Reperfusion injury after Vandenbos procedure in the primary care office

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Figure 1.
Appearance and course of resolution of reperfusion injury to the right great toe before and after the Vandenbos procedure:A) Before the procedure, B) postoperative day 2, C) postoperative day 4, D) postoperative day 19, E) postoperative day 28, and F) postoperative day 37.

Table 1.

Proposed theories for the pathophysiology of reperfusion injury

PROPOSED THEORY	DESCRIPTION
Oxidative stress^3,5,6	During ischemia, there is increased production of free radicals by local tissues and damaged mitochondria. On reperfusion, free radicals accumulate and destroy tissue because cellular antioxidants have been depleted
Intracellular calcium overload^3,5	ATP is depleted during ischemia. Consequently, function of membrane sodium-potassium ATPase pumps is compromised, leading to electrolyte disturbances and cell swelling. Intracellular hypercalcemia triggers pro-apoptotic signaling pathways that are further exacerbated when ATP supply is restored during reperfusion
Inflammation^3,7	Macrophages and damaged tissue secrete cytokines that promote neutrophilic recruitment. During reperfusion, this leads to accelerated neutrophilic extravasation of healthy tissue
Complement activation therapy^3–5	When ischemic tissue is reperfused, immunoglobulin M antibodies that were deposited onto ischemic tissues bind to complement proteins, upregulating local inflammation. Organ dysfunction and systemic inflammatory response syndrome have been reported in cases of major surgery or traumatic injury⁴