Polymorphonuclear Cells Show Features of Dysfunctional Activation During Fatal Sepsis

Sepsis and septic shock remain leading causes of morbidity and mortality for patients in the intensive care unit. During the early phase, immune cells produce various cytokines leading to prompt activation of the immune system. Polymorphonuclear leukocytes (PMNs) respond to different signals producing inflammatory factors and executing their antimicrobial mechanisms, resulting in the engulfment and elimination of invading pathogens. However, excessive activation caused by various inflammatory signals produced during sepsis progression can lead to the alteration of PMN signaling and subsequent defects in their functionality. Here, we analyzed samples from 34 patients in septic shock, focusing on PMNs gene expression and proteome changes associated with septic shock. We revealed that, compared to those patients who survived longer than five days, PMNs from patients who had fulminant sepsis were characterized by a dysfunctional hyper-activation, show altered metabolism, and recent exit from the cell cycle and signs of cellular lifespan. We believe that this multi-omics approach, although limited, pinpoints the alterations in PMNs’ functionality, which may be rescued by targeted treatments.

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Fatal Sepsis and Septic Shock Secondary to Aeromonas hydrophila Pneumonia

Clinical Pulmonary Medicine ◽

10.1097/cpm.0000000000000315 ◽

2019 ◽

Vol 26 (4) ◽

pp. 114-117

Author(s):

Kanishan Chaithra ◽

Veena A. Shetty ◽

Rekha R. Rai ◽

Raghav R. Sharma ◽

Avinash K. Shetty

Keyword(s):

Septic Shock ◽

Aeromonas Hydrophila ◽

Sepsis And Septic Shock ◽

Fatal Sepsis

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

MedPharmRes ◽

10.32895/ump.mpr.2.3.27 ◽

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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