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

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Grand Rounds 4.34 at Health Business Blog!

Thanks to David E. Williams at Health Business Blog for a most entertaining Grand Rounds and for including a link to my recent post regarding Consequences of Decreased Amniotic Fluid in pregnancy. This is the 4th post in my series on amniotic fluid that aims to provide a very basic understanding of what the 'bag of waters' is all about and the causes, complications, and managemnt of amniotic fluid abnormalities during pregnancy.

Thanks for reading and do check out this week's Grand Rounds!

Labels: amniotic fluid; AFV, oligohydramnios

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Amniotic Fluid - 5 - Evaluation and Management of Oligohydramnios

Just as the fetal outcome depends on the degree, underlying cause, timing during development and longevity of decreased amniotic fluid, to some extent, so do the management options. When the baby has complete absence of both kidneys (bilateral renal agenesis), or absence of functional kidneys (bilateral multicystic or polycystic renal dysplasia), and no amniotic fluid, then as we pointed out yesterday, the fetal outcome is clear – the condition (Potter’s sequence) is lethal. Since this outcome is inevitable, regardless of the gestational age at delivery, interruption of the pregnancy is a reasonable option if the patient wishes to proceed with that. When I trained, that was considered to be a reasonable option at any gestational age as well (whenever the patient was ready to proceed) and, in my mind, it still should be, however, there are many individuals and state regulations that consider this a ‘pregnancy termination’ and practitioners are reluctant to perform labor inductions in such women beyond the gestational age at which the state limits such procedures. Unfortunately, this might require a woman to carry her nonviable baby for 4-5 months after she has been given the diagnosis.

Another option under these circumstances is to offer the patient a program of ‘fetal hospice care.’ The goal of such programs is to allow women and their families the opportunity to spend as much time with the baby, before and after birth, as possible. We structure this with frequent office and ultrasound visits (for those who prefer) and ongoing counseling before and after delivery. In addition, we try to identify other families who have been through the same or a similar situation as a means of additional support. We will often identify one physician to lead the care of the pregnancy, avoid unnecessary testing and interventions, try to create a sensitive birth experience without fetal monitoring and with experienced nursing staff, have a neonatologist available to rapidly confirm the baby’s status following delivery, and allow the patient and any family members she welcomes to be present at the delivery to spend as much time with the baby as possible after birth. Although this approach is not for everyone, those that go through with it are almost always rewarded by the experience.

Less clear is the management of the ‘obstructive uropathies’ that are accompanied by reduced amniotic fluid and, indeed, discussion is beyond the scope of what we need to present herein. In brief, management and outcome depends on when in pregnancy the obstruction is detected and the extent of residual kidney function. As an example, if one is fortunate enough to detect an over-distended bladder and oligohydramnios as the result of posterior urethral valves (bladder out let obstruction) very early in pregnancy, there is the option to place a bladder shunt, diverting urine from the bladder into the space around the baby. Theoretically, this might help reduce the risk of pulmonary hypoplasia. However, the fetal outcome under these circumstances is highly variable. Sometimes the kidneys and the bladder have been too damaged by the obstruction to recover, sometimes the shunts have to be replaced repeatedly, and sometimes the babies still develop abdomens that remain distended and poorly muscularized as the result of the over-distention during critical stages of development – a condition called ‘prune belly syndrome' – and/or respiratory insufficiency. Complete, bilateral ureteral obstructions (between the kidneys and the bladder) are even more of a challenge, but fortunately these are very rare.

Management of premature rupture of membranes (PROM) also depends to a large extent on the timing in pregnancy. If this occurs prior to 20 (or even 22) weeks, the risk of fetal complications related to pulmonary hypoplasia and fetal deformations and the risks of maternal complications secondary to infection are so high that many practitioners will simply advise their patients to undergo pregnancy termination. Unfortunately, for counseling purposes, the outcome under these circumstances can be difficult to predict, particularly if the baby is able to maintain, even intermittently, a small amount of fluid within the uterine cavity. But it is likely that less than 5% of babies with PROM before 20 weeks have any chance at all of intact survivial.

For the patient who is reluctant to undergo pregnancy termination, an option is to simply counsel regarding risks and signs of infection (and the absolute necessity of proceeding with delivery once infection is suspected) and to follow the pregnancy over time. After initial stabilization and evaluation in the hospital, we offer most of these women outpatient management. Other than counseling there is no more that can be offered except perhaps antibiotics. There is no standard of care in the use of antibiotics under these circumstances (in fact some would decry it) but after several unexpectedly good outcomes under these circumstances, I have gotten into the routine of beginning, empirically, a broad spectrum IV cephalosporin antibiotic or penicillin to cover Group B Streptococcus, pending results of cervical-vaginal and urine cultures, as well as a 5-day course of azithromycin, and prolonged prophylactic therapy with metronidazole (the latter being given orally until delivery). Once the baby reaches the point of potential viability, hospitalization can be considered, if the patient desires more aggressive fetal surveillance.

Management of PPROM after viability has been obtained usually involves hospitalization from the outset, careful assessment for infection (even to the extent of including amniocentesis to evaluate the fluid around the baby for evidence of infection and inflammatory markers) and ongoing fetal monitoring to try to balance the risks and benefits of continuing intrauterine management versus delivery. Again, this topic is best suited for another entire post alone.

One of the more challenging, and more common, situations involving the management of pregnancies with reduced amniotic fluid is in the setting of ‘placental insufficiency’ that usually is the late culmination of abnormalities of placentation that occurred very early in pregnancy. As we discussed in our last post, when babies are not getting enough across the placenta to meet metabolic demands and to maintain normal patterns of symmetrical growth, they are able to ‘redistribute’ blood flow to essential organs such as the brain and heart. One sign that this is occurring is progressive growth of the fetal head out of proportion to that of the abdomen – asymmetrical fetal growth restriction. Eventually a critical stage is reached at which point so much blood flow is diverted away from the nonessential organs such as the kidneys, that fetal urine production drops and subsequently the amniotic fluid volume, placing the baby at risk for both cord compromise and too little oxygen. When babies truly start to become unhappy in these situations, it is not uncommon for their mothers to develop hypertensive complications of pregnancy (preeclampsia) and these frequently accompany intrauterine growth restriction.

One of the most effective means we have of ascertaining that these blood flow changes are occurring, sometimes even before significant growth abnormalities have taken place, is Doppler flow velocimetry. This is a noninvasive ultrasound-based technique that allows us to measure resistance to flow (and at times velocity of the flow) in blood vessels. In normal pregnancies, resistance to blood flow from the baby to the placenta as measured in the umbilical arteries is usually very low – indeed, blood normally continues to flow to the placenta even between beats (end diastole) of the fetal heart. At the same time, under normal conditions, resistance to blood flow to the fetal brain (usually measured in the middle cerebral artery, or MCA) is usually high. Though this resistance often decreases as pregnancy progresses, resistance to intracranial blood flow should always exceed resistance indices found in the umbilical arteries. In contrast, when there is decreased resistance in the MCA, this suggests fetal blood flow redistribution and it is often accompanied by increased resistance in the umbilical arteries reflecting the abnormalities in placentation (invasion of the maternal spiral arterioles) that led the pregnancy to this point. When the resistance in the MCA actually falls below that found in the umbilical arteries, the baby may well be at a critical stage requiring delivery, regardless of the gestational age.

When we follow the pregnancy with reduced amniotic fluid, there is not necessarily going to be a single test that tells us the baby is better off out than in. It is one of those situations where we may have to use several of the antepartum testing modalities – nonstress test (NST), contraction stress test (CST), biophysical profile (BPP), and Doppler flow velocimetry - we have at our disposal to aid in the decision-making process. This is especially important when there are complications related to oligohydramnios in the very premature baby. There are many times when the maternal condition must be factored into the decisions as well, particularly, when there is evidence of preeclampsia accompanying intrauterine fetal growth restriction associated with placental insufficiency. One must also be very cautious in the pregnancy with placental insufficiency because the baby often has had time to adapt to the chronic stress of its environment and can often appear better off than it really is even just before decompensating completely.

This concludes an overview of the pregnancy with decreased amniotic fluid. I apologize if I over-simplified some aspects of this discussion, but I wanted to present the information in a way that most of our readers could grasp the basic concepts. In the next post we will begin a discussion of increased amniotic fluid – polyhydramnios (or, simply hydramnios)...

Labels: Doppler flow velocimetry, oligohydramnios, preeclampsia, premature rupture of membranes

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Amniotic Fluid - 4 - Consequences of Decreased Amniotic Fluid

In the last three posts, we have reviewed basic aspects of amniotic fluid production and measurement and common causes of decreased amniotic fluid, or oligohydramnios. Now let’s look at reasons decreased amniotic fluid increases the risk for fetal (and newborn) complications and death. Complications related to decreased amniotic fluid depend on the underlying cause, the degree of the decrease, the timing during pregnancy, and the longevity during fetal development. First, let’s look at the worst case scenario – the baby that has no fluid (anhydramnios) from very early in the pregnancy on…

As mentioned in our last post, the most common conditions that lead to anhydramnios include absence of the fetal kidneys (bilateral renal agenesis), nonfunctional kidneys secondary to bilateral renal dysplasia (polycystic and multicystic kidneys), and complete bladder outlet obstruction (posterior urethral valves, or other anomalies associated with maldevelopment of the fetal bladder or urethra). In rare circumstances, complete bilateral obstruction of the ureters (ureteropelvic or ureterovesical junction obstruction) can also be found. Under these conditions, where the baby has essentially no amniotic fluid from late first trimester on, the outcome is uniformly LETHAL.

Interestingly, it is not the absence of kidney function that kills these babies – it is the fact that in the absence of amniotic fluid, the fetal lungs do not develop sufficiently to support breathing once they are actually born! Any of these conditions associated with early and sustained anhydramnios result in the same outcome secondary to pulmonary hypoplasia and insufficiency, and this has been labeled ‘Potter’s syndrome (or sequence)’ after the physician who first described it. Although, it is not known why the absence of fluid results in Potter’s syndrome, it is thought that the constant compression of the thorax contributes, that the production of fluid by the fetal lungs is suppressed, and even that some movement of amniotic fluid (fetal urine) into the lungs is essential for normal development of functional alveoli. Most babies who are born with Potter’s syndrome cannot even make any kind of respiratory effort at birth, and those that do, cannot get sufficient oxygen into their bodies to allow survival.

If you notice, I did not include premature and prolonged rupture of membranes (PPROM) in this category of inevitable lethal outcome. It is true that if PPROM occurs prior to 20-22 weeks, the baby is at risk for the full consequences of Potter’s syndrome, and the earlier the PPROM and the more severe the oligohydramnios, the greater the likelihood is that this will occur. Indeed, during my training, we were taught simply to offer such women induction of labor, not only because the fetal outcome was expected to be dismal but also because the risk of infection to the mother was so high. (Of course, when I trained, it was the rare baby born before 27 weeks that had any chance of survival anyway). But, I must admit, many patients I have had over the years have proven that old teaching to be incorrect, or at least not a certain death sentence for their babies. Some of these women will carry their babies to a point where there is potential viability (today, 23 weeks and beyond) and, though they are at risk for pulmonary hypoplasia, the degree of this is very difficult to predict and it may not be lethal. However, these babies may also be at increased risk for fetal deformations (particularly of the skeleton, thorax, and head) secondary to compression during development and in its most severe form, a condition termed the fetal akinesia/hypokinesia deformation sequence in which there are not only compression malformations but poor development of muscle, tendons, and enervation secondary to the lack of fetal movement in utero.

Although the above conditions are very serious, they are also all the least common complications related to oligohydramnios. Indeed, most babies will not develop decreased amniotic fluid until beyond 24 weeks gestation, so the issues related to pulmonary hypoplasia and major deformations are, fortunately, rare. The most common reasons for oligohydramnios in the latter part of pregnancy are PROM and placental insufficiency. In the case of the former, this can lead to the acute (sudden) decrease in amniotic fluid and in the latter, a more gradual reduction. Leaving infection out of the equation (as a common cause of PROM and associated with its own morbidity and mortality), the primary cause of fetal complications under these circumstances are related to umbilical cord compromise, and in the case of placental insufficiency, decreased fetal oxygenation (ultimately the cause with its own consequences, not the effect, of decreased amniotic fluid).

Normally, I tell patients that the umbilical cord is a lot like a fire hose. It is a ‘closed system’ and the blood contained within it is under some pressure. In other words, just because it is wrapped around the baby’s neck, or other body parts, or even tied into a knot, does not mean the baby is going to necessarily die as the result – in fact most don’t. At least one-third of all babies are born with the cord looped around the neck (nuchal cord) and most do just fine. However, the blood in the umbilical cord vessels is under differential ‘pressures’ depending on whether it is the poorly oxygenated arterial blood (higher pressure) coming from the baby to the placenta or the well-oxygenated venous blood (low pressure) coming back to the baby from the placenta. Obviously, when there is compression on the umbilical cord, the venous blood flow is much more likely to be impeded than the arterial blood flow.

Even if the blood in the umbilical cord is under pressure, in the presence of decreased or absent amniotic fluid it is possible for the baby to trap the cord in a position where blood flow is significantly reduced and the baby can be damaged or even die as the result of too little oxygen. I always worry about this most when there is sudden rupture of the membranes, or if the cord falls (prolapses) through the cervix, and, particularly, in women who are very heavy. It is also one of the causes of fetal morbidity and mortality in placental insufficiency sequences (accompanied by intrauterine growth restriction) because oftentimes in these circumstances, not only is the placenta poorly developed (and has less ‘reserve’), but the cord is often thinner and smaller and not endowed with adequate cushioning due to a reduction in the amount of Wharton’s jelly surrounding the blood vessels (normally two arteries and one vein) in the umbilical cord and, therefore, more likely to be significantly compromised when compressed.

Intermittent (and incomplete) umbilical cord compression can often be identified by distinct abnormalities of the fetal heart rate (FHR) tracing (most commonly, ‘variable decelerations’). These are quite common in labor, particularly after the membranes have ruptured either spontaneously or as the result of the provider’s intervention (artificial rupture of membranes, or AROM). FHR monitoring is, therefore, one means of identifying the baby ‘at risk’ for umbilical cord compromise. Most babies that have decreased fluid and normal placental function tolerate this type of FHR deceleration quite well, although they are still at increased risk for cesarean delivery if the FHR tracing begins to develop signs of ‘nonreassurance’ and spontaneous vaginal delivery is still remote. Since we seem to have spent a fair amount of time on this topic today, I will reserve further discussion on the evaluation and management of pregnancies with oligohydramnios to our next post…

Labels: amniotic fluid; AFV, anhydramnios, oligohydramnios, Potter's syndrome

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Amniotic Fluid - 3 - Oligohydramnios: Causes of Too Little Amniotic Fluid

Having discussed where amniotic fluid comes from and how we assess amniotic fluid volume, let’s address the most common amniotic fluid abnormality – too little fluid or oligohydramnios. There are 3 primary reasons why there is too little amniotic fluid: 1) rupture of membranes; 2) fetal abnormalities; 3) placental abnormalities.

Spontaneous rupture of membranes (SROM) can occur at any time in pregnancy. Most of the time, the membranes remain intact until the onset of labor, or just before labor, after the cervix has begun to change (efface and dilate). If membranes rupture prior to the onset of uterine contractions, it is called premature rupture of membranes or PROM, and if they are ruptured for more than 24 hours, prolonged premature rupture of membranes or PPROM. There are lots of things that can lead to rupture of membranes, but the ones we worry about most are infection, fetal anomalies that result in too much fluid (polyhydramnios or hydrammnios) and uterine overdistention, and cervical incompetence. The earlier in pregnancy that the membranes rupture, the greater the likelihood that it is associated with infection (with or without cervical incompetence) and this is usually infection with organisms that the mother carries in her body that get inside the uterus by ascending vaginal, blood-borne, or lymphatic transmission. However, the focus of this discussion is not to discuss SROM, but to remind readers that it is a very common cause of decreased amniotic fluid and when it occurs, the baby and the mother need to be evaluated carefully to look for causes. Since infection is often associated with PROM, that is usually what constitutes the greatest risk to the baby.

The least common, but often most serious, causes of decreased amniotic fluid are fetal abnormalities. If you recall in our first post on this subject, most of the amniotic fluid from early midtrimester on is fetal urine. Abnormalities of the fetal kidneys and urinary tract can lead to decreased urine output or the complete absence of amniotic fluid (anhydramnios) in the most severe cases. Babies can have the complete absence of both kidneys (bilateral renal agenesis), nonfunctioning kidneys associated with polycystic or multicystic renal dysplasia, or obstructive uropathies where there is blockage of urine at the urethra (usually the result of ‘posterior urethral valves’ in male children), or blockage of the ureters at various levels between the kidneys and the bladder (e.g., ureteropelvic junction (UPJ) or ureterovesical junction (UVJ)obstructions). An important point to note here is that if the baby only has ONE nonfunctioning kidney, or a blockage that affects only ONE side, the amniotic fluid is usually normal and the consequences of too little fluid for too long do not develop. However, if both kidneys are affected, this can lead to the complete absence of amniotic fluid and a condition that has been named “Potter’s sequence” which will be detailed in our next post on this subject.

Other causes of decreased fluid that may be transient (and therefore less serious) and/or reversible are congenital viral infections, such as cytomegalovirus (CMV) which has a predilection for the fetal kidneys, or conditions that affect maternal hydration. With regard to the latter, as we pointed out previously, if the mother becomes very dehydrated, or if she has a condition that severely decreases her plasma volume, the fluid around the baby, which depends so much on passive distribution from the mother across the placenta, can acutely decrease. Common conditions in which this is seen include: hyperemesis (too much vomiting), diarrhea, maternal sepsis, hemorrhage, placental abruption or previa, diabetic ketoacidosis, excessive fluid loss during fever or heat exposure, and severe preeclampsia. Oligohydramnios resulting from many of these conditions can be reversed or improved with expansion of the maternal plasma volume.

The last conditions I would like to discuss that lead to decreased amniotic fluid are those that result in decreased perfusion (blood flow) to the fetal kidneys. When it comes right down to it, the kidneys are ‘nonessential organs’ with regard to survival of the baby while it is inside its mother. For example, babies that have bilateral renal agenesis (no kidneys at all) can go all the way to term because the placenta and the mother serve as the means of removing ‘waste products’ from the baby. (They cannot survive after delivery for the reasons I will detail in my next post). Production of urine by the baby requires blood flow through the kidneys. When babies become dehydrated, or when they have to, preferentially, send blood to ‘essential organs’ such as the brain and the heart because they are not receiving enough oxygen and nutrients to support their whole bodies’ needs, their regulatory mechanisms of survival shut down blood flow to the kidneys, thereby, curtailing the production of urine.

This can occur as the result of primary fetal problems such as severe anemia associated with isoimmunization or parvovirus infections, or cardiac malformations or dysfunction from a variety of different causes. More commonly, however, this occurs as the result of abnormalities of placentation (small placentas and/or placentas that have not had normal invasion of the maternal spiral arterioles in the placental bed), wherein the babies have outgrown the capacity of the placenta to provide sufficient oxygen and/or nutrients. When ‘placental insufficiency’ occurs it is usually accompanied by intrauterine fetal growth restriction (IUGR). This usually means the baby is small for its gestational age, but there are occasions when this can occur in large babies, such as those seen in uncontrolled diabetic mothers, whose size also exceeds the capacity of the placenta to maintain their metabolic demands. When the amniotic fluid starts to go down in circumstances of placental insufficiency, this is also usually the result of ‘fetal blood flow redistribution’ away from the kidneys and to the essential organs necessary for survival.

Having discussed some of the more common causes of oligohydramnios, in our next installment of this series, we will address the evaluation, management, and consequences decreased amniotic fluid in pregnancy ….

Labels: amniotic fluid; AFV, IUGR, oligohydramnios, premature rupture of membranes

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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

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