Massive ascites in a patient with preeclampsia

Introduction

Preeclampsia (PE) affects about 2–3% of pregnancies, and is a major contributor to maternal mortality with an estimate of 100,000 deaths annually worldwide. So far, increased endothelial dysfunction, vascular permeability, and microvascular damage are considered the most important pathogenetic contributors [1–4].

Hypertension is considered hallmark of PE; however, in some patients with PE, disease can manifest as either capillary leak (proteinuria, ascites, pulmonary edema, and excessive weight gain), or a spectrum of hemostasis abnormalities with multiple organ dysfunction. Severe ascites complicates 8% of patients with haemolysis elevated liver enzymes and low platelets syndrome (HELLP syndrome) [1, 2, 5, 6], that is not always believed to be the same disease process as PE.

We present an unusual case of massive ascites in a term pregnancy which was misdiagnosed during antenatal surveillance and confused with hematoperitoneum after vaginal delivery.

Case report

A 25-year-old primigravida was admitted to the obstetric and gynecology department in the 35^th week of pregnancy because of PE. The history of the patient and the antenatal record showed normal course of pregnancy until the 32^ndweek, when urine examination showed proteinuria (+++ on dipstick). In the next 2 weeks blood pressure (BP) rose from 160 to 170/110 to 120 mm Hg. Amlopine 5 mg and aspirine 100 mg were administered, keeping the BP in the normal range. Laboratory analyses were reported within normal limits. Monitored fetal heart rate (FHR) tracing via cardiotocography (CTG) were optimal. Ultrasound (US) scan 3 days prior to delivery showed no free intra-abdominal fluid. Color Doppler analyses were normal [umbilical artery resistance index (AURI) 0.56; fetal middle cerebral artery resistance index (ACMRI) 0.91], as well as biophysical profile (score 9). Fetal biometry corresponded with gestational age and no signs of uteroplacental insufficiency were present.

At the 38^th week of pregnancy, FHR tracing was non-reassuring. BP was 170/120 mm Hg. The vaginal delivery was induced, and a male newborn was delivered (2900 g/50 cm; >10^th percentile, Apgar score in 1^st and 5^th min was 10). After delivery of the placenta, the patient became pale, edematous, dyspneic with massive (>1000 mL) vaginal hemorrhaging. Systolic BP was 50 mm Hg, and diastolic was immeasurable. US scan revealed the presence of intra-abdominal fluid. After the measures of hemodynamic stabilization, and transfusion of 1500 mL of RBC concentrate, under clinical suspicion of uterine rupture, the patient underwent immediate explorative laparotomy. After the peritoneal cavity was opened, massive ascites measuring 4.5 L were evacuated. The uterus was intact and no bleeding site in abdomen was found. Exploration of the birth canal was performed; minor ruptures of the cervix and the vagina were sutured, and firmly packed. Fluids and albumins with oxygen inhalation were administered. Urine output was satisfactory. Twelve hours after hemodynamic stabilization, hypertension reappeared. It was controlled with antihypertensive therapy and magnesium sulfate.

On the 5^th day after surgery antihypertensive therapy was stopped. No signs of ascites, pleural, and pericardial effusion were detected. In next 5 days severe proteinuria decreased five-fold with stabilization of other laboratory analyses. The patient was discharged normotensive in a clinically good condition.

Discussion

Our article reports the case of a patient who was misdiagnosed 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 appearance of the patient and suggestive laboratory analyses, 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 pregnancy was a low concentration of proteins with an altered albumin/globulin ratio <1.5 [7]. The paucity of reports in the literature may be due to under-reporting and also the difficulty in recognizing this condition clinically. Due to this under-reporting, the incidence of massive ascites in 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 capillary leak, and hence 3^rd space fluid collection appears in the form of massive ascites. The increased capillary leak may be due to a combination of increased post-capillary resistance and endothelial disruption resulting in disordered protein movement and reduced intravascular oncotic pressure. The low colloid oncotic pressure results in effusions such as ascites. It is supposed that the trigger for sudden development of massive ascites is hypoproteinemia originated from excessive renal protein loss [7]. There is evidence that PE is associated with changes in maternal systemic inflammatory response with different leukocyte subpopulations found in ascites and peripheral blood of the same woman [8]. In the majority, massive ascites develop between the 27^th and 33^th 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 pregnancy management. With additional findings of massive ascites, imposing the need for very early pregnancy termination, this group of patients shows very high perinatal 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 fetomaternal surveillance. Cautious fluid administration and observation for cardiopulmonary deterioration are mandatory to avoid maternal/fetal hypoxia.