Diagnostic ultrasound ( PDFDrive )

CHAPTER 41 Fetal Hydrops 1437
Predelivery Aspiration Procedures
Fetal luid collections may be drained under ultrasound guidance
just before delivery to assist with neonatal resuscitation. his
is particularly relevant if large fetal pleural efusions are present. 115
Massive ascites may also be drained to prevent abdominal dystocia
(when vaginal birth is planned) and aid in fetal breathing when
ascites has caused elevation of the diaphragms.
Postnatal Outcome
Because of the high incidence of in utero demise, the cause
of hydrops in utero is diferent from that with a live neonate.
In a review of 30 cases of hydrops diagnosed between 10 and
14 weeks of pregnancy, all pregnancies with nonimmune
hydrops resulted in abortion, intrauterine fetal death, or
pregnancy termination. 136 A 2007 national database review
of live-born neonates with hydrops found heart problems
(13.7%), abnormalities in heart rate (10.4%), TTTS (9%), congenital
anomalies (8.7%), chromosomal abnormalities (7.5%),
congenital viral infections (6.7%), isoimmunization (4.5%),
and congenital chylothorax (3.2%). 226 Mortality rates were
highest among neonates with congenital anomalies (57.7%)
and lowest among those with congenital chylothorax (5.9%),
and a cause could not be determined in 26%. Factors associated
independently with death were younger gestational age,
low 5-minute Apgar score, and high levels of support needed
the irst day ater birth. 226 his study reported a 36% death rate
before discharge or transfer to another hospital. he severity
of hydrops and birth gestational age of the infant are the key
determinants for survival. his is important because delivering
a fetus early to treat worsening hydrops may not improve
survival.
Data are limited regarding long-term outcome of children
surviving ater hydrops. In one series, 13 in 19 (68%) children
surviving beyond 1 year of age were normal; two had mild
developmental delay at 1 year of age; one 8-year-old child was
mentally retarded; and three (16%) had severe psychomotor
impairment with marked growth failure. 227 Haverkamp et al. 228
found that 86% of patients had normal psychomotor development,
86% showed normal neurologic status, 7% had minor neurologic
dysfunction, and 4% had spastic cerebral paresis.
CONCLUSION
Hydrops represents a terminal stage for many conditions, the
vast majority of which are fetal in origin. he onset of hydrops
signiies fetal decompensation. Immune causes can be successfully
treated in utero, as can an increasing number of nonimmune
causes. Whereas in the past, nonimmune hydrops carried virtually
100% mortality, this is no longer the case. A team approach
using obstetric imagers, maternal fetal medicine specialists,
neonatologists, and geneticists can help to decide which cases
are suitable for therapeutic intervention. A comprehensive
approach must be taken to the investigation of hydrops, both
for the management of the index case and for future counseling.
Cornerstones of this investigation are detailed ultrasound,
including echocardiography, fetal karyotyping, and other
diagnostic interventions as appropriate, and pathologic examination
of the fetus and placenta.
REFERENCES
1. Shulman LP, Phillips OP, Emerson DS, et al. Fetal ‘space-suit’ hydrops in
the irst trimester: diferentiating risk for chromosome abnormalities by
delineating characteristics of nuchal translucency. Prenat Diagn. 2000;20(1):
30-32.
2. Freda VJ, Gorman JG, Pollack W, et al. Prevention of Rh isoimmunization.
Progress report of the clinical trial in mothers. JAMA. 1967;199(6):
390-394.
3. Macafee CA, Fortune DW, Beischer NA. Non-immunological hydrops fetalis.
J Obstet Gynaecol Br Commonw. 1970;77(3):226-237.
4. Bellini C, Donarini G, Paladini D, et al. Etiology of non-immune hydrops
fetalis: an update. Am J Med Genet A. 2015;167a(5):1082-1088.
5. Derderian SC, Jeanty C, Fleck SR, et al. he many faces of hydrops. J Pediatr
Surg. 2015;50(1):50-54.
6. Ng ZM, Seet MJ, Erng MN, et al. Nonimmune hydrops fetalis in a children’s
hospital: a six-year series. Singapore Med J. 2013;54(9):487-490.
7. Yeom W, Paik ES, An JJ, et al. Clinical characteristics and perinatal outcome
of fetal hydrops. Obstet Gynecol Sci. 2015;58(2):90-97.
8. Hashimoto BE, Filly RA, Callen PW. Fetal pseudoascites: further anatomic
observations. J Ultrasound Med. 1986;5(3):151-152.
9. Derderian SC, Trivedi S, Farrell J, et al. Outcomes of fetal intervention for
primary hydrothorax. J Pediatr Surg. 2014;49(6):900-903.
10. Di Salvo DN, Brown DL, Doubilet PM, et al. Clinical signiicance of isolated
fetal pericardial efusion. J Ultrasound Med. 1994;13(4):291-293.
11. Bukowski R, Saade GR. Hydrops fetalis. Clin Perinatol. 2000;27(4):
1007-1031.
12. Nicolaides KH, Fontanarosa M, Gabbe SG, Rodeck CH. Failure of ultrasonographic
parameters to predict the severity of fetal anemia in rhesus
isoimmunization. Am J Obstet Gynecol. 1988;158(4):920-926.
13. Fleischer AC, Killam AP, Boehm FH, et al. Hydrops fetalis: sonographic
evaluation and clinical implications. Radiology. 1981;141(1):163-168.
14. Hoddick WK, Mahony BS, Callen PW, Filly RA. Placental thickness.
J Ultrasound Med. 1985;4(9):479-482.
15. Lee AJ, Bethune M, Hiscock RJ. Placental thickness in the second trimester:
a pilot study to determine the normal range. J Ultrasound Med.
2012;31(2):213-218.
16. Nicolaides KH, Warenski JC, Rodeck CH. he relationship of fetal plasma
protein concentration and hemoglobin level to the development of hydrops
in rhesus isoimmunization. Am J Obstet Gynecol. 1985;152(3):341-
344.
17. Nicolaides KH. Studies on fetal physiology and pathophysiology in rhesus
disease. Semin Perinatol. 1989;13(4):328-337.
18. Soothill PW, Nicolaides KH, Rodeck CH. Efect of anaemia on fetal acid-base
status. Br J Obstet Gynaecol. 1987;94(9):880-883.
19. Mari G, Deter RL, Carpenter RL, et al. Noninvasive diagnosis by Doppler
ultrasonography of fetal anemia due to maternal red-cell alloimmunization.
Collaborative Group for Doppler Assessment of the Blood Velocity in Anemic
Fetuses. N Engl J Med. 2000;342(1):9-14.
20. Ruma MS, Swartz AE, Kim E, et al. Angle correction can be used to measure
peak systolic velocity in the fetal middle cerebral artery. Am J Obstet Gynecol.
2009;200(4):397.e1-397.e3.
21. Pretlove SJ, Fox CE, Khan KS, Kilby MD. Noninvasive methods of detecting
fetal anaemia: a systematic review and meta-analysis. BJOG. 2009;116(12):
1558-1567.
22. Zimmerman R, Carpenter Jr RJ, Durig P, Mari G. Longitudinal measurement
of peak systolic velocity in the fetal middle cerebral artery for monitoring
pregnancies complicated by red cell alloimmunisation: a prospective
multicentre trial with intention-to-treat. BJOG. 2002;109(7):746-752.
23. Society for Maternal-Fetal Medicine, Norton ME, Chauhan SP, Dashe JS.
Society for Maternal-Fetal Medicine (SMFM) clinical guideline #7: nonimmune
hydrops fetalis. Am J Obstet Gynecol. 2015;212(2):127-139.
24. Oepkes D, Brand R, Vandenbussche FP, et al. he use of ultrasonography
and Doppler in the prediction of fetal haemolytic anaemia: a multivariate
analysis. Br J Obstet Gynaecol. 1994;101(8):680-684.