2006Ultrasound in Obstetrics and GynecologyRequires access

P04.14: Nonimmune hydrops fetalis—case report

Jiří Kučera, I. Kučerová, V. Cunat

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Abstract

28 year old gravida I para I was referred to our institution in 31th week of gestation. Fetal biometry corresponded to one week younger pregnancy. Extreme fetal cardiomegaly with tricuspidal regurgitation (CTI 0.6), pericardial effusion and ascites were observed. Doppler parameters (PSV MCA) were suggestive of severe fetal anemia. No other abnormalities were found. Amount of amniotic fluid was normal. Admission with subsequent cordocentesis and fetal transfusion was offered to the family. Induction of fetal lung maturity was initiated by steroids. Pregnancy was terminated by acute cesarian section indicated by reason of fetal hypoxia detected by CTG. Male newborn was delivered with Apgar score 5–4–6 and normal umbilical cord acid base analysis. Severe fetal anemia was confirmed postnatally. Ventilatory support with extremely high setting was needed to maintain normal blood gases during first hours of life. Ascites puncture dramatically improved situation with subsequent reduction of peak inspiratory pressure. Circulatory support by catecholamines and volume administration was required during first days of life. Echocardiography revealed extreme cardiomegaly with impaired ventricular function. This finding was followed by severe myocardial hypertrophy during first week of life. Echocardiogram was normal after 4 weeks. No underlying reason for severe fetal anemia was found. Baby recovered without having further serious complications. No developmental abnormalities were found during follow-up so far. Non-imunne hydrops is a severe condition associated with high neonatal mortality and morbidity. Fetal hydrops was caused by severe fetal anemia in our case. Fetus was at high risk if intrauterine death. Severely impaired cardiac function fully recovered despite unfavorable initial course. Baby survived without apparent developmental abnormalities.

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What this paper is about

28 year old gravida I para I was referred to our institution in 31th week of gestation. Fetal biometry corresponded to one week younger pregnancy. Extreme fetal cardiomegaly with tricuspidal regurgitation (CTI 0.6), pericardial effusion and ascites were observed. Doppler parameters (PSV MCA) were suggestive of severe fetal anemia. No other abnormalities were found. Amount of amniotic fluid was normal. Admission with subsequent cordocentesis and fetal transfusion was offered to the family. Induction of fetal lung maturity was initiated by steroids. Pregnancy was terminated by acute cesarian section indicated by reason of fetal hypoxia detected by CTG. Male newborn was delivered with Apgar score 5–4–6 and normal umbilical cord acid base analysis. Severe fetal anemia was confirmed postnatally. Ventilatory support with extremely high setting was needed to maintain normal blood gases during first hours of life. Ascites puncture dramatically improved situation with subsequent reduction of peak inspiratory pressure. Circulatory support by catecholamines and volume administration was required during first days of life. Echocardiography revealed extreme cardiomegaly with impaired ventricular function. This finding was followed by severe myocardial hypertrophy during first week of life. Echocardiogram was normal after 4 weeks. No underlying reason for severe fetal anemia was found. Baby recovered without having further serious complications. No developmental abnormalities were found during follow-up so far. Non-imunne hydrops is a severe condition associated with high neonatal mortality and morbidity. Fetal hydrops was caused by severe fetal anemia in our case. Fetus was at high risk if intrauterine death. Severely impaired cardiac function fully recovered despite unfavorable initial course. Baby survived without apparent developmental abnormalities.

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Available abstract

28 year old gravida I para I was referred to our institution in 31th week of gestation. Fetal biometry corresponded to one week younger pregnancy. Extreme fetal cardiomegaly with tricuspidal regurgitation (CTI 0.6), pericardial effusion and ascites were observed. Doppler parameters (PSV MCA) were suggestive of severe fetal anemia. No other abnormalities were found. Amount of amniotic fluid was normal. Admission with subsequent cordocentesis and fetal transfusion was offered to the family. Induction of fetal lung maturity was initiated by steroids. Pregnancy was terminated by acute cesarian section indicated by reason of fetal hypoxia detected by CTG. Male newborn was delivered with Apgar score 5–4–6 and normal umbilical cord acid base analysis. Severe fetal anemia was confirmed postnatally. Ventilatory support with extremely high setting was needed to maintain normal blood gases during first hours of life. Ascites puncture dramatically improved situation with subsequent reduction of peak inspiratory pressure. Circulatory support by catecholamines and volume administration was required during first days of life. Echocardiography revealed extreme cardiomegaly with impaired ventricular function. This finding was followed by severe myocardial hypertrophy during first week of life. Echocardiogram was normal after 4 weeks. No underlying reason for severe fetal anemia was found. Baby recovered without having further serious complications. No developmental abnormalities were found during follow-up so far. Non-imunne hydrops is a severe condition associated with high neonatal mortality and morbidity. Fetal hydrops was caused by severe fetal anemia in our case. Fetus was at high risk if intrauterine death. Severely impaired cardiac function fully recovered despite unfavorable initial course. Baby survived without apparent developmental abnormalities.

Key concepts: Medicine, Hydrops fetalis, Fetus, Anemia, Pericardial effusion, Pregnancy, Obstetrics, Gestational age

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