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The diabetic foot and ankle
FOOT AND ANKLE
The diabetic foot and ankle
redicted to be around 750,000 higher for those with undiagp nosed disease. The ratio of type I : type II diabetes is around 1:10, with type II becoming more prevalent due to Britain having the fastest growing rate of obesity in the developed world (the risk of developing type II diabetes is around 10x greater with a body mass index of >30) and an ever aging population. The Department of Health states that the current cost of treating diabetes and its complications is around 5% of the NHS budget, or around £10 million a day, with this figure set to rise 10% by 2011.1 Around half of this figure is spent on the complications of diabetes, with diabetic foot disease being responsible for around 10 to 20% of all diabetic admissions to hospital. Although foot and ankle pathology is common in the nondiabetic population, the orthopaedic surgeon should remain vigilant for patients with undiagnosed diabetes. A high index of suspicion should be used when reviewing patients in the outpatients and emergency departments for apparently simple pathology such as paronychia, slow healing wounds or similar conditions. Simple urine glucose and serum tests will provide early diagnosis of diabetes and may crucially influence decisions on patients requiring surgery.
James C Stanley Andrew M Collier
Abstract Diabetes mellitus is a common malady of our time with ever increasing numbers of patients presenting with diabetic foot and ankle pathology. Diabetes requires treatment by a multidisciplinary team and vascular disease requires management involving vascular surgeons. There is, however, an increasing burden on the orthopaedic surgeon with ulceration, foot deformity, osteomyelitis and Charcot osteo-arthropathy being direct complications of diabetes. Potential severe complications following fracture and elective surgery require an understanding of diabetes and its effects on soft tissue and bone. The key topics are: Pathophysiology effects of hyperglycaemia on vascular, neuronal and immune systems, Assessment - examination of diabetic foot pathology and how to spot the ‘at risk foot’, Ulceration - management of foot and ankle ulceration and indications for intervention, Charcot osteo-arthropathy - brief overview of Charcot-type foot and ankle disease, and Management of ankle fractures - overview of current trends in options for conservative and surgical intervention.
The effects of hyperglycaemia on the foot and ankle Hyperglycaemia promotes changes in the microvasculature secondary to thickening of the basement membrane, sorbitol accumulation and loss of nitric oxide auto-regulation. This ultimately leads to reduced nutrient and oxygen exchange. In the foot this is commonly seen with fat pad atrophy, inability to form skin callus, nerve ischaemia, tissue necrosis, muscle atrophy, and poor healing potential. The ischaemic injury alone is insufficient to fully explain the tissue dysfunction seen in the diabetic foot and ankle. Nerve ischaemic injury is also compounded by cellular structural changes secondary to non-enzymic glycation and damage to essential signal pathways, the degree of which is proportional to the magnitude of hyperglycaemia. All types of peripheral nerve are affected including sensory, motor and autonomic, with each leading to specific changes seen in the diabetic foot and ankle. Sensory nerve damage leads to a typical glove and stocking distribution of sensory loss, resulting in a loss of protective sensation to pressure/traumatic injury. Motor loss causes small muscle atrophy and forefoot deformity with toe deformity and increased prominence of the metatarsal heads. Non-enzymic cross-linking of collagen in the presence of hyperglycaemia makes soft tissues inflexible causing stiff joints and a tight Achilles tendon, worsening the forefoot pressure related to motor dysfunction. Autonomic dysfunction reduces sweating, leading to dry cracked skin and producing potential access for pathological organisms to deeper structures. Autonomic loss also causes arterial dilatation of diseased vessels with a paradoxical hyperaemia, resulting in the deceptive appearance of a well perfused foot. The hyperaemia leads to increased osseous blood flow, ultimately causing a demineralization of the bone matrix (one of the processes thought to be involved in the development of Charcot-type destruction).2 Loss of autonomic control over the venous system also causes venous congestion and further ulceration complications. Innate immunity, essential for initiation of healing and fighting infection, is impaired due to changes in neutrophil activity. The high tissue concentrations of glucose are also an ideal culture
Keywords diabetic ankle fractures; diabetic foot; diabetic ulceration
Introduction Diabetic care requires a multidisciplinary team approach with general practitioners, podiatrists and endocrinologists mediating the majority of care. Vascular disease is common and requires vascular surgical assessment; however, there is an increasing burden on the orthopaedic surgeon in the management of neuropathic ulceration and deformity. While the term ‘diabetic foot and ankle’ often refers to ulceration, gangrene and Charcot osteo-arthropathy, diabetes also has a significant influence on the management of foot and ankle fractures/soft tissue injury. The management of foot and ankle pathology in diabetics requires an understanding of hyperglycaemic tissue injury to predict, prevent and treat complications of soft tissue ulceration, deformity and traumatic injury. The number of people in the UK diagnosed with diabetes mellitus in 1996 was 1.4 million; it has now exceeded 2.3 million (equivalent to ∼3% of the population) with the true figure
James C Stanley MBBS MRCS is Specialist Registrar at the Department of Orthopaedics, Harrogate District Hospital, North Yorkshire, UK. Andrew M Collier MB ChB FRCS(Tr & Orth) is Consultant Orthopaedic Surgeon at the Department of Orthopaedics, Harrogate District Hospital, North Yorkshire, UK.
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general malaise may be the overriding feature of sepsis and standard observations (BP, HR and temp) are required. Surveillance within the community of diabetic patients reduces significant complications by identifying the ‘at risk foot’ and is the cornerstone of a diabetic foot management program. Examination of the skin quality, bony deformity or tight Achilles tendon, sensation and vascularity can identify the ‘at risk foot’ and instigate early referral. Inspection of the diabetic foot will often illustrate common findings. Thin, shiny, dry skin which is hairless and often discoloured due to dependant rubor will require moisturizers, surgical shoes with total contact insoles and regular review. Hypertrophic nails are often misshapen and require chiropody to reduce paronychia and spreading infection. Individual inspection of the web spaces may reveal pathology easily missed by the more casual examiner. Pulses and blood pressure measurements (ankle brachial pressure index or ABPI) are taken, with absent pulses and/or low ABPIs being indicative of poor arterial supply, prompting referral to a vascular surgeon for further assessment. Normal or high ABPI measurements may, however, not reflect the true patency of the vessels as Monckeberg’s sclerosis may occur, with calcification of the tunica media leading to incompressible vessels. Colour Doppler imaging is useful and should be requested via a vascular surgical team. Neurological assessment using Semmes-Weinstein monofilament hairs (size 5.07) is still considered to be the most reliable and reproducible test for protective sensation.3 The filament is pressed against the skin and allowed to bend, which roughly equates to 10 g pressure. It is then repeated in three places. Positive response to 2 out of 3 is considered sufficient to indicate protective sensation is present. This is tested over specific weight bearing areas on the sole of the foot and is easily documented using a simple diagram (Figure 1), with sensation under the 1st metatarsal head being the single most predictive site. It must be noted that any skin callus should be removed before documenting a loss of protective sensation. Further testing with a 75 g filament can then be used to describe profound sensory loss. Specific documentation then needs to be made regarding any deformity, ‘at risk areas’ or ulcerations and signs of infection, with an appreciation of areas requiring surgical intervention. Table 2 summarizes the necessary documentation in the assessment of the diabetic foot (Figure 2).
medium for bacterial colonization. Thus, even in the presence of an apparently adequate blood supply ulceration, infection and poor healing may prevail, leading to the high complication rates seen following traumatic injury and surgical intervention in the diabetic foot and ankle. Table 1 summarizes the various tissue injuries caused by hyperglycaemia and the potential associated pathologies. Delayed fracture healing in diabetics is well described. Although the exact mechanism is unclear, it is likely to be multifactorial involving insulin effects on callus formation, alterations in neutrophil activity and osseous blood flow and glycation of enzymic pathways. Wound healing is similarly affected resulting in high complication rates for open wounds and surgical incisions around the foot and ankle.
Assessment of the foot and ankle in diabetics General assessment of the patient’s condition by the multidisciplinary team includes looking for evidence of retinal and cerebro-vascular pathology, which is relevant to foot and ankle pathology as these contribute to falls, traumatic injury and poor foot hygiene. Renal and cardiac disease may also contribute to poor healing potential and should be optimised as part of the management of diabetic foot pathology. Pyrexia, tachycardia and
Summary of hyperglycaemic tissue injury and potential associated pathology Hyperglycaemic Injury
Potential foot pathology
Arterial wall thickening
• Poor O2/nutrient delivery • Fat pad atrophy • Vessel infarct/tissue necrosis • Poor healing potential • Loss of sensory protection • Unrecognised traumatic/ pressure injury • Small muscle wasting of the foot • Claw toes/prominent metatarsal heads • Loss of sweating with atrophic, dry, cracked skin Arterial • Increased osseous blood flow/demineralization • Paradoxical apparent satisfactory blood flow Venous • Congestion/swelling/ dependant ulceration • Poor tissue perfusion/ nutrient exchange • Neutrophil dysfunction • Infection risk/poor healing potential
Sensory nerve
Motor nerve
Autonomic
Innate immunity
Diabetic foot ulceration Diabetic foot ulceration is not in itself a diagnosis but is a manifestation of a spectrum of co-morbidities. During normal stance there is approximately 3000 mmHg pressure under the metatarsal heads, increasing 2- to 3-fold in the presence of fat pad necrosis. Tightening of the tendoAchillis is also a common finding in diabetics, which further increases pressure under the metatarsal heads. It is understandable therefore that foot pathology associated with diabetes is common, with 15% of all diabetics having a foot ulcer or deep infection in their lifetime (Figure 3).4 Around the world approximately half of ulceration and amputation cases are thought to be preventable5 and thus a high index of suspicion, monitoring and prevention by a multi-disciplinary team for all diagnosed diabetics is vital. The importance of
Table 1
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Summary of necessary documentation in the assessment of the diabetic foot General assessment Lab tests
Blood pressure (BP) Heart Rate (HR) Temperature (Temp) Full blood count/CRP Blood and urine glucose Blood HbA1c
Indicators of sepsis
Vascular assessment
Pulses & capillary refill Swelling and varicosities Doppler
Neurological
Atrophic, dry skin Semmes-Weinstein monofilament testing (10 g in 2 out of 3 areas)
Indictors of infection Indication of current diabetes control Indication of longer term diabetes control Indicators of arterial insufficiency Indicators of venous insufficiency Ankle-brachial pressure index (ABPI) may have to used with caution but is valid if low Indicates risk of barrier breakdown Indicates loss of protective sensation
Table 2 Figure 1 a simple method for illustrating protective sensation is to place a tick in the circle if protective sensation is present (10 g), a dot if it is not and a dot with a circle around it if profound sensory loss (75 g) is noted. Ulceration may also be annotated on the same diagram if necessary.
Management of diabetic foot ulceration Appropriate multidisciplinary team input is always advised to optimise the medical management of the patient’s diabetes. The diabetic foot should be monitored regularly as early treatment of at risk areas can prevent many ulcerations. The simplest treatments include basic foot hygiene and regular moisturising to prevent fissuring secondary to autonomic sweat dysfunction. Toe nails should be regularly trimmed to prevent pressure on the surrounding soft tissues resulting in tissue barrier failure. Dietician input should also be utilized as often diabetic patients require zinc, magnesium and protein supplements to aid the healing process. Close attention to shoe wear is also essential. A loss of protective sensation leads to inadvertent shearing injury from shoe wear. Motor dysfunction often leads to bunions, cavus, claw toes and hammer toe deformities, which produce prominent areas more susceptible to injury, often worsened by fat pad atrophy and venous insufficiency. This further exacerbates poorly fitting shoes due to swelling and skin thinning due to stretching. The majority of patients who develop ulceration will require colour Doppler imaging for evidence of vascular insufficiency, and vascular surgical input. With modern techniques distal revascularization is possible and although often prone to poor long term results, it may provide sufficient support to allow adequate healing and save a potentially threatened limb. Offloading the affected area should redistribute pressure to larger areas, prevent shear and protect from inadvertent trauma and is best achieved with either the current gold standard of total contact casting (TCC) or with a walker boot/modified footwear along with partial weight bearing. Traditionally non-weight
iagnosis and correct management cannot be over emphasised as d over 1 in 10 foot ulcerations ultimately results in amputation. In the UK this approximately equates to 100 diabetic patients undergoing minor and major lower limb amputations every week. 40% of ulcers are neuropathic in nature, 25% arterial and 35% mixed, with around 1/3 being deep and 5% having osteomyelitis. Foot ulceration in diabetics is multi-factorial but is often described as being mainly arterial (approx. 25%), neuropathic (approx 40%) or mixed (approx 35%) in origin. Foot ulcers usually occur in prominent areas caused by deformity where the overlying skin is subjected to high or prolonged pressure. The resultant shear stresses lead to a detachment of the skin from the underlying tissue and superficial lacerations. The skin often has a bed with a necrotic cap or ulcer. Ulcers with a mainly neuropathic aetiology will have a healthy granulating bed whilst those with a significant arterial component will have a necrotic bed. The Wagner classification (modified by Brodsky)6 is the most commonly used descriptive classification of diabetic foot ulcerations (Table 3), providing useful guidance to the management of each class of ulcer. A more comprehensive scale has been developed at the University of Texas, which includes risk stratification and expresses tissue breakdown, infection and gangrene separately and this may become more commonly utilized in the future.
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Figure 2 Sensation being testing under the metatarsal heads. The Semmes-Weinstein monofilament is pressed against the skin until the filament bends. Various thicknesses of filaments are available each of which bends with a predetermined pressure documented in grams.
bearing was considered helpful, however, walking may actually improve vascular flow and improve healing provided the ulcer itself is protected from pressure. TCC provides an excellent environment for healing as it prevents point pressure and minimizes shearing of the skin. However, walker boots and modified footwear are also often used as TCC is a specialized technique not available in all centres and is time consuming to apply. The TCC should be changed every 5 to 14 days to allow dressing changes and accommodate any swelling problems and has a reported mean healing time of around 39 days.7,8 TCC is not advised in patients with active infection, significant arterial occlusion, extremely thin skin, swollen skin or in patients with poor compliance (Figure 4). Superficial ulcerations without significant infection should be identified early and treated with ulcer preparation and off-loading. Normal saline dressings, or absorbent dressings (Alignate, Hydrofibre etc) are often all that is required. Occlusive hydrocolloids, hydrogels or hypertonic saline gels can help remove necrotic tissue, with the Cochrane systematic review suggesting that available trials favour the use of hydrogel dressings for the removal of slough and callus.9 Foams and calcium alginate are also useful for ulcers producing moderate volumes of exudates. Iodine and silver impregnated dressings have also been used. More recently, biologically active dressings that encourage wound healing have been used with some success, including Promogran (cellulose
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Figure 3 Photograph illustrating a typical plantar ulceration seen in diabetic feet. The pressure area has become necrotic exposing granulation tissue without significant infection or tendon/bone exposure (Wagner 1). This is best treated by orthotics and offloading.
and collagen matrix), hyaluronic acid ester (Hyalofill), platelet derived growth factor impregnated dressings (Regranex) and those that apply living foetal foreskin cells (Dermagraft, Apligraft). Ulcer debridement can often be performed in the outpatients due to sensory neuropathy diminishing any discomfort. Simple debridement of necrotic skin edges and necrotic caps will expose tissue capable of healing. In cases where operative intervention is required for extensive infection a long incision is recommended, with Brunner incisions and minimal undermining to reduce iatrogenic soft tissue traction/injury. Tendon sheaths should be opened and washed to clear tracking pus. Vacuum assisted dressings have also been used to aid healing but are usually reserved for patients with ulcers resistant to more simple measures or for large areas. Laval or maggot therapy has been suggested by some authors, however, review articles suggest this to be no more beneficial than hydrocolloid dressings and surgical debridement when indicated.9 Surgical management of ulceration is required for deep infections, osteomyelitis and recalcitrant ulcers. Following debridement 64
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The Wagner classification of diabetic foot ulceration, modified by Brodsky. The original Wagner classification is in italics after the relevant modified classification category Depth Classification 0
At risk with no ulceration
1
Superficial ulceration Not infected (Wagner 1)
2
Deep Ulceration exposing bone or tendon (Wagner 2)
3
Extensive ulceration or abscess (Wagner 3)
Ischaemia Classification A Not ischaemic B Ischaemia without gangrene
C
Partial (forefoot) gangrene (Wagner 4)
D
Complete foot gangrene (Wagner 5)
Education and footwear Regular review Offloading with total contact casting (TCC), Walking brace or footwear modification Surgical debridement and wound care Offloading Culture specific antibiotics Debridement +/− partial amputation Offloading Culture specific antibiotics Regular review Non-invasive vascular testing (Doppler) vascular consultation if symptomatic Vascular consultation for possible re-vascularisation Debridement as above Amputation and vascular consultation
Table 3 Figure 4 Aircast diabetic walker boot. The air bladders inside the boot are inflated to reduce shear stresses on the skin. The rigid outer shell and rocker bottom sole and duel density insole help eliminate pressure points, aid mobility and reduce stresses further.
correction of deformity may be indicated to relieve pressure areas and allow ulcers to heal. Percutanous Achilles lengthening, metatarsal osteotomies, Keller’s arthroplasty, interphalangeal arthroplasty and hammer toe correction may be appropriate. Using this strategy the majority of ulcers will heal within 2 to 3 months. A chronic ulcer recalcitrant to standard treatment should be biopsied to rule out Marjolin’s ulcer (squamous cell carcinoma of a chronic wound) and may require plastic surgical input for local rotational flaps and skin cover. Split skin grafts should be avoided in load bearing areas or those susceptible to shear stress. The presence of an ulcer does not per-se require antibiotics, even with a positive microbiology swab, as colonization by a multitude of different bacteria is common. More important signs of significant infection include spreading cellulitis/lymphangitis, pus/abscess or if systemic illness and pyrexial. Infected ulcers will require surgical debridement down to healthy, viable tissue and broad spectrum intravenous antibiotics should be administered to treat both anaerobic and aerobic organisms. These are often continued as oral medication for approximately 12 weeks, but this should be discussed with the microbiology team. Soft tissue gas in diabetes is most commonly caused by aerobic organisms or by mixed gram-negative rods (rather than Clostridium perfringens), but necrotizing fasciitis must be ruled out as between
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20 to 40% of all cases of necrotising fasciitis are in patients with known diabetes mellitus. Necrotising fasciitis is a progressive, rapidly spreading infection of the deep fascial layers that affects both the overlying skin and underlying muscle. It may be secondary to many types of bacteria, often in synergism, but the commonest isolated organism is Group A Streptococcus. Initial presentation is often itching or pain which progresses to anaesthesia as the overlying skin vessels infarct. Cellulitis may be present initially, although this usually gives way to purplish skin and gangrene over only a couple of hours. Tissue necrosis, putrid discharge, severe pain and general systemic signs (pyrexia, malaise, diarrhoea, vomiting) then become apparent. Soft tissue gas may be felt clinically as crepitus but is often easiest to identify on plain X-ray. Ultimately, the mortality rate of necrotising fasciitis is 80 to 90%, thus early identification and treatment are vital. Following resuscitation early, aggressive surgical debridement and opening of the fascial planes is required. Biospies should be taken from the spreading periphery as within the central gangrenous 65
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area there will be organisms present which neither cause nor add to necrotising fasciitis. The antibiotic of choice would be intravenous penicillin, or clindamycin as an alternative, to treat Group A Streptococcus, but this may need to be altered subsequently according to microbiology test results. Hyperbaric oxygen therapy may also be considered but is not available in most centres. The diagnosis of deeper purulent infections and osteomyelitis is based on both clinical and radiographic grounds. Although the exposure of bone at the base of an ulcer does not automatically lead to the diagnosis of osteomyelitis, its presence is highly suggestive and plain X-ray (looking for bone destruction) is indicated. Some care should be made with the diagnosis of osteomyelitis not associated with ulceration because any radiographic changes may be due to Charcot osteo-arthropathy, which requires very different treatment. MRI and white cell labelled scans may aid diagnosis but should be used with caution as many imaging findings are common to both conditions.10 If any doubt remains a biopsy and culture will be required. Septic arthritis may mimic a number of conditions which are similar to those found with other inflammatory or neoplastic conditions, or with Charcot osteo-arthropathy, and when the area is painless due to neuropathy the definitive diagnosis is notoriously difficult.10 However, there should be a high index of suspicion and again biopsy/aspiration will often be required. Amputation will ultimately be required for uncontrolled infection and sepsis, recalcitrant osteomyelitis or unreconstructable vascular insufficiency with gangrene. Amputation of the 1st ray or 4th/5th rays are well tolerated in the diabetic population. Amputations of the 3rd ray are less well tolerated and usually require more proximal amputations, either through the Lisfranc, mid-tarsal (Chopart) or hindfoot (Symes) if there is sufficient soft tissue cover. Otherwise, a transtibial amputation is performed. In mid-tarsal amputations insertion of the dorsi-flexion tendons into the neck of the talus is required to prevent significant equinus from the pull of the tendoAchillis. Hindfoot amputations have the advantage of improving ambulation over short distances without a prosthesis (eg to the toilet), however, prosthetic fitting is more difficult and close collaboration with the patient and orthotist is required in choosing a hindfoot amputation over a transtibial amputation. Previously, below knee re-vascularisation was thought to be futile as microangiopathic occlusive disease was thought to be responsible for tissue necrosis in the diabetic foot. It is now considered that tissue necrosis results more from narrowing and occlusion of larger vessels with the practical implication that infections and ulceration are amenable to treatment and potentially cure through revascularization of below knee vessels.
mediated vascular reflex ultimately resulting in a hyperaemia. Thus, in addition to repetitive unrecognized trauma it is thought that the hyperaemia causes an osteopenia (secondary to a mismatch in bone destruction and synthesis2) which weakens bone making it more susceptible to the repeated minor trauma. The commonest joints to be affected by Charcot osteo-arthropathy are those in the foot due to an increase in inadvertent trauma from walking, greater forces through the joints of the lower limb and a greater degree of sensory loss. Charcot osteo-arthropathy occurs in stages, as described by Sidney N Eichenholtz in 1966, resulting in fragmentation, coalescence and consolidation12 which typically occur over a 6-month period . The details of Charcot osteo-arthropathy diagnosis and management are discussed in a separate article, however, in general Charcot osteo-arthropathy causes mid-foot (Rocker bottom foot) and ankle deformity and is usually seen only in a neuropathic which is well perfused with good pulses.
Diabetic foot and ankle fractures The treatment of ankle fractures in diabetes is a notorious challenge due to high complication rates, particularly of surgical and soft tissue wounds. Historically surgical intervention lead to high amputation rates, with more recent reports continuing to highlight significant complication rates of around 45%.13,14 The patient with significant co-morbidities is particularly at risk and a multidisciplinary approach is essential to optimise the patient’s condition. However, in the absence of neuropathy, vascular insufficiency or co-morbidities diabetic patients appear to have an overall risk of complication similar to that for a matched population.14,15 Non-operative management may also lead to significant infective wound complications16 and close attention to ill-fitting casts and patient compliance is essential with regular review. Non-operative treatment is also associated with a higher rate of Charcot osteo-arthropathy17 and hence debate still continues as to the best form of management. There are some principles which must however be followed. In general there should be a low tolerance for any displacement as incongruity of the ankle can cause rapidly progressing post-traumatic arthritis or Charcot osteo-arthropathy. Even if neuropathy is not seen at presentation it cannot be assumed that it will not develop in the future. With loss of sensory protection to the ankle joint a mal-union may cause more significant long term problems and arise in a shorter timeframe. Closed reduction and casting of displaced fractures generally leads to displacement and merely delays surgical intervention, and better results are usually obtained with open reduction and internal fixation.18 If a fracture presents with pre-existing Charcot osteo-arthropathy or significant osteoarthritis then primary fusion is often indicated. Of the other fractures of the foot and ankle the general principle should be “do no harm”. Minimally displaced fractures are thus often treated conservatively. Calcaneal fractures are generally best treated conservatively except in the severely displaced as there can be potentially catastrophic wound complications. Talar fractures will require operative intervention if displaced or associated with significant collapse from avascular necrosis. Metatarsal fractures generally do well if treated conservatively and although mid-tarsal injuries are rare they often require
Charcot osteo-arthropathy Although tertiary syphilis was one of the leading causes of Charcot joints in the late 1800s, the commonest cause in modern society is diabetes mellitus. It is thought that the loss of proprioception and deep sensation ultimately leads to progressive joint degeneration, destruction, and disorganization secondary to repetitive unrecognized trauma. Using scintigraphy, it has been shown that in patients with diagnosed neuropathy there is increased blood flow within bone,11 thought to be due to an autonomic, neurally
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treatment for displacement and collapse and should be treated using similar protocols as to those for Charcot osteo-arthropathy in this region. Osteoporosis19,20 and delayed fracture healing21 are potential complications of diabetes. The exact aetiology is poorly understood but is likely to be multi-factorial, and can lead to spinal and hip fractures as well as those in the foot and ankle. It has, however, been shown that fasting hypoglycaemia may be the overriding risk factor for fracture development, and that a well controlled blood sugar level is important.22 The exact increase in fracture healing time in humans is difficult to assess and again is multi-factorial. The type and severity of diabetes is implicated as are associated co-morbidities including vascular insufficiency, renal disease and hyper-lipidaemia. Smoking, diet and age are all also likely to influence the rate of fracture healing. A young fit type II diabetic may well heal at a normal rate whilst an elderly smoker with insulin dependence and co-morbidities may require immobilisation 2 to 3 times longer. The presence of a neuropathy is often used as an appropriate marker in deciding on doubling immobilization time.15,21 Weight bearing status (or not) should follow similar protocols as for those patients without diabetes as excessive non-weight bearing may predispose the patient to developing disuse osteopenia and potentially provoke Charcot osteo-arthropathy. In the presence of significant vascular insufficiency any orthopaedic intervention to treat a fracture will be compromised and a vascular surgical assessment should be requested. Although re-cannulation of distal vessels often produces only short term success, the improved blood supply may be sufficient to promote healing and prevent infection.
References 1 Sue Roberts (National Director for Diabetes). Working together for better diabetes care, clinical case for change. Department of Health, 16 May 2007, p. 1–16. 2 Brower AC, Allman RM. The neuropathic joint: a neurovascular bone disorder. Radiol Clin North Am 1981; 19(4): 571–580. 3 Jerosch-Herold C. Assessment of sensibility after nerve injury and repair: a systematic review of evidence for validity, reliability and responsiveness of tests. J Hand Surg [Br ] 2005; 30(3): 252–264. 4 Pham H, Armstrong DG, Harvey C, Harkless LB, Giurini JM, Veves A. Screening techniques to identify people at high risk for diabetic foot ulceration: a prospective multicenter trial. Diabetes Care 2000; 23(5): 606–611. 5 National Diabetes Support Team. Diabetic foot guide. NHS Clinical Governance Support Team. 2006, p. 1–12. 6 Brodsky JW. The diabetic foot. In: Coughlin MJ, Mann RA, eds. Surgery of the foot and ankle. Mosby, 1999, p. 895–969. 7 Trepman E, Pinzur MS, Shields NN. Application of the total contact cast. Foot Ankle Int 2005; 26(1): 108–112. 8 Myerson M, Papa J, Eaton K, Wilson K. The total-contact cast for management of neuropathic plantar ulceration of the foot. J Bone Joint Surg Am 1992; 74(2): 261–269. 9 Edwards J. Debridement of diabetic foot ulcers. Issue 4. Art. No.: CD003556. Cochrane Database Syst Rev 2002. 10 Jones EA, Manaster BJ, May DA, Disler DG. Neuropathic osteoarthropathy: diagnostic dilemmas and differential diagnosis. Radiographics 2000(20 Spec No): S279–S293. 11 Edmonds ME, Clarke MB, Newton S, Barrett J, Watkins PJ. Increased uptake of bone radiopharmaceutical in diabetic neuropathy. Q J Med 1985; 57(224): 843–855. 12 Eichenholtz Sidney N. Charcot joints. Springfield, Ill., C.C. Thomas, 1966. 13 McCormack RG, Leith JM. Ankle fractures in diabetics. Complications of surgical management. J Bone Joint Surg Br 1998; 80(4): 689–692. 14 Jones KB, Maiers-Yelden KA, Marsh JL, Zimmerman MB, Estin M, Saltzman CL. Ankle fractures in patients with diabetes mellitus. J Bone Joint Surg Br 2005; 87(4): 489–495. 15 Costigan W, Thordarson DB, Debnath UK. Operative management of ankle fractures in patients with diabetes mellitus. Foot Ankle Int 2007; 28(1): 32–37. 16 Flynn JM, Rodriguez-del RF, Piza PA. Closed ankle fractures in the diabetic patient. Foot Ankle Int 2000; 21(4): 311–319. 17 Holmes Jr. GB, Hill N. Fractures and dislocations of the foot and ankle in diabetics associated with Charcot joint changes. Foot Ankle Int 1994; 15(4): 182–185. 18 Schon LC, Easley ME, Weinfeld SB. Charcot neuroarthropathy of the foot and ankle. Clin Orthop Relat Res 1998; 349: 116–131. 19 Levin ME, Boisseau VC, Avioli LV. Effects of diabetes mellitus on bone mass in juvenile and adult-onset diabetes. N Engl J Med 1976; 294(5): 241–245. 20 Krakauer JC, McKenna MJ, Buderer NF, Rao DS, Whitehouse FW, Parfitt AM. Bone loss and bone turnover in diabetes. Diabetes 1995; 44(7): 775–782. 21 Marks RM. Complications of foot and ankle surgery in patients with diabetes. Clin Orthop Relat Res 2001; 391: 153–161. 22 Holmberg AH, Nilsson PM, Nilsson JA, Akesson K. The association between hyperglycemia and fracture risk in middle age. A Prospective, Population-Based Study of 22,444 men and 10,902 women. J Clin Endocrinol Metab 2008; 93(3): 815–822.
Summary • The diabetic foot and ankle is a complex problem requiring a multidisciplinary approach. • Diabetes reduces oxygen and nutrient delivery through chan ges in the vascular system. • Neuropathy causes loss of protective sensation, deformity and swelling. • Arteriopathy and changes in innate immunity reduce healing potential. • Ulcerations mainly due to vascular insufficiency, rather than neuropathy, should be treated by the vascular surgeons. • Superficial ulcerations often only require off loading with total contact casting and regular review. • Infected, extensive or deep ulcerations may require surgical debridement +/− antibiotics. • Necrotising fasciitis should be suspected in diabetics with rapidly worsening infection and treated expectantly. • Prominent areas secondary to deformity often require surgical correction or excision to aid ulcer healing. • Fractures of the foot and ankle require anatomical reduction and in high risk patients a doubling of immobilisation time. • Distal vascular reconstruction is becoming increasingly available to improve soft tissue and bony healing. • Operative intervention is associated with high complication rates, however, poor reduction leads to post-traumatic arthropathy or Charcot osteo-arthropathy and thus further surgical intervention with again high complication rates. ◆ ORTHOPAEDICS AND TRAUMA 23:1
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Learning points
Necrotising fasciitis is most commonly due to Group A Streptococcus. Treatment includes fluid resuscitation, intravenous penicillin or clindamycin, wide surgical debridement of necrotic tissue and incision of fascial planes into healthy tissue. Second review in theatres is required at 24 hours with further debridement if necessary. Delayed primary closure may be possible following successful treatment.
An ABPI >0.7 and <1.3 may be used to determine adequate blood flow. A transcutaneous oxygen pressure of >40 mmHg also suggests adequate arterial flow. Whilst neuropathic ulcers may be tackled by the orthopaedic surgeon, ischaemic ulcers require vascular surgical input as arterial reconstruction may be required for the resolution of ulceration and limb salvage.
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The diabetic foot and ankle
redicted to be around 750,000 higher for those with undiagp nosed disease. The ratio of type I : type II diabetes is around 1:10, with type II becoming more prevalent due to Britain having the fastest growing rate of obesity in the developed world (the risk of developing type II diabetes is around 10x greater with a body mass index of >30) and an ever aging population. The Department of Health states that the current cost of treating diabetes and its complications is around 5% of the NHS budget, or around £10 million a day, with this figure set to rise 10% by 2011.1 Around half of this figure is spent on the complications of diabetes, with diabetic foot disease being responsible for around 10 to 20% of all diabetic admissions to hospital. Although foot and ankle pathology is common in the nondiabetic population, the orthopaedic surgeon should remain vigilant for patients with undiagnosed diabetes. A high index of suspicion should be used when reviewing patients in the outpatients and emergency departments for apparently simple pathology such as paronychia, slow healing wounds or similar conditions. Simple urine glucose and serum tests will provide early diagnosis of diabetes and may crucially influence decisions on patients requiring surgery.
James C Stanley Andrew M Collier
Abstract Diabetes mellitus is a common malady of our time with ever increasing numbers of patients presenting with diabetic foot and ankle pathology. Diabetes requires treatment by a multidisciplinary team and vascular disease requires management involving vascular surgeons. There is, however, an increasing burden on the orthopaedic surgeon with ulceration, foot deformity, osteomyelitis and Charcot osteo-arthropathy being direct complications of diabetes. Potential severe complications following fracture and elective surgery require an understanding of diabetes and its effects on soft tissue and bone. The key topics are: Pathophysiology effects of hyperglycaemia on vascular, neuronal and immune systems, Assessment - examination of diabetic foot pathology and how to spot the ‘at risk foot’, Ulceration - management of foot and ankle ulceration and indications for intervention, Charcot osteo-arthropathy - brief overview of Charcot-type foot and ankle disease, and Management of ankle fractures - overview of current trends in options for conservative and surgical intervention.
The effects of hyperglycaemia on the foot and ankle Hyperglycaemia promotes changes in the microvasculature secondary to thickening of the basement membrane, sorbitol accumulation and loss of nitric oxide auto-regulation. This ultimately leads to reduced nutrient and oxygen exchange. In the foot this is commonly seen with fat pad atrophy, inability to form skin callus, nerve ischaemia, tissue necrosis, muscle atrophy, and poor healing potential. The ischaemic injury alone is insufficient to fully explain the tissue dysfunction seen in the diabetic foot and ankle. Nerve ischaemic injury is also compounded by cellular structural changes secondary to non-enzymic glycation and damage to essential signal pathways, the degree of which is proportional to the magnitude of hyperglycaemia. All types of peripheral nerve are affected including sensory, motor and autonomic, with each leading to specific changes seen in the diabetic foot and ankle. Sensory nerve damage leads to a typical glove and stocking distribution of sensory loss, resulting in a loss of protective sensation to pressure/traumatic injury. Motor loss causes small muscle atrophy and forefoot deformity with toe deformity and increased prominence of the metatarsal heads. Non-enzymic cross-linking of collagen in the presence of hyperglycaemia makes soft tissues inflexible causing stiff joints and a tight Achilles tendon, worsening the forefoot pressure related to motor dysfunction. Autonomic dysfunction reduces sweating, leading to dry cracked skin and producing potential access for pathological organisms to deeper structures. Autonomic loss also causes arterial dilatation of diseased vessels with a paradoxical hyperaemia, resulting in the deceptive appearance of a well perfused foot. The hyperaemia leads to increased osseous blood flow, ultimately causing a demineralization of the bone matrix (one of the processes thought to be involved in the development of Charcot-type destruction).2 Loss of autonomic control over the venous system also causes venous congestion and further ulceration complications. Innate immunity, essential for initiation of healing and fighting infection, is impaired due to changes in neutrophil activity. The high tissue concentrations of glucose are also an ideal culture
Keywords diabetic ankle fractures; diabetic foot; diabetic ulceration
Introduction Diabetic care requires a multidisciplinary team approach with general practitioners, podiatrists and endocrinologists mediating the majority of care. Vascular disease is common and requires vascular surgical assessment; however, there is an increasing burden on the orthopaedic surgeon in the management of neuropathic ulceration and deformity. While the term ‘diabetic foot and ankle’ often refers to ulceration, gangrene and Charcot osteo-arthropathy, diabetes also has a significant influence on the management of foot and ankle fractures/soft tissue injury. The management of foot and ankle pathology in diabetics requires an understanding of hyperglycaemic tissue injury to predict, prevent and treat complications of soft tissue ulceration, deformity and traumatic injury. The number of people in the UK diagnosed with diabetes mellitus in 1996 was 1.4 million; it has now exceeded 2.3 million (equivalent to ∼3% of the population) with the true figure
James C Stanley MBBS MRCS is Specialist Registrar at the Department of Orthopaedics, Harrogate District Hospital, North Yorkshire, UK. Andrew M Collier MB ChB FRCS(Tr & Orth) is Consultant Orthopaedic Surgeon at the Department of Orthopaedics, Harrogate District Hospital, North Yorkshire, UK.
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general malaise may be the overriding feature of sepsis and standard observations (BP, HR and temp) are required. Surveillance within the community of diabetic patients reduces significant complications by identifying the ‘at risk foot’ and is the cornerstone of a diabetic foot management program. Examination of the skin quality, bony deformity or tight Achilles tendon, sensation and vascularity can identify the ‘at risk foot’ and instigate early referral. Inspection of the diabetic foot will often illustrate common findings. Thin, shiny, dry skin which is hairless and often discoloured due to dependant rubor will require moisturizers, surgical shoes with total contact insoles and regular review. Hypertrophic nails are often misshapen and require chiropody to reduce paronychia and spreading infection. Individual inspection of the web spaces may reveal pathology easily missed by the more casual examiner. Pulses and blood pressure measurements (ankle brachial pressure index or ABPI) are taken, with absent pulses and/or low ABPIs being indicative of poor arterial supply, prompting referral to a vascular surgeon for further assessment. Normal or high ABPI measurements may, however, not reflect the true patency of the vessels as Monckeberg’s sclerosis may occur, with calcification of the tunica media leading to incompressible vessels. Colour Doppler imaging is useful and should be requested via a vascular surgical team. Neurological assessment using Semmes-Weinstein monofilament hairs (size 5.07) is still considered to be the most reliable and reproducible test for protective sensation.3 The filament is pressed against the skin and allowed to bend, which roughly equates to 10 g pressure. It is then repeated in three places. Positive response to 2 out of 3 is considered sufficient to indicate protective sensation is present. This is tested over specific weight bearing areas on the sole of the foot and is easily documented using a simple diagram (Figure 1), with sensation under the 1st metatarsal head being the single most predictive site. It must be noted that any skin callus should be removed before documenting a loss of protective sensation. Further testing with a 75 g filament can then be used to describe profound sensory loss. Specific documentation then needs to be made regarding any deformity, ‘at risk areas’ or ulcerations and signs of infection, with an appreciation of areas requiring surgical intervention. Table 2 summarizes the necessary documentation in the assessment of the diabetic foot (Figure 2).
medium for bacterial colonization. Thus, even in the presence of an apparently adequate blood supply ulceration, infection and poor healing may prevail, leading to the high complication rates seen following traumatic injury and surgical intervention in the diabetic foot and ankle. Table 1 summarizes the various tissue injuries caused by hyperglycaemia and the potential associated pathologies. Delayed fracture healing in diabetics is well described. Although the exact mechanism is unclear, it is likely to be multifactorial involving insulin effects on callus formation, alterations in neutrophil activity and osseous blood flow and glycation of enzymic pathways. Wound healing is similarly affected resulting in high complication rates for open wounds and surgical incisions around the foot and ankle.
Assessment of the foot and ankle in diabetics General assessment of the patient’s condition by the multidisciplinary team includes looking for evidence of retinal and cerebro-vascular pathology, which is relevant to foot and ankle pathology as these contribute to falls, traumatic injury and poor foot hygiene. Renal and cardiac disease may also contribute to poor healing potential and should be optimised as part of the management of diabetic foot pathology. Pyrexia, tachycardia and
Summary of hyperglycaemic tissue injury and potential associated pathology Hyperglycaemic Injury
Potential foot pathology
Arterial wall thickening
• Poor O2/nutrient delivery • Fat pad atrophy • Vessel infarct/tissue necrosis • Poor healing potential • Loss of sensory protection • Unrecognised traumatic/ pressure injury • Small muscle wasting of the foot • Claw toes/prominent metatarsal heads • Loss of sweating with atrophic, dry, cracked skin Arterial • Increased osseous blood flow/demineralization • Paradoxical apparent satisfactory blood flow Venous • Congestion/swelling/ dependant ulceration • Poor tissue perfusion/ nutrient exchange • Neutrophil dysfunction • Infection risk/poor healing potential
Sensory nerve
Motor nerve
Autonomic
Innate immunity
Diabetic foot ulceration Diabetic foot ulceration is not in itself a diagnosis but is a manifestation of a spectrum of co-morbidities. During normal stance there is approximately 3000 mmHg pressure under the metatarsal heads, increasing 2- to 3-fold in the presence of fat pad necrosis. Tightening of the tendoAchillis is also a common finding in diabetics, which further increases pressure under the metatarsal heads. It is understandable therefore that foot pathology associated with diabetes is common, with 15% of all diabetics having a foot ulcer or deep infection in their lifetime (Figure 3).4 Around the world approximately half of ulceration and amputation cases are thought to be preventable5 and thus a high index of suspicion, monitoring and prevention by a multi-disciplinary team for all diagnosed diabetics is vital. The importance of
Table 1
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Summary of necessary documentation in the assessment of the diabetic foot General assessment Lab tests
Blood pressure (BP) Heart Rate (HR) Temperature (Temp) Full blood count/CRP Blood and urine glucose Blood HbA1c
Indicators of sepsis
Vascular assessment
Pulses & capillary refill Swelling and varicosities Doppler
Neurological
Atrophic, dry skin Semmes-Weinstein monofilament testing (10 g in 2 out of 3 areas)
Indictors of infection Indication of current diabetes control Indication of longer term diabetes control Indicators of arterial insufficiency Indicators of venous insufficiency Ankle-brachial pressure index (ABPI) may have to used with caution but is valid if low Indicates risk of barrier breakdown Indicates loss of protective sensation
Table 2 Figure 1 a simple method for illustrating protective sensation is to place a tick in the circle if protective sensation is present (10 g), a dot if it is not and a dot with a circle around it if profound sensory loss (75 g) is noted. Ulceration may also be annotated on the same diagram if necessary.
Management of diabetic foot ulceration Appropriate multidisciplinary team input is always advised to optimise the medical management of the patient’s diabetes. The diabetic foot should be monitored regularly as early treatment of at risk areas can prevent many ulcerations. The simplest treatments include basic foot hygiene and regular moisturising to prevent fissuring secondary to autonomic sweat dysfunction. Toe nails should be regularly trimmed to prevent pressure on the surrounding soft tissues resulting in tissue barrier failure. Dietician input should also be utilized as often diabetic patients require zinc, magnesium and protein supplements to aid the healing process. Close attention to shoe wear is also essential. A loss of protective sensation leads to inadvertent shearing injury from shoe wear. Motor dysfunction often leads to bunions, cavus, claw toes and hammer toe deformities, which produce prominent areas more susceptible to injury, often worsened by fat pad atrophy and venous insufficiency. This further exacerbates poorly fitting shoes due to swelling and skin thinning due to stretching. The majority of patients who develop ulceration will require colour Doppler imaging for evidence of vascular insufficiency, and vascular surgical input. With modern techniques distal revascularization is possible and although often prone to poor long term results, it may provide sufficient support to allow adequate healing and save a potentially threatened limb. Offloading the affected area should redistribute pressure to larger areas, prevent shear and protect from inadvertent trauma and is best achieved with either the current gold standard of total contact casting (TCC) or with a walker boot/modified footwear along with partial weight bearing. Traditionally non-weight
iagnosis and correct management cannot be over emphasised as d over 1 in 10 foot ulcerations ultimately results in amputation. In the UK this approximately equates to 100 diabetic patients undergoing minor and major lower limb amputations every week. 40% of ulcers are neuropathic in nature, 25% arterial and 35% mixed, with around 1/3 being deep and 5% having osteomyelitis. Foot ulceration in diabetics is multi-factorial but is often described as being mainly arterial (approx. 25%), neuropathic (approx 40%) or mixed (approx 35%) in origin. Foot ulcers usually occur in prominent areas caused by deformity where the overlying skin is subjected to high or prolonged pressure. The resultant shear stresses lead to a detachment of the skin from the underlying tissue and superficial lacerations. The skin often has a bed with a necrotic cap or ulcer. Ulcers with a mainly neuropathic aetiology will have a healthy granulating bed whilst those with a significant arterial component will have a necrotic bed. The Wagner classification (modified by Brodsky)6 is the most commonly used descriptive classification of diabetic foot ulcerations (Table 3), providing useful guidance to the management of each class of ulcer. A more comprehensive scale has been developed at the University of Texas, which includes risk stratification and expresses tissue breakdown, infection and gangrene separately and this may become more commonly utilized in the future.
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Figure 2 Sensation being testing under the metatarsal heads. The Semmes-Weinstein monofilament is pressed against the skin until the filament bends. Various thicknesses of filaments are available each of which bends with a predetermined pressure documented in grams.
bearing was considered helpful, however, walking may actually improve vascular flow and improve healing provided the ulcer itself is protected from pressure. TCC provides an excellent environment for healing as it prevents point pressure and minimizes shearing of the skin. However, walker boots and modified footwear are also often used as TCC is a specialized technique not available in all centres and is time consuming to apply. The TCC should be changed every 5 to 14 days to allow dressing changes and accommodate any swelling problems and has a reported mean healing time of around 39 days.7,8 TCC is not advised in patients with active infection, significant arterial occlusion, extremely thin skin, swollen skin or in patients with poor compliance (Figure 4). Superficial ulcerations without significant infection should be identified early and treated with ulcer preparation and off-loading. Normal saline dressings, or absorbent dressings (Alignate, Hydrofibre etc) are often all that is required. Occlusive hydrocolloids, hydrogels or hypertonic saline gels can help remove necrotic tissue, with the Cochrane systematic review suggesting that available trials favour the use of hydrogel dressings for the removal of slough and callus.9 Foams and calcium alginate are also useful for ulcers producing moderate volumes of exudates. Iodine and silver impregnated dressings have also been used. More recently, biologically active dressings that encourage wound healing have been used with some success, including Promogran (cellulose
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Figure 3 Photograph illustrating a typical plantar ulceration seen in diabetic feet. The pressure area has become necrotic exposing granulation tissue without significant infection or tendon/bone exposure (Wagner 1). This is best treated by orthotics and offloading.
and collagen matrix), hyaluronic acid ester (Hyalofill), platelet derived growth factor impregnated dressings (Regranex) and those that apply living foetal foreskin cells (Dermagraft, Apligraft). Ulcer debridement can often be performed in the outpatients due to sensory neuropathy diminishing any discomfort. Simple debridement of necrotic skin edges and necrotic caps will expose tissue capable of healing. In cases where operative intervention is required for extensive infection a long incision is recommended, with Brunner incisions and minimal undermining to reduce iatrogenic soft tissue traction/injury. Tendon sheaths should be opened and washed to clear tracking pus. Vacuum assisted dressings have also been used to aid healing but are usually reserved for patients with ulcers resistant to more simple measures or for large areas. Laval or maggot therapy has been suggested by some authors, however, review articles suggest this to be no more beneficial than hydrocolloid dressings and surgical debridement when indicated.9 Surgical management of ulceration is required for deep infections, osteomyelitis and recalcitrant ulcers. Following debridement 64
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The Wagner classification of diabetic foot ulceration, modified by Brodsky. The original Wagner classification is in italics after the relevant modified classification category Depth Classification 0
At risk with no ulceration
1
Superficial ulceration Not infected (Wagner 1)
2
Deep Ulceration exposing bone or tendon (Wagner 2)
3
Extensive ulceration or abscess (Wagner 3)
Ischaemia Classification A Not ischaemic B Ischaemia without gangrene
C
Partial (forefoot) gangrene (Wagner 4)
D
Complete foot gangrene (Wagner 5)
Education and footwear Regular review Offloading with total contact casting (TCC), Walking brace or footwear modification Surgical debridement and wound care Offloading Culture specific antibiotics Debridement +/− partial amputation Offloading Culture specific antibiotics Regular review Non-invasive vascular testing (Doppler) vascular consultation if symptomatic Vascular consultation for possible re-vascularisation Debridement as above Amputation and vascular consultation
Table 3 Figure 4 Aircast diabetic walker boot. The air bladders inside the boot are inflated to reduce shear stresses on the skin. The rigid outer shell and rocker bottom sole and duel density insole help eliminate pressure points, aid mobility and reduce stresses further.
correction of deformity may be indicated to relieve pressure areas and allow ulcers to heal. Percutanous Achilles lengthening, metatarsal osteotomies, Keller’s arthroplasty, interphalangeal arthroplasty and hammer toe correction may be appropriate. Using this strategy the majority of ulcers will heal within 2 to 3 months. A chronic ulcer recalcitrant to standard treatment should be biopsied to rule out Marjolin’s ulcer (squamous cell carcinoma of a chronic wound) and may require plastic surgical input for local rotational flaps and skin cover. Split skin grafts should be avoided in load bearing areas or those susceptible to shear stress. The presence of an ulcer does not per-se require antibiotics, even with a positive microbiology swab, as colonization by a multitude of different bacteria is common. More important signs of significant infection include spreading cellulitis/lymphangitis, pus/abscess or if systemic illness and pyrexial. Infected ulcers will require surgical debridement down to healthy, viable tissue and broad spectrum intravenous antibiotics should be administered to treat both anaerobic and aerobic organisms. These are often continued as oral medication for approximately 12 weeks, but this should be discussed with the microbiology team. Soft tissue gas in diabetes is most commonly caused by aerobic organisms or by mixed gram-negative rods (rather than Clostridium perfringens), but necrotizing fasciitis must be ruled out as between
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20 to 40% of all cases of necrotising fasciitis are in patients with known diabetes mellitus. Necrotising fasciitis is a progressive, rapidly spreading infection of the deep fascial layers that affects both the overlying skin and underlying muscle. It may be secondary to many types of bacteria, often in synergism, but the commonest isolated organism is Group A Streptococcus. Initial presentation is often itching or pain which progresses to anaesthesia as the overlying skin vessels infarct. Cellulitis may be present initially, although this usually gives way to purplish skin and gangrene over only a couple of hours. Tissue necrosis, putrid discharge, severe pain and general systemic signs (pyrexia, malaise, diarrhoea, vomiting) then become apparent. Soft tissue gas may be felt clinically as crepitus but is often easiest to identify on plain X-ray. Ultimately, the mortality rate of necrotising fasciitis is 80 to 90%, thus early identification and treatment are vital. Following resuscitation early, aggressive surgical debridement and opening of the fascial planes is required. Biospies should be taken from the spreading periphery as within the central gangrenous 65
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area there will be organisms present which neither cause nor add to necrotising fasciitis. The antibiotic of choice would be intravenous penicillin, or clindamycin as an alternative, to treat Group A Streptococcus, but this may need to be altered subsequently according to microbiology test results. Hyperbaric oxygen therapy may also be considered but is not available in most centres. The diagnosis of deeper purulent infections and osteomyelitis is based on both clinical and radiographic grounds. Although the exposure of bone at the base of an ulcer does not automatically lead to the diagnosis of osteomyelitis, its presence is highly suggestive and plain X-ray (looking for bone destruction) is indicated. Some care should be made with the diagnosis of osteomyelitis not associated with ulceration because any radiographic changes may be due to Charcot osteo-arthropathy, which requires very different treatment. MRI and white cell labelled scans may aid diagnosis but should be used with caution as many imaging findings are common to both conditions.10 If any doubt remains a biopsy and culture will be required. Septic arthritis may mimic a number of conditions which are similar to those found with other inflammatory or neoplastic conditions, or with Charcot osteo-arthropathy, and when the area is painless due to neuropathy the definitive diagnosis is notoriously difficult.10 However, there should be a high index of suspicion and again biopsy/aspiration will often be required. Amputation will ultimately be required for uncontrolled infection and sepsis, recalcitrant osteomyelitis or unreconstructable vascular insufficiency with gangrene. Amputation of the 1st ray or 4th/5th rays are well tolerated in the diabetic population. Amputations of the 3rd ray are less well tolerated and usually require more proximal amputations, either through the Lisfranc, mid-tarsal (Chopart) or hindfoot (Symes) if there is sufficient soft tissue cover. Otherwise, a transtibial amputation is performed. In mid-tarsal amputations insertion of the dorsi-flexion tendons into the neck of the talus is required to prevent significant equinus from the pull of the tendoAchillis. Hindfoot amputations have the advantage of improving ambulation over short distances without a prosthesis (eg to the toilet), however, prosthetic fitting is more difficult and close collaboration with the patient and orthotist is required in choosing a hindfoot amputation over a transtibial amputation. Previously, below knee re-vascularisation was thought to be futile as microangiopathic occlusive disease was thought to be responsible for tissue necrosis in the diabetic foot. It is now considered that tissue necrosis results more from narrowing and occlusion of larger vessels with the practical implication that infections and ulceration are amenable to treatment and potentially cure through revascularization of below knee vessels.
mediated vascular reflex ultimately resulting in a hyperaemia. Thus, in addition to repetitive unrecognized trauma it is thought that the hyperaemia causes an osteopenia (secondary to a mismatch in bone destruction and synthesis2) which weakens bone making it more susceptible to the repeated minor trauma. The commonest joints to be affected by Charcot osteo-arthropathy are those in the foot due to an increase in inadvertent trauma from walking, greater forces through the joints of the lower limb and a greater degree of sensory loss. Charcot osteo-arthropathy occurs in stages, as described by Sidney N Eichenholtz in 1966, resulting in fragmentation, coalescence and consolidation12 which typically occur over a 6-month period . The details of Charcot osteo-arthropathy diagnosis and management are discussed in a separate article, however, in general Charcot osteo-arthropathy causes mid-foot (Rocker bottom foot) and ankle deformity and is usually seen only in a neuropathic which is well perfused with good pulses.
Diabetic foot and ankle fractures The treatment of ankle fractures in diabetes is a notorious challenge due to high complication rates, particularly of surgical and soft tissue wounds. Historically surgical intervention lead to high amputation rates, with more recent reports continuing to highlight significant complication rates of around 45%.13,14 The patient with significant co-morbidities is particularly at risk and a multidisciplinary approach is essential to optimise the patient’s condition. However, in the absence of neuropathy, vascular insufficiency or co-morbidities diabetic patients appear to have an overall risk of complication similar to that for a matched population.14,15 Non-operative management may also lead to significant infective wound complications16 and close attention to ill-fitting casts and patient compliance is essential with regular review. Non-operative treatment is also associated with a higher rate of Charcot osteo-arthropathy17 and hence debate still continues as to the best form of management. There are some principles which must however be followed. In general there should be a low tolerance for any displacement as incongruity of the ankle can cause rapidly progressing post-traumatic arthritis or Charcot osteo-arthropathy. Even if neuropathy is not seen at presentation it cannot be assumed that it will not develop in the future. With loss of sensory protection to the ankle joint a mal-union may cause more significant long term problems and arise in a shorter timeframe. Closed reduction and casting of displaced fractures generally leads to displacement and merely delays surgical intervention, and better results are usually obtained with open reduction and internal fixation.18 If a fracture presents with pre-existing Charcot osteo-arthropathy or significant osteoarthritis then primary fusion is often indicated. Of the other fractures of the foot and ankle the general principle should be “do no harm”. Minimally displaced fractures are thus often treated conservatively. Calcaneal fractures are generally best treated conservatively except in the severely displaced as there can be potentially catastrophic wound complications. Talar fractures will require operative intervention if displaced or associated with significant collapse from avascular necrosis. Metatarsal fractures generally do well if treated conservatively and although mid-tarsal injuries are rare they often require
Charcot osteo-arthropathy Although tertiary syphilis was one of the leading causes of Charcot joints in the late 1800s, the commonest cause in modern society is diabetes mellitus. It is thought that the loss of proprioception and deep sensation ultimately leads to progressive joint degeneration, destruction, and disorganization secondary to repetitive unrecognized trauma. Using scintigraphy, it has been shown that in patients with diagnosed neuropathy there is increased blood flow within bone,11 thought to be due to an autonomic, neurally
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treatment for displacement and collapse and should be treated using similar protocols as to those for Charcot osteo-arthropathy in this region. Osteoporosis19,20 and delayed fracture healing21 are potential complications of diabetes. The exact aetiology is poorly understood but is likely to be multi-factorial, and can lead to spinal and hip fractures as well as those in the foot and ankle. It has, however, been shown that fasting hypoglycaemia may be the overriding risk factor for fracture development, and that a well controlled blood sugar level is important.22 The exact increase in fracture healing time in humans is difficult to assess and again is multi-factorial. The type and severity of diabetes is implicated as are associated co-morbidities including vascular insufficiency, renal disease and hyper-lipidaemia. Smoking, diet and age are all also likely to influence the rate of fracture healing. A young fit type II diabetic may well heal at a normal rate whilst an elderly smoker with insulin dependence and co-morbidities may require immobilisation 2 to 3 times longer. The presence of a neuropathy is often used as an appropriate marker in deciding on doubling immobilization time.15,21 Weight bearing status (or not) should follow similar protocols as for those patients without diabetes as excessive non-weight bearing may predispose the patient to developing disuse osteopenia and potentially provoke Charcot osteo-arthropathy. In the presence of significant vascular insufficiency any orthopaedic intervention to treat a fracture will be compromised and a vascular surgical assessment should be requested. Although re-cannulation of distal vessels often produces only short term success, the improved blood supply may be sufficient to promote healing and prevent infection.
References 1 Sue Roberts (National Director for Diabetes). Working together for better diabetes care, clinical case for change. Department of Health, 16 May 2007, p. 1–16. 2 Brower AC, Allman RM. The neuropathic joint: a neurovascular bone disorder. Radiol Clin North Am 1981; 19(4): 571–580. 3 Jerosch-Herold C. Assessment of sensibility after nerve injury and repair: a systematic review of evidence for validity, reliability and responsiveness of tests. J Hand Surg [Br ] 2005; 30(3): 252–264. 4 Pham H, Armstrong DG, Harvey C, Harkless LB, Giurini JM, Veves A. Screening techniques to identify people at high risk for diabetic foot ulceration: a prospective multicenter trial. Diabetes Care 2000; 23(5): 606–611. 5 National Diabetes Support Team. Diabetic foot guide. NHS Clinical Governance Support Team. 2006, p. 1–12. 6 Brodsky JW. The diabetic foot. In: Coughlin MJ, Mann RA, eds. Surgery of the foot and ankle. Mosby, 1999, p. 895–969. 7 Trepman E, Pinzur MS, Shields NN. Application of the total contact cast. Foot Ankle Int 2005; 26(1): 108–112. 8 Myerson M, Papa J, Eaton K, Wilson K. The total-contact cast for management of neuropathic plantar ulceration of the foot. J Bone Joint Surg Am 1992; 74(2): 261–269. 9 Edwards J. Debridement of diabetic foot ulcers. Issue 4. Art. No.: CD003556. Cochrane Database Syst Rev 2002. 10 Jones EA, Manaster BJ, May DA, Disler DG. Neuropathic osteoarthropathy: diagnostic dilemmas and differential diagnosis. Radiographics 2000(20 Spec No): S279–S293. 11 Edmonds ME, Clarke MB, Newton S, Barrett J, Watkins PJ. Increased uptake of bone radiopharmaceutical in diabetic neuropathy. Q J Med 1985; 57(224): 843–855. 12 Eichenholtz Sidney N. Charcot joints. Springfield, Ill., C.C. Thomas, 1966. 13 McCormack RG, Leith JM. Ankle fractures in diabetics. Complications of surgical management. J Bone Joint Surg Br 1998; 80(4): 689–692. 14 Jones KB, Maiers-Yelden KA, Marsh JL, Zimmerman MB, Estin M, Saltzman CL. Ankle fractures in patients with diabetes mellitus. J Bone Joint Surg Br 2005; 87(4): 489–495. 15 Costigan W, Thordarson DB, Debnath UK. Operative management of ankle fractures in patients with diabetes mellitus. Foot Ankle Int 2007; 28(1): 32–37. 16 Flynn JM, Rodriguez-del RF, Piza PA. Closed ankle fractures in the diabetic patient. Foot Ankle Int 2000; 21(4): 311–319. 17 Holmes Jr. GB, Hill N. Fractures and dislocations of the foot and ankle in diabetics associated with Charcot joint changes. Foot Ankle Int 1994; 15(4): 182–185. 18 Schon LC, Easley ME, Weinfeld SB. Charcot neuroarthropathy of the foot and ankle. Clin Orthop Relat Res 1998; 349: 116–131. 19 Levin ME, Boisseau VC, Avioli LV. Effects of diabetes mellitus on bone mass in juvenile and adult-onset diabetes. N Engl J Med 1976; 294(5): 241–245. 20 Krakauer JC, McKenna MJ, Buderer NF, Rao DS, Whitehouse FW, Parfitt AM. Bone loss and bone turnover in diabetes. Diabetes 1995; 44(7): 775–782. 21 Marks RM. Complications of foot and ankle surgery in patients with diabetes. Clin Orthop Relat Res 2001; 391: 153–161. 22 Holmberg AH, Nilsson PM, Nilsson JA, Akesson K. The association between hyperglycemia and fracture risk in middle age. A Prospective, Population-Based Study of 22,444 men and 10,902 women. J Clin Endocrinol Metab 2008; 93(3): 815–822.
Summary • The diabetic foot and ankle is a complex problem requiring a multidisciplinary approach. • Diabetes reduces oxygen and nutrient delivery through chan ges in the vascular system. • Neuropathy causes loss of protective sensation, deformity and swelling. • Arteriopathy and changes in innate immunity reduce healing potential. • Ulcerations mainly due to vascular insufficiency, rather than neuropathy, should be treated by the vascular surgeons. • Superficial ulcerations often only require off loading with total contact casting and regular review. • Infected, extensive or deep ulcerations may require surgical debridement +/− antibiotics. • Necrotising fasciitis should be suspected in diabetics with rapidly worsening infection and treated expectantly. • Prominent areas secondary to deformity often require surgical correction or excision to aid ulcer healing. • Fractures of the foot and ankle require anatomical reduction and in high risk patients a doubling of immobilisation time. • Distal vascular reconstruction is becoming increasingly available to improve soft tissue and bony healing. • Operative intervention is associated with high complication rates, however, poor reduction leads to post-traumatic arthropathy or Charcot osteo-arthropathy and thus further surgical intervention with again high complication rates. ◆ ORTHOPAEDICS AND TRAUMA 23:1
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Learning points
Necrotising fasciitis is most commonly due to Group A Streptococcus. Treatment includes fluid resuscitation, intravenous penicillin or clindamycin, wide surgical debridement of necrotic tissue and incision of fascial planes into healthy tissue. Second review in theatres is required at 24 hours with further debridement if necessary. Delayed primary closure may be possible following successful treatment.
An ABPI >0.7 and <1.3 may be used to determine adequate blood flow. A transcutaneous oxygen pressure of >40 mmHg also suggests adequate arterial flow. Whilst neuropathic ulcers may be tackled by the orthopaedic surgeon, ischaemic ulcers require vascular surgical input as arterial reconstruction may be required for the resolution of ulceration and limb salvage.
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