Pressure-Induced Ischemic Wound Healing
Tissue hypoxia in a pressure-induced ischemic wound has been shown to facilitate bacterial proliferation and tissue destruction. However, no adequate animal models of pressure-induced ischemic wounding have been developed, and the effects of bacteria on the healing process of such wounds have yet to be clarified. Therefore, this study aimed to develop a pressure-induced ischemic wound model and to clarify the effects of bacteria on wound healing. Two incisions that extended to the peritoneal cavity were created in the flank region of rats, and a metal plate was passed through 1 incision under the peritoneum and then exited from the other. From the exterior surface, 8 kg of pressure were applied for 6 hours to the flank skin and abdominal muscle to create an ischemic wound. The wound was observed for 2 weeks, and histological tissue sections were prepared on Days 1, 3, 7, and 14. Wound healing was compared between 2 groups: a bacterial-inoculation group (5.3 x 10/mL of Staphylococcus aureus was inoculated into the epidermis, subcutaneous tissue, and abdominal muscle before and after preparing the ischemic wound) and a control group (only pressure was applied to prepare an ischemic wound). In the bacterial-inoculation group, epidermal loss and dermal, subcutaneous, and muscular tissue necrosis were seen; further, an abscess covered by a U-shaped membrane was formed and persisted to Day 14, appearing to extrude from the wound. In the control group, ischemia caused partial loss of epidermis and partial necrosis of the subcutaneous tissue and abdominal muscle; however, by Day 14, the epidermis had regenerated, granulation tissue formed, and the structure and alignment of collagen fibers in the dermal layer were normal. These findings may suggest that when a pressure-induced ischemic wound is complicated by bacterial infection, the collagen fibers in the dermal layer, which resist ischemia, become necrotic from bacterial proliferation and neutrophilic infiltration, thus delaying wound healing.
With unrelieved pressure, tissue ischemia develops, and metabolic wastes accumulate in the interstitial tissue, resulting in anoxia and cellular death. This pressure-induced ischemia also leads to excessive tissue hypoxia, further promoting bacterial proliferation and tissue destruction. In clinical settings, some pressure-induced ischemic wounds are caused by support surfaces, and some lower-limb diabetic pressure ulcers are caused by footwear. Infection of these wounds considerably impairs the healing process. For example, with pressure ulcers, the prevalence of infection is 1.4 per 1,000 ulcer days or 27% of studied pressure ulcers. Moreover, the mortality rate for bacteremia due to pressure ulcer infection has been reported at 15.4%. In another study, 48% of patients with pressure ulcers died of sepsis. The results of the aforementioned studies suggest that if a bacterial infection develops in a pressure-induced ischemic wound, medical conditions can easily deteriorate and possibly become life threatening. Although the relationship between bacteria and acute wounds using animal models has been closely examined at the postoperative stage, no such animal model has been studied to examine the relationship between bacteria and pressure-induced ischemic wounds.
The purpose of this study was to develop an animal model of pressure-induced ischemic wounds and to clarify the effects of bacteria on the healing process of such wounds.
Tissue hypoxia in a pressure-induced ischemic wound has been shown to facilitate bacterial proliferation and tissue destruction. However, no adequate animal models of pressure-induced ischemic wounding have been developed, and the effects of bacteria on the healing process of such wounds have yet to be clarified. Therefore, this study aimed to develop a pressure-induced ischemic wound model and to clarify the effects of bacteria on wound healing. Two incisions that extended to the peritoneal cavity were created in the flank region of rats, and a metal plate was passed through 1 incision under the peritoneum and then exited from the other. From the exterior surface, 8 kg of pressure were applied for 6 hours to the flank skin and abdominal muscle to create an ischemic wound. The wound was observed for 2 weeks, and histological tissue sections were prepared on Days 1, 3, 7, and 14. Wound healing was compared between 2 groups: a bacterial-inoculation group (5.3 x 10/mL of Staphylococcus aureus was inoculated into the epidermis, subcutaneous tissue, and abdominal muscle before and after preparing the ischemic wound) and a control group (only pressure was applied to prepare an ischemic wound). In the bacterial-inoculation group, epidermal loss and dermal, subcutaneous, and muscular tissue necrosis were seen; further, an abscess covered by a U-shaped membrane was formed and persisted to Day 14, appearing to extrude from the wound. In the control group, ischemia caused partial loss of epidermis and partial necrosis of the subcutaneous tissue and abdominal muscle; however, by Day 14, the epidermis had regenerated, granulation tissue formed, and the structure and alignment of collagen fibers in the dermal layer were normal. These findings may suggest that when a pressure-induced ischemic wound is complicated by bacterial infection, the collagen fibers in the dermal layer, which resist ischemia, become necrotic from bacterial proliferation and neutrophilic infiltration, thus delaying wound healing.
With unrelieved pressure, tissue ischemia develops, and metabolic wastes accumulate in the interstitial tissue, resulting in anoxia and cellular death. This pressure-induced ischemia also leads to excessive tissue hypoxia, further promoting bacterial proliferation and tissue destruction. In clinical settings, some pressure-induced ischemic wounds are caused by support surfaces, and some lower-limb diabetic pressure ulcers are caused by footwear. Infection of these wounds considerably impairs the healing process. For example, with pressure ulcers, the prevalence of infection is 1.4 per 1,000 ulcer days or 27% of studied pressure ulcers. Moreover, the mortality rate for bacteremia due to pressure ulcer infection has been reported at 15.4%. In another study, 48% of patients with pressure ulcers died of sepsis. The results of the aforementioned studies suggest that if a bacterial infection develops in a pressure-induced ischemic wound, medical conditions can easily deteriorate and possibly become life threatening. Although the relationship between bacteria and acute wounds using animal models has been closely examined at the postoperative stage, no such animal model has been studied to examine the relationship between bacteria and pressure-induced ischemic wounds.
The purpose of this study was to develop an animal model of pressure-induced ischemic wounds and to clarify the effects of bacteria on the healing process of such wounds.