Modelling the cost-effectiveness of electric stimulation therapy in non-healing venous leg ulcers
Catalyst Health Economics Consultants, Northwood, UK. Journal of Wound Care
(Impact Factor: 1.07).
10/2011; 20(10):464, 466, 468-72. DOI: 10.12968/jowc.2011.20.10.464
Objective: To estimate the cost-effectiveness of using electric stimulation (ES) therapy (Accel-Heal) plus dressings and compression bandaging compared with dressings and compression bandaging alone in treating chronic, non-healing venous leg ulcers (VLUs) of > 6 months' duration from the perspective of the National Health Service (NHS) in the UK. Method:A 5-month Markov model was constructed, depicting the management of a chronic, non-healing VLU of > 6 months' duration. The model considers the decision by a clinician to continue with a patient's previous care plan (comprising dressings and compression bandaging) or treating with ES therapy plus dressings and compression bandaging. The model was used to estimate the relative cost-effectiveness of ES therapy at 2008-2009 prices. Results: According to the model, 38% of VLUs are expected to heal within 5 months after starting ES therapy, with a further 57% expected to improve. This improvement in clinical outcome is expected to lead to a 6% health gain of 0.017 QALYs (from 0.299 to 0.316 QALYs) over 5 months. The model also showed that using ES therapy instead of continuing with a patient's previous care plan is expected to reduce the NHS cost of managing them by 15%, from 880 pound to 749 pound, due in part to a 27% reduction in the requirement for nurse visits (from mean 49.0 to 35.9 visits per patient) over the first 5 months after the start of treatment. Hence, use of ES therapy was found to be a dominant treatment (improved outcome for less cost). Conclusion: Within the model's limitations, use of ES therapy potentially affords the NHS a cost-effective treatment, compared with patients remaining on their previous care plan in managing chronic, non-healing VLUs of > 6 months' duration. However, this is dependant on the number of ES therapy units per treatment, the unit cost of the device, and the number of nurse visits required to manage patients in clinical practice.
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ABSTRACT: Transient areolar ischemia occurs as a consequence of all breast lift/reduction procedures. Most commonly, it results in no complications or cosmetic consequences. Prolonged or more moderate ischemia results in cutaneous edema and epidermolysis in approximately 5–11% of patients. Complete full-thickness areolar necrosis has been reported to occur in approximately 0.5–7.3% of all cases of cosmetic, oncologic, or reconstructive breast surgery. Despite this unavoidable fact, there does not appear to be any literature focused on the diagnosis and management of this well-documented complication. We present this paper as a review of the current literature and as a way to establish a standard of management of areolar ischemia and necrosis. T ransient areolar ischemia occurs as a consequence of all breast lift/reduction procedures. Most com-monly, it results in no complications or cosmetic consequences. Prolonged or more moderate ischemia results in cutaneous edema and epidermolysis in approximately 5–11% of patients. 1–3 Complete full-thickness areolar necrosis has been reported to occur in approximately 0.5–7.3% of all patients of cosmetic, oncologic, or reconstructive breast surgery. 4–7 Normal anatomic variation, venous congestion, arterial insuf-Þ ciency, surgical misadventure, pedicle kinking, suture obstruction, edema, simultaneous implant prosthesis placement, hematoma, thrombosis, and infection have been reported as causative. 8 Factors associated with increased risk of areolar ischemia are listed in Table 1. The literature is replete with publications focused on anatomic study to improve predictability of the venous and arterial vasculature of the nipple areolar complex (NAC). 9–14 Others have attempted to identify risk factors and develop risk stratiÞ cation of patients undergoing breast surgery in order to assist in aware-ness for patients and surgeons of the inherent risks of surgery. The undeniable fact remains that up to 7.3% of all patients undergoing breast lift or reduction result in ischemia and possible complete necrosis. 4–7 Despite this unavoidable fact, there does not appear to be any literature focused on the diagnosis and management of this well-documented complication. We present this paper as a review of the current literature and to estab-lish a standard of management of areolar ischemia and necrosis.
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ABSTRACT: Background Tendon repair involves a slow repair process, which results in inferior repair of tissue and failure to obtain full active range of motion. Microcurrent therapy (MCT) is a new therapy after arthroplasty. Stem cells with capacity of self-renewal are ideal for tissue engineering. Aim The present work aimed at investigating the effect of MCT and the possible role of endogenous stem cells in repair of induced tendon injury in albino rat. Materials and methods Twenty-four male albino rats were classified into: Control group, tenotomy group, 5 rats were sacrificed 2 weeks and 5 rats sacrificed 4 weeks following achillis tendon injury (Subgroups IIa and IIb respectively). MCT group of 10 rats subjected to tendon injury followed by MCT, 5 rats sacrificed 2 weeks and 5 rats sacrificed 4 weeks following MCT (Subgroups IIIa and IIIb respectively). Tendon sections were stained with H&E and CD44 and CD105 immunostains. A morphometric study was performed. Results Subgroup IIa demonstrated multiple areas of widely separated collagen fibers, infiltrating cells and multiple congested vessels. Subgroup IIb showed multiple areas of disorganized collagen bundles, less infiltrating cells and few congested vessels. MCT subgroup IIIa revealed some areas of parallel collagen bundles, some infiltrating cells and some dilated congested vessels. MCT subgroup IIIb showed multiple areas of parallel collagen bundles, few infiltrating cells and occasional congested vessels. CD44 +ve and CD105 +ve cells were seen among disorganized, parallel collagen fibers and inside blood vessels. A significant increase in the area of regenerated collagen bundles was recorded in MCT subgroup IIIb. The area% of CD44 +ve and CD105 +ve MSCs denoted a significant increase in MCT subgroup IIIa. Conclusion MCT activated endogenous bone marrow derived MSCs migration to the injured achillis tendon, which stimulated tendon repair following induced tenotomy.
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ABSTRACT: Electrical stimulation (ES) profoundly affects angiogenesis by modulating the production of angiogenic factors. We evaluated the effect of sensory (direct current, 600 microamperes) and motor (monophasic pulse current, 2.5 to 3 milliamperes, 300-microsecond pulse duration, 100 Hz) intensities of cathodal current on the release of fibroblastic growth factor-2 (FGF-2) at the wound site and also the biomechanical and histological properties of healed skin. Ninety-six male, Sprague-Dawley rats were randomly assigned into one control and two experimental groups. A full-thickness skin incision was made on the dorsal region of each animal. The experimental groups received 10 sessions of ES (sensory or motor) for 1 hour per day every other day. The results showed that FGF-2 levels in the sensory group were significantly greater than in the other groups on the third day. In the motor group, FGF-2 levels were significantly decreased compared with the control group. There were no significant differences between the normalized ultimate strength and stiffness in the groups, but they tended to be higher in the motor ES group. We conclude that the application of sensory ES during the early stage of wound healing may have a beneficial effect on wound healing by inducing the release of angiogenic factors and decreasing the duration of the inflammation phase.
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