Infrared thermography and ulcer prevention in the high-risk diabetic foot: data from a single-blind multicentre controlled clinical trial.

AIM: To assess the usefulness of monthly thermography and standard foot care to reduce diabetic foot ulcer recurrence. METHODS: People with diabetes (n = 110), neuropathy and history of ≥ 1 foot ulcer participated in a single-blind multicentre clinical trial. Feet were imaged with a novel thermal imaging device (Diabetic Foot Ulcer Prevention System). Participants were randomized to intervention (active thermography + standard foot care) or control (blinded thermography + standard foot care) and were followed up monthly until ulcer recurrence or for 12 months. Foot thermograms of participants from the intervention group were assessed for hot spots (areas with temperature ≥ 2.2°C higher than the corresponding contralateral site) and acted upon as per local standards. RESULTS: After 12 months, 62% of participants were ulcer-free in the intervention group and 56% in the control group. The odds ratios of ulcer recurrence (intervention vs control) were 0.82 (95% CI 0.38, 1.8; P = 0.62) and 0.55 (95% CI 0.21, 1.4; P = 0.22) in univariate and multivariate logistic regression analyses, respectively. The hazard ratios for the time to ulcer recurrence (intervention vs control) were 0.84 (95% CI 0.45, 1.6; P = 0.58) and 0.67 (95% CI 0.34, 1.3; P = 0.24) in univariate and multivariate Cox regression analyses, respectively. CONCLUSIONS: Monthly intervention with thermal imaging did not result in a significant reduction in ulcer recurrence rate or increased ulcer-free survival in this cohort at high risk of foot ulcers. This trial has, however, informed the design of a refined study with longer follow-up and group stratification, further aiming to assess the efficacy of thermography to reduce ulcer recurrence.

Barriers to foot care in patients with diabetes as identified by healthcare professionals.

AIMS: To seek the views of healthcare professionals as to the barriers to foot care that they perceive as having an impact on clinical outcomes and contributing to the number of amputations. METHODS: The study involved healthcare professionals from the UK attending our 2015 and 2016 Masterclass diabetic foot conferences. Admission to these conferences was open to all members of the multidisciplinary spectrum who provide care of people with diabetes and foot problems. Attendees were asked to write down concerns that they considered to constitute barriers to foot care for people with diabetes. RESULTS: A total of 425 responses were received (90.8% of the total attendance at the 2015/2016 conferences). Analysis of the responses produced eight key subject areas in which barriers to care were identified: patient referrals, communication between disciplines, access to specialist services, patient care, funding, organization of care, education and infection. Within these key areas, respondents reported poor recognition and diagnosis of foot problems, lack of awareness of the need for referral both by the person with diabetes and healthcare professionals, difficulties in the referral pathway, lack of access to multidisciplinary care, shortage of resources and lack of education of both people with diabetes and healthcare professionals. The respondents identified these barriers as contributing to delay in people with diabetes receiving specialist help. Such a delay can lead to amputation. CONCLUSIONS: The crucial barrier to diabetic foot care is delay in accessing specialist care. Until this is addressed, care will be less than optimum and amputations will continue.

Acute Charcot neuro-osteoarthropathy.

Charcot neuro-osteoarthropathy (CN) is one of the most challenging foot complications in diabetes. Common predisposing and precipitating factors include neuropathy and increased mechanical forces, fracture and bone resorption, trauma and inflammation. In the last 15 years, considerable progress has been made in the early recognition of the acute Charcot foot when the X ray is still negative (stage 0 or incipient Charcot foot). Recent advances in imaging modalities have enabled the detection of initial signs of inflammation and underlying bone damage before overt bone and joint destruction has occurred. Casting therapy remains the mainstay of medical therapy of acute CN. If timely instituted, offloading can arrest disease activity and prevent foot deformity. In cases with severe deformity, modern surgical techniques can correct the unstable deformity for improved functional outcome and limb survival. Emerging new studies into the cellular mechanisms of severe bone destruction have furthered our understanding of the mechanisms of pathological bone and joint destruction in CN. It is hoped that these studies may provide a scientific basis for new interventions with biological agents.

Undiagnosed severe sleep apnoea and diabetic foot ulceration - a case series based hypothesis: a hitherto under emphasized factor in failure to heal.

BACKGROUND: Although great progress has been made in managing diabetic foot disease, it continues to carry significant morbidity and mortality. Obstructive sleep apnoea (OSA) and diabetes frequently coexist and recent studies suggest significant under-recognition of OSA in those with diabetes. There are no current reports on the direct clinical impact of OSA on acute or chronic diabetic foot ulcer healing. CASE REPORT: We describe three cases with Type 2 diabetes and a mean BMI of 50 kg/m(2) in whom we believe undiagnosed severe OSA may have impeded the rate of recovery of acutely infected foot ulcers. Despite standard care whilst in hospital with optimization of glycaemia, daily wound care, ulcer offloading techniques including casting, it was difficult to achieve satisfactory granulation in the first two cases with previously unrecognized and hence untreated severe OSA (Apnoea-Hypopnea Index > 30) until correction had been achieved through continuous positive airway pressure therapy (CPAP). In the third case, despite all optimization techniques, healing has not been achieved and individuals' reluctance to consider CPAP may be one possible factor. DISCUSSION: We observe in three severely obese individuals with diabetes that untreated severe OSA may have contributed to delayed wound healing. We also observed an improvement in two individuals after institution of CPAP therapy. Clinicians managing the diabetic foot should consider investigating the presence of OSA in non-healing or slowly progressive foot ulcers when all other factors have been fully optimized.

Inflammatory and bone turnover markers in a cross-sectional and prospective study of acute Charcot osteoarthropathy.

AIMS: To assess markers of inflammation and bone turnover at presentation and at resolution of Charcot osteoarthropathy. METHODS: We measured serum inflammatory and bone turnover markers in a cross-sectional study of 35 people with Charcot osteoarthropathy, together with 34 people with diabetes and 12 people without diabetes. In addition, a prospective study of the subjects with Charcot osteoarthropathy was conducted until clinical resolution. RESULTS: At presentation, C-reactive protein (P = 0.007), tumour necrosis factor-α (P = 0.010) and interleukin-6 (P = 0.002), but not interleukin-1ß, (P = 0.254) were significantly higher in people with Charcot osteoarthropathy than in people with and without diabetes. Serum C-terminal telopeptide (P = 0.004), bone alkaline phosphatase (P = 0.006) and osteoprotegerin (P < 0.001), but not tartrate-resistant acid phosphatase (P = 0.126) and soluble receptor activator of nuclear factor-κß ligand (P = 0.915), were significantly higher in people with Charcot osteoarthropathy than in people with and without diabetes. At follow-up it was found that tumour necrosis factor-α (P = 0.012) and interleukin-6 (P = 0.003), but not C-reactive protein (P = 0.101), interleukin-1ß (P = 0.457), C-terminal telopeptide (P = 0.743), bone alkaline phosphatase (P = 0.193), tartrate-resistant acid phosphatase (P = 0.856), osteoprotegerin (P = 0.372) or soluble receptor activator of nuclear factor-kß ligand (P = 0.889), had significantly decreased between presentation and the 3 months of casting therapy time point, and all analytes remained unchanged from 3 months of casting therapy until resolution. In people with Charcot osteoarthropathy, there was a positive correlation between interleukin-6 and C-terminal telopeptide (P = 0.028) and tumour necrosis factor-α and C-terminal telopeptide (P = 0.013) only at presentation. CONCLUSIONS: At the onset of acute Charcot foot, serum concentrations of tumour necrosis factor-α and interleukin-6 were elevated; however, there was a significant reduction in these markers at resolution and these markers may be useful in the assessment of disease activity.

Medical management of Charcot arthropathy.

Charcot arthropathy is a major complication of diabetes and it poses management challenges to health care professionals. Early diagnosis and timely intervention are essential for improved outlook of these patients. Casting therapy has been accepted as the mainstay treatment of the acute Charcot foot, although there are still controversies regarding its duration, the choice of removable and non-removable device and weight-bearing casts vs. non-weight-bearing casts. Two groups of antiresorptive therapies have been evaluated in the treatment of the acute Charcot foot, bisphosphonates (intravenous and oral) and calcitonin. These therapies have clearly shown a reduction of bone turnover, although, they have not shown a significant effect on temperature reduction. Current evidence to support their use is weak. An anabolic agent to speed up clinical resolution and fracture healing may be helpful and a clinical trial to evaluate the possible benefit of 1-84 recombinant human parathyroid hormone on fracture healing in the acute Charcot foot is in progress. This paper summarises the current approach to medical management of acute Charcot arthropathy with specific emphasis on casting and pharmacological therapy. Emerging new studies of the pathogenesis of this condition are also discussed.

Five-year follow-up of a cohort of people with their first diabetic foot ulcer: the persistent effect of depression on mortality.

AIMS/HYPOTHESIS: Depressive disorders are associated with mortality within 18 months of presentation of diabetic foot ulcers (DFU). The main aim of this study was to determine whether depressive disorder is still associated with increased mortality in people with their first foot ulcer at 5 years. METHODS: This is a 5-year follow-up of a cohort of 253 patients presenting with their first DFU. At baseline, the Schedules for Clinical Assessment in Neuropsychiatry (SCAN) 2.1 was used to define those who met DSM-IV (Diagnostic and Statistical Manual 4th edition) criteria for depressive disorder. Cox regression analysis controlled for potential covariates: age, sex, marital status, socioeconomic status, smoking, mean HbA(1c), diabetes complications and ulcer severity. The main outcome was mortality at 5 years. RESULTS: The prevalence of DSM-IV depressive disorder at baseline was 32.2% (n = 82). There were 92 (36.4%) deaths over the 5 years of follow-up. In the Cox regression (n = 246), after adjusting for covariates, baseline DSM-IV depressive disorder was significantly associated with a twofold increased risk of mortality for any depressive episode (HR 2.09, 95% CI 1.34, 3.25), minor (HR 1.93, 95% CI 1.00, 3.74) or major depressive disorders (HR 2.18, 95% CI 1.31, 3.65), compared with patients who were not depressed. CONCLUSIONS/INTERPRETATION: Depression is associated with a persistent twofold increased risk of mortality in people with their first DFU at 5 years.

Audit of acute Charcot's disease in the UK: the CDUK study.

AIMS/HYPOTHESIS: We studied factors associated with the development and resolution of acute Charcot foot using a web-based observational study. METHODS: Clinicians managing cases of acute Charcot foot in the UK and Ireland between June 2005 and February 2007 were invited to register anonymised details on a secure website. RESULTS: A total of 288 cases (age 57.0 ± 11.3 years [mean ± SD]; 71.2% male) were registered from 76 centres. Of these, 36% of patients recalled an episode of relevant trauma in the preceding 6 months, while 12% had had surgery to the affected foot. In 101 (35%) cases, ulceration was present at registration and 20% of these had osteomyelitis. Non-removable off-loading devices were used at presentation in 35.4% of cases, with removable off-loading used in 50%. Data on resolution were available for 219 patients. The median time to resolution was 9 months in patients whose initial management included the use of non-removable off-loading, compared with 12 months in the remainder (p = 0.001). Bisphosphonates were administered intravenously in 25.4% and orally in 19.4% of cases. The median time to resolution in patients who received bisphosphonates was 12 months and was longer than in those who did not (10 months, p = 0.005). CONCLUSIONS/INTERPRETATION: The median time to resolution was longer than in earlier series. Although limited by being observational and non-randomised, these data suggest that the use of non-removable off-loading at presentation may shorten the time to resolution. They provide no evidence to indicate that the use of bisphosphonates is beneficial.

Thiazolidinediones induce osteocyte apoptosis and increase sclerostin expression.

AIMS: Thiazolidinediones (TZDs) are associated with a higher risk of bone fracture in women compared with men. The aim of the present study was to investigate whether TZDs could influence osteocyte behaviour and contribute to the skeletal phenotype observed in TZD-treated patients. METHODS: The murine MLO-Y4 cell line was used as a source of osteocytes. These cells were cultured for 24 h with 0, 10(-8) m, 10(-7) m, 10(-6) m, 10(-5) m or 10(-4) m of pioglitazone, rosiglitazone or troglitazone in the presence or absence of 17beta-oestradiol. The extent of osteocyte apoptosis was assessed, as was the expression of the bone formation inhibitor sclerostin and receptor activator for nuclear factor kappaB ligand (RANKL) also. RESULTS: In the absence of 17beta-oestradiol, pioglitazone, rosiglitazone and troglitazone induced osteocyte apoptosis dose-dependently even at the lowest concentration of 10(-8) m. Furthermore, the expression of sclerostin but not RANKL was significantly increased in TZD-treated cultures compared with untreated cultures. The presence of 17beta-oestradiol significantly reduced TZD-induced osteocyte apoptosis and also sclerostin up-regulation. CONCLUSIONS: These findings therefore raise the potential concern of using TZDs in post-menopausal women where the lack of oestrogen would not prevent osteocyte apoptosis and sclerostin up-regulation and may aggravate the reduction in bone mass in these patients.

Role of neuropathy on fracture healing in Charcot neuro-osteoarthropathy.

Charcot neuro-osteoarthropathy (CNO) is a devastating condition affecting most commonly the foot/ankle joint in diabetic patients and may lead to severe deformities and amputation. Peripheral sensory neuropathy seems to be a pre-requisite to the development of CNO. The aim of this review article is to summarise the skeletal effects of the nervous system on bone remodelling and fracture healing of normal and damaged joints and to describe how neuropathy, in the context of modern concept of neuro-osteopathology, is crucial in the predisposition of the patient to develop acute CNO.

Day-case angioplasty in diabetic patients with critical ischemia.

AIM: Recent studies have shown that percutaneous transluminal angioplasty (PTA) can be safely performed as a day-case procedure. Many centers consider diabetes mellitus as a contraindication to day-case PTA. In this study, the safety and efficacy of 95 day-case PTA in 66 diabetic patients with critical leg ischemia (CLI) were evaluated. METHODS: Diabetic patients with CLI were assessed in a one-stop multidisciplinary outpatient clinic. Sixty-six outpatients with CLI deemed suitable for radiological intervention by non-invasive imaging (ultrasound angiology or magnetic resonance angiography) were scheduled for day-case PTA. RESULTS: PTA was initially successful in 63 out of 66 patients (95%). In 3 patients (5%), PTA was not possible because the lesion could not be balloon dilated or crossed with a guide wire. Clinically suspected first, second and third re-stenosis confirmed by non-invasive studies occurred in 20 out of 63 (31%), 7 out of 20 (35%) and 2 out of 7 (28%) patients, respectively. Following PTA, debridement was performed in 11 patients (17%), minor amputation in 8 (13%) and major amputation in 3 (5%). Relief of the primary symptom of rest pain or healing of ulcers was achieved in 23 out of 32 (72%) and 25 out of 27 (92.5%) patients, respectively. No peri-interventional morbidity or mortality was encountered. CONCLUSION: PTA is feasible and safe as a day-case procedure in diabetic patients with CLI. Re-stenosis can be managed by repeat day-case PTA.

Reliability of a novel thermal imaging system for temperature assessment of healthy feet.

BACKGROUND: Thermal imaging is a useful modality for identifying preulcerative lesions ("hot spots") in diabetic foot patients. Despite its recognised potential, at present, there is no readily available instrument for routine podiatric assessment of patients at risk. To address this need, a novel thermal imaging system was recently developed. This paper reports the reliability of this device for temperature assessment of healthy feet. METHODS: Plantar skin foot temperatures were measured with the novel thermal imaging device (Diabetic Foot Ulcer Prevention System (DFUPS), constructed by Photometrix Imaging Ltd) and also with a hand-held infrared spot thermometer (Thermofocus® 01500A3, Tecnimed, Italy) after 20 min of barefoot resting with legs supported and extended in 105 subjects (52 males and 53 females; age range 18 to 69 years) as part of a multicentre clinical trial. The temperature differences between the right and left foot at five regions of interest (ROIs), including 1st and 4th toes, 1st, 3rd and 5th metatarsal heads were calculated. The intra-instrument agreement (three repeated measures) and the inter-instrument agreement (hand-held thermometer and thermal imaging device) were quantified using intra-class correlation coefficients (ICCs) and the 95% confidence intervals (CI). RESULTS: Both devices showed almost perfect agreement in replication by instrument. The intra-instrument ICCs for the thermal imaging device at all five ROIs ranged from 0.95 to 0.97 and the intra-instrument ICCs for the hand-held-thermometer ranged from 0.94 to 0.97. There was substantial to perfect inter-instrument agreement between the hand-held thermometer and the thermal imaging device and the ICCs at all five ROIs ranged between 0.94 and 0.97. CONCLUSIONS: This study reports the performance of a novel thermal imaging device in the assessment of foot temperatures in healthy volunteers in comparison with a hand-held infrared thermometer. The newly developed thermal imaging device showed very good agreement in repeated temperature assessments at defined ROIs as well as substantial to perfect agreement in temperature assessment with the hand-held infrared thermometer. In addition to the reported non-inferior performance in temperature assessment, the thermal imaging device holds the potential to provide an instantaneous thermal image of all sites of the feet (plantar, dorsal, lateral and medial views). TRIAL REGISTRATION: Diabetic Foot Ulcer Prevention System NCT02317835, registered December 10, 2014.

Novel Semiquantitative Bone Marrow Oedema Score and Fracture Score for the Magnetic Resonance Imaging Assessment of the Active Charcot Foot in Diabetes.

There are no accepted methods to grade bone marrow oedema (BMO) and fracture on magnetic resonance imaging (MRI) scans in Charcot osteoarthropathy. The aim was to devise semiquantitative BMO and fracture scores on foot and ankle MRI scans in diabetic patients with active osteoarthropathy and to assess the agreement in using these scores. Three radiologists assessed 45 scans (Siemens Avanto 1.5T, dedicated foot and ankle coil) and scored independently twenty-two bones (proximal phalanges, medial and lateral sesamoids, metatarsals, tarsals, distal tibial plafond, and medial and lateral malleoli) for BMO (0-no oedema, 1-oedema < 50% of bone volume, and 2-oedema > 50% of bone volume) and fracture (0-no fracture, 1-fracture, and 2-collapse/fragmentation). Interobserver agreement and intraobserver agreement were measured using multilevel modelling and intraclass correlation (ICC). The interobserver agreement for the total BMO and fracture scores was very good (ICC = 0.83, 95% confidence intervals (CI) 0.76, 0.91) and good (ICC = 0.62; 95% CI 0.48, 0.76), respectively. The intraobserver agreement for the total BMO and fracture scores was good (ICC = 0.78, 95% CI 0.6, 0.95) and fair to moderate (ICC = 0.44; 95% CI 0.14, 0.74), respectively. The proposed BMO and fracture scores are reliable and can be used to grade the extent of bone damage in the active Charcot foot.

Increased Mortality in Diabetic Foot Ulcer Patients: The Significance of Ulcer Type.

Diabetic foot ulcer (DFU) patients have a greater than twofold increase in mortality compared with nonulcerated diabetic patients. We investigated (a) cause of death in DFU patients, (b) age at death, and (c) relationship between cause of death and ulcer type. This was an eleven-year retrospective study on DFU patients who attended King's College Hospital Foot Clinic and subsequently died. A control group of nonulcerated diabetic patients was matched for age and type of diabetes mellitus. The cause of death was identified from death certificates (DC) and postmortem (PM) examinations. There were 243 DFU patient deaths during this period. Ischaemic heart disease (IHD) was the major cause of death in 62.5% on PM compared to 45.7% on DC. Mean age at death from IHD on PM was 5 years lower in DFU patients compared to controls (68.2 ± 8.7 years versus 73.1 ± 8.0 years, P = 0.015). IHD as a cause of death at PM was significantly linked to neuropathic foot ulcers (OR 3.064, 95% CI 1.003-9.366, and P = 0.049). Conclusions. IHD is the major cause of premature mortality in DFU patients with the neuropathic foot ulcer patients being at a greater risk.

Medial localization of mineralization-regulating proteins in association with Mönckeberg's sclerosis: evidence for smooth muscle cell-mediated vascular calcification.

BACKGROUND: Calcification of the media of peripheral arteries is referred to as Mönckeberg's sclerosis (MS) and occurs commonly in aged and diabetic individuals. Its pathogenesis is unknown, but its presence predicts risk of cardiovascular events and leg amputation in diabetic patients. Several studies have documented expression of bone-associated genes in association with intimal atherosclerotic calcification, leading to the suggestion that vascular calcification may be a regulated process with similarities to developmental osteogenesis. Therefore, we examined gene expression in vessels with MS to determine whether there was evidence for a regulated calcification process in the vessel media. METHODS AND RESULTS: In situ hybridization, immunohistochemistry, and semiquantitative reverse-transcription polymerase chain reaction were used to examine the expression of mineralization-regulating proteins in human peripheral arteries with and without MS. MS occurred in direct apposition to medial vascular smooth muscle cells (VSMCs) in the absence of macrophages or lipid. These VSMCs expressed the smooth muscle-specific gene SM22alpha and high levels of matrix Gla protein but little osteopontin mRNA. Compared with normal vessels, vessels with MS globally expressed lower levels of matrix Gla protein and osteonectin, whereas alkaline phosphatase, bone sialoprotein, bone Gla protein, and collagen II, all indicators of osteogenesis/chondrogenesis, were upregulated. Furthermore, VSMCs derived from MS lesions exhibited osteoblastic properties and mineralized in vitro. CONCLUSIONS: These data indicate that medial calcification in MS lesions is an active process potentially orchestrated by phenotypically modified VSMCs.

Lower limb venous pressure in diabetic neuropathy.

OBJECTIVE: Distended turgid veins have been noted in the feet of patients with diabetic neuropathy. This study assessed the supine venous pressure and its correlation with diabetic neuropathy and arteriovenous (AV) shunting in the feet of type I and type II diabetic subjects. RESEARCH DESIGN AND METHODS: Seventeen patients with chronic Charcot joints, 11 patients with a history of neuropathic foot ulceration, 14 diabetic control subjects, and 11 normal control subjects were studied. Neuropathy was assessed by vibration and thermal thresholds and standard cardiovascular autonomic neuropathy tests. Supine venous pressure was measured by insertion of a 21-gauge needle connected to a strain gauge manometer into the veins on the dorsum of the foot. Venous PO2 was used as a measure of AV shunting. RESULTS: Venous pressure was raised in the group with chronic Charcot joints (18.9 +/- 4.2 mmHg, P < 0.001 vs. the diabetic control group [11.3 +/- 2.6 mmHg]), the normal control group (12.3 +/- 2.3 mmHg, mean +/- SD), and the diabetic group with a history of neuropathic foot ulceration (16.0 +/- 3.7 mmHg, P = 0.008 vs. diabetic control subjects and P = 0.04 vs. normal control subjects), with a maximum of 28 mmHg. Venous pressure was correlated with heart rate variation to deep breathing, r = -0.61 (P = 0.001), vibration threshold, r = 0.56 (P = 0.001), Valsalva ratio, r = -0.64 (P -= 0.001), warm threshold, r = 0.69 (P = 0.001), and venous PO2, r = 0.43 (P = 0.02). There was no correlation with skin temperature, duration of diabetes, age, HbA1c, random blood glucose, ankle/brachial Doppler index, height, or serum creatinine. CONCLUSIONS: Venous pressure is much higher in the neuropathic diabetic limb and is correlated with the severity of neuropathy and with AV shunting.

Plantar pressures are elevated in the neuroischemic and the neuropathic diabetic foot.

OBJECTIVE: Clinical observation has noted that diabetic neuropathic ulcers occur frequently on the plantar surface, whereas neuroischemic ulcers seem to occur often on the foot margins. The reason for this difference in the site of ulceration is unknown, but it may be related to differences in pressure loading. The aim of the study was to compare vertical in-shoe foot pressures measured during walking (using the F-SCAN system) in four groups of patients whose degree of neuropathy was measured by vibration perception threshold (VPT). RESEARCH DESIGN AND METHODS: Subjects included 14 neuroischemic diabetic patients (VPT 29.3 +/- 13.5 V) with history of ulceration on the margins of the foot, 18 patients with neuropathy alone (VPT 38.7 +/- 12.7 V) and previous history of ulceration on the plantar surface, 10 diabetic control patients (VPT 9.9 +/- 2.7 V), and 15 nondiabetic control subjects (VPT 7.0 +/- 0.5 V). RESULTS: When compared with the other three groups, neuroischemic patients had higher foot pressures when measured as mean peak pressures and highest peak pressures under four areas of the foot: medial and lateral forefoot, hallux, and heel. Furthermore, when measuring the maximum pressures developed at any point under the plantar surface, the neuroischemic patients also had the most elevated pressures (757.6 +/- 135.9 kPa), significantly higher than those found in the neuropathic group (482.8 +/- 68.6 kPa, P = 0.04) and in both diabetic control patients (310.2 +/- 34.7 kPa, P = 0.008) and nondiabetic controls subjects (365.1 +/- 49.8 kPa, P = 0.007). CONCLUSIONS: Despite having increased plantar pressures and a comparable degree of neuropatny, the neuroischemic patients did not have a history of ulceration on the plantar surface. These observations may have relevance to different mechanisms of ulcer formation in the neuroischemic and neuropathic foot.

Is neuropathic ulceration the key to understanding increased mortality due to ischaemic heart disease in diabetic foot ulcer patients? A population approach using a proportionate model.

Ischaemic heart disease (IHD) is the commonest cause of death in diabetic foot ulcer patients and non-ulcerated diabetic patients, yet the mortality rate of diabetic foot ulcer patients is over twice that of non-ulcerated patients. As the cause of this increased mortality is not understood, we plotted the ratio of deaths due to ischaemic heart disease (IHDn) to other causes of death (i.e. IHDn:OCDn) against age for 242 diabetic foot ulcer patients and 121 controls (non-ulcerated diabetic patients). The IHDn:OCDn ratio rose above 1.0 from age 40 years onwards for diabetic foot ulcer patients, but from age 70 years onwards for controls, demonstrating differentially increased mortalities due to IHD. A population model involving summation of IHDn:OCDn ratios for neuropathic and neuroischaemic diabetic foot ulcer patients calculated an overall increased mortality rate of 1.8 compared with that of non-ulcerated diabetics. The model predicted that a 25% reduction in neuropathic diabetic foot ulcer patients dying from IHD would eliminate the increased mortality, demonstrating that neuropathic rather than ischaemic ulceration defines the cause of increased mortality among diabetic foot ulcer patients.

Pathology of the Diabetic Foot.

The diabetic foot can be divided into two entities - the neuropathic foot and the neuro-ischaemic foot. It is essential to differentiate between the two, because each has characteristic complications including different types of ulcer, which require distinct therapeutic strategies.

Comparing two dressings in the treatment of diabetic foot ulcers.

A report of a study that compared a polyurethane foam dressing with an alginate dressing for foot ulcers in patients with diabetes.