Curbing Inflammation in Burn Patients

Farina, Jayme Adriano; Rosique, Marina Mínguez; Rosique, Rodrigo G.

doi:10.1155/2013/715645

Cited by 94 publications

(69 citation statements)

References 85 publications

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“…Additionally, an increased susceptibility to infection due to altered immune status may lead to sepsis, further exacerbating systemic inflammation [16]. Sustained hypermetabolism and inflammation impair wound healing through delayed re-epithelialization [17, 18].…”

Section: Pathophysiology Of Burn Woundsmentioning

confidence: 99%

Burn wound healing and treatment: review and advancements

et al. 2015

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Burns are a prevalent and burdensome critical care problem. The priorities of specialized facilities focus on stabilizing the patient, preventing infection, and optimizing functional recovery. Research on burns has generated sustained interest over the past few decades, and several important advancements have resulted in more effective patient stabilization and decreased mortality, especially among young patients and those with burns of intermediate extent. However, for the intensivist, challenges often exist that complicate patient support and stabilization. Furthermore, burn wounds are complex and can present unique difficulties that require late intervention or life-long rehabilitation. In addition to improvements in patient stabilization and care, research in burn wound care has yielded advancements that will continue to improve functional recovery. This article reviews recent advancements in the care of burn patients with a focus on the pathophysiology and treatment of burn wounds.

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Section: Pathophysiology Of Burn Woundsmentioning

confidence: 99%

Burn wound healing and treatment: review and advancements

et al. 2015

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“…In addition to contributing to acute mortality, the development of SIRS post-burn injury has significant impacts on wound healing/repair and susceptibility to secondary infection, thereby affecting surgical outcome and long-term patient morbidity [2]. However, as with SIRS produced by infectious (sepsis) or other non-infectious/sterile causes (trauma, pancreatitis or extensive surgical insults), our mechanistic understanding of post-burn inflammation and its systemic propagation, and our ability to manipulate this response, are limited [3]. Clinical trials based on inhibiting soluble pro-inflammatory mediators in sepsis patients have failed, suggesting that although such soluble mediators function optimally in regulating local inflammatory responses, their long-range systemic activities may be fundamentally constrained by dilution, degradation and other neutralizing effects within the circulation [4, 5].…”

Section: Introductionmentioning

confidence: 99%

“…Burn injury is a unique form of trauma with very well defined etiology, onset of insults and early clinical course, producing acute sterile SIRS in virtually all patients with a moderate to severe degree of injury [1, 3, 16]. Therefore, it may represent an optimal study population to evaluate acute MV release and its relationship to the development of SIRS.…”

Section: Introductionmentioning

confidence: 99%

Circulating Microvesicles Are Elevated Acutely following Major Burns Injury and Associated with Clinical Severity

et al. 2016

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Microvesicles are cell-derived signaling particles emerging as important mediators and biomarkers of systemic inflammation, but their production in severe burn injury patients has not been described. In this pilot investigation, we measured circulating microvesicle levels following severe burns, with severe sepsis patients as a comparator group. We hypothesized that levels of circulating vascular cell-derived microvesicles are elevated acutely following burns injury, mirroring clinical severity due to the early onset and prevalence of systemic inflammatory response syndrome (SIRS) in these patients. Blood samples were obtained from patients with moderate to severe thermal injury burns, with severe sepsis, and from healthy volunteers. Circulating microvesicles derived from total leukocytes, granulocytes, monocytes, and endothelial cells were quantified in plasma by flow cytometry. All circulating microvesicle subpopulations were elevated in burns patients on day of admission (day 0) compared to healthy volunteers (leukocyte-microvesicles: 3.5-fold, p = 0.005; granulocyte-microvesicles: 12.8-fold, p<0.0001; monocyte-microvesicles: 20.4-fold, p<0.0001; endothelial- microvesicles: 9.6-fold, p = 0.01), but decreased significantly by day 2. Microvesicle levels were increased with severe sepsis, but less consistently between patients. Leukocyte- and granulocyte-derived microvesicles on day 0 correlated with clinical assessment scores and were higher in burns ICU non-survivors compared to survivors (leukocyte MVs 4.6 fold, p = 0.002; granulocyte MVs 4.8 fold, p = 0.003). Mortality prediction analysis of area under receiver operating characteristic curve was 0.92 (p = 0.01) for total leukocyte microvesicles and 0.85 (p = 0.04) for granulocyte microvesicles. These findings demonstrate, for the first time, acute increases in circulating microvesicles following burns injury in patients and point to their potential role in propagation of sterile SIRS-related pathophysiology.

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“…Moreover, in these children, chronic mental disability was correlated to the size of burn injury (Rosenberg et al, ). Systemic manifestations within the first hours after burns include capillary permeability of protein into the interstitial space, generalized edema, and a tendency of hypovolemic shock (Farina, Rosique, & Rosique, ).…”

Section: Systemic Inflammationmentioning

confidence: 99%

Animal models of neuroinflammation secondary to acute insults originated outside the brain

Hamasaki

Machado

Silva

2017

J of Neuroscience Research

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The term "neuroinflammation" has been widely used to describe a series of acute or chronic conditions that cause inflammation in the central nervous system (CNS). Neurological damage can be a consequence of direct local injury or, secondary, of systemic or even distant inflammatory processes. In this respect, animal models have been developed to better understand the pathophysiology and, possibly, to evaluate more effective methods of treatment for these disorders. Animal models that promote alterations in blood-brain barrier permeability-the activation of microglia or astrocytes, modifications in neuropeptide expression, oxidative stress, increased apoptosis, release of inflammatory mediators, leukocyte infiltration, and brain edema-are likely to involve neuroinflammation and therefore can serve as useful models for human inflammatory CNS injury. This review describes the major animal models of neuroinflammation triggered by systemic or distant inflammatory processes. We will focus on animal models of acute neurologic damage; experimental models that lead to chronic neuroinflammation will not be addressed here.

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Curbing Inflammation in Burn Patients

Cited by 94 publications

References 85 publications

Burn wound healing and treatment: review and advancements

Burn wound healing and treatment: review and advancements

Circulating Microvesicles Are Elevated Acutely following Major Burns Injury and Associated with Clinical Severity

Animal models of neuroinflammation secondary to acute insults originated outside the brain

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