Discussion:
Preeclampsia is a life threating disorder with various symptoms. It is important to decide appropriate timing for delivery to prevent adverse outcome for mother and infant. There are several severe features which are key symptoms to decide this [Table1]. The pathophysiology of preeclampsia is increased vascular permeability and vascular spasm caused by endothelial dysfunction. Because effusion into the body cavity in preeclampsia is generally explained by increased capillary permeability due to endothelial cell dysfunction and reduced intravascular oncotic pressure, ascites is thought to be an early event in aggravated preeclampsia 2). Cong KJ et al. reported that the incidence of ascites in severe preeclampsia was 21.6/1000 during pregnancy3). On the other hand, Vaijyanath AM et al. estimated the incidence of ascites was 8 in 1000 during pregnancy and ascites usually develops from 27 to 31 weeks gestation in preeclampisa4). They also reported that preeclampsia with massive ascites and respiratory distress due to pleural effusion during pregnancy should be signal pregnancy termination4).
In this case, massive ascites was observed after delivery. However, we may speculate that a certain level of ascites had accumulated before delivery based upon the 7 kg weight gain in the final month before delivery, and normal weight gain during the third trimester of pregnancy is about 0.5kg per one week5). Indeed, one described a relationship between ascites and rapid weight gain can occur in association with preeclampsia6). Thus, it is necessary to anticipate the development or aggravation of preeclampsia when we see excessive weight gain during pregnancy.
The principal finding of this case is the acute retention of massive ascites occurring two days after delivery. Intra-abdominal hypertension is defined as a sustained intra-abdominal pressure (IAP) greater than 15cmH20. Antepartum IAP levels are thought to be significantly higher in patients with preeclampsia7). The abdominal cavity can be considered as a semi-closed compartment, and any volume change in abdominal content can affect IAP.
In the present case, we speculate that the IAP level was elevated with the development of PE and existence of ascites before delivery. After delivery IAP decreased significantly because of a sudden involvement of the uterus which occupied most of the abdominal cavity. Finally, according to rapid decreased IAP levels at the time of delivery, a large amount of ascites leaked into the abdominal cavity. Thus, massive ascites was detected postpartum.
The level of soluble fms-like tyrosine kinase-1 (sFlt-1) in this case was higher in postpartum period. There is no diagnostic criteria for sFlt-1 values, but current reports describe the level of sFlt-1 as gradually decreasing after delivery and stabilized around 77 pg/ml. In this case, it was suggested that sFlt-1 was high at the time of delivery8). sFlt-1 is known as important factor for microvascular damage. The model suggests elevated sFlt-1 and associated microvascular damage may be severe during delivery and ascites was likely to accumulate.
There are several reports relating PE with massive ascites. One cohort study reported that ascites was associated with maternal events such as eclampsia, pulmonary edema, renal failure, and disseminated intravascular coagulation9). A secondd prospective cohort study showed an association between ascites and both maternal and perinatal outcomes such as premature obstetrics and low birth weight10). Although both studies described patients diagnosed with severe PE, the case described here did not show severe hypertension nor any other related pathological features. However, this case was associated with FGR and neonatal distress. Thus, the accumulation of ascites itself may indicate that severe PE and/or aggravation of PE.
There is no clear evidence for management of PE associated with ascites. According to one report, early termination may improve the outcome in cases of preeclampsia associated with ascites11). Moreover, another report showed that development of ascites in preeclampsia warrants immediate termination of pregnancy in a study of 21 patients with pregnancy induced hypertension. Based on the existing literature and this case, earlier termination should be considered to improve both maternal and infant outcomes if obvious ascites is observed with preeclampsia.
In addition, critical actions, such as albumin replacement therapy or abdominal puncture to remove ascites, may be required if serious complications including respiratory distress accompany massive ascites in postpartum. In this case, massive ascites decreased naturally as preeclampsia improved, and no medical intervention was needed for the management of massive ascites.