Assessing outcome of diabetic foot ulcers and multidisciplinary foot clinic.

Foot problem has been increasingly recognised as a major complication of diabetes, which is associated with a very high mortality and morbidity. Therefore Multi-Disciplinary Foot Clinics (MDFC) have been established all over the world to provide holistic care to these patients. There is a wide variation in the availability of a range of professional skills in the MDFC in different health economy. Therefore the care provided by these MDFC can vary from one place to other. It is very important to measure the outcome of these MDFC so that patients, regulatory authorities and funding bodies can compare them. Traditionally ulcer related outcomes such as the healing rate and the proportion of ulcers healed have been measured in many foot ulcer studies. Similarly the amputation rate is measured to determine the efficacy of diabetic foot management in an area of the health economy. However, these measures do not take into account other important factors such as the functional ability and the quality of life of patients. Therefore patient related outcomes such as the recurrence of ulcer, number of working days lost, the mobility of patient following treatment, survival following first episode of ulceration etc also needs to be measured, which are very important from the patient's perspective. This review looks into various patient related outcomes that can and should be measured to assess the quality of care provided by the MDFC.

Conservative management of diabetic foot osteomyelitis.

In this retrospective study, 130 patients with diabetic foot osteomyelitis were analysed. 66.9% of these healed with antibiotic treatment alone and 13.9% needed amputation, of which 1.5% were major. Presence of MRSA was associated with adverse outcome (53.3% vs 21.1%, p=0.04) which was defined as death, amputation and failure to heal.

Insensate foot of diabetic foot ulcer can have underlying silent neuropathic pain.

Subjects with diabetic foot ulcer (DFU) are believed to be less likely to complain of symptoms of painful diabetic peripheral neuropathy (PDPN). When we assessed this using Leeds Assessment of Neuropathic Symptoms and Signs questionnaire (s-LANSS) we found that out of total 44 subjects with DFU, 19 (43·2%) had possible neuropathic discomfort. s-LANSS score was significantly higher in DFU group (8·1 ± 7·7 versus 4·7 ± 4·6; P = 0·04). However, there was no difference in the perception of pain in 10-point Likert scale (3·9 ± 3·6 versus 3·3 ± 3·0; P = NS) between these two groups. This study suggests that subjects with DFU may suffer from PDPN, but do not perceive it. Further studies are needed to assess if treatment of PDPN in these subjects is beneficial.

Sural nerve pathology in diabetic patients with minimal but progressive neuropathy.

AIMS/HYPOTHESIS: The early pathological features of human diabetic neuropathy are not clearly defined. Therefore we quantified nerve fibre and microvascular pathology in sural nerve biopsies from diabetic patients with minimal neuropathy. METHODS: Twelve diabetic patients underwent detailed assessment of neuropathy and fascicular sural nerve biopsy at baseline, with repeat assessment of neuropathy 8.7+/-0.6 years later. RESULTS: At baseline, neuropathic symptoms, neurological deficits, quantitative sensory testing, cardiac autonomic function and peripheral nerve electrophysiology showed minimal abnormality, which deteriorated at follow-up. Myelinated fibre density, fibre and axonal area, and g-ratio were normal but teased fibre studies showed paranodal abnormalities (p<0.001), segmental demyelination (p<0.01) and remyelination (p<0.01) without axonal degeneration. Unassociated Schwann cell profile density (p<0.04) and unmyelinated axon density (p<0.001) were increased and axon diameter was decreased (p<0.007). Endoneurial capillaries demonstrated basement membrane thickening (p<0.006), endothelial cell hyperplasia (p<0.004) and a reduction in luminal area (p<0.007). CONCLUSIONS/INTERPRETATION: The early pathological features of human diabetic neuropathy include an abnormality of the myelinated fibre Schwann cell and unmyelinated fibre degeneration with regeneration. These changes are accompanied by a significant endoneurial microangiopathy.

Charcot neuroarthropathy in diabetes mellitus.

Charcot neuroarthropathy has been recognised for over 130 years and yet it remains a major cause of morbidity for patients with diabetes mellitus and a continuing challenge for physicians. It is rare but it seems to be increasing in prevalence and this provides hope that with larger studies it will soon be possible to clarify the natural history and optimal treatment regimens. The underlying cause is thought to be trauma in a neuropathic foot that leads to a complex series of pathological processes culminating in bone and joint destruction and subsequent deformity. The acute reaction is often misdiagnosed and many patients present late with established deformity. Even when the diagnosis is considered at an early stage there are no definitive criteria or tests to confirm charcot neuroarthropathy and a high index of suspicion is necessary in any diabetic patient with a swollen warm foot in the presence of somatic or autonomic neuropathy. Treatment has traditionally involved the use of various methods to avoid weight bearing but recent work has begun to suggest that bisphosphonates might be able to arrest the acute process. In the long term, treatment involves a multidisciplinary approach aimed at providing appropriate footwear to reduce plantar pressures and avoid foot ulceration; in some circumstances this involves surgical correction of deformities before adequate footwear can be supplied. Further studies of the emerging treatments for Charcot neuroarthropathy are needed to provide long-term outcome data on morbidity and deformity.

Spinal-cord involvement in diabetic peripheral neuropathy.

The pathogenesis of diabetic distal symmetrical polyneuropathy (DSP) is poorly understood but there is some evidence that the disease process might extend beyond peripheral nerves. We used magnetic-resonance imaging to measure spinal-cord cross-sectional area in diabetic patients with and without DSP and in healthy controls. There were significant differences in cord area between the groups at C4/5 and T3/4 (p=0.004 and p=0.033, respectively), with a smaller cord area in those with DSP compared with controls (p=0.001 and p=0.016 for C4/5 and T3/4, respectively). These results indicate that DSP is not simply a disease of the peripheral nerve and that there is substantial involvement of the spinal cord.

'Sausage toe': a reliable sign of underlying osteomyelitis.

AIMS: To follow-up patients with a 'sausage' deformity of the toe associated with local neuropathic ulceration to confirm the diagnosis of underlying osteomyelitis. This was based on our observation that some diabetic patients with suspected pedal osteomyelitis with a local neuropathic ulcer have a 'sausage' deformity of a toe. METHODS: Over a period of 2 years, 14 patients with foot ulcers, who were observed to have the 'sausage' deformity of a toe in the diabetic foot clinic were followed up and investigated. RESULTS: Underlying osteomyelitis was confirmed in six on the very first X-ray examination. A further seven had osteomyelitis diagnosed on bone scanning. Both the X-ray and the bone scan were equivocal in one patient, whose ulcer only healed after an 8-week course of antibiotics. Antibiotic therapy was successful in 11 patients and three patients required amputation of the affected toe. Following successful treatment, there was full resolution of the 'sausage toe' in the majority. CONCLUSIONS: The appearance of a 'sausage toe' should alert the physician of the possibility of underlying osteomyelitis in diabetic foot, so that prompt treatment can be commenced with antibiotics.

Diabetic neuropathic pain in a leg amputated 44 years previously.

The mechanism of neuropathic pain in the diabetic limb is far from clear. Phantom limb pain likewise is of obscure aetiology. The development of typical pain in an absent leg in a patient with diabetes many years after the amputation stimulates thought as to the mechanism, not only of neuropathic pain, but also of phantom limb pain. A 58-year-old man was diagnosed with type 2 diabetes 44 years after having undergone left below knee amputation for congenital AV malformation, at the age of 13. Eight months before the diagnosis of diabetes he began to complain of pain in the leg on the amputated side-pain very similar to that described in typical diabetic neuropathy. This was followed by similar pain in the right leg. MR scan of the spine revealed a small syringohydromyelia of the thoracic cord in addition to a prolapse of disc at L(5)/S(1) level on the left side, which was first noted 5 years previously. There were no other features of S(1) compression. The typical neuropathic character of the pain involving both the amputated and the intact limbs that developed with the diagnosis of type 2 diabetes suggest that the neuropathic pain may originate from centres higher than peripheral nerves.

Early identification of diabetic foot ulcers that may require intervention using the micro lightguide spectrophotometer.

OBJECTIVE: Adequate tissue oxygenation is known to be essential for the healing of diabetic foot ulcers, but hypoxia has also been shown to be a potent stimulus for growth. There are no studies looking specifically at ulcer oxygen levels during the healing process. We measured the serial microvascular oxygen saturation (SaO2) of the foot ulcer, the ulcer margin, and a control site using the Erlangen micro lightguide spectrophotometer (EMPHO II; Bodenseewerk Geratetechnik, Erlangen, Germany) to study serial changes during healing. RESEARCH AND DESIGN METHODS: Studied over 9 months were 14 patients with neuropathy with a total of 24 foot ulcer sites. Of these patients, four (seven ulcers) had significant ischemia as determined by the ankle-brachial pressure index (ABPI) and transcutaneous oxygen tension. RESULTS: Of 21 ulcer sites with serial measurements, only 13 ulcers healed. In those ulcers, a significant reduction (P<0.05) in SaO2 occurred with healing. SaO2 dropped from 58% at initial presentation (mean area 2.6 cm2) to 47% at midsize (mean area 1.2 cm2 at 5.2 weeks) and finally reduced to 45% just before it healed. Similar trends were also seen around the margin of the ulcers (initial 49%, midsize 45%, and final 41%; P = 0.1). However, there were no such changes on the control sites (43, 40, and 40%; P = 0.5) or within the eight ulcers that did not heal (46, 42, and 53%; P = 0.2). CONCLUSIONS: Serial microvascular oxygen measurements may be used to identify at an early stage those ulcers that are unlikely to heal and, therefore, need surgical intervention.

Digital imaging: an accurate and easy method of measuring foot ulcers.

AIMS: A progressive reduction in the area of foot ulcer on serial measurement is traditionally done by tracing the margin of the ulcer on a transparent film and counting the number of squares on a graph paper underneath. We set out to use and validate the measurement of foot ulcers using a digital imaging technique and compare this with the traditional method. METHODS: Thirty diabetic foot ulcers (18 patients) were studied over 10 weeks. Each ulcer was traced by three independent observers with a pen over a flexigrid Opsite film and digital photographs were taken. Each observer calculated the area of an ulcer first using a 1-mm2 graph paper and then with the computer software. For each ulcer we calculated the mean area using measurements from all the observers. We then calculated the deviation from this mean for each observer. RESULTS: There was significantly less interobserver variation using the digital image than the traditional method with mean coefficient of variation (CV) 16% vs. 27%; P = 0.05. CONCLUSIONS: The digital imaging method was faster and easier to use and the patients preferred it, as it was a noncontact method. In addition it also provides a photographic record for comparison.

Unusual infections in diabetes.

Infection with rare organisms or at unusual sites occur more frequently in people with diabetes. If not recognised and treated promptly, morbidity and mortality are high in such cases. Here we report cases of necrotising fascitis, malignant otitis externa, Fournier's gangrene and psoas abscess occurring in diabetics that needed intensive treatment with antibiotics, surgical debridement and insulin. Literature reviews suggest that cellular defence mechanisms may be impaired in people with diabetes.

Central pontine myelinolysis and ataxia: an unusual manifestation of hypoglycaemia.

Hypoglycaemia is common in people with diabetes who aim to achieve good blood glucose control. Severe hypoglycaemia presents with evidence of neurological dysfunction, such as inability to concentrate, confusion, seizures, and coma. Such disturbances are reversible on correction of the hypoglycaemia. Infrequently there may be a focal neurological deficit and we report one such case presenting with cerebellar symptoms following an episode of severe hypoglycaemia. A magnetic resonance scan showed features consistent with the presence of central pontine myelinolysis. The symptoms resolved within a few months with only minimal residual neurological deficit.