Impaired Wound Healing In Patients Research Articles

Sulfated hyaluronic acid/collagen-based biomimetic hybrid nanofiber skin for diabetic wound healing: Development and preliminary evaluation

Diabetic foot ulcers (DFUs) are one of the most serious and devastating complication of diabetes, manifesting as foot ulcers and impaired wound healing in patients with diabetes mellitus. To solve this problem, sulfated hyaluronic acid (SHA)/collagen-based nanofibrous biomimetic skins was developed and used to promote the diabetic wound healing and skin remodeling. First, SHA was successfully synthetized using chemical sulfation and incorporated into collagen (COL) matrix for preparing the SHA/COL hybrid nanofiber skins. The polyurethane (PU) was added into those hybrid scaffolds to make up the insufficient mechanical properties of SHA/COL nanofibers, the morphology, surface properties and degradation rate of hybrid nanofibers, as well as cell responses upon the nanofibrous scaffolds were studied to evaluate their potential for skin reconstruction. The results demonstrated that the SHA/COL, SHA/HA/COL hybrid nanofiber skins were stimulatory of cell behaviors, including a high proliferation rate and maintaining normal phenotypes of specific cells. Notably, SHA/COL and SHA/HA/COL hybrid nanofibers exhibited a significantly accelerated wound healing and a high skin remodeling effect in diabetic mice compared with the control group. Overall, SHA/COL-based hybrid scaffolds are promising candidates as biomimetic hybrid nanofiber skin for accelerating diabetic wound healing.

Chemotherapy-Mediated Complications of Wound Healing: An Understudied Side Effect.

Significance: Chemotherapy is a primary method to treat cancer. While chemotherapeutic drugs are designed to target rapidly dividing cancer cells, they can also affect other cell types. In the case of dermal cells and macrophages involved in wound healing, cytotoxicity often leads to the development of chronic wounds. The situation becomes even more severe when chemotherapy is combined with surgical tumor excision. Recent Advances: Despite its significant impact on patients' recovery from surgery, the issue of delayed wound healing in individuals undergoing chemotherapy remains inadequately explored. Critical Issues: This review aims to analyze the harmful impact of chemotherapy on wound healing. The analysis showed that chemotherapy drugs could inhibit cellular metabolism, cell division, and angiogenesis and lead to nerve damage. They impede the migration of cells into the wound and reduce the production of extracellular matrix. At the molecular level, they interfere with replication, transcription, translation, and cell signaling. This work reviews skin problems that patients may experience during and after chemotherapy and demonstrates insights into the cellular and molecular mechanisms of these pathologies. Future Directions: In the future, the problem of impaired wound healing in patients treated with chemotherapy may be addressed by cell therapies like autologous keratinocyte transplantation, which has already proved effective in this case. Epigenetic intervention to mitigate the side effects of chemotherapy is also worth considering, but epigenetic consequences of chemotherapy on skin cells are largely unknown and should be investigated.

Therapeutic TNF Inhibitors Exhibit Differential Levels of Efficacy in Accelerating Cutaneous Wound Healing

Adalimumab but neither etanercept nor certolizumab-pegol has been reported to induce a wound-healing profile invitro by regulating macrophage differentiation and matrix metalloproteinase expression, which may underlie the differences in efficacy between various TNF-α inhibitors in impaired wound healing in patients with hidradenitis suppurativa, a chronic inflammatory skin disease. To examine and compare the efficacy of various TNF inhibitors in cutaneous wound healing invivo, a human TNF knock-in Leprdb/db mouse model was established to model the impaired cutaneous wound healing as seen in hidradenitis suppurativa. The vehicle group exhibited severe impairments in cutaneous wound healing. In contrast, adalimumab significantly accelerated healing, confirmed by both histologic assessment and a unique healing transcriptional profile. Moreover, adalimumab and infliximab showed similar levels of efficacy, but golimumab was less effective, along with etanercept and certolizumab-pegol. In line with histologic assessments, proteomics analyses from healing wounds exposed to various TNF inhibitors revealed distinct and differential wound-healing signatures that may underlie the differential efficacy of these inhibitors in accelerating cutaneous wound healing. Taken together, these data revealed that TNF inhibitors exhibited differential levels of efficacy in accelerating cutaneous wound healing in the impaired wound-healing model invivo.

Effect of cold atmospheric plasma/NO gas application with different exposure times on healing in wounds with tissue loss in diabetic rats.

Applications of cold atmospheric plasma/nitric oxide (CAP/NO) gas have recently garnered popularity when treating impaired wound healing in patients with diabetes. In this study, we aimed to investigate the effects of NO gas application for 60 and 120 s on wound healing in diabetic rats. A dorsal excision 3 cm in diameter was performed in 15 diabetic rats; these rats were categorized into the following 3 groups: DC (untreated diabetic control); DNO/60 (exposure to 200 ppm NO gas for 60 s/day); and DNO/120 (exposure to 200 ppm NO gas for 120 s/day). Wound contraction on days 0, 3, 7, 11, and 14 and wound contraction rate between days 0 and 14 were evaluated. On day 14, tissue samples were collected for histopathologic assessment of inflammation, epithelial regeneration, angiogenesis congestion, and collagen fiber organization. Normality of distribution was assessed using the Shapiro-Wilk test, and intergroup comparisons were performed using the Mann-Whitney U test (NPar Test) and the Kruskal-Wallis test (non-parametric ANOVA). Wound contraction during treatment days 7-14 was significantly greater in the NO-treatment groups than in the DC group (p<0.05). The NO60 s and NO120 s groups showed a significantly higher wound contraction rate than the DC group (p=0.033, p=0.049, respectively). Significant differences were noted between the control and NO groups in terms of inflammation (p<0.05) and between the control group and DNO/60 and DNO/120 groups in terms of collagen organization (p<0.05, p<0.01, respectively). Evaluation of epithelialization revealed significant intergroup differences between the control and NO treatment groups (p<0.01). In this study, the application of NO once a day for 60 seconds and 120 seconds in diabetic wounds contributed equally to wound healing.

Topical Administration of a Marine Oil Rich in Pro-Resolving Lipid Mediators Accelerates Wound Healing in Diabetic db/db Mice through Angiogenesis and Macrophage Polarization.

Impaired wound healing in patients with type 2 diabetes (DM2) is characterized by chronic inflammation, which delays wound closure. Specialized pro-resolving lipid mediators (SPMs) are bioactive molecules produced from essential polyunsaturated fatty acids (PUFAs), principally omega-3 docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). SPMs are potent regulators of inflammation and have been used to suppress chronic inflammation in peripheral artery disease, non-alcoholic fatty liver disease, and central nervous system syndromes. LIPINOVA® is a commercially available safe-grade nutritional supplement made from a fractionated marine lipid concentrate derived from anchovy and sardine oil that is rich in SPMs and EPA, as well as DHA precursors. Here, we assessed the effect of LIPINOVA® in wound dressing applications. LIPINOVA® showed biocompatibility with keratinocytes and fibroblasts, reduced the abundance of pro-inflammatory macrophages (Mφ1), and promoted in vitro wound closure. Daily application of the marine oil to open wounds made by punch biopsy in db/db mice promoted wound closure by accelerating the resolution of inflammation, inducing neoangiogenesis and Mφ1/Mφ2 macrophage polarization. In conclusion, LIPINOVA® displays pro-resolutive properties and could be exploited as a therapeutic agent for the treatment of diabetic ulcers.

Transdermal deferoxamine administration improves excisional wound healing in chronically irradiated murine skin

BackgroundRadiation-induced skin injury is a well-known risk factor for impaired wound healing. Over time, the deleterious effects of radiation on skin produce a fibrotic, hypovascular dermis poorly suited to wound healing. Despite increasing understanding of the underlying pathophysiology, therapeutic options remain elusive. Deferoxamine (DFO), an iron-chelating drug, has been shown in prior murine studies to ameliorate radiation-induced skin injury as well as improve wound healing outcomes in various pathologic conditions when administered transdermally. In this preclinical study, we evaluated the effects of deferoxamine on wound healing outcomes in chronically irradiated murine skin.MethodsWild-type mice received 30 Gy of irradiation to their dorsal skin and were left to develop chronic fibrosis. Stented excisional wounds were created on their dorsal skin. Wound healing outcomes were compared across 4 experimental conditions: DFO patch treatment, vehicle-only patch treatment, untreated irradiated wound, and untreated nonirradiated wounds. Gross closure rate, wound perfusion, scar elasticity, histology, and nitric oxide assays were compared across the conditions.ResultsRelative to vehicle and untreated irradiated wounds, DFO accelerated wound closure and reduced the frequency of healing failure in irradiated wounds. DFO augmented wound perfusion throughout healing and upregulated angiogenesis to levels observed in nonirradiated wounds. Histology revealed DFO increased wound thickness, collagen density, and improved collagen fiber organization to more closely resemble nonirradiated wounds, likely contributing to the observed improved scar elasticity. Lastly, DFO upregulated inducible nitric oxide synthase and increased nitric oxide production in early healing wounds.ConclusionDeferoxamine treatment presents a potential therapeutic avenue through which to target impaired wound healing in patients following radiotherapy.

Isatis glauca subsp. sivasica extract contributes to diabetic wound healing process via increased collagen and nitric oxide content

Isatis L. genus highly endemic and that is traditionally suggested for wound management in Turkey. In this study, we have reported the effect of I. glauca subsp. sivasica extract on diabetic wound healing process. A diabetic model was generated in Wistar rats using streptozotocin injection. Rats were divided into two main groups: control group and Isatis group. Full thickness excisional skin wounds were created by using a biopsy punch. The Isatis group was treated with single daily dose I. glauca subsp. sivasica extract (50 mg/kg). Rats were sacrificed day 3 or 7 after wounding. The dominant phenolic compounds identified with RP-HPLC-DAD from Isatis extract were the benzoic acid and vanillic acid. Isatis extract significantly accelerated wound healing process considering the wound closure rates (WCR). Moreover, the levels of collagen and nitric oxide were elevated on days 3 and 7 by Isatis administration in the diabetic wound tissue. These data suggest that, for the first time, I. glauca subsp. sivasica extract may have the potential to promote the impaired wound healing in patients with diabetes.

Polymeric micelle mediated follicular delivery of spironolactone: Targeting the mineralocorticoid receptor to prevent glucocorticoid-induced activation and delayed cutaneous wound healing

Impaired wound healing in patients receiving glucocorticoid therapy is a serious clinical concern: mineralocorticoid receptor (MR) antagonists can counter glucocorticoid-induced off-target activation of MR receptors. The aim of this study was to investigate the cutaneous delivery of the potent MR antagonist, spironolactone (SPL), from polymeric micelle nanocarriers, prepared using a biodegradable copolymer, methoxy-poly(ethylene glycol)-di-hexyl-substituted-poly(lactic acid). Immunofluorescent labelling of the MR showed that it was principally located in the pilosebaceous unit (PSU), justifying the study rationale since polymeric micelles accumulate preferentially in appendageal structures. Cutaneous biodistribution studies under infinite and finite dose conditions, demonstrated delivery of pharmacologically relevant amounts of SPL to the epidermis and upper dermis. Preferential PSU targeting was confirmed by comparing amounts of SPL in PSU-containing and PSU-free skin biopsies: SPL nanomicelles showed 5-fold higher delivery of SPL in the PSU-containing biopsies, 0.54 ± 0.18 ng/mm2vs. 0.10 ± 0.03 ng/mm2, after application of a hydrogel in finite conditions. Canrenone, an active metabolite of SPL, was also quantified in skin samples. In addition to being used for the treatment of delayed cutaneous wound healing by site-specific antagonism of the MR, the formulation might also be used to treat pilosebaceous androgen-related skin diseases, e.g. acne vulgaris, since SPL is a potent androgen receptor antagonist.

Inhibition of 11β-HSD1 Expression by Insulin in Skin: Impact for Diabetic Wound Healing.

Chronic, non-healing wounds impose a great burden on patients, professionals and health care systems worldwide. Diabetes mellitus (DM) and obesity are globally highly prevalent metabolic disorders and increase the risk for developing chronic wounds. Glucocorticoids (GCs) are endogenous stress hormones that exert profound effects on inflammation and repair systems. 11-beta-hydroxysteroid dehydrogenase 1 (11β-HSD1) is the key enzyme which controls local GC availability in target tissues such as skin. Since treatment with GCs has detrimental side effects on skin integrity, causing atrophy and delayed wound healing, we asked whether the dysregulated expression of 11β-HSD1 and consequently local GC levels in skin contribute to delayed wound healing in obese, diabetic db/db mice. We found increased expression of 11β-HSD1 during disturbed wound healing and in the healthy skin of obese, diabetic db/db mice. Cell analysis revealed increased expression of 11β-HSD1 in fibroblasts, myeloid cells and dermal white adipose tissue from db/db mice, while expression in keratinocytes was unaffected. Among diabetes- and obesity-related factors, insulin and insulin-like growth factor 1 down-regulated 11β-HSD1 expression in fibroblasts and myeloid cells, while glucose, fatty acids, TNF-α and IL-1β did not affect it. Insulin exerted its inhibitory effect on 11β-HSD1 expression by activating PI3-kinase/Akt-signalling. Consequently, the inhibitory effect of insulin is attenuated in fibroblasts from insulin-resistant db/db mice. We conclude that insulin resistance in obesity and diabetes prevents the down-regulation of 11β-HSD1, leading to elevated endogenous GC levels in diabetic skin, which could contribute to impaired wound healing in patients with DM.

591-P: Macrophage IL-1beta–Dependent VEGF-A Expression Is Required for Inflammatory Arteriogenesis and Wound Healing in Type 2 Diabetes

Impaired wound healing in patients with diabetes mellitus (DM) is a major source of morbidity and mortality. Current treatments for diabetic wounds are modestly effective at promoting healing. Recently, we identified an important role for inflammatory macrophage VEGF-A production in consequent angiogenesis/arteriogenesis required for adequate wound healing. We sought to understand the impact of diabetes on inflammatory angiogenesis and consequent healing. We hypothesized that diabetes mellitus (DM) results in reduced inflammatory macrophage VEGF-A expression with consequent impairments in angiogenesis-dependent wound healing. Mice with experimental diabetes demonstrated profound delays both in wound healing using a dermal punch biopsy model and in perfusion recovery using the femoral artery ligation model of hind limb ischemia. VEGF-A expression is highly upregulated in “classic inflammatory” macrophages relative to “alternatively activated” or wound healing macrophages. This is supported by a strong association between IL-1β and VEGF-A expression. In order to understand whether this relationship between IL-1β and VEGF-A was causal, we generated a novel mouse with a LoxP flanked IL-1β allele to create an inducible macrophage deletion of IL-1β. Myeloid IL-β deletion resulted in severely impaired macrophage VEGF-A expression and consequent decreases in angiogenesis and wound healing, consistent with the experimental model of DM. Moreover, macrophages from diabetic mice demonstrated reduced expression of IL-1R signaling complex components along with consequent reductions in VEGF-A expression. Defining inflammatory macrophages as key, early drivers of angiogenesis supports a paradigm shift away from inflammation-suppression for adequate wound healing, allowing for macrophage reprograming strategies that promote appropriate inflammation-dependent healing responses. Disclosure C.S. Mantsounga: None. Funding National Institutes Health (1R01HL139795)

Additional Risk Stratification Using Local and Systemic Factors for Patients with Critical Limb Ischaemia Undergoing Endovascular Therapy in the WIfI Era

While current guidelines describe the importance of assessing limb characteristics for predicting limb prognosis in patients with critical limb ischaemia (CLI), several reports have also suggested that systemic factors are associated with limb prognosis. The aim of this study was to evaluate whether systemic factors have the same impact on wound healing as limb characteristics in CLI patients undergoing endovascular therapy. A total of 735 patients who were treated for the first time for CLI with tissue loss between April 2010 and December 2015 were extracted from a prospective registry and data for the Wound, Ischaemia, and foot Infection (WIfI) classification were searched retrospectively. The predictors of wound healing were explored with Cox proportional hazards regression. The one year wound healing rate was 60.2% in WIfI stage 1–3 patients and 53.6% in WIfI sstage 4 (p = .01). In WIfI stage 1–3, no systemic factors were significantly associated with wound healing, whereas, in WIfI stage 4 patients. Non-ambulatory status [hazard ratio (HR) 1.98; 95% confidence interval (CI) 1.37–2.84], haemodialysis (HR 1.90; 95% CI 1.33–2.72) and an albumin level under 3.0 g/dL (HR 1.53; 95% CI 1.02–2.31), were identified as independent risk factors for failure to achieve wound healing. If none or one of these risk factors were present, wound healing was comparable with WIfI 4 and WIfI 1–3 patients (67.7% vs. 63.6%, p = .89), whereas in patients with two or more risk factors wound healing was worse in WIfI 4 than in WIfI 1–3 patients (35.7% vs. 49.5%, p = .01). Non-ambulatory status, haemodialysis, and a low albumin level were additional systemic risk factors for impaired wound healing in patients with WIfI stage 4. The wound healing rate in WIfI stage 4 patients with one or fewer of these risk factors was comparable to that in WIfI stage 1–3.

Chronic hyperglycemia as a risk factor in implant therapy

It has been estimated that by 2030, the number of patients with diabetes aged > 64years will be > 82million in underdeveloped countries, and > 48million in developed countries. Chronic hyperglycemia delays wound healing by reducing the expression of growth factors in the wound fluid and re-epithelialization. Impaired wound healing in patients with diabetes has also been associated with inhibition of the production of stromal cell-derived factor-1alpha by several tissues including bone marrow, brain, heart, spleen, and gingivae. Chronic hyperglycemia interferes with the osseointegration of implants by deferring the expression of fibronectin and integrins. Results from experimental studies have shown a significantly higher bone-to-implant contact around implants placed in healthy animals compared with animals with streptozotocin-induced diabetes. Moreover, persistent hyperglycemia plays a role in abnormal differentiation of osteoclasts, thereby making bone tissue more susceptible to resorption. Furthermore, persistent hyperglycemia has also been associated with increased peri-implant soft tissue inflammation (increased peri-implant bleeding on probing and probing depth) and crestal bone loss. Clinical studies have shown that under optimal glycemic control dental implants can show success and survival rates of up to 100% in patients diagnosed with diabetes. Although patients with diabetes can undergo dental implant therapy and can exhibit implant survival similar to those in systemically healthy individuals, the contribution of glycemic control and regular oral hygiene maintenance cannot be disregarded.

Additional Risk Stratification Using Local and Systemic Factors for Patients with Critical Limb Ischaemia Undergoing Endovascular Therapy in the WIfI Era

While current guidelines describe the importance of assessing limb characteristics for predicting limb prognosis in patients with critical limb ischaemia (CLI), several reports have also suggested that systemic factors are associated with limb prognosis. The aim of this study was to evaluate whether systemic factors have the same impact on wound healing as limb characteristics in CLI patients undergoing endovascular therapy. A total of 735 patients who were treated for the first time for CLI with tissue loss between April 2010 and December 2015 were extracted from a prospective registry and data for the Wound, Ischaemia, and foot Infection (WIfI) classification were searched retrospectively. The predictors of wound healing were explored with Cox proportional hazards regression. The one year wound healing rate was 60.2% in WIfI stage 1-3 patients and 53.6% in WIfI stage 4 (p=.01). In WIfI stage 1-3, no systemic factors were significantly associated with wound healing, whereas, in WIfI stage 4 patients, non-ambulatory status [hazard ratio (HR) 1.98; 95% confidence interval (CI) 1.37-2.84], haemodialysis (HR 1.90; 95% CI 1.33-2.72) and an albumin level under 3.0g/dL (HR 1.53; 95% CI 1.02-2.31), were identified as independent risk factors for failure to achieve wound healing. If none or one of these risk factors were present, wound healing was comparable with WIfI 4 and WIfI 1-3 patients (67.7% vs. 63.6%, p=.89), whereas in patients with two or more risk factors wound healing was worse in WIfI 4 than in WIfI 1-3 patients (35.7% vs. 49.5%, p=.01). Non-ambulatory status, haemodialysis, and a low albumin level were additional systemic risk factors for impaired wound healing in patients with WIfI stage 4. The wound healing rate in WIfI stage 4 patients with one or fewer of these risk factors was comparable to that in WIfI stage 1-3.

Gene Expression Markers of Impaired Wound Healing in Patients with Pain after Vaginal Mesh

Gene Expression Markers of Impaired Wound Healing in Patients with Pain after Vaginal Mesh

Diabetes: Epigenetic changes lead to impaired wound healing in patients with T2DM.

Diabetes: Epigenetic changes lead to impaired wound healing in patients with T2DM.

Skin wound healing in diabetic β6 integrin‐deficient mice

Integrin αvβ6 is a heterodimeric cell surface receptor, which is absent from the normal epithelium, but is expressed in wound-edge keratinocytes during re-epithelialization. However, the function of the αvβ6 integrin in wound repair remains unclear. Impaired wound healing in patients with diabetes constitutes a major clinical problem worldwide and has been associated with the accumulation of advanced glycated endproducts (AGEs) in the tissues. AGEs may account for aberrant interactions between integrin receptors and their extracellular matrix ligands such as fibronectin (FN). In this study, we compared healing of experimental excisional skin wounds in wild-type (WT) and β6-knockout (β6(-/-) ) mice with streptozotocin-induced diabetes. Results showed that diabetic β6(-/-) mice had a significant delay in early wound closure rate compared with diabetic WT mice, suggesting that αvβ6 integrin may serve as a protective role in re-epithelialization of diabetic wounds. To mimic the glycosylated wound matrix, we generated a methylglyoxal (MG)-glycated variant of FN. Keratinocytes utilized αvβ6 and β1 integrins for spreading on both non-glycated and FN-MG, but their spreading was reduced on FN-MG. These findings indicated that glycation of FN and possibly other integrin ligands could hamper keratinocyte interactions with the provisional matrix proteins during re-epithelialization of diabetic wounds.

3‐Deoxyglucosone‐collagen alters human dermal fibroblast migration and adhesion: Implications for impaired wound healing in patients with diabetes

The interaction of fibroblasts with the extracellular matrix is critical for wound healing. Advanced glycation end products (AGEs) occur through nonenzymatic glycation of long-lived proteins such as collagens. One precursor to these modifications, 3-deoxyglucosone (3DG), is elevated in patients with diabetes and contributes to the accumulation of AGEs on collagen with increasing chronological age. Because wound repair is dependent on fibroblast migration, proliferation, and expression of extracellular matrix proteins, we examined the role of 3DG-treated collagen and the subsequent response of fibroblasts to this modification. We found that fibroblasts adhere more strongly to 3DG-treated collagen and do not migrate efficiently into the wound site. We further show that 3DG-treated collagen induces perinuclear localization of focal adhesion kinase and paxillin, indicative of decreased association of these proteins with the cytoskeleton. Additionally, these cells expressed higher levels of the misfolded indicator protein growth arrest and DNA damage inducible gene 153. These data suggest that fibroblast/matrix interactions are altered as AGEs accumulate and affect focal adhesion formation. Furthermore, 3DG may be a factor mediating chronic wounds observed in patients with diabetes and in the elderly by altering the signaling within the fibroblast and inducing the misfolding of proteins.

Hyperglycaemic conditions decrease cultured keratinocyte mobility: implications for impaired wound healing in patients with diabetes

Elevated blood glucose in patients with diabetes mellitus (DM) leads to complications including poor wound healing. Proper keratinocyte migration and proliferation are the crucial steps during re-epithelialization. We hypothesize that the impaired wound healing in patients with DM is due to the disruption of proper re-epithelialization. We aimed to explore the effects of high glucose on keratinocytes in terms of cell migration and proliferation. Keratinocytes were cultivated in normal and high glucose conditions. Their viability was evaluated by MTS assay. Transwell migration and in vitro scratch assays were used to evaluate their mobility. The mRNA expressions and activities of matrix metalloproteinase (MMP)-2 and MMP-9 were determined. The mRNA of their respective physiological inhibitors, tissue inhibitor of MMP (TIMP)-1 and TIMP-2, was also evaluated. Immunofluorescent staining and Western blotting were used to examine the expression of phosphorylated focal adhesion kinase (pp125(FAK)). The impacts of high glucose on keratinocyte proliferation were assessed by 5-bromo-2'-deoxyuridine incorporation assay. High glucose treatment did not affect keratinocyte viability up to 3 days. In contrast, the mobility of keratinocytes, the activities and gene expressions of MMP-2 and MMP-9, the expression of pp125(FAK), and the cell proliferation after 5 days were significantly downregulated after hyperglycaemic treatments while the mRNA expression of TIMP-1 increased. Under hyperglycaemic conditions, keratinocytes demonstrate reduced migration and decreased proliferation capacities. These impairments of keratinocyte functions are likely to result in inadequate re-epithelialization. These defective physiological events provide a reasonable explanation for the poor wound healing commonly observed in patients with DM.

Depression, Healing, and Recovery From Coronary Artery Bypass Surgery

Effects of postoperative depression on recovery from coronary artery bypass grafting have not been widely studied. To evaluate emotional and physical recovery after bypass surgery and investigate associations between depressive symptoms and infections and impaired wound healing in patients with high and low levels of depressive symptoms. A nonrandomized, comparative, longitudinal design was used to study 72 bypass surgery patients without serious noncardiac comorbidities who were available for follow-up after discharge. Patients completed questionnaires to assess depressive symptoms, emotional recovery, and physical recovery within 48 hours after extubation, at discharge from the hospital, and 6 weeks later and performed 6-minute walk tests at the last 2 times. Infections and impaired wound healing (as indicated by positive cultures, antibiotic treatment, or extra treatments, such as debridements or incisions and drainage) were identified by chart audit. At discharge, patients with higher depressive symptom scores (indicating more symptoms) reported poorer emotional recovery (P<.001) and poorer physical recovery (P=.007) and achieved shorter walking distances (P<.001) than did patients with lower scores (indicating fewer symptoms). Six weeks after discharge, emotional and physical recovery remained lower in patients with more depressive symptoms (P<.001). Infections and impaired wound healing were more common among patients with higher depressive symptom scores (46%) than among patients with lower scores (19%, P=.03). After bypass surgery, depressive symptoms are associated with infections, impaired wound healing, and poor emotional and physical recovery.

Impaired wound healing in patients with diabetes.

This article reviews a cross-section of literature on wound healing and highlights how diabetes mellitus can cause deviations from usual healing patterns. Nursing interventions can either enhance or delay the healing process. Nurses need to understand the defective processes to optimise the available healing potential.