Pathophysiology of burns

Keck, Maike; Herndon, David; Kamolz, Lars‐Peter; Frey, Manfred; Jeschke, Marc G.

doi:10.1007/s10354-009-0651-2

Cited by 112 publications

(130 citation statements)

References 69 publications

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“…Burn injuries often cause extravasation of interstitial fluids into burn wounds and surrounding tissues. 20 By nature of the collagen damage, these injuries often exhibit abnormal osmotic and hydrostatic pressure gradients that worsen with burn depth and normal inflammatory response. 4 As suggested by Stamatas et al in their hyperspectral imaging study of controlled skin inflammation, the interstitial fluid accumulation can eventually exert enough pressure upon both blood and lymphatic vessels leading to further proliferation of ischemia and edema buildup.…”

Section: Water Concentrationmentioning

confidence: 99%

Spatial frequency domain imaging of burn wounds in a preclinical model of graded burn severity

et al. 2013

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Abstract. Frequent monitoring of early-stage burns is necessary for deciding optimal treatment and management. Both superficial and full thickness burns are relatively easy to diagnose based on clinical observation. In between these two extremes are superficial-partial thickness and deep-partial thickness burns. These burns, while visually similar, differ dramatically in terms of clinical treatment and are known to progress in severity over time. The objective of this study was to determine the potential of spatial frequency domain imaging (SFDI) for noninvasively mapping quantitative changes in chromophore and optical properties that may be an indicative of burn wound severity. A controlled protocol of graded burn severity was developed and applied to 17 rats. SFDI data was acquired at multiple near-infrared wavelengths over a course of 3 h. Burn severity was verified using hematoxylin and eosin histology. From this study, we found that changes in water concentration (edema), deoxygenated hemoglobin concentration, and optical scattering (tissue denaturation) to be statistically significant at differentiating superficial partial-thickness burns from deep-partial thickness burns.

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Section: Water Concentrationmentioning

confidence: 99%

Spatial frequency domain imaging of burn wounds in a preclinical model of graded burn severity

et al. 2013

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“…sepsis, urinary tract, pneumonia, and abscess) [123,144] Trauma [50,83], surgery [12,76] Burns [71] Neoplasm (primary, metastasis and paraneoplastic syndrome) [80] Cardiac Myocardial infarction [90], cardiac surgery [6] Haematological Leukaemia, stem cell transplant [129] Renal Renal failure [128] Hepatic Hepatitis, cirrhosis, hepatic failure [121] Orthopaedic Fractures [140] Acta Neuropathol changes in BBB. Increased BBB permeability and altered expression of tight-junctional proteins were reported in three different inflammatory models (Table 3).…”

Section: Disruption Of Blood-brain Barriermentioning

confidence: 99%

The neuroinflammatory hypothesis of delirium

et al. 2010

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Delirium is a neuropsychiatric syndrome characterized by a sudden and global impairment in consciousness, attention and cognition. It is particularly frequent in elderly subjects with medical or surgical conditions and is associated with short-and long-term adverse outcomes. The pathophysiology of delirium remains poorly understood as it involves complex multi-factorial dynamic interactions between a diversity of risk factors. Several conditions associated with delirium are characterized by activation of the inflammatory cascade with acute release of inflammatory mediators into the bloodstream. There is compelling evidence that acute peripheral inflammatory stimulation induces activation of brain parenchymal cells, expression of proinflammatory cytokines and inflammatory mediators in the central nervous system. These neuroinflammatory changes induce neuronal and synaptic dysfunction and subsequent neurobehavioural and cognitive symptoms. Furthermore, ageing and neurodegenerative disorders exaggerate microglial responses following stimulation by systemic immune stimuli such as peripheral inflammation and/or infection. In this review we explore the neuroinflammatory hypothesis of delirium based on recent evidence derived from animal and human studies.

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“…Animals in the sham-operated group received no fluid resuscitation. Six random rats were collected from each of the IF and DF groups at different time points (3,6,12,24,48,72, and 120 h) following scalding and immediately sacrificed to collect 0.4 g of left ventricle tissues, which were stored at -80 °C for further mRNA and protein purification, and 0.1 g of fresh left ventricle tissues for immunohistochemical staining.…”

Section: Animals and Treatmentmentioning

confidence: 99%

The expression profile of aquaporin 1 in rat myocardium after severe burns

Li¹,

Zha²,

Li³

et al. 2015

Turk J Med Sci

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Background/aim: To investigate the myocardial expression profile of aquaporin 1 (AQP1) in rats after severe burns.Materials and methods: Ninety healthy male adult Wistar rats were randomly assigned to the following treatments: sham operation (control group, n = 6), immediate fluid resuscitation treatment post scalding (IF group, n = 42), and delayed fluid resuscitation treatment after scalding (DF group, n = 42). At 3, 6, 12, 24, 48, 72, and 120 h after scalding, myocardial water contents were assayed and AQP1 expressions were detected by real-time polymerase chain reaction and western blot. The AQP levels in the myocardium at 12 h after scalding were assayed by gene microarrays.Results: Scald injuries resulted in significantly synchronized increases in the myocardial water contents and the myocardial mRNA and protein expression of AQP1, with a peak at 12 h after scalding. Rats receiving delayed fluid resuscitation treatment had more severe myocardial edema and significantly higher myocardial AQP1 expressions than the rats receiving immediate fluid resuscitation treatment. The mRNAs of 6 other AQPs (AQP2, 3, 4, 6, 7, and 12b) were found to be changed in the myocardium among rats with different treatments. Conclusion:AQP1 may play a functional role in the development of myocardial edema after scalding. Targeting AQP1 may provide opportunities for therapeutic intervention in myocardial edema following severe burns.

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Pathophysiology of burns

Cited by 112 publications

References 69 publications

Spatial frequency domain imaging of burn wounds in a preclinical model of graded burn severity

Spatial frequency domain imaging of burn wounds in a preclinical model of graded burn severity

The neuroinflammatory hypothesis of delirium

The expression profile of aquaporin 1 in rat myocardium after severe burns

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