Charcot neuroarthropathy is a rare but serious complication of diabetes, causing progressive destruction of the bones and joints of the foot leading to deformity, altered biomechanics and an increased risk of ulceration. Management is complicated by a lack of consensus on diagnostic criteria and an incomplete understanding of the pathogenesis. In this review, we consider recent insights into the development of Charcot neuroarthropathy. It is likely to be dependent on several interrelated factors which may include a genetic pre-disposition in combination with diabetic neuropathy. This leads to decreased neuropeptides (nitric oxide and calcitonin gene-related peptide), which may affect the normal coupling of bone formation and resorption, and increased levels of Receptor activator of nuclear factor kappa-B ligand, potentiating osteoclastogenesis. Repetitive unrecognized trauma due to neuropathy increases levels of pro-inflammatory cytokines (interleukin-1β, interleukin-6, tumour necrosis factor α) which could also contribute to increased bone resorption, in combination with a pre-inflammatory state, with increased autoimmune reactivity and a profile of monocytes primed to transform into osteoclasts - cluster of differentiation 14 (CD14). Increased blood glucose and loss of circulating Receptor for Advanced Glycation End-Products (AGLEPs), leading to increased non-enzymatic glycation of collagen and accumulation of AGLEPs in the tissues of the foot, may also contribute to the pathological process. An understanding of the relative contributions of each of these mechanisms and a final common pathway for the development of Charcot neuroarthropathy are still lacking. Cite this article: S. E. Johnson-Lynn, A. W. McCaskie, A. P. Coll, A. H. N. Robinson. Neuroarthropathy in diabetes: pathogenesis of Charcot arthropathy. Bone Joint Res 2018;7:373–378. DOI: 10.1302/2046-3758.75.BJR-2017-0334.R1

Aim. Forefoot ulcers in patients with diabetic neuropathy are a result of factors that result in increased forefoot plantar pressures. Progressive hindfoot equinus from contraction of gastrocnemius-soleus-tendo-Achilles complex and progressive plantar flexed metatarsal heads secondary to claw toe deformity results callus at the metatarsal heads which break down to ulceration. The aim is to describe 2-stage treatment pathway for managing these ulcers. Methods. Consecutive patients, who presented with forefoot ulcers since February 2019 were treated with a 2-stage treatment pathway. The first stage of this is an out-patient tendo-Achilles lengthening (TAL). The second stage is surgical proximal dorsal closing wedge metatarsal osteotomy for patients with persistent or recurrent ulcers. Patients were followed for a minimum of 12 months. Results. 112 patients (146 feet) underwent TAL by 3 consultants. Of these, 96 patients were followed for a minimum of 12 months (range 12–36 months). None had infection or wound related problems at the tenotomy sites; complete transection of the tendon was noted in 4 patients (4%) and one-patient developed heel callosity suggestive of over-lengthening. In 92 patients (96%), the ulcers healed within 10 weeks (± 4 weeks). Additional z-lengthening of peroneal longus and tibialis posterior tendons helped in patients with 1. st. metatarsal and 5. th. metatarsal head ulcers respectively. In 12 patients (10%), the ulcer failed to heal or recurred. MRI scan in these patients showed plantar flexed metatarsals from progressive claw toe deformity. The ulcer in this group healed after surgical offloading with proximal dorsal closing wedge osteotomy of the metatarsal/s, with no recurrence at a minimum 12months of follow-up. Conclusion. The described 2-stage treatment pathway results in long-term healing of neuropathic forefoot ulcers, and in 96% of patients, the ulcer healed after the first stage out-patient percutaneous TAL

Diabetes is a poor prognostic indicator after an ankle fracture. Many surgeons avoid operating due to concerns regarding complications. We performed a retrospective analysis of complication rates for acute ankle fractures in diabetics with a control non-diabetic patient treated by all surgeons in our unit and assessed factors for success including long-segment fixation. Patient records were cross-referenced with departmental databases and a review of all ankle fractures managed in our department was conducted from 2012. All patients subjected to a retrospective-review of their follow-up for at least 6-months. Radiographs were assessed of the ankle before and at completion of treatment being reviewed independently (RA & FR). We identified the HB1Ac (diabetic-control) and systematic co-morbidities. Fractures were classified into unimalleolar, bi malleolar and trimalleolar and surgery grouped into standard or long-segment-rigid fixation. Statistical analysis was conducted using absolute/relative risk (RR); numbers needed to treat (NNT) were calculated. We compared a control-group, a diabetic group managed conservatively, and undergoing surgery; comparing the concept of rigid fixation and prolonged imobilisation in isolation or combined. Further sub-analysis conducted assessing diabetic neuropathy, retinopathy and nephropathy. Ethics approval was granted as per our institutional policy by our governance lead. We identified 154 diabetic ankle fractures, seventy-six had conservative-treatment; 78 had operative fixation of which 23 had rigid-long-segment-fixation. The diabetic-groups had a higher risk-relative-risk of complication − 3.2 (P< 0.03) being linked to systematic complications of diabetes e.g. neuropathy 5.8 (P< 0.003); HBA1c 4.6 P< 0.004); and neuropathy or retinopathy 6.2 (P< 0.0003). Relative-risk reduction of complications occurred following surgery with prolonged immobilization (0.86) and rigid-fixation (0.65). The Number-Needed-to-Treat required to see a benefit from rigid fixation was 7. Diabetics have a higher risk for complications, however the risk is not as great as previously reported. We provide evidence of rigid-long-segment-fixation with prolonged-immobilization improving-outcomes

In developed nations Charcot arthropathy is most commonly caused by diabetes mellitus. Worldwide, leprosy remains the primary cause. All evidence points to a relationship between neurologic loss, continued loading activities and the development of unrecognized bone fragmentation. In type 2 diabetes, dysregulation of leptin biology causes bone loss and may be an important factor in precipitating Charcot events. Bone density studies show massive loss of bone in patients with ankle and hindfoot Charcot problems, but not midfoot problems. This suggests a different mechanism for collapse. Stable collapse with ulcer development in the midfoot can be treated with exostectomy. Realignment and fusion remain the mainstays of treatment for diabetic Charcot neuropathy, especially in the ankle and hindfoot. Bone mineralization deficiencies require special consideration of fixation techniques. Thin wire external fixation – either as primary fixation or to reinforce/neutralize other methods can be very helpful. Large bridging screws and carefully selected bridging plates are frequently also valuable to consider. Excessive immobilization periods (often double the normal amount of time) are generally required. The goal may be limited to a braceable, plantigrade foot

Aims

Calcaneal osteomyelitis remains a difficult condition to treat with high rates of recurrence and below-knee amputation, particularly in the presence of severe soft-tissue destruction. This study assesses the outcomes of single-stage orthoplastic surgical treatment of calcaneal osteomyelitis with large soft-tissue defects.

Charcot neuro-osteoarthropathy (CN) of the midfoot presents a major reconstructive challenge for the foot and ankle surgeon. The Synthes 6 mm Midfoot Fusion Bolt is both designed and recommended for patients who have a deformity of the medial column of the foot due to CN. We present the results from the first nine patients (ten feet) on which we attempted to perform fusion of the medial column using this bolt. Six feet had concurrent hindfoot fusion using a retrograde nail. Satisfactory correction of deformity of the medial column was achieved in all patients. The mean correction of calcaneal pitch was from 6° (-15° to +18°) pre-operatively to 16° (7° to 23°) post-operatively; the mean Meary angle from 26° (3° to 46°) to 1° (1° to 2°); and the mean talometatarsal angle on dorsoplantar radiographs from 27° (1° to 48°) to 1° (1° to 3°).

However, in all but two feet, at least one joint failed to fuse. The bolt migrated in six feet, all of which showed progressive radiographic osteolysis, which was considered to indicate loosening. Four of these feet have undergone a revision procedure, with good radiological evidence of fusion. The medial column bolt provided satisfactory correction of the deformity but failed to provide adequate fixation for fusion in CN deformities in the foot.

In its present form, we cannot recommend the routine use of this bolt.

Cite this article: Bone Joint J 2015; 97-B:809–13

We studied a cohort of 26 diabetic patients with chronic ulceration under the first metatarsal head treated by a modified Jones extensor hallucis longus and a flexor hallucis longus transfer. If the first metatarsal was still plantar flexed following these two transfers, a peroneus longus to the peroneus brevis tendon transfer was also performed. Finally, if ankle dorsiflexion was < 5° with the knee extended, a Strayer-type gastrocnemius recession was performed.

The mean duration of chronic ulceration despite a minimum of six months’ conservative care was 16.2 months (6 to 31). A total of 23 of the 26 patients were available for follow-up at a mean of 39.6 months (12 to 61) after surgery. All except one achieved complete ulcer healing at a mean of 4.4 weeks (2 to 8) after surgery, and there was no recurrence of ulceration under the first metatarsal.

We believe that tendon balancing using modified Jones extensor hallucis longus and flexor hallucis longus transfers, associated in selected cases with a peroneus longus to brevis transfer and/or Strayer procedure, can promote rapid and sustained healing of chronic diabetic ulcers under the first metatarsal head.

We compared the clinical and radiographic results of total ankle replacement (TAR) performed in non-diabetic and diabetic patients. We identified 173 patients who underwent unilateral TAR between 2004 and 2011 with a minimum of two years’ follow-up. There were 88 male (50.9%) and 85 female (49.1%) patients with a mean age of 66 years (sd 7.9, 43 to 84). There were 43 diabetic patients, including 25 with controlled diabetes and 18 with uncontrolled diabetes, and 130 non-diabetic patients. The clinical data which were analysed included the Ankle Osteoarthritis Scale (AOS) and the American Orthopaedic Foot and Ankle Society (AOFAS) scores, as well the incidence of peri-operative complications.

The mean AOS and AOFAS scores were significantly better in the non-diabetic group (p = 0.018 and p = 0.038, respectively). In all, nine TARs (21%) in the diabetic group had clinical failure at a mean follow-up of five years (24 to 109), which was significantly higher than the rate of failure of 15 (11.6%) in the non-diabetic group (p = 0.004). The uncontrolled diabetic subgroup had a significantly poorer outcome than the non-diabetic group (p = 0.02), and a higher rate of delayed wound healing.

The incidence of early-onset osteolysis was higher in the diabetic group than in the non-diabetic group (p = 0.02). These results suggest that diabetes mellitus, especially with poor glycaemic control, negatively affects the short- to mid-term outcome after TAR.

Cite this article: Bone Joint J 2014;96-B:1674–80.

It is difficult to determine the safe timing of weight-bearing or reconstructive surgery in patients with Charcot arthropathy of the foot and ankle. In this study the Doppler spectrum of the first dorsal metatarsal artery was used to monitor the activity of the disease activity and served as a guideline for management. A total of 15 patients (seven men and eight women) with acute diabetic Charcot arthropathy of the foot and ankle were immobilised in a non-weight-bearing cast. They were followed at two-week intervals and bilateral Doppler spectra of the first dorsal metatarsal arteries were obtained using a 10 MHz linear ultrasound probe. The patients were allowed to start weight-bearing or undergo surgery after the Doppler spectrum had returned to normal pattern. The Doppler spectra in the unaffected limbs were triphasic in pattern, whereas those in limbs with active Charcot arthropathy showed monophasic forward flow. They returned to normal after a mean of 13.6 weeks (6 to 20) of immobilisation. Three patients underwent pan-talar arthrodesis to correct gross instability and deformity.

Doppler spectrum analysis of the foot may reflect the activity of the disease in patients with Charcot arthropathy, and may be used as a guide to begin weight-bearing or undergo reconstructive surgery.

We present the results of ankle fusion using the Ilizarov technique for bone loss around the ankle in 20 patients. All except one had sustained post-traumatic bone loss. Infection was present in 17. The mean age was 33.1 years (7 to 71). The mean size of the defect was 3.98 cm (1.5 to 12) and associated limb shortening before the index procedure varied from 1 cm to 5 cm. The mean time in the external fixator was 335 days (42 to 870). Tibiotalar fusion was performed in 19 patients and tibiocalcaneal fusion in one. Associated problems included diabetes in one patient, pelvic and urethral injury in one, visual injury in one patient and ipsilateral tibial fracture in five. At the final mean follow-up of 51.55 months (24 to 121) fusion had been achieved in 19 of 20 patients. A total of 16 patients were able to return to work. The results were graded as good in 11 patients, fair in six and poor in three. The mean external fixation index was 8.8 days/mm (0 to 30). One patient with diabetes developed severe infection which required early removal of the fixator. Refractures occurred in three patients, two of which were at the site of fusion and one at a previous tibial shaft fracture site. Equinus deformity of the ankle fusion occurred after a further fracture in one patient. There were two patients with residual forefoot equinus, and one developed late valgus at the fusion site.

Poor consolidation of the regenerated bone in two patients was treated by bone grafting in one and by bone and fibular strut grafting in the other. Residual soft-tissue infection was still present in two patients.