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Pulmonary changes in liver transplant candidates with Hepatitis C Cirrhosis
  Mohamede S Al-Moamaryt,  Tanja  Gorka,  Ibrahime H Al-Traif,  Hamdane H Al-Jahdalit,  Abdullah A Al-Shimemeri ,  Bandere  Al-Kanway,  Abdulmajedt A Abdulkareeem ,  Abdulmajedt A Abdulkareeem

Objectives: Several studies have shown that pulmonary abnormalities are common in patients with end-stage liver disease. However, most of these studies were conducted on patients with heterogeneous etiologies. Therefore, we studied these changes in a homogenous group of hepatitis C cirrhotic patients who were potential candidates for liver transplantation.
Methods: The charts of 81 patients from King Fahad National Guard Hospital, Riyadh, Kingdom of Saudi Arabia with hepatitis C cirrhosis who were evaluated for liver transplantation were reviewed. The following data was retrieved: echocardiography with micro-bubble study, arterial blood gases, and pulmonary function tests of 81 candidates and reviewed over 3 years from 1994 to 1997.
Results: The mean age was 53 (±9) years with male to female ratio of 1.4:1. Echocardiographic micro-bubble study, revealed 4 of 62 (7%) had an intrapulmonary shunt. Arterial blood gases results were pH of 7.44 (±0.4), partial arterial tension of carbon dioxide of 33 mm Hg (±4), partial arterial tension of oxygen of 84 mm Hg (±12), and alveolar-arterial gradient of 30 mm Hg (±10). Eleven percent had obstructive airway disease, 17% had restrictive lung impairment, and 43% had reduced diffusion capacity. Seventy five percent of patients with reduced diffusion capacity had normal lung volumes. Various pulmonary function test abnormalities did not lead to significant differences in arterial blood gases.
Conclusions: Pulmonary changes were frequent in liver transplant candidates with hepatitis C virus cirrhosis with reduced diffusion capacity being the most. Apart from the effect of hepatopulmonary syndrome on arterial oxygenation, other pulmonary abnormalities were not significantly different.

Saudi Medical Journal 2001; Vol. 22 (12): 1069-1072


End-stage liver disease (ESLD) is associated with a variety of pulmonary changes. According to the degree of liver failure, patients with cirrhosis exhibit progressive abnormalities of the systemic and pulmonary hemodynamics which reflect a complex interaction between intrapulmonary and extrapulmonary factors.1,2 This explains the frequent occurrence of arterial oxygenation and pulmonary function tests (PFT) abnormalities in ESLD. Intrapulmonary shunt (IPS) is another cause of significant arterial oxygenation abnormalities in ESLD. It occurs uncommonly in ESLD and can be diagnosed reliably by contrast trans-thoracic echocardiography.3,4 These changes mandate careful pre-transplantation evaluation to avoid intra-operative or post-operative complications. Most of the studies that evaluated cardiopulmonary changes in chronic liver disease were conducted on a group of patients with different etiologies. Therefore, we evaluated the pulmonary changes in a homogenous cohort of liver transplant (LT) candidates with ESLD due to hepatitis C virus infection (HCV) with special emphasis on the prevalence and features of intra-pulmonary shunt.P> FONT>

Methods.FONT> FONT>Study population.B>I>FONT> FONT>King Fahad National Guard Hospital (KFNGH) is a tertiary care center in the Kingdom of Saudi Arabia where approximately 25-30 LTs are performed each year. From January 1994 to October 1997, 263 patients with ESLD were evaluated for possible LT. Of these, the study group consisted of 81 patients (31%) with advanced ESLD due to HCV. All patients had biopsy-proven liver cirrhosis consistent with HCV. All patients were anti-HCV positive using a 2nd generation enzyme linked immunosorbent assay (ELISA) test and the HCV infection was confirmed by the presence of hepatitis C ribonucleic acid. Comprehensive investigations were carried out to exclude other etiologies.P>

Pulmonary function tests.B>I>FONT> FONT>The majority of patients had pulmonary function tests (Jaeger Master lab, Germany) that included spirometry, lung volumes by either body box or helium dilution methods, and diffusion capacity. Spirometric values were calculated from the best of at least 3 trials as recommended by the American Thoracic Society criteria.5 All PFT values were reported as a percentage of the predicted values. Forced expiratory volume in 1 second (FEV1) to forced expiratory capacity (FVC) ratio of less than 70% was considered an obstructive impairment and total lung capacity (TLC) of less than 80% of predicted was considered a restrictive lung impairment.6 A reduced lung diffusion capacity (DLco) of less than 80% of predicted was considered abnormal when corrected DLco to alveolar volume was less than predicted.6 P>

Arterial blood gases.B>I>FONT> FONT>Sixty-seven arterial blood gases (ABG) were performed on room air. The Alveolar-arterial oxygen gradient (A—a) PO2, was calculated by the simplified version of the alveolar air equation.6 Partial arterial tension of oxygen (PAO2)=149-partial arterial tension of carbon dioxide (PaCO2)/0.8 The (A—a) PO2 was then obtained by calculating the difference between calculated PAO2 and measured PaO2. Orthodeoxia was defined as drop in PaO2 by 10% upon standing up from lying position.4P>

Echocardiographic measurements.B>I>FONT> FONT>As part of the LT work up, all patients had a contrast trans-thoracic echocardiography (TTE) with micro-bubble study to assess cardiac structure and function and to exclude the presence of shunt. All the echocardiographs were carried out by one operator


From the Department of Medicine (Al-Moamary, Al-Traif, Al-Jahdali, Al-Shimemeri, Al-Kanway), Department of Cardiac Sciences (Gorka), Department of Hepatobiliary Sciences (Al-Abdulkareem), King Fahad National Guard Hospital, Riyadh, Kingdom of Saudi Arabia.

Received 27th March 2001. Accepted for publication in final form 21st July 2001.

Address correspondence and reprint request to: Dr. Mohamed S. Al-Moamary, Department of Medicine (1443), King Fahad National Guard Hospital, PO Box 84252, Riyadh, Kingdom of Saudi Arabia. Tel. +966 (1) 2520088 Ext. 4196. Fax. +966 (1) 2635128. E-mail:




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