Amniotic Fluid - 4 - Consequences of Decreased Amniotic Fluid
Sunday, May 11, 2008
Kenneth F. Trofatter, Jr., MD, PhD
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
18 Comments:
At Sun May 11, 01:06:00 PM 2008,
nina.nunez said…
Hi, my name is Nina.
I know I'm not posting in the right spot, but I hope you don't mind. I've looked over your archive and I'm very grateful that you take the time to address reader concerns. Here's a new one..maybe a bit challenging one for you...
I am 29 years old and have had two successful pregnancies..at 18 years of age and at 21. I am very healthy and active. When I was 24,three hemangiomas were found on my liver incidently after surgery for gallbladder removal. I saw a liver specialist who advised that I stop taking birth control pills, which I did. I recently had a liver resection (my right lobe) due to a growing, symptomatic hemangioma (7cm). It was growing near my diaphragm and caused intense shoulder and sometimes breathing pain. The surgery went very well (It was in Dec 2007). I did not need a blood transfusion and am now just about fully recovered. Prior to surgery, my LFT was completely normal. My Liver Functions are almost completely back to normal now. Of course everything was sky high immediately after surgery. The two I still have two small hemangiomas on the left lobe (1.5 cm and 2cm respectively). I still have a little bit of shoulder pain and we did a recent scan of the liver. The concern is that one of the hemangiomas that are left might still be symptomatic. It is in a subdiaphragmatic location on the left lobe. I recently remarried and would love to have another child or two. My liver surgeon thinks it would be fine with monitoring of the existing hemangiomas. My OB/GYN said he didn' think it was a great idea, but he would send me to a specialist. What are your thoughts/experiences on this? Without empirical evidence that hormones make hemangiomas grow, would pregnancy be a contraindication? How long should you wait after abdominal surgery to get pregnant? My incision ran from my sternum straight down with a slight curve towards my right rib. Approximately 12 inches long.
Thank you for your time and I look forward to hearing from you.
At Tue May 13, 06:12:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
To Nina: I would tend to agree with your surgeon. The remaining hemangiomas are small and could be easily followed during a pregnancy. I did write a post on March 2, 2008 in which I discuss "Hereditary Hemorrhagic Telangiectasias in Pregnancy." You might want to read that and ask your doctor if he/she thinks you might have this condition! With regard to another pregnancy, the surgery you had should not significantly increase your risk for complications at this point and, in your case, it may be better to try sooner than later while the hemangiomas are still small. Good luck and let us know what you decide to do and how things turn out! Dr T
At Tue May 13, 06:48:00 PM 2008,
nina said…
Thank you for your quick response. It is very interesting to read about HHT. I do know my mother had a single hemangioma on her liver. But, beyond that, we don't know of anyone else in the family that has one. I will talk to my liver specialist in Dallas about it. Thank you so much for your insight! I appreciate it!
At Thu May 15, 06:05:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
To Nina: You're welcome. Please let me know what the liver specialist thinks! Dr T
At Tue May 20, 11:43:00 AM 2008,
marti said…
Hi. I have been diagnoised with oligohydraminos at 16 weeks and anhydraminos at 24 weeks, not due to PPROM. The dr's say my baby's chances are poor once he is born. He does have some problems, they can only find one kidney. Is there anything you can do once there is no fluid? I am so devestated.
At Tue May 20, 07:11:00 PM 2008,
Anonymous said…
Hi Dr. Trofatter!
Thank you for your thorough responses to everyone's questions. I am 35 yrs old and had a very difficult first pregnancy that ended in miscarriage five weeks ago. I had bleeding at 3-7 weeks, oligohydraminos and severe hyperemesis gradvidarum the entire 4.5 mos resulting in several ER visits and hospitalizations, a CVS at 12 weeks which showed mosaic turner's syndrome, an amnio which confirmed the turner's diagnosis and my water broke at 18 weeks. My OB said it was okay to try after 1 cycle and the geneticist after 2 cycles, yet I am afraid of having another miscarriage and/or another baby with a genetic defect. I have a couple of questions regarding future pregnancies. What is the best time frame to start trying again? I could not take prenatal vitamins or folic acid during my pregnancy (it would make the nausea and hyperemesis even worse), how detrimental is this to the baby? I was taking zofran (once a day) as well as vistaril and reglan (twice a day) could these medications and the severe vomiting led to oligohydraminos.
Thank you for your assistance with my questions.
At Sun May 25, 05:40:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
To Marti May 20: No, I am afraid that if there is anhydramnios now, either the one kidney is dysplastic and nonfunctional or there is severe placental insufficiency related to whatever problem caused the baby's abnormalities. We cannot replace the fluid and hope for a better outcome under these circumstances. I am so sorry, but we are very limited in terms of being able to help under these circumstances except to pray with you. Best wishes to you, and if you think about it, please let us know what happens. Dr T
At Sun May 25, 05:47:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
To anonymous May 20: Fortunately, the risk of recurrence of the Turner's is relatively low. You should not get pregnant again until YOU are READY to do so, regadless of when it might be safe to try. That may take some counseling from what you have told me. It is hard to say if the hyperemesis was simply the result of the abnormal fetal karytoype or if this is something you will be at risk for again. I would strongly suggest at leats 2-3 months of supplemental folic acid (4 mg/day) and a multivitamin with extra Vitamin D and calcium in anticipation of the worst from the hyperemesis standpoint. I doubt the medications caused the decreased fluid. More likely there was something innately wrong with the baby and/or the placenta secondary to the chromosomal abnormality. If you do get pregnant again and have problems with hyperemesis, write back and I will give you my thoughts on what you can try. Sorry for your recent loss. Best wishes and thanks for writing! Dr T
At Thu May 29, 02:48:00 PM 2008,
Anonymous said…
Hi Doctor,
My name is Tricia and I was looking for information on low amniotic fluid for months to get a better understanding. I got pregnant in August '07 and in November '07 I started bleeding a lot. I went to the emergency room and verified that my child was still alive and that I had a blood clot in my uterus. I bled on and off for three more weeks. When I went to the OB/GYN it was discovered that I had less than 1cm of amniotic fluid (4 1/2 mths). I was put on bed rest immediately with weekly appointments to check if my baby was still alive. I was hospitalised at 23 weeks by my OB so that I could be under 24hr monitoring just in case I went into labor. I went into labor at 28wks and 6 days. Labor & Delivery lasted 2 1/2 hours. she was 2lbs 2ozs and she was not able to breathe on her own and died half an hour after.
I have a 7 year old daughter and that pregnancy went very well - no complications what so ever.
I would like to try again in spring '09. Is there anything that I can do to prevent the anhydramnios. My fluids never went over 2cm. Can this happen again.
Also in the first trimester, I would always feel something sharp stick me in my belly whenever I got up out of a chair, could there have been something inside of me sticking my uterus. I have three very, very small fibroids.
At Thu May 29, 05:47:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
Hi Tricia: Do you remember the events surrounding the bleeding at 4 and a half months? Was this after intercourse or after having fallen? Are you a smoker? Did you have any pain with the bleeding? Did they find anything wrong with the baby after it was born - abnormalities of the kidneys, heart, face , etc.? Did your doctor suspect you had ruptured the bag of waters along with the bleeding or afterwards?
Regardless, it sounds as if you had an early placental abruption (separation of the placenta from the lining of the uterus). Your baby had decreased fluid because there was not enough blood flow going through the placenta to keep the baby happy - it shut down flow to its kidneys and just stopped making urine. Unfortunately, this occurred at a critical time in the fetal lung development and without the fluid around the baby, the lungs never developed properly (pulmonary hypoplasia). That's why you baby could not breathe after birth.
I do not know if the fibroids contributed to the placental abruption, but they could have. Sometimes fibroids will be a source of inflammation and if they sit right underneath the placenta, they can cause problems, but I suspect something else happened. I am so sorry for your loss and thank you for writing. Best wishes! Dr T
At Fri Jun 06, 10:30:00 AM 2008,
Anonymous said…
Hi, my name is Denise:
4.5 years ago I was pregnant with twins. We had twin to twin transfusion. We had considerd the surgery to disconnect to two veins so this wouldn't be a concern. We decided not to and thought that a reduction of amniotic fluid later would be better for us. I was seeing a specialist a couple hours aways from where I live and with the bumps and everything i started having contractions, luckly they stopped with some medicine. My specialist wanted me to spend the rest of my pregnacy up at the hospital, several months. Considering I had a 6 year old son, whom was extremely attached to me and his dad wasn't very close to him and i didn't have anyone to watch him I said no. My husband and I decided to get a dr closer, still being over 1 hour away. I was having pains when i got up so the dr recommended me get a reduction asap, in november. During to reduction I noticed that he was taking alot of fluid 2.5 jars. Is that alot? After, they didn't give my my rh shot right away. Before christmas I told my dr I wanted to have the babies before the new year, he said that it wouldn'd be a good idea to just wait. 1.5 months after the amniotic reduction we found out the donor baby died severy days earlier. We found that out on Jan 9 my babies were 32 weeks they would have been 30 weeks if they were delivered when I wanted them to be. After my daughter was born on that day they asked me if i wanted a otopsy done while the dr was there and he said that there was no need that the baby died from not having enough fluid in her sack. my mind cannot forget and wonder if taking too much fluid from the recipient baby put too much presure on the donor baby and that's why she died. What should i do? should i investigate and find out what happened or should i just let it go?
At Sat Jun 07, 08:38:00 AM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
To Denise: I think you should just let it go, but that is so much easier said than done... I know that. TTTS is a very serious condition and even in the most experienced hands, there is a high rate of fetal loss and/or long-term complications. It sounds like you were in good hands and handled appropriately and despite everyone's best efforts, the rsults were not the best. If you have not done so already, it might be a good idea to get a counselor to hlp you work through these issues. I am sorry for your loss, even that many years ago, it still hurts. Dr T
At Wed Jun 11, 06:06:00 AM 2008,
Anonymous said…
hi,My name is lakshmi.i am 12 weeks pragnant.doctor told fluid is less around the baby. i am fearing about it.will it be a problem to the baby?what i need to do.. please advice me.
At Wed Jun 11, 07:08:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
To lakshmi: I am sorry, but I would need more information first. Why does your doctor think the fluid is too low at 12 weeks?
Dr T
At Wed Jun 11, 10:45:00 PM 2008,
Anonymous said…
Hi Doctor,I am Lakshmi....Thank u so much for your time andquick reply.Doctor adviced to take NT scan at 12 week.doctor checked the scan report and said that liquor is less for the gestational age.and also she said that baby is so tiered inside.she has given THRIVE capsules to increse the liquor.asked me to take rest in the afternoon time. But i am working as a software engineer.so if it is compulsary to take rest then i will take. she told that take the tablets and also lots of water,then come for the checkup on 28th so that i will let u know whether rest is need or not.
but i have seen in some sites and some of friends and relatives are saying that baby is not at good condition if there is no fluid at this stage. I wolud like to clear on this.now i am taking that tablet and lots of water.i will wokr for 9 hours in the office.and what could be the resons for less fluid around the baby. can you plz reply me .. and if u need the scanned reports i will attach and send u as a mail.This is my first pragnancy.so i am very fearig about it.please do reply me.
Thank u in advance.
At Sun Jun 15, 02:03:00 PM 2008,
Kenneth F. Trofatter, Jr., MD, PhD said…
Lakshmi: If there really is no fluid at this point. that is VERY bad. Either the baby has no kidneys (bilateral renal agenesis), or has dysplastic kidneys (polycystic or multicystic), or has urethral obstruction (could they see a fetal bladder), or another anomaly such as a limb-body-wall complex, or such a poor placenta that it cannot support the health of a baby even this early. Have you seen a specialist yet in Maternal-Fetal Medicine? If not, please do. Best of luck to you and let us know what you find out! Dr T
At Sat Jun 21, 12:32:00 AM 2008,
shruti said…
Hi doctor,
I am Shruti,age 28 years i had lost my 2 pregnancies due to lesser amnotic fluid.
now i am still pregnenat & Gestational age is 25 weeks 2 days my lmv is 25-12-07
i hav a similar problem in all pregnancy(problem of lessing Amnotic fluid)
Ist pregnancy supervised & detected IUGR & severe oligohydraminos(USG) at 22 weeks and the later IUD at 28 weeks.Birth weight 1.2kg,no obivious congenitial malformations and autopsy was not done.
I was detected PIH at 26 weeks and was on ALPHA METHYL DOPA 250 mg TDS & other investigation was normal.
IInd pregnancy LMP.15.5.2005 detected Hypertension at 20 weeks and is on nifedipine. On evaluation found to hav severe oligohydraminos and IUGR and reffered for targeted anomaly scan to look for the fetal pathology.
Other investigatins done are: Antiphospholipid anti body : Negative,Torch titer:Neagtive, Triple Test: i in 68,karyotype(30-11-05) 44 autosomes&2 sex cromosomes.Fetal karotype:Normal,24 hr urinary protien-203mg/24hrs,Antinuclear Anti body:+++ve Homogenous at 1:10,Anti cardiolipin anti body IgG:0.24 GPL Factor V Ledien mutation: Negative,platelet count: 276,000,APTT:31 SEC
(gone to immunology department for counselling and there was clinically no evidence of SLE.....
and when the Fetus was no more final diagnosis was that:
Fetus with Intrauterine growth retardation due to chronic placental insufficiency? secondray to Maternal Hypertension.Internal examination: there was no abnormality detected in internal organs,Placenta was shrunken, shriveled and hard,Histopathology: Multiple placental infarcts,.....
so now before my 3rd pegnancy some tests as Reproductive Immunophenotype...Natural killer cell Activity: CD3(Pan T Cell) 83.7% (63-86)CD19(B Cells) 8.6*% (3-8) CD56+CD+16+Cell9.4% (3-12) CD56 Cells 23.6* %(3-12) EStimation of CyTOkines: TH1 type cytokine estimation: TNF-594.999pg/ml (high:400-600pg/ml),Interferon assay of Latent tuberculosis: Positive for latent tuberculosis-2.209IU/ml(<0.35 IU/ml)
this is my third Pregnancy now(12.06.08) my weight is 64 kgs. B.P is 140/90, blood group is B+ve,Triple Test- Triple Test-Trisomy21 screen: Negative,NTD screening: positive>=1:50,Trisomy18 screening : Negative on 12.5.08 my AFI was approx 9.0cms but on 19.06.08 my AFI becomes 5.2cms, foetal heart rate is 176b/m.& is regular in rythm.foetal movments r sluggish.gestational age is 24 weeks 3 daysof foetus. weight is 627 gms approx. umblical cord is showing normal Cerbral ventricles r not dilated. postion of the heart within thorax is normal, foetal abdomen is normal, utres & adnexa shows no abnormality.....
But a less liquir makes my pregnancy at high risk.....
please advice me:1. how could the level of amnotic fluid could be increased ???? with the help of any capsules vaccine or any therapy.
2.did maternal hydration therapy work on me??
3. hav u got any conclusion for me that why every time amnotic fluid goes less to me in all of my pregnancy.
Please ans fast I will be thankful to u ...
At Sun Jun 22, 03:02:00 AM 2008,
shruti said…
Hi doctor,
I am Shruti,age 28 years i had lost my 2 pregnancies due to lesser amnotic fluid.
now i am still pregnenat & Gestational age is 25 weeks 2 days my lmv is 25-12-07
i hav a similar problem in all pregnancy(problem of lessing Amnotic fluid)
Ist pregnancy supervised & detected IUGR & severe oligohydraminos(USG) at 22 weeks and the later IUD at 28 weeks.Birth weight 1.2kg,no obivious congenitial malformations and autopsy was not done.
I was detected PIH at 26 weeks and was on ALPHA METHYL DOPA 250 mg TDS & other investigation was normal.
IInd pregnancy LMP.15.5.2005 detected Hypertension at 20 weeks and is on nifedipine. On evaluation found to hav severe oligohydraminos and IUGR and reffered for targeted anomaly scan to look for the fetal pathology.
Other investigatins done are: Antiphospholipid anti body : Negative,Torch titer:Neagtive, Triple Test: i in 68,karyotype(30-11-05) 44 autosomes&2 sex cromosomes.Fetal karotype:Normal,24 hr urinary protien-203mg/24hrs,Antinuclear Anti body-+++ve Homogenous at 1:10,Anti cardiolipin anti body IgG: 0.24 GPL Factor V Ledien mutation: Negative,platelet count: 276,000,APTT:31 SEC
(gone to immunology department for counselling and there was clinically no evidence of SLE.....
and when the Fetus was no more final diagnosis was that:
Fetus with Intrautterine growth retardation due to chronic placental insufficiency? secondray to Maternal Hypertension.Internal examination: there was no abnormality detected in internal organs,Placenta was shrunken, shriveled and hard,Histopathology: Multiple placental infarcts,.....
so now before my 3rd pegnancy some tests as Reproductive Immunophenotype...Natural killer cell Activity: CD3(Pan T Cell) 83.7% (63-86)CD19(B Cells) 8.6*% (3-8) CD56+CD+16+Cell9.4% (3-12) CD56 Cells 23.6* %(3-12) EStimation of CyTOkines: TH1 type cytokine estimation: TNF-594.999pg/ml (high:400-600pg/ml),Interferon assay of Latent tuberculosis: Positive for latent tuberculosis-2.209IU/ml(<0.35 IU/ml)
this is my third Pregnancy now(12.06.08) my weight is 64 kgs. B.P is 140/90, blood group is B+ve,Triple Test- Triple Test-Trisomy21 screen: Negative,NTD screening: positive>=1:50,Trisomy18 screening : Negative on 12.5.08 my AFI was approx 9.0cms but on 19.06.08 my AFI becomes 5.2cms, foetal heart rate is 176b/m.& is regular in rythm.foetal movments r sluggish.gestational age is 24 weeks 3 daysof foetus. weight is 627 gms approx. umblical cord is showing normal Cerbral ventricles r not dilated. postion of the heart within thorax is normal, foetal abdomen is normal, utres & adnexa shows no abnormality.....
But a less liquir makes my pregnancy at high risk.....
please advice me:1. how could the level of amnotic fluid could be increased ???? with the help of any capsules vaccine or any therapy.
2.did maternal hydration therapy work on me??
3. hav u got any conclusion for me that why every time amnotic fluid goes less to me in all of my pregnancy.
Please ans fast I will be thankful to u ...
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