Maternal acute renal failure and non-immune hydrops
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《美国医学杂志》
Division of Neonatology, Department of Pediatrics, PGIMER, Chandigarh-160012, India
With the control of Rh isoimmunisation, non-immune hydrops is assuming increasing importance in perinatal medicine. In this case report, we present an unusual association of maternal acute renal failure and neonatal non-immune hydrops.
A 26-year-old primigravida mother was referred to our hospital at 37 weeks of gestation with problems of oliguria and edema of face and limbs for 3 days. Her blood pressure and blood sugar were normal and she was on regular hematinics and calcium. There was no history of rash or fever in the 1st trimester. Routine antenatal ultrasound done at 16 weeks revealed a single live fetus of appropriate gestation. Veneral disease research laboratory test (VDRL) done in the 1st trimester was non-reactive. At admission she was of average built, had facial puffiness and pitting edema of limbs. Her blood pressure was 140/90 mm of Hg. Uterus was relaxed and fetal heart was 136/min and regular. Blood group was B positive. Urine routine showed 3+ RBCs and 20 pus cells/high per field. There were no casts or eosinophils. Urine was negative for albumin on many occasions and culture was sterile. Serum urea was 44mg/dl and creatinine 2.2 mg/dl. ASO and C reactive protein were negative. She was diagnosed as a case of acute renal failure either secondary to post infectious glomerulonephritis or acute interstitial nephritis. Ultrasound of abdomen revealed a single live fetus of 37 weeks with oligohydramnios (Amniotic Fluid Index of 5cm). The non stress test (NST) was non-reactive. In view of oligohydramnios and nonreactive NST an emergency caesarian section was done. She did not-receive any extra fluid to cause fetal hydrops or any medication that could cause fetal renal failure and oligohydramnios.
A liveborn female baby weighing 2.7 kg was delivered. Placenta was complete with normal morphology and weighed 350 gm. The baby was depressed at birth and required intermittent positive pressure ventilation and chest compressions during resuscitation. In view of continuing poor respiratory efforts the baby was shifted to neonatal intensive care unit for mechanical ventilation. Apgar scores at 1, 5 and 10 minutes of life were 2, 6 and 9 respectively. Immediately after birth the baby was noted to have puffiness of face, swollen neck and pitting edema of both upper and lower limbs. There was no dysmorphism, pallor, hepatosplenomegaly, rash or petechiae or abdominal masses. There was no evidence of intrauterine infection and chromosomal abnormalities. Chest X ray revealed bilateral diffuse haziness, which cleared in next 2 days. The baby was ventilated in Neonatal Intensive Care Unit (NICU) for respiratory distress with a maximum Peak Inspiratory Pressure (PIP) of 22 and Positive End Expiratory Pressure (PEEP) of 5 cm of water and FiO2 of 80%. The baby was given injection frusemide 1mg/kg 12 hourly on day 1 and day 2. The generalized edema subsided by day 3 and the baby had a weight loss of 80gm on day 1 and 72gm on day 2 (cumulative 5.5%of birth weight). The baby was extubated at 60 hours of life and respiratory distress settled by end of day 3. The baby did not manifest any features of hypoxic ischemic encephalopathy. Day 1 serum sodium was 117meq/L and repeat Na on day 2 was 132 meq/L. Cord blood PCV was 40% which rose to 52% after edema subsided. Ultrasound abdomen revealed mild ascites and small pleural effusion. Toxoplasma, other Rubella, Cytomegalovirus, herpes simplex (TORCH) work-up was negative. Echocardiography and electrocardiogram did not suggest any cardiac abnormality. Renal functions were deranged on day 1 probably reflecting maternal renal function but became normal by 48hr. Liver function tests were normal. Mother's urine output and renal function improved by day 3 and edema subsided by day 4 of postpartum. The baby was discharged home on day 8 of life with a weight of 2784 gm. On follow up at 3 months the baby did not have any stigmata of intrauterine infection or chromosomal abnormality.
Non-immune hydrops occurs in nearly 1 in 3500 live births.[1] The important causative factors include cardiovascular abnormalities (19.3%), chromosomal abnormalities (13%), cystic hygroma (10.7%), hematological disorders (10%), pulmonary, genitourinary and gastrointestinal malformations (15%). Intrauterine infections account for nearly 3% of non-immune hydrops. In the rest even after extensive investigations no cause is identified.[2] To the best of our knowledge, no case of renal failure in the mother associated with hydrops in the baby has been reported.
The exact etiopathogenesis of hydrops in our baby is unclear. But one can hypothesize that the hydropic manifestation is secondary to fluid overload in the mother and fetal anoxia. Fluid overload in the mother leads to increased shift of fluids to the fetus, as the placenta is freely permeable to free water.[3] However in a normal fetus the urine output increases proportionately to keep pace with increased fluid transfer. In the presence of fetal anoxia as seen in the index case there is renal vasoconstriction with decreased urine output.[4] In the presence of this oliguria any increase in fluid transfer to the fetus would invariably lead to fluid overload in the baby and subsequent hydropic manifestations. The features of fetal anoxia in the index case were manifesting in the form of acute onset oligohydramnios, non-reactive NST and need for resuscitation at birth. The dramatic resolution of postnatal edema to diuretics and ventilatory support suggest the possibility of a mild variant of hydrops.
References
1. Hutchison A A, Drew JH, Victor Yu, Williams M L, Fortune DW, Beischer NA. Non-immune Hydrops Fetalis. A review of 61 cases. Obstet Gynaecol 1982; 59 : 347-352.
2. Hansman M, Gembrush U, Bald R. In Harrison Mr, Golbus MS, Filly, eds. Management of the fetus with nonimmune hydrops. The Unborn Patient . Philadelphia; WB Saunders Co. 1991; 248.
3. Battaglia F, Prystowsky H, Hellergens A, Brun P. the effect of aministration of fluids intravenously to mothers upon the concentrations of water and electrolytes in plasma of human fetuses. Pediatrics 1960; 25 : 2-10.
4. Nicolaides KH, Peters MT, Vyas S. Rabinowitz R, Rosen D J D, Campbell S. Relation of rate of urine production to oxygen tension in small for gestational age fetuses. Am J Obstet Gynecol 1990; 162 : 387-391.(Murki Srinivas, Mukhopadh)
With the control of Rh isoimmunisation, non-immune hydrops is assuming increasing importance in perinatal medicine. In this case report, we present an unusual association of maternal acute renal failure and neonatal non-immune hydrops.
A 26-year-old primigravida mother was referred to our hospital at 37 weeks of gestation with problems of oliguria and edema of face and limbs for 3 days. Her blood pressure and blood sugar were normal and she was on regular hematinics and calcium. There was no history of rash or fever in the 1st trimester. Routine antenatal ultrasound done at 16 weeks revealed a single live fetus of appropriate gestation. Veneral disease research laboratory test (VDRL) done in the 1st trimester was non-reactive. At admission she was of average built, had facial puffiness and pitting edema of limbs. Her blood pressure was 140/90 mm of Hg. Uterus was relaxed and fetal heart was 136/min and regular. Blood group was B positive. Urine routine showed 3+ RBCs and 20 pus cells/high per field. There were no casts or eosinophils. Urine was negative for albumin on many occasions and culture was sterile. Serum urea was 44mg/dl and creatinine 2.2 mg/dl. ASO and C reactive protein were negative. She was diagnosed as a case of acute renal failure either secondary to post infectious glomerulonephritis or acute interstitial nephritis. Ultrasound of abdomen revealed a single live fetus of 37 weeks with oligohydramnios (Amniotic Fluid Index of 5cm). The non stress test (NST) was non-reactive. In view of oligohydramnios and nonreactive NST an emergency caesarian section was done. She did not-receive any extra fluid to cause fetal hydrops or any medication that could cause fetal renal failure and oligohydramnios.
A liveborn female baby weighing 2.7 kg was delivered. Placenta was complete with normal morphology and weighed 350 gm. The baby was depressed at birth and required intermittent positive pressure ventilation and chest compressions during resuscitation. In view of continuing poor respiratory efforts the baby was shifted to neonatal intensive care unit for mechanical ventilation. Apgar scores at 1, 5 and 10 minutes of life were 2, 6 and 9 respectively. Immediately after birth the baby was noted to have puffiness of face, swollen neck and pitting edema of both upper and lower limbs. There was no dysmorphism, pallor, hepatosplenomegaly, rash or petechiae or abdominal masses. There was no evidence of intrauterine infection and chromosomal abnormalities. Chest X ray revealed bilateral diffuse haziness, which cleared in next 2 days. The baby was ventilated in Neonatal Intensive Care Unit (NICU) for respiratory distress with a maximum Peak Inspiratory Pressure (PIP) of 22 and Positive End Expiratory Pressure (PEEP) of 5 cm of water and FiO2 of 80%. The baby was given injection frusemide 1mg/kg 12 hourly on day 1 and day 2. The generalized edema subsided by day 3 and the baby had a weight loss of 80gm on day 1 and 72gm on day 2 (cumulative 5.5%of birth weight). The baby was extubated at 60 hours of life and respiratory distress settled by end of day 3. The baby did not manifest any features of hypoxic ischemic encephalopathy. Day 1 serum sodium was 117meq/L and repeat Na on day 2 was 132 meq/L. Cord blood PCV was 40% which rose to 52% after edema subsided. Ultrasound abdomen revealed mild ascites and small pleural effusion. Toxoplasma, other Rubella, Cytomegalovirus, herpes simplex (TORCH) work-up was negative. Echocardiography and electrocardiogram did not suggest any cardiac abnormality. Renal functions were deranged on day 1 probably reflecting maternal renal function but became normal by 48hr. Liver function tests were normal. Mother's urine output and renal function improved by day 3 and edema subsided by day 4 of postpartum. The baby was discharged home on day 8 of life with a weight of 2784 gm. On follow up at 3 months the baby did not have any stigmata of intrauterine infection or chromosomal abnormality.
Non-immune hydrops occurs in nearly 1 in 3500 live births.[1] The important causative factors include cardiovascular abnormalities (19.3%), chromosomal abnormalities (13%), cystic hygroma (10.7%), hematological disorders (10%), pulmonary, genitourinary and gastrointestinal malformations (15%). Intrauterine infections account for nearly 3% of non-immune hydrops. In the rest even after extensive investigations no cause is identified.[2] To the best of our knowledge, no case of renal failure in the mother associated with hydrops in the baby has been reported.
The exact etiopathogenesis of hydrops in our baby is unclear. But one can hypothesize that the hydropic manifestation is secondary to fluid overload in the mother and fetal anoxia. Fluid overload in the mother leads to increased shift of fluids to the fetus, as the placenta is freely permeable to free water.[3] However in a normal fetus the urine output increases proportionately to keep pace with increased fluid transfer. In the presence of fetal anoxia as seen in the index case there is renal vasoconstriction with decreased urine output.[4] In the presence of this oliguria any increase in fluid transfer to the fetus would invariably lead to fluid overload in the baby and subsequent hydropic manifestations. The features of fetal anoxia in the index case were manifesting in the form of acute onset oligohydramnios, non-reactive NST and need for resuscitation at birth. The dramatic resolution of postnatal edema to diuretics and ventilatory support suggest the possibility of a mild variant of hydrops.
References
1. Hutchison A A, Drew JH, Victor Yu, Williams M L, Fortune DW, Beischer NA. Non-immune Hydrops Fetalis. A review of 61 cases. Obstet Gynaecol 1982; 59 : 347-352.
2. Hansman M, Gembrush U, Bald R. In Harrison Mr, Golbus MS, Filly, eds. Management of the fetus with nonimmune hydrops. The Unborn Patient . Philadelphia; WB Saunders Co. 1991; 248.
3. Battaglia F, Prystowsky H, Hellergens A, Brun P. the effect of aministration of fluids intravenously to mothers upon the concentrations of water and electrolytes in plasma of human fetuses. Pediatrics 1960; 25 : 2-10.
4. Nicolaides KH, Peters MT, Vyas S. Rabinowitz R, Rosen D J D, Campbell S. Relation of rate of urine production to oxygen tension in small for gestational age fetuses. Am J Obstet Gynecol 1990; 162 : 387-391.(Murki Srinivas, Mukhopadh)