414 maternal hydration affects amniotic fluid index (afi)

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414 415 Volume 164 Number I, Part MATERNAL HYDRATION AFFECfS AMNIOTIC FLUID INDEX (API) University of California & Childrens' Hospital, San Francisco, CA S.I.Kilpatrick,MD.PhD, K.Safford,RN!' L. L.Scheerer.MD & R.K.Laros,MD. Adequate amniotic fluid volume is considered an important aspect of fetal well being. However, the dynamics involved in control of amniotic fluid volume are not well IDlderstood. The purpose of this study was to examine our hypothesis that maternal hydration would increase AF\ in women With low AFIs. A prospective, randomized, blinded trial was designed. Women seen in our antenatal testing centers were eligible to be randomized If; 1) AFI was 2.1 - 6.0 (AFI1); 2) there were no indications for delivery; and 3) membranes were mtact. Patients who consented were randomized mto either control (C) or hydration (H) groups. The control group was instructed to drink their normal amount of fluid, while the hydration group was instructed to drink 2 liters of water two to four hours prior to the repeat AFI. The women returned for a second AFI (AF\2) the same or following day. LlAFI refers to AFI2 - AFI 1. Maternal urine specific gravity (SO) was obtained after each AFI (SOl, S02). The investigator recording AFI was blinded to the patient's group. Means ± standard deviations analyzed with Student's T test. AFll AFI2 Ll AFI SOl S02 4.8±.87 5.1±l.0 .31±.86 l.012± .009 H N;20 4.7±.80 6.6±2.5* l.92±2.4* l.01l± * p:C .01 H vs C .006 l.013± .007 1.005± .008* Conclusjogs; We have shown that AFI varies little within one patient over approximately 24 hours as illustrated by our control group. This supports the reliability and reproducibility of AFI. But perhaps most intriguing are the results that AF\ may be elevated simply by increasing maternal water intake. The clinical importance of augmenting amniotic fluid volume with maternal hydration merits further investigation. AMNIOTIC FLUID INDEX (AFI) AND OUTCOME IN POSTDATES PREONANCIES Children's Hospital & University of California, San Francisco, CA. S.I.Kilpatrick MD PhD, T.Pomeroy,RNX, C.lohnson,RNx, E.Main,MD & L.Scheerer,MD. AFI 5.Ocm has been shown to be associated with higher perinatal morbidity in county hospital patients seen for antenatal testing for various indications. We were interested in whether this relationship exists specifically in postdates patients from a private hospital setting as well. Between 8/1/89 and 7/31/90 all patients referred for postdates antenatal testing had an AFI recorded. Delivery data were entered into a comprehensive computer database program (Main et aI., SPO, 1989) at the time of patient discharge. Outcome variables were compared between patients, whose last AFI was days before delivery, in three AFI groups: 1) 2) 2.1-5.Ocm; and 3) The mean gestational age was 41.1, 41.8, and 41.6 weeks, in the 2.1-5.0, and >5.1 respectively. Thick CIS Fetal distress ICN Meconium in labor admission N;ll 30% 55% 18% 18% 2.1-5.0cm N;24 36% 50% 21% 8% N;159 15%* 29%* 9% 4% Chi Square Conclusion' In a private hospital setting AFI in postdates patients was associated with a significant increase in the incidence of thick meconium and Cesarean delivery. Further, there was a trend for an increase in fetal distress in labor and admission to the ICN. Although the N was small, it is noteworthy that the morbidity in the group is no different than that in the 2.1-5.Ocm group. Our data suggest induction should be considered in postdates patients with an 416 417 SPO Abstracts 36 FETAL URINE PRODUCTION IN PATIENTS WITH OLIGOHYDRAMNIOS_ LJ Groome, J Owen, CL Neelyx, JC Hauth_ University of Alabama School of Medicine, Birmingham, Alabama. Oligohydramnios (oligo) may be the result of a hypoxemia-induced reduction in renal blood flow, impairing fetal urine production. To assess the clinical significance of this observation, we compared the intrapartum fetal heart rate (FHR) patterns in 51 women with oligo at 38 weeks gestation to the proximate antepartum rate of fetal urine production. The mean hourly fetal urine production rate (HFUPR) was found to decrease significantly with increasing degrees of fetal compromise (Figure): the mean HFUPR was 95 ml/hr in the absence of fetal distress (FD); this fell to 59 ml/hr for fetuses who had an abnormal intrapartum FHR pattern but responded to i n t r aut e r i n e resuscitation, and to 33 ml/hr for fetuses delivered abdominally (C/S) for fetal distress_ These results suggest that oligo associated with a low . E •• 1- ;. I:: . i: 1: , 0 FD Fl.' HFUPR may identify those fetuses with less intrinsic or uteroplacental reserve than those with oligo and a higher rate of fetal urine production. The former fetuses are more likely to develop a significantly abnormal FHR pattern in the intrapartum period. DEVELOPMENT OF THE FETAL RESPONSE DECREMENT. LJ Groome, SJ Gotlieb x , CL Neelyx, MD Waters x , GD Colwell x _ The University of Alabama School of Medicine, Birmingham, Alabama Fetal response to acoustic stimulation (AS) assesses the acoustic startle response (ASR) , whereas repeated AS tests the neural circuitry governing motor inhibition. Response decrement is a measure of the ability to inhibit motor response and is a more mature form of behavior than is persistenb response. Here we examine developmental changes in the nature of the fetal ASR to repeated AS. Eighty-seven normal fetuses (28-32 wks; >32-36 wks; 36-40 wks) received a 2 sec on/5 sec off sound stimulus (74dB at 1m air) for a total of 14 trials. Fetal movement was graded according to intensity: fast general (3); fast local (2) ; slow roll 2 (1); and no movement rql Q.l 26-32 (N-32) .. 32-36 (N-33) - 36-40 (N-22) (0) . Fetuses responded similarly to the first stimulus regardless of age (Figure)_ However, there is a significant I..L.. 1 3 5 7 9 11 13 16 Trial developmental trend (p < 0.05) in response decrement: response decrement occurred faster in fetuses> 32 wks. Thus, although the neural mechanism governing the ASR is functional by 28 wks, maturation of the motor-inhibition circuitry does not occur until later in gestation.

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414

415

Volume 164 Number I, Part ~

MATERNAL HYDRATION AFFECfS AMNIOTIC FLUID INDEX (API) University of California & Childrens' Hospital, San Francisco, CA S.I.Kilpatrick,MD.PhD, K.Safford,RN!' T.Pomeroy,RN~ L. Hoedt,RN~ L.Scheerer.MD & R.K.Laros,MD.

Adequate amniotic fluid volume is considered an important aspect of fetal well being. However, the dynamics involved in control of amniotic fluid volume are not well IDlderstood. The purpose of this study was to examine our hypothesis that maternal hydration would increase AF\ in women With low AFIs. ~: A prospective, randomized, blinded trial was designed. Women seen in our antenatal testing centers were eligible to be randomized If; 1) AFI was 2.1 - 6.0 (AFI1); 2) there were no indications for delivery; and 3) membranes were mtact. Patients who consented were randomized mto either control (C) or hydration (H) groups. The control group was instructed to drink their normal amount of fluid, while the hydration group was instructed to drink 2 liters of water two to four hours prior to the repeat AFI. The women returned for a second AFI (AF\2) the same or following day. LlAFI refers to AFI2 - AFI 1. Maternal urine specific gravity (SO) was obtained after each AFI (SOl, S02). The investigator recording AFI was blinded to the patient's group. ~: Means ± standard deviations analyzed with Student's T test.

AFll AFI2 Ll AFI SOl S02

4.8±.87 5.1±l.0 .31±.86 l.012± .009

H N;20 4.7±.80 6.6±2.5* l.92±2.4* l.01l± * p:C .01 H vs C .006

l.013± .007

1.005± .008*

Conclusjogs; We have shown that AFI varies little within one patient over approximately 24 hours as illustrated by our control group. This supports the reliability and reproducibility of AFI. But perhaps most intriguing are the results that AF\ may be elevated simply by increasing maternal water intake. The clinical importance of augmenting amniotic fluid volume with maternal hydration merits further investigation.

AMNIOTIC FLUID INDEX (AFI) AND OUTCOME IN POSTDATES PREONANCIES Children's Hospital & University of California, San Francisco, CA. S.I.Kilpatrick MD PhD, T.Pomeroy,RNX, C.lohnson,RNx, E.Main,MD & L.Scheerer,MD.

AFI ~ 5.Ocm has been shown to be associated with higher perinatal morbidity in county hospital patients seen for antenatal testing for various indications. We were interested in whether this relationship exists specifically in postdates patients from a private hospital setting as well. ~: Between 8/1/89 and 7/31/90 all patients referred for postdates antenatal testing had an AFI recorded. Delivery data were entered into a comprehensive computer database program (Main et aI., SPO, 1989) at the time of patient discharge. Outcome variables were compared between patients, whose last AFI was ~7 days before delivery, in three AFI groups: 1) ~2.Ocm; 2) 2.1-5.Ocm; and 3) ~5.1cm. ~: The mean gestational age was 41.1, 41.8, and 41.6 weeks, in the ~2.0, 2.1-5.0, and >5.1 ~roups, respectively.

Thick CIS Fetal distress ICN Meconium in labor admission

~2.0cm N;ll 30% 55% 18% 18%

2.1-5.0cm N;24 36% 50% 21% 8%

~5.1cm N;159 15%* 29%* 9% 4%

*~.05 Chi Square Conclusion' In a private hospital setting AFI ~5.0cm in postdates patients was associated with a significant increase in the incidence of thick meconium and Cesarean delivery. Further, there was a trend for an increase in fetal distress in labor and admission to the ICN. Although the N was small, it is noteworthy that the morbidity in the ~2.Ocm group is no different than that in the 2.1-5.Ocm group. Our data suggest induction should be considered in postdates patients with an AFI~5.0cm.

416

417

SPO Abstracts 36

FETAL URINE PRODUCTION IN PATIENTS WITH OLIGOHYDRAMNIOS_ LJ Groome, J Owen, CL Neelyx, JC Hauth_ University of Alabama School of Medicine, Birmingham, Alabama.

Oligohydramnios (oligo) may be the result of a hypoxemia-induced reduction in renal blood flow, impairing fetal urine production. To assess the clinical significance of this observation, we compared the intrapartum fetal heart rate (FHR) patterns in 51 women with oligo at ~ 38 weeks gestation to the proximate antepartum rate of fetal urine production. The mean hourly fetal urine production rate (HFUPR) was found to decrease significantly with increasing degrees of fetal compromise (Figure): the mean HFUPR was 95 ml/hr in the absence of fetal distress (FD); this fell to 59 ml/hr for fetuses who had an abnormal intrapartum FHR pattern but responded to i n t r aut e r i n e resuscitation, and to 33 ml/hr for fetuses delivered abdominally (C/S) for fetal distress_ These results suggest that oligo associated with a low

~:[i . E •• 1- •

~' ~ ;. ~w I:: ~ I·

. i: 1: , 0 FD Fl.' ~F.cD_-';"I7'i

HFUPR may identify those fetuses with less intrinsic or uteroplacental reserve than those with oligo and a higher rate of fetal urine production. The former fetuses are more likely to develop a significantly abnormal FHR pattern in the intrapartum period.

DEVELOPMENT OF THE FETAL RESPONSE DECREMENT. LJ Groome, SJ Gotliebx, CL Neelyx, MD Watersx, GD Colwellx_ The University of Alabama School of Medicine, Birmingham, Alabama

Fetal response to acoustic stimulation (AS) assesses the acoustic startle response (ASR) , whereas repeated AS tests the neural circuitry governing motor inhibition. Response decrement is a measure of the ability to inhibit motor response and is a more mature form of behavior than is persistenb response. Here we examine developmental changes in the nature of the fetal ASR to repeated AS. Eighty-seven normal fetuses (28-32 wks; >32-36 wks; 36-40 wks) received a 2 sec on/5 sec off sound stimulus (74dB at 1m air) for a total of 14 trials. Fetal movement was graded according to intensity: fast general (3); fast ~ local (2) ; slow roll ~ 2

(1); and no movement rql Q.l

• 26-32 (N-32) .. 32-36 (N-33) - 36-40 (N-22)

(0) . Fetuses responded similarly to the first stimulus regardless of age (Figure)_ However, there is a significant

I..L.. o'L~~--'----L-,=~:El 1 3 5 7 9 11 13 16

Trial

developmental trend (p < 0.05) in response decrement: response decrement occurred faster in fetuses> 32 wks. Thus, although the neural mechanism governing the ASR is functional by 28 wks, maturation of the motor-inhibition circuitry does not occur until later in gestation.