BACKGROUND: One of the severe complications of liver disease is hepatopulmonary syndrome (HPS). There is paucity in literature regarding the various factors associated with the development of HPS. This study was conducted to analyze the prevalence and determinants of HPS among patients with decompensated chronic liver disease (CLD). METHODS: This study was a cross-sectional-observational study conducted in a tertiary care center. Decompensated CLD patients admitted for pre-liver transplant workup were included in the study. Demographic data, clinical findings, and biochemical and hematologic parameters were collected. Pulse oximetry, arterial blood gas analysis, bubble contrast echocardiogram, diffusion capacity of the lungs for carbon monoxide (DLCO), and spirometry were done to get the needed parameters. All data were entered into a Microsoft Excel sheet and analyzed using the statistical software SPSS for Windows, version 22.0. RESULTS: Among 64 subjects, 58 were men (90.6%). Mean age was 54.5 years. HPS was present in 26 (40.6%) patients. Platypnea and orthodeoxia were present more often in HPS patients. DLCO was significantly impaired among patients with HPS. Portopulmonary hypertension was seen in 8 (12.5%) subjects with no difference between HPS and non-HPS patients. Subjects with HPS had more severe liver disease. A model for end-stage liver disease (MELD)-Na score > 19 was associated with HPS (sensitivity 73.08%, specificity 65.79%, PPV 59.4%, and NPV 78.1%). Multivariate analysis (binary logistic regression) revealed that a higher MELD-Na score, hepatic encephalopathy, and impaired DLCO were independently associated with HPS. CONCLUSIONS: HPS is associated with more severe liver disease (as per Child-Turcotte-Pugh [CTP] stage and MELD-Na score). There was no relation between HPS and causes of CLD. Higher MELD-Na score, hepatic encephalopathy, impaired DLCO, clubbing, and spider naevi were independently associated with HPS.
BACKGROUND: One of the severe complications of liver disease is hepatopulmonary syndrome (HPS). There is paucity in literature regarding the various factors associated with the development of HPS. This study was conducted to analyze the prevalence and determinants of HPS among patients with decompensated chronic liver disease (CLD). METHODS: This study was a cross-sectional-observational study conducted in a tertiary care center. Decompensated CLD patients admitted for pre-liver transplant workup were included in the study. Demographic data, clinical findings, and biochemical and hematologic parameters were collected. Pulse oximetry, arterial blood gas analysis, bubble contrast echocardiogram, diffusion capacity of the lungs for carbon monoxide (DLCO), and spirometry were done to get the needed parameters. All data were entered into a Microsoft Excel sheet and analyzed using the statistical software SPSS for Windows, version 22.0. RESULTS: Among 64 subjects, 58 were men (90.6%). Mean age was 54.5 years. HPS was present in 26 (40.6%) patients. Platypnea and orthodeoxia were present more often in HPS patients. DLCO was significantly impaired among patients with HPS. Portopulmonary hypertension was seen in 8 (12.5%) subjects with no difference between HPS and non-HPS patients. Subjects with HPS had more severe liver disease. A model for end-stage liver disease (MELD)-Na score > 19 was associated with HPS (sensitivity 73.08%, specificity 65.79%, PPV 59.4%, and NPV 78.1%). Multivariate analysis (binary logistic regression) revealed that a higher MELD-Na score, hepatic encephalopathy, and impaired DLCO were independently associated with HPS. CONCLUSIONS: HPS is associated with more severe liver disease (as per Child-Turcotte-Pugh [CTP] stage and MELD-Na score). There was no relation between HPS and causes of CLD. Higher MELD-Na score, hepatic encephalopathy, impaired DLCO, clubbing, and spider naevi were independently associated with HPS.