Background: Ultraviolet (UV)-A therapy is a simple, inexpensive, and effective modality for wound healing, with tremendous potential to improve healing and reduce clinical infections in a number of clinical settings. To date, application of UV-A relies on bulky and hard-to-dose lamps that provide inconsistent therapy, thus making it difficult to apply therapy that is appropriate for the patient.
Methods: This study was designed to test the effectiveness of a novel wound therapy device that combines UV-A with traditional negative-pressure wound therapy (NPWT) to promote wound healing. Furthermore, we tested the ability of fiberoptic UV-A delivery to inhibit bacterial proliferation. Finally, we assayed the level of DNA damage that results from UV-A as compared to established UV-C therapies. Wound healing studies were performed in a porcine model using an articulated therapy arm that allows for continued therapy administration over an extended time course. Negative-pressure wound therapy was administered alone or with UV-A fiberoptic therapy for 2 weeks. Dressings were changed twice a week, at which time wound area was assessed.
Results: Data demonstrate that UV-A with NPWT treatment of wounds results in greater healing than NPWT alone. Using the same therapy device, we demonstrate that exposure of Staphylococcus aureus and Pseudomonas aeruginosa to fiberoptic UV-A results in decreased colony area and number of both bacterial strains. Finally, we show that UV-A induces minimal DNA damage in human fibroblasts and no more DNA damage in wound tissue as compare to intact skin.
Conclusions: These data demonstrate that UV-A can decrease bacterial proliferation and promote wound healing when coupled with NPWT.
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.
Background: The aim of this study was to evaluate the incidence and recovery of acute kidney injury (AKI) in patients admitted to the hospital with and without diabetes mellitus (DM) with foot infections.
Methods: We retrospectively reviewed 294 patients with DM and 88 without DM admitted to the hospital with foot infections. The Kidney Disease: Improving Global Outcomes guidelines were used to define AKI. Recovery was divided into three categories: full, partial, and no recovery within 90 days of the index AKI.
Results: The AKI incidence was 3.0 times higher in patients with DM (DM 48.5% versus no DM 23.9%; 95% confidence interval [CI], 1.74–5.19; P < .01). Acute kidney injury incidence was similar at each stage in people with and without DM (stage 1, DM 58.1% versus no DM 47.6%; stage 2, DM 23.3% versus no DM 33.3%, and stage 3, DM 18.6% versus no DM 19.1%). Twenty-nine patients with diabetes had a second AKI event and four had a third event. In patients without DM, one patient had a second AKI. Cumulative AKI incidence was 4.7 times higher in people with DM (DM 60.9% versus no DM 25.0%; 95% CI, 2.72–8.03; P < .01). Patients with diabetes progressed to chronic kidney disease or in chronic kidney disease stage 39.4% of the time. Patients without diabetes progressed 16.7% of the time, but this trend was not significant (P = .07). Complete recovery was 3.8 times more likely in patients without diabetes (95% CI, 1.26–11.16; P = .02).
Conclusions: Acute kidney injury incidence is higher in patients with diabetes, and complete recovery after an AKI is less likely compared to patients without diabetes.
Objective: To investigate the predictive value of erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) in persons with and without diabetes with osteomyelitis (OM).
Methods: We evaluated 455 patients in a retrospective cohort study of patients admitted to the hospital with diabetic foot OM (n = 177), diabetic foot soft-tissue infections (STIs) (n = 176), nondiabetic OM (n = 51), and nondiabetic STIs (n = 51). Infection diagnosis was determined through bone culture, histopathologic examination for OM, and/or imaging (magnetic resonance imaging/single-photon emission computed tomography) for STI. The optimal cutoff values of ESR and CRP in predicting OM were determined by receiver operating characteristic curve analysis. Sensitivity, specificity, positive and negative predictive values, and positive and negative likelihood ratios were determined through contingency tables.
Results: In persons without diabetes with STI or OM, the mean ESR and CRP differences were 10.0 mm/h and 2.6 mg/dL, respectively. In contrast, persons with diabetes had higher levels of each: 24.8 mm/h and 6.8 mg/dL, respectively. As a result, ESR and CRP predicted OM better in patients with diabetes. However, when patients were stratified by neuropathy status, ESR remained predictive of OM in diabetic patients with neuropathy (75% sensitivity, 58% specificity) but not in diabetic patients without neuropathy (50% sensitivity, 44% specificity). Also, CRP remained predictive irrespective of neuropathy status. A similar trend was observed in patients without diabetes.
Conclusions: Previous studies have reported that ESR and CRP are predictive of OM. However, this study suggests that neuropathy influences the predictive value of inflammatory biomarkers. The underlying mechanisms require further study.