Amniotic Fluid - 8 - Evaluation and Management of Polyhydramnios
Sunday, May 25, 2008
Kenneth F. Trofatter, Jr., MD, PhD
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
13 Comments:
At Sun Sep 21, 02:20:00 PM 2008,
Anonymous said…
Dear Dr. T.,
I am 30 weeks pregnant and was diagnosed with polyhydramnios around week 25. I do not know what the AFI was at this week. At week 29 it was 28.5cm and at week 30 it increased to 33cm. Should I be concerned that it increased so much in one week? The baby is also measuring on the large size. I have a 2 vessel cord, which was found during the 20 week u/s. Screenings for trisomy 21, 18, and open neural tube defect showed very low risk and gest diabetes was negative. Are there particular abnormalities typical of polyhydramnios I should be especially concerned about?
Thank you.
At Tue Oct 07, 04:15:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
To anonymous Sept 21: You may simply have a large baby who has a tendency to make a lot of urine! You might also now be gestational diabetic, since about 10-15% of women who become gestational diabetic pass their initial diabetes screening and it is only picked up because they arte rescreened (or give a full 3 hour GTT) at 32-odd weeks. Babies who have gastrointestinal abnormalities and don't get the fluid they swallow into the part of the GI tract that absorbs fluid will develop polyhydramnios and babies who do not swallow well for reasons of certian anomalies (e.g. tracheoesophageal fistulas) or neuromuscular disorders may also develop polphydramnios. Certain genetic syndromes such as Beckwith-Wiedemann are associated with large babies and hydramnios. The most common cause is still "idiopathic polyhydramnios" which means we just aren't smart enough to figure out why it's there. So, let us know how things turn out and best wishes! Dr T
At Wed Oct 22, 07:26:00 AM 2008,
Anonymous said…
Dr. Trofatter,
I am so glad I found your extremely informative posts!
I found out 2 weeks ago that my AFI was 34.1 (I was 31 weeks). I was brought back in for a BPP yesterday (33 weeks) and my AFI dropped to 27. My dr. looked closely at the baby and reviewed all my tests and everything looks normal, so it looks like I fall in the "idiopathic" category of causes. I took my 1-hour GD test at 29 weeks and passed "with flying colors". Also, I've only gained 12 pounds so far, so I really don't think GD is a factor.
I will continue to go in weekly for a BPP until the numbers are back in the normal range.
I know that 27 is still considered "high", but what are your thoughts as far as my risks? I should mention that my stomach is measuring 38 weeks, and the baby is a good 3 weeks larger than true GA. (weight was estimated over 4 pounds at the 31 week ultrasound). My first son was 8 pounds, 5 ounces when he was born at 38 weeks.
My main concerns are:
1) Placental abruption- we believe this occured with my first child(though I had no risk factors). I delivered him under general anesthesia via a C-section (I wasn't even in labor, just happened to be in the hospital for a non-stress test when his heart rate dropped).
2) Uterine abruption- Since I had a previous C-section, and since my tummy/baby are measuring so big, is this a genuine risk?
3) Abruption of membranes and cord prolapse- what should one do in this situation if the fluid levels are known to be high? I've heard that I should get on all fours to take the pressure off the cord which may be in the cervix, but I'm curious to hear a doctor's opinion on this.
Thanks again for your insight and support. I look forward to your response.
At Thu Oct 30, 07:29:00 AM 2008,
Anonymous said…
Dr. Trofatter,
As a follow-up to my Oct 22nd post:
I had another BPP this week (33 weeks) and the AFI was back up to 33. The baby's scores were an 8 out of 8. I went in for a fasting and 2-hour postprandial glucose test yesterday and those came back fine.
I am scheduled to meet with the perinatologist next week.
I still have the same questions from my last post, but also, would it be wise to schedule my c-section for 37-38 weeks?? I'm leaning towards this, but I am carrying a boy and want to make sure his lungs are fully developed.
Thanks!
At Fri Oct 31, 04:25:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
To anonymous Oct 22: If you get close to term this time, it looks like you are cruising for a 9-10lb baby! The combination of polyhydramnios and a 'macrosomic' baby will increase your risk for uterine rupture but so much of that depends on how well your uterus was repaired and how well it healed. Your greatest risk for placental abruption comes if you develop pregnancy-induced hypertension and at the time your membranes rupture. Rapid decompression of the uterus (i.e., the acute fluid loss) can cause premature separation of the placenta. It can also increase your risk for a cord prolapse if the presenting part is not engaged in the pelvis at the time membranes rupture. You need to contact your doctor with any regular uterine activity, leakage of fluid, pain, bleeding or decrease in the baby's activity. If you do suddenly rupture membranes completely, assuming a knee-chest position (on all fours with the chest and head bent forward) may be a sensible thing to do until you can get to your doctor's office or hospital. Thanks for all the great questions! Best wishes and let us know how things turn out! Dr T
At Wed Dec 17, 05:03:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
To anonymous Oct 30: I just now got your follow-up question so you are probably already delivered and I hope everything turned out fine. My only recommendation before delivery at 37 weeks would have been to first document fetal lung maturity. Let us know how you did if you find your way back to this site! Kind regards and thanks for reading! Dr T
At Sun Apr 26, 06:35:00 PM 2009,
Cori said…
Dear Dr. Trofatter,
I am 35 weeks and at my 31 wk ultrasound they said my amniotic fluid was on the high side of normal. At one measurement it was 23.1 and then last week at my 34 wk appointment, I was told my afi was at 16, but there was 10 cm of fluid in the middle that was immeasurable because it wasn't in one of the four pockets. At my 34 wk appointment, I measured at 38 weeks. At my 31 wk appointment, I measured at 34 weeks. This is my second baby, with the first my waters went at 38 weeks. No gestational diabetes, am overweight this pregnancy (about 215 lbs, gained 20 so far). Have googled polyhydraamnios and have scared myself. Is this baby going to be huge? Am I likely to have him early? Was told from 31 wk u/s that he is in 66th percentile for growth.
At Sat May 02, 03:54:00 PM 2009,
Anonymous said…
Dear Dr. Trofatter,
Thank you for all of your very helpful articles!
I am 22 weeks and was just told that the results of my 22 week ultrasound came back showing my AFI at 30. To my knowledge, I did not have this condition, or any complications, with my first pregnancy. The Dr. recommended I be screened for gestational diabetes (the 1 hr glucose test) immediately because the baby appeared to be completely healthy on the ultrasound - they checked EVERYTHING. My blood sugar came back normal and they keep "re-assuring" me that the baby looks fine.
1) That is great that they think the baby is fine, but what about the AFI level? Isn't it double what it should be? I am in much pain and discomfort... at 22 weeks!!! I am concerned about PROM and delivering the baby prematurely. Are these concerns valid?
2) Is it likely that my AFI levels will continue to increase? and
3) Is it necessary to try to reduce the amount of fluid somehow?
4) I am also concerned because I never had the "quad screening". Could there be something wrong with the baby that was not seen during the ultrasound?
5) Lastly, I have just recovered from being extremely sick with a pretty severe virus for about 9 days that went into a sinus infection for another 10 or so days (had to be treated with amoxil). During this 2-3 week time is when I started to notice very rapid belly growth and discomfort & pain upon touching my abdomen. Could this infection be a factor?
Any information would be helpful because my doctor's office seems to be fairly unconcerned.
Thank you,
Holli
At Tue May 12, 06:13:00 AM 2009,
Anonymous said…
Dr. T,
I am just writing an update for you! I was the anonymous poster on Oct 22 and Oct 30.
I ended up having a healthy baby boy via planned C-section at 38 weeks. At 34 weeks I went into preterm labor (contractions 3 minutes apart), and then was able to "manage" them for the remaining 4 weeks so they were only 12 minutes apart. That last month was awful! I had to get on sleeping pills just so I could sleep at night because the pressure of the water/baby made me feel like I couldn't breathe when I laid down!
But, we made it and the baby was a healty 8 pounds, 15 ounces with an Apgar score of 8/9. There was a comical side of the delivery too, when my AF squirted out and hit a nurse. Luckily I have a great OB who was absolutely wonderful throughout the whole ordeal and the nurse had a good sense of humor.
The joys of motherhood... :)
Thanks again for this wonderful thread. It was a great source of information for me!
At Fri Aug 14, 08:11:00 PM 2009,
Anonymous said…
Dr. T,
I am 38 weeks and 5 days pregnany with my first baby. It was discovered at 37 weeks that I have high fluid, and it was an index of 26 at that time. I was checked again this week, and it went up to 28.6. I will be checked again in 3 days, and now we are faced with the decision of a possible c-section. Is that wise, with the risk of cord prolapse when my membranes rupture?
Our OB laid out everything, and is leaving the decision to us. We are leaning towards a c-section. What do you think?
KB
At Sat Nov 21, 08:16:00 AM 2009,
Anonymous said…
Dear Dr. T.,
I am 23 weeks, 4 days. I am carring twins. Baby B, was found to have Diaphagmatic Hernia. We are now finding large amounts of amniotic fluid in his sac. I am very worried, I know there are risks with them "tapping off" his sac. I need to also worry about his sister, baby a. My uturus is measuring at 33 weeks and again i'm only 23.5 weeks. What am I in for? What can I do if anything to lower his fluid levels?
Thanks so much for any advice you can give me.
Liz
At Sat Jan 09, 10:46:00 AM 2010,
Anonymous said…
I have heard from my mother-in-law (who is a RN) and an ENT, that polyhydramnios could cause deafness due to the pressure of the fluid. Is this true?
I recently had a 10 9.5oz baby girl and sufferred from this. Only my OB did not care. My baby is deaf on one side. She was also born with Unilateral Choanal Atresia. Only on the opposite side to the deaf ear. I guess i'm just looking for some answers and closure.
Could you please tell me what you think??
At Mon Jan 18, 05:40:00 PM 2010,
Kenneth F. Trofatter, Jr., MD, PhD said…
To anonymous Jan 9: I have never heard of that association and could not find it in the literature. Polyhydramnios often occurs when there are certain congenital birth defects or neurologic and neuromuscular disorders are present in the fetus. Those might be associated with the congenital deafness, but I doubt that is secondary to the polyhydramnios. Great question though and thanks for reading!
Dr T
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