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Amniotic fluid and cord prolapse
Dr. Wajeih ALAali, SSCOG, ABOG, MFMConsultant OBGYN and Fetal medicine
Amniotic fluid
❖ Protects the fetus from mechanical trauma
❖ Bacteriostatic
❖ Development of both the lungs and the limbs.
❖ Fetal diagnosis
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
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 161:382–388, 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
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
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
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 161:382–388, 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
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
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
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.
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
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
Oligohydramnios
Laboratory Workup:
❖ Nitrazine test
❖ Ferning test
❖ PAMG-1 test
❖ placental insufficiency tests
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.
Cord prolapse
Cord prolapse
❖ The cord lies in front of the presenting part and the fetal membranes are ruptured
❖ umbilical cord passes through the cervix at the same time as or in advance of the fetal presenting part.
Cord prolapse
❖ Occult: cord passes through the cervix alongside the fetal presenting part; it is neither visible nor palpable.
❖ Overt: cord presents in advance of the fetus and is visible or palpable within the vaginal vault or even past the labia.
Risk factors
9/8/16, 10:25 PMUmbilical cord prolapse | Contemporary OB/GYN
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UCP can be occult or overt. Occult prolapse occurs when the cord passes through the
cervix alongside the fetal presenting part; it is neither visible nor palpable. In overt
prolapse, the cord presents in advance of the fetus and is visible or palpable within the
vaginal vault or even past the labia.
Prolapse of the cord often leads to cord compression which, in turn, leads to abnormal
findings on fetal heart rate (FHR) tracings in 41% to 67% of cases. These changes may
present as a severe, sudden deceleration, often with prolonged bradycardia, or recurrent
moderate-to-severe variable decelerations. The diagnosis of overt UCP is made on vaginal
examination, which will reveal a palpable umbilical cord (usually a soft, pulsating mass)
within or visibly extruding from the vagina. A confirmed diagnosis of occult UCP is rare,
because it cannot be definitively diagnosed even when Doppler ultrasound imaging is
employed. Attempts to identify occult prolapse with imaging could delay necessary
treatment for this emergent condition. Occult UCP likely is the cause of some cases of
urgent cesarean delivery for unexplained fetal bradycardia.
NEXT: RISK FACTORS >>NEXT: RISK FACTORS >>
Risk factorsRisk factors
Several factors increase the risk of cord prolapse. The main precipitating event is rupture of
membranes (ROM), either spontaneous or performed artificially by a healthcare provider.
Most risk factors for UCP can be separated into two categories: spontaneous and
iatrogenic (Table 1).
Spontaneous causes may be related to fetal factors, uterine distention, or pregnancy
complications. Fetal risk factors include malpresentation, fetal anomalies, fetal growth
restriction/small for gestational age, funic presentation, and cord abnormalities. Factors
related to uterine distention include polyhydramnios, multiple gestation (although this may
3,5ANSWER
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HOME PUBLICATIONS BUSINESS EDUCATION CAREERS CONTACT US LOG IN | REGISTER Prevention
❖ Avoid amniotomy unless the fetal head is well-engaged
Diagnosis
❖ Fetal heart rate abnormalities
❖ Visual of prolapsed cord
Management
❖ It is a top emergency
❖ NEEDS URGENT DELIVERY
❖ However, Lethal anomaly, demised foetus.
Management
9/8/16, 10:25 PMUmbilical cord prolapse | Contemporary OB/GYN
Page 4 of 9http://contemporaryobgyn.modernmedicine.com/contemporary-obgyn/content/tags/bradley-holbrook-md/umbilical-cord-prolapse?page=full
Elevation of the presenting fetal part. The key first step after identifying a UCP is to elevate
the presenting fetal part off the prolapsed cord. This is generally performed manually, with
the physician placing 2 fingers or an entire hand into the vagina to elevate the fetus off the
cord. Care should be taken to avoid palpation of the cord because that may cause
vasospasm, potentially leading to a worse outcome. Placing the patient in steep
Trendelenburg or in knee-chest position is believed to be helpful by taking advantage of
gravity to further relieve pressure on the cord.
In cases in which the interval to delivery is likely to be prolonged (that is, requiring maternal
transport to a facility where cesarean delivery can be performed), bladder filling may be a
better option. With this technique—commonly called Vago’s method, in reference to the
physician who first described the technique—a Foley catheter is placed and the bladder is
filled with 500 to 750 mL of saline, and then clamped. The patient’s enlarging bladder
provides upward pressure on the fetus, thus alleviating the compression on the cord. Vago
described this as an alternative to manual elevation, which he described as “effective, but .
. . unpleasant for the mother and wearying for the doctor.” He also noted that in his
experience, filling the bladder tends to calm uterine contractions, which would certainly
further relieve pressure on the cord. Over the years, studies have shown Vago’s method to
be effective. To employ this strategy requires that a cord prolapse tray be immediately
available (Figure 1). Comparison of manual elevation of the presenting part versus bladder
filling shows essentially equal outcomes between the 2 groups. It should be noted that
the combination of the 2 methods does not lead to any improvement over using either
alone.
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9
10
10,11
12
Management
Management9/8/16, 10:25 PMUmbilical cord prolapse | Contemporary OB/GYN
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ReferencesReferences
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2. Lin MG. Umbilical cord prolapse. Obstet Gynecol Surv. 2006;61:269–277.
3. Koonings PP, Paul RH, Campbell K. Umbilical cord prolapse. A contemporary look. J Reprod Med.
1990;35:690–692.
4. Boyle JJ, Katz VL. Umbilical cord prolapse in current obstetric practice. J Reprod Med. 2005;50:303–306.
5. Murphy DJ, MacKenzie IZ. The mortality and morbidity associated with umbilical cord prolapse. Br JObstet Gynaecol. 1995;102:826–830.
6. Usta IM, Mercer BM, Sibai BM. Current obstetrical practice and umbilical cord prolapse. Am J Perinatol.1999;16:479–484.
7. Holbrook BD, Phelan ST. Umbilical cord prolapse. Obstet Gynecol Clin North Am. 2013;40:1–14.
8. Critchlow CW, Leet TL, Benedetti TJ, Daling JR. Risk factors and infant outcomes associated with
umbilical cord prolapse: a population-based case-control study among births in Washington State. Am JObstet Gynecol. 1994;170:613–618.
9. Katz Z, Lancet M, Borenstein R. Management of labor with umbilical cord prolapse. Am J ObstetGynecol. 1982;142:239–241.
10. Vago T. Prolapse of the umbilical cord: a method of management. Am J Obstet Gynecol. 1970;107:967–
969.
11. Caspi E, Lotan Y, Schrever Pl. Prolapse of the cord: reduction of perinatal mortality by bladder instillation
and cesarean section. Isr J Med Sci. 1983;19:541–545.
12. Bord I, Gemer O, Anteby EY, Shenhav S. The value of bladder filling in addition to manual elevation of
presenting fetal part in cases of cord prolapse. Arch Gynecol Obstet. 2011;283:989–991.
13. Barrett JM. Funic reduction for the management of umbilical cord prolapse. Am J Obstet Gynecol.1991;165:654–657.
14. Leong A, Rao J, Opie G, Dobson P. Fetal survival after conservative management of cord prolapse for
three weeks. BJOG. 2004;111:1476–1477.
15. Siassakos D, Hasafa Z, Sibanda T, et al. Retrospective cohort study of diagnosis-delivery interval with
umbilical cord prolapse: the effect of team training. BJOG. 2009;116:1089–1096.
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