scholarly journals Cortisol Is an Associated-Risk Factor of Brain Dysfunction in Patients with Severe Sepsis and Septic Shock

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Duc Nam Nguyen ◽  
Luc Huyghens ◽  
Haibo Zhang ◽  
Johan Schiettecatte ◽  
Johan Smitz ◽  
...  
Keyword(s):  
Septic Shock ◽  
Risk Factor ◽  
Severe Sepsis ◽  
Serum Cortisol ◽  
Brain Dysfunction ◽  
Sedation Scale ◽  
Richmond Agitation Sedation Scale ◽  
Cortisol Levels ◽  
Sepsis And Septic Shock ◽  
Mortality Hazard Ratio

Objectives. To investigate cortisol levels in brain dysfunction in patients with severe sepsis and septic shock.Methods. In 128 septic and sedated patients, we studied brain dysfunction including delirium and coma by the evaluation of Richmond Agitation Sedation Scale (RASS), the Confusion Method Assessment in the ICU (CAM-ICU) after sedation withdrawal and the measurement of serum S100B biomarker of brain injury. Serum cortisol and S100B were measured within 12 hours after ICU admission and daily over the next four days.Results. Brain dysfunction was observed in 50% (64/128) before but in 84% (107/128) of patients after sedation withdrawal, and was more common in the patients older than 57 years (P= 0.009). Both cortisol (P= 0.007) and S100B levels (P= 0.028) were higher in patients with than patients without brain dysfunction. Cortisol levels were associated with ICU mortality (hazard ratio = 1.17,P= 0.024). Multivariate logistic regression showed that cortisol (odds ratio (OR): 2.34, 95% CI (2.01, 3.22),P= 0.02) and the combination effect of cortisol with age (OR: 1.004, 95% CI (1.002, 1.93),P= 0.038) but not S100B were associated with brain dysfunction.Conclusions. Cortisol was an associated-risk factor of brain dysfunction in patients with severe sepsis and septic shock.

scholarly journals Presence of Hypogammaglobulinemia – A Risk Factor of Mortality in Patients with Severe Sepsis, Septic Shock, and SIRS

2013 ◽  
Vol 114 (4) ◽  
pp. 246-257 ◽  
Author(s):  
Miroslav Průcha ◽  
R. Zazula ◽  
I. Herold ◽  
M. Dostál ◽  
T. Hyánek ◽  
...  
Keyword(s):  
Septic Shock ◽  
Risk Factor ◽  
Severe Sepsis ◽  
Retrospective Study ◽  
Independent Factor ◽  
High Incidence ◽  
Sepsis And Septic Shock ◽  
The Relationship

In this retrospective study we assessed the frequency of hypogammaglobulinemia in 708 patients with SIRS, severe sepsis and septic shock. We evaluated the relationship between hypogammaglobulinemia IgG, IgM and 28 day mortality. Total of 708 patients and 1,513 samples were analyzed. In the three subgroups we investigated, patients met the criteria of SIRS, severe sepsis and septic shock. IgG hypogammaglobulinemia was demonstrated in 114 patients with severe sepsis (25.2%), 11 septic shock patients (24.4%), and in 29 SIRS patients (13.9%). IgM hypogammaglobulinemia was documented in 55 patients with severe sepsis (12.2%), 6 septic shock patients (13.3%), and in 17 SIRS patients (8.1%). Mortality of patients with severe sepsis and normal IgG levels was significantly lower (111 patients; 32.8%) compared with those with IgG hypogammaglobulinemia (49 patients; 43.0%; p=0.001). Mortality of patients with septic shock and IgG hypogammaglobulinemia (n=5) was significantly higher compared with those with normal IgG levels (45.5% vs. 38.2%; p=0.001). Mortality of patients with severe sepsis and IgM hypogammaglobulinemia did not differ from that of patients with normal IgM levels (37.0 vs. 41.8%). Mortality of patients with septic shock and IgM hypogammaglobulinemia was significantly higher compared with those with normal IgM levels (50% vs. 38.5%; p=0.0001). This study documented relatively high incidence of hypogammaglobulinemia IgG and IgM in patients with severe sepsis, septic shock and SIRS respectively. The presence of IgG hypogammaglobulinemia in patients with severe sepsis is independent factor of mortality.

scholarly journals A multicentre case-control study of nonsteroidal anti-inflammatory drugs as a risk factor for severe sepsis and septic shock

Critical Care ◽  
2009 ◽  
Vol 13 (2) ◽  
pp. R43 ◽  
Author(s):  
Annick Legras ◽  
Bruno Giraudeau ◽  
Annie-Pierre Jonville-Bera ◽  
Christophe Camus ◽  
Bruno François ◽  
...  
Keyword(s):  
Septic Shock ◽  
Risk Factor ◽  
Severe Sepsis ◽  
Case Control Study ◽  
Case Control ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Sepsis And Septic Shock ◽  
Control Study

Effect of fluid bolus triggers and their combination on fluid responsiveness in optimization phase of severe sepsis and septic shock resuscitation

MedPharmRes ◽  
2018 ◽  
Vol 2 (3) ◽  
pp. 27-32
Author(s):  
Bien Le ◽  
Dai Huynh ◽  
Mai Tuan ◽  
Minh Phan ◽  
Thao Pham ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Septic Shock ◽  
Severe Sepsis ◽  
Fluid Responsiveness ◽  
Statistical Significance ◽  
Venous Pressure ◽  
Fluid Bolus ◽  
Low Blood Pressure ◽  
Low Central Venous Pressure ◽  
Sepsis And Septic Shock

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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