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Amniotic fluid IUGR Post date

Dr. Wajeih ALAali, SSCOG, ABOG, MFMConsultant OBGYN and Fetal medicine

1

Amniotic fluid

Protects the fetus from mechanical trauma

Bacteriostatic

Development of both the lungs and the limbs.

Fetal diagnosis

2

Volume

10 mL at 8 weeks

630 mL at 22 weeks

770 mL at 28 weeks

After 30 weeks, the increase slows

515 mL at 41 weeks

3

48 PART 1 Scientific Basis of Perinatal Biology

mechanisms act to maintain AF volume, and there is some evidence that they may be regulated to normalize AF volume in pathologic conditions.

The major contributors to AF volume in the latter portion of pregnancy are fetal urine and fluid produced by the fetal lung. Minor contributors are transudation across the umbilical cord and skin and water produced as a result of fetal metabo-lism. Although some data on these processes in the human fetus are available, the bulk of the information about fetal AF circula-tion derives from animal models, primarily the sheep.

URINE PRODUCTION

Although the mesonephros can produce urine by 5 weeks of gestation, the metanephros (the adult kidney) develops later, with nephrons formed at 9 to 11 weeks,20 at which time fetal urine is excreted into the AF. The amount of urine produced increases progressively with advancing gestation, and it consti-tutes a significant proportion of the AF in the second half of pregnancy.21 The amount of urine produced by the human fetus has been estimated by the use of ultrasound assessment of fetal bladder volume.22 Although there continues to be uncertainty regarding the accuracy of noninvasive measurements, human fetal urine output appears to increase from 110 mL/kg/24 hr at 25 weeks to almost 200 mL/kg/24 hr at term,22,23 in the range of 25% of body weight per day or almost 1000 mL/day near term.22,24-26 In near-term fetal sheep, with direct methods used for measuring urine production rates, similar high values have been found.27-29 There may be a tendency for the urine flow rate to decrease after 40 weeks gestation, particularly if oligohy-dramnios is present.30

Reduction or absence of fetal urine flow is commonly associ-ated with oligohydramnios, indicating that urine flow is

latter half of pregnancy, most commonly in the sheep model. Evidence suggests that the entire volume of AF turns over on a daily basis,18 making this a highly dynamic system. The volume of AF is influenced by a complex interplay of productive and absorptive mechanisms (Fig. 3-2).19 These

Figure 3-1 Amniotic fluid volumes from 8 to 44 weeks of human gestation. Dots repre-sent mean measurements for each 2-week interval. Shaded area indicates the 95% confi-dence interval (2.5 to 97.5 percentiles). (From Brace RA, Wolf EJ: Normal amniotic fluid volume changes throughout pregnancy, Am J Obstet Gynecol 161:382388, 1989.)

Am

niot

ic fl

uid

volu

me

(mL)

Gestational age (weeks)

0

500

1000

1500

2000

2500

8 12 16 20 24 28 32 36 40 44

1%5%25%50%

75%

95%

99%

Figure 3-2 Circulation of amniotic fluid water to and from the fetus. (Modified from Seeds AE: Current concepts of amniotic fluid dynamics, Am J Obstet Gynecol 138:575, 1980.)

Lung fluid

Swallowing

Urine

Intramembranouspathway

Amnion

Chorionlaeve

Placenta

Amniotic fluid

4AF, IUGR, IUFD - November 3, 2016

Composition of Amniotic Fluid

First trimester: isotonic with maternal or fetal plasma minimal protein components. extremely low oxygen tension and an increased concentration of sugar alcohols

Second half of pregnancy: urea, creatinine, and uric acid increase

5

Production of Amniotic Fluid Early pregnancy:

nonkeratinized fetal skin

From the mother across the uterine decidua or the placenta surface

Second half of pregnancy

Urine production

Fetal lung fluid

6

48 PART 1 Scientific Basis of Perinatal Biology

mechanisms act to maintain AF volume, and there is some evidence that they may be regulated to normalize AF volume in pathologic conditions.

The major contributors to AF volume in the latter portion of pregnancy are fetal urine and fluid produced by the fetal lung. Minor contributors are transudation across the umbilical cord and skin and water produced as a result of fetal metabo-lism. Although some data on these processes in the human fetus are available, the bulk of the information about fetal AF circula-tion derives from animal models, primarily the sheep.

URINE PRODUCTION

Although the mesonephros can produce urine by 5 weeks of gestation, the metanephros (the adult kidney) develops later, with nephrons formed at 9 to 11 weeks,20 at which time fetal urine is excreted into the AF. The amount of urine produced increases progressively with advancing gestation, and it consti-tutes a significant proportion of the AF in the second half of pregnancy.21 The amount of urine produced by the human fetus has been estimated by the use of ultrasound assessment of fetal bladder volume.22 Although there continues to be uncertainty regarding the accuracy of noninvasive measurements, human fetal urine output appears to increase from 110 mL/kg/24 hr at 25 weeks to almost 200 mL/kg/24 hr at term,22,23 in the range of 25% of body weight per day or almost 1000 mL/day near term.22,24-26 In near-term fetal sheep, with direct methods used for measuring urine production rates, similar high values have been found.27-29 There may be a tendency for the urine flow rate to decrease after 40 weeks gestation, particularly if oligohy-dramnios is present.30

Reduction or absence of fetal urine flow is commonly associ-ated with oligohydramnios, indicating that urine flow is

latter half of pregnancy, most commonly in the sheep model. Evidence suggests that the entire volume of AF turns over on a daily basis,18 making this a highly dynamic system. The volume of AF is influenced by a complex interplay of productive and absorptive mechanisms (Fig. 3-2).19 These

Figure 3-1 Amniotic fluid volumes from 8 to 44 weeks of human gestation. Dots repre-sent mean measurements for each 2-week interval. Shaded area indicates the 95% confi-dence interval (2.5 to 97.5 percentiles). (From Brace RA, Wolf EJ: Normal amniotic fluid volume changes throughout pregnancy, Am J Obstet Gynecol 161:382388, 1989.)

Am

niot

ic fl

uid

volu

me

(mL)

Gestational age (weeks)

0

500

1000

1500

2000

2500

8 12 16 20 24 28 32 36 40 44

1%5%25%50%

75%

95%

99%

Figure 3-2 Circulation of amniotic fluid water to and from the fetus. (Modified from Seeds AE: Current concepts of amniotic fluid dynamics, Am J Obstet Gynecol 138:575, 1980.)

Lung fluid

Swallowing

Urine

Intramembranouspathway

Amnion

Chorionlaeve

Placenta

Amniotic fluid

7

Amniotic fluid abnormality

Polyhydraqmnios: Amniotic fluid index (AFI) > 24 cm or a single pocket of fluid at least 8 cm in depth that results in an amniotic fluid volume of more than 2000 mL

Oligohydramnios: AFI < 7 cm or the absence of a fluid pocket 2-3 cm in depth.


Polyhydramnios Causes:

Poorly controlled maternal diabetes mellitus

Fetal anomalies: CNS abnormalities and neuromuscular diseases

Congenital cardiac-rhythm anomalies , hydrops

twin-to-twin transfusion syndrome

Fetal infection- TORCH

Chromosomal abnormalities

Fetal akinesia syndrome

Idiopathic

9

Polyhydramnios Laboratory Workup:

OGTT

Kleihauer-Betke test to evaluate fetal-maternal hemorrhage

Hemoglobin Bart in patients of Asian descent (who may be heterozygous for alpha-thalassemia)

Fetal karyotyping for trisomy 21, 13, and 18

TORCH

Blood group and antibody assessment

10

Polyhydramnios Ultrasound Workup:

Evaluate the fetal anatomy; assess for diaphragmatic hernia, lung masses, and the absence of the stomach bubble. The double-bubble sign!

A macrosomic fetus is observed in association with poorly controlled maternal diabetes.

Assess the blood flow velocity in the middle cerebral artery of the fetus for fetal anemia.

Test for fetal arrhythmias and malformations

Large abdominal circumference may be observed with ascites and hydrops fetalis.

11

Polyhydramnios

Medical care:

Higher incidence of preterm labor secondary to overdistention of the uterus.

Weekly or twice weekly perinatal visits and cervical examinations.

Bed rest to decrease the likelihood of preterm labor.

Serial ultrasonography to determine the AFI and document fetal growth.

Fetal anemia


Oligohydramnios

13

Oligohydramnios Causes:

PROM and chronic leakage of the amniotic fluid

Fetal urinary tract anomalies, such as renal agenesis, polycystic kidneys, or any urinary obstructive lesion

Placental insufficiency, as seen in pregnancy-induced hypertension (PIH), maternal diabetes, or postmaturity syndrome

Maternal use of prostaglandin synthase inhibitors or ACE inhibitors

14

Oligohydramnios

Laboratory Workup:

Nitrazine test

Ferning test

PAMG-1 test

placental insufficiency tests

15

Oligohydramnios Ultrasound Workup:

Visualize the fetal kidneys, collecting system, and bladder. If these are normal, suspect the chronic leakage of amniotic fluid or hypertensive disorders.

Assess fetal growth. If PROM or urinary tract anomalies are absent, consider placental insufficiency and IUGR.

Uterine artery Doppler study findings may aid in the diagnosis of placental insufficiency.


Intrauterine Growth Restriction

17

Intrauterine Growth Restriction

Definition:

Birth weight of a newborn infant is below the 10th percentile for a given gestational age

18

Growth-restricted fetuses at risk of:

meconium aspiration

asphyxia

polycythemia

hypoglycemia

mental retardation.

Adult onset conditions such as hypertension, diabetes, and atherosclerosis

19

ETIOLOGY

Maternal

Placental

Fetal


ETIOLOGY Maternal:

poor nutritional intake

cigarette smoking

drug abuse

early cardiovascular disease

hypertension & diabetes

obesity

alcoholism

cyanotic heart disease

pulmonary insufficiency

antiphospholipid syndrome

thrombophilias

21

ETIOLOGY Placental:

placental insufficiency; essential hypertension, obesity (associated with leptin resistance which leads to placental dysfunction), chronic renal disease, and gestational hypertension

placental or cord abnormalities Fetal

Intrauterine infection (listeriosis and TORCH)

Congenital anomalies.

22

23

Types of IUGR Symmetrical:

Early onset

HC/AC ratio may be normal

Intrauterine infections, congenital fetal anomalies or chromosomal abnormality

Asymmetrical:

Late in pregnancy

Normal head size, small AC.

Inadequate nutrition, low glycogen in liver.


DIAGNOSIS

Accurate dating LMP

First trimester US: CRL

Clinical assessment

FH Audible, FM perception

25

DIAGNOSIS Ultrasound

Fetal weight parameters: BPD, HC, AC, FL

Serial fetal growth assessment

AFI

Umbilical Artery Doppler

MCA Doppler

DV Doppler

26

Figure 2: Abnormal Development of the umbilical artery

A review of 12 randomized, controlled trials of Doppler ultrasonography of the umbilical artery in high-risk pregnancies reported that, in the Doppler group, there was a significant reduction in the number of antenatal admissions (44%, 95% confidence interval (CI) 2857%), induction of labor (20%, 95% CI 1028%), and Cesarean

section for fetal distress (52%, 95% CI 2469%) 37. Furthermore, the clinical action guided by Dopplerultrasonography reduced the odds of perinatal death by 38% (95% CI 1555%). Post hoc analyses revealed a statistically significant reduction in elective delivery, intrapartum fetal distress, and hypoxic encephalopathy in the Doppler group. It was concluded that there is now compelling evidence that women with high-risk pregnancies, including pre-eclampsia and suspected intrauterine growth restriction, should be offered Doppler ultrasonographic

study of umbilical artery waveforms 37.

In terms of monitoring growth-restricted pregnancies, abnormal waveforms in the umbilical artery are an early sign of fetal impairment. For example, Bekedam et al. followed up growth-restricted fetuses longitudinally and reported thatabnormalities in the umbilical artery preceded the occurrence of cardiotocographic signs of fetal hypoxemia in more

than 90% of cases 38. The median time interval between absence of end-diastolic frequencies and the onset of late decelerations was 12 days (range 049 days).

Fetal arterial blood flow redistribution

In fetal hypoxemia, there is an increase in the blood supply to the brain, myocardium and the adrenal glands and reduction in the perfusion of the kidneys, gastrointestinal tract and the lower extremities (Figure 3 and 4, Table 1 )3966. Although knowledge of the factors governing circulatory readjustments and their mechanism of action is incomplete, it appears that partial pressures of oxygen and carbon dioxide play a role, presumably through their action on chemoreceptors. This mechanism allows preferential delivery of nutrients and oxygen to vital organs, thereby compensating for diminished placental resources. However, compensation through cerebral vasodilatation islimited and a plateau corresponding to a nadir of pulsatility index (PI) in cerebral vessels is reached at least 2 weeks before the development of the fetus is jeopardized. Consequently, arterial vessels are unsuitable for longitudinalmonitoring of growth-restricted fetuses. Cardiac and venous velocity waveforms give more information regarding fetal well-being or compromise.

Abnormal Development of the umbilical artery

Umbilical arteries - high pulsatility index

Umbilical arteries - high pulsatility index

Umbilical arteries - very high pulsatility index. - end diastolic velocity - pulsation in the umbilical vein

Umbilical arteries Severe cases absence of reversal of end diastolic frequencies

27

Management

Prevention

Previous history: Uterine artery Doppler, Previous workup. Start ASA

Optimise general health condition

APL ASA

Thombophilia LMWH


Management Antepartum

Assess modifiable risks

US

Fetal well being tests: NST, BPP, Doppler study, Fetal kick chart

Amniocentesis

TORCH

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abnormalities in flow can identify fetuses with the worstoutcomes. Further research is needed to evaluate the optimaltiming of delivery with the above abnormalities in fetal bloodflow.

Fetal Kick CountsThere is insufficient evidence (no trials) to assess the effect offetal kick counts specifically for FGR fetuses.

NST/CardiotocographyMonitoring of the fetal heart rate is commonly referred to asNST, or as cardiotocography (CTG). CTG has not been well-evaluated with high-quality studies in FGR. When comparingCTG with no CTG, there is no difference in the prediction ofperinatal mortality, preventable deaths, or cesarean sections(154). Computerized CTG may improve perinatal mortalitywhen compared to traditional CTG (154). However, this anal-ysis was not limited to FGR fetuses, and the benefit of ante-natal CTG has yet to be fully investigated in this population. Inmany management schemas, CTG has been cited as a standardmonitoring tool, despite the lack of rigorous studies proving itsefficacy (1). Nonreactive and abnormal CTG has been associ-ated with acidosis and hypoxemia, (155,156) and this justifiesits use as a screening tool for fetal well-being.

Biophysical ProfileEvidence from RCTs does not support the use of BPP as a testof fetal well-being in high-risk pregnancies (157). In high-

risk pregnancies (including FGR, post-term pregnancies,hypertensive disorders, or other conditions), when comparinga BPP to other tests of fetal well-being, there is no difference inperinatal deaths or low Apgar scores (157). Although theoverall incidence of adverse outcomes was low, there is nosignificant differences between the groups in perinatal deaths(RR 1.33, 95% CI 0.602.98) or in Apgar score

IUFD

Fetal death after 20 weeks gestation but before the onset of labor.

1% of pregnancies.

33

Risk factors


non-Hispanic black race, nulliparity or multiparity (>5),unmarried status, low socioeconomic status, low education,multiple gestation, assisted reproductive technology, and pastobstetric history (previous stillbirth, preterm delivery, orgrowth restriction) (616). Obesity, smoking, drug, and alco-hol abuse are common modifiable risk factors for fetal death.Pesticides, radiation, and fertility drugs have also been asso-ciated with fetal death. In developing countries, the mostcommon causes of stillbirths are complications of labor andinfections. Basic emergency obstetric care, births in adequatefacilities with option for safe cesarean delivery (CD), improve-ment in nutrition, and prevention and treatment of syphilisand malaria are the most feasible and cost-effective interven-tions in developing countries to decrease the incidence ofstillbirth (17).

PREVENTIONSome of the risk factors listed in Table 54.1, in particularobesity, smoking, and drug and alcohol abuse, are modifiable,and should be avoided. As the vast majority of fetal deathsoccur in developing countries, interventions should be focusedon prevention in these settings, and include (18) the following:

l Periconception folate fortificationl Insecticide-treated bed nets or intermittent preventative

treatment for malarial Syphilis detection and treatmentl Detection and treatment of hypertensive disordersl Detection and management of diabetes in pregnancyl Detection and management of FGRl Induction at 41 weeks (prevention of postterm pregnancy)l Skilled care at birthl Basic and comprehensive emergency obstetric care

PREGNANCY MANAGEMENTCounselingCounseling should include review of possible etiologies(Table 54.1), workup (Table 54.2), delivery options, as well as

Table 54.1 Associations/Risk Factors/Possible Etiologies of Fetal Death

Maternal risk factors Fetal risk factors

Chronic hypertensionPreeclampsiaDiabetes mellitus, thyroid disordersRenal diseaseSystemic lupus erythematosusAutoimmune diseaseAntiphospholipid syndromeCholestasis of pregnancyAlloimmunizationObesitySubstance abuse (especially cocaine, alcohol, coffee:>3 cups/day, etc.)

SmokingViral infections:

Parvovirus B19CytomegalovirusEnteroviruses (e.g., coxsackie virus)EchovirusesHSV-1, HSV-2HIV

Bacterial infections:Listeria monocytogenesEscherichia coliGroup B streptococciUreaplasma urealyticumTreponema pallidum

Parasitic infections:Toxoplasma gondii

Uterine malformationsAbdominal trauma

Congenital malformations (1520%)Chromosomal/genetic abnormalities (813%): monosomy X,trisomy 21, trisomy 18, and trisomy 13

Single gene disorders: hemoglobinopathies (e.g., alpha-thalasse-mia); metabolic diseases (e.g., SmithLemliOpitz syndrome)

Glycogen storage diseasesPeroxisomal disorders amino acid disordersConfined placental mosaicism (aneuploidy in placenta with a euploidfetus)

Placental abruption, placenta and vasa previaPlacental pathology

Chronic villitisMassive chorionic intervillositis

Complications of multifetal gestation (e.g., twin-twin transfusion, twinreversed arterial perfusion syndrome, and discordant growth)

Umbilical cord complications, fetomaternal hemorrhageFetal growth restrictionUteroplacental insufficiencyIntrauterine asphyxiaPreterm labor or rupture of membranesPostterm

In bold, most common associations.

Table 54.2 Maternal and Fetal Investigation for Fetal Death

Predeliveryl Amniotic fluid for cytogeneticsl Screen for coagulopathy (only if fetal death > 4 wk from delivery)l CBC, antibody screen, urine drug screenl KleihauerBetke testing or flow cytometryl Lupus anticoagulant, anticardiolipin antibodies (IgM, IgG) and

anti-b2-glycoprotein antibodies (IgM, IgG)l Parvovirus B19 titers (IgM, and IgG)a

l Syphilis testing (RPR or VDRL)l Thyroid-stimulating hormonel Glucose screening (oral glucose tolerance test, hemoglobin

A1C) (if glucose screening not done in pregnancy)l Thrombophilia workup only to be considered in cases of severe

placental infarcts, fetal growth restriction, or in the setting of apersonal history of thrombosis (factor V Leiden mutation;G20210A prothrombin gene mutation; antithrombin III)

Postdeliveryl Cord blood for cytogeneticsl Autopsy and placental examinationl Protein C, protein S activity (in selected cases as described

above for other thrombophilia workup)

aConsider workup for parvovirus especially in cases with fetal hydrops orother signs of this viral infection

FETAL DEATH 391

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Diagnosis Suspect

Absence of fetal movements

Uterus is small for dates

Fetal heart tones are not detected

Confirm by US

NO FH activity

Overlapping of skull bones (Spalding sign)

Gas shadow in fetal heart (Robert sign)

35

Management

Expectant management: weekly coagulation

IOL: Prostaglandin, Misoprostol


Work up


non-Hispanic black race, nulliparity or multiparity (>5),unmarried status, low socioeconomic status, low education,multiple gestation, assisted reproductive technology, and pastobstetric history (previous stillbirth, preterm delivery, orgrowth restriction) (616). Obesity, smoking, drug, and alco-hol abuse are common modifiable risk factors for fetal death.Pesticides, radiation, and fertility drugs have also been asso-ciated with fetal death. In developing countries, the mostcommon causes of stillbirths are complications of labor andinfections. Basic emergency obstetric care, births in adequatefacilities with option for safe cesarean delivery (CD), improve-ment in nutrition, and prevention and treatment of syphilisand malaria are the most feasible and cost-effective interven-tions in developing countries to decrease the incidence ofstillbirth (17).

PREVENTIONSome of the risk factors listed in Table 54.1, in particularobesity, smoking, and drug and alcohol abuse, are modifiable,and should be avoided. As the vast majority of fetal deathsoccur in developing countries, interventions should be focusedon prevention in these settings, and include (18) the following:

l Periconception folate fortificationl Insecticide-treated bed nets or intermittent preventative

treatment for malarial Syphilis detection and treatmentl Detection and treatment of hypertensive disordersl Detection and management of diabetes in pregnancyl Detection and management of FGRl Induction at 41 weeks (prevention of postterm pregnancy)l Skilled care at birthl Basic and comprehensive emergency obstetric care

PREGNANCY MANAGEMENTCounselingCounseling should include review of possible etiologies(Table 54.1), workup (Table 54.2), delivery options, as well as

Table 54.1 Associations/Risk Factors/Possible Etiologies of Fetal Death

Maternal risk factors Fetal risk factors

Chronic hypertensionPreeclampsiaDiabetes mellitus, thyroid disordersRenal diseaseSystemic lupus erythematosusAutoimmune diseaseAntiphospholipid syndromeCholestasis of pregnancyAlloimmunizationObesitySubstance abuse (especially cocaine, alcohol, coffee:>3 cups/day, etc.)

SmokingViral infections:

Parvovirus B19CytomegalovirusEnteroviruses (e.g., coxsackie virus)EchovirusesHSV-1, HSV-2HIV

Bacterial infections:Listeria monocytogenesEscherichia coliGroup B streptococciUreaplasma urealyticumTreponema pallidum

Parasitic infections:Toxoplasma gondii

Uterine malformationsAbdominal trauma

Congenital malformations (1520%)Chromosomal/genetic abnormalities (813%): monosomy X,trisomy 21, trisomy 18, and trisomy 13

Single gene disorders: hemoglobinopathies (e.g., alpha-thalasse-mia); metabolic diseases (e.g., SmithLemliOpitz syndrome)

Glycogen storage diseasesPeroxisomal disorders amino acid disordersConfined placental mosaicism (aneuploidy in placenta with a euploidfetus)

Placental abruption, placenta and vasa previaPlacental pathology

Chronic villitisMassive chorionic intervillositis

Complications of multifetal gestation (e.g., twin-twin transfusion, twinreversed arterial perfusion syndrome, and discordant growth)

Umbilical cord complications, fetomaternal hemorrhageFetal growth restrictionUteroplacental insufficiencyIntrauterine asphyxiaPreterm labor or rupture of membranesPostterm

In bold, most common associations.

Table 54.2 Maternal and Fetal Investigation for Fetal Death

Predeliveryl Amniotic fluid for cytogeneticsl Screen for coagulopathy (only if fetal death > 4 wk from delivery)l CBC, antibody screen, urine drug screenl KleihauerBetke testing or flow cytometryl Lupus anticoagulant, anticardiolipin antibodies (IgM, IgG) and

anti-b2-glycoprotein antibodies (IgM, IgG)l Parvovirus B19 titers (IgM, and IgG)a

l Syphilis testing (RPR or VDRL)l Thyroid-stimulating hormonel Glucose screening (oral glucose tolerance test, hemoglobin

A1C) (if glucose screening not done in pregnancy)l Thrombophilia workup only to be considered in cases of severe

placental infarcts, fetal growth restriction, or in the setting of apersonal history of thrombosis (factor V Leiden mutation;G20210A prothrombin gene mutation; antithrombin III)

Postdeliveryl Cord blood for cytogeneticsl Autopsy and placental examinationl Protein C, protein S activity (in selected cases as described

above for other thrombophilia workup)

aConsider workup for parvovirus especially in cases with fetal hydrops orother signs of this viral infection

FETAL DEATH 391

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Questions ?

38

AF, IUGR, IUFD - November 3, 2016

af, iugr, iufd - wikispaces iugr, iufd .pdf... · pathway amnion chorion laeve placenta amniotic...

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