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  • 1. FOOT AND ANKLEThe diabetic foot and ankle p ­ redicted to be around 750,000 higher for those with undiag- nosed disease. The ratio of type I : type II diabetes is around 1:10, with type II becoming more prevalent due to Britain hav-James C Stanley ing the fastest growing rate of obesity in the developed world (the risk of developing type II diabetes is around 10x greaterAndrew M Collier 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.Abstract Although foot and ankle pathology is common in the non-Diabetes mellitus is a common malady of our time with ever increasing d ­ iabetic population, the orthopaedic surgeon should remainnumbers of patients presenting with diabetic foot and ankle pathology. vigilant for patients with undiagnosed diabetes. A high indexDiabetes requires treatment by a multidisciplinary team and vascular dis- of suspicion should be used when reviewing patients in theease requires management involving vascular surgeons. There is, how- outpatients and emergency departments for apparently simpleever, an increasing burden on the orthopaedic surgeon with ulceration, pathology such as paronychia, slow healing wounds or similarfoot deformity, osteomyelitis and Charcot osteo-arthropathy being direct conditions. Simple urine glucose and serum tests will providecomplications of diabetes. Potential severe complications following frac- early diagnosis of diabetes and may crucially influence decisionsture and elective surgery require an understanding of diabetes and its on patients requiring surgery.effects on soft tissue and bone. The key topics are: Pathophysiology -effects of hyperglycaemia on vascular, neuronal and immune systems, The effects of hyperglycaemia on the foot and ankleAssessment - examination of diabetic foot pathology and how to spotthe ‘at risk foot’, Ulceration - management of foot and ankle ulceration Hyperglycaemia promotes changes in the microvasculature sec-and indications for intervention, Charcot osteo-arthropathy - brief over- ondary to thickening of the basement membrane, sorbitol accu-view of Charcot-type foot and ankle disease, and Management of ankle mulation and loss of nitric oxide auto-regulation. This ultimatelyfractures - overview of current trends in options for conservative and leads to reduced nutrient and oxygen exchange. In the foot this issurgical intervention. commonly seen with fat pad atrophy, inability to form skin callus, nerve ischaemia, tissue necrosis, muscle atrophy, and poor heal-Keywords diabetic ankle fractures; diabetic foot; diabetic ulceration ing 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 struc- tural changes secondary to non-enzymic glycation and damage toIntroduction essential signal pathways, the degree of which is proportional toDiabetic care requires a multidisciplinary team approach with the magnitude of hyperglycaemia. All types of peripheral nervegeneral practitioners, podiatrists and endocrinologists mediating are affected including sensory, motor and autonomic, with eachthe majority of care. Vascular disease is common and requires leading to specific changes seen in the diabetic foot and ankle.vascular surgical assessment; however, there is an increas- Sensory nerve damage leads to a typical glove and stockinging burden on the orthopaedic surgeon in the management of distribution of sensory loss, resulting in a loss of protective sensa-neuropathic ulceration and deformity. While the term ‘diabetic tion to pressure/traumatic injury. Motor loss causes small musclefoot and ankle’ often refers to ulceration, gangrene and Charcot atrophy and forefoot deformity with toe deformity and increasedosteo-arthropathy, diabetes also has a significant influence on the prominence of the metatarsal heads. Non-enzymic cross-linkingmanagement of foot and ankle fractures/soft tissue injury. The of collagen in the presence of hyperglycaemia makes soft tis-management of foot and ankle pathology in diabetics requires an sues inflexible causing stiff joints and a tight Achilles tendon,understanding of hyperglycaemic tissue injury to predict, prevent worsening the forefoot pressure related to motor dysfunction.and treat complications of soft tissue ulceration, deformity and Autonomic dysfunction reduces sweating, leading to dry crackedtraumatic injury. skin and producing potential access for pathological organisms to The number of people in the UK diagnosed with diabetes deeper structures. Autonomic loss also causes arterial dilatationmellitus in 1996 was 1.4 million; it has now exceeded 2.3 mil- of diseased vessels with a paradoxical hyperaemia, resulting inlion (equivalent to ∼3% of the population) with the true figure the deceptive appearance of a well perfused foot. The hyperae- mia leads to increased osseous blood flow, ultimately causing a demineralization of the bone matrix (one of the processes thoughtJames C Stanley MBBS MRCS is Specialist Registrar at the Department of to be involved in the development of Charcot-type destruction).2Orthopaedics, Harrogate District Hospital, North Yorkshire, UK. Loss of autonomic control over the venous system also causes venous congestion and further ulceration complications.Andrew M Collier MB ChB FRCS(Tr & Orth) is Consultant Orthopaedic Innate immunity, essential for initiation of healing and fight-Surgeon at the Department of Orthopaedics, Harrogate District ing infection, is impaired due to changes in neutrophil activity.Hospital, North Yorkshire, UK. The high tissue concentrations of glucose are also an ideal cultureORTHOPAEDICS AND TRAUMA 23:1 61 © 2008 Elsevier Ltd. All rights reserved.
  • 2. FOOT AND ANKLEmedium for bacterial colonization. Thus, even in the presence of general malaise may be the overriding feature of sepsis and stan-an apparently adequate blood supply ulceration, infection and dard observations (BP, HR and temp) are required.poor healing may prevail, leading to the high complication rates Surveillance within the community of diabetic patientsseen following traumatic injury and surgical intervention in the reduces significant complications by identifying the ‘at risk foot’diabetic foot and ankle. and is the cornerstone of a diabetic foot management program. Table 1 summarizes the various tissue injuries caused by Examination of the skin quality, bony deformity or tight Achilleshyperglycaemia and the potential associated pathologies. tendon, sensation and vascularity can identify the ‘at risk foot’ Delayed fracture healing in diabetics is well described. and instigate early referral.Although the exact mechanism is unclear, it is likely to be multi- Inspection of the diabetic foot will often illustrate commonfactorial involving insulin effects on callus formation, alterations findings. Thin, shiny, dry skin which is hairless and often discol-in neutrophil activity and osseous blood flow and glycation of oured due to dependant rubor will require moisturizers, surgicalenzymic pathways. Wound healing is similarly affected resulting shoes with total contact insoles and regular review. Hypertrophicin high complication rates for open wounds and surgical inci- nails are often misshapen and require chiropody to reduce paro-sions around the foot and ankle. nychia and spreading infection. Individual inspection of the web spaces may reveal pathology easily missed by the more casual examiner.Assessment of the foot and ankle in diabetics Pulses and blood pressure measurements (ankle brachialGeneral assessment of the patient’s condition by the multi- pressure index or ABPI) are taken, with absent pulses and/or lowdisciplinary team includes looking for evidence of retinal and ABPIs being indicative of poor arterial supply, prompting refer-cerebro-vascular pathology, which is relevant to foot and ankle ral to a vascular surgeon for further assessment. Normal or highpathology as these contribute to falls, traumatic injury and poor ABPI measurements may, however, not reflect the true patencyfoot hygiene. Renal and cardiac disease may also contribute to of the vessels as Monckeberg’s sclerosis may occur, with calci-poor healing potential and should be optimised as part of the fication of the tunica media leading to incompressible of diabetic foot pathology. Pyrexia, tachycardia and Colour Doppler imaging is useful and should be requested via a vascular surgical team. Neurological assessment using Semmes-Weinstein monofila- Summary of hyperglycaemic tissue injury and ment hairs (size 5.07) is still considered to be the most reliable potential associated pathology and reproducible test for protective sensation.3 The filament is pressed against the skin and allowed to bend, which roughly Hyperglycaemic Injury Potential foot pathology equates to 10 g pressure. It is then repeated in three places. Posi- tive response to 2 out of 3 is considered sufficient to indicate Arterial wall thickening • Poor O2/nutrient delivery protective sensation is present. This is tested over specific weight pad atrophy • Fat bearing areas on the sole of the foot and is easily documented • Vessel infarct/tissue necrosis using a simple diagram (Figure 1), with sensation under the 1st • Poor healing potential metatarsal head being the single most predictive site. It must be Sensory nerve • Loss of sensory protection noted that any skin callus should be removed before document- • Unrecognised traumatic/ ing a loss of protective sensation. Further testing with a 75 g pressure injury filament can then be used to describe profound sensory loss. Spe- Motor nerve • Small muscle wasting of the cific documentation then needs to be made regarding any defor- foot mity, ‘at risk areas’ or ulcerations and signs of infection, with • Claw toes/prominent an appreciation of areas requiring surgical intervention. Table 2 metatarsal heads summarizes the necessary documentation in the assessment of Autonomic • Loss of sweating with the diabetic foot (Figure 2). atrophic, dry, cracked skin Arterial • Increased osseous blood Diabetic foot ulceration flow/demineralization Diabetic foot ulceration is not in itself a diagnosis but is a mani- • Paradoxical apparent festation of a spectrum of co-morbidities. During normal stance satisfactory blood flow there is approximately 3000 mmHg pressure under the metatarsal Venous heads, increasing 2- to 3-fold in the presence of fat pad ­necrosis. • Congestion/swelling/ Tightening of the tendoAchillis is also a common finding in dia- dependant ulceration betics, which further increases pressure under the metatarsal • Poor tissue perfusion/ heads. It is understandable therefore that foot pathology associ- nutrient exchange ated with diabetes is common, with 15% of all diabetics having a Innate immunity • Neutrophil dysfunction foot ulcer or deep infection in their lifetime (Figure 3).4 • Infection risk/poor healing Around the world approximately half of ulceration and ampu- potential tation cases are thought to be preventable5 and thus a high index of suspicion, monitoring and prevention by a multi-­disciplinaryTable 1 team for all diagnosed diabetics is vital. The importance ofORTHOPAEDICS AND TRAUMA 23:1 62 © 2008 Elsevier Ltd. All rights reserved.
  • 3. FOOT AND ANKLE Summary of necessary documentation in the assessment of the diabetic foot General Blood pressure (BP) Indicators of sepsis assessment Heart Rate (HR) Temperature (Temp) Lab tests Full blood count/CRP Indictors of infection Blood and urine Indication of current glucose diabetes control Blood HbA1c Indication of longer term diabetes control Vascular Pulses capillary Indicators of arterial assessment refill insufficiency Swelling and Indicators of venous varicosities insufficiency Doppler Ankle-brachial pressure index (ABPI) may have to used with caution but is valid if low Neurological Atrophic, dry Indicates risk of skin barrier breakdown Semmes-Weinstein Indicates loss of monofilament testing protective sensation (10  g in 2 out of 3 areas) Table 2Figure 1 a simple method for illustrating protective sensation is toplace a tick in the circle if protective sensation is present (10 g), a dot Management of diabetic foot ulcerationif it is not and a dot with a circle around it if profound sensory loss Appropriate multidisciplinary team input is always advised to(75 g) is noted. Ulceration may also be annotated on the same optimise the medical management of the patient’s diabetes. Thediagram if necessary. diabetic foot should be monitored regularly as early treatment of at risk areas can prevent many ulcerations. The simplest treat-d­ iagnosis and correct management cannot be over emphasised as ments include basic foot hygiene and regular moisturising to pre-over 1 in 10 foot ulcerations ultimately results in amputation. In vent fissuring secondary to autonomic sweat dysfunction. Toethe UK this approximately equates to 100 diabetic patients under- nails should be regularly trimmed to prevent pressure on the sur-going minor and major lower limb amputations every week. rounding soft tissues resulting in tissue barrier failure. Dietician 40% of ulcers are neuropathic in nature, 25% arterial and 35% input should also be utilized as often diabetic patients requiremixed, with around 1/3 being deep and 5% having osteomyelitis. zinc, magnesium and protein supplements to aid the healing pro- Foot ulceration in diabetics is multi-factorial but is often cess. Close attention to shoe wear is also essential. A loss of pro-described as being mainly arterial (approx. 25%), neuropathic tective sensation leads to inadvertent shearing injury from shoe(approx 40%) or mixed (approx 35%) in origin. Foot ulcers wear. Motor dysfunction often leads to bunions, cavus, claw toesusually occur in prominent areas caused by deformity where and hammer toe deformities, which produce prominent areasthe overlying skin is subjected to high or prolonged pressure. more susceptible to injury, often worsened by fat pad atrophyThe resultant shear stresses lead to a detachment of the skin from and venous insufficiency. This further exacerbates poorly fittingthe underlying tissue and superficial lacerations. The skin often shoes due to swelling and skin thinning due to stretching.has a bed with a necrotic cap or ulcer. Ulcers with a mainly neuro- The majority of patients who develop ulceration will requirepathic aetiology will have a healthy granulating bed whilst those colour Doppler imaging for evidence of vascular insufficiency,with a significant arterial component will have a necrotic bed. and vascular surgical input. With modern techniques distal The Wagner classification (modified by Brodsky)6 is the most revascularization is possible and although often prone to poorcommonly used descriptive classification of diabetic foot ulcer- long term results, it may provide sufficient support to allow ade-ations (Table 3), providing useful guidance to the management quate healing and save a potentially threatened limb.of each class of ulcer. A more comprehensive scale has been Offloading the affected area should redistribute pressure todeveloped at the University of Texas, which includes risk strati- larger areas, prevent shear and protect from inadvertent traumafication and expresses tissue breakdown, infection and gangrene and is best achieved with either the current gold standard ofseparately and this may become more commonly utilized in the total contact casting (TCC) or with a walker boot/modified foot-future. wear along with partial weight bearing. Traditionally non-weightORTHOPAEDICS AND TRAUMA 23:1 63 © 2008 Elsevier Ltd. All rights reserved.
  • 4. FOOT AND ANKLEFigure 2 Sensation being testing under the metatarsal heads. TheSemmes-Weinstein monofilament is pressed against the skin until thefilament bends. Various thicknesses of filaments are available each ofwhich bends with a predetermined pressure documented in grams.bearing was considered helpful, however, walking may actu-ally improve vascular flow and improve healing provided the Figure 3 Photograph illustrating a typical plantar ulceration seenulcer itself is protected from pressure. TCC provides an excel- in diabetic feet. The pressure area has become necrotic exposinglent environment for healing as it prevents point pressure and granulation tissue without significant infection or tendon/boneminimizes shearing of the skin. However, walker boots and exposure (Wagner 1). This is best treated by orthotics and offloading.modified footwear are also often used as TCC is a specializedtechnique not available in all centres and is time consuming to and collagen matrix), hyaluronic acid ester (Hyalofill), plateletapply. The TCC should be changed every 5 to 14 days to allow derived growth factor impregnated dressings (Regranex) anddressing changes and accommodate any swelling problems and those that apply living foetal foreskin cells (Dermagraft, Apli-has a reported mean healing time of around 39 days.7,8 TCC is graft). Ulcer debridement can often be performed in the outpa-not advised in patients with active infection, significant arterial tients due to sensory neuropathy diminishing any discomfort.occlusion, extremely thin skin, swollen skin or in patients with Simple debridement of necrotic skin edges and necrotic capspoor compliance (Figure 4). will expose tissue capable of healing. In cases where operative Superficial ulcerations without significant infection should be intervention is required for extensive infection a long incision isidentified early and treated with ulcer preparation and off-­loading. recommended, with Brunner incisions and minimal underminingNormal saline dressings, or absorbent dressings (Alignate, Hydro- to reduce iatrogenic soft tissue traction/injury. Tendon sheathsfibre etc) are often all that is required. Occlusive hydrocolloids, should be opened and washed to clear tracking pus. Vacuumhydrogels or hypertonic saline gels can help remove necrotic tis- assisted dressings have also been used to aid healing but aresue, with the Cochrane systematic review suggesting that avail- usually reserved for patients with ulcers resistant to more simpleable trials favour the use of hydrogel dressings for the removal measures or for large areas. Laval or maggot therapy has beenof slough and callus.9 Foams and calcium alginate are also useful suggested by some authors, however, review articles suggest thisfor ulcers producing moderate volumes of exudates. Iodine and to be no more beneficial than hydrocolloid dressings and surgicalsilver impregnated dressings have also been used. More recently, debridement when indicated.9biologically active dressings that encourage wound healing have Surgical management of ulceration is required for deep infec-been used with some success, including Promogran (cellulose tions, osteomyelitis and recalcitrant ulcers. Following debridementORTHOPAEDICS AND TRAUMA 23:1 64 © 2008 Elsevier Ltd. All rights reserved.
  • 5. FOOT AND ANKLE 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 Education and footwear Regular review 1 Superficial ulceration Offloading with total contact casting (TCC), Not infected (Wagner 1) Walking brace or footwear modification 2 Deep Ulceration exposing Surgical debridement and bone or tendon (Wagner 2) wound care Offloading Culture specific antibiotics 3 Extensive ulceration or Debridement +/− partial abscess (Wagner 3) amputation Offloading Culture specific antibiotics Ischaemia Classification A Not ischaemic Regular review B Ischaemia without gangrene Non-invasive vascular testing (Doppler) vascular consultation if symptomatic C Partial (forefoot) gangrene Vascular consultation for (Wagner 4) possible re-vascularisation Debridement as above D Complete foot gangrene Amputation and vascular (Wagner 5) consultationTable 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 shellcorrection of deformity may be indicated to relieve pressure areas and rocker bottom sole and duel density insole help eliminate pressureand allow ulcers to heal. Percutanous Achilles lengthening, meta- points, aid mobility and reduce stresses further.tarsal osteotomies, Keller’s arthroplasty, interphalangeal arthro-plasty and hammer toe correction may be appropriate. Using thisstrategy the majority of ulcers will heal within 2 to 3 months. 20 to 40% of all cases of necrotising fasciitis are in patients with A chronic ulcer recalcitrant to standard treatment should be known diabetes mellitus.biopsied to rule out Marjolin’s ulcer (squamous cell carcinoma of Necrotising fasciitis is a progressive, rapidly spreading infec-a chronic wound) and may require plastic surgical input for local tion of the deep fascial layers that affects both the overlying skinrotational flaps and skin cover. Split skin grafts should be avoided and underlying muscle. It may be secondary to many types ofin load bearing areas or those susceptible to shear stress. bacteria, often in synergism, but the commonest isolated organ- The presence of an ulcer does not per-se require antibiotics, ism is Group A Streptococcus. Initial presentation is often itchingeven with a positive microbiology swab, as colonization by a or pain which progresses to anaesthesia as the overlying skinmultitude of different bacteria is common. More important signs vessels infarct. Cellulitis may be present initially, although thisof significant infection include spreading cellulitis/lymphangitis, usually gives way to purplish skin and gangrene over only a cou-pus/abscess or if systemic illness and pyrexial. Infected ulcers will ple of hours. Tissue necrosis, putrid discharge, severe pain andrequire surgical debridement down to healthy, viable tissue and general systemic signs (pyrexia, malaise, diarrhoea, vomiting)broad spectrum intravenous antibiotics should be administered then become apparent. Soft tissue gas may be felt clinically asto treat both anaerobic and aerobic organisms. These are often crepitus but is often easiest to identify on plain X-ray.continued as oral medication for approximately 12 weeks, but Ultimately, the mortality rate of necrotising fasciitis is 80 tothis should be discussed with the microbiology team. Soft tissue 90%, thus early identification and treatment are vital. Followinggas in diabetes is most commonly caused by aerobic organisms resuscitation early, aggressive surgical debridement and open-or by mixed gram-negative rods (rather than Clostridium per- ing of the fascial planes is required. Biospies should be takenfringens), but necrotizing fasciitis must be ruled out as between from the spreading periphery as within the central gangrenousORTHOPAEDICS AND TRAUMA 23:1 65 © 2008 Elsevier Ltd. All rights reserved.
  • 6. FOOT AND ANKLEarea there will be organisms present which neither cause nor mediated vascular reflex ultimately resulting in a hyperaemia.add to necrotising fasciitis. The antibiotic of choice would be Thus, in addition to repetitive unrecognized trauma it is thoughti­ntravenous penicillin, or clindamycin as an alternative, to treat that the hyperaemia causes an osteopenia (secondary to a mis-Group A Streptococcus, but this may need to be altered subse- match in bone destruction and synthesis2) which weakens bonequently according to microbiology test results. Hyperbaric oxy- making it more susceptible to the repeated minor trauma. Thegen therapy may also be considered but is not available in most commonest joints to be affected by Charcot osteo-arthropathy arecentres. those in the foot due to an increase in inadvertent trauma from The diagnosis of deeper purulent infections and osteomyelitis walking, greater forces through the joints of the lower limb and ais based on both clinical and radiographic grounds. Although the greater degree of sensory loss. Charcot osteo-arthropathy occursexposure of bone at the base of an ulcer does not automatically in stages, as described by Sidney N Eichenholtz in 1966, result-lead to the diagnosis of osteomyelitis, its presence is highly sug- ing in fragmentation, coalescence and consolidation12 whichgestive and plain X-ray (looking for bone destruction) is indicated. typically occur over a 6-month period . The details of CharcotSome care should be made with the diagnosis of osteomyelitis osteo-arthropathy diagnosis and management are discussed in anot associated with ulceration because any radiographic changes separate article, however, in general Charcot osteo-arthropathymay be due to Charcot osteo-arthropathy, which requires very causes mid-foot (Rocker bottom foot) and ankle deformity and isdifferent treatment. MRI and white cell labelled scans may aid usually seen only in a neuropathic which is well perfused withdiagnosis but should be used with caution as many imaging find- good pulses.ings are common to both conditions.10 If any doubt remains abiopsy and culture will be required. Diabetic foot and ankle fractures Septic arthritis may mimic a number of conditions which aresimilar to those found with other inflammatory or neoplastic con- The treatment of ankle fractures in diabetes is a notorious chal-ditions, or with Charcot osteo-arthropathy, and when the area is lenge due to high complication rates, particularly of surgicalpainless due to neuropathy the definitive diagnosis is notoriously and soft tissue wounds. Historically surgical intervention leaddifficult.10 However, there should be a high index of suspicion to high amputation rates, with more recent reports continuingand again biopsy/aspiration will often be required. to highlight significant complication rates of around 45%.13,14 Amputation will ultimately be required for uncontrolled infec- The patient with significant co-morbidities is particularly at risktion and sepsis, recalcitrant osteomyelitis or unreconstructable and a multidisciplinary approach is essential to optimise thevascular insufficiency with gangrene. Amputation of the 1st ray patient’s condition. However, in the absence of neuropathy, vas-or 4th/5th rays are well tolerated in the diabetic population. cular insufficiency or co-morbidities diabetic patients appear toAmputations of the 3rd ray are less well tolerated and usually have an overall risk of complication similar to that for a matchedrequire more proximal amputations, either through the Lisfranc, population.14,15mid-tarsal (Chopart) or hindfoot (Symes) if there is sufficient soft Non-operative management may also lead to significanttissue cover. Otherwise, a transtibial amputation is performed. In infective wound complications16 and close attention to ill-fittingmid-tarsal amputations insertion of the dorsi-flexion tendons into casts and patient compliance is essential with regular review.the neck of the talus is required to prevent significant equinus Non-operative treatment is also associated with a higher ratefrom the pull of the tendoAchillis. Hindfoot amputations have of Charcot osteo-arthropathy17 and hence debate still continuesthe advantage of improving ambulation over short distances as to the best form of management. There are some principleswithout a prosthesis (eg to the toilet), however, prosthetic fit- which must however be followed. In general there should be ating is more difficult and close collaboration with the patient and low tolerance for any displacement as incongruity of the ankleorthotist is required in choosing a hindfoot amputation over a can cause rapidly progressing post-traumatic arthritis or Charcottranstibial amputation. osteo-arthropathy. Even if neuropathy is not seen at presenta- Previously, below knee re-vascularisation was thought to tion it cannot be assumed that it will not develop in the futile as microangiopathic occlusive disease was thought to With loss of sensory protection to the ankle joint a mal-unionbe responsible for tissue necrosis in the diabetic foot. It is now may cause more significant long term problems and arise in aconsidered that tissue necrosis results more from narrowing and shorter timeframe. Closed reduction and casting of displacedocclusion of larger vessels with the practical implication that fractures generally leads to displacement and merely delays sur-infections and ulceration are amenable to treatment and poten- gical intervention, and better results are usually obtained withtially cure through revascularization of below knee ­vessels. open reduction and internal fixation.18 If a fracture presents with pre-existing Charcot osteo-arthropathy or significant osteoarthri- tis then primary fusion is often ­indicated.Charcot osteo-arthropathy Of the other fractures of the foot and ankle the general principleAlthough tertiary syphilis was one of the leading causes of Charcot should be “do no harm”. Minimally displaced fractures are thusjoints in the late 1800s, the commonest cause in ­modern society often treated conservatively. Calcaneal fractures are ­ generallyis diabetes mellitus. It is thought that the loss of proprioception best treated conservatively except in the severely displacedand deep sensation ultimately leads to progressive joint degen- as there can be potentially catastrophic wound ­ complications.eration, destruction, and disorganization secondary to repetitive Talar fractures will require operative intervention if displacedunrecognized trauma. Using scintigraphy, it has been shown that or ­associated with significant collapse from avascular patients with diagnosed neuropathy there is increased blood Metatarsal fractures generally do well if treated conservativelyflow within bone,11 thought to be due to an autonomic, neurally and although mid-tarsal injuries are rare they often requireORTHOPAEDICS AND TRAUMA 23:1 66 © 2008 Elsevier Ltd. All rights reserved.
  • 7. FOOT AND ANKLEt­reatment for displacement and collapse and should be treated Referencesusing similar protocols as to those for Charcot osteo-arthropathy 1 Sue Roberts (National Director for Diabetes). Working together forin this region. better diabetes care, clinical case for change. Department of Health, Osteoporosis19,20 and delayed fracture healing21 are potential 16 May 2007, p. 1–16.complications of diabetes. The exact aetiology is poorly under- 2 Brower AC, Allman RM. The neuropathic joint: a neurovascular bonestood but is likely to be multi-factorial, and can lead to spinal disorder. Radiol Clin North Am 1981; 19(4): 571–580.and hip fractures as well as those in the foot and ankle. It has, 3 Jerosch-Herold C. Assessment of sensibility after nerve injury andhowever, been shown that fasting hypoglycaemia may be the repair: a systematic review of evidence for validity, reliability andoverriding risk factor for fracture development, and that a well responsiveness of tests. J Hand Surg [Br ] 2005; 30(3): 252–264.controlled blood sugar level is important.22 4 Pham H, Armstrong DG, Harvey C, Harkless LB, Giurini JM, Veves A. The exact increase in fracture healing time in humans is dif- Screening techniques to identify people at high risk for diabeticficult to assess and again is multi-factorial. The type and severity foot ulceration: a prospective multicenter trial. Diabetes Care 2000;of diabetes is implicated as are associated co-morbidities includ- 23(5): 606– vascular insufficiency, renal disease and hyper-lipidaemia. 5 National Diabetes Support Team. Diabetic foot guide. NHS ClinicalSmoking, diet and age are all also likely to influence the rate of Governance Support Team. 2006, p. 1–12.fracture healing. A young fit type II diabetic may well heal at a 6 Brodsky JW. The diabetic foot. In: Coughlin MJ, Mann RA, eds.normal rate whilst an elderly smoker with insulin dependence Surgery of the foot and ankle. Mosby, 1999, p. 895–969.and co-morbidities may require immobilisation 2 to 3 times lon- 7 Trepman E, Pinzur MS, Shields NN. Application of the total contactger. The presence of a neuropathy is often used as an appropriate cast. Foot Ankle Int 2005; 26(1): 108–112.marker in deciding on doubling immobilization time.15,21 Weight 8 Myerson M, Papa J, Eaton K, Wilson K. The total-contact cast forbearing status (or not) should follow similar protocols as for management of neuropathic plantar ulceration of the foot. J Bonethose patients without diabetes as excessive non-weight bearing Joint Surg Am 1992; 74(2): 261–269.may predispose the patient to developing disuse osteopenia and 9 Edwards J. Debridement of diabetic foot ulcers. Issue 4. Art. No.:potentially provoke Charcot osteo-arthropathy. CD003556. Cochrane Database Syst Rev 2002. In the presence of significant vascular insufficiency any ortho- 10 ones EA, Manaster BJ, May DA, Disler DG. Neuropathic Jpaedic intervention to treat a fracture will be compromised and osteoarthropathy: diagnostic dilemmas and differential diagnosis.a vascular surgical assessment should be requested. Although Radiographics 2000(20 Spec No): S279– of distal vessels often produces only short term 11 dmonds ME, Clarke MB, Newton S, Barrett J, Watkins PJ. Increased Esuccess, the improved blood supply may be sufficient to promote uptake of bone radiopharmaceutical in diabetic neuropathy. Q J Medhealing and prevent infection. 1985; 57(224): 843–855. 12 ichenholtz Sidney N. Charcot joints. Springfield, Ill., C.C. Thomas, E 1966.Summary 13 cCormack RG, Leith JM. Ankle fractures in diabetics. Complications M • The diabetic foot and ankle is a complex problem requiring a of surgical management. J Bone Joint Surg Br 1998; 80(4): 689–692. multidisciplinary approach. 14 ones KB, Maiers-Yelden KA, Marsh JL, Zimmerman MB, Estin M, J • Diabetes reduces oxygen and nutrient delivery through chan­ Saltzman CL. Ankle fractures in patients with diabetes mellitus. ges in the vascular system. J Bone Joint Surg Br 2005; 87(4): 489–495.• Neuropathy causes loss of protective sensation, deformity and 15 ostigan W, Thordarson DB, Debnath UK. Operative management C swelling. of ankle fractures in patients with diabetes mellitus. Foot Ankle Int• Arteriopathy and changes in innate immunity reduce healing 2007; 28(1): 32–37. potential. 16 lynn JM, Rodriguez-del RF, Piza PA. Closed ankle fractures in the F• Ulcerations mainly due to vascular insufficiency, rather than diabetic patient. Foot Ankle Int 2000; 21(4): 311–319. neuropathy, should be treated by the vascular surgeons. 17 olmes Jr. GB, Hill N. Fractures and dislocations of the foot and H• Superficial ulcerations often only require off loading with total ankle in diabetics associated with Charcot joint changes. Foot Ankle contact casting and regular review. Int 1994; 15(4): 182–185.• Infected, extensive or deep ulcerations may require surgical 18 chon LC, Easley ME, Weinfeld SB. Charcot neuroarthropathy of the S debridement +/− antibiotics. foot and ankle. Clin Orthop Relat Res 1998; 349: 116–131.• Necrotising fasciitis should be suspected in diabetics with 19 evin ME, Boisseau VC, Avioli LV. Effects of diabetes mellitus on L r ­ apidly worsening infection and treated expectantly. bone mass in juvenile and adult-onset diabetes. N Engl J Med 1976; • Prominent areas secondary to deformity often require surgical 294(5): 241–245. correction or excision to aid ulcer healing. 20 rakauer JC, McKenna MJ, Buderer NF, Rao DS, Whitehouse FW, K • Fractures of the foot and ankle require anatomical reduction Parfitt AM. Bone loss and bone turnover in diabetes. Diabetes 1995; and in high risk patients a doubling of immobilisation time. 44(7): 775–782.• Distal vascular reconstruction is becoming increasingly 21 arks RM. Complications of foot and ankle surgery in patients with M a ­ vailable to improve soft tissue and bony healing. diabetes. Clin Orthop Relat Res 2001; 391: 153–161. • Operative intervention is associated with high complication 22 olmberg AH, Nilsson PM, Nilsson JA, Akesson K. The association H rates, however, poor reduction leads to post-traumatic ar- between hyperglycemia and fracture risk in middle age. thropathy or Charcot osteo-arthropathy and thus further sur- A Prospective, Population-Based Study of 22,444 men and 10,902 gical intervention with again high complication rates. ◆ women. J Clin Endocrinol Metab 2008; 93(3): 815–822.ORTHOPAEDICS AND TRAUMA 23:1 67 © 2008 Elsevier Ltd. All rights reserved.
  • 8. FOOT AND ANKLE Learning points Necrotising fasciitis is most commonly due to Group A Streptococcus. Treatment includes fluid resuscitation, An ABPI 0.7 and 1.3 may be used to determine adequate intravenous penicillin or clindamycin, wide surgical debridement blood flow. A transcutaneous oxygen pressure of 40 mmHg of necrotic tissue and incision of fascial planes into healthy also suggests adequate arterial flow. tissue. Second review in theatres is required at 24 hours with Whilst neuropathic ulcers may be tackled by the orthopaedic further debridement if necessary. Delayed primary closure may surgeon, ischaemic ulcers require vascular surgical input as be possible following successful treatment. arterial reconstruction may be required for the resolution of ulceration and limb salvage.ORTHOPAEDICS AND TRAUMA 23:1 68 © 2008 Elsevier Ltd. All rights reserved.