scholarly journals Alkaline phosphatase treatment improves renal function in patients with severe sepsis or septic shock

Critical Care ◽  
2007 ◽  
Vol 11 (Suppl 2) ◽  
pp. P14 ◽  
Author(s):  
S Heemskerk ◽  
R Masereeuw ◽  
O Moesker ◽  
M Bouw ◽  
J van der Hoeven ◽  
...  
2009 ◽  
Vol 37 (2) ◽  
pp. 417-e1 ◽  
Author(s):  
Suzanne Heemskerk ◽  
Rosalinde Masereeuw ◽  
Olof Moesker ◽  
Martijn P. W. J. M. Bouw ◽  
Johannes G. van der Hoeven ◽  
...  

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
C. Chelazzi ◽  
G. Villa ◽  
A. R. De Gaudio

The cardiorenal syndrome is a clinical and pathophysiological entity defined as the concomitant presence of renal and cardiovascular dysfunction. In patients with severe sepsis and septic shock, acute cardiovascular, and renal derangements are common, that is, the septic cardiorenal syndrome. The aim of this paper is to describe the pathophysiology and clinical features of septic cardiorenal syndrome in light of the actual clinical and experimental evidence. In particular, the importance of systemic and intrarenal endothelial dysfunction, alterations of kidney perfusion, and myocardial function, organ “crosstalk” and ubiquitous inflammatory injury have been extensively reviewed in light of their role in cardiorenal syndrome etiology. Treatment includes early and targeted optimization of hemodynamics to reverse systemic hypotension and restore urinary output. In case of persistent renal impairment, renal replacement therapy may be used to remove cytokines and restore renal function.


2006 ◽  
Vol 34 ◽  
pp. A18 ◽  
Author(s):  
Saman Hayatdavoudi ◽  
Daniel Ikeda ◽  
Adam Seiver ◽  
John Winchell ◽  
Alexandra Rojas ◽  
...  

2015 ◽  
Vol 61 (01+02/2015) ◽  
Author(s):  
Michael Drey ◽  
Michael Behnes ◽  
Robert Kob ◽  
Dominic Lepiorz ◽  
Stefan Hettwer ◽  
...  

MedPharmRes ◽  
2018 ◽  
Vol 2 (3) ◽  
pp. 27-32
Author(s):  
Bien Le ◽  
Dai Huynh ◽  
Mai Tuan ◽  
Minh Phan ◽  
Thao Pham ◽  
...  

Objectives: to evaluate the fluid responsiveness according to fluid bolus triggers and their combination in severe sepsis and septic shock. Design: observational study. Patients and Methods: patients with severe sepsis and septic shock who already received fluid after rescue phase of resuscitation. Fluid bolus (FB) was prescribed upon perceived hypovolemic manifestations: low central venous pressure (CVP), low blood pressure, tachycardia, low urine output (UOP), hyperlactatemia. FB was performed by Ringer lactate 500 ml/30 min and responsiveness was defined by increasing in stroke volume (SV) ≥15%. Results: 84 patients were enrolled, among them 30 responded to FB (35.7%). Demographic and hemodynamic profile before fluid bolus were similar between responders and non-responders, except CVP was lower in responders (7.3 ± 3.4 mmHg vs 9.2 ± 3.6 mmHg) (p 0.018). Fluid response in low CVP, low blood pressure, tachycardia, low UOP, hyperlactatemia were 48.6%, 47.4%, 38.5%, 37.0%, 36.8% making the odd ratio (OR) of these triggers were 2.81 (1.09-7.27), 1.60 (0.54-4.78), 1.89 (0.58-6.18), 1.15 (0.41-3.27) and 1.27 (0.46-3.53) respectively. Although CVP < 8 mmHg had a higher response rate, the association was not consistent at lower cut-offs. The combination of these triggers appeared to raise fluid response but did not reach statistical significance: 26.7% (1 trigger), 31.0% (2 triggers), 35.7% (3 triggers), 55.6% (4 triggers), 100% (5 triggers). Conclusions: fluid responsiveness was low in optimization phase of resuscitation. No fluid bolus trigger was superior to the others in term of providing a higher responsiveness, their combination did not improve fluid responsiveness as well.


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