The early association of water irrigation with negative pressure wound therapy does not more efficiently reduce the depth of the alkali infiltration progress into the burn

Abstract

Water irrigation is an efficacious decontaminating method for dermis exposures to corrosive agents and hence has been widely applied to treat especially alkali burns. Nevertheless, once alkali has infiltrated the deep subcutaneous tissue, washing the tissue surface with water irrigation does not attenuate the damage progress. Therefore, significant efforts have been devoted to promising strategies aimed at removing the deeply infiltrated lye. According to a recent report, the negative pressure wound therapy (NPWT) reduces the pH value of the exudate from alkali-provoked burns thus accelerating wound healing. However, it remains to be ascertained whether or not NPWT coupled with water irrigation, that is, iNPWT, more effectively hinders the alkali injury deepening. In this study, we compared the effectiveness of an early application of water irrigation with or without NPWT in preventing the progressive deepening of the alkali burn in an animal model. Our histological examination results showed no appreciable difference in tissue injury depth, dermal retention, inflammatory cell infiltration, re-epithelization, and cellular function between iNPWT and water irrigation alone treatments. Thus, our results prove that the more expensive NPWT coupled with water irrigation does not more effectively hinder the alkali's injury deepening. Hence, iNPWT use should be more cautious in clinical practice.

Keywords: NPWT; alkali burn; water irrigation; wound healing.

FIGURE 1

A, (A) Representative gross image of the rat alkali burn model at D0 and D3; and (B) HE stained sections of D3. B, (A) A schematic representation of iNPWT application. (B) The rat was applied with a KCI black sponge covered by 3 M film and attached to a negative pressure pump, generating a pressure between 100–120 mmHg. An injection hose was inserted into the surface of the skin to achieve a solution flow of 30 mL/min

FIGURE 2

A, Representative gross image of the differently treated burn wounds on day 1 and day 3. Scale bar, 1 cm. B, Quantification of the surface areas of the eschar formation at post‐burn day 1 and day 3. P > 0.05

FIGURE 3

A, Representative CK14 IHC staining microscopic image at post‐burn day 3. B, High‐power microscopic image of CK14 IHC staining and quantification of the epithelialization percentages of wounds at post‐burn day 3. P > 0.05

FIGURE 4

A, Post‐burn day 3 Masson staining of the wound tissue sections. The retained collagen was marked with arrows. Scale bar, 1 mm. B, The percentage of the collage retention area at day 3 after injury. P > 0.05

FIGURE 5

A, Post‐burn day 3 HE stains of the wound sections. B, The percentage of tissue loss at day 3 after injury. P > 0.05

FIGURE 6

Inflammatory cells in different layers of the burn wound skin. Scale bar, 50 μm. P > 0.05

FIGURE 7

LDH‐staining of dead/live rat skin cells at post‐burnt day 3. The blue‐purple precipitate/particle marks the LDH enzyme activity

FIGURE 8

TUNEL‐staining of apoptotic rat skin sections at post‐burnt day 3. Positive cells are marked with white arrows. Scale bar, 100 μm