Repeated paracentesis and i.v. albumin infusion to treat ‘tense’ ascites in cirrhotic patients

Journal of Hepatology, 1987;5:102-108

102

Elsevier

HEP 00306

Repeated paracentesis and i.v. albumin infusion to treat 'tense' ascites in cirrhotic patients A safe alternative therapy Francesco Salerno 1, Salvatore Badalamenti I , Pierluigi Incerti l, Silvana Tempini 1, Bruno Restelli 2, Savino Bruno 2, Giorgio Bellati 3 and Luigi Roffi 4 l lstituto di Medicina lnterna della Universitg~ degli Studi di Milano, 2Divisione di Medicina delr Ospedale San Paolo di Milano, 3Divisione di Medicina dell'Ospedale Sant'Anna di Como and 4Divisione di Medicina dell'Ospedale San Gerardo di Monza (Italy)

(Received 11 November, 1986) (Accepted 24 February, 1987)

Summary To investigate the usefulness of paracentesis as an alternative treatment for ascites, 41 cirrhotic patients with 'tense' ascites were randomly assigned to treatment with either repeated paracenteses plus i.v. albumin infusion (n = 20) or diuretics (n = 21). Satisfactory mobilization of ascites was obtained with paracentesis in all but one case and with diuretics in all but two cases. Ascites disappeared within 3 or 4 days with paracentesis, but only after 15 days with diuretics. The rate of reaccumulation of ascites following paracentesis, without diuretic administration, exceeded 300 g/day in only 5 patients. The incidence of complications and the mortality rate were similar in both groups of patients during hospital stay and during follow-up. This was corroborated by the evidence that no negative changes were induced in clinical and laboratory parameters of hemodynamic, hepatic and renal function after evacuation of the ascites. These results confirm that repeated paracenteses combined with human albumin replacement are safe and effective for treating 'tense' ascites, and more rapid than traditional diuretic theraPY.

Introduction Large-volume paracentesis was employed for a long time to mobilize ascites in patients with liver cirrhosis [1], but was abandoned as the treatment of

choice of ascites after the introduction of modern diuretic therapy because of fear of severe adverse effects. It was widely believed that large-volume paracentesis increases the risk of hypotension, hyponatremia, renal failure and encephalopathy in cirrhotic

This work was supported by Regione Lombardia, Progetto di Ricerca No. 824, delibera No. 9783. Correspondence: F. Salerno, M.D., Medicina Interna, Universit~ di Milano, via Pace, 9, 20122 Milan, Italy. 0168-8278/87/$03.50I~) 1987 Elsevier Science Publishers B.V. (BiomedicalDivision)

PARACENTESIS VS. DIURETIC THERAPY patients [2-5]. However, it has recently been reported that paracentesis is a safe procedure for cirrhotic patients with 'tense' ascites. Kao et al. [6] showed that a single paracentesis of 5 liters from ascitic patients with peripheral edema was not followed by adverse effects on systemic hemodynamics or plasma sodium concentration, while Quintero et al. [7] showed that consecutive paracenteses combined with i.v. albumin infusion can resolve 'tense' ascites with the same incidence of side effects as that observed in similar patients treated with diuretics. In this paper, we report the results of a randomized controlled trial comparing repeated paracenteses with diuretic therapy as treatment for massive ascites in patients with liver cirrhosis. The aim of the study was to further investigate the safety and efficacy of paracentesis and to estimate the rate of reaccumulation of ascites after treatment in patients not taking diuretics.

Materials and Methods

All cirrhotic patients hospitalized for 'tense' ascites in our four departments between January 1985 and May 1986 were considered for the present study. Study criteria. The following criteria were required for admission to the study: (1) massive ascites confirmed by ultrasound scanning; (2) urinary sodium excretion rate lower than 20 meq/day on a sodium-restricted diet and without diuretics; (3) no cancer, encephalopathy, active gastrointestinal bleeding, renal failure, diabetes, infection or primary cardiac disorders; (4) hemoglobin higher than 9 g/dl; (5) total bilirubin lower than 6 mg/di; (6) aminotransferases lower than 200 U/l; (7) serum urea lower than 60 mg/dl; (8) serum creatinine lower than 1.5 mg/dl. Study design. The study was approved by the local ethics committee. After informed consent was obtained, patients were placed on a sodium- and waterrestricted diet (less than 40 meq/day and 1000 ml/day). Any diuretic that had been previously prescribed was discontinued at least 5 days before the beginning of any treatment. Among 74 patients considered, 41 patients were finally enrolled in the trial.

103 The diagnosis of liver cirrhosis was based on clinical, laboratory and, for 18 cases, histological criteria. Twenty patients had alcoholic cirrhosis, 12 postnecrotic (7 HBsAg+ve) cirrhosis and 9 cryptogenic cirrhosis. Thirty-four patients had already had one or more episodes of ascites, while ascites developed for the first time in 7 cases. The 41 patients were randomly assigned to two groups. The 20 group A subjects were treated with consecutive paracenteses (4 liters per day until disappearance of ascites) and i.v. human albumin infusion (20-60 g after each paracentesis, depending approximately on the amount of albumin lost during ascites evacuation). Under local anesthesia and with aseptic precautions, paracenteses were performed in the left lower abdominal quadrant using a 16- or 18-gauge needle. Ascitic fluid was drawn by gravity into a receptacle resting on the floor. The time required for completion of paracentesis varied from 60 to 120 min. Samples of ascitic fluid were taken for cell counts, cultures and protein and electrolyte determinations. In order to better ascertain the incidence of early complications, patients remained hospitalized at least until day 15, and were given no diuretic therapy. Group B included 21 subjects treated with diuretics: spironolactone was given daily (200 mg/day), the dosage was doubled on day 5, and furosemide (50 mg/day) was added on day 9 when there was no response to the previous regimens (loss of body weight lower than 200 g/day). Body weight (BW), blood pressure (BP), heart rate (HR) and urine flow rate were measured daily. The accuracy of 24-h urine collection was checked by the determination of daily creatinine excretion. On days 1 (immediately before starting the treatment), 5, 10 and 15, fasting blood samples and urinary 24-h samples were taken for standard liver and renal tests, and hemoglobin (Hb), hematocrit (Ht), blood cell count, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were also determined. PRA and PAC were determined for 25 cases (12 of group A and 13 of group B) in blood drawn into.tubes containing disodium EDTA, after at least 2 h of bed rest. PRA was measured by radioimmunoassay of angiotensin I generated at pH 6.0; bound and free

104 antigens were separated by addition of a second antibody coupled to magnetic particles, and sedimentation after application of a magnetic field, using materials from Biodata (Milan, Italy). The minimum detectable angiotensin I concentration was 0.2 ng/ml; the intra- and interassay coefficients of variation were 4% and 7.3%, respectively. Normal values in the supine position range from 0.50 to 2.60 ng/ml/h. P A C was measured by solid phase r a d i o i m m u n o a s say (Diagnostic Product C o r p . , Los Angeles, C A ) . The minimum detectable aldosterone concentration was 15 pg/ml; intra- and interassay coefficients of variations were 5.5 and 6.9%, respectively. Normal values in recumbent subjects range from 15 to 160, pg/ml. Normal values for P R A and P A C refer to people on normal dietary sodium intake (120-150 meq/day). Osmolality was m e a s u r e d by the m e t h o d of freezing point depression, with a Fiske o s m o m e ter; sodium and potassium concentration was determined by flame p h o t o m e t r y in an IL243. Urea, creatinine, bilirubin, Hb, Ht and blood cell count were determined by autoanalyzer. Plasma a m m o n i a levels were measured by the m e t h o d of Miller and Rice [8]. Daily' sodium balance was calculated as follows: sodium balance = N a i+, - ( N a u+ + Naas + c + 10) in which Na~, is the dietary sodium intake, N a ,+ is the urinary sodium excretion, Naa~ c is the sodium lost with the ascites, and 10 is the a p p r o x i m a t e insensible daily sodium loss in milliequivalents. Sodium concentration was d e t e r m i n e d in samples of fluid obtained from every tap for the first 7 patients. All these samples showed sodium concentrations equal to the concentrations in peripheral plasma. Therefore, for the rest of the patients we assumed that sodium concentration in the ascitic fluid was equal to that in the plasma. The results were analyzed statistically by S t u d e n t ' s t-test and paired t-test, and the Z2-test of Yates.

Results

Table 1 shows that the two groups of cirrhotic pa-

F. SALERNO et al. TABLE 1 CLINICAL AND LABORATORY DATA FOR 41 CIRRHOTIC PATIENTS SELECTED FOR THE TRIAL OF PARACENTESIS VS. DIURETICS

Age (yr) Sex (m/f) Weight (kg) Alcoholic etiology (n) Bilirubin (mg/dl) Albumin (g/dl) Urea (mg/dl) Creatinine (mg/dl) Hemoglobin (g/dl) Hematocrit (%) Plasma sodium (meq/I) Plasma potassium (meq/I) Urine sodium (meq/day) Urine potassium (meq/day) PRA (ng/ml/h) a PAC (pg/ml) a Duration of ascites prior to treatment (days)

Group A (n = 20)

Group B (n = 21)

53.7 + 2.8 15/5 71.7 + 2.7 10 3.1 + 0.4 2.86 + 0.11 29.8 + 3.6 0.95 + 0.06 11.9 + 0.5 34 + 0.9 133 + 1.3 4.2 + 0.12 5.7 + 1.4 21.7 + 3.5 12.6 + 1.5 648 + 118

56.4 + 2.1 17/4 73.7 + 3.0 10 2.9 + 0.3 2.82 + 0.10 33.4 + 3.2 0.95 + 0.06 11.8 + 0.4 34 + 0.8 136 + 0.8 4.3 + 0.11 8.2 + 1.8 25.6 + 4.1 10.0 + 2.4 415 + 88

39 + 4.4

37 + 4.3

PRA (plasma renin activity) and PAC (plasma aldosteronc concentration) were measured for 12 patients in group A and 13 patients in group B.

tients studied were h o m o g e n e o u s for a wide variety of clinical and l a b o r a t o r y p a r a m e t e r s . In addition to ascites, a few cases had p e r i p h e r a l e d e m a (2 cases in • group A and 2 in group B). Eight patients (3 in group A and 5 in group B) had not had any diuretic treatment prior to hospitalization; the o t h e r patients had taken diuretics for 4 days to 2 months with little or no effect. Satisfactory mobilization of ascites was obtained for all except one patient of group A . F o r this patient. evacuation of ascites was incomplete because of compartmentalization of ascitic fluid, as d o c u m e n t e d by ultrasound scanning. The mean volume of ascites removed was 12.2 + 0.6 liters (range 6 . 2 - 1 6 ) , the mean loss of body weight 9.7 + 0.6 kg (range 4.5-15.2) and the mean a m o u n t of albumin infused 109 + 10 g (range 40-260). No patient d e v e l o p e d complications during the 15 days following the start of treatment. T h e rate of ascites reaccumulation, estimated a p p r o x i m a t e l y from the body weight increases from day 5 to day 15, was

PARACENTESIS VS, DIURETIC THERAPY

105

variable. F o u r p a t i e n t s did n o t r e a c c u m u l a t e ascites,

(95% vs. 9 0 . 4 % , Z2 = 0.35; P > 0.50). T a b l e s 2 and 3

as c o n f i r m e d with u l t r a s o u n d scanning, w h i l e the oth-

show the values for the clinical and l a b o r a t o r y pa-

er 15 r e a c c u m u l a t e d ascites, gaining w e i g h t at a rate

r a m e t e r s for p a t i e n t s r e s p o n s i v e to t r e a t m e n t .

of 364 + 67 g/day ( r a n g e 9 0 - 1 1 0 0 ) ; h o w e v e r , only 5 patients r e g a i n e d w e i g h t at a rate faster than 300

g r o u p A , m e a n b o d y w e i g h t was significantly red u c e d at all times after paracentesis. F o r the o t h e r

g/day. T h e b o d y w e i g h t increase was u n r e l a t e d to any

p a r a m e t e r s i n v e s t i g a t e d , p a r a c e n t e s i s c o m b i n e d with

of the clinical and l a b o r a t o r y p a r a m e t e r s

i.v. a l b u m i n infusion caused a slight d e c r e a s e in H R

investi-

In

gated o r to the a m o u n t s of ascitic fluid e v a c u a t e d o r

(day 10) and u r i n e o s m o l a l i t y (day 10), and increases

h u m a n a l b u m i n infused. T h e r e f o r e , the r a t e of as-

in p l a s m a a l b u m i n c o n c e n t r a t i o n (days 5 and 10) and

cites r e a c c u m u l a t i o n after p a r a c e n t e s i s was u n p r e -

urine flow rate (days 5, 10 and 15). I n c r e a s e d urine

dictable f r o m o u r data. In g r o u p B, r e s o l u t i o n of as-

flow rates w e r e o b s e r v e d in 14 patients. T h e s e cases

cites was o b t a i n e d in 19 of 21 patients. T h e final b o d y

had significantly l o w e r baseline urine e x c r e t i o n s than

weight loss was 8.9 + 2.1 kg (not d i f f e r e n t f r o m that

the o t h e r 5 (414 + 57 vs. 780 + 174 ml/day, P <

o b t a i n e d with p a r a c e n t e s i s ) , but the t i m e r e q u i r e d

0.02).

was 19 + 5 days. T h e d i u r e t i c r e g i m e n s r e q u i r e d

In the 19 r e s p o n d i n g patients of g r o u p B, signifi-

were: 200 rag/day of s p i r o n o l a c t o n e for 8 cases, 400

cant B W r e d u c t i o n s w e r e o b s e r v e d on days 10 and

nag/day for 5 cases, s p i r o n o l a c t o n e plus f u r o s e m i d e

15. M e a n B P and H R did not c h a n g e . F o r the o t h e r

for 6 cases. D i u r e t i c t r e a t m e n t was unsuccessful for

p a r a m e t e r s i n v e s t i g a t e d , significant increases w e r e

two cases b e c a u s e of d e v e l o p m e n t of r e n a l failure in

o b s e r v e d in u r i n e flow rate, s o d i u m and p o t a s s i u m

one and no w e i g h t loss in the o t h e r . B o t h t h e s e cases

e x c r e t i o n , p l a s m a a l b u m i n and p o t a s s i u m c o n c e n t r a -

were t a k i n g the highest d o s a g e of diuretics.

tions, with significant d e c r e a s e s in urine osmolality.

T h e p e r c e n t a g e s of p a t i e n t s r e s p o n d i n g to treat-

T a b l e 4 shows the s o d i u m b a l a n c e during the 15

ment did n o t differ significantly in the two g r o u p s

days of o b s e r v a t i o n . B e f o r e starting the t r e a t m e n t ,

FABLE 2 BLOOD AND URINE TEST, BLOOD PRESSURE, H E A R T RATE AND WEIGHT DATA FOR 19 RESPONDING PATIENTS (GROUP A), PRE- AND POST-PARACENTESIS

BW (kg) a MBP (mm Hg) b HR (bpm) ¢ V (ml/day) a Ux~V (meq/day) e UKV (meq/day) f U,~m(mosm/l)g Plasma urea (mg/dl) Plasma Na ÷ (meq/l) Plasma K ÷ (meq/l) Ammonemia (/,tg/dl) Hematocrit (%) Albumin (g/all) Plasma osm (mosm/l) PRA (ng/ml/h) h PAC (pg/ml) ~

Day 1

Day 5

72.7 + 2.6 87.2 + 2.3 87.8 + 2.5 510 + 70 5.9 + 1.5 23.3 + 4.2 640 + 51 31 + 4 133 _+ 1.4 4.2 + 1.4 82 + 10 33 + 2 2.87 + 0.11 298 + 10 13 + 1.6 679 + 125

62.9 + 84.3 + 83.3 + 705 + 7.7 + 24.6 + 602 + 39 + 132 + 4.2 + 90 + 34 + 3.17 + 286 + 13.1 + 762 +

2.6*** 2.4 2.5 75* 2.4 5.1 63 6 1.2 1.3 7 1 0.14"** 4 1.6 129

Day 10

Day 15

63.7 + 2.6*** 87.7 + 1.8 80.3 + 2.6*** 776 + 90** 5.6 --- 1.6 29.3 + 5.3 463 + 52* 38 + 5 132 + 1.2 4.4 + 1.4 90 + 6 34 + 1 3.13 + 0.09** 284 + 4 12.2 + 1.8 805 + 106

65.1 + 86.5 + 86.5 + 925 + 9.5 + 30.5 + 520 + 38 + 132 + 4.2 + 79 + 33 + 3.08 + 285 + 9.5 + 811 +

2.6*** 2.4 2.4 127"** 3.8 4.7 58 5 1.1 0.2 5 1 0.13 3 3.8 121

" Body weight; b mean blood pressure; c heart rate; d urine voluane; e urine sodium excretion; f urine potassium excretion; g urine osmolality; h plasma renin activity; i plasma aldosterone concentration. *P < 0.05; **P < 0.02; ***P < 0.01 (statistical significance vs. respective baseline values).

106

F. SALERNO et al.

TABLE 3 BLOOD AND URINE TEST, BLOOD PRESSURE, H E A R T RATE AND WEIGHT DATA FOR 19 RESPONDING PATIENTS (GROUP B), BEFORE AND DURING THERAPY WITH DIURETICS Day 1 BW (kg) a MBP (mm Hg) b HR (bpm) c V (ml/day) d UNaV (meq/day) c UKV (meq/day) f Uosm (mosm/l)g Plasma urea (mg/dl) Plasma Na + (meq/I) Plasma K ÷ (meq/l) Ammonemia (ug/dl) Hematocrit (%) Albumin (g/dl) Plasma osm (mosm/l) PRA (ng/ml/h)h PAC (pg/ml) ~

73.5 + 90.8 + 78.2 + 726 + 8.7 + 25.8 + 627 + 33 + 136 + 4.1 + 68 + 34 + 2.80 + 297 + 10 + 429 +

Day 5 2.9 1.7 2.4 103 2.0 4.6 78 3 1 0.2 7 1 0.10 7.6 2.4 95

72.7 + 91.8 + 79.7 + 1176 + 63.4 + 30.0 + 532 + 31 + 134 + 4.2 + 74 + 33 + 2.78 + 293 + 9.0 + 369 +

Day 10 2.9 2.4 2.2 130"** 11"** 6.2 58 2 1 0.3 8 1 0.11 6 1.7 97

69.7 + 89.3 + 77.9 + 1513 + 112 + 39.7 + 474 + 32 + 134 + 4.7 + 73 + 34 + 3.00 + 296 + 12.1 + 383 +

Day 15 2.7*** 1.2 2.3 160"** 18"** 4.4 53*** 4 1 0.1"** 7 1 0.10" 6 1.9 92

67.4 + 89.7 + 81.5 + 1600 + 107 + 44.7 + 426 + 36 + 134 + 4.6 + 75 + 35 + 3.11 + 300 + 13.5 + 505 +

2.8*** 1.6 2.2 120"** 13"** 5.0 52*** 4 1 0.1" 7 1 0.11"* 4 1.3 89

a Body weight; b mean blood pressure; c heart rate; d urine volume; c urine sodium excretion; f urine potassium excretion; g urine osmolality; h plasma renin activity; i plasma aldosterone concentration. *P < 0.05; **P < 0.02; ***P < 0.01 (statistical significance vs. respective baseline values).

t h e t w o g r o u p s d i d n o t d i f f e r in m e a n d a i l y s o d i u m balance (+23.6

+ 1.4 vs. + 2 1 . 7

+

c u r r e d in 3 p a t i e n t s in g r o u p A (2 e p i s o d e s o f e n c e p h -

1.8 m e q / d a y ) .

a l o p a t h y a n d 1 o f r e n a l f a i l u r e ) a n d 4 in g r o u p B (2

D u r i n g t h e first 5 d a y s , p a t i e n t s o f g r o u p A h a d

episodes of gastrointestinal bleeding with encepha-

m a r k e d l y n e g a t i v e s o d i u m b a l a n c e s d u e to t h e g r e a t

iopathy, 1 of encephalopathy and 1 of renal failure).

loss of s o d i u m r e m o v e d in t h e ascitic fluid. A l t h o u g h ,

T h e c o m p l i c a t i o n s a p p e a r e d a f t e r t h e first 15 d a y s of

a f t e r d a y 5, p a t i e n t s o f g r o u p A r e t u r n e d t o a s t a t e o f

t r e a t m e n t in all t h e cases o f g r o u p A a n d in 3 o f g r o u p

n e t s o d i u m r e t e n t i o n , t h e i r final c u m u l a t i v e s o d i u m

B. F i v e o f t h e s e p a t i e n t s (2 o f g r o u p A a n d 3 o f g r o u p

b a l a n c e was s i g n i f i c a n t l y m o r e n e g a t i v e t h a n t h a t o f

B ) d i e d b e f o r e b e i n g d i s c h a r g e d f r o m h o s p i t a l . All

p a t i e n t s o f g r o u p B.

t h e r e m a i n i n g p a t i e n t s w e r e p e r i o d i c a l l y c h e c k e d as

S e r i o u s c o m p l i c a t i o n s d u r i n g h o s p i t a l i z a t i o n oc-

o u t p a t i e n t s . T h i s f o l l o w - u p h a s c o n t i n u e d f o r 19.8 +

TABLE 4 MEAN SODIUM BALANCES IN PATIENTS WITH LIVER CIRRHOSIS AND 'TENSE' ASCITES, D U R I N G AND AFTER PARACENTESIS (GROUP A) a OR DURING DIURETIC THERAPY (GROUP B) b Days

Group A (n = 19) Group B (n = 19)

1-5

6-10

11-15

1-15 c

-1428 + 73* -79 + 38

+89 + 33* -410 + 91

+71 + 36* -409 + 69

-1267 + 106"* -897 + 124

* P < 0.001; **P < 0.05.

a These patients had had three or four consecutive paracenteses before day 5. b These patients were treated with spironolactone or spironolactone plus furosemide for all 15 days. ¢ Cumulative sodium balance.

PARACENTESIS VS. DIURETIC THERAPY

107

The present study provides evidence that for patients with liver cirrhosis and 'tense' ascites repeated paracenteses are a safe and effective procedure to mobilize ascites, being at least as good as traditional diuretic therapy. Paracentesis was satisfactory for 95% of the cases, compared to 90.4% success with diuretic therapy. The procedure was well tolerated by all our patients. The frequency of complications and the mortality rate during the follow-up were similar to those observed in patients treated with diuretics. These results confirm those of Quintero et al. [7]. However, it is advisable to take into account some essential features of our protocol: (1) the selection criteria excluded patients with high risks of complications from the trial; (2) human albumin was infused z~fter each paracentesis to replace the 60-80% of protein lost; (3) daily water and salt intake was restricted over the entire period of the study; (4) patients had not taken diuretics for at least 5 days before and for at least 15 days after starting paracentesis. Therefore, we cannot be sure whether the present results can be extrapolated to other cirrhotic patients and whether the same results can be obtained without albumin infusion and/or water and salt restriction. In this context, the importance of albumin replacement is suggested by a recent preliminary report of Gin6s et al. [9], who observed a higher incidence of complications after paracentesis in patients who were not infused with albumin than in those who were infused. The incidence of complications was lower in our

patients treated with paracentesis occurred late in the procedure. This suggests that paracentesis did not cause rapid changes in the systemic hemodynamics of our patients. This conclusion is corroborated by the laboratory evidence that paracentesis induced no changes in serum electrolyte, urea, creatinine or ammonia concentrations, in Ht, or in PRA, a sensitive measure of effective plasma volume. These results are in accord with the recent evidence that large-volume paracentesis in cirrhotic patients with ascites and peripheral edema does not affect plasma volume measured by the 125I-labeled albumin dilution technique [6]. Not only were there none of the feared severe adverse effects, but some clinical and laboratory findings seem to indicate improved cardiovascular and renal function after paracentesis. In fact, urine volume was significantly and stably increased and urine osmolality was decreased after the procedure. These changes were more evident in patients with low basal urine excretion rates. A slight but significant decrease in H R was also observed without any change in blood pressure. These results might be attributed to beneficial effects on cardiac output and renal perfusion, according to a previous demonstration that cardiac output and circulatory function improve progressively in cirrhotic patients during paracentesis of 5 - 8 liters [10]. A further interesting finding in the present study was that ascites evacuation did not cause hyponatremia, even though it caused a markedly negative sodium balance. Stability of the plasma sodium concentration might have been favored by the albumin replacement and restriction of water intake. Finally, ascites reaccumulation, estimated from the body weight increase, was slow in most patients treated with paracentesis, and exceeded 300 g/day in only 5 of 19 cases. Although body weight gain may underestimate the amount of ascites reaccumulated

p~tients than in those previously studied by Quintero et al. [7]. The difference is due, in our opinion, to the more restricted criteria of selection which we employed, to the delay in giving diuretics after ascites tap. and to the lower doses of diuretics used. In particular, it is worth noting that the three complications (encephalopathy and renal failure) in the group of

in some cases because of shifting of edema fluid into the peritoneal cavity after paracentesis, peripheral edema was present in only two of the 20 patients of group A. The finding of a slow rate of ascites rea.ccumulation is in contrast with that of several other investigators, who reported a more rapid reaccumulation of ascites in the first 3 days following paracente-.

2.6 weeks for group A and 14 + 2.2 weeks for group B. During this period, 3 patients of group A and 4 of group B have died.

Discussion

108

F. SALERNO et al.

sis [11,12]. In the present trial we did not find any

torily treated with consecutive paracenteses and al-

correlation between the rate of ascites reaccumula-

bumin infusion. Results from the follow-up suggest

tion and any other p a r a m e t e r studied, but it is likely

that ascites reaccumulation is slow in most cases and

that the human albumin infusion delayed ascites for-

that the incidence of complications and the mortality

mation by increasing the oncotic pressure of the

rates are similar to those observed in patients treated

blood. In conclusion, our study shows that cirrhotic pa-

with diuretics. T h e r e f o r e , paracentesis may be used

tients with 'tense' ascites can be rapidly and satisfac-

needing ascites resolution without additional risk.

to shorten the duration of hospitalization for patients

References 1 Dawson, AD. Historical notes on ascites. Gastroenterology 1960; 30: 790-791. 2 Nelson WP, Rosenbaum JD, Strauss MB. Hyponatremia in hepatic cirrhosis following paracentesis. J. Clin Invest 1951; 3: 738-740. 3 Liebowitz HR. Hazards of abdominal paracentesis in the cirrhotic patient (Part III). NY State J Med 1962; 62: 2223-2229. 4 Baldus WP, Summerskill WHJ. The kidney in hepatic disease. Postgrad Med 1967; 41: 103-112. 5 Papper S, Belsky JL, Bleifer KH. Renal failure in Laennec's cirrhosis of the liver. I. Description of clinical and laboratory features. Ann Int Med 1959; 57: 759-773. 6 Kao HW, Rakov NE, Savage E, Reynolds TB. The effect of large volume paracentesis on plasma volume - A cause of hypovolemia? Hepatology 1985; 5: 403-407. 7 Quintero E, Gin6s P, Arroyo V, et al. Paracentesis vs di-

8

9

10

11

12

uretics in the treatment of cirrhotics with tense ascites. Lancet 1985; i: 611-612. Miller GE, Rice JD Jr. Determination of the concentration of ammonia nitrogen in plasma by means of a simple ion exchange method. Am J Clin Pathol 1963; 39: 97-103. Gin6s P, Tit6 LL, Pan6s J, et al. Paracentesis vs paracentesis plus i.v. albumin in the treatment of ascites. Preliminary results of a comparative study [Abstract]. J Hepatol 1986; 3 (suppl. I): $23. Guazzi M, Polese A, Magrini F, Fiorentini C, Olivari MT. Negative influence of ascites on the cardiac function of cirrhotic patients. Am J Med 1975; 59: 165-170. Shear L, Ching S, Gabudza GJ. Compartmentalization of ascites and edema in patients with hepatic cirrhosis. N Engl J Med 1970; 282: 1391-1396. Mankin H, Lowell A. Osmotic factors influencing the formation of ascites in patients with cirrhosis of the liver. J Clin Invest 1948; 27: 145-153.