Influence of ascites in the pulmonary function of patients with portal hypertension

Abstracts

BACKGROUND: Oxygen deficiency in patients with portal hypertension may be secondary to changes in respiratory mechanics due to ascites. OBJECTIVES: Evaluate pulmonary function in patients with portal hypertension before and after reduction of the ascites. METHOD: Fifteen patients with portal hypertension and ascites were submitted to pulmonary function tests, comprising spirometry and arterial blood gas determination, before and after reduction of ascites. The analysed parameters were: forced vital capacity (FVC); forced expiratory volume in one second (FEV1); forced expiratory flow between 25-75% of the forced vital capacity (FEF 25-75%); expiratory reserve volume (ERV); FEV1/CVF; arterial oxygen pressure (PaO2); arterial carbon-dioxide pressure (PaCO2) and arterial oxygen saturation (SaO2). RESULTS: There was remarkable improvement in pulmonary volumes after decrease of ascites by treatment with diuretics associated or not to paracentesis. CONCLUSION: We concluded, that in patients with portal hypertension and ascites, there is a decrease of pulmonary volumes compared to predicted values, with significant improvement after decrease of ascites. Similarly, an increase of the arterial oxygen pressure and of the arterial oxygen saturation was perceived.

Ascite; Hypertension, portal; Respiratory function tests

INTRODUÇÃO: A oxigenação inadequada nos pacientes com hipertensão portal pode ser secundária a alterações na mecânica respiratória, determinadas pela presença da ascite. OBJETIVO: Avaliar a função pulmonar de doentes com hipertensão portal antes e após redução do volumeda ascite. Método: Quinze doentes com hipertensão portal e ascite foram submetidos a provas de função pulmonar, constituindo-se de espirometria e gasometria arterial, antes e após redução do volume da ascite. Os parâmetros analisados foram: capacidade vital forçada (CVF); volume expiratório no primeiro segundo (VEF1); fluxo expiratório entre 25 e 75% da CVF (FEF 25-75% ); volume de reserva expiratória (VRE); relação VEF1 / CVF; pressão arterial de oxigênio (PaO2), pressão arterial de dióxido de carbono (PaCO2) e saturação arterial de oxigênio (SaO2). RESULTADOS: Houve melhora significativa dos volumes pulmonares analisados após a diminuição da ascite com o tratamento diurético associado ou não à paracentese. CONCLUSÃO: Concluímos que nos doentes com hipertensão portal e ascite, há diminuição dos volumes pulmonares emrelação aos valores preditos, com melhora significativa após diminuição da ascite. Do mesmo modo, observamos aumento na PaO2 e na SaO2.

Ascite; Hipertensão portal; Testes de função respiratória

ORIGINAL ARTICLE

Influence of ascites in the pulmonary function of patients with portal hypertension ^*

Angela Maria Stiefano Nitrini; Roberto Stirbulov^{(TE SBPT)}; Ernani Geraldo Rolim

^{Correspondence}

ABSTRACT

BACKGROUND: Oxygen deficiency in patients with portal hypertension may be secondary to changes in respiratory mechanics due to ascites.

OBJECTIVES: Evaluate pulmonary function in patients with portal hypertension before and after reduction of the ascites.

METHOD: Fifteen patients with portal hypertension and ascites were submitted to pulmonary function tests, comprising spirometry and arterial blood gas determination, before and after reduction of ascites. The analyzed parameters were: forced vital capacity (FVC); forced expiratory volume in one second (FEV₁); forced expiratory flow between 25% - 75% of forced vital capacity (FEF _25-75%); expiratory reserve volume (ERV); FEV₁/FVC; arterial oxygen pressure (PaO₂); arterial carbon-dioxide pressure (PaCO₂) and arterial oxygen saturation (SaO₂).

RESULTS: There was remarkable improvement in pulmonary volumes after decrease of ascites by treatment with diuretics associated or not to paracentesis.

CONCLUSION: We concluded, that in patients with portal hypertension and ascites, there is a decrease of pulmonary volumes compared to predicted values, with significant improvement decrease of ascites. Similarly, an increase of the arterial oxygen pressure and of the arterial oxygen saturation was perceived.

Key words: Ascites/therapy. Hypertension, portal. Respiratory function tests.

Abbreviations used in this paper:

TLC – Total lung capacity

FVC – Forced vital capacity

COPD – Chronic obstructive pulmonary disease

RLD – Restrictive lung disease

FEF_25-75% – Forced expiratory flow between 25% and 75% of forced vital capacity

ISCMSP – Irmandade da Santa Casa de Misericórdia de São Paulo

PaCO₂ – Arterial carbon dioxide tension

PaO₂ – Arterial oxygen tension

SaO₂ – Arterial oxygen saturation

FV – Flow volume

FEV₁ – Forced expiratory volume in one second

V/Q – Ventilation/perfusion ratio

RV – Residual volume

ERV – Expiratory reserve volume

Introduction

Hepatic cirrhosis is the main cause of portal hypertension and ascites. Ascites is found in 50% of cirrhotic patients by approximately 10 years after they have been diagnosed with compensated cirrhosis.^(1-3)

Various changes can be detected by pulmonary function tests in patients diagnosed with chronic hepatic diseases, mainly in those diagnosed with cirrhosis. These changes, which characterize the “hepatopulmonary syndrome” result in hypoxemia and affect one-third of all patients diagnosed with cirrhosis.⁽⁴⁾

In patients diagnosed with cirrhosis, inadequate oxygenation is caused by various physiopathological mechanisms, such as inadequate vascular tonus, pulmonary vasodilation, altered ventilation/perfusion (V/Q) ratio, more arterial-venous shunts, and changes in the diffusion/perfusion ratio.^(4-9)

In addition to the expected changes in cirrhotic patients, we can observe restrictive and obstructive changes in pulmonary function tests when there is ascites.⁽¹⁰⁾ The hypoxemia and decreased pulmonary volume seen in such cases improves after the ascites has been reduced.^(11-15)

The increased intra-abdominal volume and pressure caused by the ascites results in decreased lung expansion, and consequent hypoventilation, mainly in the lung bases. Together with the interstitial edema seen in cirrhotic patients, alveolar collapse and microatelectasis may also occur, a situation which could explain the changes in spirometry and blood gas analysis ⁽¹⁰⁾.

Therefore, ascites, especially when severe and when combined with cirrhosis, impairs pulmonary function in patients with portal hypertension. The nature and degree of this impairment varies depending upon the etiology of the ascites. This study evaluates and quantifies the effect that reducing ascitic fluid has on the pulmonary function of patients diagnosed with portal hypertension.

Methods

Using spirometry and blood gas analysis, we evaluated pulmonary function in adult male and female patients diagnosed with portal hypertension and ascites and admitted to the Central Hospital and to the Hospital São Luiz Gonzaga between March 1996 and October 2000. Both institutions operate under the auspices of the Irmandade Santa Casa de Misericórdia de São Paulo (ISCMSP).

All patients were admitted to the study group after having the proposed treatment fully explained and agreeing to be submitted to spirometry and blood gas analysis.

Exclusion criteria included: history of prior heart and lung diseases, unstable hemodynamics, neoplasias, renal insufficiency with serum creatinine values > 3.5 mg/dL, gastrointestinal hemorrhage, encephalopathy, bacterial peritonitis, and difficulty to cooperate during the spirometric exam. Smokers were included in the group only when they presented no clinical or radiograph signs of prior pulmonary impairment.

In all of the patients studied, chest radiographs were normal, although decreased lung expansion (due to abdomen volume increase) was observed.

In the cirrhotic patients studied, severity of the cirrhosis was determined by using the Child-Pugh classification system (Chart 1).

All patients presented with moderate to severe ascites, which was characterized by physical examination and tomography. Large volume ascites was diagnosed by simple abdomen examination. Ascites with increased abdominal wall tension was diagnosed through palpation. Ascites causing respiratory distress, especially when in supine position was confirmed through sonograms evidencing large volume ascites.

All patients were submitted to pulmonary function tests before and after treatment for ascites. The clinical treatment prescribed included rest, salt restriction (2 g/day) and diuretics. The chosen diuretic was spironolactone, combined with furosemide in some cases. Patients were not submitted to pulmonary physiotherapy.

Therapeutic paracentesis was performed in patients diagnosed with ascites and presenting signs and symptoms of respiratory distress or abdominal discomfort, as well as in patients who were not responding well to the clinical treatment with diuretics (good response = continuous weight loss of ± 500g/day).

A mean volume of 6.5 L of ascitic fluid was removed from each patient, with a parenteral replacement of 1 plasma unit (300 mL) for every 2 liters of drained fluid. Patients were submitted to spirometry on the day following paracentesis.

Spirometric tests were performed in the Pulmonary Function Tests Laboratory of the ISCMSP using the MedGraphics Breeze Cardiorespiratory Diagnostic Software, system 1070 (Medical Graphics, St. Paul, MN, USA), a 2.15 Koko spirometer (PDS Instrumentation, Louisville, CO, USA) and a model 113 pH/blood gas analyzer (Instrumentation Laboratory, Lexington, MA, USA).

The methodology used in the test and the parameters analyzed are in accordance with the guidelines set forth by the Brazilian Consensus on Spirometry (routine determined by the Pulmonary Function Tests Laboratory in the Santa Casa de São Paulo).

The parameters analyzed were forced vital capacity (FVC), forced expiratory volume in one second (FEV₁), forced expiratory flow between 25% and 75% of forced vital capacity (FEF_25-75%), expiratory reserve volume (ERV) and the FEV₁ to FVC ratio.

Slow vital capacity (SVC) was used to evaluate volume and lung capacity. The adopted predictive values were those suggested by Crapo.⁽¹⁶⁾

The volume-time curves (forced spirometry) were produced according to the acceptability and reproducibility criteria established by the American Thoracic Society. Of a total of 8 curves, the best of 3 acceptable curves was chosen. The predictive values were those suggested by Knudson.⁽¹⁷⁾

The flow-volume curves were also submitted to the acceptability and reproducibility criteria of the ATS and the best of 3 acceptable curves was also chosen. An envelope curve was also created.

In patients who were submitted to arterial blood gas tests, the parameters analyzed were arterial oxygen tension (PaO₂), arterial carbon dioxide tension (PaCO₂), and arterial oxygen saturation (SaO₂).

Results from the studied variables were analyzed using the paired Student’s t-test. Values of p < 0.050 (5%) were considered statistically significant.

Results

Of the 15 patients with portal hypertension and ascites analyzed, 9 (60%) were male and 6 (40%) were female. Ages ranged from 31 to 67 (mean, 51 ± 9.5). The most common diagnosis was alcoholic liver cirrhosis, which was found in 5 (33.3%) of the patients studied. Portal hypertension combined with hepatitis B, hepatitis C or schistosomiasis was diagnosed in 9 (60%) of the patients (Table 1), a history of prior alcoholism was reported in 10 (67%), and 5 (33.3%) were smokers.

According to the Child-Pugh classification system, which was applied in 13 of the patients, our study group was mainly composed of class B patients (11 patients; 84.6%). Only 2 patients (15.4%; patients 1 and 3, who were diagnosed with schistosomiasis) belonged to class C. None scored low enough to be considered class A.

Twelve patients were submitted to therapeutic paracentesis, and, on average, 6.5 L of ascitic fluid were removed. Average weight loss within the group was 6.9 kg. Three patients had excellent response to the clinical treatment, with substantial reduction of abdominal volume and an average weight loss of 6.4 kg. They were submitted to a second battery of spirometric tests without the need for therapeutic paracentesis. Spirometric results can be seen in Table 2.

Prior to paracentesis or clinical therapy, FVC values were lower than the predicted mean values. After treatment, these numbers improved. This was also true of FEV₁ values. There were no statistically significant differences in FEV₁/FVC ratios after treatment. The FEF_25-75% values were also lower than the predictive mean before paracentesis or clinical treatment and increased after treatment, although the increase was not statistically significant. There was, however, a statistically significant improvement in ERV values after treatment. Table 3 summarizes the main variables analyzed and their significance.

Six patients were submitted to blood gas tests. Prior to paracentesis, mean PaO₂ = 68 ± 17 mmHg, mean PaCO₂ = 32 ± 17 mmHg; and mean SaO₂ = 92±6%. After paracentesis, mean PaO₂ = 76 ± 17 mmHg, mean PaCO₂ = 29 ± 5 mmHg and mean SaO₂ = 94±4%. The increases in PaO₂ and SaO₂ attained a level of statistical significance (Table 3).

Discussion

Even though the number of patients studied was small, we observed a higher prevalence of male patients diagnosed with alcoholic liver cirrhosis. This is in accordance with data found in the literature.^(1,2,18)

According to various studies,^(4,9,19,20) the pulmonary changes seen in cirrhotic patients are closely related to the degree of hepatic involvement. This is important for the interpretation of the results in our study, since most of our patients were cirrhotic (60%), suffering from moderate to severe forms of the disease (Child-Pugh scores of B or C in 13 patients; 86.66%). These patients could present with pulmonary manifestations due to the baseline disease, as well as with other symptoms caused by the ascites-induced increase in intra-abdominal pressure.

We observed a higher prevalence of chronic obstructive pulmonary disease (COPD; 8 patients; 53.32%), whereas other authors have reported a higher prevalence of restrictive lung disease (RLD).^{(10,14,21-,23)}

According to Yao et al.,⁽¹⁰⁾ ascites causes elevation of the diaphragm, with lung volume reduction and increased intrathoracic pressure. This, together with the pulmonary edema found in cirrhotic patients, may result in pulmonary tissue compression and the attendant microatelectasis, which are responsible for the hypoxemia and restrictive pattern observed in the pulmonary function tests. Similarly to our study, Yao et al.⁽¹⁰⁾ also reported COPD and concluded that this may be related to the degree of hepatic involvement. In patients with more severe hepatic disease, there is greater interstitial lung edema and therefore more extensive involvement of alveoli and bronchioles, causing premature closure of the airways during expiration, as well as obstructive disorders.

According to Chao et al.,⁽²¹⁾ the effects of ascites on the respiratory system are probably mediated by the hydrostatic pressure exerted on the diaphragm. Under these circumstances, the extent to which gas exchange is altered is closely related to lung volume reduction.

Since only 3 of the 8 patients with obstructive defects were smokers, we were unable to establish a correlation between smoking and COPD. We believe, in agreement with Yao et al.,⁽¹⁰⁾ that pulmonary changes due to severe chronic hepatic disease alone can better explain our findings.

In evaluating the pulmonary function of cirrhotic patients with and without ascites, Ordialez Fernandez et al.⁽²²⁾ observed restrictive patterns and reduced ERV. When respiratory muscle force was measured in patients with and without ascites, the authors found decreases in the evaluated parameters, indicating that the accessory muscles in the chest wall were less effective, which could have contributed to the functional changes observed.

In concordance with our findings, most studies in the literature show that FVC, FEV₁, ERV, and functional residual capacity decrease before and increase after paracentesis.^{(10,12,14,15,21,24)}

In some patients, we observed that spirometric results returned to normal after paracentesis or after clinical treatment with diuretics, demonstrating that reduction of ascites improves respiratory parameters.

There were no significant differences between pretreatment and posttreatment FEV₁/FVC ratios. This indicates that the increase in FEV₁ was proportional to the FVC increase, approximating the predicted value of 80%. Such decreases in FEV₁ and FVC, together with FEV₁/FVC ratios remaining at the predicted value, are seen in RLD and could therefore be related to the obstructive disorders observed in our patients.

The small decrease in FEF_25-75% found before treatment may be related to the bronchiolar involvement and lung compression, involving premature narrowing of the small airways, which can occur in patients with hepatic diseases and ascites.

In our study, ERV values were markedly below normal prior to ascites treatment. In accordance with previous studies, we observed significant improvement after treatment. We also believe that the lower intra-abdominal pressure resulting from reduction of the ascites volume was responsible for the ERV improvement.^(11,14,22)

According to Chao et al.,⁽²¹⁾ ascites may impair pulmonary perfusion by reducing blood flow in the lung bases, which are mechanically compressed, thereby aggravating hypoxemia in cirrhotic patients. Some studies have reported hypoxemia in patients with ascites prior to the treatment and considerable improvement in PaO₂ after therapy with diuretics.^(15,23) According to the authors, the use of diuretics may reduce interstitial lung edema and yield a more favorable V/Q ratio.

In the present study, we observed mild hypoxemia, which improved after treatment. There was also improvement in SaO₂ after the reduction of ascites, but PaCO₂ was unaffected. Increased lung volume, combined with improved pulmonary ventilation, may have contributed to better oxygenation. All patients were prescribed diuretics during the study and this may have contributed to PaO₂ improvement, in accordance with the previously cited studies.

In summation, the reduction of ascites volume significantly improved pulmonary ventilation in the patients evaluated in this study. Therapeutic paracentesis seems to be an alternative treatment for rapid relief of symptoms such as dyspnea and abdominal discomfort, or for patients who do not satisfactorily respond to diuretic therapy.

References

Submitted: 31/07/2003.

Accepted, after revision: 16/10/2003.

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*

Study carried out at the Medical Clinic of the Hospital São Luiz Gonzaga, - Irmandade da Santa Casa de Misericórdia de São Paulo.

Publication Dates

• Publication in this collection
  19 May 2004
• Date of issue
  Feb 2004

History

• Received
  31 July 2003
• Accepted
  16 Oct 2003