Faculty Opinions recommendation of Continuing chronic beta-blockade in the acute phase of severe sepsis and septic shock is associated with decreased mortality rates up to 90 days.

Author(s):  
André Coetzee
2017 ◽  
Vol 119 (4) ◽  
pp. 616-625 ◽  
Author(s):  
C. Fuchs ◽  
S. Wauschkuhn ◽  
C. Scheer ◽  
M. Vollmer ◽  
K. Meissner ◽  
...  

2006 ◽  
Vol 17 (4) ◽  
pp. 423-432
Author(s):  
Jan Powers ◽  
Judith Jacobi

Severe sepsis is a complex syndrome often resulting in multiple organ dysfunction. This is an extremely challenging problem to manage in the intensive care unit, with mortality rates remaining at unacceptably high levels. Death of patients afflicted by this condition generally results from organ dysfunction syndromes related to hypoperfusion abnormalities. Management of patients with severe sepsis or septic shock can be very complex and challenging, utilizing a significant amount of resources. Pharmacologic support of patients with severe sepsis or septic shock primarily involves agents to support and improve perfusion at the microvascular level. It is important to understand the pharmacologic properties of the medications utilized to manage patients with these conditions. The information presented in this article is based on the best evidence currently available in order to assist the critical care nurse in understanding the pharmacologic therapy related to treatment of severe sepsis and septic shock.


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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