Frances L. Game
University of Nottingham
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Diabetes Care | 2011
Lee C. Rogers; Robert G. Frykberg; David Armstrong; Andrew J.M. Boulton; Michael Edmonds; Georges Ha Van; A. Hartemann; Frances L. Game; William Jeffcoate; A. Jirkovska; Edward B. Jude; Stephan Morbach; William B. Morrison; Michael S. Pinzur; Dario Pitocco; Lee J. Sanders; Luigi Uccioli
The diabetic Charcot foot syndrome is a serious and potentially limb-threatening lower-extremity complication of diabetes. First described in 1883, this enigmatic condition continues to challenge even the most experienced practitioners. Now considered an inflammatory syndrome, the diabetic Charcot foot is characterized by varying degrees of bone and joint disorganization secondary to underlying neuropathy, trauma, and perturbations of bone metabolism. An international task force of experts was convened by the American Diabetes Association and the American Podiatric Medical Association in January 2011 to summarize available evidence on the pathophysiology, natural history, presentations, and treatment recommendations for this entity.
Diabetes-metabolism Research and Reviews | 2008
R. J. Hinchliffe; Gerlof D. Valk; Jan Apelqvist; David Armstrong; K. Bakker; Frances L. Game; A. Hartemann-Heurtier; Magnus Löndahl; Patricia Elaine Price; W. H. van Houtum; William Jeffcoate
The outcome of management of diabetic foot ulcers is poor and there is uncertainty concerning optimal approaches to management. We have undertaken a systematic review to identify interventions for which there is evidence of effectiveness. A search was made for reports of the effectiveness of interventions assessed in terms of healing, ulcer area or amputation in controlled clinical studies published prior to December 2006. Methodological quality of selected studies was independently assessed by two reviewers using Scottish Intercollegiate Guidelines Network (SIGN) criteria. Selected studies fell into the following categories: sharp debridement and larvae; antiseptics and dressings; chronic wound resection; hyperbaric oxygen (HBO); reduction of tissue oedema; skin grafts; electrical and magnetic stimulation and ultrasound. Heterogeneity of studies prevented pooled analysis of results. Of the 2251 papers identified, 60 were selected for grading following full text review. Some evidence was found to support hydrogels as desloughing agents and to suggest that a systemic (HBO) therapy may be effective. Topical negative pressure (TNP) may promote healing of post‐operative wounds, and resection of neuropathic plantar ulcers may be beneficial. More information was needed to confirm the effectiveness and cost‐effectiveness of these and other interventions. No data were found to justify the use of any other topically applied product or dressing, including those with antiseptic properties. Further evidence to substantiate the effect of interventions designed to enhance the healing of chronic ulcers is urgently needed. Until such evidence is available from robust trials, there is limited justification for the use of more expensive treatments and dressings. Copyright
Diabetes-metabolism Research and Reviews | 2012
Frances L. Game; R. J. Hinchliffe; Jan Apelqvist; David Armstrong; K. Bakker; A. Hartemann; Magnus Löndahl; Patricia Elaine Price; William Jeffcoate
The outcome of management of diabetic foot ulcers is poor, and there is continuing uncertainty concerning optimal approaches to management. It was for these reasons that in 2006 the International Working Group of the Diabetic Foot (IWGDF) working group on wound healing undertook a systematic review of the evidence to inform protocols for routine care and to highlight areas which should be considered for further study. The same working group has now updated this review by considering papers on the interventions to improve the healing of chronic ulcers published between December 2006 and June 2010. Methodological quality of selected studies was independently assessed by two reviewers using Scottish Intercollegiate Guidelines Network criteria. Selected studies fell into the following ten categories: sharp debridement and wound bed preparation with larvae and hydrotherapy; wound bed preparation using antiseptics, applications and dressing products; resection of the chronic wound; hyperbaric oxygen therapy (HBOT); compression or negative pressure therapy; products designed to correct aspects of wound biochemistry and cell biology associated with impaired wound healing; application of cells, including platelets and stem cells; bioengineered skin and skin grafts; electrical, electromagnetic, lasers, shockwaves and ultrasound; other systemic therapies which did not fit in the above categories. Heterogeneity of studies prevented pooled analysis of results.
Diabetic Medicine | 2005
N. Pound; Susan Chipchase; K. Treece; Frances L. Game; William Jeffcoate
Aims Measures of healing rate may not give a complete indication of the effectiveness of overall management of diabetic foot ulcers. Apart from healing and speed of healing, the outcomes of greatest importance to the patient are avoidance of any amputation and remaining free from any recurrence. We have documented the number of patients presenting with diabetic foot ulcers who become ulcer free and examined the value of documenting ulcer‐free survival.
Diabetic Medicine | 2004
K. Treece; R.M. Macfarlane; N. Pound; Frances L. Game; William Jeffcoate
Objective The lack of a simple, robust classification of diabetic foot ulcers has critically hampered research into optimum patterns of care. We have therefore attempted validation of the previously published S(AD) SAD system, which is based on grading of ulcer features using simple clinical methods.
Diabetic Medicine | 2004
A. Gazis; N. Pound; R.M. Macfarlane; K. Treece; Frances L. Game; William Jeffcoate
Objective To determine the mortality of a population of patients diagnosed with Charcot neuropathic osteoarthropathy managed by a single specialist unit and to compare the results with a control population.
Diabetic Medicine | 2007
P. Ince; Denise Kendrick; Frances L. Game; William Jeffcoate
Aims To explore the relationships between time to healing of diabetic foot ulcers and baseline characteristics of both patients and their ulcers.
Regenerative Medicine | 2007
Manar Moustafa; Anthony J. Bullock; Fionuala M Creagh; Simon Heller; William Jeffcoate; Frances L. Game; Carol Amery; Soloman Tesfaye; Zoe Ince; David Haddow; Sheila MacNeil
AIM To compare the rate of healing of diabetic neuropathic ulcers using cultured autologous keratinocytes delivered on chemically defined transfer discs (Myskin) (active treatment) versus healing obtained with cell-free discs (placebo). MATERIALS AND METHODS After a 4-week lead-in period patients (randomly assigned) received active or placebo treatments weekly for 6 weeks. All patients then received active treatments for a maximum of 12 treatments where required. Altogether, 16 patients with a total of 21 ulcers resistant to conventional therapy were recruited from four specialist diabetic centers in three cities. RESULTS All 21 ulcers were treated and of these ten healed and eight improved, with two failing to respond (one ulcer was lost due to autoamputation). For analysis according to the study criteria, however, only the 12 patients with 12 index ulcers who completed treatment protocols were eligible - five in the placebo group and seven in the active group. Of these, five ulcers healed completely and seven were reduced by more than 50%. Complete healing took a median of ten active applications. CONCLUSIONS Repeated regular applications of the patients keratinocytes, delivered on the carrier dressing, initiated wound healing in ulcers resistant to conventional therapy, with 18 out of 21 ulcers responding. The healing observed did not appear attributable to patient recruitment or the cell-free carrier dressing but to the delivery of the cultured cells.
Journal of the American Podiatric Medical Association | 2011
Lee C. Rogers; Robert G. Frykberg; David Armstrong; Andrew J.M. Boulton; Michael Edmonds; Georges Ha Van; A. Hartemann; Frances L. Game; William Jeffcoate; A. Jirkovska; Edward B. Jude; Stephan Morbach; William B. Morrison; Michael S. Pinzur; Dario Pitocco; Lee J. Sanders; Luigi Uccioli
The diabetic Charcot foot syndrome is a serious and potentially limb-threatening lower-extremity complication of diabetes. First described in 1883, this enigmatic condition continues to challenge even the most experienced practitioners. Now considered an inflammatory syndrome, the diabetic Charcot foot is characterized by varying degrees of bone and joint disorganization secondary to underlying neuropathy, trauma, and perturbations of bone metabolism. An international task force of experts was convened by the American Diabetes Association and the American Podiatric Medical Association in January 2011 to summarize available evidence on the pathophysiology, natural history, presentations, and treatment recommendations for this entity.
Diabetic Medicine | 2004
Frances L. Game; William Jeffcoate
A 52-year-old man is referred to the diabetic clinic by his general practitioner (GP). He has a history of Type 2 diabetes diagnosed 8 years ago which is treated with a combination of Metformin and Gliclazide (last HbA1c 8.6%). He also has hypertension for which he takes aspirin and Ramipril. The referral is prompted by the presence of a foot ulcer that has failed to heal over an 8-week period. The patient has had repeated courses of Co-Fluampicil prescribed by the GP. The referral is accompanied by a wound swab result that demonstrates isolation of methicillin-resistant Staphylococcus aureus (MRSA). Clinically the patient is well. Both feet appear neuropathic and are insensate, while peripheral pulses are palpable. On the right foot there is an ulcer under the first metatarso-phalangeal joint with surrounding callus, this foot is 3° hotter than the left. After debridement bone is palpable at the base of the wound. • What is the immediate management plan? • What is the clinical relevance of the wound swab result? • Should the patient be started on antibiotics? If so, which antibiotics are appropriate? • What is the long-term management of MRSA in the diabetic foot?