rarely results in a poor outcome unless the congenital infection is the result of a primary (first time) infection in the mother during the pregnancy. Overall, among seronegative women, there is about a 0.5-1% risk of a primary CMV infection in each pregnancy, although this is much higher in 'at risk' groups such as day care workers, health care providers, and women with young children. Primary maternal infections carry an overall transmission risk to the baby of 25-50% and recurrent infections about 2-3%. Maternal antibody to CMV is incompletely protective against transmission to the baby, but it does play a major role in reducing the severity of infection in both fetus and newborn.

A high percentage of primary maternal infections are asymptomatic, or simply confused with another illness, or even written off as normal symptoms of pregnancy, so usually the diagnosis is not considered. Indeed, perhaps, the hardest part of making the diagnosis of CMV infection during pregnancy in mother and baby is simply suspecting that it might be a problem. If a woman develops a prolonged (weeks) illness with fever, resembling infectious mononucleosis (caused by another herpes virus, Epstein-Barr virus (EBV)), and the latter cannot be confirmed by routine testing, then CMV should be high on the differential diagnosis. The ante goes up considerably if the mother is a young teen having her first baby (especially if she conceived shortly after becoming sexually active or changing partners), or if she works, or has another young child, in a high risk setting such as a daycare center.

Serologic testing, as we discussed at the outset, can often help to confirm a primary infection when it is obtained coincident with maternal symptoms. Virus detection by culture, immunofluorescent, or polymerase chain reaction (PCR) techniques, best done by sampling maternal urine, may be positive (and almost always will be for months after a primary infection), but this alone does not tell us if this is a primary symptomatic CMV infection or a recurrent infection accompanying another illness. Unfortunately, in most cases maternal infection with CMV is usually not suspected until the baby is found to be growth restricted or has subtle physical abnormalities, or a thickened placenta, to suggest it has either a chromosomal abnormality or a congenital infection, sometimes months after the maternal exposure. Under these circumstances, maternal serologic testing might not be helpful in establishing either the fetal diagnosis or the diagnosis of a primary maternal infection during pregnancy.

Congenital CMV infections associated with primary maternal infections early in pregnancy and accompanied by growth restriction and detectable abnormalities by fetal ultrasound, generally, have a very poor prognosis, but even then, the outcome is not entirely predictable. Establishing the presence of fetal infection, when fetal abnormalities are identified, requires an 'invasive' procedure. Performing a simple amniocentesis, and using a CMV-specific PCR or shell vial culture technique, can confirm fetal infection with CMV in nearly 100% of cases. (Remember, the amniotic fluid from midtrimester on is mostly fetal urine, and CMV is excreted in large amounts from the kidneys following congenital infection, and often for years afterwards, even in 'asymptomatic' cases). However, unless we have confirmatory maternal serologic information, or symptomatic infection confirmed to be the result of CMV during the pregnancy, we still may not know if the congenital infection is the result of primary or recurrent maternal disease. If the diagnosis of CMV is not suspected until late in pregnancy, or not until after the birth of the baby, detection of CMV in a urine sample taken from the baby within the first two weeks'(preferably, the first 48-72 hours) of life also suffices to confirm congenital infection. CMV is a VERY slow growing virus, so any detection of virus in this time frame most certainly represents intrauterine infection.

Congenital CMV infections are asymptomatic or unrecognized in about 90% of cases, including 85-90% of babies acquiring the virus as a consequence of primary maternal infection and 99% of those resulting from recurrent infections. Most of the asymptomatic infections pose no immediate life threat, but 10-15% of these babies are at risk for long-term complications such as sensorineural hearing loss, chorioretinitis, and dental abnormalities, usually apparent by two years' of age. Of these, the hearing loss is by far the most significant because delay in its detection can contribute to psychomotor retardation. More than 90% of congenitally infected infants, regardless of the severity of their infection, will shed infectious virus at birth, and may do so for 6 or more years longer, even in the presence of specific immunity.

About 5-10% of congenitally infected babies will have significant evidence of infection at birth. Approximately half of these will have classic 'cytomegalic inclusion disease (CMID)' (described below) and half will have atypical involvement. Virtually 100% of these infants excrete CMV at birth and will continue to do so for many years afterwards. Infants in this group have a 20-30% eventual mortality and account for 90% of the significant mental and psychomotor retardation associated with congenital CMV infections. The most severely affected children are usually the result of primary maternal infections during pregnancy and should be suspected in instances of unexplained intrauterine growth restriction and fetal death beyond 20 weeks' gestation.

The most common findings in babies with CMID include symmetrical growth restriction, multiple small skin hemorrhages (petechiae), enlargement of the liver and spleen (hepatosplenomegaly), jaundice, microcephaly (small head), abnormalities of the dental enamel, and chorioretinitis. They can have numerous associated birth defects involving virtually any organ system, a catalog of which is not necessary for our discussion today. Prenatal detection by ultrasound of fetal growth delay and gross or subtle, nonspecific physical abnormalities of the baby may be the only clues that a congenital CMV infection has occurred. Unfortunately, these often manifest themselves only weeks or even months after fetal infection has occurred because the virus is very slow growing, and it is relatively nondestructive, compared to other herpes viruses.

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With the above information as background, let me answer our reader’s questions:

Could this virus have caused my miscarriages? It is unlikely. Although I did not address this specific point above, many people over many years have tried to implicate CMV in recurrent miscarriages and I have never seen an article that found good evidence to do so.

Is there a period of time I should wait before trying to conceive again? The TORCH screen and your CMV seropositivity should not preclude your getting pregnant again soon. You already have ‘protective immunity’ and you will probably have the virus for the rest of your life. However, if you have had recurring miscarriages, perhaps you should wait to conceive until you have had a more thorough evaluation for that.

If I do become pregnant again am I at risk of having a baby affected by CMV? Yes, you have a 2-3% chance of having a baby with a congenital CMV infection. But, the presence of your antibody to CMV will decrease the risk of serious complications from the infection. Most (99%) babies who get CMV as the result of a recurrent maternal infection are asymptomatic, but 10-15% of these babies are at risk for long-term complications such as sensorineural hearing loss, chorioretinitis, and dental abnormalities, usually apparent by two years' of age. Your baby can be screened within 48-72 hours of birth by simply checking his/her urine for CMV to determine if there was a congenital infection. Almost all babies with a congenital CMV infection will excrete the virus in their urine. If CMV is present, the baby simply needs to be followed more closely for the hearing and eye problems noted above to prevent correctible sources of developmental delay. These children usually do not have problems with growth or mental retardation.

Labels: CMV, cytomegalovirus, RPL

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More Queries About Rh-Negative Blood

The following two comments recently appeared on my post addressing Implications of a Negative Blood Type. The first reader's question is worth repeating because MANY readers have asked the same question (in various forms) and the explanation is fairly simple. The second reader's questions revolve around potential complications of Rh-sensitization in someone who is attempting to conceive by in vitro fertilization with donor sperm. Her situation is NOT unique today and many other women may be interested in my responses to her queries as well...

Anonymous said...
Hi,I have a daughter who is
O negative. I also have a son who is O positive.
I am O positive and my wife is O negative. Is this possible?

Kenneth F. Trofatter, Jr., MD, PhD said...
To anonymous Sept 24: Yes, it simply means that you are heterozygous for the Rh D antigen. That means you have one chromosome that carries the gene for D and one that does not. Your wife has two that do not because she is Rh-negative and if she had even one dose of D, she would be phenotypically Rh-positive just like you because D is a dominant allele. Anyway, odds are that half of your kids (male and female) would be expected to be Rh-positive and half Rh-negative based on percentages alone (and no other extenuating circumstances). Sounds like that's what's happened so far in your family. Hope that helps. Thanks for reading! Dr T


lotsofdecisions said...
Hi. I became sensitized to Rh during my pregnancy with my daughter. My questions:

1) Does the fact that I was sensitized at my daughter's birth impact the problems I may have with a future pregnancy? I'm using donor sperm and know that the donor is O+ and heterozygous. How great is the risk? My titers are around 1:4.

2) After 2 unsuccessful IVFs to avoid having a second O+ child, I am about to admit defeat re: giving my daughter a full sibling. My question: should I consider only O- donors? It seems like using an A- or B- donor could result in as great of issues as if I used my daughter's donor.

3) How concerned should I be about CMV? I'm CMV negative. I've lived in the Northeast as well as the South. It seems like I'd have contracted CMV if I were susceptible to it.

Sorry this is so long. Thanks in advance.

Kenneth F. Trofatter, Jr., MD, PhD said...
To lots of decisions Sept 20:
1) Yes, your Rh-isoimmunization could have an impact on a future pregnancy. If your donor is heterozygous for Rh-positivity, there is a 50% chance your babies from that donor will be Rh-positive and potentially at risk for "Rh disease." You are currently at relatively low risk for complications with a titer of only 1:4. The risk begins to rise dramatically once your titer exceeds 1:16. During a pregnancy, I would recommend you have your titer checked every 4-6 weeks, especially if it begins to rise. In fact, if it does rise during a pregnancy, that probably confirms the baby is Rh-positive. We can currently assess risk for fetal anemia by a noninvasive study called Doppler flow velocimetry of the peak systolic velocity in the baby's middle cerebral artery. It's not as hard to do as it is to pronounce!

2) If you are using an Rh-positive donor, you cannot be sure that the baby is not Rh-positive until you test fetal cells by some sort of invasive procedure (chorionic villus sampling, amniocentesis, percutaneous umbilical cord blood sampling). You would be better starting off with an Rh-negative donor because then the baby CANNOT be Rh-positive. It does not matter whether that donor is A-, B-, O-, or AB-. The problem is with Rh, not the major blood group antigens.

3) CMV negativity is a BIG concern to me in your situation. (Check out a couple of my earlier blogs on that subject as well). You may be at risk for contracting that from your donor or you could simply contract it from someone else, especially your daughter, who is VERY likely to pick it up if she spends time around other kids. It is spread by all kinds of body fluids (e.g., blood, urine, and drool) and it is unlikely you are "not susceptible" to catching it; you probably have just been UNLUCKY enough not to have been exposed to it earlier in your life. I say unlucky, because if you did happen to catch it during a pregnancy, the results could be quite devastating to the baby. Thanks for reading and the great questions and BEST of luck to you too! Dr T

Labels: CMV, cytomegalovius, Rh-isoimmunization, Rh-negative blood type, Rhogam

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