黑料网

ISSN: 2329-910X
Clinical Research on Foot & Ankle
Make the best use of Scientific Research and information from our 700+ peer reviewed, 黑料网 Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.

Review Article 黑料网

Diabetic Foot Ulcer-Diagnosis and Management

Simerjit Singh*Dinker R Pai,Chew Yuhhui
Department of Orthopaedics, Melaka Manipal Medical College, Jalan Batu Hampar, Bukit Baru, Melaka, Malaysia
Corresponding Author : Dr. Simerjit Singh
Department Of Orthopaedics, Melaka Manipal Medical College
Jalan Batu Hampar, Bukit Baru, Melaka, Malaysia
Tel: (606) 2925849/50/51
Fax: (606) 2817977
E-mail: Simer1980@Yahoo.Com
Received September 27, 2013; Accepted October 30, 2013; Published November 07, 2013
Citation: Singh S, Pai DR, Yuhhui C (2013) Diabetic Foot Ulcer - Diagnosis and Management. Clin Res Foot Ankle 1:120. doi:10.4172/2329-910X.1000120
Copyright: © 2013 Singh S, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Related article at
DownloadDownload

Visit for more related articles at Clinical Research on Foot & Ankle

View PDF Download PDF

Abstract

Diabetes Mellitus is known to have many complications and one of the most distressing is diabetic foot ulcer which affects 15% of people with diabetes. It puts enormous financial burden on the patient and the health care services, even though it is preventable. Diabetic foot ulcer is characterized by a classical triad of neuropathy, ischemia, and infection. Each of these has a multifactorial aetiopathogenesis. These factors are compounded by mechanical stress created by foot deformities. The most commonly used classification systems are the Wagner-Ulcer Classification system and the University of Texas Wound Classification. These classifications help to predict the outcome of this condition. Prevention of this condition is paramount to prevent long term morbidity and sometimes mortality. This can be achieved by patient self-awareness and emphasis on regular foot examinations during follow-up. Care of the diabetic foot should be multidisciplinary. Debridement, dressings and offloading are the pillars of local management. Simultaneous glycemic and infection control is also essential. Amputations are usually the treatment of last resort but occasionally can be considered early to allow for faster mobilization and rehabilitation. Causative factors like peripheral vasculopathy and neuropathy must also be appropriately treated.

style="padding-left:40px;">
Keywords
Diabetes mellitus; Vasculopathy; Amputations; Multifactorial aetiopathogenesis; Neuropathy; Ischemia; Infection
Introduction
Diabetes mellitus (DM) is a serious and complex disease affecting almost all the vital organs in the body. About 347 million people in the world are diagnosed with DM [1] and majority of them are due to DM type 2 [2]. In recent years, studies have substantiated the relationship of sugar sweetened beverages and cardiovascular diseases, type 2 DM and long term weight gain [3]. The incidence of DM is on the rise and it has been predicted that it will increase by a double by the year 2030 [4]. DM is known to have many complications and one of the most distressing is Diabetic Foot Ulcer (DFU) which affects 15% of people with diabetes [5]. The incidence and importance of this complication is highlighted by the fact that papers on diabetic foot in Pub-Med have increased from 0.7% in the 1980-88 to 2.6% in 1998-2004 [6]. DFU is prone to infections, chronicity and recurrence which eventually affect the mental health of patients [7]. A benign looking ulcer in a patient with diabetes often ends up in amputation. A study in the United States reported that 38% of all the amputations were associated with DM [8]. This can lead to severe morbidity and mortality. Therefore DFU puts enormous financial burden on the patient and the health care services, even though it is preventable [9]. The successful DFU management strategies involve intensive prevention, early assessment and aggressive treatment by a multi-disciplinary team of experts. The aim of this review is to discuss the current diagnostic and management options for diabetic foot ulcer.
Aetiopathogenesis
DFU is characterized by a classical triad of neuropathy, ischemia, and infection [5]. Due to the impaired metabolic mechanisms in DM, there is an increased risk of infection and poor wound healing due to a series of mechanisms which include decreased cell and growth factor response, diminished peripheral blood flow and decreased local angiogenesis [10]. Thus, the feet are predisposed to peripheral vascular disease, damage of peripheral nerves, deformities, ulcerations and gangrene.
Neuropathy
Neuropathy causes more than 60% of the foot ulcers [11] and affects patients with both type 1 and type 2 DM. Rise in blood glucose levels leads to increased enzyme production such as aldose reductase and sorbitol dehydrogenase. These enzymes convert glucose into sorbitol and fructose. As these sugar products accumulate, the synthesis of nerve cell myoinositol is decreased, affecting nerve conduction [11]. Furthermore, hyperglycaemia induced microangiopathy leads to reversible metabolic, immunologic and ischemic injury of autonomic, motor and sensory nerves [12]. This causes a decrease in peripheral sensation and damages the nerve innervations of small muscles of the foot and fine vasomotor control of the pedal circulation [13].
When the nerve gets injured, the patient is at a higher risk of getting a minor injury without noticing it until it becomes an ulcer. The risk of developing foot ulcers in patients with sensory loss is increased up to seven-fold, compared to non-neuropathic patients with diabetes [4]. DM also affects the autonomic nervous system, leading to dryness and fissuring of skin, making it prone to infection. Autonomic system also controls the microcirculation of skin. These changes ultimately contribute to the development of ulcers, gangrene, and limb loss [14,15]. Peripheral neuropathy has also been implicated in Charcot neuroarthropathy [16,17].
Vasculopathy
Hyperglycemia causes endothelial cell dysfunction and smooth cell abnormalities in peripheral arteries. Endothelial cells synthesize nitric oxide which causes vasodilation and protects the blood vessels from endogenous injury. Hence, in hyperglycemia, there is perturbation of the physiological properties of nitric oxide which usually regulates the endothelial homeostasis, anticoagulation, leukocyte adhesion, smooth muscle cell proliferation and antioxidant capacity. Endothelium-derived vasodilators and nitric oxide are decreased hence leading to constriction of the blood vessels [18] and propensity for atherosclerosis [19], eventually leading to ischemia. Ischemia can also occur even in the presence of palpable pedal pulses [13]. The microcirculation is also disturbed due to arteriolar-venular shunting, reducing the blood circulation to the area of need [13]. Hyperglycemia in DM is also associated with increase in thromboxane A2 leading to plasma hypercoagulability [20]. Clinically the patient may have signs of vascular insufficiency such as claudication, night pain or rest pain, absent peripheral pulses, thinning of skin, loss of limb hair etc. [21].
Immunopathy
Compared to a healthy person’s immune system, that of a patient with diabetes is much weaker. Thus, foot infection in a patient with diabetes is a limb threatening and debilitating condition. The hyperglycaemic state causes an elevation of pro-inflammatory cytokines and impairment of polymorphonuclear cell functions like chemotaxis, adherence, phagocytosis and intracellular killing [22]. Besides that, high blood glucose is a good medium for the growth of bacteria. The predominant organisms in diabetic foot infections are mainly aerobic gram positive cocci like S. aureus and β-hemolytic streptococci [23] but in one research conducted in India, gram-negative aerobes were the common microorganisms in diabetic foot [24]. The soft tissues of foot like plantar aponeurosis, tendons, muscles sheaths and fascia cannot resist infections. Furthermore, several compartments in the foot are interconnected and could not limit the spread of infection from one into another. This soft tissue infection can rapidly spread to the bones, causing osteitis. Thus a simple ulcer on the foot can easily result in complications such as osteitis/osteomyelitis and gangrene without appropriate care.
Mechanical stress
Insensate limbs are prone to injury which is often overlooked. The movements of the foot like flexion and extension are affected due to the damage to innervations of the foot muscles. Gradually, it leads to an alteration of the anatomical framework of the foot and formation of deformities. The deformities in turn create abnormal bony prominences and pressure points eventually predisposing to ulcers. Metatarsal fat pads are displaced distally, reducing the cushioning effects of the metatarsal heads and increase the pressure points which lead to callus formations that cause skin breakdown and ulceration [25,26]. Peripheral neuropathy promotes callus formation. The callus (callosity) contributes to high pressure areas and ulcer formation [27]. In the words of Duckworth et al. [28] “abnormally high pressures are more common in patients with diabetic neuropathy and almost all patients with a history of ulceration show high-pressure areas which correlate well with the site of previous ulceration.” Usually, ulcers occur on the plantar aspect of great toe and heel. However, ill-fitting shoes (which are the most common source of trauma) [29] can cause ulcers on the dorsal aspect [30]. Hence neuropathic foot ulcer formation in patients with diabetes has a complex multifactorial aetiopathogenesis wherein areas of high pressure complimented by peripheral neuropathy and associated skin changes lead to ulcer formation.
Neuroarthropathy
Charcot neuroarthropathy (CN) is a chronic painless progressive degenerative arthropathy resulting from the disturbance in sensory innervations of the affected joint. The impairment of the autonomic nervous system due to DM causes an increase in local blood supply and the resting blood flow is much higher than in the normal patient. The sudden increase in blood flow causes calcium to dissolve, leading to osteoclastic activity of the bone and thus damaging the bone [31]. Another theory is that the repetitive minor trauma to the insensate joints leads to fracture and disintegration [32]. The production of proinflammatory cytokines leads to uncontrolled osteolysis in CN. The cytokines such as tumor necrosis factor-α and interleukin-1β increase the expression of receptor activator of nuclear factor-κb (RANKL), which in turn causes maturation of osteoclasts by triggering production of nuclear factor-κb [32]. The hallmark deformity associated with this condition is midfoot collapse, also known as “rocker-bottom” foot. There might be hallux valgus deformity and loose bodies in the joint cavity. The deformities associated with CN also predispose for recurrent ulcerations.
Classification
To date, there are many classifications of Diabetic foot. However, the most commonly used classification systems are the Wagner-Ulcer Classification system [33] (Table1) and the University of Texas Wound Classification [34]. The University of Texas Wound Classification is a simple classification that considers grade (depth of the lesion) and stage (presence or absence of infection and ischaemia). The ‘grade’ ranges from 0 (pre- or post-ulcerative completely epithelized lesion) to III (involvement of bone or joint). ‘Stage’ ranges from A (absence of both infection and ischaemia), B (infection), C (ischaemia) and D (infection and ischaemia). The ‘grade and stage’ are combined to give the final classification (Table 2).
In both classifications, the higher the grade, the higher the risk of amputation with a longer healing time. Samson et al. found ‘The University of Texas Wound classification system’ to be better predictor of outcome [35]. However both the systems do not take into account the severity of infection [36]. Another validated classification system for DFUs that includes the severity of infection is The PEDIS (perfusion, extent, depth, infection, and sensation) system [36].
Diagnosis
History and physical examination
A proper investigation should be carried out in all patients with diabetes. A good history should include the duration of DM, neuropathic and peripheral vascular disease symptoms, previous ulcers or amputations and any other complication of DM like retinopathy or nephropathy [37]. A complete history will aid in assessing the severity and risk of foot ulceration.
Foot examinations are reported to be effective in reducing the risk of amputations [38]. The foot should be carefully inspected for abnormalities like dry skin, fissures, deformities, and callosities. Ulcerations, prominent veins, and nail lesions should be looked out for. Changes in the foot temperature must be noted. An increase in temperature might suggest inflammation [39] while a decrease may indicate ischemia. Capillary refilling time should be assessed. All peripheral pulses must be examined. Pain, redness and swelling of the insensate foot/ankle should alert the examiner for CN, which can be easily confused with septic or gouty arthritis.
Examination of ulcer
A sterile stainless steel probe is used for assessing the ulcer to determine the depth and if there are sinus tracts present [40]. The location, size, shape, depth, base and margins of the ulcer should be examined clinically. Presence of granulation tissue or slough should be looked for in the floor of the ulcer to determine subsequent management (Figure1 and 2). Diagnosing a soft tissue infection in patient with diabetes is sometimes difficult, as the signs of inflammation of the overlying ulcer may be absent. The infection is mainly diagnosed based on presence of clinical signs and symptoms such as redness, warmth, tenderness, purulent secretions and fever [9] (Figure3). Palpation of the bone at the base of the ulcer with a sterile, blunt stainless steel probe has been suggested as positive predictor of underlying osteomyelitis [40].
Neurological testing
Sensory neuropathy can be tested by using monofilaments and biothesiometer. Semmes-Weinstein monofilaments are reported to be easy to use and help in predicting the risk of ulceration and amputation [41]. Caputo et al. [42] suggested annual testing of all patients with diabetes with a nylon monofilament to detect peripheral neuropathy. A 128 Hz tuning fork can also be used to test for vibratory sensation over the tip of the great toe bilaterally since metabolic neuropathies are more severe distally. Pain sensation should be tested as well. The Heart Rate Variability (HRV) with deep breathing or orthostatic blood pressure is measured to detect autonomic neuropathy [43] and any decrease or absence of HRV is considered the earliest sign of autonomic neuropathy in DM [44]. Specialised tests for sudomotor dysfunction include thermoregulatory sweat testing, quantitative sudomotor axon reflex testing, silicone impressions, the Sympathetic Skin Response (SSR), and the quantitative direct and indirect axon reflex testing [45]. These tests can be used in various combinations to localise the lesion of autonomic dysfunction (pre-ganglionic or post-ganglionic) [45].
Laboratory investigations
The standard procedure involves measuring blood glucose level and urine for glucose and ketones. Other investigations like full blood count, blood urea, electrolytes, and creatinine levels should be monitored regularly. Glycosylated hemoglobin (HbA1C) is important to gauge the patient’s overall glycemic control as HbA1c shows the mean blood sugar concentration best over previous weeks to months [46]. Hepatic and renal function tests are necessary for monitoring the patient’s metabolic status. ESR can be done to assess the presence and response to treatment of infections like osteomyelitis [47]. Routine wound cultures are not recommended since all wounds harbour microorganisms [9]. However in the presence of invasive infection, cultures from the deeper tissue will help to identify the causative microorganisms.
Imaging
In case of diabetic foot, it is hard to assess the depth of the ulcer especially when there is pus and slough covering it. Also, it is hard to determine the extent of deep infection as the rubor of inflammatory response is minimal in subfascial sepsis [48]. X rays are helpful to determine the depth of foot ulceration and to assess presence of bone infection or neuroarthropathy. In CN, radiographs may reveal bony erosions, fractures, subluxation/dislocation of multiple joints, osteosclerotic features or united fractures [17]. Magnetic Resonance Imaging has emerged as a popular investigation for many of the foot problems. In Diabetic foot it is especially useful to detect infection and CN. It is used to evaluate the extent of foot infection by revealing the depth of ulceration, edema and localized fluid collections in the soft tissues, joints and tendon sheaths. Positron emission tomography demonstrates a high specificity for osteomyelitis [32].
Other investigations
Most of the DFUs may have silent osteomyelitis. Newman et al. found Indium-111 leukocyte scan to be 89% sensitive for diagnosing osteomyelitis in DFUs [49]. The treatment of ischaemic ulcers invariably requires surgical revascularization and hence differentiating them from neuropathic ulcers is paramount. Ankle brachial index (ABI) or toe-brachial index can be used to determine the extent of the vascular problem [50]. Values below 0.9 suggests an obstruction [51] while ABI less than 0.4 is associated with tissue necrosis and a significant risk for amputation [52]. Screening ABI every 5 years in patients with diabetes without any signs/symptoms of vascular insufficiency has been recommended. Pulse oximetry has also been reported to be as effective as ABI and the sensitivity of the test will be improved if used together with ABI [53]. The transcutaneous oxygen tension method is a reliable indicator of skin perfusion as periwound cutaneous perfusion is the critical physiological determinant of ulcer healing. TcPO2 less than 20mmHg has been associated with early wound healing failure [54]. Other investigations to detect vascular insufficiency include measuring absolute toe pressure, continuous-wave Doppler Ultrasonography, duplex ultrasonography, pulse volume recordings and angiography (CT, MRI or contrast). Pedobarography is a study of foot pressure and has been widely used in the research of diabetic foot [55]. In-shoe and barefoot peak plantar pressure measurement has also been suggested to assess foot at-risk and prevent ulcers [56].
In summary, DM affects multiple systems such as CVS, CNS, urinary, eye etc. Investigations in patients with DFU should be performed not only to assess local foot problems but also to assess the patient as a whole. Local investigations should be used to differentiate vascular from neurological problems, as the treatment of each is different. Detecting CN requires special investigations to differentiate it from other inflammatory conditions.
Management
Standard care for DFU is ideally provided by a multidisciplinary team by ensuring glycemic control, adequate perfusion, local wound care and regular debridement, off-loading of the foot, control of infection by appropriate antibiotics and management of comorbidities. Educating patients helpas in preventing ulcers and their recurrence.
Debridement
Ulcers heal faster when the wound is clean as the devitalized necrotic tissues hinder cell migration and predispose it to infection and prohibit healing. Debridement of the wound may hasten healing by removing the dead necrotic tissue, particulate matter, or foreign materials, and reducing bacterial load [57]. The conventional way is to use a scalpel and excise all unwanted tissues including callus and eschar (sharp debridement). Since the necrotic tissue often extends beyond the ulcer bed, some authors recommend liberal debridement of deeper tissue beyond the ulcer boundary [58]. Using repeated ‘piecemeal’ debridements and herbal drinks, Wong et al. [59] reported 87% success rate in limb salvage. They stated that the radical debridement causes inadvertent damage to the vascularity of local tissue. Another approach is to completely excise the chronic ulcer and the underlying bony prominences and convert it to a fresh ulcer. Some authors have reported good results with this approach [60,61]. The limiting factors of sharp debridement include inadvertent bleeding, poor pain tolerance by the patient and lack of any objective markers to differentiate impaired and healthy tissue to ascertain the extent of debridement [57]. Other methods of wound debridement include physical debridement using wet-to-dry dressings; hydrodissection or hydrocision with the use of high pressure saline beam; enzymatic debridement using enzymes like collagenase and papain as ointment preparations; autolytic debridement with the use of moisture retaining dressings; and biological debridement with use of larvae of common green bottle fly (Lucilia sericata). Maggot therapy is recommended for DFUs when surgical debridement and antibiotics fail to improve tissue healing [62]. Occasionally sharp debridement is combined with other forms of debridement to achieve ulcer healing.
Dressings
Dressing materials used include saline-moistened gauze dressings (wet-to-dry); moisture retaining dressings (hydrogels, hydrocolloids, hydrofibres, transparent films and alginates) that provide physical and autolytic debridement respectively; and antiseptic dressings (silver dressings, cadexomer). New advanced dressings are being researched, for example Vulnamin© gel made of amino acids and hyaluronic acid are used along with elastocompression has shown favourable results [63]. Promogran© by Johnson and Johnson’s is a freeze dried matrix composed of collagen and oxidized regenerated cellulose [64]. When in contact with wound exudates, it forms a biodegradable gel that physically binds and inactivates matrix metalloproteases that affects wound healing. A randomized control trial found it to be efficacious especially for ulcers of less than six months duration [65]. Medicated honey has antiinflammatory, antiseptic and osmotic properties and has been used as such or in combination with sterile dressings [66].
Offloading
Total contact cast (TCC), removable cast walkers, custom shoes, half-shoes, soft heel shoes, padded socks, and shoe inserts, wheelchairs, crutches etc. have been used for offloading the foot to prevent and treat the DFUs. The aim is to reduce the plantar pressure by redistributing it to a larger area, to avoid shear and friction, and to accommodate the deformities. A randomized control trial compared the efficacy of a TCC, removable cast walker and half-shoe in patients with DFUs found TCC to be the most effective modality [67]. TCC was also found to be superior to traditional dressings in treatment of plantar DFUs [68]. However, the limiting factors for TCC include requirement of trained personnel for its application and high costs due to need for frequent cast changings. Removable cast walkers such as Aircast walkers allow for surveillance of skin and dressing changes. One study [69] found them to be more cost effective than TCC. A recent systematic review found non-removable offloading devices (for example TCC) to be more effective for ulcer healing than removable off-loading devices (for example, removable cast walker) [70].
Medical treatment
Strict glycaemic control should be maintained with the use of diabetic diet, oral hypoglycaemic agents and insulin. Infections of the soft tissue and bone are the leading cause of hospital admissions in patients with DFUs [71]. As stated earlier, the diagnosis of infection in DFUs is primarily clinical. Culture from the deeper tissues aids in selecting appropriate antibiotics. While awaiting the results of wound culture, patients can be given empirical broad spectrum antibiotic regimen. Antibiotics are preferably given intravenously for limb threatening infections.
Gabapentin and pregabalin have been used for symptomatic relief for painful neuropathy in DM [72]. A recent study in Greece found pregabalin to be more cost effective as compared to gabapentin [73]. A double blinded randomised trial study of tramadol has been proven to be successful in alleviating pain symptoms in diabetic neuropathy [74]. Aldose reductase inhibitors are being studied and have shown to be effective in inhibiting progression of peripheral neuropathy [75,76]. Autonomic dysfunction may require the use of beta-blockers [14]. Medical management of symptoms of vascular insufficiency like intermittent claudication includes Cilostazol or Pentoxifylline besides exercise therapy.
Adjuvant therapy
Management strategies that target the defective extracellular matrix (ECM) in DFUs include the skin substitutes that are derived from growing skin cells of autologous or allogenic source onto collagen or polylactic acid [77]. They contain matrix which can be cellular for example DermagraftW (Shire Regenerative Medicine, Inc. La Jolla, California, United States) and Apligraf® (Novartis Pharma AG, Basel, Switzerland) or acellular like OasisW (Healthpoint, Ltd Fort Worth, Texas, United States) and Matriderm® (MedSkin Solutions Dr Suwelack AG, Germany) [78-80]. They promote wound healing by “promoting revascularization, cellular migration, and repopulation of wound fields through provision of an appropriate scaffold material to facilitate these processes” [81]. They should not be used as replacement to skin grafting or flap coverage as stressed by Brem et al. [82]. The high cost, limited availability, risk of transmissible diseases and immunological rejection limit their widespread use [77].
Hyperbaric Oxygen (HBO) has been found to be a useful adjunctive therapy for DFUs and is associated with decrease in amputation rates [83,84]. The beneficial role of topical oxygen therapy in treating chronic wounds has also been documented [85,86]. Negative pressure wound therapy involves creating a sub-atmospheric pressure at the wound site and draining out the exudates. It improves oxygenation, cellular proliferation and wound granulation and reduces bacterial load and inhibitory cytokines [87]. A study found better efficacy and decreased amputation rate with the use of negative pressure wound therapy compared to moist dressings (hydrogels, alginates) in the management of DFUs [88]. Extracorporeal shock wave therapy acts by increasing angiogenesis and blood supply, cellular proliferation and thus hastening wound healing. Some studies have found improved results with the use of shock therapy in DFUs [89,90]. Low energy lasers have also been used as an adjunctive therapy for DFUs [91,92]. They act by increasing microcirculation and improving healing of the ischaemic DFU. Growth factors for example recombinant human platelet derived growth factor (rhPDGF) [93], topical platelets [94] and platelet rich plasma [95] have also been used in treating DFUs and have shown favourable results.
Surgical management
Wound closure: Wound closure is attempted once the ulcer is clean with healthy granulation tissue. Primary closure is possible for small wounds; tissue loss can be covered with the help of skin graft, flap or commercially available skin substitutes. Split-thickness skin grafts are preferred over full thickness grafts. In one study [96], topical phenytoin application before autografting promoted granulation tissue formation and was found to enhance graft uptake in large DFUs. Yamaguchi et al. [97] used a combined method of treating DFUs by scraping the exposed bone till it bled and covered it with epidermal sheets obtained from suction blisters of patients. The authors stated 100% success rate with this technique. Another study [98] comparing skin grafting and standard dressing in the management of DFUs found better results in skin graft group in terms of decreased healing time and length of hospital stay. DFUs with exposed tendon, ligament or bone require coverage with muscle flaps [99]. Flaps can be either local (for smaller wounds) or freeflaps (for large area). Latissimus dorsi, gracilis or rectus abdominis are the commonly used free flaps [100]. The limitations of standard flaps include donor site morbidity, difficulty in shaping the flaps and interference with footwear [100].
Revascularization surgery: Patients with peripheral ischemia who have significant functional disability should undergo surgical revascularization if medical management fails. This may decrease the amputation risk in patients with ischaemic DFUs [101]. Brem et al. [102] advocated early revascularization after controlling the infection in cases of ischaemic DFUs. The procedures include open (bypass grafting or endarterectomy) or endovascular techniques (angioplasty with or without stent) [103].
The traditional method of treatment for ischemic limbs is surgical bypass. Autologous vein (preferably) or synthetic grafts may be used. Peroneal and dorsalis pedis bypass have been used and have acceptable limb salvage rates [104]. With regard to angioplasty, good results in terms of low post procedure amputation rate (5.2%) have been reported with the use of percutaneous transluminal angioplasty of infrapopliteal artery [105]. However a Cochrane review by Berridge et al. found no difference in limb salvage or death at one year between initial surgery and initial thrombolysis [106]. The authors concluded that the higher risk of complications associated with thrombolysis must be balanced against risks of surgery in every case.
Amputation: Amputations are generally used as a treatment of last resort when other measures fail. However, they may be also performed earlier to allow for earlier return to work or better functional status. For example, amputation is preferred over prolonged antibiotic therapy in case of toe infections (except for the great toe) [107]. Patients with DM account for around 40-60% of all the lower extremity amputations and most of them result from deterioration of foot ulcer [108]. Schaper et al. [36] mentioned that patients with diabetes who have a foot infection are around 50 times more likely to be hospitalized and 150 times more likely to undergo lower extremity amputation than those without foot infections. Determining the level of amputation requires the tradeoffs between vascularity and limb length. As a general principle, it is imperative to save as much limb length as possible. Clinical examination, ABI and transcutaneous oxygen measurements (before and after inhalation of oxygen) can be used to decide the level of amputation, but of these transcutaneous oxygen measurements are preferred [109]. The commonly performed amputations for ischaemic DFUs include toe, Ray, transmetatarsal, tarsometatarsal (Lisfranc), midtarsal (Chopart), hindfoot and ankle (Pirogoff, Boyd, Syme’s) and trans-tibial. A two-stage technique of Syme’s amputation has been described to decrease the risk of infection and wound healing reported with it in patients with diabetes [110]. However Pinzur et al. in a randomized control trial found singlestage Syme’s amputation as effective as two-stage amputation [111]. Tenectomy of the Achilles tendon is preferred along with Lisfranc and Chopart amputations to avoid equinus deformity. Tourniquet, thin skin flaps and suturing of muscles to bones (myodesis) are avoided [109]. Avoiding hematoma formation by meticulous haemostasis is desired. Post-amputation, simple moistened gauze dressings are preferred. Depression and anxiety are the common psychiatric illness in amputees [112,113] and the decision to amputate a patient’s limb must be made in consultation with the patient and with comprehensive counselling. Exostectomies, arthrodesis and amputation are done to manage complications such as CN. The indications for surgery in CN are failed conservative management with deformity, joint instability, infection and recurrent ulceration [32]. Osteomyelitis usually responds to antibiotics without the need for surgery. However, if required the infected bone can be resected if it does not affect the architecture of the foot [114].
Prevention
Patient education and self-care practices like maintaining foot hygiene and nail care should be promoted. Skin is kept moisturized with the application of topical moisturizers after washing the feet gently with soap and water [21]. Harsher measures like hot soaks, heating pads and topical agents such as hydrogen peroxide, iodine and astringents are better avoided [21]. There is direct correlation between glycemic control and ulcer formation [115]. Neuropathic feet are warmer and temperature differences of 2-7°C have been noted between neuropathic and nonneuropathic feet [116]. Hence self-monitoring may reduce the risk of ulceration [39]. Smoking and alcohol consumption should be minimized, though the direct link between them and DFUs is weak [115,116]. Offloading and appropriate footwear to relieve focal high pressure areas is recommended for foot at-risk. Other comorbidities like hypertension and hyperlipidaemia which predispose to vascular occlusion should be treated. Prevention of ulcer recurrence may also require corrective surgical interventions.
Factors Affecting Healing
Picwell et al. [117] studied factors affecting healing of diabetic foot ulcers that included the location of ulcer, duration of diabetes, ulcer duration, the presence of heart failure and peripheral arterial disease. The proximal location of the ulcer corresponded with maximal healing time with no difference in healing times between plantar and nonplantar ulcers. Sheehan et al. [118] noted that the percentage change in foot ulcer area after 4 weeks can predict of healing at the end of 12 weeks and can be used as an early indicator of unresponsiveness to treatment. Increased size and depth of ulcer have been associated with poor healing [119].
Summary
Diabetic foot is a chronic complication of DM which is not accorded the “glamour” status of its more illustrious sisters like coronary heart disease, cerebrovascular disease, nephropathy or retinopathy. Nonetheless it is responsible for a significant proportion of morbidity in DM, causing severe patient distress and frequently permanent disability. It is therefore necessary to pay special attention to this complication when reviewing, or counselling, patients with DM. This is all the more so as it is a complication that is preventable by simple measures that can largely be taken by the patient himself. Frequent clinical examination of the feet and related systems forms the mainstay of detecting diabetic foot; investigations are only an adjunct to clinical examination. The treatment is usually conservative and a limb sparing approach is used, along with proper diabetic control. Management of aetiological factors like vasculopathy, neuropathy and infection is essential to get good outcomes. Amputation is usually used as a last resort in non-salvageable limbs. Above all, this is one condition which proves the maxim that “prevention is better than cure”.
References

References

  1. value="1" id="Reference_Titile_Link">Danaei G, Finucane MM, Lu Y, Singh GM, Cowan MJ, et al. (2011)

  2. value="2" id="Reference_Titile_Link">

  3. value="3" id="Reference_Titile_Link">Malik VS, Popkin BM, Bray GA, Després JP, Hu FB (2010)

  4. value="4" id="Reference_Titile_Link">Wild S, Roglic G, Green A, Sicree R, King H (2004)

  5. value="5" id="Reference_Titile_Link">Pendsey SP (2010)

  6. value="6" id="Reference_Titile_Link">Boulton AJ (2004)

  7. value="7" id="Reference_Titile_Link">Carrington AL, Mawdsley SK, Morley M, Kincey J, Boulton AJ (1996)

  8. value="8" id="Reference_Titile_Link">Ziegler-Graham K, MacKenzie EJ, Ephraim PL, Travison TG, Brookmeyer R (2008)

  9. value="9" id="Reference_Titile_Link">Boulton AJ, Kirsner RS, Vileikyte L (2004)

  10. value="10" id="Reference_Titile_Link">Brem H, Tomic-Canic M (2007)

  11. value="11" id="Reference_Titile_Link">Clayton W, Elcasy TA (2009)

  12. value="12" id="Reference_Titile_Link">Younger DS, Rosoklija G, Hays AP (1998)

  13. value="13" id="Reference_Titile_Link">Jeffcoate WJ, Harding KG (2003)

  14. value="14" id="Reference_Titile_Link">Vinik AI, Maser RE, Mitchell BD, Freeman R (2003)

  15. value="15" id="Reference_Titile_Link">Boyko EJ, Ahroni JH, Stensel V, Forsberg RC, Davignon DR, et al. (1999)

  16. value="16" id="Reference_Titile_Link">Perrin BM, Gardner MJ, Suhaimi A, Murphy D (2010)

  17. value="17" id="Reference_Titile_Link">Rajbhandari SM, Jenkins RC, Davies C, Tesfaye S (2002)

  18. value="18" id="Reference_Titile_Link">Creager MA, Lüscher TF, Cosentino F, Beckman JA (2003)

  19. value="19" id="Reference_Titile_Link">Dokken BB (2008)

  20. value="20" id="Reference_Titile_Link">Paraskevas KI, Baker DM, Pompella A, Mikhailidis DP (2008)

  21. value="21" id="Reference_Titile_Link">Armstrong DA, Lavery LA (1998)

  22. value="22" id="Reference_Titile_Link">Gupta S, Koirala J, Khardori R, Khardori N (2007)

  23. value="23" id="Reference_Titile_Link">Lipsky BA, Berendt AR, Deery HG, Embil JM, Joseph WS, et al. (2004)

  24. value="24" id="Reference_Titile_Link">Gadepalli R, Dhawan B, Sreenivas V, Kapil A, Ammini AC, et al. (2006)

  25. value="25" id="Reference_Titile_Link">Bowering CK (2001)

  26. value="26" id="Reference_Titile_Link">Murray HJ, Young MJ, Hollis S, Boulton AJ (1996)

  27. value="27" id="Reference_Titile_Link">Rosen RC, Davids MS, Bohanske LM, Lemont H (1985)

  28. value="28" id="Reference_Titile_Link">Duckworth T, Boulton AJ, Betts RP, Franks CI, Ward JD (1985)

  29. value="29" id="Reference_Titile_Link">Macfarlane RM, Jeffcoate WJ (1997)

  30. value="30" id="Reference_Titile_Link">Peters EJ, Armstrong DA, Lavery LA (2007)

  31. value="31" id="Reference_Titile_Link">Rogers LC, Frykberg RG, Armstrong DG, Boulton AJM, Edmonds M, et al. (2011)

  32. value="32" id="Reference_Titile_Link">Madan SS, Pai DR (2013)

  33. value="33" id="Reference_Titile_Link">Wagner FW Jr (1981)

  34. value="34" id="Reference_Titile_Link">Lavery LA, Armstrong DG, Harkless LB (1996)

  35. value="35" id="Reference_Titile_Link">Oyibo SO, Jude EB, Tarawneh I, Nguyen HC, Harkless LB, et al. (2001)

  36. value="36" id="Reference_Titile_Link">Schaper NC, Dryden M, Kujath P, Nathwani D, Arvis P, et al. (2013)

  37. value="37" id="Reference_Titile_Link">Lavery LA, Armstrong DG, Vela SA, Quebedeaux TL, Fleischli JG (1998)

  38. value="38" id="Reference_Titile_Link">Mayfield JA, Reiber GE, Nelson RG, Greene T (2000)

  39. value="39" id="Reference_Titile_Link">Armstrong DG, Holtz-Neiderer K, Wendel C, Mohler MJ, Kimbriel HR, et al. (2007)

  40. value="40" id="Reference_Titile_Link">Grayson ML, Gibbons GW, Balogh K, Levin E, Karchmer AW (1995)

  41. value="41" id="Reference_Titile_Link">Mayfield JA, Sugarman JR (2000)

  42. value="42" id="Reference_Titile_Link">Caputo GM, Cavanagh PR, Ulbrecht JS, Gibbons GW, Karchmer AW (1994)

  43. value="43" id="Reference_Titile_Link">Rogers LC, Bevilacqua NJ (2008)

  44. value="44" id="Reference_Titile_Link">Unger J, Cole BE (2007)

  45. value="45" id="Reference_Titile_Link">Illigens BM, Gibbons CH (2009)

  46. value="46" id="Reference_Titile_Link">Koenig RJ, Peterson CM, Jones RL, Saudek C, Lehrman M, et al. (1976)

  47. value="47" id="Reference_Titile_Link">Rabjohn L, Roberts K, Troiano M, Schoenhaus H (2007)

  48. value="48" id="Reference_Titile_Link">Naraynsingh V, Maharaj R, Dan D, Hariharan S (2011)

  49. value="49" id="Reference_Titile_Link">Newman LG, Waller J, Palestro CJ, Schwartz M, Klein MJ, et al. (1991)

  50. value="50" id="Reference_Titile_Link">Shin JB, Seong YJ, Lee HJ, Kim SJ, Park JR (2000)

  51. value="51" id="Reference_Titile_Link">Doobay AV, Anand SS (2005)

  52. value="52" id="Reference_Titile_Link">Reiber GE, Pecoraro RE, Koepsell TD (1992)

  53. value="53" id="Reference_Titile_Link">Parameswaran GI, Brand K, Dolan J (2005)

  54. value="54" id="Reference_Titile_Link">Pecoraro RE, Ahroni JH, Boyko EJ, Stensel VL (1991)

  55. value="55" id="Reference_Titile_Link">Lobmann R, Kayser R, Kasten G, Kasten U, Kluge K, et al. (2001)

  56. value="56" id="Reference_Titile_Link">Patry J, Belley R, Côté M, Chateau-Degat ML (2013)

  57. value="57" id="Reference_Titile_Link">Pai, DR, Madan SS (2013) Techniques in Chronic Wound Management: Review of the Literature and Recent Concepts. J Nov Physiother 3: 2.

  58. value="58" id="Reference_Titile_Link">Shi JY, Zhou SL (1996) Diabetic teno-necrosis—a clinical study [in Chinese]. Shanghai J Trad Chin Med 5: 27-31.

  59. value="59" id="Reference_Titile_Link">Wong MW, Leung PC, Wong WC (2001)

  60. value="60" id="Reference_Titile_Link">Piaggesi A, Schipani E, Campi F, Romanelli M, Baccetti F, et al. (1998)

  61. value="61" id="Reference_Titile_Link">Armstrong DG, Lavery LA, Vazquez JR, Short B, Kimbriel HR, et al. (2003)

  62. value="62" id="Reference_Titile_Link">Mumcuoglu KY, Ingber A, Gilead L, Stessman J, Friedmann R, et al. (1998)

  63. value="63" id="Reference_Titile_Link">Abbruzzese L, Rizzo L, Fanelli G, Tedeschi A, Scatena A, et al. (2009)

  64. value="64" id="Reference_Titile_Link">

  65. value="65" id="Reference_Titile_Link">Veves A, Sheehan P, Pham HT (2002)

  66. value="66" id="Reference_Titile_Link">Shukrimi A, Sulaiman AR, Halim AY, Azril A (2008)

  67. value="67" id="Reference_Titile_Link">Armstrong DG, Nguyen HC, Lavery LA, Van Schie CH, Boulton AJ, et al. (2001)

  68. value="68" id="Reference_Titile_Link">Mueller MJ, Diamond JE, Sinacore DR, Delitto A, Blair VP 3rd, et al. (1989)

  69. value="69" id="Reference_Titile_Link">Verity S, Sochocki M, Embil JM, Trepman E (2008)

  70. value="70" id="Reference_Titile_Link">Morona JK, Buckley ES, Jones S, Reddin EA, Merlin TL (2013)

  71. value="71" id="Reference_Titile_Link">Gibbons GW (1987)

  72. value="72" id="Reference_Titile_Link">Backonja M, Beydoun A, Edwards KR, Schwartz SL, Fonseca V, et al. (1998)

  73. value="73" id="Reference_Titile_Link">Athanasakis K, Petrakis I, Karampli E, Vitsou E, Lyras L, et al. (2013)

  74. value="74" id="Reference_Titile_Link">Harati Y, Gooch C, Swenson M, Edelman S, Greene D, et al. (1998)

  75. value="75" id="Reference_Titile_Link">Hotta N, Kawamori R, Fukuda M, Shigeta Y; Aldose Reductase Inhibitor-Diabetes Complications Trial Study Group (2012)

  76. value="76" id="Reference_Titile_Link">Hotta N, Akanuma Y, Kawamori R, Matsuoka K, Oka Y, et al. (2006)

  77. value="77" id="Reference_Titile_Link">Rizzi SC, Upton Z, Bott K, Dargaville TR (2010)

  78. value="78" id="Reference_Titile_Link">Lev-Tov H, Li CS, Dahle S, Isseroff RR (2013)

  79. value="79" id="Reference_Titile_Link">Redekop WK, McDonnell J, Verboom P, Lovas K, Kalo Z (2003)

  80. value="80" id="Reference_Titile_Link">Jeon H, Kim J, Yeo H, Jeong H, Son D, et al. (2013)

  81. value="81" id="Reference_Titile_Link">Greaves NS, Iqbal SA, Baguneid M, Bayat A (2013)

  82. value="82" id="Reference_Titile_Link">Brem H, Young J, Tomic-Canic M, Isaacs C, Ehrlich HP (2003)

  83. value="83" id="Reference_Titile_Link">Faglia E, Favales F, Aldeghi A, Calia P, Quarantiello A, et al. (1996)

  84. value="84" id="Reference_Titile_Link">Liu R, Li L, Yang M, Boden G, Yang G (2013)

  85. value="85" id="Reference_Titile_Link">Kalliainen LK, Gordillo GM, Schlanger R, Sen CK (2003)

  86. value="86" id="Reference_Titile_Link">Sen CK, Khanna S, Gordillo G, Bagchi D, Bagchi M, et al. (2002)

  87. value="87" id="Reference_Titile_Link">Plikaitis CM, Molnar JA (2006)

  88. value="88" id="Reference_Titile_Link">Blume PA, Walters J, Payne W, Ayala J, Lantis J (2008)

  89. value="89" id="Reference_Titile_Link">Wang CJ, Wu RW, Yang YJ (2011)

  90. value="90" id="Reference_Titile_Link">Moretti B, Notarnicola A, Maggio G, Moretti L, Pascone M, et al. (2009)

  91. value="91" id="Reference_Titile_Link">Schindl A, Schindl M, Schön H, Knobler R, Havelec L, et al. (1998)

  92. value="92" id="Reference_Titile_Link">Landau Z, Schattner A (2001)

  93. value="93" id="Reference_Titile_Link">Hollinger JO, Hart CE, Hirsch SN, Lynch S, Friedlaender GE (2008)

  94. value="94" id="Reference_Titile_Link">Scherer SS, Tobalem M, Vigato E, Heit Y, Modarressi A, et al. (2012)

  95. value="95" id="Reference_Titile_Link">Villela DL, Santos VL (2010)

  96. value="96" id="Reference_Titile_Link">Younes N, Albsoul A, Badran D, Obedi S (2006)

  97. value="97" id="Reference_Titile_Link">Yamaguchi Y, Yoshida S, Sumikawa Y, Kubo T, Hosokawa K, et al. (2004)

  98. value="98" id="Reference_Titile_Link">Mahmoud SM, Mohamed AA, Mahdi SE, Ahmed ME (2008)

  99. value="99" id="Reference_Titile_Link">Attinger CE, Ducic I, Cooper P, Zelen CM (2002)

  100. value="100" id="Reference_Titile_Link">Schirmer S, Ritter RG, Fansa H (2013)

  101. value="101" id="Reference_Titile_Link">LoGerfo FW, Gibbons GW, Pomposelli FB Jr, Campbell DR, Miller A, et al. (1992)

  102. value="102" id="Reference_Titile_Link">Brem H, Sheehan P, Rosenberg HJ, Schneider JS, Boulton AJ (2006)

  103. value="103" id="Reference_Titile_Link">Albayati MA, Shearman CP (2013)

  104. value="104" id="Reference_Titile_Link">DarlingRC 3rd, Chang BB, Shah DM, Leather RP (1997)

  105. value="105" id="Reference_Titile_Link">Faglia E, Mantero M, Caminiti M, Caravaggi C, De Giglio R, et al. (2002)

  106. value="106" id="Reference_Titile_Link">Berridge DC, Kessel DO, Robertson I (2013)

  107. value="107" id="Reference_Titile_Link">Benton GS, Kerstein MD (1985)

  108. value="108" id="Reference_Titile_Link">Apelqvist J, Larsson J (2000) What is the most effective way to reduce incidence of amputation in the diabetic foot? Diabetes Metab Res Rev 16: 75-83.

  109. value="109" id="Reference_Titile_Link">Canale ST, Beaty JH (2008) Surgical principles of amputations: Campbell’s operative orthopaedics. (11thedn.) Mosby Elssevier, Philadelphia, Pennsylvania, USA.

  110. value="110" id="Reference_Titile_Link">Pinzur MS, Morrison C, Sage R, Stuck R, Osterman H, et al. (1991)

  111. value="111" id="Reference_Titile_Link">Pinzur MS, Smith D, Osterman H (1995)

  112. value="112" id="Reference_Titile_Link">Atherton R, Robertson N (2006)

  113. value="113" id="Reference_Titile_Link"> Singh R, Ripley D, Pentland B, Todd I, Hunter J, et al. (2009)

  114. value="114" id="Reference_Titile_Link">Lipsky BA (1997)

  115. value="115" id="Reference_Titile_Link">Moss SE, Klein R, Klein BE (1992)

  116. value="116" id="Reference_Titile_Link">Mayfield JA, Reiber GE, Sanders LJ, Janisse D, Pogach LM (1998)

  117. value="117" id="Reference_Titile_Link">Pickwell KM, Siersma VD, Kars M, Holstein PE, Schaper NC, et al. (2013)

  118. value="118" id="Reference_Titile_Link">Sheehan P, Jones P, Caselli A, Giurini JM, Veves A (2003)

  119. value="119" id="Reference_Titile_Link">Margolis DJ, Kantor J, Santanna J, Strom BL, Berlin JA (2000)

--
Diabetic Foot Ulcer-Diagnosis and Management
Post your comment

Share This Article

Relevant Topics

Recommended Journals

View More

Article Tools

Article Usage

  • Total views: 27524
  • [From(publication date):
    November-2013 - Nov 24, 2024]
  • Breakdown by view type
  • HTML page views : 22167
  • PDF downloads : 5357

Post your comment

captcha   Reload  Can't read the image? click here to refresh
Peer Reviewed Journals

Make the best use of Scientific Research and information from our 700 + peer reviewed, 黑料网 Journals

Journals by Subject

Agri and Aquaculture Biochemistry Bioinformatics & Systems Biology Biomedical Sciences Business & Management Chemical Engineering Chemistry Clinical Sciences Computer Science Economics & Accounting Engineering Environmental Sciences Food & Nutrition General Science Genetics & Molecular Biology
Geology & Earth Science Immunology & Microbiology Informatics Materials Science Mathematics Medical Sciences Nanotechnology Neuroscience & Psychology Nursing & Health Care Pharmaceutical Sciences Physics Plant Sciences Social & Political Sciences Veterinary Sciences

Clinical & Medical Journals

Anesthesiology Cardiology Clinical Research Dentistry Dermatology Diabetes & Endocrinology Gasteroenterology Genetics Haematology Healthcare Immunology Infectious Diseases Medicine Microbiology
Molecular Biology Nephrology Neurology Nursing Nutrition Oncology Ophthalmology Orthopaedics Pathology Pediatrics Physicaltherapy & Rehabilitation
Psychiatry Pulmonology Radiology Reproductive Medicine Surgery Toxicology
International Conferences 2024-25
 
Meet Inspiring Speakers and Experts at our 3000+ Global

Conferences by Country

Netherlands
New Zealand Philippines

Medical & Clinical Conferences

Conferences By Subject

Top