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.