Mechanism of Edema and Congestion in Partial-Thickness Burns
Bradykinin is the primary mediator responsible for edema and congestion in partial-thickness burns, as it directly causes increased vascular permeability and vasodilation leading to fluid extravasation into tissues.
Pathophysiology of Burn-Induced Edema
The development of edema and congestion in partial-thickness burns involves a complex inflammatory cascade, but bradykinin plays the central role:
Bradykinin causes direct microvascular changes including increased vascular permeability and decreased blood flow in burn zones, which are independent of leukocyte-mediated injury 1
Bradykinin antagonist administration significantly reduces tissue edema in burn injuries, with experimental studies showing reduced wet/dry weight ratios in treated animals compared to controls (P < 0.05) 1
Bradykinin antagonist treatment improves blood flow in partial-thickness burns and zones of stasis compared to saline-treated controls, demonstrating its role in the microvascular dysfunction that characterizes burn edema 1
The Inflammatory Mediator Cascade
While bradykinin is the primary answer, burns trigger release of multiple vasoactive substances that work synergistically:
The "cytokine storm" in burn shock releases kinins (histamine, serotonin, and bradykinin) along with inflammatory mediators including thromboxanes, prostacyclins, prostaglandins, and leukotrienes 2
These mediators cause temporary endothelial failure, leading to massive fluid escape from the vascular space into tissues according to Landis-Starling law 2
The fluid shift can be massive, with severe burns requiring up to 25,000 ml of intravenous fluids in the first 48 hours, and tissue water accumulation reaching 300-400% of blood flow volume 2
Clinical Significance
The edema formation is most pronounced in the first 48 hours after burn injury, when bradykinin and other mediators are most active 2
Inadequate cooling immediately after injury may lead to progression of burn depth, suggesting that early intervention can modulate the inflammatory cascade 3
Answer: D. Bradykinin is the correct mechanism, as it is the key mediator directly responsible for the microvascular permeability changes and edema formation characteristic of partial-thickness burns.