The only enzymatic debridement in China-collagenase ointment

Deep second-degree burn wound tissue necrosis reaches the dermis. The persistence of necrotic tissue hinders epithelial crawling, can also easily cause bacterial infection, aggravate inflammatory reaction, and hinder wound repair. Therefore, the first step in repairing burn wounds is to remove necrotic tissue. Complete debridement often results in loss of adjacent normal tissue, while incomplete debridement is the source of postoperative infection. Collagenase can not only act on denatured collagen, but also act on undenatured collagen fibers between necrotic tissue and normal tissue, thereby more thoroughly removing necrotic tissue. Research in recent years has found that in addition to having a good scab removal effect, it can also accelerate the response of repair cells to damage and promote wound healing.

20 male SD rats were randomly divided into 4 groups after numbering, with 5 rats in each group. Two deep second-degree burn wounds were made on the back of each rat, and one wound was randomly selected as the experimental group and the other wound as the control group. The experimental group used collagenase ointment to change the dressing, and the control group used Vaseline gauze to change the dressing, once for 1 day until the wound healed.

As a result, the wound healing time of the experimental group (20.75±1.71) days was significantly shorter than that of the control group (25.25±1.71) days. The healing rates on 7d, 10d, 14d, and 21d were (37.60±7.42)%, (54.52±7.20)%, (77.72±8.50)%, and (98.04±3.92)% respectively, which were all higher than those in the control group (19.06± 4.26)%, (35.96±5.88)%, (49.48±6.04)%, (81.80±6.04)% (t values are 8.200, 9.116, 10.102, 5.294 respectively, P values are all less than 0.05).

Conclusion: Collagenase ointment can significantly promote healing of deep II-degree wounds, and its mechanism is related to accelerating the separation of necrotic tissue, reducing local inflammatory reaction, and increasing the expression of EGF and bFCF.

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