Evolution of intrapulmonary vascular dilatations in cirrhosis

Current Gastroenterology Reports, 2000

Hypoxemia is common in patients with cirrhosis but the natural history of this syndrome is unknown. This study was conducted to evaluate the natural history of arterial oxygenation in patient with end stage liver cirrhosis. Sixty eight patients with liver cirrhosis were followed up for 6-12 months. Arterial blood gas (ABG) and pulse oximetry were obtained on day of presentation and follow up. There were no significant changes in the oxygen saturation by pulse oximetry (SpO2), partial pressure of oxygen (PaO2) and alveolar arterial oxygen gradient (A-a O2) after 6-12 months. Mean arterial oxygen saturation (SaO2) in 46 patients was 95.42±1.92, and after follow up changed to 95.45±2.96. Thirty eight patients had SaO2 > 94% (mean 96.12±1.08 after 6-12 months changed to 95.66±2.58) ; 8 patients had SaO2 = 94 (mean 92.08±1.44 after 6-12 months changed to 94.46±4.47). There were no significant changes in the SpO2, PaO2 and A-a O2 after 6-12 months.

2000

Journal of Hepatology, 1999

Background/Aims: Hepatopuhnonary syndrome is defined as a clinical triad including chronic liver disease, abnormal pulmonary gas exchange resulting ultimately in profound arterial hypoxaemia, and evidence of intrapulmonary vascular dilatations. We report five patients with liver cirrhosis diagnosed with hepatopulmonary syndrome who had associated chronic obstructive or restrictive respiratory diseases. Methods: Clinical, radiographic and constrast-enhanced echocardiographic findings, and systemic and pulmonary haemodynamic and gas exchange, including ventilation-perfusion distributions, measurements were assessed in all five patients. Results: Echocardiography was consistent with the presence of intrapulmonary vasodilation without intracardiac abnormalities, and high resolution computed tomographic scan features were compatible with clinical (3 cases) or histopathological diagnoses (2 cases) of associated respiratory disorders. The most common prominent functional findings were moderate W E HAVE SUGGESTED that the hepatopulmonary syndrome (HPS) should be defined as a clinical triad characterized by the association of an advanced, chronic liver disorder, pulmonary gas exchange disturbances leading ultimately to intense hypoxaemia, and widespread intrapulmonary vascular dilatations, in the absence of intrinsic cardiopulmonary disease (1). This definition is challenged in part by Krowka & Cortese (2) and Lange & Stoller (3), who support the view that HPS can coexist with any other respiratory conditions commonly associated with liver diseases,

Background and Aims: The determination of the prevalence of cardiopulmonary complications at a liver transplant center in Iran. Methods: Ninety-nine patients (61 male and 38 female) with a mean age of 36.5 (15-66) years with proven cirrhosis were enrolled in this study. Patients with primary cardiac disease, current smokers, those with sepsis, hepatocellular carcinoma, recently ruptured esophageal varices and chronic pulmonary or renal diseases were excluded from the study. Sixty-nine patients had ascites. Forty-four patients had grade C Child-Pugh classification. All patients were evaluated for respiratory function by chest X-ray (CXR), room air arterial blood gas, simultaneous pulse oximetry, cardiac echocardiography and spirometry. Results: Sixty-one patients (66.1%) had a widened alveolar-arterial O2 difference ( > 20 mmHg); 14 (14.1%) had hypoxemia; 6 (6.1%) had mean pulmonary arterial pressure (MPAP) = 25-40 mmHg; 12 (12.1%) had tricuspid regurgitation; pleural effusion and lung restriction were detected in 4 (4%) and 50 (50.5%), respectively. P(A-a)O2 was negatively associated with pulmonary hypertension (P < 0.03) and tricuspid regurgitation (P < 0.005). Portal hypertension and portal vein thrombosis were detected in 91 and 8 patients, respectively. Conclusions: A widened alveolar-arterial oxygen difference was common in our patients, but hypoxemia occurred in 14% of patients. Portopulmonary hypertension was preponderant in those patients of male gender.

Journal of Hepatology, 1999

Background/Aims: The use of transesophageal contrast echocardiography (TOCE) in the diagnosis of intrapuhnonary vascular dilatation (IVD) and hepatopulmonary syndrome (HPS) needs to be studied. We tested the specificity of TOCE using traditional criteria and the value of a new method based on TOCE, a grading scale and a selected contrast. Methods: 1) Several solutions were tested and two were selected: 20% mannitol and 0.9% saline. 2) 71 cirrhotic patients and 20 controls were studied. Left atrium opacitication with contrast was classified into 6 degrees by TOCE. Mild and significant IVD were considered in relation to results in controls. Patients were studied with saline and mannitol-TOCE. Results were compared to transthoracic contrast echocardiography (TTCE), to gas exchange abnormalities and to Child class. Results: The reproducibility of TOCE grading was excellent, (Kappa BO.9). IVD detection using TTCE, mannitol-TOCE and saline-TOCE was 29.5%, 55% (25% mild and 30% significant), and 45% (38% mild and 7% significant), respectively. The best agreement with TTCE (reference method) was obtained with manmtol-TOCE, using significant IVD as the cut point. By this criterion, 18% reached the criteria of .

World Journal of Gastroenterology Wjg, 2006

AIM: To study the presence of sustained low diffusing capacity (DL(CO)) after liver transplantation (LT) in patients with hepatopulmonary syndrome (HPS).METHODS: Six patients with mild-to-severe HPS and 24 without HPS who underwent LT were prospectively followed before and after LT at mid-term (median, 15 mo). HPS patients were also assessed at long-tem (median, 86 mo).RESULTS: Before LT, HPS patients showed lower PaO(2) (71 +/- 8 mmHg), higher AaPO(2) (43 +/- 10 mmHg) and lower DL(CO) (54% +/- 9% predicted), due to a combination of moderate-to-severe ventilation-perfusion (V(A)/Q) imbalance, mild shunt and diffusion limitation, than non-HPS patients (94 +/- 4 mmHg and 19 +/- 3 mmHg, and 85% +/- 3% predicted, respectively) (P<0.05 each). Seven non-HPS patients had also reduced DL(CO) (70% +/- 4% predicted). At mid- and long-term after LT, compared to pre-LT, HPS patients normalized PaO(2) (91 +/- 3 mmHg and 87 +/- 5 mmHg), AaPO(2) (14 +/- 3 mmHg and 23 +/- 5 mmHg) and all V(A)/Q descriptors (P<0.05 each) without changes in DL(CO) (53% +/- 8% and 56% +/- 7% predicted, respectively). Post-LT DL(CO) in non-HPS patients with pre-LT low DL(CO) was unchanged (75% +/- 6% predicted).CONCLUSION: While complete V(A)/Q resolution in HPS indicates a reversible functional disturbance, sustained low DL(CO) after LT also present in some non-HPS patients, points to persistence of sub-clinical liver-induced pulmonary vascular changes.

Gastroenterology, 2003

Background & Aims: The hepatopulmonary syndrome (HPS) has been defined by chronic liver disease, arterial deoxygenation, and widespread intrapulmonary vasodilation. Mortality of patients with HPS is considered to be high, but the effect of HPS on survival in patients with cirrhosis remains unclear. Methods: A total of 111 patients with cirrhosis were studied prospectively by using transthoracic contrast echocardiography for detection of pulmonary vasodilation, blood gas analysis, and pulmonary function test. Twenty different clinical characteristics and survival times were noted. Results: Twentyseven patients (24%) had HPS. Their mortality was significantly higher (median survival, 10.6 months) compared with patients without HPS (40.8 mo, P < 0.05), even after adjusting for liver disease severity (2.9 vs. 14.7 months in Child-Pugh class C with [n ‫؍‬ 15] and without HPS [n ‫؍‬ 35, P < 0.05]; 35.3 vs. 44.5 months in Child-Pugh class B with [n ‫؍‬ 7] and without HPS [n ‫؍‬ 23, P ‫؍‬ NS]), and exclusion of patients who underwent liver transplantation during follow-up (median survival 4.8 vs. 35.2 months, P ‫؍‬ 0.005). Causes of death were mainly nonpulmonary and liver-related in the 19 patients with and the 35 patients without HPS who died. In multivariate analysis, HPS was an independent predictor of survival besides age, Child-Pugh class, and blood urea nitrogen. Mortality correlates with severity of HPS. Conclusions: The presence of HPS independently worsens prognosis of patients with cirrhosis. This should influence patient management and scoring systems and accelerate the evaluation process for liver transplantation.

Journal of Clinical Gastroenterology, 2006

Goals: We aimed to determine the role of thorax high-resolution computed tomography (HRCT) in demonstrating the pulmonary vasodilatation in patients with hepatopulmonary syndrome (HPS). Background: Traditionally, the presence of intrapulmonary vascular dilatations can be detected by using one of the three diagnostic modalities: contrast-enhanced echocardiography, technetium 99 mlabeled macroaggregated albumin scan, and pulmonary angiography. Study: The study group included 10 patients with HPS (Group 1), 12 patients with normoxemic cirrhosis (Group 2), and 12 healthy controls (Group 3). All of the subjects underwent conventional and HRCT of thorax. The diameters of pulmonary trunk, main pulmonary arteries, and right lower lobe basal segmental arteries were measured. The ratios of right lower lobe basal segmental pulmonary artery to bronchus diameter were calculated. Results: The mean diameters of the main pulmonary trunk, right and left main pulmonary arteries were not different between the groups. Mean diameters of right lower lobe basal segmental pulmonary arteries were significantly higher in Group 1 compared with Group 2 (P = 0.01) and Group 3 (P = 0.002). Mean right lower lobe basal segmental pulmonary artery to bronchus ratios were significantly higher in Group 1 compared with Group 2 (P = 0.03) and Group 3 (P , 0.001). Group 2 had significantly higher pulmonary artery to bronchus ratios than Group 3 (P , 0.001). Conclusions: Thorax HRCT may be helpful in the diagnosis of HPS by demonstrating the dilated peripheral pulmonary vessels or increased pulmonary artery to bronchus ratios in patients with liver disease and hypoxemia.

Critical Care, 2002

Purpose: To describe the epidemiology of the acute respiratory distress syndrome (ARDS) in a Brazilian ICU. Methods: This prospective observational, non-interventional study, included all consecutive patients with ARDS criteria [1] admitted in the ICU of a Brazilian tertiary hospital, between January 1997 and September 2001. Were collected in a prospective fashion the following variables: age, gender, APACHE II score at ICU admission and at ARDS diagnosis, cause of ARDS, presence of AIDS, cancer and immunosuppression, occurrence of barotrauma, performance of traqueostomy, mortality, duration of mechanical ventilation (MV), length of stay (LOS) in ICU and in hospital. The lung injury score (LIS) [2] was used to quantify the degree of pulmonary injury in the first week of ARDS. Results: There was 2182 patients (P) admitted in ICU during the study period, of whom 141 (6.46%) had ARDS criteria. Seventy-six (54%) were men, the mean age was 46 ± 18 years, APACHE II 18 ± 7 and 19 ± 7 at admission and at ARDS diagnosis, respectively. Septic shock accounted for 42% (60 P) of the ARDS causes, sepsis 22% (31 P), diffuse pulmonary infection 16% (23 P), aspiration pneumonia 11% (15 P), non-septic shock 5% (7 P) and others 4% (5 P). Ten percent (14 P) had AIDS, 30% (43 P) cancer and 25% (36 P) immunosuppression. All patients were mechanically ventilated with Tidal Volume between 4 and 8 ml/kg. Only 3.5% (5 P) had barotrauma and 10% (14 P) performed traqueostomy. Mortality rate was 79% in the ICU. The patients required 12 ± 10 days on MV, ranging from 1 to 55 days. The LOS in ICU and hospital was 14 ± 13 (1-69) days and 28 ± 32 (1-325) days, respectively. There was a time delay of 3.7 ± 4.5 days between admission in ICU and the onset of ARDS. The Murray score (mean ± SD) was 3.2 ± 0.4, 3 ± 0.5, 3 ± 0.5, 2.9 ± 0.6, 2.8 ± 0.7, 2.7 ± 0.7 and 2.6 ± 0.8 in the first 7 days, respectively. Conclusions: ARDS in our hospital has a similar incidence of reports in the USA and Europe. There was a higher mortality, which could be explained by a high incidence of infection causes of ARDS, mainly septic shock, and elevated combined occurrence of AIDS, cancer and immunosuppression, along the degree of LIS. The incidence of barotrauma was low, as a consequence of the current mechanical ventilation strategies.