Prognostic Factors and Clinical Features in

Liveborn Neonates with Hydrops Fetalis

Hsuan-Rong Huang, M.D.,1 Pei-Kwei Tsay, Ph.D.,2 Ming-Chou Chiang, M.D.,1
Reyin Lien, M.D.,1 and Yi-Hung Chou, M.D.1

ABSTRACT

The purpose of this study was to delineate the etiology and the clinical features of
liveborn neonates with hydrops fetalis, and to explore the prognostic factors for survival.
Medical records of 28 liveborn neonates with hydrops fetalis between April 1995 and
March 2005 were reviewed retrospectively. Demographic data, clinical manifestations,
laboratory findings, and outcomes were analyzed. Most patients presented with pleural
effusions (21 of 28) and ascites (22 of 28). The majority of patients had hydrops due to
cardiovascular diseases (seven of 28), hematologic disorders (six of 28), lymphatic
malformations (six of 28), and idiopathic origins (six of 28). The overall survival rate
was 50% and was highest (83%) in infants with lymphatic malformations. By univariate
analysis, risk factors for mortality are earlier ages at diagnosis and at birth, low Apgar
scores, need for resuscitation in the delivery room, low serum albumin level, and severe
acidemia. After using stepwise multiple logistic regression analysis, the most significant
factors associated with fatality were younger gestational age at birth and lower serum
albumin level. Hydrops fetalis remains a complex condition with a high mortality rate.
Hydrops resulting from lymphatic malformations has a favorable outcome. Preterm birth at
less than 34 weeks and serum albumin concentration lower than 2 g/dL are two poor
prognostic factors for survival.

KEYWORDS: Albumin, hydrops fetalis, lymphatic malformations, neonates, outcome

Hydrops fetalis (HF) is an abnormal accumu-
lation of fluid in a fetus due to diverse etiologies. The
infants frequently present severely ill and the mortality
rate is very high. HF is usually classified into two
categories: immune HF (IHF) and nonimmune HF
(NIHF). The former was caused mainly by Rh incom-
patibility, but the occurrence has steadily declined because
of maternal treatment with anti-D globulin. At present,
NIHF appears more frequently, and it accounts for 90%
of HF.1 The survival rate for fetuses with HF ranges from
12% to 24%,2 but is much higher (40% to 50%) in
liveborn neonates.3 Most patients with HF diagnosed
in early fetal life have chromosomal anomalies, whereas
those occurrences diagnosed after the second trimester are
caused mainly by cardiovascular diseases.4–6 The prog-
nosis is dependent partly on the underlying disease, but
with aggressive postnatal care, the survival rate is
increased in selected cases. The purpose of this study
is to identify the prognostic factors for liveborn neonates
with HF. In addition to underlying diseases, we also focus
on the clinical features and biochemical data of these
newborns. By doing so, we may provide additional

1
Division of Neonatology, Department of Pediatrics, Chang Gung
Memorial Hospital, Chang Gung University College of Medicine;
2
Department of Public Health and Center of Biostatistics, Chang
Gung University College of Medicine, Taoyuan, Taiwan.
Address for correspondence and reprint requests: Ming-Chou
Chiang, M.D., Division of Neonatology, Department of Pediatrics
Chang Gung Memorial Hospital, Chang Gung University College of
Medicine 5, Fushing Street, Gueishan Shiang, Taoyuan, Taiwan 333,
Republic of China.
Am J Perinatol 2007;24:33–38. Copyright # 2007 by Thieme
Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001,
USA. Tel: +1(212) 584-4662.
Accepted: August 11, 2006. Published online: December 27, 2006.
DOI 10.1055/s-2006-958158. ISSN 0735-1631.
33
34 AMERICAN JOURNAL OF PERINATOLOGY/VOLUME 24, NUMBER 1
information for postnatal care to improve the survival rate
and to identify significant prognostic factors to better
counsel the parents.
MATERIALS AND METHODS
Medical records of liveborn neonates with HF admitted
to the neonatal intensive care unit at Chang Gung
Children’s Hospital were reviewed retrospectively for
the period between April 1995 and March 2005. HF
was defined as the presence of general anasarca (sub-
cutaneous thickening > 5 mm) revealed on real-time
fetal ultrasonography plus at least two of the following
conditions: pleural effusion, ascites, pericardial effusion,
placental edema, or polyhydramnios. NIHF was defined
as infants with HF without evidence of isoimmuniza-
tion. In our patient population, we divided the diagnosis
into the following categories according to the classifica-
tion by Forouzan7: hematologic disorders, cardiovas-
cular diseases, lymphatic malformations, chromosomal
anomalies, thoracic abnormalities, and idiopathic ori-
gins. Hematologic disorders were evaluated by complete
blood count, blood smear, Coombs test, blood typing,
hemoglobin electrophoresis, and Kleihauer-Betke stain.
Cardiovascular diseases and thoracic abnormalities were
investigated by radiography and ultrasonography. In
addition to a predominance of lymphocytes presented
in visceral effusions, lymphatic malformations were es-
tablished by computed tomography (CT) or magnetic
resonance imaging (MRI).8 Karyotyping was offered to
identify the chromosomal anomalies. Furthermore,
screening for congenital infection (including toxoplas-
mosis, rubella, cytomegalovirus, herpes simplex virus,
syphilis, and parvovirus B19) was performed in some
patients who lacked a definitive diagnosis. If there were
no results of the prenatal and postnatal workup that
could explain the cause of hydrops, it was regarded as
having an idiopathic origin.
Demographic data, such as gender, maternal age,
gestational ages (GA) at diagnosis and at birth, mode of
delivery, birthweight (BW), and Apgar scores were
recorded. In addition, the following information was
collected: numbers and locations of body cavities with
fluid accumulation, whether the excess fluid was tapped
in the delivery room (DR), need for resuscitation in the
DR, administration of inotropic agents, ventilator mode
and settings if used, vital signs, and underlying etiology.
Hemogram, biochemical data, and blood gas analysis
from the first blood sampling were obtained. The com-
position of effusions, hematologic and immunologic
studies, bacterial and viral cultures, and chromosomal
results were collated. The volume of pleural effusions
was identified according to the appearance of effusions
on a chest radiograph: small (not more than one fourth
of the lung field), moderate (one fourth to one half of the
lung field), large (more than half of the lung field), or
2007
massive (the entire lung with mediastinal shift).9 Ma-
ternal records were reviewed to determine the prenatal
diagnosis and interventions.
Statistical analysis was performed using SPSS for
Windows, version 10.0 (SPSS, Inc., Chicago, IL). Dis-
crete variables were analyzed by x2 test. Continuous
variables were analyzed by Student’s t-test. Data are
expressed as mean
standard deviation. Statistical sig-
nificance was defined as p < 0.05. After univariate anal-
ysis to screen for statistically significant variables, a
stepwise multiple logistic regression analysis was per-
formed to adjust confounding variables simultaneously.
RESULTS
Demographic Data
Twenty-eight liveborn neonates were eligible for our
study with a sex distribution of 11 boys and 17 girls.
During 1995 to 2005, there were 18,976 newborns
admitted to the neonatal intensive care unit in this
tertiary-center population, giving an approximate prev-
alence of HF of 1.5 per 1000 admissions. Fourteen
patients survived, yielding an overall survival rate of
50%. Among the 28 neonates, the maternal age was
28.9
6.0 years. GA at diagnosis and at birth was
32.5
3.7 and 33.9
3.3 weeks, respectively, and the
BW was 2600
844 g. Apgar scores were 3
2 at 1
minute and 5
2 at 5 minutes, respectively. Seventy-five
percent of patients (21 of 28) were delivered via cesarean
section.
Clinical Features
Twenty-one of 28 neonates (75%) presented with pleural
effusions, 22 newborns (79%) presented with ascites, two
newborns (7%) presented with pericardial effusions, and
seven newborns (25%) presented with cardiomegaly. A
total of 16 neonates (57%) had two or more serous cavity
effusions. Seven patients (25%) received intrauterine
therapy. Fetal pleurocentesis was performed in three
cases, a pleuroamniotic shunt was placed in three cases,
and digoxin was prescribed for a fetus with supraven-
tricular tachycardia. Among those with prenatal therapy,
three patients (43%), including the one with fetal ar-
rhythmia, survived. Forty-three percent of the patients
required resuscitation in the DR after birth. Ninety-
three percent of all patients underwent ventilator support
for respiratory distress and 79% received inotropic agents
for unstable vital signs.
The clinical features are summarized in Table 1.
Laboratory findings disclosed hypoalbuminemia
(2.1
0.6 g/dL) and acidemia (pH, 7.005
0.25). Pro-
found anemia was noted in two patients with isoimmune
hemolytic anemia in which hemoglobin (Hb) 4.1 g/dL
was found in one with Rh type (E, c) incompatibility,
 LIVEBORN NEONATES WITH HYDROPS FETALIS/HUANG ET AL 35

Table 1 Summary of the Clinical Features of Liveborn Table 2 Etiology and Outcome of Liveborn Neonates
Neonates with Hydrops Fetalis with Hydrops Fetalis
Surviving Fatal Cases Total Patients
Clinical Features Cases (n ¼ 14) (n ¼ 14) (n ¼ 28)
Survived Died Total
Intrauterine fetal 7 (25%) Etiology and Outcome (n ¼ 14) (n ¼ 14) (n ¼ 28)
therapy Idiopathic origins 3 3 6
Pleurocentesis 1 2 Hematologic disorders 6
Pleuroamniotic 1 2 Rh type (E, c) 1
shunt
incompatibility
Digoxin 1
Anti-M alloantibodies 1
Resuscitation in 2 10 12 (43%) Homozygous 1
the DR a-thalassemia
Mechanical 12 14 26 (93%) Fetomaternal 2
ventilation hemorrhage
IMV 9 9 Twin–twin transfusion 1
HFOV 3 5 syndrome
Inotropic agents 9 13 22 (79%)
Cardiovascular diseases 7
used
Structural anomalies
Pleural effusions 11 10 21 (75%) Ebstein anomaly 1 1
Small 4 1 Atrioventricular 1 2
Moderate 5 3 septal defect
Large 2 3 Arrhythmias, PSVT 1
Massive 3 Hemangioma of 1
Ascites 10 12 22 (79%) iliac artery
 2 serous cavity 8 8 16 (57%)
Lymphatic malformations 5 1 6
effusions
Chromosomal anomalies 2
HFOV, high-frequency oscillatory ventilator; IMV, intermittent Trisomy 21 1
mandatory ventilation.
Chromosome 1
22p deletion
and Hb 1.8 g/dL was found in one with anti-M alloanti-
Thoracic abnormalities, 1 1
bodies. Three infants presented with nonimmune ane-
CCAM
mia: one due to thalassemia (Hb, 6.3 g/dL), and two
infants with fetomaternal hemorrhage (Hb, 3.3 and 7.7 PSVT, paroxysmal supraventricular tachycardia; CCAM, congenital
cystic adenomatoid malformation.
g/dL, respectively). White blood cell counts, platelet
counts, and C-reactive protein levels were within normal
limits. from those with hematologic disorders, there would be
no surviving infants with NIHF secondary to hemato-
logic disorders. Eleven of the 14 infants who died in the
Etiology and Outcome neonatal period did so within 2 weeks.
There were two patients with IHF and 26 patients with
NIHF. The majority of patients had hydrops due to
cardiovascular diseases (seven of 28), hematologic dis- Prognostic Factors
orders (six of 28), lymphatic malformations (six of 28), By univariate analysis, the risk factors for mortality are
and idiopathic origins (six of 28). Table 2 summarizes younger GAs at diagnosis (30.9
4.0 versus 33.9
3.1
the etiology and outcome of liveborn neonates with HF. weeks; p ¼ 0.036) and at birth (32.0
3.4 versus
Infants with lymphatic malformations had a favorable 35.9
1.7 weeks; p ¼ 0.001), low Apgar scores (2
2
survival rate (83%) in this study. The survival rate was versus 4
2 at 1 minute; p ¼ 0.015; and 4
2 versus
33% in infants with hematologic disorders because only 6
2 at 5 minutes; p ¼ 0.030), need for resuscitation in
two infants with isoimmune hemolytic anemia survived. the DR (p ¼ 0.006), low serum albumin level (1.7
0.3
No fetal transfusion was provided but exchange trans- versus 2.4
0.6 g/dL; p ¼ 0.001), and severe acidemia
fusion therapy was done in the patient with Rh type (6.862
0.21 versus 7.136
0.20; p ¼ 0.001; Table 3).
(E, c) incompatibility. The remaining four infants, in- Using stepwise multiple logistic regression analysis, the
cluding one with homozygous a-thalassemia, two with most significant factors associated with fatality are
fetomaternal hemorrhage, and one with twin–twin younger GA at birth and lower serum albumin level.
transfusion syndrome, all died as a result of severe By using receiver operating characteristics analysis, the
underlying disease. If infants with IHF were separated area under the curve is 0.964. The cutoff points of GA at
36 AMERICAN JOURNAL OF PERINATOLOGY/VOLUME 24, NUMBER 1 2007

Table 3 Comparison of Clinical Characteristics between Surviving and Fatal Cases in Liveborn Neonates with
Hydrops Fetalis
Characteristic Surviving Cases (n ¼ 14) Fatal Cases (n ¼ 14) p

Sex, male/female 6/8 5/9 0.99

Gestational age (wk)
At diagnosis 33.9
3.1 30.9
4.0 0.036
At birth 35.9
1.7 32.0
3.4 0.001
Gestational age  34 wk 3 10 0.008
BW (g) 2802
690 2397
957 0.210
Apgar score
1 minute 4
2 2
2 0.015
5 minutes 6
2 4
2 0.030
Intubation in the DR 11 14 0.222
Resuscitation in the DR 2 10 0.006
Chest taping in the DR 6 5 0.99
Chest tube insertion 7 9 0.704
Inotropic agents usage 9 13 0.165
Pleural effusions 11 10 0.99
Ascites 10 12 0.648
Cardiomegaly 2 5 0.385
 2 serous cavity effusions 8 8 0.648
Hb (g/dL) 13.3
5.1 10.2
3.3 0.066
Albumin (g/dL) 2.4
0.6 1.7
0.3 0.001
pH 7.136
0.20 6.862
0.21 0.001
BW, birthweight; DR, delivery room; Hb, hemoglobin.

birth and of serum albumin concentration for survival are
34 weeks (sensitivity, 1.00; specificity, 0.71) and 2.0 g/
dL (sensitivity, 0.86; specificity, 0.64), respectively.
DISCUSSION
NIHF accounted for the majority of HF. Cardiovascular
diseases are one of the main causes for NIHF. Seventy-
one percent of infants with cardiovascular diseases had
structural anomalies including Ebstein anomaly and
atrioventricular septal defects (AVSDs). Although
many cardiac malformations have been reported, the
most common were AVSDs.10–12 Intrauterine conges-
tive heart failure with high hydrostatic pressure secon-
dary to inadequate cardiac output with right atrial
overload leads to fetal hydrops.4–6 Prenatal intervention
has not been offered to fetuses with structural anomalies
in our institution to date, but fetal arrhythmia can be
treated medically. In one of our patients, transplacental
digitalization successfully converted paroxysmal supra-
ventricular tachycardia to normal sinus rhythm. Large
series have shown improved survival rates following
appropriate maternal drug administration in hydropic
fetuses with arrhythmia.4,5 One hydropic fetus was
diagnosed with a bulky hemangioma over the external
and internal iliac arteries after birth. We speculate that
the hemangioma functions as a huge arteriovenous
shunt, leading to cardiac overload and high-output
cardiac failure. It is difficult to diagnose prenatally, and
clinicians should be aware that hemangiomas and arte-
riovenous malformations can be a rare cause of HF.13
Two patients had chromosomal anomalies. In our
series, all hydropic patients were diagnosed during the
second or third trimesters; we speculate that the true
incidence of abnormal fetal karyotypes associated with
HF is probably higher, because if a chromosomal anom-
aly is confirmed in early pregnancy, the parents select
termination or there is an increased tendency for sponta-
neous abortion or delivery as a stillbirth. In our clinical
observation, there was no definitive case resulting from
an infectious disease. Rodrı́guez et al14,15 reported that
cardiovascular diseases are more common in the live-
born, whereas congenital infections are the most com-
mon causes for stillborn fetuses with NIHF. Our results
concur with these authors for liveborn series.
In our study, 7% of HF was IHF, which is similar
to a previous report by Heinonen et al.2 In contrast with
other observations, minor group incompatibility, instead
of Rh incompatibility, is the major cause of IHF. Wu
et al16 reported that anti-E and anti-E þ c antibodies
play an important role in maternal irregular antibodies to
result in neonatal hemolytic diseases in Taiwan. How-
ever, anti-M alloantibody is seldom the cause of neonatal
hemolytic disease.17 Exchange transfusion therapy and
intensive neonatal care can provide a better outcome in
this situation.
HF caused by a lymphatic malformation present-
ing as a chylothorax had favorable prognosis, which is in

agreement with other investigators.5,18,19 In addition to
CT and MRI, lymphatic malformations can be also
confirmed by lymphangiography, lymphoscintigraphy,
and lung biopsy. These diagnostic methods are accurate
to distinguish the congenital errors of lymphatic devel-
opment (such as lymphangiomas, lymphangiectasis, or
lymphatic dysplasia syndrome).20 We adopted conserva-
tive management in most patients, including pleural
drainage and a high-protein, medium-chain triglyceride
diet, and symptoms resolved spontaneously in surviving
cases. In addition, prenatal interventions by either in-
termittent thoracocentesis or an in-dwelling pleuro-
amniotic shunt are warranted in severe progressive
cases to minimize the risk of pulmonary hypoplasia
resulting from intrathoracic compression.21
Various poor prognostic factors for mortality have
been described, including the presence of a pleural
effusion,22  two serous cavity effusions, a need for chest
compressions at birth,6 and lower Apgar scores at 1 and
5 minutes.23 By univariate analysis, the fatal cases had a
tendency to lower Apgar score, need for resuscitation in
the DR, and more severe acidemia than the surviving
group. These parameters suggesting a poor condition at
birth reflect the severity of hydrops, and strongly influ-
ence outcome. Moreover, using stepwise multiple logis-
tic regression analysis, we conclude that the most
significant factors for fatality are GA at birth younger
than 34 weeks and a serum albumin level < 2 g/dL. A
hydropic fetus who is delivered prematurely is subject to
the additional complications of prematurity. Poor re-
sponse to neonatal resuscitation in premature infants
with hydrops is attributed to the decreased lung com-
pliance (secondary either to hyaline membrane disease or
extrapulmonary compression), cardiovascular compro-
mise, and even intracranial hemorrhage.24 Prenatal in-
tervention to prolong pregnancy in selected patients
might improve the survival rate.
Phibbs et al25 have demonstrated a close correla-
tion between serum albumin concentration and severity
of HF. They proposed that anemia or cardiac disorders
lead to congestive heart failure with elevated central
venous pressure, which results in increased capillary
filtration pressure and restriction of lymphatic return.
Heart failure leads to congestion of the liver, causing a
decrease in albumin synthesis. In addition, hypoxia
increases capillary permeability to albumin in asphyxi-
ated hydropic infants. Finally, hypoalbuminemia causes
a significant decrease in plasma colloid osmotic pressure,
allowing edema formation and serous effusion.25 Except
for albumin transfusion after birth, Shimokawa et al26
reported that intrauterine albumin infusion is effective in
treating idiopathic HF. In our observation, there is no
evidence that transfusing albumin aggressively in the
postnatal period is effective. However, albumin trans-
fusion, in selective cases, might be beneficial in removing
fluid from lungs and subsequently to improve pulmonary
LIVEBORN NEONATES WITH HYDROPS FETALIS/HUANG ET AL 37
function, and could support the cardiovascular circula-
tion in hydropic infants with hypotension.
In conclusion, hydrops fetalis remains a complex
condition with high mortality and morbidity. The out-
come of HF is dependant mainly on the underlying
etiology, GA at birth, and serum albumin level. Our
observation suggests that hydrops resulting from lym-
phatic malformations has a favorable outcome. Preterm
birth at < 34 weeks and a serum albumin concen-
tration < 2 g/dL are two poor prognostic factors for
survival.
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