Case report:
A 26-year-old primigravid women was followed by an obstetrics practitioner over the course of a naturally conceived pregnancy. Proteinuria without hypertension was observed after 35 weeks of gestation. Ultrasonography (USG) did not detect ascites until 39 weeks of gestation. From 36 to 40 weeks of gestation the gained 7 kg. At 40 weeks of gestation, she was admitted due to the premature rupture of the membrane. A vacuum delivery with Kristeller maneuver was performed because of fetal distress and maternal severe hypertension. The newborn was fetal growth restricted, weighing 2758 gram, with Apgar score of 8 and 9 at 1 and 5 minutes, and Umbilical pH of 7.084. Maternal blood pressure improved rapidly after delivery. No maternal abdominal symptoms were observed on the day of delivery. Two days after delivery, the mother exhibited increased abdominal volume. USG detected massive ascites, and she was transferred to our hospital.
Maternal blood pressure fluctuated around 140/80mmHg, with heart rate of 106bpm, and SpO2 99% (room air) without respiratory distress. Massive ascites was confirmed by USG, Computed Tomography (CT) and abdominal puncture [Figure1]. Biochemical analysis revealed abnormal serum albumin (1.8g/dl) and creatinine (0.97mg/dl) levels. Serum AST/ALT was within normal limits and not applicable to HELLP syndrome. A spot urine sample protein and creatinine ratio was 1.19g/g Cre [Figure2].
Based on the above clinical condition, the admitting diagnosis was preeclampsia with massive ascites. If the patient had ascites due to preeclampsia, we expected to recover spontaneously after delivery. Blood pressure and blood creatinine levels recovered over a few days. The urine volume also increased and body weight and waist circumference decreased significantly. The patient was discharged on the seventh day of postpartum in good general condition. At the three month follow up, urine protein had improved to normal level and ascites was not detectable.