Abstract:
:Severe burn injury remains a major burden on patients and healthcare systems. Following severe burns, the injured tissues mount a local inflammatory response aiming to restore homeostasis. With excessive burn load, the immune response becomes disproportionate and patients may develop an overshooting systemic inflammatory response, compromising multiple physiological barriers in the lung, kidney, liver, and brain. If the blood-brain barrier is breached, systemic inflammatory molecules and phagocytes readily enter the brain and activate sessile cells of the central nervous system. Copious amounts of reactive oxygen species, reactive nitrogen species, proteases, cytokines/chemokines, and complement proteins are being released by these inflammatory cells, resulting in additional neuronal damage and life-threatening cerebral edema. Despite the correlation between cerebral complications in severe burn victims with mortality, burn-induced neuroinflammation continues to fly under the radar as an underestimated entity in the critically ill burn patient. In this paper, we illustrate the molecular events leading to blood-brain barrier breakdown, with a focus on the subsequent neuroinflammatory changes leading to cerebral edema in patients with severe burns.
journal_name
Crit Carejournal_title
Critical care (London, England)authors
Flierl MA,Stahel PF,Touban BM,Beauchamp KM,Morgan SJ,Smith WR,Ipaktchi KRdoi
10.1186/cc7794subject
Has Abstractpub_date
2009-01-01 00:00:00pages
215issue
3eissn
1364-8535issn
1466-609Xpii
cc7794journal_volume
13pub_type
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