Abstract
Aim of the study: Negative pressure wound therapy is thought to improve wound healing by altering capillary perfusion. However, despite many theories, the underlying mechanism of action remains controversial. Recent evidence suggests an increased tissue pressure and a temporary decreased microvascular blood flow as the main reasons for the good clinical results [1]. In an attempt to further ...
Abstract
Aim of the study: Negative pressure wound therapy is thought to improve wound healing by altering capillary perfusion. However, despite many theories, the underlying mechanism of action remains controversial. Recent evidence suggests an increased tissue pressure and a temporary decreased microvascular blood flow as the main reasons for the good clinical results [1]. In an attempt to further explain the mechanism of action, we investigated the pressure distribution on the foam interface, and the influence on perfusion in a pre-experimental design. Materials and methods: Pressure distribution was measured using a sensor based on a capacitive dielectric elastomer with flexible electrodes. In vitro flow measurements were done with vessel imitations in a block of 300 bloom ballistic gel to simulate soft tissue. Results: A peak pressure of up to 187 mmHg (255 g/cm2) within the foam interface, as well as decreased perfusion, were found using a standard negative pressure wound therapy setup. In conclusion, negative pressure wound therapy applies positive pressure to adjacent tissue and decreases local flow. The amount of suction applied is proportional to the pressure on the foam interface and reduction in flow. Conclusion: In line with previous studies investigating the underlying mechanism of action, these findings may contribute to possible alterations in the use of negative pressure wound therapy, e.g. lowering suction pressure in patients with diminished peripheral blood flow.
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