Indications for Doppler Flow Velocimetry During Pregnancy

Recently, I received a phone call from our billing office reporting that an insurance company had declined to reimburse us for a claim that included charges for Doppler flow velocimetry for the indication of intrauterine growth restriction (IUGR). My response to the office personnel was simply that that is the most widely accepted indication we have for these procedures and that I would compose a letter of explanation to the insurance company, the contents of which are detailed below...

Doppler flow velocimetry (DFV) is a noninvasive method to assess resistance to, and velocity of, blood flow using ultrasound technology. In pregnancy, it has been proven to be a valuable adjunct to fetal assessment because often DFV abnormalities will precede detectable fetal abnormalities of growth, amniotic fluid, and placental insufficiency and can help assess the severity of fetal compromise when these abnormalities are suspected.

The principles underlying the most common indications for DFV are as follows:

Under normal conditions, the placenta offers little resistance to fetal and maternal blood flow, even during diastole (i.e., between heart beats); and, there is no preferential blood flow to the brain as reflected in normally high resistance, especially from late midtrimester on, at the expense of perfusion of other organs...

Under abnormal conditions, blood flow to the placenta may be reduced and accompanied by increased resistance to perfusion (fetal and/or maternal) and/or there is preferential blood flow to preserve ‘essential’ organs such as the brain (‘brain-sparing effect’) as manifested by low resistance Doppler patterns to these organs and eventually reduced perfusion (fetal blood flow redistribution) of ‘nonessential’ organs such as the kidneys.

Some factors that lead to aberrations in DFV patterns include:

• Abnormalities in placentation or of the umbilical cord
• ‘Placental insufficiency’ regardless of fetal size
• Fetal anemia resulting from maternal isoimmunization, viral infection (e.g., parvovirus B19 and CMV), twin-twin transfusion syndrome, fetal-maternal hemorrhage…
• Chromosomal abnormalities
• Cardiac and intracranial malformations

When indicated, DFV evaluation of the following may contribute valuable information with regard evaluation of the pregnancy, but should be performed by individuals trained and experienced in the performance and interpretation of the results:

Maternal:
Uterine arteries

Fetal:
Umbilical arteries
Middle cerebral arteries
Ductus venosus
Umbilical vein

Common indications for Doppler flow velocimetry studies include:

• Abnormalities of growth (both intrauterine growth restriction(IUGR) and excessive fetal growth (macrosomia)
• Fetal anomalies (e.g., cystic hygromas, cardiac, thoracic, diaphragmatic, neural tube, renal, and abdominal wall)
• Fetal hydrops
• Oligohydramnios (decreased fluid) and polyhydramnios (increased fluid)
• Poor OB history (e.g., preeclampsia, IUGR, previous stillborn…)
• Known maternal risk factors: hypertension, preeclampsia, diabetes, autoimmune disorders (overt and subclinical), thrombophilias (acquired and genetic)
• Abnormal maternal serum screening (e.g. elevated MSAFP and/or increased risk for fetal chromosomal abnormality)
• Multiple gestation
• Maternal trauma (fetal-maternal hemorrhage)
• Suspected placental abruption
• Known maternal isoimmunization
• Exposure to parvovirus B19

In recent years, DFV has become the primary means of screening related to fetal anemia. This is done by evaluating the peak systolic velocity (PSV) in the fetal middle cerebral artery. Its negative predictive value is so high that it has obviated the need for, and the expense of, repetitive invasive procedures when there is known maternal isoimmunization, Parvovirus B19 exposure, or other potential causes of severe fetal anemia such as trauma or placental abruption or placenta previa that might lead to fetal-maternal hemorrhage or fetal blood loss.

It is also the primary means of ruling out fetal anemia as a cause of hydrops fetalis and it is the mainstay in the assessment of multiple gestations as a means of screening and staging possible twin-to-twin transfusion syndrome. DFV of the fetal ductus venosus in early pregnancy has also proven useful in the identification of fetuses at risk for chromosomal abnormalities and major congenital heart defects. DFV of the branch pulmonary arteries can help predict the risk of fetal pulmonary hypoplasia in cases of premature and prolonged rupture of membranes.

DFV is no longer considered ‘experimental’ and it has become a ‘standard of care’ in the hands of specialist in Maternal-Fetal Medicine for the evaluation and management of complicated pregnancies.

Labels: Doppler flow velocimetry, fetal hydrops, isoimmunization, IUGR, oligohydramnios, polyhydramnios

Permalink | 10 Comments| Email Post

Post your comment

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

Permalink | 9 Comments| Email Post

Post your comment

Amniotic Fluid - 7 - Complications Related to Polyhydramnios

When excessive amniotic fluid (polyhydramnios or, simply, hydramnios) is present, there are increased risks of complications for both mother and baby. Some of the risks to the baby are obvious if there is an identifiable etiology for the hydramnios, such as maternal diabetes, multiple gestation, congenital malformation, chromosomal abnormality, severe fetal anemia secondary to isoimmunization or Parvovirus B19, neuromuscular disorders, or congenital infection. Indeed, past reviews confirm the risk for poor outcomes when an etiology is found. For example, Stoll and colleagues (Community Genet 1999;2:36-42) identified 290 cases of polyhydramnios in 225,669 consecutive pregnancies and diagnosed congenital malformations prenatally in 44.5% of the cases. Among these, 10.3% of the infants were stillborn, 41% had more than one malformation, 14.5% had a chromosomal abnormality.

Similarly, Biggio and colleagues (Obstet Gynecol 1999;94:773-7) compared 370 women with singleton pregnancies beyond 20 weeks' gestation and hydramnios with 36,426 controls who had normal amniotic fluid volumes. “The perinatal mortality rate in all women with hydramnios was 49 per 1000 births, compared with 14 per 1000 births in the control group (P < .001). Women with hydramnios had 25 times more anomalies than controls (8.4% versus 0.3%; P < .001)…the cesarean rate was three times higher in women with hydramnios compared with controls (47.0% versus 16.4%; P < .001).” Interestingly, in their study, the increased risks were concentrated in the nondiabetic women with hydramnios.

However, as we mentioned previously, 50-60% of hydramnios is idiopathic (without an identifiable cause). So the question remains, are there increased risks to the baby if no identifiable etiology for the hydramnios is found? In other words, does the excessive fluid alone seem to contribute to or be associated with poor perinatal outcome. The scientific literature would indicate that it does. For example, Magann and colleagues (Obstet Gynecol Surv 2007;62:795-802) recently presented an extensive review dating back more than 50 years and found that idiopathic hydramnios was linked “to fetal macrosomia (in the absence of diagnosed maternal diabetes), an increase in the risk of adverse pregnancy outcomes, and a 2- to 5-fold increase in the risk of perinatal mortality.” So, what are some of the pregnancy risks, irrespective of the cause of the excessive amniotic fluid.

Common risks secondary to overdistention of the uterus include abdominal pain, premature labor and delivery, and premature rupture of membranes. There is also an increased risk of uterine rupture, although this is rare in the absence of a previous cesarean delivery or other operative uterine procedure. In the presence of severe hydramnios, especially in a woman of small stature, overdistention of the uterus can put so much pressure on the mother’s diaphragm that she has difficulty breathing in ANY position and maternal cardiorespiratory decompensation may occur under these circumstances.

Often under these circumstances, placental perfusion is also reduced, the baby develops relative placental insufficiency, and as a consequence of the baby’s (and probably the placenta’s) unhappiness, the mother develops preeclampsia. Doppler flow studies have shown a greater incidence of fetal blood flow ‘redistribution’ (an indirect indicator of ‘placental insufficiency’) in the presence of hydramnios and this is most likely due to the excessive pressure on the umbilical vessels and the placenta itself resulting in decreased fetal perfusion. Indeed, any fetal condition associated with hydramnios that places the baby in a ‘distressed’ situation, particularly, severe fetal anemia and other causes of hydrops fetalis, increases the risk for maternal preeclampsia.

Indeed, the very first obstetrical patient I ever saw die (30 years ago) had a baby with hydrops secondary to severe maternal Rh-isoimmunization and polyhydramnios. An attempt was made to transfuse the baby in utero and afterwards she was sent to the antepartum unit for monitoring. I noticed her blood pressure was elevated and checked her urine to also find 4+ proteinuria. I remember notifying her attending physician ( I was a second year resident at the time) that she appeared to be developing severe preeclampsia and was brushed off that this was simply the ‘stress of the procedure that she had just been through.’ When I came in to round on her the next morning, she was not in her bed and when I asked if she had been discharged, I was told that she had had a hypertensive crisis in the middle of the night, a cerebrovascular accident, and could not be resuscitated. The occurrence of severe maternal preeclampsia in the presence of fetal hydrops has come to be known as “mirror syndrome” in which the mother’s condition reflects (and is probably driven by) the dire fetal condition (Vidaeff, et al. J Reprod Med 2002;47:770-4). Needless to say, there are some things one NEVER forgets!

Hydramnios can also cause several complications related to the onset and course of labor. Too much fluid often leads to lack of ‘engagement’ of the fetal head in the pelvis and/or an unstable fetal lie (breech or transverse). This can be a special problem when the membranes rupture (spontaneously or artificially) because if there is no ‘presenting part’ obstructing the cervix, the umbilical cord can suddenly prolapse with the gush of fluid through the cervix into the vagina turning a relatively uncomplicated situation into an emergency. Acute release of the fluid and decompression of the uterus can also cause sudden separation of the placenta (placental abruption) from the uterine wall. Stretching of the uterine muscle (myometrium) can also result in abnormal labor patterns secondary to poor contractility (myometrial dysfunction) and at times can result in poor contraction (involution) of the uterus following delivery, a situation that is usually accompanied by post-partum hemorrhage. All of these complications contribute to the increased rate of cesarean deliveries in pregnancies with hydramnios and the increased rate of maternal and fetal complications.

One other complication which occurs frequently (and is often not thought about) in the presence of hydramnios, particularly if this is associated with diabetes or simply, with fetal macrosomia, is immaturity of fetal lung development. As we have pointed out in earlier posts, late preterm (near-term) elective delivery of a baby just because it is “too big” can have tragic consequences. It is not unusual for macrosomic babies to have a 2-3 week lag in the functional ability of their lungs at birth because excessive insulin production (hyperinsulinemia) that often accompanies macrosomia can delay the production of the lung surfactants that reduce surface tension in the alveoli and are necessary for expansion of these so that oxygen exchange can occur normally. There is nothing sadder than seeing a 10 lb baby of a diabetic mother laying in the neonatal intensive care unit struggling to survive with severe respiratory distress syndrome and persistent fetal circulation as a consequence of an elective (often cesarean) delivery.

Having discussed some of the more common complications of polyhydramnios, in our next (and final!?!) post on the topic of amniotic fluid, we will address the evaluation and management of the pregnancy with too much amniotic fluid…

Labels: diabetes, hydramnios, polyhydramnios, Rh-isoimmunization

Permalink | 14 Comments| Email Post

Post your comment

Grand Rounds 4.35 at Musings of a Dinosaur!

Thanks to Musings of a Dinosaur for the effort and "Jurassic Park" spectacular presentation of this week's Grand Rounds 4.35. Thanks too for including a link to my recent post on "Polyhydramnios: Causes of Too Much Amniotic Fluid."

Grand Rounds offers us the opportunity to sample the diversity of ideas and perspectives currently circulating throughout the medical community at all levels of involvement. This week's offering certainly represents the community well and it was a pleasure to peruse. So, don't be shy, check it out and see how the whole world looks at this incomparable profession!

Labels: amniotic fluid; AFV, polyhydramnios

Permalink | 0 Comments| Email Post

Post your comment

Amniotic Fluid - 6 - Polyhydramnios: Causes of Too Much Amniotic Fluid

Polyhydramnios (excessive amniotic fluid), also termed hydramnios, is usually defined by vertical pockets of amniotic fluid > 8 cm or as a 4-quadrant amniotic fluid index (AFI) > 95th percentile for the gestational age. Polyhydramnios has a multitude of causes and associations but is seen in only about 1-2% of all pregnancies. It can occur gradually or rapidly depending on the underlying etiology. About 50-60% of polyhydramnios is ‘idiopathic’ which means we haven’t been smart enough to figure out why there is too much fluid. It is not necessarily associated with increased urine production by the baby, but it may have a genetic basis because it can recur in sequential pregnancies, even without an etiology being identified. In some instances there is just excessive fluid and it doesn’t necessarily increase significantly over time and in other cases, it gets progressively worse and may cause both fetal and maternal complications.

There are some specific conditions in which polyhydramnios is frequently associated. The easiest to understand are the fetal anomalies that inhibit or prevent fetal swallowing or block the passage of fluid through the fetal bowel. (Recall, much of the amniotic fluid around the baby is urine and the baby must be able to swallow that and move it through the bowel to the colon where it can be reabsorbed). Common structural gastrointestinal abnormalities that are accompanied by polyhydramnios include esophageal atresia (incomplete development of the esophagus), tracheoesophageal fistulas (aberrant connections, sometimes ending in ‘blind pouches’, between the trachea and the esophagus), duodenal atresia with the classic “double bubble” seen by ultrasound in the upper abdomen (and at least 30% of these associated with Down syndrome – trisomy 21), other small bowel atresias and obstructions (the lower in the small bowel the obstruction, the greater the number of fluid-filled loops of bowel), gastroschisis (a condition in which much of the small bowel is outside the abdomen through a small defect adjacent to the fetal umbilical cord insertion site), gastrointestinal ‘malrotations’ and ‘midgut volvulus’.

Other fetal anomalies associated with polyhydramnios probably have different reasons for contributing to the excessive fluid. Large neural tube defects and certain neuromuscular disorders (such as myotonic dystrophy), for example, probably exert their effects by impairing the ability of the baby to actually swallow fluid, even if the esophagus and gastrointestinal tract are patent. Certain cardiac defects and fetal arrhythmias may contribute by virtually putting the baby into congestive heart failure. Heart failure is also likely to be a major contributing factor when the baby has severe anemia secondary to maternal isoimmunization, a fetal hemoglobinopathy, or bone marrow suppression of red blood cell synthesis as is seen with congenital Parvovirus B19 infections.

Other congenital infections (e.g., syphilis, toxoplasmosis, cytomegalovirus) may also result in excessive amniotic fluid although the actual causes of this may be different depending on the organism involved. Indeed, any condition that results in immune or nonimmune fetal hydrops, including chromosomal abnormalities and inborn errors associated with severe metabolic or cardiac dysfunction, may be accompanied by polyhydramnios. One of the more unusual conditions that is associated with polyhydramnios and fetal hydrops is the so-called “mirror syndrome” that occurs in some cases of severe maternal preeclampsia. Lithium toxicity appears to cause polyhydramnios by causing the baby to have a condition called diabetes insipidus which results from inadequate vasopressin (antidiuretic hormone – ADH) secretion by the posterior pituitary gland and, subsequently, massive production of very dilute (unconcentrated) urine.

The most common clinical condition that is often accompanied by polyhydramnios is diabetes, particularly, gestational diabetes and type 2 diabetes. It is much less likely to be found in long-standing diabetics, particularly, if they have significant kidney, cardiac, or vascular disease. In diabetics, polyhydramnios is more common if the diabetes is poorly-controlled and/or the baby is macrosomic. At times, even improving the diabetic control will not reduce the increased amniotic fluid. The etiology of the increased fluid in certain diabetics is unclear, but when present, it increases the risk for a poor fetal outcome.

In the next post, we will continue with a discussion of polyhydramnios – pregnancy complications, evaluation, and management….

Labels: fetal hydrops, fetal macrosomia, isoimmunization, polyhydramnios

Permalink | 55 Comments| Email Post

Post your comment

Amniotic Fluid - 2 - Assessment of Amniotic Fluid Volume

We closed our last post with the comment that BOTH too much fluid (polyhydramnios, otherwise termed hydramnios) or too little fluid (oligohydramnios) are associated with fetal abnormalities and/or poor perinatal outcome. In fact, the greater the amniotic fluid abnormality, one way or the other, the greater the likelihood is of fetal complications or loss and, for that matter, maternal complications as well. The maternal complications are (usually) not related to the fluid abnormalities themselves (except in cases of severe polyhydramnios), but to the reasons the amniotic fluid volumes are abnormal to start with. That will become clearer as we proceed with these posts.

With the widespread use of ultrasound, we have come to use ‘semi-objective’ measures of amniotic fluid volume (AFV). Although what is “abnormal” has gone through various permutations over time, most practitioners assess AFV by one of two methods. The first method is to simply measure the depth of the single largest vertical pocket of fluid (free of umbilical cord and body parts) with the ultrasound transducer oriented perpendicular to the uterus and not just perpendicular to the abdominal wall and with a minimum of pressure on the transducer itself. If the single largest pocket is < 2 cm, the AFV is considered to be ‘decreased’ at anytime from midtrimester until term. If the single largest pocket is > 8 cm, the AFV is considered to be ‘increased’.

The second method that has gained perhaps the most popularity over time is the “amniotic fluid index (AFI).” This technique involves dividing the uterus into four ‘quadrants’ by imagining perpendicular lines running through the umbilicus of the mother, and then simply measuring the single deepest pocket of fluid in each quadrant and adding up the 4 results. At term, the mean AFI is 11.5 cm with 5th and 95th percentiles of 6.8 and 19.6 cm, respectively, and quite frankly, there is not much variation in those values from late midtrimester on. Oligohydramnios is then defined as an AFI < 5th percentile and polyhydramnios as > 95th percentile.

Either approach can be performed quickly and though the AFI technique would intuitively seem to give you a better total picture of AFV, in reality, there probably is no real difference in the reliability of the methods. Indeed, in experienced hands, subjective assessment of amniotic fluid by simply looking is probably just as good (may the lord of evidence-based medicine please not strike me down)! If there are only very small pockets of free fluid, the baby appears crowded, or in the most extreme cases, there is absolutely no fluid (severe oligohydramnios or anhydramnios) and the baby has gross pressure deformations of the head or extremities, or overlapping of the ribs, the diagnosis of too little fluid is readily apparent. In a similar vein, if the baby appears to be freely floating or turning and has no restriction of extremity extension, there is probably too much fluid. With all that said and done, since not everyone has ‘experienced hands’ and there is some beauty to numbers, we use the 4-quadrant AFI as our routine approach to the assessment of AFV.

In the next post in this series we will discuss specific conditions and complications associated with decreased amniotic fluid….

Labels: amniotic fluid; AFV, anhydramnios, hydramnios, oligohydramnios, polyhydramnios

Permalink | 3 Comments| Email Post

Post your comment