ꢀꢀꢀꢁ
110ꢀ ꢀStanić et al., Massive ascites and preeclampsia
canal was performed; minor ruptures of the cervix and the may be due to a combination of increased post-capillary
vagina were sutured, and firmly packed. Fluids and albu- resistance and endothelial disruption resulting in dis-
mins with oxygen inhalation were administered. Urine ordered protein movement and reduced intravascular
output was satisfactory. Twelve hours after hemodynamic oncotic pressure. The low colloid oncotic pressure results
stabilization, hypertension reappeared. It was controlled in effusions such as ascites. It is supposed that the trigger
with antihypertensive therapy and magnesium sulfate.
for sudden development of massive ascites is hypopro-
On the 5th day after surgery antihypertensive therapy teinemia originated from excessive renal protein loss
was stopped. No signs of ascites, pleural, and pericardial [7]. There is evidence that PE is associated with changes
effusion were detected. In next 5 days severe proteinuria in maternal systemic inflammatory response with dif-
decreased five-fold with stabilization of other laboratory ferent leukocyte subpopulations found in ascites and
analyses. The patient was discharged normotensive in a peripheral blood of the same woman [8]. In the majority,
clinically good condition.
massive ascites develop between the 27th and 33th week
of pregnancy. Clinical findings supporting this condition
include significant respiratory distress of the mother, dry
cough and dyspnea, respiratory acidosis and a fall in pO2
[6]. Evident maternal respiratory insufficiency imposes a
high-risk condition for the fetus. In patients with PE, a
transitory portal hypertension with transudation of the
fluid with low protein content into peritoneal cavity is
noted [3]. Patients with intrauterine growth restriction
and PE present a challenging group for high-risk preg-
nancy management. With additional findings of massive
ascites, imposing the need for very early pregnancy ter-
mination, this group of patients shows very high perina-
tal mortality, up to 42%. We conclude that massive ascites
in women with PE presents a rare complication that
mandates active pregnancy termination within 24 to 48
h. Medicament therapy and drainage of ascites have no
value. Evaluation of peritoneal fluid quantity in women
with PE could warn the obstetrician of the potential risks
demanding more intensive and more frequent fetoma-
ternal surveillance. Cautious fluid administration and
observation for cardiopulmonary deterioration are man-
datory to avoid maternal/fetal hypoxia.
Discussion
Our article reports the case of a patient who was mis-
diagnosed for hematoperitoneum due to presence of
massive ascites that were not visible 3 days before
delivery, and hence were confused with massive intra-
abdominal bleeding due to uterine rupture. Due to this
misjudgment that was supported by the clinical appear-
ance of the patient and suggestive laboratory analy-
ses, an unnecessary laparotomy was performed. It is,
however, intriguing why uterine rupture was not ruled
out by simple uterine cavity exploration. We assume
that the clinical aspect of the patient was indicative for
hemorrhagic shock, so it was decided to do an urgent
laparotomy and suture of uterine rupture, to prevent the
life-threatening condition.
Some amount of peritoneal fluid can be seen during
cesarean section in patients with PE and in women with
normal pregnancies, but the presence of massive ascites
is a rare finding. Although there is no clear definition of
massive ascites, arbitrarily it is defined as the presence of
an amount equal to or more than 2 L of peritoneal fluid.
In 1949, Golden stated that the cause of ascites in preg-
nancy was a low concentration of proteins with an altered
References
albumin/globulin ratio ꢀ<ꢀ1.5 [7]. The paucity of reports in [1] Sibai BM, Stella CL. Diagnosis and management of
atypical preeclampsia-eclampsia. Am J Obstet Gynecol.
the literature may be due to under-reporting and also the
2009;200:481–7.
difficulty in recognizing this condition clinically. Due to
[2] Scazzocchio E, Figueras F. Contemporary prediction of preec-
this under-reporting, the incidence of massive ascites in
lampsia. Curr Opin Obstet Gynecol. 2011;23:65–71.
PE has different estimations ranging from eight to twenty
one point six cases in 1000 patients with PE [4]. The
modern concept of pathophysiology of PE includes renal
retention of sodium and fluid together with generalized
endothelial cell dysfunction. Gradually, expansion of
interstitial compartment develops due to generalized cap-
illary leak, and hence 3rd space fluid collection appears in
the form of massive ascites. The increased capillary leak
[3] Smith GC, Wear H. The perinatal implications of angiogenic fac-
tors. Curr Opin Obstet Gynecol. 2009;21:111–6.
[4] Duckitt K, Harrington D. Risk factors for pre-eclampsia at ante-
natal booking: systematic review of controlled studies. Br Med J.
2005;330:565.
[5] Myatt L, Webster RP. Vascular biology of preeclampsia. J Thromb
Haemost. 2009;7:375–84.
[6] Woods JB, Blake PG, Perry KG Jr, Magann EF, Martin RW,
Martin JN Jr. Ascites: a portent of cardiopulmonary
- 10.1515/crpm-2015-0014
Downloaded from De Gruyter Online at 09/12/2016 10:39:13AM
via University of Exeter
Wenska
