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      Alteraciones gasométricas en pacientes cirróticos hospitalizados Translated title: Gasometric alterations in hospitalized cirrhotic patients

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          Abstract

          Introducción y objetivos: Aunque se ha descrito la existencia de diversas alteraciones del intercambio gaseoso en la cirrosis, existen pocos estudios que las hayan estudiado de forma prospectiva. El objetivo de este trabajo fue conocer la frecuencia y gravedad de dichas alteraciones en los pacientes cirróticos hospitalizados, correlacionándolas con el grado de disfunción hepática. Pacientes y métodos: Se estudiaron 50 pacientes cirróticos consecutivos (41 varones) que requirieron ingreso hospitalario por descompensación de su hepatopatia (ascitis, encefalopatía hepática, hepatitis alcohólica y hemorragia digestiva alta), y que no presentaban procesos pulmonares ni cardiacos agudos o crónicos que pudiesen producir hipoxemia. Los pacientes fueron agrupados según su estadio de Child-Pugh (A, n = 13; B, n = 21; C, n = 16). En siete pacientes se constató la presencia de una hepatitis alcohólica sobreañadida grave (HAAG). En todos ellos se realizó una gasometría arterial basal antes de ser dados de alta, y se efectuó un ecocardiograma transtorácico con contraste en caso de sospecha de síndrome hepatopulmonar (SHP). Resultados: Se observó una discreta hipoxemia global (80,9 mmHg) sin diferencias según el grado de Child-Pugh. La hipocapnia fue significativamente más marcada en los pacientes con estadio Child C que en aquellos con estadios A y B (31,2 ± 3,1 frente a 38,1 ± 4,3 y 36,3 ± 5 mmHg; p < 0,05), respectivamente. En cambio, los pacientes cirróticos con HAAG presentaron un hipocapnia significativamente menor que aquellos otros sin HAAG (31,2 ± 3,1 frente a 36,3 ± 5 mmHg; p < 0,05). En el análisis multivariante, las variables con valor pronóstico independiente para la presencia de hipocapnia fueron la protrombina, la albúmina y el sodio plasmáticos. Se constató la presencia de SHP en 8 pacientes (16%). Conclusiones: La alteración gasométrica más frecuentes de la cirrosis es la alteración del gradiente alvéolo-arterial de oxígeno, que se acentúa conforme empeora la función hepática. La hipocapnia, aunque su patogenia no es bien conocida, podría constituir una mecanismo compensador de la hipoxemia o bien ser el resultado de la activación de los centros respiratorios centrales por sustancias no aclaradas en el hígado.

          Translated abstract

          Background and objectives: Gas exchange alterations have been described in cirrhotic patients; but by the moment, a few prospective studies have focused in them. The aim of this study was to describe the frequency and severity of gasometric alterations in hospitalized cirrhotic patients, a their correlationwith hepatocellular disfunction. Patients and methods: 50 consecutive cirrhotic patients (41 males) admited for liver decompensation (ascites, liver encephalopathy, alcoholic hepatitis and upper gastrointestinal bleeding) without acute or chronic cardiopulmonary disfunction were included in the study. Patients were classificated according with Child-Pugh score (A, n = 13; B, n = 21; C, n = 16). Severe alcoholic hepatitis (SAH) was confirmed in 7 patients. Arterial gasometry was performed in all patients before discharge. Contrast echocardiography was performed in any case of suspicion of hepatopulmonary syndrome (HPS). Results: Light hypoxemia was observed (80.9 mmHg), without differences with Child-Pugh. Hypocapnia was significantly more evident in Child C than in A and B (31.2 ± 3.1 vs. 38.1 ± 4.3 y 36.3 ± 5 mmHg; p < 0,05), respectively. Cirrhotic patients with SAH showed a significantly higher hypocapnia by comparison with others (31.2 ± 3.1 vs. a 36.3±5 mmHg; p < 0.05). In multivariate analysis, independent prognostic variables for hypocapnica were plasmatic levels of protrombin time, albumin and sodium. HPS was confirmed in 8 patients (16%). Conclusions: The most prevalent gas exchange abnormality in cirrhosis was the alteration of alveolar-arterial oxygen tension gradient, directly correlated with hepatocellur disfunction. Hypocapnia could be a compensatory mechanism or the result of the activation of central respiratory centres by non-depurated substances by the liver.

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          Most cited references 39

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          Diagnostic utility of contrast echocardiography and lung perfusion scan in patients with hepatopulmonary syndrome.

          Two modalities, contrast echocardiography and lung perfusion scan, are used to identify intrapulmonary vascular dilatation and diagnose hepatopulmonary syndrome (HPS), but a comparison of these two procedures has not been performed. The aim of this study was to compare the use of these diagnostic modalities in detecting intrapulmonary vascular dilatation and diagnosing HPS. Forty consecutive outpatients with biopsy-proven cirrhosis had contrast echocardiography, a lung perfusion scan, and arterial blood gases analyzed. Fifteen of 40 cirrhotics (38%) had positive contrast echocardiogram results. Seven patients with positive echocardiogram results had gas exchange abnormalities and could be considered to have HPS (7 of 40 [17.5%]). Three of these patients were hypoxemic and had no concurrent cardiopulmonary disease, and each had positive contrast echocardiogram and lung perfusion scan results and were readily diagnosed as having HPS. The other 4 patients (3 hypoxemic and 1 normoxemic with an elevated alveolar-arterial gradient) had coexisting intrinsic lung disease and/or chest radiograph abnormalities complicating the diagnosis of HPS, and each had positive echocardiogram and negative lung scan results. The remaining 8 patients with positive echocardiogram results had normal lung scan and normal gas exchange results. No patient had positive lung scan and negative contrast echocardiogram results. Contrast echocardiography is the most useful screening test for intrapulmonary vasodilatation and may be positive more frequently than lung perfusion scans in patients with HPS.
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            Hepatopulmonary syndrome: prevalence and predictive value of various cut offs for arterial oxygenation and their clinical consequences.

             V Fuhrmann,  O Kandel,  S Lehr (2002)
            The hepatopulmonary syndrome (HPS) is defined as the triad of liver disease, arterial deoxygenation, and pulmonary vascular dilatation. The reported prevalence of HPS in cirrhotic patients varies between 4% and 19%, and various threshold values defining arterial deoxygenation have been used and recommended previously. However, it is not known how the prevalence of HPS differs using different cut off values for arterial deoxygenation. We studied 127 patients for the presence of HPS using transthoracic contrast echocardiography for detection of pulmonary vasodilation, pulmonary function tests, and blood gas analysis. Ninety eight patients were included in the study, of whom 33 (34%) had a positive contrast echocardiography. Using an increased alveolar-arterial difference for the partial pressure of oxygen (AaDO(2)) as an indication of hypoxaemia, the prevalence of HPS was considerably higher (>15 mm Hg, 32%; >20 mm Hg, 31%; and >age related threshold, 28%) than using reduced partial pressure of arterial oxygen (PaO(2)) as a threshold (<80 mm Hg, 19%; <70 mm Hg, 15%; and
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              Hepatopulmonary syndrome. Clinical observations and lack of therapeutic response to somatostatin analogue.

              We retrospectively studied 22 patients with hepatopulmonary syndrome (HPS) evaluated at the Mayo Medical Center from 1984 to 1991. All patients had hepatic cirrhosis with clinical evidence of portal hypertension; 13 (59 percent) had severe hypoxemia while breathing room air in the supine position (PaO2 < 60 mm Hg), and 14 of 16 (88 percent) had orthodeoxia breathing room air. On the basis of angiographic observations, we defined type 1 and type 2 patterns of pulmonary vascular abnormalities in HPS. Response to 100 percent oxygen and therapeutic regimens may differ in the angiographic patterns. Substantial deterioration in PaO2 associated with clinically stable hepatic dysfunction was documented in five of seven patients studied with sequential arterial blood gas testing; four subsequently died within 48 months. Overall mortality was 41 percent, occurring a mean of 2.5 years after diagnosis. In 7 of the 22 patients, we prospectively studied the effect of somatostatin analogue given subcutaneously for 4 consecutive days. No significant improvement in PaO2 was documented while breathing room air or 100 percent oxygen (p < 0.05). We conclude that in selected patients with clinically stable hepatic dysfunction and deteriorating oxygenation, the prognosis is poor. Our data in combination with recent surgical reports suggest that liver transplantation may be the treatment of choice in patients with HPS and worsening oxygenation.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                ami
                Anales de Medicina Interna
                An. Med. Interna (Madrid)
                Arán Ediciones, S. L. (, , Spain )
                0212-7199
                May 2005
                : 22
                : 5
                : 209-212
                Affiliations
                Badalona Barcelona orgnameHospital Universitari Germans Trias i Pujol orgdiv1Servicio de Aparato Digestivo
                Article
                S0212-71992005000500002
                10.4321/s0212-71992005000500002

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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