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Chronic and non-healing wounds are a global health issue with limited effective treatments. Wound care costs continue to rise, highlighting the need for new therapies. Medicinal plants, particularly African species, show promise for enhancing wound healing. This review analysed 93 studies and identified 37 relevant to wound healing, covering 39 plant species. Ten species were identified for their rich phytochemical content, specifically flavonoids, terpenoids, and alkaloids (plant-derived compounds). These compounds act synergistically, enhancing the wound healing process at each stage. Flavonoids reduce inflammation and support tissue turnover, while terpenoids enhance collagen production and wound closure. Alkaloids offer antimicrobial benefits and support wound contraction. Notable plants include Ageratum conyzoides and Aspilia africana (Asteraceae family); promoting haemostasis by lowering plasma fibrinogen and enhancing platelet-derived growth factors; Withania somnifera (Solanaceae); and Entada africana (Fabaceae), effectively regulating inflammation. In the proliferative phase, Ocimum gratissimum (Lamiaceae), Calendula officinalis (Asteraceae), and Centella asiatica (Apiaceae) although C. officinalis is native to Southern Europe, and C. asiatica an Asian-native; they are widely used in African traditional medicine and included here for their relevance in African wound healing practices; Justicia flava (Acanthaceae), Alternanthera sessilis (Amaranthaceae), and Acalypha indica (Euphorbiaceae); play key roles in enhancing collagen production, angiogenesis, and re-epithelialisation. This comprehensive analysis highlights the role of African medicinal plants in wound healing and their potential to improve wound care therapy.
Diabetes related foot ulcers (DFUs) are complex and costly to manage, with the prevalence of non-healing wounds steadily increasing across the globe. Non-healing wounds can occur when clinicians fail to undertake an appropriate assessment, fail to recognise the importance of systemic or local complications, or provide the optimal treatment. The aetiological causes behind non-healing wounds are multifactorial; however, the purpose of this article is to focus on the role of oxygen in non-healing wounds and to introduce readers to advances in the delivery of topical oxygen therapy (TOT) via a haemoglobin spray. Importantly, this article incorporates a clinical decision support tool (CDST) to help clinicians identify the most appropriate individuals for whom topical haemoglobin may be most beneficial and the most appropriate time for introducing the intervention to improve wound healing outcomes.
To investigate risk factors for re-infection and compare the outcomes in people with diabetic foot infections. A retrospective chart review was conducted, and 294 hospitalised patients with moderate to severe diabetic foot infections (DFIs) were analysed for this study. The diagnosis and classification of the severity of infection was based on the International Working Group on the Diabetic Foot (IWGDF) infection guidelines. Skin and soft tissue infections were diagnosed based on clinical observations as per IWGDF classification in addition to ruling out any suspected osteomyelitis (OM) through negative bone culture, MRI or WBC SPECT CT. OM was confirmed by bone culture or histopathology. Clinical outcomes were based on a 12-month follow-up period. All dichotomous outcomes were compared using χ 2 with an alpha of 0.05. The result of this study shows a 48% rate of re-infection in people admitted to our hospital with moderate and severe diabetic foot infections (DFI). Patients with osteomyelitis present during the index admission were 2.1 times more likely to experience a re-infection than patients with soft tissue infection (56.7% vs. 38.0% respectively). In the univariate analysis, risk factors for re-infection included osteomyelitis, non-healing wounds, prolonged wound healing, antidepressants and leukocytosis. In the regression analysis, the only risk factor for re-infection was wounds that were not healed >90 days (HR =2.0, CI: 1.5, 2.7, p = 0.001). Re-infection is very common in patients with moderate and severe diabetic foot infections. Risk factors include osteomyelitis, non-healing wound, prolonged wound healing, antidepressants and leukocytosis.
The objective of this paper was to investigate erythrocyte sedimentation rate (ESR) and c-reactive protein (CRP) in diagnosing pedal osteomyelitis (OM) in patients with and without diabetes, and with and without severe renal impairment (SRI). This was a retrospective cohort study of patients with moderate and severe foot infections. We evaluated three groups: Subjects without diabetes (NDM), subjects with diabetes and without severe renal insufficiency (DM-NSRI), and patients with diabetes and SRI (DM-SRI). SRI was defined as eGFR <30. We evaluated area under the curve (AUC), cutoff point, sensitivity and specificity to characterize the accuracy of ESR and CRP to diagnose OM. A total of 408 patients were included in the analysis. ROC analysis in the NDM group revealed the AUC for ESR was 0.62, with a cutoff value of 46 mm/h (sensitivity, 49.0%; specificity, 76.0%). DM-NSRI subjects showed the AUC for ESR was 0.70 with the cutoff value of 61 mm/h (sensitivity, 68.9%; specificity 61.8%). In DM-SRI, the AUC for ESR was 0.67, with a cutoff value of 119 mm/h (sensitivity, 46.4%; specificity, 82.40%). In the NDM group, the AUC for CRP was 0.55, with a cutoff value of 6.4 mg/dL (sensitivity, 31.3%; specificity, 84.0%). For DM-NSRI, the AUC for CRP was 0.70, with a cutoff value of 8 mg/dL (sensitivity, 49.2%; specificity, 80.6%). In DM-SRI, the AUC for CRP was 0.62, with a cutoff value of 7 mg/dL (sensitivity, 57.1%; specificity, 67.7%). While CRP demonstrated relatively consistent utility, ESR's diagnostic cutoff points diverged significantly. These results highlight the necessity of considering patient-specific factors when interpreting ESR results in the context of OM diagnosis.
There is an increasing use of non-medicated wound dressing with claims of irreversible bacterial binding. Most of the data are from in vitro models which lack clinical relevance. This study employed a range of in vitro experiments to address this gap and we complemented our experimental designs with in vivo observations using dressings obtained from patients with diabetes-related foot ulcers. A hydrophobic wound dressing was compared with a control silicone dressing in vitro. Test dressings were placed on top of a Pseudomonas aeruginosa challenge suspension with increasing concentrations of suspension inoculum in addition to supplementation with phosphate buffered saline (PBS) or increased protein content (IPC). Next, we used the challenge suspensions obtained at the end of the first experiment, where bacterial loads from the suspensions were enumerated following test dressing exposure. Further, the time-dependent bacterial attachment was investigated over 1 and 24 h. Lastly, test dressings were exposed to a challenge suspension with IPC, with or without the addition of the bacteriostatic agent Deferiprone to assess the impacts of limiting bacterial growth in the experimental design. Lastly, two different wound dressings with claims of bacterial binding were obtained from patients with chronic diabetes-related foot ulcers after 72 h of application and observed using scanning electron microscope (SEM). Bacteria were enumerated from each dressing after a 1-h exposure time. There was no statistical difference in bacterial attachment between both test dressings when using different suspension inoculum concentrations or test mediums. Bacterial attachment to the two test dressings was significantly lower (p < 0.0001) when IPC was used instead of PBS. In the challenge suspension with PBS, only the hydrophobic dressing achieved a statistically significant reduction in bacterial loads (0.5 ± 0.05 log colony forming units; p = 0.001). In the presence of IPC, there was no significant reduction in bacterial loads for either test dressing. When bacterial growth was arrested, attachment to the test dressings did not increase over time, suggesting that the number of bacteria on the test dressings increases over time due to bacterial growth. SEM identified widespread adsorption of host fouling across the test dressings which occurred prior to microbial binding. Therein, microbial attachment occurred predominantly to host fouling and not directly to the dressings. Bacterial binding is not unique to dialkylcarbamoyl chloride (DACC) dressings and under clinically relevant in vitro conditions and in vivo observations, we demonstrate (in addition to previously published work) that the bacterial binding capabilities are not effective at reducing the number of bacteria in laboratory models or human wounds.
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