Nonimmune Hydrops Fetalis: Report of 22 Cases Including Three Siblings

ABSTRACT. Twenty-two casesof nonimmune hydrops fetalis (NIHF) seen over a three-year period are described. Eight cases were associated with major congenital anom alies, seven cases with minor anomalies or other disease entities, and seven idiopathic cases. The overall mortality rate was 50%, greatest in those cases complicated by major anomalies. The clinical problems commonly en countered in management of these patients are reviewed, and include prenatal detection, perinatal asphyxia, dis seminated intravascular coagulopathy, fluid and electro

lyte imbalance, and respiratory difficulty. A review of the

literature for those entities found in association with NIHF is also included. The case studies of three consec utive siblings with NIHF born to the same parents are briefly analyzed. Pediatrics 64:326—332,1979; hydrops

fetalis, edema, ascites, nonimmune hydrops, polyhy dramnios.

Nonimmune fetal hydrops (generalized body

edema secondary to factors other than isoimmuni zation) was first distinguished from erythroblastosis fetalis (secondary to Rh or other blood type incom patibility) by Potter in 1943.' In describing 17 such cases, she noted the lack of hepatosplenomegaly, the absence of abnormal erythropoiesis, the fre quency of prima gravida Rh-positive mothers, and the good prognosis for future pregnancies. In 1970 it was estimated that approximately 20% of cases of hydrops fetalis in Western countries are nonimmu nologic.2 However, with the decline in the frequency of Rh isoimmunization,3 4 nonimmune hydrops may

become the predominant form of fetal hydrops

which must be recognized and managed by the

medical community. Such nonimmune hydrops has

been associated with a large number of maternal and fetal conditions (Table 1) as well as a high

mortality rate (95% in the largest single reported series) 5-3@iThis report describes 22 cases of nonim mune hydrops seen in six Denver hospitals since 1975, with an overall (peninatal, neonatal, and in fant) mortality rate of 50%.

CASE REPORTS

The case records of six Denver hospitals that possess intensive care newborn nurseries were reviewed over a three-year period from July 1975 through June 1978 in an attempt to identify all cases of nonimmunologic hy

drops fetalis (NIHF). Because these hospitals serve a

large geographical referral area, and because there may well have been infants who died before or shortly after birth in community hospitals, it is probable that there are other cases that escaped our attention. A total of 22 cases are described, representing an incidence of at least 1.4

cases for each 10,000 births. The data are presented in

Tables 2 to 4. Table 2 delineates details of eight cases in which NIHF was associated with major congenital anom alies. Table 3 describes seven cases in which there were minor anomalies or other pathologic conditions, such as congenital infection. Table 4 describes seven idiopathic

cases.

RESULTS

Of the 22 cases there were one intrauterine death, nine neonatal deaths, and one later infant death, resulting in an overall mortality rate of 50% (11 of 22). This is a higher survival rate than that reported by Beischer et al (42 of 44 infant deaths),5 and may

reflect either improved peninatal management or

biased population evidenced by later referral to tertiary care centers or both. In this regard, 12 of the int'ants were born in the Denver hospitals pos sessing tertiary care facilities for both mother and newborn. Eight of these 12 infants died, while two of the ten patients transferred in from outlying hospitals died. Of the eight infants born with major anomalies, seven died; two of seven died in the Received for publication Dec 27, 1978; accepted Feb 22, 1979.

Reprint requests to (J.A.L.), Indiana University Medical Center

and the James Whitcomb Riley Hospital for Children, 1100 West Michigan St. Indianapolis, IN 46223.

Nonimmune Hydrops Fetalis: Report of 22

Cases Including Three Siblings

P. C. Etches, MB, MRCP, and James A. Lemons, MD

TABLE 1. NIHF: Causesand Associations

Fetal

1. Hematologic

Homozygous a-thalassemia Chronic fetomaternal transfusion

Twin to twin transfusion (recipient or donor) Multiple gestation with “¿parasitic―fetus 2. Cardiovascular

Severe congenital heart disease

(atrial septal defect, ventricular septal defect, hy

poplastic left heart, pulmonary valve insuffi ciency, Ebstein's, subaortic stenosis)

Premature closure of foramen ovale Myocarditis

Large arteriovenous malformation

Tachyarrhythmias: paroxysmal SVT, atrial flutter Bradyarrhythmias: heart block

Fibroelastosis 3. Pulmonary

Cystic adenomatoid malformation of lung Pulmonary lymphangiectasia

Pulmonary hypoplasia (diaphragmatic hernia) 4. Renal

Congenital nephrosis Renal vein thrombosis 5. Intrauterine infections

Syphilis Toxoplasmosis Cytomegalovirus Leptospirosis Chagas disease Congenital hepatitis

6. Congenital anomalies

Achrondroplasia E trisomy

Multiple anomalies Turner's syndrome

7. Miscellaneous

Meconium peritonitis Fetal neuroblastomatosis Dysmaturity

Tuberous sclerosis Storage disease Small bowel volvulus Placental

Umbilical vein thrombosis Chorionic vein thrombosis Chorioangioma

Maternal

Diabetes mellitus Toxemia

Idiopathic

group with minor anomalies and associated condi tions; one of seven patients died with idiopathic hydrops. There were 12 male and ten female infants; 20 infants were white and two were black.

It is of note that the possibility of hydrops fetalis was suspected antenatally in eight cases, either

because of acute onset polyhydramnios (seven

cases), or as a result of ultrasound diagnosis of ascites or pleural fluid (five cases) or both. The anticipation of a potentially hydropic infant in these instances may have led to more vigorous intrapar

tum and postnatal management. Although 12 of 22

cases were delivered by cesarean section, birth as phyxia was almost universal in that 17 babies had an Apgar score of 3 or less at one minute, and 18 had an Apgar score of 6 or less at five minutes. Ascites, or hydroathoraces, or both were noted in 14 cases, necessitating emergency abdominal para centesis in six cases and thoracentesis in two cases in the delivery room.

Eight of the 22 cases demonstrated major con genital anomalies (Table 2), an incidence of 36% and similar to that in previous reports.5 However, in contrast to other series, only one major cardiac

malformation (large ventricular septal defect

(VSD), patent ductus artenosus (PDA)) was found in the present group of patients. Other major ma! formations were noted in seven additional patients, and involved the pulmonary, gastrointestinal, and lymphatic systems.

A second group of seven infants demonstrated minor congenital anomalies or other pathologic con ditions or both. Two infants revealed disturbances of cardiac rhythm, one case of paroxysmal supra ventricular tachycardia and one of congenital heart block. The duration of the cardiac arrhythmia pre natally is unknown in both cases. In the second case, the mother possessed a weakly positive anti nuclear antibody titer, although lupus erythemato sus (LE) preparations were negative. The associa tion between congenital heart block and maternal connective tissue disease has been documented and the case we describe here is a subject of a single

previous case 637 Another infant was born

to a mother with systemic lupus although there was no evidence of lupus in the infant; he later suffered

from microcephaly and died unexpectedly at 13

months of age. A single case of intrauterine cyto megalovirus infection was found, as evidenced by culture from the urine and stool, with histologic evidence of severe cytomegalovirus (CMV) hepati tis on liver biopsy, and myocarditis on the basis of enzyme changes and clinical course.

Three of the 22 cases reported were siblings, born consecutively to the same parents. The first preg nancy in 1975 was uneventful until 23 weeks gesta tion at which time acute polyhydramnios was nec

ognized. At approximately 26 weeks gestation, a

stillborn infant weighing 1,095 gm was delivered.

Pathologic examination revealed a female fetus

with severe hydrops and symmetrical cystic lym

phangiomas on both sides of the neck. The placenta

was fragmented and weighed 580 gm. The second

TABLE2. NIHF Associatedwith Major CongenitalAnomalies*

Case Mater- Gray

nal Age ida

(yr) Para

1 25 G2

P1

2 26 Gi

Pg

3 29 Gi

Pg

4 18 Gi

Pg

5 34 G6

P3

7 21 Gi

Pg

8 19 Gi

P0 Ges ta tion (wk) Birth Weight (gm) Lowest Weight (gm) Mode of Delivery, Complications Apgar Clinical Score Findings

0/0 Hydrops, still birth

2/0 Hydrops, ascites,

DIC, intestinal

obstruction with perfora tion, peritonitis 1/1 Hydrops

2/2 Hydrops, ascites,

hyaline mem

brane disease

1/2 Hydrops, pleural effusions, DIC Outcome and Pathologic Findings Pla cent al Weight (gm)

2/2 Hydrops, anemic, Died 24 hr—VSD,

DIC

36 2,650

26 1,095

33 2,580

. . . Vaginal-precipi

tous

. . . Vaginal

Polyhydramnios 1,610 590 Vaginal

Twin pregnancy, fetal distress PDA, corneal opacities Stillbirth—bilateral cystic hygromata Survived—ileal atresia, meco nium peritonitis secondary to in utero perforation Died 1 hr—cystic

adenomatoid malformation of lung

Died 13 hr—pneu

mothoraces, hy

poplastic lungs, pulmonary se questration Died 4'/2 hr—hypo

plastic lungs

Died 13 min—hy poplastic kidneys,

microcephaly

Died 4 wk—uniden tified storage dis ease (? GM gan gliosidosis) mes enteric lymphan giectasia multiple

arterial and ye

nous thromboses

34 2,940 2,250 734 Cesarean section Breech, polyhy

dramnios, ultra sound—? hy drops

34 3,160 . . . Cesarean section Polyhydramnios

6 27 G2

SB1

34 2,400

34 3,175

. . . 700 Cesarean section Acute polyhy dramnios, fetal distress, ultra sound-pleural effusions, hy drops

. . . . . . Cesarean section

Toxemia

. . . Cesarean section

Fetal distress, ul trasound—? hy drops and as cites

39 3,960 1,500

1/1 Hydrops

7/9 Hydrops, ascites, respiratory dis tress

a Abbreviationused:DIC, disseminated intravascular coagulopathy.

amination revealed a thin anterior placenta, poly hydramnios, fetal edema, and ascites. At 34 weeks gestation, the mother went into spontaneous labor, but because of fetal distress underwent cesarean section. At birth the baby weighed 2,500 gm and

was severely asphyxiated, requiring paacentesis

and thoracentesis in the delivery room. In spite of continued intensive support the infant expired at

4'/2 hours of age. Autopsy examination revealed a

premature infant with generalized hydrops, bilat eral pleural effusions, and ascites. The lungs were hypoplastic; the placenta weighed 700 gm and con tamed areas that were markedly thinned. The third pregnancy in 1977 again proceeded normally until

23 weeks gestation when there was evidence of

polyhydramnios by clinical evaluation and ultra sound. Again, extensive evaluation of the patient failed to reveal any abnormalities that might be causally related to the fetal hydrops. At 30 weeks

gestation, ultrasound revealed evidence of pleural fluid in the fetus. Betamethasone was given to the mother and two days later an elective cesarean section was performed. At birth the baby weighed 1,940 gm with generalized edema, and was imme diately intubated and provided ventilator support. Thoracentesis was performed at 3 hours of age. The baby had mild respiratory distress but recovery was uneventful and the baby was discharged at 4 weeks

of age. The placenta weighed 560 gm and demon

strated an irregular pattern of extreme thinning with large membraneous areas intervening between

the cotyledons. In summary, these parents had

TABLE 3. NIHF Associatedwith Minor Anomaliesand Other Conditions*

Apgar Clinical

Score Findings

1/1 Hydrops, anemia,

DIC, heart fail ure (left side),

CMV hepatitis,

myocarditis, by

drocephalus

1/1 Hydrops, anemia,

DIC, ascites,

pleural effusion and pericardial effusion

6/6 Hydrops, PDA, NEC, donor of

twin to twin

transfusion 6/7 Hydrops, anemia,

pleural effu sions, ascites, DIC, sepsis (Staphylococ cus aureus) Outcome and Pathologic Findings

Case Mater- Gray- Ges- Birth Lowest Pla- Mode of nal ida ta- Weight Weight cent- Delivery, Age Para tion (gm) (gm) al Complications

(yr) (wk) Weight

(gm)

9 21 Gi 36 3,700 2,500 . . . Vaginal 2/6 Hydrops, paroxys- Survived

mal supraven tricular tachy cardia

1/4 Hydrops, anemia, Survived—single

hyperbilirubine- umbilical artery mia

3/2 Hydrops, anemia, Survived—pace congenital maker (tempo heart block, rary X4 days)

DIC

Survived

P0

10 22 G2

P0

SB1

11 31 G4

P3

12 25 G1

P0

13 24 G3

l@1

14 32 G4

P2

SBI

15 34 G3

P2

34 2,180 1,450 498 Cesarean section

Breech, fetal dis tress

33 3,340 1,900 623 Cesarean section

Breech, fetal dis

tress, maternal

ANA

32 1,900 1,370 . . . Vaginal Fetal distress

38 3,720 . . . 1,120 Cesarean section

Decreased fetal movement, me conium staining

. . - 500 Vaginal

Polyhydramnios,

ultrasound—fe tal pleural effu

sion and ? hy

drops

Died 48 hr—severe asphyxial changes, single umbilical artery

Survived

Died 72 hr

Ritter's disease

with severe as phyxial changes, imperforate by men, hypoplastic uterus, bilateral accessory renal arteries 32 1,050 680 580 Cesarean section

Twin (2nd)—

transverse lie

36 2,940

* Abbreviations used: DIC, disseminated intravascular coagulopathy.

newborn with NIHF. Prenatal diagnosis was estab lished or suggested in one third of the cases. When uterine growth rate increases disproportionately to gestational age, ultrasound examination is indicated to diagnose possible underlying causes. If fetal as cites, pleural fluid or tissue edema is apparent, then a possible diagnosis of fetal hydrops should be en tertained. A further search should then be made for abnormalities associated with NIHF, eg, fetal heart rate disturbances and congenital infection. Once recognized as a high risk pregnancy, frequent eva!-uation of fetal well-being is warranted through the remainder of gestation. Delivery of the infant must be anticipated whenever possible, and undertaken in an optimal environment within a maternal and neonatal intensive care setting. The appropriate

timing of delivery is not known, although with

evidence of progressive hydrops, premature deliv ery by induction or cesarean section may be mdi cated. As severe depression at birth is almost uni

form, preparations must be made beforehand for

immediate, vigorous resuscitation and stabilization DISCUSSION

The number of conditions that have been recog nized in association with NIHF is extensive (Table 1). However, it is difficult to speculate on, much less confirm, a cause and effect relationship in most of these situations. As elegantly reviewed by Barnes et al,@ the underlying common pathologic mecha nisms responsible for edema formation in the fetus

and newborn remain unclear. Edema has been at

tributed commonly to one of three factors: conges tive heart failure, decreased colloid osmotic pres

sure, and anemia. Based upon both clinical and

experimental evidence, however, none of these fac tors is singularly or uniformly related to the for mation of edema. In the present series of patients,

no common underlying physiologic abnormality

could be identified which may have been responsi ble for the NIHF (Table 5).

CaseMater-Gravandnalidata Ges BirthLowestPla Mode ofApgarClinicalOutcome WeightWeightcent

Delivery,ScoreFindingsPathologicAgeParation(gm)(gm)atComplicationsFindings(yr)(wk)Weight

(gm)1619G2

P1342,3001,760.

. .Vaginal8/9Hydrops, necro

tizing entercoli tisSurvived1720Gi

P0331,9201,600390Cesarean

section

Maternal lupus

nephritis, tox

emia, fetal

bradycardia2/5Hydrops,

DIC,

LE, ANA nega

tiveDied

13 mo—mi

crocephaly, cere

bral hemorrhage

(old)1821GI

P0332,600.

. .. . .Vaginal

Edema, normal

blood pressure3/4Hydrops,

DIC,

pleural effu sionsDied

11/2 hr1928Gi394,7203,700650Cesarean

section7/8HydropsSurvivedP0Polyhydramnios,

ultrasound—?

hydrops2033G3

P2342,9402,200734Vaginal Polyhydramnios0/1Hydrops,

DICSurvived—pro

longed ascites (chylous)2128G3

P2331,9401,540.

. .Elective cesarean

section Polyhydramnios,

ultrasound pleural effu

sions—?by drops4/6Mild

hydrops,

pleural effu sions, hyaline membrane dis

ease, ascitesSurvived—placenta

membranacea2227G2

P1362,4001,880.

. .Vaginal2/4Hydrops, hyaline

membrane dis ease, DIC, as

citesSurvived

TABLE4. NIHF—IdiopathicCases*

a Abbreviations used: DIC, disseminated intravascular coagulopathy; LE, lupus erythematosus.

TABLE 5. Laboratory Tests to be Consideredin

Evaluation of NIHF

Complete blood cell count, platelet count Betke-Kleihauer test on maternal blood Electrolytes, renal and liver function tests Blood type, Coombs' (direct and indirect) Hemoglobin electrophoresis

X-rays of chest, abdomen, long bones, and skull ECG, echocardiogram

Bacterial, viral cultures

Serology for congenital infections (mother and baby) Diagnostic thoracentesis/paracentesis

Placental anatomy/histology

Chromosomal karyotype Other tests as indicated

of the infant. Decisions concerning viability of a hydropic infant should not be made at the time of delivery unless lethal anomalies are obvious. In the delivery room, abdominal paracentesis or thoracen tesis or both may be life-saving in the presence of marked ascites and inadequate response to intuba tion and positive pressure ventilation.

During the ensuing period of stabilization several factors must be considered. Adequate oxygenation

and ventilation may require high ventilatory rate (40 to 60/mm), peak inspiratory pressures (25 to 50 cm H2O), and positive end expiratory pressure (6 to 8 cm H2O). Perfusion must also be supported. De spite the marked increase in total body water and extracellular fluid, infants with Rh isoimmune hy drops (and possibly NIHF) frequently have normal or reduced blood volumes.39 40 Therefore, volume expansion (preferably with whole blood or partially packed cells) may be indicated if peripheral perfu sion is compromised.

Once initial stabilization is complete, three par ticular management problems are frequently en countered. First, inadequate ventilation, or oxygen ation, or both often persist despite vigorous venti lator and circulatory support. In these instances, massive hydrops with ascites, pleural effusions, and pulmonary edema are usually present and may warrant repeated paracentesis, or thoracentesis, or both. Further, the pulmonary edema is optimally managed by continuous positive airway pressure with judicious use of diuretics (furosemide) and

digitalis. Management of the generalized body

conservatively by mild to moderate fluid restriction (60 to 80 mi/kg/day) after initial stabilization. Spontaneous diuresis usually ensues between three and five days after birth, resulting in a maximal weight loss by 7 to 12 days. The mean weight loss of the surviving babies during the neonatal period in the present series was 28% of birth weight (range 17 to 43%). During the process of diuresis, which may be brisk and massive, a metabolic alkalosis may be noted, referred to as “¿contraction alka losis―.4'A third problem that occurred in 50% of the infants within 24 hours of age was disseminated intravascular coagulopathy. Perhaps on the basis of the severe perinatal asphyxia and associated prob lems, the disseminated intravascular coagulation (DIC) often required prompt, sometimes repeated, exchange transfusions with fresh CPD blood (< 48 hours old). If thrombocytopenia is severe, platelet transfusion (5 ml/kg of platelet pack) may be re

quired midway through and at the completion of

the exchange transfusion. Throughout the stabii zation period, plans for a comprehensive diagnostic

evaluation must be made (Table 3). Blood and

serum analyses should be obtained before beginning an exchange transfusion.

In view of a possible relative increase in frequency

of NIHF and the perhaps improved outlook for

survival of these infants, vigorous efforts to provide

optimal support should be made for both the hy

dropic fetus and newborn. A thorough understand ing of related conditions and expected clinical prob lems is necessary.

ACKNOWLEDGMENT

This investigation was supported in part by a grant from the National Foundation/March of Dimes.

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19. Bates HR, Jr: Coxsackie virus B3 calcific pancarditis and hydrops fetalis. Am J Obstet Gynecol 106:629, 1970

20. Ito T, Engle MA, Holswade GR: Congenital insuffi ciency of the pulmonic valve. Pediatrics 28:712, 1961 21. Arcilla RA, Thilenius OG, Ranniger K: Congestive

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TEENAGE PREGNANCY: WHY THE EPIDEMIC?

It is the age of the Pill, yet over a million American teenagers will get pregnant this year. About 600,000 of these young women will give birth . . . . In the 1950s, of course, contraception was illegal in many states even for married adults . ... By the mid- 1960s, contraceptive services were available to some resourceful adolescents, and residents of a few states could obtain reasonably inexpensive legal abortions—though the popular press still shied away from passing along information about either one. Court decisions in the 1970s have made contra ception and abortion even more widely available. Now, about 400,000 teenage girls have abortions each year. But of the 600,000 teenagers who give birth, a staggering 94% keep their children. More than a third of these young mothers do not marry. Many are struggling with medical, social, and economic problems. The teenage pregnancy epidemic of the 1970s turns out to be more of a teenage baby-keeping epidemic.

From Working Papers For a Neu' Society 6:64 (March/April), 1979.

1979;64;326

Pediatrics

P. C. Etches and James A. Lemons

Nonimmune Hydrops Fetalis: Report of 22 Cases Including Three Siblings

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