Effect of intravenous albumin on systemic and hepatic hemodynamics and vasoactive neurohormonal systems in patients with cirrhosis and spontaneous bacterial peritonitis
Introduction
Spontaneous bacterial peritonitis (SBP) in cirrhosis is frequently associated with an impairment in circulatory function and renal failure. Circulatory dysfunction is characterized by arterial hypotension and a marked activation of the renin–angiotensin and sympathetic nervous systems [1], [2], [3]. Renal failure has the characteristics of hepatorenal syndrome. In most patients, it follows a rapidly progressive course and, if not treated, is associated with a 100% hospital mortality rate. Other patients develop a steady type of renal failure. The hospital mortality rate in these patients is four-fold (30%) higher than that observed in patients with SBP not developing renal failure (7%). The most important predictor of renal failure and hospital mortality after SBP is the presence of renal impairment at infection diagnosis [1], [2].
The pathogenesis of circulatory dysfunction in SBP is not well established. It was initially suggested to be related to a cytokine-mediated accentuation of the arterial vasodilation already present in these patients [2]. However, a recent study suggests that the mechanism is far more complex [3]. Without any doubt, disturbances at the level of the peripheral arterial circulation play an important role, since patients developing circulatory dysfunction after SBP show normal or reduced systemic vascular resistance despite an intense stimulation of the endogenous vasoconstrictor systems. However, circulatory dysfunction in SBP is also associated with a significant fall in cardiac output, indicating the participation of the heart in the pathogenesis of this abnormality. Renal failure in SBP is secondary to this impairment in circulatory function.
Another important feature that is presently unclear is the mechanism by which the intravenous administration of albumin prevents circulatory dysfunction and renal failure in SBP. In patients treated with antibiotics alone the prevalence of circulatory dysfunction and renal failure is of approximately 35%. This is reduced to 10% in patients receiving albumin at infection diagnosis and during antibiotic therapy [4].
This article reports the results of a pilot study assessing systemic and hepatic hemodynamics and the activity of endogenous neurohormonal vasoactive systems prior to and following albumin administration in a consecutive series of patients with SBP. The aim of the study was to characterize the mechanism of the therapeutic effect of albumin administration in SBP.
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Patients
Twelve consecutive patients with cirrhosis and SBP (polymorphonuclear cell count in ascitic fluid ≥250 mm−3 in the absence of findings suggestive of secondary peritonitis) [5] treated with ceftriaxone (2 g i.v. immediately after diagnosis followed by 1 g i.v. every 24 h) were included in the study. Criteria for inclusion were: age between 18 and 80 years; no antibiotics (except for prophylactic oral norfloxacin), β-blockers or therapeutic paracentesis within one week before inclusion; no
Clinical, hemodynamic and laboratory data at infection diagnosis
SBP was community-acquired in 10 patients and culture-positive in 7 and was associated with an intense inflammatory response as indicated by the large number of patients with systemic inflammatory response syndrome (7), the high concentration of polymorphonuclear leucocytes in ascitic fluid (Table 1) and very high plasma and ascitic fluid levels of IL-6 (Table 2) in most cases.
Liver function was markedly deteriorated (Table 3). Five patients had renal impairment and four hepatic encephalopathy
Discussion
The results of this study are consistent with the concept that treatment with third generation cephalosporins and albumin prevents circulatory and renal dysfunction and reduces hospital mortality in patients with SBP [4]. Five of our patients had renal impairment at infection diagnosis and were, therefore, at high risk for developing progressive renal failure and death. However, all patients included in the study were discharged from hospital alive after resolution of the infection. Moreover,
Acknowledgements
This study was supported in part by grants from the Fondo de Investigación Sanitaria (FIS 00/0921), the Instituto de Salud Carlos III (BEFI 00/9380 and C03/2) and the Hospital Clı́nic. The authors are indebted to Ms M.A. Baringo and L. Rocabert for expert technical assistance in hemodynamic studies.
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