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.