The diabetic foot is a complication of diabetes affecting 15% of diabetics in their lives. It is associated to diabetic neuropathy and peripheral vascular disease and its incidence has increased. The ulceration is the initial cause of a dramatic process leading, if not correctly treated, to amputations. Both neuropathy, neuro-ischemia and infections have a role in determining healing or worsening of the lesions and 85% of all amputations in diabetic patients are preceded by a foot ulceration deteriorating to a severe gangrene or infection. The different causative agents and the different clinical presentations of diabetic foot ask a multidisciplinary approach in order to address treatments to the final goals, the prevention of the amputations and the maintenance of a functional foot able with weight-bearing ability. Many professional figures, diabetologists, surgeons (both general and vascular and orthopedics), interventional radiologists, infectious diseases specialists, specialized nurses, podiatrists, orthotic technicians, are called to apply their knowledges to the diabetic patients affected by diabetic foot in a virtuous circle leading to reach the goals, with the imperative action of the multidisciplinary team. The so organized center will allow both a correct and rapid diagnosis, the use in ambulatorial environments of modern tools, or the hospitalization in multitasking wards, in which all the complications and the necessary treatments are possible, both in emergencies or in elective way, considering both revascularizations and surgery.

No abstract

Diabetic patients are at increased risk of developing foot ulcers which may cause bone infections associated with a high probability of both amputation and mortality. Therefore, prompt diagnosis and adequate treatment are of key importance. In our Diabetic Foot Unit, effective multidisciplinary treatment of osteomyelitis secondary to diabetes involves the application of a gentamicin-eluting calcium sulphate/hydroxyapatite bone graft substitute to fill residual bone voids after debridement. The data of all patients treated with the gentamicin-eluting calcium sulphate/hydroxyapatite bone graft substitute for diabetic foot infections with ulcer formation and osteomyelitis at metatarsals, calcaneus and hindfoot at our institute from July 2013 to September 2016 were retrospectively collected and evaluated. A total of 35 patients were included in this retrospective single-arm case series and were either continuously followed up for at least one year or until healing was confirmed. Nineteen lesions affected the distal row of tarsus/talus, ten the calcaneus and a further six were located at the metatarsals. While all of the metatarsal lesions had healed at 1-year follow-up, the healing rate in the hindfoot region was lower with 62.5% at the calcaneus and 72.2% at the distal tarsus and talus at 12 months, respectively. The overall cure rate for ulcerous bone infection was 81.3%. In two calcaneal lesions (25%) and two lesions of distal tarsus/talus (11.1%) amputation was considered clinically necessary. Promising results were achieved in the treatment of diabetic foot infections with soft tissue ulcers by a multidisciplinary approach involving extensive debridement followed by adequate dead space management with a resorbable gentamicin-eluting bone graft substitute.

This study is a retrospective epidemiological assessment of bacterial species isolated from a cohort of out-patients with diabetic foot infections referred to our “Diabetic Foot Unit” over one year, with particular attention to index pathogens, as identified by the EARS Network. Staphylococcus aureus and Pseudomonas aeruginosa accounted for 33.5% and 11.9% of cases, respectively. MRSA was isolated in 27.1% of patients, with 14.06% showing additional resistance to three antimicrobial classes. Pseudomonas aeruginosa presented extensive resistance to fluoroquinolones (57.3%), which was associated with resistance to piperacillin in 17.6% or to carbapenems in 23.5% of cases. Other pathogens, such as methicillin resistant Staphylococcus epidermidis, Escherichia coli and Morganella morganii ESBL and Enterococcus faecium VRE, were also found.

Introduction: Diabetes mellitus is characterised by a clearcut progression with time of carotid artery wall thickness and atherosclerosis show, its magnitude being attenuated by blood pressure lowering interactions including those based on the effect of ACE inhibition. Limited information is available on the effect of ACE inhibition on carotid thickening in diabetic patients with no other risk factors kept under effective strict metabolic control by treatment. Methods: This was a double blind study on 47 normotensive normolipaemic patients with a IDDM ( mean duration of disease 13±6 years, mean ±SD) who were studied if 1) there was no evidence of micro and macrovascular implications and 2) insulin treatment and clinical conditions were stable. Patients were randomised to Quinapril (Q, n=24) or placebo (P, n=23) and kept on treatment for 24 months. Intensive life style modifications were implemented in both groups by means of frequent visits (every 4 weeks). Measurements were made at randomisation as well as after 13 weeks and 24 months of treatment and consisted of carotid IMT by echo colour Doppler, office and 24 hour ambulatory blood pressure and lipid and glucose metabolic variables. Results: Age was similar in the Q and P groups (37.2±vs 35.8±6.8 years) which also showed no significant between group differences, as baseline office blood pressure (124±11/80±6 vs 123±13/ 77±8 mmHg) mean 24 hour blood pressure (127±9/78±8 vs 128±7/79±6 mmHg), serum total cholesterol (172±26 vs 183±34 mg/dl) and serum triglycerides (76±30 vs 80±63 mg/dl) values. Baseline glycated haemoglobin was not significantly different in the two groups (7.8±1.1 vs 7.8±1.1%), this being the case also for fasting blood glucose (158±51 vs 180± 68 mg/dl). Baseline IMT was 0.47± 0.10 mm in the placebo group and 0.46±0.16 in the Q group. Neither after 13 weeks nor after 2 years Q or P administration was associated with significant alterations in office or ambulatory blood pressure, lipid variables, fasting blood glucose and glycated haemoglobin. In the P group IMT remained unchanged both after 3 mouths and after 2 years (0.47±0.12 mm and 0.47 ±0.12 respectively) whereas in the Q group it showed a modest reduction (0.41±0.1 and 0.44 ±0.15mm) which was statistically significant only after 3 months (p<0.01). Conclusions: In uncomplicated, normotensive, normolipaemic patients with type I diabetes mellitus under effective glycaemic control, long term progression of carotid artery wall thickness can be prevented with only additional small benefit by ACE inhibition.