31.10.20 Impact of Ascites in Pulmonary Function of Patients with Portal Hypertension

Original Article


Impact of Ascites on Pulmonary Function

Impact of Ascites in Pulmonary Function of Patients with Portal Hypertension

Muhammad Mahboob Alam1, Umar Usman2, Umair Ahmad2, Muhammad Arif2,
Saqib Musharraf3 and
Noor ul Huda Mehboob4


Objective: To evaluate the pulmonary function of patients having portal hypertension with altered volume of ascites.

Study Design: Cross-sectional study

Place and Duration of Study: This study was conducted at the Department of Pulmonology, Faisalabad Medical University, Faisalabad and Abwa Hospital / Research centre Faisalabad from July, 2019 to December, 2019.

Materials and Methods: Fifteen patients with portal hypertension and ascites underwent pulmonary function tests, consisting of spirometry and arterial blood gases, before and after reducing the volume of ascites. The parameters analyzed were: forced vital capacity (FVC); expiratory reserve in the first second (FEV 1); expiratory flow between 25 and 75% of FVC (FEF25-75%); Force expiratory volume 6(FEV6); FEV1 ratio/ FVC; PEF, arterial oxygen pressure (PaO2), carbon dioxide arterial pressure (PaCO2) and oxygen saturation (SaO2).

Results: There was a significant improvement in the lung volumes analyzed after decreasing ascites with diuretic treatment associated or not with paracentesis.

Conclusion: We conclude that in patients with portal hypertension and ascites, there is a decrease in lung volumes in relation to the predicted values, with significant improvement after a decrease in ascites. Likewise, we observed an increase in PaO2 and SaO2.

Key Words: Ascites, Portal hypertension, Pulmonary function tests, Compensated cirrhosis, Hypoxemia

Citation of article: Alam MM, Usman U, Ahmad U, Arif M, Musharraf S, Mehboob NH. Impact of Ascites in Pulmonary Function of Patients with Portal Hypertension. Med Forum 2020;31(10):83-87.




Liver cirrhosis is the main cause of portal hypertension and ascites, which in turn is the main complication found in cirrhotic patients after approximately ten years of diagnosis of compensated cirrhosis, affecting 50% of patients 1-3.

Several changes can be detected by pulmonary function tests in patients with chronic liver disease, especially in those with cirrhosis. These changes, which together characterize the "hepatopulmonary syndrome", cause hypoxemia and occur in one third of patients with cirrhosis 4. Inadequate oxygenation in patients with cirrhosis is caused by several pathophysiological mechanisms,    such    as    inadequate    vascular    tone,



1. Abwa Hospital & Research Centre / Abwa Medical College,  Faisalabad.

2. Faisalabad Medical University, Faisalabad.

3. Gulab Devi Educational Complex, Lahore.

4. Aziz Fatima Medical & Dental College, Faisalabad.



Correspondence: Dr. Umar Usman, Associate Professor / HOD (Pulmonology), Faisalabad Medical University, Faisalabad.

Contact No: 0300-6627988

Email: drumarusman33@yahoo.com



Received:    March, 2020

Accepted:    July, 2020

Printed:        October, 2020



pulmonary vasodilation, altered ventilation-perfusion ratio (V/Q), increased arteriovenous shunts and changes in the diffusion-perfusion ratio 5-9.

In addition to the changes already expected in cirrhotics, when ascites occurs, we can observe restrictive and obstructive changes in pulmonary function tests with decreased lung volumes &hypoxemia, that improve after reducing ascites10-14.

The increase in volume and intra-abdominal pressure resulting from ascites leads to a decrease in lung expansion, with consequent hypoventilation, especially in the lung bases. Along with the interstitial edema present in cirrhotic patients, there may be alveolar collapse and micro atelectasis that may explain the spirometric and gasometric changes found. Therefore, ascites, especially when high in volume, impairs the pulmonary function of patients with portal hypertension of different etiologies in a variable way, especially when associated with cirrhosis 15. This work aims to evaluate and quantify the influence of reduction in the volume of ascetic fluid on the pulmonary function of patients with portal hypertension.


We analyzed lung function using spirometry and measurement of arterial gases in adult patients, of both sexes, diagnosed with portal hypertension and ascites, admitted to the Department of Pulmonology, Faisalabad Medical University, Faisalabad and Abwa Hospital / Resarch centre Faisalabad for the period from 1st July, 2019 to 31st December, 2019. All participants included after being properly informed about proposed treatment and having agreed to the spirometry and arterial blood gas tests.

Exclusion Criteria: Those having previous cardiac and pulmonary diseases, hemodynamic instability, neoplasms, renal failure with serum creatinine >3.5mg/dl, gastrointestinal hemorrhage, encephalopathy, bacterial peritonitis and difficulty in collaborating with the spirometric examination. Smokers were included only when they had no clinical or radiological symptoms or signs of previous pulmonary involvement.

Chest radiographs were found to be within normal limits, with a decrease in lung expansibility as a consequence of the large abdominal volume presented by the patients. The cirrhotic patients classified according to the Child-Pugh criteria for establishing severity of the disease Pic 1.

The patients had moderate to severe ascites, which was characterized by data from the physical and ultrasound examination: high-volume ascites, by simple inspection of the abdomen; ascites with increased abdominal wall tension, as evidenced by palpation; ascites which, due to its proportion, caused respiratory distress to the patient, especially when in the supine position; and ultrasound showing massive ascites.

All patients underwent a pulmonary function study before starting treatment for ascites. The clinical treatment consisted of a prescription for rest, a diet with 2.0 g of salt and diuretics. The diuretic used was spironolactone, associated or not with furosemide. The patients were not submitted to pulmonary physiotherapy. Therapeutic paracentesis was indicated in patients who presented ascites with signs and symptoms of abdominal and respiratory discomfort or in patients who were not responding satisfactorily to clinical treatment with diuretics (continuous weight loss of about 500 g / day).

An average of 6.5 liters of ascitic fluid was removed per patient, with parenteral replacement of a plasma unit (300 ml) for every liters of ascitic fluid drained. After paracentesis, patients were submitted to spirometry, performed the day after the procedure. The spirometric tests were performed at the Pulmonology Department of     DHQ Hospital Faisalabad with devices:MIR spirolabIII version 3.1.

The technique used to perform the exam and the parameters obtained and analyzed are in accordance with American Thoracic Society(ATS). The parameters analyzed were: FVC (forced vital capacity); FEV 1 (expiratory volume in the first second); FEF     25-75% (forced expiratory flow between 25 and 75% of FVC); force expiratory volume 6(FEV6), peak expiratory flow (PEF) and FEV 1 / FVC ratio. The slow vital capacity curve (VCC) evaluated lung volumes and capacities and the predicted values adopted were those of Crapo11.

The volume-time curve (forced spirometry) was performed according to the acceptance and reproducibility criteria of curves recommended by the American Thoracic Society, and the best of three acceptable curves, of eight performed, was chosen. The predicted values were those of Wang WT 12.  Patients undergoing arterial blood gas analysis were analyzed for their arterial oxygen pressure (PaO2), arterial carbon dioxide pressure (PaCO2) and arterial oxygen saturation (SaO2). The results of the variables found were analyzed by the Student's t test for paired data. Statistically significant differences were considered when p<0.050(5%).


We analyzed 15 patients with portal hypertension and ascites, 9(60%) were male and   6(40%)were females, with ages ranging from 31 to 67 years and mean of 51 ± 9.5 years old. A higher prevalence of patients with diagnosis of liver cirrhosis was observed in 33.33% cases. Portal hypertension associated with hepatitis B or C virus, had a prevalence of 60% (Table-1). Ten patients had a history of Hepatitis C (67%) and 5patients were smokers (33.3%).





Albumin, g/dl




Bilirubin, umol/dl




Bilirubin, mg/dl




(s above normal)




Prothrombin level, % Ascites


mild controlled

Moderate refractory

Encephalopathy (grade)







Figure No.1: Child Pugh Score

Table No.1: Distribution according to the frequency of etiological diagnosis of patient


Number of patient


Cirrhosis with hep c



Cirrhosis with hep b






Hep b with hep c



Hepb with alcoholism






Hep c with alcoholism



Portal vein thrombosis with hep-c







According to Child-Pugh criteria, applied to 13 patients, except for patients 1 and 3, with cryptogenic cirrhosis, our group was formed mostly by patients with score B (11 patients / 84.6%), with only 2 patients had a C score (15.4%) and no patient had an A score.

Twelve patients underwent therapeutic paracentesis, with removal of 6.5 liters of ascitic fluid and an average loss of 6.9 kg of weight. Three patients showed an excellent response to clinical treatment, with a significant decrease in abdominal volume, with an average loss of 6.4 kg of weight, and were then referred to a new spirometry without undergoing therapeutic paracentesis. The spirometric diagnoses found in the patients analyzed are shown in Table-2.

Table No.2: Spirometry Results Obtained Pre & Post Paracentesis and Clinical Treatment of Ascities Patients



Post treatment














































OVDSA= Obstructive ventilatory disorder of small airway, LOVD= mild obstructive ventilatory disorder, RVD= restrictive ventilatory disorder, MOVD= moderate obstructive ventilatory disorder, MVD= mixed ventilatory disorder, NL= normal.

Our patients, before paracentesis and / or clinical treatment of ascites, presented FVC results below the expected average measurements and obtained a significant improvement in this parameter after treatment. FEV1 values were also reduced before ascites treatment and improved after paracentesis and / or clinical treatment. The FEV 1 ratio / FVC showed no statistically significant difference after treatment. The FEF values 25-75% before paracentesis and / or clinical treatment of ascites were also reduced in relation to the predicted average.

Although we observed an increase after treatment, it was not statistically significant. We can observe that there was an improvement in the FEV6 and PEF after reduction of ascites, with statistical significance. The results in Table 3 briefly demonstrate all the main variables analyzed by us and their degree of significance for the study in question.

Six patients underwent arterial blood gas analysis. Before paracentesis, the mean values found in these patients were: PaO 2 = 68 ± 17mmHg; PaCO 2 = 32 ± 17mmHg; and SaO 2 = 92 ± 6%. After paracentesis, the means were: PaO 2 = 76 ± 17mmHg; PaCO 2 = 29 ± 5mmHg and SaO 2 = 94 ± 4%.

The increase in values of PaO2 and SaO2 showed statistical significance (Table 3).

Table No.3: Comparison of spirometric variables and air gases pre and post paracentesis and clinical treatment of ascities


Pre- paracentesis

Post paracentesis























FEF 25/75(L/S)




FEF 25-75 (%)


























FEV=forced expiratory volume FVC=forced vital capacity FEF=Forced expiratory flow PaO2=partial pressure of oxygen PaCO2=partial pressure of carbon dioxide SaO2=oxygen saturation PEF=peak expiratory flow FEV6 =forced expiratory flow in 6 seconds.


According to other studies 4-9, the pulmonary changes found in cirrhotic patients are closely related to the degree of impaired liver function. This data is important for the interpretation of the results of our work, since our patients were mostly cirrhotic (60%) with a moderate to advanced degree of disease (Child-Pugh B or C in 86.66% of the cases -13 patients), and may present pulmonary manifestations resulting from their underlying disease, in addition to those caused by increased intra-abdominal pressure as a consequence of ascites. We observed a higher prevalence of obstructive ventilatory disorder (eight patients-53.32%), and in the literature the reports point to a higher prevalence of restrictive ventilatory disorder 12.

As in our work, Zampiet al13 reported the presence of obstructive ventilatory disorder and concluded that this finding could be related to the degree of hepatic impairment of the patients analyzed. In patients with more advanced liver disease, there would be greater pulmonary interstitial edema and, therefore, greater involvement of the alveoli and bronchioles, causing early closure of the airways on expiration and obstructive disorders.

According to Ramalingam et al 14, the effects of ascites on the respiratory system are probably mediated by the hydrostatic pressure exerted on the diaphragm and the severity of the damage caused by gas exchange is closely related to the decrease in lung volumes that occurs in these circumstances. We were unable to establish a relationship between smoking and obstructive ventilatory disorder, as only three patients, out of eight with an obstructive pattern, were smokers.

We believe, like other authors, that decrease in intra-abdominal pressure due to reduced volume of ascites, was responsible for the improvement 14,15. Some studies found hypoxemia in ascitic patients before treatment and reported a significant increase in PaO2 after diuretic therapy. Possibly the use of diuretics, according to the authors, reduced pulmonary interstitial edema, leading to a more favorable ventilation / perfusion ratio.

A study conducted by Yigitet al 16 documented the presence of a restrictive pattern, with increased in FEV6 and PEF in the pulmonary functional assessment, in cirrhotic patients with and without ascites. They found a decrease in the parameters analyzed when measuring respiratory muscle strength in patients with and without ascites, indicating less effectiveness of the rib cage muscles, which could contribute to the functional changes found. In most of reviewed studies, it was observed, like us, a decrease in FVC, FEV 1, FEV, in addition to PEF before, and significant increases after paracentesis17-20.

We observed that several patients had a normal spirometric examination after clinical treatment with diuretics, or after paracentesis, showing an evident improvement in respiratory parameters by decreasing the volume of ascites. The FEV 1 / FVC ratio did not show significant differences before and after treatment, which shows that the increases in FEV 1 were proportional to the FVC increases, being very close to the 80% expected for the relationship. The decrease in FEV 1 and FVC with maintenance of the predicted values for the FEV 1 / FVC ratio is found in restrictive pulmonary disorders, which may therefore be associated with the observed obstructive disorders. The small decrease in FEF25-75% found before treatment may be associated with bronchiolar involvement and pulmonary compression with early closure of the small airways, which can occur in patients with liver disease with ascites. The FEV6 and PEF was significantly reduced in our study before the treatment of ascites with significant improvement after its treatment, in agreement with the reviewed studies 21.

In the present study, we found mild hypoxemia in our patients with improvement after treatment. SaO2 also improved after reducing ascites, but we did not see the same when assessing PaCO2. Probably the improvement in lung volumes, with a consequent improvement in pulmonary ventilation, contributed to better oxygenation. As all patients used diuretics during the study, this may have contributed to an improvement in PaO2.


Reduced ascites volume significantly improves pulmonary ventilation and therapeutic paracentesis seems to be a treatment alternative for rapid relief of symptoms of dyspnea and abdominal discomfort, or for cases in which therapy diuretics is not entirely satisfactory. We concluded that in patients with portal hypertension and ascites, there is a decrease in lung volumes in relation to the predicted values, with significant improvement after a decrease in ascites.

Author’s Contribution:

Concept & Design of Study:

Muhammad Mahboob Alam


Umar Usman, Umair Ahmad

Data Analysis:

Muhammad Arif, Saqib Musharraf and Noor ul Huda Mehboob

Revisiting Critically:

Muhammad Mahboob Alam, Umar Usman

Final Approval of version:

Muhammad Mahboob Alam

Conflict of Interest: The study has no conflict of interest to declare by any author.


1.      Adebayo D, Neong SF, Wong F. Refractory ascites in liver cirrhosis. Am J Gastroenterol 2019;114(1): 40-7.

2.      Bernts LH, Drenth JP, Tjwa ET. Management of portal hypertension and ascites in polycystic liver disease. Liver Int 2019;39(11):2024-33.

3.      Sinha R, Lockman KA, Mallawaarachchi N, Robertson M, Plevris JN, Hayes PC. Carvedilol use is associated with improved survival in patients with liver cirrhosis and ascites. J Hepatol 2017; 67(1):40-6.

4.      Soulaidopoulos S, Cholongitas E, Giannakoulas G, Vlachou M, Goulis I. Update on current and emergent data on hepatopulmonary syndrome. World J Gastroenterol 2018; 24(12):1285-98.

5.      Fu L, Wang Q, Wu J, Guo Y, Huang M, Liu T, et al. Congenital extrahepatic porto-systemic shunt: an under diagnosed but treatable cause of hepato-pulmonary syndrome. Eur J Pediatr 2016; 175(2):195-201.

6.      Grilo-Bensusan I, Pascasio-Acevedo JM. Hepatopulmonary syndrome: What we know and what we would like to know. World J Gastroenterol 2016;22(25):5728-41.

7.      Chang CC, Lee WS, Hsieh HG, Chuang CL, Huang HC, Lee FY, et al. Selective cyclooxygenase inhibition by SC-560 improves hepatopulmonary syndrome in cirrhotic rats. PloS one. 2017;12(6):e0179809.

8.      Waseem N, Chen PH. Hypoxic hepatitis: a review and clinical update. J Clin Translational Hepatol 2016;28;4(3):263-8.

9.      Iqbal S, Smith KA, Khungar V. Hepatopulmonary syndrome and portopulmonary hypertension: implications for liver transplantation. Clinics in Chest Med 2017;38(4):785-95.

10.  Awad NF, Elbalsha AA, Abo Amer MZ, Ibrahim MH. Study of The Relationship between Severity of Liver Cirrhosis and Pulmonary Function Tests. Egyptian J Hospital Med 2019;76(7):4570-6.

11.  Fernandez JJ, Castellano MV, Vianna FD, Nacif SR, Rodrigues Junior R, Rodrigues SC. Clinical and functional correlations of the difference between slow vital capacity and FVC. JornalBrasileiro de Pneumologia. 2020;46(1).

12.  Wang WT, Ko HK, Lin CC, Shu JH, Hsu HC, Liang Y, et al. Spirometric reference values in heathy Chinese adults in Taiwan: The secular changes and comparison with other Asian populations. JFMA 2020;119(1):290-9.

13.  Zampi G, Pergolini A, Pontillo D, Cottini M. Abdominal ascitic fluid: tricky concealing of the electrocardiogram. Kardiologia Polska (Polish Heart J) 2017;75(8):814.

14.  Ramalingam V, Ansari S, Truwit J. Respiratory Complications in Acute and Chronic Liver Disease. In: Nanchal R, Subramanian R, editors. Hepatic Critical Care. Springer, Cham; 2018. https://doi.org/10.1007/978-3-319-66432-3_11

15.  Moore CM, Van Thiel DH. Cirrhotic ascites review: Pathophysiology, diagnosis and management. World J Hepatol 2013;5(5):251-63.

16.  Yigit IP, Hacievliyagil SS, Seckin Y, Oner RI, Karıncaoglu M. The relationship between severity of liver cirrhosis and pulmonary function tests. Digestive Dis Sci 2008;53(7):1951-6.

17.  Kraus MS, Teufel M, Esser M, Kiefer LS, Fleischer S, Graepler-Mainka U, et al. Differing Pulmonary Structural Abnormalities Detected on Pulmonary MR Imaging in Cystic Fibrosis Patients with Varying Pancreatic Function. In RoFo-Fortschritte auf demGebiet der Rontgenstrahlen und der bildgebendenVerfahren 2020;192(6):

18.  Pan MM, Zhang HS, Sun TY. Value of forced expiratory volume in 6 seconds FEV(6) in the evaluation of pulmonary function in Chinese elderly males 2017;97(20):1556-61.

19.  Wittmer VL, Lima RT, Maia MC, Duarte H, Paro FM. Respiratory and symptomatic impact of ascitis relief by paracentesis in patients with hepatic cirrhosis. Arq Gastroenterol 2020;57:64–8.

20.  Surani SR, Mendez Y, Anjum H, Varon J. Pulmonary complications of hepatic diseases.  World J Gastroenterol 2016;22(26):6008-15.

21.  Lenz K, Buder R, Kapun L, Voglmayr M. Treatment and management of ascites and hepatorenal syndrome: an update. Therap Adv Gastroenterol 2015;8(2):83-100.