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Pleural effusion and ascites in severe preeclampsia: Frequency and

correlation with plasma colloid osmotic pressure and renal filtration function

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 Cir Cir 2011;79:299-305

Pleural effusion and ascites in severe preeclampsia:

frequency and correlation with plasma colloid
osmotic pressure and renal filtration function
Juan Gustavo Vázquez-Rodríguez* and María Guadalupe Veloz-Martínez**

Abstract

Background: Capillary leak with pleural effusion and/or ascites in severe preeclampsia (SP) may be a reason for low
plasma colloid osmotic pressure (PCOP) and deterioration of renal filtration function. The objective of this study was to
report the frequency of pleural effusion and/or ascites in patients with SP and to compare the correlation with PCOP and
renal filtration function. We conducted a cross-sectional study.
Methods: Ninety-two pregnant women with SP were studied. In 52 patients, no fluid collections were demonstrated
and in 40 patients the findings were positive. Correlation with PCOP and endogenous creatinine clearance (CrCl) was
calculated. Student t test and Pearson correlation coefficient (r) were used for statistical analysis.
Results: Frequency of fluid collections was 43.48% (ascites, 16 cases; pleural effusion, 12 cases; and ascites with pleu-
ral effusion, 12 cases). PCOP in patients without and with collections were different (20.12 ± 2.16 vs. 18.78 ± 2.58 mmHg,
respectively; p = 0.009) as well as with endogenous CrCl (111.69 ± 37.61 vs. 95.27 ± 34.22 ml/min/1.73 m2 SC × 0.85;
p = 0.03). Correlation coefficient (r) of PCOP was negative with all the fluid collections (ascites -0.25, pleural effusion
-0.29, ascites with pleural effusion -0.02 and -0.30) as well as the r of endogenous CrCl (ascites -0.01, pleural effusion
-0.13, ascites with pleural effusion -0.27 and -0.67).
Conclusions: Frequency of collections was very high (43.48%). A weak negative correlation with PCOP and endog-
enous CrCl was found.

Key words: ascites, pleural effusion, plasma colloid osmotic pressure, renal filtration, severe preeclampsia, pregnancy.

Introduction common factor seems to be an anomaly of the stages of

Preeclampsia-eclampsia (PE) is a disease of human preg-
nancy recognized by the appearance of new hypertension af-
ter 20 weeks of gestation (blood pressure ≥140/90 mmHg),
abnormal proteinuria (≥300 mg/24 h) and generalized ede-
ma.1 There are several theories to explain its cause.2 The
* Unidad de Cuidados Intensivos de Adultos,
** Coordinación Local de Investigación en Salud, Hospital de
Ginecología y Obstetricia 3, Centro Médico Nacional La Raza,
Instituto Mexicano del Seguro Social, México, D.F., Mexico
Correspondence:
Juan Gustavo Vázquez-Rodríguez
Allende 116 interior 13, Col. Centro
56100 Texcoco, Estado de México, México
Tel: (595) 954 9944; (55) 5782 1088, ext. 23667
E-mail: juangustavovazquez@hotmail.com
Received for publication: 7-27-2010
Accepted for publication: 11-25-2010
invasion of the cytotrophoblast on the wall of the uterine
spiral arterioles causing turbulence, hypoperfusion and
ischemia of the sinusoidal spaces. The release of various
substances of placental origin to the maternal circulation
causes arteriolar and capillary endothelial damage, base-
ment membrane fragmentation and increased permeability
that favor the phenomenon of capillary leakage of water,
solutes and macromolecules (albumin) to the interstices.2,3
Thus, the balance of forces described by Starling in the mi-
crocirculation is altered from a reduction in plasma colloid
osmotic pressure (PCOP) of proteins4,5 and the relative in-
crease in capillary hydrostatic pressure, which justifies the
presence of local and then generalized edema.4-8
In preeclamptic patients, capillary leakage may be as-
sociated with abnormal collections of fluid in the pleura or
peritoneum. The most important factor for its development
seems to be reduced PCOP of proteins.8 However, it has
been documented that increased mean arterial pressure,5
extensive structural damage of the microvasculature in
patients complicated by HELLP syndrome,9 intracapillary
coagulopathy,10 platelet count ≤100,000/mm,3,11 proteinuria

Volume 79, No. 4, July-August 2011 299


>5 g/24  h,11 serum creatinine (Cr) ≥120  mOsm/l,11 portal
hypertension,9 presence of acute cardiogenic pulmonary
edema,9,10 uncontrolled systolic arterial pressure (SAP)11
and adult respiratory insufficiency syndrome (ARIS)9,10
may favor their formation. The aim of this study was to re-
port the frequency of pleural effusion or ascites in pregnant
women with severe preeclampsia (SP) and compare their
correlation with total PCOP of proteins and renal filtration
function.
Materials and Methods
We designed a cross-sectional study that included 92 preg-
nant patients with SP treated in the Intensive Care Unit
(ICU) of the Gynecology and Obstetrics Hospital #3, Na-
tional Medical Center La Raza, IMSS, Mexico City. Exclu-
sion criteria were as follows: chronic liver disease, heart
failure, chronic renal insufficiency (CRI), cholangiopathy,
pancreatitis, malignancies, pelvic infections or severe mal-
nutrition.
All patients had an upper abdominal ultrasound per-
formed and the baby was delivered by caesarean section
with documentation of the presence of pleural effusion
and/or ascites. Based on the findings, two groups were
formed: patients without fluid collections and patients
with fluid collections. In the case of pleural effusion, the
quantification estimated by the physician who performed
the ultrasound was recorded and the amount of ascites flu-
id (ml) was taken from the operative description done by
the obstetrician-gynecologist who performed the cesarean
section.
The following general data were recorded: age, parity,
gestational weeks, SAP, diastolic blood pressure (DAP),
mean arterial pressure (MAP), central venous pressure
(CVP), uresis (ml/h), glucose (Glu) (mg/dl), urea (mg/dl),
Cr (mg/dl), uric acid (UA) (mg/dl), total protein (TP), albu-
min (Alb) (g/dl), serum globulin (Glob) (g/dl), Alb PCOP
(mmHg), Glob PCOP (mmHg), total PCOP of proteins
(mmHg), Briones index (BI) (the ratio between the total
PCOP proteins/MAP) and complications of pleural effusion
and/or ascites fluid, as appropriate.
We compared the total PCOP of proteins, Cr and cal-
culated endogenous creatinine clearance (CrCl) (ml/
min/1.73 m2 SC × 0.85) between groups and the correlation
for each was calculated with the quantity (ml) of ascites
fluid and/or pleural effusion.
To determine the total PCOP of proteins (mmHg), the
following formula was used:12
[Serum albumin (g/dl)  × 5.54] +
[serum globulin (g/dl)  × 1.43]
300 Cirugía y Cirujanos
Vázquez-Rodríguez JG and Veloz-Martinez MG
The median normal value of the total PCOP of pro-
teins in healthy nonpregnant patients is 25.4 ± 2.3 mmHg.
In women with an uncomplicated pregnancy at term it is
22.4 ± 0.5 mmHg (5), in preeclamptic pregnant patients it
is 17.9 ± 0.7 mmHg and in women with preeclampsia in the
postpartum period it is 13.7 mmHg.5-7
Cr (mg/dl) value was obtained from the report developed
by the Clinical Laboratory Department at the same institu-
tion from a blood sample processed upon patient admission
to the ICU. Endogenous CrCl was obtained using the Cock-
croft-Gault formula, multiplying the result by the correction
constant of 0.85 for female gender:
Endogenous CrCl (ml/min/1.73 m2 SC) =
[140 –age (years) × weight (kg)/Cr (mg/dl) × 72] 0.85
For statistical analysis we calculated descriptive statis-
tics (mean, median, range and standard deviation). Student
t test and Pearson correlation coefficient (r) were used;
p <0.05 was accepted as statistically significant.
Results
Findings of collections (ascites, pleural effusion, or both)
were negative in 56.52% (52 cases) and positive in 43.48%
(40 cases). The main general data of both groups are shown
comparatively in Table 1. As can be seen, the parameters of
interest were similar.
Laboratory results of both groups upon admission to the
ICU are shown in Table 2. As can be seen, significant dif-
ferences were found when comparing the median of the TP
(p  =  0.01) and total PCOP of proteins (p  =  0.009) from a
low concentration of globulins (p = 0.005) and of its PCOP
(p = 0.007) in patients with collections. Similarly, BI was
lower in this group of patients (p = 0.009).
In the 40 patients with collections, the most common
finding was ascites in 40% (16 cases) followed by solitary
pleural effusion in 30% (12 cases) and ascites together with
pleural effusion in the same patient in 30% (12 cases) (Fig-
ure 1). In patients with ascites, the median fluid collection
was 231.25  ±  26  ml. In patients with solitary pleural ef-
fusion it was 133.33  ±  11.54  ml, and in women who had
ascites together with a pleural effusion the medians were
275 ± 28.95 ml and 100 ml, respectively.
When the median of ascites was found in an isolated
manner (231.25 ± 26 ml) vs. the median ascites accompa-
nied by pleural effusion (275  ±  28.95  ml), similar results
were found (p  =  0.67). Similarly, when comparing mean
pleural fluid alone (133.33 ± 11.54) vs. the average amount
of pleural effusion accompanied by ascites (100 ml) no dif-
ference was found (p = 0.32).
Pleural effusion and ascites in severe preeclampsia

Table 1. General data

Patients without collections Patients with collections

Parameter n = 52 n = 40 p

Age (years) 29.76 ± 5.67 28.382 ± 6.27 0.45

Parity (median) 2 1 0.29
Weeks of gestation 32.85 ± 3.74 32 ± 3.22 0.25
Systolic blood pressure (mmHg) 127.59 ± 15.06 128.33 ± 16.31 0.82
Median arterial pressure (mmHg) 94.20 ± 11.55 95.69 ± 10.23 0.53
Diastolic arterial pressure (mmHg) 77.94 ± 11.58 78.74 ± 9.43 0.72
Central venous pressure (cm water) 10.38 ± 2.56 11.20 ± 2.79 0.15

n = number of cases; mmHg, millimeters of mercury.

Table 2. Clinical laboratory results

Patients without collections Patients with collections

Parameter n = 52 n = 40 p

Glucose (mg/dl) 126.30 ± 59.30 108.05 ± 29.81 0.08

Uric acid (mg/dl) 6.39 ± 1.58 6.71 ± 1.81 0.38
Total proteins (g/dl) 5.38 ± 0.70 4.99 ± 0.70 0.01
Albumin (g/dl) 3.03 ± 0.34 2.88 ± 0.43 0.07
Globulins (g/dl) 2.40 ± 0.51 2.11 ± 0.39 0.005
Colloid osmotic albumin pressure (mmHg) 16.76 ± 1.89 15.96 ± 2.41 0.09
Colloid osmotic globulin pressure (mmHg) 3.38 ± 0.70 3.01 ± 0.56 0.007
Colloid osmotic pressure of the total plasma proteins 20.12 ± 2.16 18.78 ± 2.58 0.009
(mmHg)
Briones Index 0.21 ± 0.03 0.19 ± 0.03 0.03
(total of the colloid osmotic pressure of plasma
proteins/mean arterial pressure)
n = number of cases.

The median of the total PCOP of proteins of patients
without collections was 20.12 ± 2.16 mmHg and of the 40
patients who did have collections it was 8.78 ± 2.58 mmHg
(p = 0.009) (Figure 2).
Figure 3 shows the comparative values of the total PCOP
of proteins of patients with positive findings by type of fluid
collection (ascites, pleural effusion and both). The compari-
son of means showed no significant difference (p >0.05).
Renal function parameters of the 92 patients studied are
shown comparatively in Table 3. As can be seen, the aver-
age uresis was similar in both groups (p = 0.23) and mean
blood urea was higher in the group with positive findings
than in the group without collections (p = 0.04) as well as
the average Cr (p = 0.03). Figure 4 shows the comparison
of the value of serum Cr according to groups of patients
(p = 0.03).
When all 92 patients were grouped by renal function
using a classification according to the level of Cr [normal
function Cr <0.9 mg dl, Cr 0.9−1.2 mg/dl injury, and acute
renal insufficiency (ARI) Cr >1.2 mg/dl], it was found that
the most frequent category was normal renal function fol-
lowed by categories of injury and ARI (Table 4). The num-
ber of cases of ARI was higher in the group with collections
(nine cases) compared with those without collections (six
cases); the comparison of means showed a significant dif-
ference (p = 0.03). From these data, the relative prevalence

Volume 79, No. 4, July-August 2011 301

 Vázquez-Rodríguez JG and Veloz-Martinez MG

16 (40%) (a similar measure of relative risk) of ARI in the 92 patients

16 studied was 1.5 (group B 9 cases/6 cases in group A = 1.5).
14 The role of renal filtration function assessed with the en-
12 (30%) 12 (30%) dogenous CrCl was lower in the group of patients with col-
Number of cases

12
lections (p = 0.03) (Figure 5).
10
In the group of patients with collections, the r of the total
8 PCOP of proteins vs. ascites was −0.25 vs. pleural effusion
6 alone (−0.29) and in patients with combined ascites and
4 pleural effusion (−0.02 and −0.30), respectively (mean for
both was −0.16). In this same group of patients, the r of the
2
endogenous CrCl vs. ascites was −0.01 vs. solitary pleural
0 effusion −0.13 and vs. ascites with pleural effusion −0.27
Ascitis Pleural Both
effusion collections and −0.67, respectively (average for both −0.47). None of
the patients with collections presented signs, symptoms or
Figure 1. Frequency of ascites fluid, pleural effusion, or both in 40 complications secondary to serous fluid.
patients with severe preeclampsia.

Discussion
20.12 ± 2.16 During normal pregnancy the increase in circulating vol-
20.5 ume and hydrostatic pressure in the venous system favors
20 the development of mild edema of the extremities and in
5% the appearance of a discrete pericardial effusion.13 As-
PCO (mm Hg)

cites fluid and/or pleural effusion are not common findings

19.5
in women with a normal pregnancy.13 This study found
19 18.78 ± 2.58 that the frequency of collections (ascites fluid, pleural ef-
fusion or both) was 43.48% (40 cases) from the analysis
18.5
of 92 pregnant patients with SP. For this total, ascites fluid
represented 17.40%, solitary pleural effusion 13% and as-
18 cites fluid in conjunction with pleural effusion 13%. The
Patients without Patients with frequency of fluid collections studied is high.
collections (n=52) collections (n=40) Derruelle et al.11 described the postpartum complications
Figure 2. Comparison of total plasma colloid osmotic pressure in 453 patients with preeclampsia and HELLP syndrome and
(PCOP) of proteins of patients without and with collections (p = 0.009). found that 16.77% (76 cases) had ascitic fluid and/or pleu-
ral effusion and were associated with a SAP  > 60  mmHg.
The frequency of ascites fluid reported in this study is
similar to that reported in the study by Derruelle et al.11
However, no difference was found in SAP values as these
20 19.74 ± 2.25 authors reported because the average SAP of patients with-
19.5 out and with collections was similar (127.59  ±  15.06 vs.
18.98 ± 2.95
19 18.78 ± 2.58 128.33 ± 16.31 mmHg, p = 0.82) (Table 1).
PCO (mm Hg)

18.5 A previous study14 in which 225 pregnant women with

PE were studied found that the finding of ascites fluid had
18
17.53 ± 1.95 a frequency of 4.89% (11 cases), which was lower than the
17.5 current rate of 17.40%, possibly due to differences exist-
17 ing in sample size and criteria for case selection. How-
16.5 ever, in both investigations11,14 the percentage of this type
16 of collection was high. In the 40 patients who developed
All Ascitis Pleural Both fluid collections, it is notable that the frequency of asci-
n=40 n=16 effusion n=12 tes fluid, pleural effusion and ascites in conjunction with
n=12
pleural effusion showed a relatively uniform distribution:
Figure 3. Total PCOP of proteins according to type of collection. 17.40, 13 and 13% in relation to all patients (92 cases), 40,

302 Cirugía y Cirujanos

Pleural effusion and ascites in severe preeclampsia

Table 3. Comparison of the parameters of renal function in patients without and

with collections upon admission to the ICU

Patients without Patients with

collections collections
Parameter n = 52 n = 40 p

Uresis (ml/h) 144.15 ± 99.06 168.90 ± 96.60 0.23

Blood urea (mg/dl) 33.54 ± 15.57 41.98 ± 23.06 0.04
Serum creatinine (mg/dl) 0.97 ± 0.23 1.25 ± 0.83 0.03
Glomerular filtration: 111.69 ± 37.61 95.27 ± 34.22 0.03
Corrected endogenous CrCl (ml/min/1.73 m2 SC × 0.85)

n = number of cases.
ICU, intensive care unit.

1.4 115
1.25 ± 0.83 111.69 ± 37.61
Endogenous CrCl (ml/min/1.73
1.2
110
Serum creatinine

1 0.97 ± 0.23 m2 SC x 0.85)

105
(mg/dL)

0.8
100
0.6
95.27 ± 34.22
95
0.4

0.2 90

0 85
Without collections With collections Without collections With collections
n= 52 n= 40 n=52 n=40
Groups of patients Groups of patients

Figure 4. Comparison of serum creatinine value according to groups Figure 5. Comparison of the value of calculated endogenous creati-
of patients (p = 0.03). nine clearance (CrCl) according to groups (p = 0.03).

Table 4. Comparison by categories of renal function according to the serum creatinine

level of patients without and with collections

Categories of renal function Patients without collections Patients with collections

n = 52 n = 40 p

Normal n = 24 n = 16
(Cr <0.9 mg/dl) 0.77 ± 0.10 0.78 ± 0.07 0.89
Injury n = 22 n = 15
(Cr 0.9-1.2 mg/dl) 1.03 ± 0.08 1.01 ± 0.04 0.53
ARI n=6 n=9
(Cr >1.2 mg/dl) 1.44 ± 0.19 2.44 ± 1.04 0.03
range 1.26-1.72 range 1.45-4.30
Total n = 52 n = 40
Median 0.97 ± 0.23 1.25 ± 0.83 0.03

n = number of cases.
Cr, serum creatinine; ARI, acute renal insufficiency.

Volume 79, No. 4, July-August 2011 303


30 and 30%, respectively, compared with the group with
fluid collections (40 cases). In this regard, it is possible
that the trend towards uniformity corresponds to a similar
biological behavior of the peritoneum and pleura in the
context of SP.
Regardless of the anatomic site of its formation, the fluid
amounts found were small in all cases and no patient had
signs, symptoms or secondary complications in contrast to
that reported by Lilford et al.15 who described the case of a
preeclamptic patient with massive ascites with pleural and
synovial effusion or the study by Foreman16 reporting on a
patient with SP who was found to have massive ascites (12
liters) without any other pathology to explain it. Similarly,
none of the patients studied had pleural effusion second-
ary to ARIS or an acute episode of cardiac insufficiency as
cited in the literature.9,10 Thus, the collections found were a
subclinical finding.
In the present study it was found that the median of the
total PCOP of proteins in patients with collections was sig-
nificantly different from patients who did not have fluid col-
lections (p = 0.009) (Figure 2). The same happened when
BI was compared, which resulted in being lower in women
with collections (p = 0.03) (Table 2). Because measurement
of the PCOP and BI can estimate the magnitude of capil-
lary leak syndrome in PE,5,14 it is possible that, from the
results, the main cause (not the only one) for fluid forma-
tion in the pleura and peritoneum of patients with SP can
be the reduced PCOP that determines a relative imbalance
(increase) in the hydrostatic pressure in the microcircula-
tion. Low concentrations of Alb, Glob and TP found in the
group of patients with collections (Table  2) support this
view as well as the negative r of its PCOP compared with
the amounts of various liquids studied. The results are con-
sistent as described in previous reports that emphasize the
role of PCOP.4-6,8,10-11,14-16
Although the reduced total PCOP of proteins and imbal-
ance (increase) in the hydrostatic pressure of the microcir-
culation are important, the involvement of structural factors
such as endothelial injury, disruption of basal membrane
and coagulation in situ10,11 remain to be assessed, which is
the phenomenon in the capillary leak that occurs simultane-
ously in PE patients.
It has been described in the literature that impaired re-
nal function may promote the development of generalized
edema and thus the formation of abnormal fluid collections
in the serosa in these types of patients.11 In this study we
found that the level of urea and Cr of the patients with col-
lections was higher when compared with those without col-
lections (p  =  0.04 and 0.03, respectively) (Table  3). Both
situations occurred secondary to a reduction of renal filtra-
tion function, which was corroborated when it was found
that endogenous CrCl, the test considered as the standard
304 Cirugía y Cirujanos
Vázquez-Rodríguez JG and Veloz-Martinez MG
for evaluating the function in clinical practice, was lower in
the group with collections than in patients without collec-
tions (p = 0.03) (Figure 5).
On the basis that the findings are indicative of impair-
ment of renal filtration function, it is recommended to keep
in mind that this condition is a factor that may contribute to
the development of collections of peritoneal or pleural fluid
of preeclamptic patients.
In conclusion, the frequency of collections of serous fluid
in the present study was 43.48%, representing a high figure.
Clinically, its presence did not produce signs, symptoms or
secondary complications. There was a weak negative cor-
relation of total PCOP of proteins with each of the types of
fluid accumulation. Patients with collections had impaired
renal filtration function. It is possible that the sum of the
effects of various mechanisms with simultaneous action
(reducing the total PCOP of proteins, increased capillary
hydrostatic pressure, structural damage of the microvascu-
lature and impaired renal filtration function) is the most vi-
able explanation that justifies the collection of fluid in the
pleura and/or peritoneum of preeclamptic patients. These
concepts should be considered for diagnosis and treatment
of these patients.
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