Diabetic foot is a common cause of acute purulent infection, chronic ulceration and blackened necrosis of the toes in the foot and shoe area, and is difficult to heal, mainly caused by bacterial infection and atherosclerotic occlusion. Diabetic patients with low immunity develop rapidly when the foot and boot area is infected, and there is peripheral neuropathy in diabetic patients, and the pain is mild when infected, and often the infection is very serious when admitted to hospital, which often leads to high level amputation if not treated correctly in time.
Diabetic foot should first be treated with active glycemic control and peripheral neuropathy. We believe that for infected ulcers without arterial ischemia, it is crucial to control the infection, and the most important measure to control the infection is to remove the infection focus. For toes that are severely infected with necrosis or have combined osteomyelitis with no possibility of cure, they should be amputated as early as possible, otherwise the infection will be difficult to control and will spread to the proximal end and spread to the surrounding relatively normal toes, and after clearing and amputating the toes, the wounds that can be closed with direct sutures should be closed as much as possible The majority of the wounds can be healed in one phase, which can significantly shorten the healing time, reduce the patient’s pain and treatment cost. For wounds that cannot be closed in one phase, we adopt local antimicrobial dressing exchange, which can rapidly control the infection of the wounds, with less exudation and the growth of fresh granulation tissue. For smaller wounds, no special treatment is needed. The new epithelium growing on the edge of the fresh granulation wound will promote rapid wound healing. For larger wounds without skin defects, we adopt direct debridement and suturing, which can significantly shorten the wound healing time. For larger wounds with tissue defects, we use punctate implants, which are less invasive and have a higher survival rate.
At present, the patients with infected diabetic foot ulcers admitted by me have adopted the above-mentioned trilogy of local treatment measures, i.e., removal of infected foci – local antimicrobial dressing change – debridement and suture or punctate skin implant, which have achieved remarkable efficacy and have completely eliminated the trauma within a short period of time with maximum preservation of the extremity. For diabetic foot ischemic ulcers caused by arteriosclerotic occlusion of the lower extremity, the most important thing is to open the main artery of the lower extremity. If the artery of the lower extremity is opened by interventional or surgical therapy and the blood supply to the ulcer wound is improved, the same trilogy therapy can be adopted to treat diabetic foot ischemic ulcers.
Patient 1 had a chronic diabetic foot ulcer secondary to severe infection, dorsal foot abscess formation, osteomyelitis of the middle toe, and exposed toe bone, and the lower leg was proposed for amputation outside the hospital.
After dorsal foot abscess incision and drainage, debridement and toe amputation, necrotic tissue was still visible on the wound surface.
Two weeks after the operation, the wound surface was neat and dry with fresh granulation after local antimicrobial dressing change.
Four weeks after surgery, the trauma surface was significantly smaller than before, and the trauma surface was neat and dry with fresh granulation and obvious growth of new epithelium at the edge.
At 6 weeks after surgery, the wound was significantly smaller than before and was about to heal completely.
At 7 weeks postoperatively, the ulcer was completely healed.
Patient 2 had a severely infected diabetic foot and a dorsalis pedis abscess after incision and drainage, and a lower leg amputation was proposed outside the hospital before surgery.
Two weeks after surgery, the wound was neat and smaller than before with significant granulation tissue growth after local antimicrobial dressing change.
At 4 weeks after surgery, the trauma was significantly smaller than before, with neat trauma, fresh granulation, and obvious growth of new epithelium at the edge.
At 6 weeks after surgery, the dorsal foot wound was completely healed.
Patient 3 had a chronic ulcer caused by diabetic foot and arteriosclerotic occlusion of the lower extremity, which had persisted for 3 months.
Ten days after admission, the ulcer wound was significantly reduced after active control of diabetes, anti-infection, vasodilatation and local antibacterial drug exchange.
Seventeen days after admission, the ulcer wound was completely healed.
Patient 4 An 82-year-old diabetic patient with a traumatic anterior knee hematoma and secondary infection with skin necrosis was admitted to the hospital after the outpatient physician removed the necrotic skin with a two-month history.
One week after admission, after aggressive control of diabetes mellitus, anti-infective therapy, hematoma removal and local antimicrobial dressing change, the wound was neat and fresh granulation with a large subcutaneous remnant cavity.
Two weeks after admission and one week after debridement and suturing, the trauma was completely healed.
Patient 5 Diabetic patient with complete infection and necrosis of the medial soft tissues of the left foot [toe], and radiographs showed [toe osteomyelitis with no possibility of healing.
One week after the debridement and toe amputation of the left foot, the incision healed well with no signs of infection.
Two weeks after the operation, the incision healed grade A.
Patient 6 had a chronic ulcer with severe infection caused by diabetic foot, with necrotic tissue and purulent exudate visible on the surface.
One week after admission, the necrotic tissue and purulent exudate on the trabecular surface had been significantly reduced by aggressive anti-infection, diabetes control and local antimicrobial dressing changes.
Two weeks after admission, the wound surface was neat and clean, with fresh granulation and new epithelium visible at the edges.
Three weeks after admission, the ulcer was significantly smaller than before, and fresh granulation tissue had filled the trabecular surface, and new epithelium was visible at the edges. Thereafter, the patient was discharged automatically and abandoned treatment at our hospital.