Diabetic foot ulcers

Introduction

Diabetes is increasingly common, and is associated with significant patient morbidity, mortality and high socioeconomic costs (Table I). Due to the increasing prevalence of diabetes, almost all clinicians will treat patients who suffer from it, or will treat a direct complication of diabetes. One of the most serious complications affecting orthopaedic surgeons is the diabetic foot ulcer (DFU). The aim of this review is to update clinicians on the optimal management of the DFU.

Aetiology of DFU

Diabetes is a metabolic disease characterised by hyperglycaemia as a result of defects in insulin secretion or action. In the long-term this leads to damage and dysfunction of organs, specifically the eyes, kidneys, heart, nerves and blood vessels.⁴ A break in the skin on the foot in the presence of diabetes is known as a diabetic foot ulcer (DFU), and is the leading cause of hospitalisation in patients with diabetes (Fig. 1).^5,6

Fig. 1

Necrotic diabetic foot ulcer of calcaneum.

There are multiple risk factors for the development of a DFU (Table II).⁵ The most common reasons are related to neuropathy, vasculopathy or a combination of both.^7-9 The vast majority of DFU seen in clinics or presenting as emergencies have combined pathology, and only 10% of DFU are due to isolated vasculopathy or peripheral vascular disease (PVD).¹⁰

Neuropathy

Diabetes is thought to cause damage to the vasa nervorum resulting in an ischaemic insult and a progressive irreversible sensory, motor and autonomic neuropathy. Most presentations of sensory neuropathy are insidious until the onset of complications. The sensory deficit usually occurs below the knee, is denser distally and is bilateral. Sensory deficit results in numbness of the feet with burning, pain or paraesthesia being less common.⁹ Autonomic neuropathy leads to stiff, dry and scaly skin, which may crack due to loss of normal skin flexibility, predisposing to softtissue infection. Motor neuropathy is rarer, but in the feet usually affects the intrinsic and extrinsic muscle balance giving claw or hammer toes. These lesser toe deformities can cause pressure points and subsequent ulceration. Motor neuropathy can also present as isolated mononeuritis. This usually affects the peroneal nerve and results in foot drop. Sensory and autonomic neuropathy leads to high foot pressures, foot deformities, and gait instability which leads to increased plantar pressures and the subsequent risk of developing ulcers.^11-13

Vasculopathy

Arteriosclerosis is more common, more aggressive and more diffuse than in non-diabetics. The vasculopathy in diabetic patients affects the large and small arteries as well as the microcirculation, with more diffuse circumferential lesions that are harder to treat in isolation. This is significant in the foot with regards to the DFU, but also explains why diabetic patients have higher risks of cardiovascular complications such as ischaemic heart disease.

In summary, the primary aetiology of a DFU is excessive pressures on softtissues in a neuropathic foot, which is exacerbated by poor vascularity and deformity.

Management of DFU

There are clear guidelines, recently updated by NICE¹⁴ for the optimal management of the DFU, but for those presenting as an emergency, standards of practice can vary. The infected emergency DFU can be life-threatening; the term ‘foot attack’ has been coined and appropriately highlights that management needs to be more aggressive.¹

There is a wealth of evidence and international consensus which demonstrates how a multidisciplinary approach reduces amputation rates, lowers costs and leads to a better quality of life for patients with DFU.^9,14-20 The key NICE recommendation is that every patient with a DFU is referred promptly to the multidisciplinary team (MDT; Table III) and the patient should have a named clinician in charge of their care, which can either be the diabetologist or the surgeon. The benefits of the MDT approach are clear in that diabetes is a multi-system disease and all comorbidities that will affect wound-healing need to be addressed. The MDT approach is preventative, reducing the risk by up to 85% of further DFU and amputation occurrances.¹⁹ In the presence of an emergency or foot attack, the best practice recommendation from NICE is that immediate stabilisation and drainage of pus should be performed by the admitting team, before referral within 24 hours to the foot MDT service.¹⁴

Assessment of the DFU

Imaging

All patients with a DFU should have weight-bearing foot and ankle radiographs taken to evaluate any gross fractures or deformities as a result of Charcot arthropathy. However with a sensitivity of between 60% and 75% for osteomyelitis, sometimes more detailed assessment is required.^28,29 If the ulcer overlies a bony prominence with radiological changes then osteomyelitis can be assumed, and pencilling of the metatarsal and phalanges occurs in diabetes and is more likely to be as a result of hyperaemia than an infective process.²⁹ More expensive and specialist imaging such as triple phase bone scans and MRI can be used to compliment clinical examination. However they all suffer from poor specificity and sensitivity and struggle in differentiating between infection and Charcot arthropathy.⁹

Charcot neuroarthropathy is a disease process that results in increased osteoclastic activity, leading to bone resorption, fragmentation and deformity. In the acute phase it is difficult to distinguish between an infection and Charcot arthropathy. Diagnosis is based on clinical findings more heavily than imaging as MRI cannot distinguish between infective oedema and oedema secondary to destructive Charcot.³⁰

Microbiological assessment

DFU infections are generally polymicrobial, and due to previous antibiotic use may harbour resistant organisms. Superficial swabs of the ulcers are often carried carried out; however we feel they are of limited value due to colonisation by commensal micro-organism. In our experience they often do not reflect micro-organisms isolated from deep infection. Ultimately, accurate microbiology can only be obtained by either a bone biopsy of suspected osteomyelitic lesions, or from deep-tissue samples during surgical debridement. Initial antibiotic treatment regimes should be broad until accurate cultures are obtained and we would advise deep-tissue sampling or bone biopsy in established cases of osteomyelitis, allowing targeted antibiotic regimes.³¹ This is supported in part by NICE, which advocates early referral to the DFU MDT if antibiotics have not worked over a period of 14 days, to allow for earlier diagnosis and assessment.¹⁴

Treatment

Medical management of uncontrolled diabetes and sepsis in the first instance is key to a successful outcome. If there is spreading infection or an accompanying abscess (a foot attack) then the DFU should be treated as an emergency and urgent decompression of the ulcer performed before transfer of care, ideally within 24 hours, to a team with a specialist interest in this treatment. In our experience, delaying urgent surgical decompression while admitting teams discuss management is associated with increased morbidity and mortality in these diabetic patients.

Wagner first classified and rationalised DFU treatments; his system was subsequently modified by Brodsky, which gives a numerical assessment for depth of ulcer (0-3) and an alphabetic grade for the vascular assessment (A-C; see Table IV).

Debridement

Debridement decreases bacterial counts, stimulates production of local growth factors and reduces pressure on the wound bed that facilitates healing. Debridement can be surgical, enzymatic, autolytic, mechanical and biological. Surgical debridement is the most effective in reducing complications from DFU, and shortens ulcer healing time.^37,38

Surgical debridement consists of the complete excision of all dead, devitalised and infected tissue in theatre; in our institution it is often undertaken with regional anaesthesia. Copious lavage and repeat microbiological sampling to determine the level of infection in the residual wound is essential. Careful antibiotic treatment driven by laboratory results optimises outcomes and closure of the ulcer, as this has been shown to speed up ulcer healing time. In our institution we pack any defects with antibiotic-loaded calcium sulphate, which we have shown shortens the length of hospital stay and speeds up ulcer healing.³¹ Non-adherent dressings are applied and wounds are initially checked at weekly intervals. A low threshold for repeat surgical debridement has also been shown to reduce duration and speed ulcer healing.³⁸

In our experience, DFU located in the forefoot responds well to prompt, aggressive surgical debridement of the infected tissue, including even ray or toe amputation as required. Reliable limb salvage (and even retention of foot length) can be achieved. Difficulties arise when the ulcers are located in the mid- or hind-foot. The aims still remain the same – salvage the foot and eliminate infection. If the ulcer has resulted in midfoot osteomyelitis and the infection cannot be controlled then a Symes or below-knee amputation can be considered as a two-stage procedure, providing there is appropriate soft-tissue coverage.

Debridement in the midfoot and Charcot collapse results in altered biomechanics, a higher rate of recurrence of ulceration and proximal migration of amputation level. Hindfoot ulcers affecting the calcaneum can be the hardest to manage due to the lack of soft-tissue coverage. Sometimes a partial calcanectomy (with negative pressure wound therapy to minimise the dead space and plastics coverage) can be successful in salvaging the foot. With these partial foot amputations, there are ankle-foot orthoses that can be applied to aid in weight-bearing.

The aim of surgical debridement, and the MDT approach in managing the DFU is to salvage the foot and limb whilst minimising the rate of amputation. Primary amputation should be the last resort after all other salvage techniques have been explored; however in certain patients a below-knee amputation may offer a better functional outcome than repeated attempts at limb salvage and reconstruction, although there are no clear consensus guidelines for this. This decision is individualised and multifactorial to match the patient’s lifestyle, medical, physical and psychological comorbidities.

There is increasingly a role for elective prophylactic surgery in the management of DFU, with the aim of correcting deformities that increase plantar pressures and predispose to repeat ulceration. Although this does carry a higher risk of infection and complications when compared with standard foot and ankle elective surgery, the benefits can be considerable. Corrective procedures can range from simple exostectomy; the removal of prominent pressure-causing bone lumps; to full deformity reconstruction via triple arthrodesis or tendon lengthening and tendon transfer. Surgery can be performed using minimally invasive techniques to minimise complications, and recent results are encouraging.³⁹

Adjunct therapies

Biodegradable fillers

Stimulan is a synthetic, purified form of calcium sulphate, which allows a wide range of antibiotics to be added into the mixture. It is then placed into soft-tissue or bone defects after ulcer debridement (as shown in Figs 2 and 3). It is biodegradable and has a more consistent elution of antibiotics delivered at high concentrations to the local soft-tissues. In our series,³¹ it has performed better as filler than gentamicin beads and we have not seen any problems with hypercalceamia, likely due to the smaller amounts being used when compared with revision joint arthroplasty, and the lack of wound leakage problems.

Fig. 2

A forefoot ulcer.

Fig. 3

Ulcer post-debridement and application of Stimulan.

Future therapies

Hyperbaric oxygen therapy (HBOT) involves intermittent administration of 100% oxygen in daily sessions in a hyperbaric chamber. It is thought that this improves wound tissue hypoxia, enhances perfusion, reduces oedema and promotes ulcer healing.⁴⁵ It has also been shown to stimulate vasculogenic stem cells from the bone marrow, ‘recruiting’ them to the skin wound.⁴⁵ However, HBOT is expensive and there is no evidence that it is superior to current treatments. It is not mainstream treatment.

Conclusion

DFU is a complicated diagnosis, expensive to treat and increasingly common. It presents a host of challenges and problems to the treating clinician. The primary goal of treatment is to limit the risk of amputation, and further complications. This is best achieved with a multidisciplinary approach. The main components of management include patient education, good blood sugar control, prompt surgical debridement, appropriate antibiotics, offloading with a total contact cast, and (where appropriate) elective prophylactic surgery to minimise future recurrence.

It is important to recognise that the acute presentation of an infected DFU requires prompt surgical drainage of pus, and the term ‘foot attack’ should be used to promote an understanding of the urgency. Once initial debridement has been carried out, local pathways should exist for the prompt transfer (within 24 hours) to the specialist MDT. On-going management should focus on prevention, then dealing with complications, otherwise the financial costs of managing ongoing complications could potentially overwhelm local healthcare budgets.