Hepatopulmonary syndrome: Is NO the right answer?
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The effects of serum estrogen levels on hypoxemia and blood nitric oxide levels in experimental hepatopulmonary syndrome
2005, Hepatology ResearchHepatopulmonary syndrome (HPS) is a well-defined cause of hypoxemia in patients who have liver disease due to abnormal intrapulmonary vascular dilatation. The pulmonary symptoms of HPS are the result of oxygenation defects that occur as a result of acquired dilatations of the pulmonary blood vessels. In this study, we investigated the effects of estrogen and nitric oxide (NO) in experimental HPS, especially in intrapulmonary vascular dilatation.
Fifty female Sprague–Dawley rats were used in this study. The animals were divided into five groups of 10. Group l (the control group): the common bile duct (CBD) was dissected but not ligated. Group 2 (the cirrhosis group): the CBD was ligated. Group 3 (the cirrhosis + oophorectomized group): the CBD was ligated and a bilateral oophorectomy performed. Group 4 (the cirrhosis + estrogen group): the CBD was ligated and exogenous estrogen (5000 U/kg) given. Group 5 (the control + estrogen group): the CBD was dissected, but not ligated and exogenous estrogen (5000 U/kg) given. A 5-week waiting period was observed for the development of cirrhosis and the rats’ lungs and liver were taken for histopathological examination. Pulmonary vessel diameters were measured. The total bilirubin, direct bilirubin, alkaline phosphatase (ALP), estrogen and serum nitric oxide (NO) levels were measured.
The mean perialveolar vessel diameters were significantly higher in the cirrhotic rats (Groups 2, 3, and 4) than the control and control + estrogen administered groups. Again, when we compared the cirrhosis + oophorectomized group and the cirrhosis + estrogen group, the mean perialveolar vessel diameter was significantly lower in the cirrhosis + oophorectomized group than the cirrhosis + estrogen administered group (p = 0.001). The mean perialveolar vessel diameter in the cirrhosis + oophorectomized group was significantly lower than the cirrhosis group (p = 0.01). When we compared the cirrhotic rats (Groups 2, 3, and 4) and the control group, the plasma NO levels were significantly higher in the cirrhotic rats than the control group (p < 0.001). Among the cirrhotic rats, the plasma NO levels were 47.2 ± 0.7 and 70.9 ± 1.5 μmol/l in the cirrhosis + oophorectomized group and the cirrhosis + estrogen administered group, respectively (p = 0.004).
We consider that raised levels of estrogen have a potential role in intrapulmonary vascular dilatation and hypoxemia in HPS. Also, we consider that this effect of estrogen is due to increased levels of NO. Antiestrogenic surgical therapy may decrease the serum estrogen and NO levels, and may decrease the diameter of perialveolar vessels in order to relieve hypoxia in cirrhotic cases.
Hepatopulmonary syndrome: Relationship with liver dysfunction and systemic hemodynamic disorder
2004, Medicina ClinicaEl síndrome hepatopulmonar (SHP), que cursa con un gradiente alvéolo-arterial de oxígeno incrementado y, en fases avanzadas, con hipoxemia, es el resultado de la vasodilatación pulmonar. En la cirrosis hepática se ha demostrado la presencia de vasodilata-ción fundamentalmente esplácnica, pero también en otras zonas. Nuestro principal objetivo fue conocer el estado hemodinámico, la función renal y el estado de algunos sistemas humorales en pacientes diagnosticados de SHP.
Analizamos consecutivamente a 32 pacientes cirróticos divididos en 2 gru-pos, uno de 18 pacientes cirróticos con intercambio gaseoso normal (C-IGN), y otro de 14 pa-cientes diagnosticados de SHP por ecocardiografía transtorácica de contraste y/o gammagrafía pulmonar-cerebral con macroagregados de albúmina, en régimen de hospitalización, sin fárma-cos de acción cardiovascular durante los 4 días previos, reposo en cama, abstinencia de alco-hol y tabaco y dieta de 50 mEq de sodio.
Los pacientes del grupo SHP se caracterizaban por un índice de Child-Pugh más avanzado, presencia de acropaquias y arañas vasculares. Presentaban mayor grado de hypoxemia en sedestación, mayor hipocapnia y menores valores de difusión (TLCO). Asimismo, mostraban un estado circulatorio hiperdinámico caracterizado por menor presión arterial, mayor índice cardíaco,menores resistencias vasculares y mayor flujo femoral, con menores aclaramiento de creatinina,excreción de Na urinario, volumen urinario/24 h e hipervolemia, acompañado de mayor activacióndel eje renina-angiotensina-aldosterona y mayor excreción urinaria de nitritos y nitratos.
La vasodilatación pulmonar que explica el SHP es parte de la vasodilatación ge-neralizada que ocurre en la cirrosis hepática, que tiene relación con el grado de disfunción he-pática medido por la clasificación de Child-Pugh. La mayor activación del sistema renina-aldos-terona y el aumento del volumen plasmático expresan un grado más alto de subllenado arterial causado por un incremento en la producción de óxido nítrico.
The hepatopulmonary syndrome (HPS) causes an increased alveolar to arterial gradient of oxygen and in advanced phases hypoxemia, as the result of pulmonary va-sodilation. In liver cirrhosis, it has been demonstrated the existence of splachnic vasodilation and also in other vascular beds. Our main objectives were to know the hemodynamic status, the renal function and the condition of some humoral systems in patient diagnosed of HPS.
We studied consecutively 32 cirrhotic patients Divided in two groups, a group of 18 cirrhotic patients with normal gaseous exchange (NGE), and another group of 14 cirrhotic patients diagnosed of HPS by contrast-enhanced transthoracic echocardiography and/or lung and brain scintigraphy with 99 Tc albumin macroaggregates. They were all in rest in bed, upon alcohol and tobacco abstinence and on a diet of 50 mEq of sodium. Cardiovascular drugs were all withheld during 4 days in order to reach steady state.
Patients of the HPS group were characterized by a more advanced index of Child-Pugh and presence of clubbing and vascular spiders. They presented a greater degree of hypoxemia in a sitting position, greater hypocapnia and smaller transference factor values (TLCO). They also showed a hyperkinetic circulatory condition characterized by smaller arterial blood pressu-re, greater cardiac index, smaller vascular resistances and greater femoral flows, with smaller clearance of creatinine, elimination of urinary sodium, urinary volume/24 h and an increased plasmatic volume, accompanied with a greater activation of the renin-angiotensin-aldosterone axis and a greater urinary elimination of nitrites and nitrates.
The pulmonary vasodilation that explains the HPS is a constitutive part of the sys-temic vasodilation occurring in liver cirrhosis, and it is related to the degree of liver dysfunction as measured by the classification of Child-Pugh. The greater activation of the renin-aldosterone system and the rise of the plasmatic volume express a highest grade of arterial underfilling cau-sed by an increment in the nitric oxide production.
Anesthesia for liver resection and transplantation
2004, EMC - Anesthesie-ReanimationLa chirurgie hépatique est une chirurgie majeure dont les indications sont principalement carcinologiques. C'est une chirurgie qui expose à un risque d'hémorragie et d'embolies gazeuses peropératoires, et a une morbidité postopératoire importante. L'amélioration des techniques chirurgicales, mais aussi des avancées importantes dans la compréhension de la physiopathologie du cirrhotique, a permis de réduire le risque de ces interventions et de proposer cette chirurgie aux patients cirrhotiques (notamment après une hépatite C), qui développent des carcinomes hépatocellulaires. La transplantation hépatique est une des greffes d'organe les plus fréquemment réalisées en France et reste une intervention à haut risque qui pose de nombreux problèmes per- et postopératoires. Le manque de greffons hépatiques et la mortalité élevée des patients inscrits sur les listes d'attente conduisent à proposer de nouvelles techniques de prélèvement sur donneur en état de mort encéphalique (partition hépatique ou split) et des prélèvements sur donneur vivant.
Liver surgery is a major surgical procedure, mainly indicated for cancer resection. Intraoperative risk includes hemorrhage and air embolism, and severe postoperative complications are frequent. Improvement in surgical technique and recent advance in the understanding of cirrhosis-related alteration in cardiovascular, pulmonary and renal function have permitted to perform hepatic surgery in cirrhotic patients, especially when cirrhosis is secondary to hepatitis C. Orthotopic liver transplantation is one of the most frequently performed transplantation in France, and it remains a high risk surgery. The inadequate supply of donor livers has lead to development of new surgical technique, including liver splitting of cadaveric graft and living related donors.
Pulmonary Arteriovenous Malformations after Cavopulmonary Anastomosis
2003, Annals of Thoracic SurgeryCitation Excerpt :Levels of NO are elevated in the exhaled air of patients with the hepatopulmonary syndrome and normalize after orthotopic liver transplantation [37, 38]. The precise mechanism by which chronic liver failure leads to upregulation of the NO biosynthetic pathway in pulmonary vascular smooth muscle is not known; however, it may be due to the lack of hepatic clearance of inflammatory mediators such as endotoxin and various cytokines [39, 40]. In patients with advanced liver failure the pulmonary vasculature presumably has increased exposure to these inflammatory cytokines.
Pulmonary arteriovenous malformations (PAVMs) are a cause of progressive cyanosis after cavopulmonary anastomosis in children with single ventricle physiology who are on the pathway leading to a Fontan procedure. Investigations into possible mechanisms for the etiology of PAVMs are ongoing and suggest that the liver might play a key regulatory role in the development of these lesions.
Occurrence of hepatopulmonary syndrome in Budd-Chiari syndrome and the role of venous decompression
2002, GastroenterologyCitation Excerpt :Abscess drainage led to reversal of HPS. Vasoactive substance imbalance,1 probably an increased local nitric oxide level due to hepatic dysfunction,27 has been implicated in the pathogenesis of HPS. However, in a series of 25 cirrhotic patients with HPS,2 15 (60%) were found to be Child–Pugh class A, indicating that factors other than severity of liver disease are also important in the pathogenesis of HPS.
Background & Aims: Hepatopulmonary syndrome (HPS) has been predominantly detected in cirrhotic patients and rarely in patients with noncirrhotic portal hypertension. The aim of this study was to determine the occurrence of HPS in patients with Budd–Chiari syndrome (only anecdotal reports available) and evaluate the role of venous decompression in its reversal. Methods: Twentynine consecutive cases of Budd–Chiari syndrome without primary cardiopulmonary disease were investigated by air contrast echocardiography and arterial blood gas analysis. Venous decompression (e.g., by balloon cavoplasty) was attempted when feasible. Results: Eight cases (27.6%) of HPS and 9 cases (31.0%) with positive contrast echocardiography but unimpaired oxygenation were detected. Duration of disease was longer (P = 0.026) among those with positive contrast echocardiography. Cavoplasty reversed 4 of 5 cases of HPS and 2 of 2 cases with positive contrast echocardiography alone. Venous decompression by drainage of amebic liver abscess (which was compressing hepatic venous outflow) also reversed 1 case of HPS. HPS was relieved by venous decompression in 5 of 6 cases. Conclusions: HPS developed in a substantial fraction of our patients with Budd–Chiari syndrome, with positive contrast echocardiography occurring mainly in the benign, slowly progressing variety. Venous decompression showed promise in reversing such cases.
GASTROENTEROLOGY 2002;122:897-903
Pulmonary dysfunction in non-cirrhotic patients with chronic viral hepatitis
2002, European Journal of Internal MedicineBackground: Hepatopulmonary syndrome (HPS), defined as hypoxemia and functional intrapulmonary right-to-left shunts in the presence of chronic liver disease, is a frequent complication of end-stage liver disease. The aim of this study was to determine the extent of pulmonary dysfunction and the prevalence of HPS in non-cirrhotic patients with chronic viral hepatitis. Methods: Lung function tests were carried out in 178 patients with chronic viral hepatitis (mean age 43.2 years, 95 smokers). To demonstrate intrapulmonary shunting, contrast echocardiography was performed in all patients with hypoxemia (paO2<70 mmHg) or a reduced diffusion capacity (DLCO<70% predicted). Results: The median results of lung function parameters (FVC, FEV1, FEV1/FVC, TLC, DLCO, and blood gas analysis) were normal. Despite normal lung function, hypoxemia and/or DLCO reduction were observed in 17 of 178 patients (9.6%). A correlation with inflammatory activity, extent of fibrosis, or etiology was not found. Intrapulmonary shunting was observed in three of 17 patients. Two of these patients fulfilled the diagnostic criteria of HPS. Conclusions: Impaired gas exchange is a common finding even in non-cirrhotic patients with chronic viral hepatitis. HPS, however, was present in 1.1% of patients with chronic viral hepatitis and is thus not restricted to patients with liver cirrhosis, portal hypertension, or acute liver failure.