Читать книгу Genetic Disorders and the Fetus - Группа авторов - Страница 91
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ОглавлениеBrace16 described three determinants of AFV: (i) movement of water and solutes across the membranes; (ii) physiologic regulation of flow rates, such as fetal urine production and swallowing; and (iii) maternal effects on transplacental fluid movement. Total water accumulation in utero during pregnancy reaches about 4 L (fetus 2,800 mL; placenta 400 mL; AF 800 mL).8 Urine production per kg of body weight increases from 110 mL/kg/24 hour at 25 weeks to 190 mL/kg/24 hour at 35 weeks.17 Interference with disposal in the routes of fluid production by a factor affecting only 1 percent of the volume may increase or decrease total AFV by as much as 1 L in 10 days. AF turnover continues even after fetal death, but it is reduced by about 50 percent,18 implying that membranes may be responsible for about half of the water exchange. This suggests that the membranes play a larger role in water disposal than in production. Indeed, electron microscopic studies19 correlate with an absorptive function of the membranes. It is unlikely that excess AF production results solely from excess urine production or a failure of the fetus to swallow AF.20 The amnion must play a role in the maintenance of AFV and composition. Earlier studies concluded that 25–50 percent of the fluid turnover takes place through the fetus in late pregnancy.21 Abramovich22 challenged the concept that swallowing and voiding are important in controlling the AFV. He showed that some anencephalics may swallow considerable amounts of AF and that normal volumes were found in esophageal atresia and in the absence of fetal kidneys. Thus, other factors are involved in controlling the AFV. Chamberlain23 has reviewed the studies done on abnormalities of AFV and altered perinatal outcome.
Ultrasonic assessment of fetal kidney function in normal and complicated pregnancies revealed that the fetal urinary production rate was 2.2 mL/h at 22 weeks, increasing to 26.3 mL/h at 40 weeks.24 The authors concluded that regulation by the central nervous system does not play a large role in fetal urination control, and that fetal polyuria does not explain polyhydramnios. Polyhydramnios was accompanied by elevated AF pressures.25
Various techniques have been used for the direct estimation of AFV. Comparable results have been reported using dilution techniques, radioactive materials, or various dyes or chemicals.26–33 Abnormal AFV is associated with increased maternal risk and perinatal morbidity and mortality, but the invasive nature of AFV assessment limited its clinical utility.34 The vertical pocket measurement (VPM) is simple but remains semiquantitative with limited accuracy. The AF Index (AFI) is the result of the sum of the four maximum vertical pockets (MVP) from each quadrant of the uterus. A meta‐analysis concluded that both AFI and VPM identified abnormal AFVs poorly. The AFI led to more false‐positive oligohydramnios findings, and more interventions without improvement in perinatal outcome.35 Population differences for the AFI may also exist.36 Sandlin et al.37 established reference ranges for AFV from 16 to 41 weeks, using dye‐dilution techniques and a quantile regression statistical approach (Table 3.1). Refinements in quantifying the noninvasive sonographic assessment of AFV have not significantly improved the predictive ability to identify at‐risk pregnancies.38, 39
Table 3.1 Amniotic fluid volume percentile values in relation to gestational age by second‐order quantile regression
| Weeks of gestation | 5th | 25th | 50th | 75th | 95th |
|---|---|---|---|---|---|
| 16 | 134.0 | 334.5 | 377.1 | 503.2 | 694.7 |
| 17 | 132.3 | 322.0 | 389.6 | 552.2 | 937.2 |
| 18 | 130.9 | 311.1 | 401.9 | 602.0 | 1233.7 |
| 19 | 129.9 | 301.7 | 414.0 | 652.1 | 1584.8 |
| 20 | 129.2 | 293.7 | 425.8 | 701.8 | 1986.6 |
| 21 | 128.9 | 286.9 | 437.2 | 750.4 | 2430.0 |
| 22 | 128.9 | 281.4 | 448.3 | 797.2 | 2900.5 |
| 23 | 129.2 | 277.0 | 459.0 | 841.5 | 3378.4 |
| 24 | 129.8 | 273.7 | 469.2 | 882.5 | 3839.9 |
| 25 | 130.8 | 271.4 | 478.9 | 919.5 | 4258.8 |
| 26 | 132.1 | 270.2 | 488.1 | 951.9 | 4609.3 |
| 27 | 133.8 | 270.0 | 496.7 | 979.1 | 4868.0 |
| 28 | 135.8 | 270.8 | 504.7 | 1000.5 | 5016.9 |
| 29 | 138.3 | 272.6 | 512.1 | 1015.9 | 5045.3 |
| 30 | 141.1 | 275.4 | 518.8 | 1024.8 | 4951.1 |
| 31 | 144.4 | 279.3 | 524.8 | 1027.1 | 4741.3 |
| 32 | 148.1 | 284.4 | 530.0 | 1022.8 | 4430.5 |
| 33 | 152.3 | 290.6 | 534.5 | 1012.0 | 4040.0 |
| 34 | 157.0 | 298.0 | 538.2 | 994.8 | 3594.8 |
| 35 | 162.3 | 306.8 | 541.1 | 971.6 | 3121.4 |
| 36 | 168.2 | 317.0 | 543.2 | 942.8 | 2644.7 |
| 37 | 174.7 | 328.8 | 544.5 | 909.0 | 2186.7 |
| 38 | 182.0 | 342.3 | 545.0 | 870.7 | 1764.2 |
| 39 | 190.0 | 357.7 | 544.7 | 828.7 | 1389.0 |
| 40 | 198.2 | 375.2 | 543.5 | 783.6 | 1067.1 |
| 41 | 207.9 | 395.0 | 541.5 | 736.2 | 800.0 |
Amniotic fluid volumes are in mL.
Source: Sandlin et al. 2014.37 Reproduced with permission of Springer Business + Science Media.
Polyhydramnios occurs in 1–2 percent of all pregnancies35 and is associated with fetal malformations in about 40 percent of cases.40 Moise defined polyhydramnios in singleton or twin pregnancies as MVP >8 cm in the late second and the third trimesters, and oligohydramnios as MVP <2 cm.41 Most common are neural tube defects (NTDs) and disorders that impair deglutition or absorption of AF (esophageal and other intestinal atresias or obstructions).26, 40, 42, 43 Myotonic dystrophy was identified in 4 of 41 patients with “idiopathic” polyhydramnios.44 The development of polyhydramnios in anencephaly is believed to result from impaired swallowing by the fetus43 or deficient antidiuretic hormone production by the fetus.45 Polyhydramnios also occurs in maternal diabetes mellitus and may appear, especially early in pregnancy, in monozygotic twins.43 Irrespective of the cause, there seems to be a risk of recurrence for polyhydramnios of between 0.06 and 8 percent.42, 43
Oligohydramnios, in contrast, is most often associated with disorders of the urinary tract that interfere with micturition, such as renal agenesis.46 Placental insufficiency and extrauterine pregnancy also may cause oligohydramnios, as can exposure to maternal hypertension treatment with renin–angiotensin system blockers.47 Sherer48 cautioned that decreased AFV is especially of concern when it occurs in conjunction with structural fetal anomalies, fetal growth restriction, or maternal disease, and others have noted an increased risk of fetal heart rate abnormalities.49 However, a normal AFV may occur even in the presence of urinary tract obstruction or bilateral renal agenesis.26 A normal AFV was found in 13 cases of hydronephrosis, eight of which had confirmed urinary tract obstruction at birth; the other five were normal.50 The authors suggest that fetal hydronephrosis associated with normal amounts of AF does not require intrauterine treatment. Appropriate intervention after birth should lead to normal renal function. Rarely, oligohydramnios may be extreme, even to the point at which there is virtually no AF. These extreme cases are frequently associated with amnion nodosum, fetal defects or placental problems.43
