FLUID RESUSCITATION INCREASES INFLAMMATORY RESPONSE TO TRAUMATIC INJURY

Intra-abdominal hypertension occurs in 50% of all patients admitted to the intensive care unit and is associated with significant morbidity and mortality. Intra-abdominal hypertension is defined as a sustained, pathologic rise in intra-abdominal pressure to 12 mm Hg or more. Patients with intra-abdominal hypertension may progress to abdominal compartment syndrome. Early identification and treatment of this condition will improve patient outcome. Patients at risk for intra-abdominal hypertension include those with major traumatic injury, major surgery, sepsis, burns, pancreatitis, ileus, and massive fluid resuscitation. Predisposing factors include decreased abdominal wall compliance, increased intraluminal contents, increased peritoneal cavity contents, and capillary leak/fluid resuscitation.

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A Levee to the Flood: Pre-injury Neuroinflammation and Immune Stress Influence Traumatic Brain Injury Outcome

Frontiers in Aging Neuroscience ◽

10.3389/fnagi.2021.788055 ◽

2022 ◽

Vol 13 ◽

Author(s):

Samuel Houle ◽

Olga N. Kokiko-Cochran

Keyword(s):

Risk Factors ◽

Traumatic Brain Injury ◽

Brain Injury ◽

Inflammatory Response ◽

Genetic Risk ◽

Traumatic Injury ◽

Genetic Risk Factors ◽

Post Injury ◽

Immune Stress ◽

Age Related

Increasing evidence demonstrates that aging influences the brain's response to traumatic brain injury (TBI), setting the stage for neurodegenerative pathology like Alzheimer's disease (AD). This topic is often dominated by discussions of post-injury aging and inflammation, which can diminish the consideration of those same factors before TBI. In fact, pre-TBI aging and inflammation may be just as critical in mediating outcomes. For example, elderly individuals suffer from the highest rates of TBI of all severities. Additionally, pre-injury immune challenges or stressors may alter pathology and outcome independent of age. The inflammatory response to TBI is malleable and influenced by previous, coincident, and subsequent immune insults. Therefore, pre-existing conditions that elicit or include an inflammatory response could substantially influence the brain's ability to respond to traumatic injury and ultimately affect chronic outcome. The purpose of this review is to detail how age-related cellular and molecular changes, as well as genetic risk variants for AD affect the neuroinflammatory response to TBI. First, we will review the sources and pathology of neuroinflammation following TBI. Then, we will highlight the significance of age-related, endogenous sources of inflammation, including changes in cytokine expression, reactive oxygen species processing, and mitochondrial function. Heightened focus is placed on the mitochondria as an integral link between inflammation and various genetic risk factors for AD. Together, this review will compile current clinical and experimental research to highlight how pre-existing inflammatory changes associated with infection and stress, aging, and genetic risk factors can alter response to TBI.

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Systemic Inflammatory Response during Cardiac Surgery: A Pilot Study

Innovations Technology and Techniques in Cardiothoracic and Vascular Surgery ◽

10.1097/imi.0000000000000123 ◽

2015 ◽

Vol 10 (2) ◽

pp. 125-132 ◽

Cited By ~ 3

Author(s):

David C. Fitzgerald ◽

Sari D. Holmes ◽

John R. St. Onge ◽

Chidima Ioanou ◽

Lisa M. Martin ◽

...

Keyword(s):

Cardiac Surgery ◽

Treatment Group ◽

Inflammatory Response ◽

Osmotic Pressure ◽

Fluid Resuscitation ◽

Fluid Therapy ◽

Fluid Management ◽

Colloid Osmotic Pressure ◽

C Reactive Protein ◽

Reactive Protein

Objective There is a growing body of evidence indicating that perioperative fluid management during cardiac surgery influences patient care and outcome. The choice of fluid therapy and the degree of systemic inflammatory response triggered during surgery control the effects of tissue edema formation and end-organ function. As such, “goal-directed” fluid resuscitation protocols that measure colloid osmotic pressure (COP) may promote improvements in patient morbidity and mortality. Methods Thirty patients scheduled for primary coronary artery bypass grafting were prospectively randomized for perioperative fluid treatment under COP guidance [albumin (ALB), n = 17] or conventional fluid protocols without COP support (control, n = 13). Whole-blood samples were drawn at four different time intervals including (A) anesthesia induction, (B) 10 minutes after the initiation of cardiopulmonary bypass, (C) at the completion of sternal skin approximation, and (D) 3 hours after admission to the cardiac intensive care unit. Interleukin 6 (IL-6) and IL-8 were measured by immunometric, enzyme-linked immunosorbent assays as well as C-reactive protein. Colloid osmotic pressure values were measured using a colloid osmometer. Results As compared with conventional fluid protocols, the patients treated in the intervention (ALB) group received significantly less total perioperative fluid [7893.6 (1874.5) vs 10,754.8 (2403.9), P = 0.001], and this relationship remained after controlling for age, sex, and The Society of Thoracic Surgeons risk score (β = −0.5, t = −3.1, P = 0.005). Colloid osmotic pressure values were significantly higher in the ALB group at time point D after surgery (P= 0.03). There were no significant differences in IL-6, IL-8, and C-reactive protein values between the groups at any of the time blood draw intervals. Perioperative outcomes were evaluated by treatment group. For both groups, the incidence of perioperative morbidity was low and did not differ by treatment group. Conclusions The use of COP-guided fluid resuscitation was associated with a significant reduction in perioperative fluid demand. However, patients prescribed to COP-guided fluid therapy did not experience a reduction in whole-body inflammation or improved surgical outcome as compared with conventional fluid management techniques.

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Differential Impact of Alcohol Abuse Patterns on Host Inflammatory Response Following Traumatic Injury

Journal of Emergency Medicine ◽

10.1016/j.jemermed.2012.09.121 ◽

2012 ◽

Vol 43 (5) ◽

pp. 940

Author(s):

L. Moreno-Walton ◽

J. Sulzer ◽

J. Engle ◽

L. Stuke ◽

P. Molina

Keyword(s):

Alcohol Abuse ◽

Inflammatory Response ◽

Traumatic Injury ◽

Differential Impact ◽

Host Inflammatory Response

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Inflammatory Response to Traumatic Injury: Clinical and Animal Researches in Inflammation

Mediators of Inflammation ◽

10.1155/2015/729637 ◽

2015 ◽

Vol 2015 ◽

pp. 1-2 ◽

Cited By ~ 1

Author(s):

Huang-Ping Yu ◽

Irshad H. Chaudry ◽

Mashkoor A. Choudhry ◽

Chung-Hsi Hsing ◽

Fu-Chao Liu ◽

...

Keyword(s):

Inflammatory Response ◽

Traumatic Injury

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Protective effect of geraniol inhibits inflammatory response, oxidative stress and apoptosis in traumatic injury of the spinal cord through modulation of NF-κB and p38 MAPK

Experimental and Therapeutic Medicine ◽

10.3892/etm.2016.3850 ◽

2016 ◽

Vol 12 (6) ◽

pp. 3607-3613 ◽

Cited By ~ 23

Author(s):

Jiansheng Wang ◽

Baishan Su ◽

Hongbin Zhu ◽

Chao Chen ◽

Gang Zhao

Keyword(s):

Oxidative Stress ◽

Spinal Cord ◽

Inflammatory Response ◽

Protective Effect ◽

P38 Mapk ◽

Traumatic Injury

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Developing a Minimally Invasive Cell-Based Model to Predict Response to Major Trauma

Proceedings of IMPRS ◽

10.18060/24607 ◽

2020 ◽

Vol 3 ◽

Author(s):

Kayla Gates ◽

Rebecca Nunge ◽

Jamila Adom ◽

Mark Kaplan ◽

Todd McKinley

Keyword(s):

Cell Death ◽

Inflammatory Response ◽

Traumatic Injury ◽

Control Group ◽

Immunologic Response ◽

Post Injury ◽

Predictive Tool ◽

Severity Of Injury ◽

Inflammatory Stimuli

Background. Physical trauma results in a systemic inflammatory response. Preliminary research in orthopedic trauma patients suggests that patients with similar demographics and severity of injury vary in their response to traumatic injury. Analysis of the immunological response post-injury showed a sustained pro-inflammatory response with delayed reparative cytokine expression in trauma sensitive patients, while the trauma tolerant patients had an early inflammatory expression with resolution by 72 hours post-injury. Thus, we hypothesize that differential response to non-traumatic injury might serve as a predictive tool for the identification of trauma tolerant and sensitive patients prior to injury. The goal of this research is to test whether immunological changes to inflammatory stimuli can predict tolerance or sensitivity to trauma using an-vitro cell-based assay. Methods. Splenocytes were isolated from naive C57BL/6 mice and subjected to biological trauma in vitro using LPS (100 ng/mL) or hypoxic trauma using hydrogen peroxide (50 µM, 100 µM, and 200 µM) with or without proinflammatory cytokines, IL-1β (1 ng/mL) , IL-6 (200 ng/mL), and IL-33 (150 ng/mL). Inflammation and hypoxia were assessed using IL-6 and HIF-1ɑ expression respectively via qPCR 24 hours post-treatment. Cell death and pro-inflammatory cytokine production using multiplex analysis were used to measure outcomes. Results. Both types of treatments showed increased cell death compared to the control group. qPCR data is pending. Conclusion. With these studies as a core of the experimental approach, this in vitro cell-based assay will be used to assess immunologic response to inflammatory stimuli across the genetic variation of mouse strains. Findings from this project could enable the development of a clinical test that accurately predicts immunologic response to trauma and related-complications based on patients’ sensitivity to pre-traumatic injury.

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