Dialysis therapy is associated with an increased incidence of lower-extremity wounds and amputations. We compared the incidence of foot ulcers and amputations before and after the start of dialysis.
We evaluated 150 consecutive diabetic patients receiving dialysis and compared the incidence of foot complications 30 months before and after initiation of hemodialysis. We used claims data for diabetes, ulceration, and dialysis and abstracted medical records to verify diagnoses and dates of ulcers and amputations. We compared initial and cumulative ulcer/amputation incidence to account for multiple events in the same person over time. We used the same formula to determine the incidence rate difference and 95% confidence intervals (CIs) to compare new ulcers and amputations during the study.
There was no significant difference in the incidence of first foot ulcers before (91.7 per 1,000 patient-years; 95% CI, 73.7–112.3 per 1,000 patient-years) and after (82.7; 95% CI, 65.7–102.3) the start of hemodialysis. The incidence of cumulative ulcers was significantly higher before (304.0 per 1,000 patient-years; 95% CI, 270.8–340.2) compared with after (210.7 per 1,000 patient-years; 95% CI, 183.0–240.9) dialysis. There was no difference in the incidence of first amputation before (29.3 per 1,000 patient-years; 95% CI, 1 9.4–41.7 per 1,000 patient-years) and after (37.3 per 1,000 patient-years; 95% CI, 19.4–41.7 per 1,000 patient-years) dialysis or in the cumulative incidence of amputations before (61.3 per 1,000 patient-years; 95% CI, 46.7–8.4 per 1,000 patient-years) and after (58.7 per 1,000 patient-years; 95% CI, 44.5–75.5 per 1,000 patient-years) dialysis.
There was no increase in the incidence of ulcers or amputations after beginning hemodialysis.
There is an increased prevalence of foot ulceration in patients with diabetes, leading to hospitalization. Early wound closure is necessary to prevent further infections and, ultimately, lower-limb amputations. There is no current evidence stating that an elevated preoperative hemoglobin A1c (HbA1c) level is a contraindication to skin grafting. The purpose of this review was to determine whether elevated HbA1c levels are a contraindication to the application of skin grafts in diabetic patients.
A retrospective review was performed of 53 consecutive patients who underwent split-thickness skin graft application to the lower extremity between January 1, 2012, and December 31, 2015. A uniform surgical technique was used across all of the patients. A comparison of HbA1c levels between failed and healed skin grafts was reviewed.
Of 43 surgical sites (41 patients) that met the inclusion criteria, 27 healed with greater than 90% graft take and 16 had a skin graft that failed. There was no statistically significant difference in HbA1c levels in the group that healed a skin graft compared with the group in which skin graft failed to adhere.
Preliminary data suggest that an elevated HbA1c level is not a contraindication to application of a skin graft. The benefits of early wound closure outweigh the risks of skin graft application in patients with diabetes.
Persons with diabetes have a higher incidence of fractures compared with persons without diabetes. However, there is little published information concerning the deleterious effect of late-stage diabetes on fracture healing. There are no studies using animal models that evaluate the effect of advanced diabetes on fracture healing. The purpose of our study was to evaluate cytokine expression, specifically macrophage inflammatory protein 1 (MIP-1) and vascular endothelial growth factor, in fracture healing in a type 2 diabetes rat model.
We evaluated biomarker expression after femur fracture using a rat model. The two groups consisted of 24 Zucker diabetic rats (study group) and 12 Zucker lean rats (control group). An independent reviewer was used to assess delayed union. We evaluated serum samples 2, 4, 7, and 14 days after surgery for MIP-1, vascular endothelial growth factor, leptin, and other cytokine levels.
At 3 weeks, Kaplan-Meier estimates showed that 45.8% of femur fractures in Zucker diabetic rats had healed, whereas 81.8% of those in Zucker lean rats had healed (P = .02). A logistic regression model to predict fast healing that included the three cytokines and diabetes status showed that the only factor achieving significance was MIP-1α. Vascular endothelial growth factor was the only biomarker to show significance compared with delayed healing.
These results confirm significant differences in biomarker expression between diabetic and nondiabetic rats during bone healing. The key factors for bone healing may appear early in the healing process, whereas differences in diabetes versus nondiabetes are seen later in the healing process. Increased levels of MIP-1α were associated with the likelihood of delayed healing.
We aimed to evaluate surrogate markers commonly used in the literature for diabetic foot osteomyelitis remission after initial treatment for diabetic foot infections (DFIs).
Thirty-five patients with DFIs were prospectively enrolled and followed for 12 months. Osteomyelitis was determined from bone culture and histologic analysis initially and for recurrence. Fisher exact and χ2 tests were used for dichotomous variables and Student t and Mann-Whitney U tests for continuous variables (α = .05).
Twenty-four patients were diagnosed as having osteomyelitis and 11 as having soft-tissue infections. Four patients (16.7%) with osteomyelitis had reinfection based on bone biopsy. The success of osteomyelitis treatment varied based on the surrogate marker used to define remission: osteomyelitis infection (16.7%), failed wound healing (8.3%), reulceration (20.8%), readmission (16.7%), amputation (12.5%). There was no difference in outcomes among patients who were initially diagnosed as having osteomyelitis versus soft-tissue infections. There were no differences in osteomyelitis reinfection (16.7% versus 45.5%; P = .07), wounds that failed to heal (8.3% versus 9.1%; P = .94), reulceration (20.8% versus 27.3%; P = .67), readmission for DFIs at the same site (16.7% versus 36.4%; P = .20), amputation at the same site after discharge (12.5% versus 36.4%; P = .10). Osteomyelitis at the index site based on bone biopsy indicated that failed therapy was 16.7%. Indirect markers demonstrated a failure rate of 8.3% to 20.8%.
Most osteomyelitis markers were similar to markers in soft-tissue infection. Commonly reported surrogate markers were not shown to be specific to identify patients who failed osteomyelitis treatment compared with patients with soft-tissue infections. Given this, these surrogate markers are not reliable for use in practice to identify osteomyelitis treatment failure.
Diabetic foot ulcers (DFUs) are a major burden to patients and to the health-care systems of many countries. To prevent or treat ulcers more effectively, predictive biomarkers are needed. We examined temperature as a biomarker and as a causative factor in ulcer development.
Thirty-seven individuals with diabetes were enrolled in this observational case-control study: nine with diabetic neuropathy and ulcer history (DFU), 14 with diabetic neuropathy (DN), and 14 nonneuropathic control participants (DC). Resting barefoot plantar temperatures were recorded using an infrared thermal camera. Mean temperatures were determined in four anatomical regions—hallux and medial, central, and lateral forefoot—and separate linear models with specified contrasts among the DFU, DN, and DC groups were set to reveal mean differences for each foot region while controlling for group characteristics.
The mean temperature reading in each foot region was higher than 30.0°C in the DFU and DN groups and lower than 30.0°C in the DC group. Mean differences were greatest between the DFU and DC groups, ranging from 3.2°C in the medial forefoot to 4.9°C in the hallux.
Increased plantar temperatures in individuals with a history of ulcers may include acute temperature increases from plantar stresses, chronic inflammation from prolonged stresses, and impairment in temperature regulation from autonomic neuropathy. Diabetic foot temperatures, particularly in patients with previous ulcers, may easily reach hazard thresholds indicated by previous pressure ulcer studies. The results necessitate further exploration of temperature in the diabetic foot and how it may contribute to ulceration.