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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 26  |  Issue : 4  |  Page : 170-175

The impact of large-volume paracentesis on renal haemodynamics in cirrhotic patients with ascites


1 Department of Tropical Medicine; Department of Hepatology, Gastroenterology and Liver Transplant, Menoufiya University, Menoufia, Egypt
2 Department of Hepatology, Gastroenterology and Liver Transplant, Menoufiya University, Menoufia, Egypt
3 Department of Radiology, Menoufiya University, Menoufia, Egypt
4 Department of Clinical Biochemistry, National Liver Institute, Menoufiya University, Menoufia, Egypt

Date of Submission09-Sep-2014
Date of Acceptance20-Oct-2014
Date of Web Publication30-Dec-2014

Correspondence Address:
Khaled Mohammad Attallah
3 Qenawy Street, Hassan Mohammad District, 12111 EL-Haram, Giza
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1110-7782.148164

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  Abstract 

Background and aim
Ascites in liver cirrhosis is associated with a poor prognosis and impairment of the quality of life and may be complicated by hepatorenal syndrome. Renal functions and haemodynamic changes after large-volume paracentesis (LVP) in cirrhotic patients with tense ascites were evaluated.
Patients and methods
A total of 50 cirrhotic patients with tense ascites were divided into two groups: group I 25 patients without renal impairment and group II 25 patients with renal impairment (type II hepatorenal syndrome).
Results
In groups I and II, the serum creatinine decreased significantly 24 h after LVP (P < 0.05 and 0.01, respectively). The glomerular filtration rate and the urine output increased significantly 24 h after LVP (P < 0.05, P < 0.01 and P < 0.01, P < 0.05, respectively, in groups I and II). The renal artery resistive index (RI) was significantly higher in group II compared with group I (P < 0.01). LVP caused a significant increase in the cardiac output, the stroke volume and the cardiac index (P < 0.01) and a significant decrease in the RI in both groups (P < 0.01). There was significant correlation between serum and ascetic fluid electrolyte levels in all patients.
Conclusion
LVP causes a significant reduction of heart rate and mean arterial pressure, serum creatinine, blood urea nitrogen and RI with a significant glomerular filtration rate increase, but had no effect on the plasma renin activity.

Keywords: Ascites, cirrhosis, hepatorenal syndrome, large-volume paracentesis, renal resistive index


How to cite this article:
Salman TA, Zaghla HE, Attallah KM, El-Haddad OM, Korayem EM, Basuni AA, El-Ezzawy HE. The impact of large-volume paracentesis on renal haemodynamics in cirrhotic patients with ascites. Egypt J Intern Med 2014;26:170-5

How to cite this URL:
Salman TA, Zaghla HE, Attallah KM, El-Haddad OM, Korayem EM, Basuni AA, El-Ezzawy HE. The impact of large-volume paracentesis on renal haemodynamics in cirrhotic patients with ascites. Egypt J Intern Med [serial online] 2014 [cited 2018 Oct 15];26:170-5. Available from: http://www.esim.eg.net/text.asp?2014/26/4/170/148164


  Introduction Top


Hepatorenal syndrome (HRS) is a clinical condition that occurs in patients with chronic liver disease, advanced hepatic failure and portal hypertension due to impaired renal function and marked abnormalities in the arterial circulation and the activity of endogenous vasoactive systems. There is marked renal vasoconstriction that results in a low glomerular filtration rate (GFR), whereas in the extrarenal circulation, there is a predominance of arterial vasodilatation, which results in the reduction of the total systemic vascular resistance and arterial hypotension [1].

HRS is characterized by a combination of liver failure, circulatory abnormalities and renal failure (RF) [2]. Type I HRS is characterized by rapidly progressive RF with a doubling of serum creatinine to a level greater than 2.5 mg/dl [3], with a median survival of 2 weeks, and type II HRS is characterized by a slowly progressive increase in the serum creatinine level to greater than 1.5 mg/dl and urine sodium less than 10 mEq/dl with a median survival of 4-6 months [4].

About 18% of the cirrhotic patients with ascites develop HRS after 1 year and 39% after 5 years, and up to 10% of the hospitalized patients with liver failure can also develop HRS [5].

Renal Doppler indices have been used to analyse renal haemodynamics for a long time, and the renal resistive index (RI) correlates with the renal function in a variety of kidney disorders [6] and increases along the clinical stages of cirrhotic renal dysfunction [7]. High values of RI predict the occurrence of HRS and have also been shown to correlate with the intra-abdominal pressure (IAP) [8].

Intra-abdominal hypertension affects kidney function and is an important factor contributing to acute RF in critical care patients [9]. Intra-abdominal hypertension may reduce the renal perfusion pressure and contribute to RF in cirrhotic patients with ascites [10].

Abnormalities of circulatory function in patients with HRS include a high cardiac output (CO), a low arterial blood pressure and decreased total systemic vascular resistance. Although it was traditionally considered that the increased vascular resistance in HRS occurred only in the renal circulation, vascular resistance is also increased in upper and lower limbs as well as in the cerebral circulation [11].

Large-volume paracentesis (LVP) is an optimum choice for the management of tense ascites. The main findings of studies comparing LVP with diuretics in patients with tense ascites are summarized as follows:

  1. LVP combined with an infusion of albumin is more effective than diuretics and shortens the duration of hospital stay significantly.
  2. LVP plus albumin is safer than diuretics as the frequency of hyponatraemia, renal impairment and hepatic encephalopathy is lower in patients treated with LVP in the majority of the studies.
  3. LVP is a safe procedure, and the risk of local complications such as haemorrhage or bowel perforation is extremely low [12].



  Patients and methods Top


This prospective open-label un-controlled study was conducted at the National Liver Institute, Menoufiya University. A total of 50 cirrhotic patients with tense ascites were enrolled in this study after obtaining their informed consent. Patients were divided according to their renal function into two groups:

  1. Group I: 25 patients with tense ascites without renal impairment.
  2. Group II: 25 patients with tense ascites and renal impairment (type II HRS).


Exclusion criteria

  1. Sepsis as spontaneous bacterial peritonitis or any other infection.
  2. Hepatocellular carcinoma, cardiac, pulmonary or intrinsic RF.
  3. Acute gastrointestinal bleeding 1 week before the study.
  4. Use of diuretics, β-blockers, plasma expanders and paracentesis within 1 month.
  5. International normalized ratio greater than 1.5 or platelet count less than 100 × 10 3 /mm 3 .


Laboratory investigations

(1) Complete blood count, biochemical liver tests: serum bilirubin (total and direct), serum albumin, prothrombin time and concentration, serum aspartate transaminase, serum alanine transaminase, alkaline phosphatase, gamma glutamyl transferase.

(2) Renal functions [blood urea, serum creatinine and blood urea nitrogen (BUN)], plasma renin activity (PRA) by the radioimmunoassay and the estimated GFR (eGFR) using the Mayo Quadratic formula [13] before and 24 h after LVP.

(3) Serum and ascetic fluid sodium (Na + ), potassium (K + ) and chloride (Cl ) and the total ascetic fluid white blood cell count for the exclusion of spontaneous bacterial peritonitis.

(4) A high-resolution machine (Philips ATL, HDI 5000 with SonoCT manufacturer, Philips Medical Systems, Nederland B.V., Amsterdam, The Netherlands) with different transducers was used to perform the following examinations:

(1) Abdominal ultrasound

Ultrasound-guided LVP was performed on all cases. About 5-8 l, with mean of 6.4 ± 1.04 l, were withdrawn. Human albumin was infused simultaneously at a dose of 1 U (100 ml) for every 3 l of ascites drained.

(2) Renal Doppler was performed to assess renal haemodynamics, especially the renal artery RI.

(3) Echocardiography was performed to assess the stroke volume (SV), the CO and the cardiac index (CI).

Statistical procedures

Descriptive statistics were presented as the mean ± SD for normally distributed data and median, range for non-normally distributed data. The Student t-test was used for normally distributed quantitative variables to measure the mean and SD. The Mann-Whitney test was used for quantitative variables that were not normally distributed. Pearson's correlation test was used to study the correlation between two normally distributed quantitative variables. The paired t-test was used to detect the mean and SD of normally distributed prevalue and postvalue of the same variable of the same group of patients. The Wilcoxon test was used to detect the mean and SD of non-normally distributed prevalue and postvalue of the same variable of the same group of patients. Repeated measures of analysis of variance test were performed to differentiate changes in different follow-up results of normally distributed studied variables, and the Friedman test was performed to differentiate changes in different follow-up results of the different studied variables. P-value less than 0.05 was considered significant for all variables.


  Results Top


The age in group I ranged between 38 and 63 years, with a mean ± SD of 52.7 ± 7.3 years: there were 8 (32%) female and 17 (68%) male participants. In group II, the age ranged between 40 and 66 years, with a mean ± SD of 54.9 ± 8.3 years: there were 11 (44%) female and 14 (56%) male participants with no significant difference.

The body weight was 74.9 ± 12.7 vs. 74.1 ± 14.7 kg, the height 168.4 ± 7.9 vs. 167.4 ± 9.04 cm and the body surface area 1.85 ± 0.19 vs. 1.83 ± 0.21 m 2 in groups I and II, respectively, with no significant difference.

Regarding baseline laboratory measurements of all patients, haemoglobin and albumin were significantly lower in group II compared with group I (P < 0.05): haemoglobin was 10.3 ± 1.45 against 9.5 ± 1.06 g/dl, whereas albumin was 2.35 ± 0.4 against 2.11 ± 0.43 g/l in groups I and II, respectively. There was no statistically significant difference regarding red blood cells, white blood cells and platelet counts, prothrombin time, prothrombin activity, total and direct bilirubin, aspartate transaminase, alanine transaminase, gamma glutamyl transferase and alkaline phosphatase.

There was a statistically significant difference in the level of serum and ascitic fluid electrolytes (Na + , K + and Cl ) between both groups. The serum Na + was 125.2 ± 7.58 against 126.4 ± 6.9 mEq/l, the ascitic fluid Na + was 126.8 ± 6.78 against 128.2 ± 6.1 mEq/l, the serum K + was 4.44 ± 0.52 against 4.67 ± 0.86 mEq/l, the ascitic fluid K + was 4.31 ± 0.54 against 4.46 ± 0.85 mEq/l, the serum Cl - was 99.4 ± 4.96 against 101.6 ± 3.62 mEq/l and the ascitic fluid Cl was 105.12 ± 4.81 against 106.8 ± 4.38 mEq/l in group I and group II, respectively. Urinary Na + was significantly lower in group II (4.79 ± 1.7 mEq/l) compared with group I (6.85 ± 3.72 mEq/l) (P < 0.05).

On comparing renal function tests [urea, creatinine, BUN, eGFR, urine output (UO) and PRA] in both groups before and 24 h after LVP, there was a highly significant increase in urea, creatinine, BUN and PRA levels in group II compared with group I (P < 0.01): before LVP, urea was 70.4 ± 46.2 against 140.9 ± 37.01 mg/dl, creatinine 0.89 ± 0.3 against 2.2 ± 0.59 mg/dl, BUN 32.9 ± 21.6 against 65.4 ± 17.6 mg/dl and PRA 4.68 ± 3.11 against 11.5 ± 3.25 ng/ml/h in groups I and II, respectively; and 24 h after LVP, urea was 68.4 ± 49.9 against 134.4 ± 42.7 mg/dl, creatinine 0.81 ± 0.32 against 1.92 ± 0.51 mg/dl, BUN 31.9 ± 23.2 against 62.4 ± 20.2 mg/dl and PRA 4.68 ± 3.14 against 11.8 ± 3.7 ng/ml/h in groups I and group II, respectively. Overall, eGFR estimates were less in group II than in group I (P < 0.01). Before LVP, eGFR was 104.8 ± 50.6 against 33.12 ± 10.1 ml/min, and 24 h after LVP, it was 120.6 ± 56.7 against 40.4 ± 16.5 ml/min in groups I and II, respectively (P < 0.01).

Serum creatinine decreased significantly 24 h after LVP in groups I and II (P < 0.05 and 0.01, respectively). However, the eGFR and the UO increased significantly 24 h after LVP (P < 0.05 and 0.01, respectively, in group I; P < 0.01 and 0.05, respectively, in group II) as shown in [Table 1].
Table 1: Renal function changes in all patients (before and 24 h after LVP)

Click here to view


The renal RI ratio was significantly higher in group II compared with group I, whether before, 1 h after or 24 h after LVP (P < 0.01), although there was a significant decrease in RI in both groups (P < 0.01). The right RI was 0.704 ± 0.0357 against 0.814 ± 0.0279 before LVP, 0.681 ± 0.0411 against 0.789 ± 0.0299 1 h after LVP and 0.6812 ± 0.0435 against 0.788 ± 0.0309 24 h after LVP in groups I and II, respectively. The left RI was 0.703 ± 0.0355 against 0.814 ± 0.0272 before LVP, 0.678 ± 0.0431 against 0.788 ± 0.0289 1 h after LVP and 0.679 ± 0.046 against 0.786 ± 0.028 24 h after LVP in groups I and II, respectively.

There was a significant increase in CO, SV and CI (P < 0.01) in group I: CO was 7486.8 ± 1265.1, 7647.04 ± 1325.9 and 7552.2 ± 1311.7 ml/min, SV was 91.4 ± 16.3, 98.8 ± 17.9 and 95.2 ± 17.3 ml/beat and CI was 4056.6 ± 570.3, 4171.9 ± 609.3 and 4090.2 ± 576.8 ml/min/m 2 . In group II, CO was 7576.5 ± 1012.3, 7886.9 ± 969.4 and 7644.6 ± 999.6 ml/min, SV was 92.04 ± 13.98, 98.4 ± 13.7 and 95.5 ± 14.23 ml/beat and CI was 4139.04 ± 522.2, 4245.4 ± 685.8 and 4175.12 ± 511.5 ml/min/m 2 before, 1 and 24 h after LVP, respectively [Table 2].
Table 2: Haemodynamic parameters before, 1 h after and 24 h after LVP

Click here to view


The heart rate (HR) (beats/min) showed a statistically significant reduction in both groups before, 1 h after and 24 h after LVP, respectively, showing values of 91.1 ± 9.8, 85.2 ± 10.3 and 88.0 ± 11.9 in group I and values of 87.9 ± 11.8, 82.7 ± 13.9 and 84.5 ± 12.8 in group II (P < 0.05).

The mean arterial pressure (MAP) (mmHg) showed a significant decrease when compared in both groups before LVP, 1 h after and 24 h after LVP, respectively, showing values of 86.3 ± 11.8, 81.7 ± 10.9 and 84.5 ± 12.1 in group I and values of 83.2 ± 12.2, 79.4 ± 11.6 and 80.7 ± 10.6 in group II (P < 0.05).


  Discussion Top


In this study, all patients showed a significant decrease in HR 1 and 24 h after LVP compared with the baseline HR. This is in agreement with a study conducted by Appenrodt et al. [14] who found a significant decrease in the HR 1 and 24 h after paracentesis compared with the baseline HR (80, 76 and 72 beats/min) in cirrhotic patients with ascites. Similarly, Umgelter et al. [15] reported that there was a reduction in the HR from 101 beats/min (85-116) before paracentesis to 91 beats/min (68-106) after paracentesis, and Savino et al. [16] found a reduction in the HR from 104.46 ± 18.36 beats/min before paracentesis to 100.4 ± 16 beats/min after paracentesis (P < 0.001).

In the current study, there was a significant reduction in the MAP after LVP. Similar to this finding, García-Compean et al. [17] observed a reduction in the MAP from 89 ± 11 mmHg before paracentesis to 84 ± 11 mmHg 24 h after paracentesis with albumin substitution (P < 0.05). Also, Appenrodt et al. [14] found a significant decrease in the MAP 1 and 24 h after paracentesis compared with that before paracentesis [77 mmHg (63-83), 73 mmHg (67-78) and 72 mmHg (65-77), respectively]. Finally, Umgelter et al. [15] showed that the MAP reduced from 81 mmHg (74-100) before paracentesis with albumin substitution to 77 mmHg (68-93) 24 h after paracentesis, and Lai et al. [18] reported a significant decrease in the MAP during the first 2 h of paracentesis. This decrease in MAP is probably due to a decreased intravascular volume as a result of rapid reformation of ascites. Furthermore, Phillip et al. [19] showed a decrease in the MAP and the systemic vascular resistance immediately, 2 h after and 6 h after paracentesis.

Regarding other haemodynamic changes in this study, the mean value of CI increased in both groups after LVP, but not to a significant level. Also, Umgelter et al. [20] reported an increase in CI from 4.12 l/min/m 2 before paracentesis to 4.55 l/min/m 2 after paracentesis with albumin substitution, and Savino et al. [16] reported an increase in CI from 3.90 ± 1.21 l/min/m 2 before paracentesis to 4.42 ± 1.21 l/min/m 2 after paracentesis, (P < 0.001) in cirrhotic patients with tense ascites. Increasing CI after paracentesis has been attributed to an improved venous return and right ventricular filling, as impingement of the elevated diaphragm on the right heart is reduced by the decreased IAP as a consequence of LVP [21]; also, as the MAP decreased, it was believed that a decrease in the afterload caused by a decrease in the systemic vascular resistance due to decreased IAP after paracentesis was the reason for the enhanced CI [20].

Singh et al. [22] observed that there was no significant increase in the PRA after LVP with albumin substitution (45.90 ± 8.59 ng/ml/h) compared with that before LVP (43.18 ± 10.73 ng/ml/h) (P = 0.273). Similarly, Appenrodt et al. [14] reported no significant difference in plasma renin before and after paracentesis (385 and 402 μU/ml, respectively). Lai et al. [18] revealed similar results. All previous results are comparable to the current study. However, comparing the PRA between both groups, a significant increase in PRA was found in the HRS group (P < 0.01). These findings were similar to Ruiz Del Arbol et al. [23], who found an increase in the PRA from 9.9 ± 5.2 ng/ml/h in cirrhotic patients without HRS to 17.5 ± 11.4 ng/ml/h in cirrhotic patients complicated by HRS. As in HRS, there is a primary peripheral arterial vasodilatation and mesenteric blood pooling, resulting in a poorly effective arterial blood volume and compensatory stimulation of endogenous vasopressor systems [15]; also, in HRS, a mild increase in portal pressures leads to the up-regulation of nitric oxide synthase [24].

The present study showed that LVP with albumin substitution improved the RI significantly in cirrhotic patients with tense ascites in both groups. Any decrease in RI may be the consequence of diminished renal vascular resistance caused by reduced IAP and retroperitoneal pressure after LVP [6]. Also, the finding of decreasing RI despite decreasing HR may be interpreted as indicating a reduced renal vascular resistance [20]. However, on comparing both groups, the RI was significantly higher in the HRS group compared with the ascitic group before or after paracentesis.

An increased UO and an enhanced haemodynamic status after paracentesis were initially observed in cirrhotic patients with an elevated IAP. Paracentesis influenced the haemodynamic status favourably as expressed by an increased CO and improved the renal function in patients with cirrhosis and tense ascites [21],[25]. Umgelter et al. [20] reported an increase in the UO from 12 ml/h before paracentesis to 16 ml/h after paracentesis with albumin substitution in cirrhotic patients with tense ascites and HRS. In addition, Garcνa-Compean et al. [17] reported that there was a significant increase in the UO from 612 ± 593 ml/day before paracentesis to 904 ± 502 ml/day after paracentesis (P < 0.05) in cirrhotic patients with tense ascites. Maslovitz et al. [26] detected a significant increase in the daily UO from 925 ± 248 ml/day before paracentesis to 1523 ± 526 ml/day after paracentesis (P < 0.001), and Savino et al. [16] found an increase in the UO from 46.74 ± 26.46 cm 3 /h before paracentesis to 54.95 ± 24.52 cm 3 /h after paracentesis (P < 0.01).

Garcνa-Compean et al. [17] reported that there was no significant difference in serum creatinine before and 24 h after LVP (0.8 ± 0.3 and 0.8 ± 0.4 mg/dl, respectively). Also, Maslovitz et al. [26] reported no significant difference in serum creatinine before and after paracentesis (0.84 ± 0.17 and 0.8 ± 0.12 mg/dl, respectively). In contrast, results of the present study showed a significant reduction in serum creatinine 24 h after LVP. Similar findings were observed by Savino et al. [16], who showed a significant decrease in serum creatinine from 1.37 ± 0.49 mg/dl before paracentesis to 1.32 ± 0.58 mg/dl after paracentesis (P < 0.001). The decrease in serum creatinine attributed to the increased CO due to increased cardiac compliance after paracentesis and the decreased IAP improved renal perfusion by lowering venous and retroperitoneal pressures [15] as the impairment of renal function caused by direct renal compression due to increased IAP. These events might be the reason for the improvement in renal perfusion and in serum creatinine as a consequence [16].

Umgelter et al. [20] reported an increase in GFR from 5 ml/h before paracentesis to 9 ml/h after paracentesis with albumin substitution in cirrhotic patients with tense ascites and HRS. Also, in another study, Umgelter et al. [15] discovered a significant elevation in GFR from 23 ml/min before paracentesis to 34 ml/min 24 h after paracentesis in cirrhotic patients with tense ascites and HRS, which is consistent with the finding of an improved renal function and GFR after LVP and albumin substitution in the current study [20].

Nguyen-Khac et al. [27] reported a strong correlation of electrolytes in the serum of cirrhotic patients with that in the ascitic fluid as the ascitic Na + was 133.1 ± 6.6, blood Na + was 131.8 ± 6.3 mmol/l (P < 0.0001), ascitic K + 4.1 ± 0.8, blood K + 4.3 ± 0.9 mmol/l (P < 0.0001) and ascitic Cl was 107.2 ± 7.6, and blood Cl - was 101 ± 7 mmol/l (P < 0.0001). Finally, in the present study, there was a positive correlation between serum and ascitic electrolytes (Na + , K + and Cl ) in both groups.


  Conclusion Top


PRA is significantly higher in patients with HRS and LVP, with albumin substitution leading to a significant reduction in HR and MAP, serum creatinine, BUN and RI and a significant increase in GFR, but there was no significant effect on the PRA. Finally, there was a significant correlation between the level of serum and ascitic fluid electrolytes.


  Acknowledgements Top


Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Salerno F, Gerbes A, Ginès P, Wong F, Arroyo V. Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. Gut 2007; 56:1310-1318.  Back to cited text no. 1
    
2.
Bataller R, Ginès P, Guevara M, Arroyo V. Hepatorenal syndrome. Semin Liver Dis 1997; 17:233-247.  Back to cited text no. 2
    
3.
Arroyo V, Guevara M, Ginès P. Hepatorenal syndrome in cirrhosis: pathogenesis and treatment. Gastroenterology 2002; 122:1658-1676.  Back to cited text no. 3
    
4.
Ginès P, Guevara M, Arroyo V, Rodés J. Hepatorenal syndrome in cirrhosis. Lancet 2003; 362:1819-1827.  Back to cited text no. 4
    
5.
Schuppan D, Afdhal NH. Liver cirrhosis. Lancet 2008; 371:838-851.  Back to cited text no. 5
    
6.
Tublin ME, Bude RO, Platt JF. The resistive index in renal doppler sonography: where do we stand? Am J Roentgenol 2003; 180:885-892.  Back to cited text no. 6
    
7.
Rivolta R, Maggi A, Cazzaniga M, Castagnone D, Panzeri A, Solenghi D, et al. Reduction of renal cortical blood flow assessed by Doppler in cirrhotic patients with refractory ascites. Hepatology 1998; 28:1235-1240.  Back to cited text no. 7
    
8.
Kirkpatrick AW, Colistro R, Laupland KB, Fox DL, Konkin DE, Kock V, et al. Renal arterial resistive index response to intraabdominal hypertension in a porcine model. Crit Care Med 2007; 35:207-213.  Back to cited text no. 8
    
9.
Dalfino L, Tullo L, Donadio I, Malcangi V, Brienza N. Intra-abdominal hypertension and acute renal failure in critically ill patients. Intensive Care Med 2007; 34:707-713.  Back to cited text no. 9
    
10.
Malbrain ML. Abdominal pressure in the critically ill: measurement and clinical relevance. Intensive Care Med 1999; 25:1453-1458.  Back to cited text no. 10
    
11.
Guevara M, Bru C, Ginès P, Fernández-Esparrach G, Sort P, Bataller R, et al. Increased cerebrovascular resistance in cirrhotic patients with ascites. Hepatology 1998; 28:39-44.  Back to cited text no. 11
    
12.
Pache I, Bilodeau M. Severe haemorrhage following abdominal paracentesis for ascites in patients with liver failure. Aliment Pharmacol Ther 2005; 21:525-529.  Back to cited text no. 12
    
13.
Rule AD, Larson TS, Bergstralh EJ, Slezak JM, Jacobsen SJ, Cosio FG. Using serum creatinine to estimate glomerular filtration rate: accuracy in good health and in chronic kidney disease. Ann Intern Med 2004; 141:929-937.  Back to cited text no. 13
    
14.
Appenrodt B, Wolf A, Grünhage F, Trebicka J, Schepke M, Rabe C, et al. Prevention of paracentesis-induced circulatory dysfunction: midodrine vs albumin. A randomized pilot study. Liver Int 2008; 28:1019-1025.  Back to cited text no. 14
    
15.
Umgelter A, Reindl W, Wagner KS, Franzen M, Stock K, Schmid RM, et al. Effects of plasma expansion with albumin and paracentesis on haemodynamics and kidney function in critically ill cirrhotic patients with tense ascites and hepatorenal syndrome: a prospective uncontrolled trial. Crit Care 2008; 12:R4.  Back to cited text no. 15
    
16.
Savino JA, Cerabona T, Agarwal N, Byrne D. Manipulation of ascitic fluid pressure in cirrhotic to optimize hemodynamic and renal function. Ann Surg 1988; 208:504-511.  Back to cited text no. 16
    
17.
García-Compean D, Blanc P, Larrey D, Daures JP, Hirtz J, Mendoza E, et al. Treatment of cirrhotic tense ascites with Dextran-40 versus albumin associated with large volume paracentesis: a randomized controlled trial. Ann Hepatol 2002; 1:29-35.  Back to cited text no. 17
    
18.
Lai KN, Li P, Law E, Swaminathan R, Nicholls MG. Large-volume paracentesis versus dialytic ultrafiltration in the treatment of cirrhotic ascites. Q J Med 1991; 78:33-41.  Back to cited text no. 18
    
19.
Phillip V, Saugel B, Ernesti C, Hapfelmeier A, Schultheiß C, Thies P, et al. Effeects of paracentesis on hemodynamic parameters and respiratory function in critically ill patients. BMC Gastroenterol 2014; 14:18.  Back to cited text no. 19
    
20.
Umgelter A, Reindl W, Franzen M, Lenhardt C, Huber W, Schmid RM. Renal resistive index and renal function before and after paracentesis in patients with hepatorenal syndrome and tense ascites. Intensive Care Med 2009; 35:152-156.  Back to cited text no. 20
    
21.
Luca A, Feu F, García-Pagán JC, Jiménez W, Arroyo V, Bosch J, et al. Favorable effects of total paracentesis on splanchnic hemodynamics in cirrhotic patients with tense ascites. Hepatology 1994; 20:30-33.  Back to cited text no. 21
    
22.
Singh V, Dheerendra PC, Singh B, Nain CK, Chawla D, Sharma N, et al. Midodrine versus albumin in the prevention of paracentesis-induced circulatory dysfunction in cirrhotics: a randomized pilot study. Am J Gastroenterol 2008; 103:1399-1405.  Back to cited text no. 22
    
23.
Ruiz-del-Arbol L, Monescillo A, Arocena C, Valer P, Ginès P, Moreira V, et al. Circulatory function and hepatorenal syndrome in cirrhosis. Hepatology 2005; 42:439-447.  Back to cited text no. 23
    
24.
Abraldes JG, Iwakiri Y, Loureiro-Silva M, Haq O, Sessa WC, Groszmann RJ. Mild increases in portal pressure up-regulate vascular endothelial growth factor and endothelial nitric oxide synthase in the intestinal microcirculatory bed, leading to a hyperdynamic state. Am J Physiol Gastrointest Liver Physiol 2006; 290:980-987.  Back to cited text no. 24
    
25.
Cade R, Wagemaker H, Vogel S, Mars D, Hood-Lewis D, Privette M, et al. Hepatorenal syndrome. Studies of the effect of vascular volume and intraperitoneal pressure on renal and hepatic function. Am J Med 1987; 82:427-438.  Back to cited text no. 25
[PUBMED]    
26.
Maslovitz S, Jaffa A, Eytan O, Wolman I, Many A, Lessing JB, et al. Renal blood flow alteration after paracentesis in women with ovarian hyperstimulation. Obstet Gynecol 2004; 104:321-326.  Back to cited text no. 26
    
27.
Nguyen-Khac E, Thevenot T, Capron D, Dharancy S, Paupart T, Thabut D, et al. Are ascitic electrolytes usable in cirrhotic patients? Correlation of sodium, potassium, chloride, urea, and creatinine concentrations in ascitic fluid and blood. Eur J Intern Med 2008; 19:613-618.  Back to cited text no. 27
    



 
 
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