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International Journal of Surgery xxx (2015) 1e4
Contents lists available at ScienceDirect
International Journal of Surgery journal homepage: www.journal-surgery.net
Review
The diabetic foot management e Recent advance Q5
Prabhu Dayal Sinwar New PG Hostel Room No 28, Sardar Patel Medical College Bikaner, Rajasthan, India
h i g h l i g h t s
Q1
Diabetic neuropathy and peripheral vascular disease are the main etiological factors in foot ulceration. Wagner's classification is one of the most widely used and universally accepted grading systems for DFU, consisting of six simplistic wound grades used to assess ulcer depth. Assessment of peripheral neuropathy and evaluation of peripheral arterial status are the two important investigations in a diabetic foot. Management of diabetic neuropathic ulcer by appropriate and timely removal of callus, control of infection and reduction of weight bearing forces. Management of diabetic ischaemic foot are medical management, surgical management and percutaneous transluminal angioplasty of stenosed and occluded lower extremity arteries.
a r t i c l e i n f o
a b s t r a c t
Article history: Received 13 October 2014 Received in revised form 22 January 2015 Accepted 26 January 2015 Available online xxx
Diabetic ulceration of the foot represents a major global medical, social and economic problem. It is the commonest major end-point of diabetic complications. Diabetic neuropathy and peripheral vascular disease are the main etiological factors in foot ulceration and may act alone, together, or in combination with other factors such as microvascular disease, biomechanical abnormalities, limited joint mobility and increased susceptibility to infection. In the diabetic foot, distal sensory polyneuropathy is seen most commonly. The advent of insulin overcame the acute problems of ketoacidosis and infection, but could not prevent the vascular and neurological complications. Management of diabetic neuropathic ulcer by appropriate and timely removal of callus, control of infection and reduction of weight bearing forces. Management of diabetic ischaemic foot are medical management, surgical management and percutaneous transluminal angioplasty of stenosed and occluded lower extremity arteries. Foot ulceration in persons with diabetes is the most frequent precursor to amputation. © 2015 Published by Elsevier Ltd on behalf of Surgical Associates Ltd.
Keywords: Diabetic foot Neuropathy Atherosclerosis Neuropathic ulcer Angioplasty Amputation
Q2
1. Introduction Diabetic ulceration of the foot represents a major global medical, social and economic problem. It is the commonest major end-point of diabetic complications. Diabetic neuropathy and peripheral vascular disease are the main etiological factors in foot ulceration and may act alone, together, or in combination with other factors such as microvascular disease, biomechanical abnormalities, limited joint mobility and increased susceptibility to infection. Ulceration rarely results from a single pathology. It is the interaction of contributory causes which leads to the breakdown of the foot at risk [1]. The neuropathic foot, for example, does not spontaneously ulcerate. It is the combination of insensitivity and
either extrinsic factors e.g. walking barefoot and stepping on a sharp object, or simply wearing ill-fitted shoes, or intrinsic factors such as diminished sensation and the development of a callosity which progresses to an ulcer on walking. Neuropathy is the most significant pathology in the pathway to ulceration [2]. Diabetic foot disease is an important problem confronting the diabetologists, internists and surgeons [3]. The advent of insulin overcame the acute problems of ketoacidosis and infection, but could not prevent the vascular and neurological complications. Foot is the most vulnerable part in a diabetic. It is exposed to frequent trauma and requires a sensitive sensory protection, which is often lacking in a diabetic. The foot, being farthest away from the central nervous system and hemodynamically disadvantageously placed, becomes the common site of complicated lesions. Foot ulceration in persons with diabetes is the most frequent precursor to amputation [4,5]. Overall, patients with diabetes are more likely to have an
E-mail address: [email protected]. http://dx.doi.org/10.1016/j.ijsu.2015.01.023 1743-9191/© 2015 Published by Elsevier Ltd on behalf of Surgical Associates Ltd.
Please cite this article in press as: P.D. Sinwar, The diabetic foot management e Recent advance, International Journal of Surgery (2015), http:// dx.doi.org/10.1016/j.ijsu.2015.01.023
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amputation than patients without diabetes [6]. 2. Etiopathogenesis In a large prospective study by Lavery et al. [7], significant independent risk factors for DFI included wounds that penetrated to bone, wounds with a long duration, recurrent wounds, wounds with a traumatic aetiology and the presence of PAD. Although the etiopathogenesis of diabetic foot disease is multifactorial, three main factors, namely neuropathy, ischaemia and infection lead to tissue necrosis and ulcer formation [8]. Other factors are foot biomechanics and weight bearing, peripheral vessel calcifications, trauma, (possibly) diabetic autonomic neuropathy and microangiopathy and diabetic skeletal disease. 2.1. Neuropathy in diabetic foot In the diabetic foot, distal sensory polyneuropathy is seen most commonly. However, motor and autonomic fibres may also be involved and combined neuropathies frequently occur. The development of a neuropathy is linked to poor glycaemic control over many years and it increases in frequency with both age and the duration of diabetes. Multiple factors such as blood glucose concentration, blood lipids, structure of myelin sheath and its permeability, axonal flow and micro and macroangiopathy of the peripheral nerves contribute to the production of diabetic neuropathy [9]. Longitudinal data from the Rochester Study [10] supported the contention that the duration and severity of exposure to hyperglycemia influenced the severity of the neuropathy. Current research on diabetic neuropathy is focused on oxidative stress, advanced glycation-end products, protein kinase C and the polyol pathway [11]. 2.2. Blood flow in diabetic neuropathic foot Recent studies have shown that the blood flow is increased in diabetic foot. The latter is due to the arterio-venous shunting and dilated and stiff peripheral arteries [12]. The pulsatility index which is inversely proportional to the quantity of the blood flow is markedly reduced in diabetic foot. The normal Doppler flow pattern is triphasic: a forward flow in systole followed by a reverse flow and a further short forward flow in diastole. In diabetics there is an increased forward flow with the absence of reverse flow. 2.3. Skeletal changes in diabetic foot Due to increased blood flow to the lower limb there in enhanced blood supply to the bones of the diabetic foot. 2.4. Stiffening of arterial wall The medial wall calcification in the peripheral vessels in the lower limb raises ankle brachial systolic pressure and shortens transit times of pulse wave. In Charcot's diabetic neuroarthropathy vascular calcification is found in about 90% [13]. Ward et al. have shown that rapid increase in flow of blood bypasses small vessels and the capillary nutrient circulation and results in a relative distal ischaemia [14]. The enhanced blood flow, vasodilatation and arteriovenous shunting, all arising out of sympathetic denervation leads to abnormal venous pooling and oedema. Atherosclerosis of the large vessels of the leg in a diabetic is often multisegmental, distal and bilateral. Diabetic angiopathy is reported to be the most frequent cause of
morbidity and mortality in diabetic patients [15]. Macroangiopathy manifests as a diffuse multisegmental involvement typically involving the infrapopliteal vessels, and is also associated with compromised collateral circulation. Parving and Resmusen have demonstrated functional abnormality in the form of leakage of albumin from the capillaries to the interstitium; however an occlusive microvascular disease in the diabetic foot has not been clearly demonstrated [16]. The presence of neuropathy makes the feet insensitive and the diabetic patient is often not aware of even a severe mechanical trauma and gross infection. 3. Presentation Patients present with a variety of complaints ranging from local to systemic signs of infections. Local signs of infection may include pain/tenderness, erythema, oedema, purulent drainage and newonset malodor. Systemic signs of infection include anorexia, nausea, vomiting, fever, chills, night sweats, change in mental status and a recent worsening of glycaemic control. Wagner's classification is one of the most widely used and universally accepted grading systems for DFU, consisting of six simplistic wound grades used to assess ulcer depth (grades 0e5) [17]. This classification is limited by the inability to recognize ischaemia and infection as independent risk factors in all classification grades [18] (Table 1). Q3 A more recently proposed and popularized DFU classification is the University of Texas Health Science Center San Antonio (UT) classification system [18]. This system incorporates a matrix structure of four grades of wound depth with subgroups to denote the presence of infection, ischaemia or both (Table 2). Wounds with frank purulence and/or two or more local signs of inflammation such as warmth, erythema, lymphangitis, lymphadenopathy, oedema, pain and loss of function may be classified as ‘infected.’ Lower extremity vascular insufficiency is made by a combination of one or more clinical signs or symptoms of claudication, restpain, absent pulses, dependent rubor, atrophic integument, absence of pedal hair or pallor on elevation. From the practical point of view the diabetic foot can be divided into two major types: (1) Ischaemic diabetic foot and (2) Non Ischaemic neuropathic diabetic foot [8]. 4. Investigations Assessment of peripheral neuropathy and evaluation of peripheral arterial status are the two important investigations in a diabetic foot. Accurate sensory testing in diabetic neuropathy is of paramount importance in the diagnosis, objective quantification and monitoring natural evolution or effects of therapy. These involve testing for (1) Vibration perception Threshold (VPT) {assessed by a Biothesiometer}, (2) Thermal Discrimination Threshold (TDT) {assessed by using 1. Marstock stimulator 2. Automated thermal
Table 1 Wagner classification system. Grade
Wound depth
0 1 2 3 4 5
Pre-ulcerative area without open lesion Superficial ulcer (partial/full thickness) Ulcer deep to tendon, capsule, bone Stage 2 with abscess, osteomyelitis or joint sepsis Localized gangrene Global foot gangrene
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P.D. Sinwar / International Journal of Surgery xxx (2015) 1e4 Table 2 The University of Texas Health Science Center San Antonio (UT) classification system.
A B C D
0
1
2
3
No open lesion With infection Ischaemic Infection/ Ischaemia
Superficial wound With infection Ischaemic Infection/ Ischemia
Tendon/Capsule With infection Ischaemic Infection/ Ischemia
Bone/Joint With infection Ischaemic Infection/ Ischemia
3
line agent for the treatment of painful neuropathy [32]. Duloxetine is an inhibitor of the re-uptake of 5-hydroxytryptamine and norepinephrine and has recently been approved by the Food and Drug Administration for the treatment of neuropathic pain. 5.3. Management of diabetic ischaemic foot
5. Treatment
1. Medical Management. 2. Surgical Management. 3. Percutaneous Transluminal Angioplasty of stenosed and occluded lower extremity arteries. Medical management: It is indicated when ulcer is small, recent and also in those patients unfit for reconstructive surgery. Surgical management: This comprises of arterial reconstruction, sympathectomy and amputation. Arterial reconstruction e Indications for reconstructive surgery are intractable rest pain and claudication, nonhealing ulcers even after good medical management. Lumbar sympathectomy e For relief of ischaemic rest pain this has an important role to play. Percutaneous transluminal angioplasty: Angioplasty is particularly useful in high risk patients where surgery is contraindicated. The lesions most amenable for angioplasty include stenoses less 4 cm long and occlusions shorter than 10 cm.
5.1. Management of diabetic neuropathic ulcer
6. Dressing
The three cardinal principles of management are [8]: 1. Appropriate and timely removal of callus. 2. Control of infection. 3. Reduction of weight bearing forces. Delbridge and Lequesne et al. [23] have shown that the formation of callus is central to the development of neuropathic ulcer in a diabetic. After removing the callus a bacterial swab may be taken from the floor of the ulcer and appropriate antibiotic instituted. Dressing materials can include natural, modified and synthetic polymers, as well as their mixtures or combinations, processed in the form of films, foams, hydrocolloids and hydrogels. Moreover, wound dressings may be employed as medicated systems, through the delivery of healing enhancers and therapeutic substances (drugs, growth factors, peptides, stem cells and/or other bioactive substances). The most important aspect of promoting healing is to remove weight bearing force from the site of ulcer and ensure a redistribution of the shearing forces [24]. A recent systematic review by Patton et al. [25] demonstrated that insoles may prevent diabetic foot ulceration, but most of the evidence is poor and inconclusive. The current state of the art in insole design primarily addresses vertical forces with the aim of reducing foot pressures [26e28]. 1. Special foots. 2. Polyethylene foam insoles (Plastozole). 3. Micro cell rubber insole (Tovey's insole) [29]. 4. “Cork cradle” shoe. 5. Special windows cut out in the shoes to accommodate the deformed foot. 6. Total contact plast cast with minimum padding [29].
Wound dressing material can be of various categories like antimicrobials, silver impregnated dressings, enzymatic debridement, negative pressure device, advanced wound dressing, skin substitute, growth factors and biologic wound product, hyperbaric oxygen etc.
threshold tester [19e21]}. Although angiography and visualisation of the vascular tree is taken as the gold standard for evaluation of peripheral arterial disease, currently, non-invasive vascular laboratory has assumed an important role in the evaluation of peripheral ischemia and the diabetic foot [22]. The various tests used consist of: 1. Doppler ultrasound (for estimation of ankle brachial ratio). 2. Photo-plethysmography. 3. Transcutaneous oximetry. 4. Laser doppler flowmetry. 5. Television microscopy.
5.2. Tricyclic drugs Several randomised clinical trials have supported the use of these agents in the management of neuropathic pain. Selective serotonin-re-uptake inhibitors e These inhibit presynaptic reuptake of serotonin. Studies suggest that treatment with paroxetine [30], but not fluoxetine [31], is associated with considerable relief from pain. Similarly, citalopram was confirmed to be efficacious in relieving neuropathic pain, but was less effective than imipramine [32]. Anticonvulsants e These have been used in the management of neuropathic pain for many years [33,34]. Gabapentin is an adjuvant anticonvulsant which is emerging as a first-
6.1. Sugar management The importance of choosing one type of long acting insulin, becoming familiar with it and sticking with it is recommended. In view of recent information from the UGDP study, oral agents should be employed with more caution. Emphasis on foot care is stressed [35]. In our institution we experience good results of diabetic foot management with proper sugar level management, proper wound care in form of daily dressing and debridement of slough, skin grafting for large chronic red granulating tissue wound. 7. Conclusion Diabetic sensorimotor polyneuropathy is common (20%e30% of diabetics). Multiple factors such as blood glucose concentration, blood lipids, structure of myelin sheath and its permeability, axonal flow and micro and macroangiopathy of the peripheral nerves contribute to the production of diabetic neuropathy. Half of patients with diabetic sensorimotor polyneuropathy are asymptomatic. It cannot be diagnosed by history alone. It is essential to examine the feet carefully and regularly. The presence of unilateral heat and swelling in a neuropathic diabetic patient should be presumed to be due to acute Charcot neuropathy until proven otherwise. Ethical approval Its review study based on the previous research work. Funding None.
Please cite this article in press as: P.D. Sinwar, The diabetic foot management e Recent advance, International Journal of Surgery (2015), http:// dx.doi.org/10.1016/j.ijsu.2015.01.023
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Author contribution All work done by the corresponding author.
[15] [16]
Conflicts of interest [17]
None. [18]
Guarantor Prabhu Dayal Sinwar. Acknowledgement No source of funding present.
[19]
[20]
[21]
References [22] [1] A.J.M. Boulton, The pathway to ulceration: aetiopathogenesis, in: A.J.M. Boulton, H. Connor, P.R. Cavanagh, et al. (Eds.), The Foot in Diabetes, third ed., John Wiley & Sons Ltd, Chichester, 2000, pp. 19e31. [2] G.E. Reiber, L. Vileikyte, E.J. Boyko, et al., Causal pathway for incident lower extremity ulcers in patients with diabetes from two settings, Diabetes Care 22 (1999) 157e162. [3] D.R.R. Williams, Hospital admissions of diabetic patients: information from hospital activity analysis, Diabet. Med. 2 (1985) 27e32. [4] L.A. Lavery, H.R. Ashry, W. van Houtum, J.A. Pugh, L.B. Harkless, S. Basu, Variation in the incidence and proportion of diabetes-related amputations in minorities, Diabetes Care 19 (1996) 48e52. [5] L.A. Lavery, W.H. van Houtum, H.R. Ashry, D.G. Armstrong, J.A. Pugh, Diabetesrelated lower-extremity amputations disproportionately affect Blacks and Mexican Americans, South Med. J. 92 (1999) 593e599. [6] G.E. Reiber, E.J. Boyko, D.G. Smith, Lower extremity foot ulcers and amputations in diabetes, in: second ed., in: M.I. Harris, C. Cowie, M.P. Stern (Eds.), Diabetes in America, vol. 95, NIH Publication, 1995, pp. 409e428. [7] L.A. Lavery, D.G. Armstrong, R.P. Wunderlich, M.J. Mohler, C.S. Wendel, B.A. Lipsky, Risk factors for foot infections in individuals with diabetes, Diabetes Care 29 (2006), 1288_93. [8] M.E. Edmonds, The diabetic foot: pathophysiology and treatment, in: P.J. Watkins (Ed.), Clinics in Endocrinology and Metabolism, W.B. Saunders, London, 1986, pp. P880eP916. [9] A.J.M. Boulton, J.D. Ward, Diabetic neuropathies and pain, in: P.J. Watkins (Ed.), Clinics in Endocrinology and Metabolism, vol. 15:4, W.B. Saunders, London, 1986. [10] P.J. Dyck, K.M. Kratz, J.L. Karnes, et al., The prevalence by staged severity of various types of diabetic neuropathy, retinopathy, and nephropathy in a population-based cohort: the Rochester Diabetic Neuropathy Study, Neurology 43 (1993) 817e824. [11] A.J.M. Boulton, R.A. Malik, J.C. Arezzo, J.M. Sosenko, Diabetic somatic neuropathies: technical review, Diabetes Care 27 (2004) 1458e1486. [12] M.E. Edmonds, The neuropathic foot in diabetics, part-1: blood flow, Diabet. Med. 3 (1986) 111e115. [13] S. Sinha, C.S. Munichoodappa, G.P. Kozak, Neuroarthropathy (Charcot's joints) in diabetes mellitus, Med. Baltim. 52 (1972) 191e210. [14] J.D. Ward, J.M. Simms, G. Knight, et al., Venous distension in the diabetic
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neuropathic foot (physical sign of arteriovenous shunting), J. Roy. Soc. Med. 76 (1983) 1011e1014. W.S. Joseph, J.L. LeFrock, The pathogenesis of diabetic foot infections immunopathy, angiopathy, and neuropathy, J. Foot Surg. 26 (1987). S7_11. H.H. Parving, S.M. Rasmussem, Transcapillary escape rate of albumin and plasma volume in short and long term juvenile diabetics, J. Clin. Lab. Invest. 32 (1973) 81e87. F.W. Wagner Jr., The dysvascular foot: a system for diagnosis and treatment, Foot Ankle 2 (1981), 64_122. S.O. Oyibo, E.B. Jude, I. Tarawneh, H.C. Nguyen, L.B. Harkless, A.J. Boulton, A comparison of two diabetic foot ulcer classification systems: the Wagner and the University of Texas wound classification systems, Diabetes Care 24 (2001), 84_8. G.A. Jamal, S. Hansen, A.I. Weir, J.P. Ballantyne, An improved automated method for the measurement of thermal threshold. 1. Normal subjects, J. Neurol. Neurosurg. Psychiatr. 48 (1985) 354e360. G.A. Jamal, A.I. Weir, S. Hansen, J.P. Ballantyne, An improved automated method for the measurement of thermal threshold. 2. Patients with peripheral neuropathy, J. Neurol. Neurosurg. Psychiatr. 48 (1985) 361e366. H. Fruhstorfur, V. Lindbloom, W.G. Schmidt, Method for quantitative estimation of thermal thresholds in patients, J. Neurol. Neurosurg. Psychiatr. 39 (1976) 1071e1075. J.J. Hurley, F.B. Hershey, A.I. Auer, H.B. Binningtoni, Noninvasive evaluation of peripheral arterial statusdthe physiologic approach, in: M.E. Levin, L.W. Oneal (Eds.), The Diabetic Foot, C.V. Mosby Company, London, 1983, p. 120. L. Delbridge, G. Ctercteko, C. Fowler, T.S. Reeve, L.P. Le Quesne, The aetiology of diabetic neuropathic foot ulceration, Br. J. Surg. 72 (1985) 1e6. A.J.M. Boulton, C.I. Franks, R.P. Betts, T. Duckworth, J.D. Ward, Reduction of abnormal foot pressures in diabetic neuropathy using a new polymer insole material, Diabetes Care 7 (1984) 42e46. J. Patton, G. Bruce, R. Jones, E. Stenhouse, Effectiveness of insoles used for the prevention of ulceration in the neuropathic diabetic foot: a systematic review, J. Diabetes Complicat. 25 (2011) 52e62. L.A. Lavery, S.A. Vela, J.G. Fleischli, D.G. Armstrong, D.C. Lavery, Reducing plantar pressure in the neuropathic foot. A comparison of footwear, Diabetes Care 20 (1997) 1706e1710. M.J. Mueller, M.J. Strube, B.T. Allen, Therapeutic footwear can reduce plantar pressures in patients with diabetes and transmetatarsal amputation, Diabetes Care 20 (1997) 637e641. G.E. Reiber, D.G. Smith, D.A. Boone, et al., Design and pilot testing of the DVA/ Seattle Footwear System for diabetic patients with foot insensitivity, J. Rehabil. Res. Dev. 34 (1) (1997) 1e8. F.I. Tovey, Establishing a diabetic shoe service, Pract. Diabetes 2 (1985) 5e8. S.H. Sindrup, L.F. Gram, K. Brosen, O. Eshoj, B.I. Mogensen, The SSRI paroxetine is effective in the treatment of diabetic neuropathy symptoms, Pain 42 (1990) 135e144. M.B. Max, S.A. Lynch, J. Muir, et al., Effects of desipramine, amitriptyline and fluoxetine on pain relief in diabetics in diabetic neuropathy, N. Engl. J. Med. 326 (1992) 1250e1256. S.H. Sindrup, U. Bjerre, A. Dejgaard, et al., The selective serotonin reuptake inhibitor citalopram relieves the symptoms of diabetic neuropathy, Clin. Pharmacol. Ther. 53 (1992) 547e552. H. McQuay, D. Carrell, A.R. Jadad, P. Wilfen, A. Moore, Anticonvulsant drugs for the management of pain: a systematic review, BMJ 311 (1995) 1047e1052. T.S. Jensen, Anticonvulsants in neuropathic pain: rationale and clinical evidence, Eur. J. Pain 6 (Suppl. A) (2002) 61e68. H.H. Epstein, The management of adult diabetes, Can. Fam. Physician 19 (10) (1973 Oct) 69e72.
Please cite this article in press as: P.D. Sinwar, The diabetic foot management e Recent advance, International Journal of Surgery (2015), http:// dx.doi.org/10.1016/j.ijsu.2015.01.023
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IJSU1735_proof ■ 29 January 2015 ■ 1/4
International Journal of Surgery xxx (2015) 1e4
Contents lists available at ScienceDirect
International Journal of Surgery journal homepage: www.journal-surgery.net
Review
The diabetic foot management e Recent advance Q5
Prabhu Dayal Sinwar New PG Hostel Room No 28, Sardar Patel Medical College Bikaner, Rajasthan, India
h i g h l i g h t s
Q1
Diabetic neuropathy and peripheral vascular disease are the main etiological factors in foot ulceration. Wagner's classification is one of the most widely used and universally accepted grading systems for DFU, consisting of six simplistic wound grades used to assess ulcer depth. Assessment of peripheral neuropathy and evaluation of peripheral arterial status are the two important investigations in a diabetic foot. Management of diabetic neuropathic ulcer by appropriate and timely removal of callus, control of infection and reduction of weight bearing forces. Management of diabetic ischaemic foot are medical management, surgical management and percutaneous transluminal angioplasty of stenosed and occluded lower extremity arteries.
a r t i c l e i n f o
a b s t r a c t
Article history: Received 13 October 2014 Received in revised form 22 January 2015 Accepted 26 January 2015 Available online xxx
Diabetic ulceration of the foot represents a major global medical, social and economic problem. It is the commonest major end-point of diabetic complications. Diabetic neuropathy and peripheral vascular disease are the main etiological factors in foot ulceration and may act alone, together, or in combination with other factors such as microvascular disease, biomechanical abnormalities, limited joint mobility and increased susceptibility to infection. In the diabetic foot, distal sensory polyneuropathy is seen most commonly. The advent of insulin overcame the acute problems of ketoacidosis and infection, but could not prevent the vascular and neurological complications. Management of diabetic neuropathic ulcer by appropriate and timely removal of callus, control of infection and reduction of weight bearing forces. Management of diabetic ischaemic foot are medical management, surgical management and percutaneous transluminal angioplasty of stenosed and occluded lower extremity arteries. Foot ulceration in persons with diabetes is the most frequent precursor to amputation. © 2015 Published by Elsevier Ltd on behalf of Surgical Associates Ltd.
Keywords: Diabetic foot Neuropathy Atherosclerosis Neuropathic ulcer Angioplasty Amputation
Q2
1. Introduction Diabetic ulceration of the foot represents a major global medical, social and economic problem. It is the commonest major end-point of diabetic complications. Diabetic neuropathy and peripheral vascular disease are the main etiological factors in foot ulceration and may act alone, together, or in combination with other factors such as microvascular disease, biomechanical abnormalities, limited joint mobility and increased susceptibility to infection. Ulceration rarely results from a single pathology. It is the interaction of contributory causes which leads to the breakdown of the foot at risk [1]. The neuropathic foot, for example, does not spontaneously ulcerate. It is the combination of insensitivity and
either extrinsic factors e.g. walking barefoot and stepping on a sharp object, or simply wearing ill-fitted shoes, or intrinsic factors such as diminished sensation and the development of a callosity which progresses to an ulcer on walking. Neuropathy is the most significant pathology in the pathway to ulceration [2]. Diabetic foot disease is an important problem confronting the diabetologists, internists and surgeons [3]. The advent of insulin overcame the acute problems of ketoacidosis and infection, but could not prevent the vascular and neurological complications. Foot is the most vulnerable part in a diabetic. It is exposed to frequent trauma and requires a sensitive sensory protection, which is often lacking in a diabetic. The foot, being farthest away from the central nervous system and hemodynamically disadvantageously placed, becomes the common site of complicated lesions. Foot ulceration in persons with diabetes is the most frequent precursor to amputation [4,5]. Overall, patients with diabetes are more likely to have an
E-mail address: [email protected]. http://dx.doi.org/10.1016/j.ijsu.2015.01.023 1743-9191/© 2015 Published by Elsevier Ltd on behalf of Surgical Associates Ltd.
Please cite this article in press as: P.D. Sinwar, The diabetic foot management e Recent advance, International Journal of Surgery (2015), http:// dx.doi.org/10.1016/j.ijsu.2015.01.023
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amputation than patients without diabetes [6]. 2. Etiopathogenesis In a large prospective study by Lavery et al. [7], significant independent risk factors for DFI included wounds that penetrated to bone, wounds with a long duration, recurrent wounds, wounds with a traumatic aetiology and the presence of PAD. Although the etiopathogenesis of diabetic foot disease is multifactorial, three main factors, namely neuropathy, ischaemia and infection lead to tissue necrosis and ulcer formation [8]. Other factors are foot biomechanics and weight bearing, peripheral vessel calcifications, trauma, (possibly) diabetic autonomic neuropathy and microangiopathy and diabetic skeletal disease. 2.1. Neuropathy in diabetic foot In the diabetic foot, distal sensory polyneuropathy is seen most commonly. However, motor and autonomic fibres may also be involved and combined neuropathies frequently occur. The development of a neuropathy is linked to poor glycaemic control over many years and it increases in frequency with both age and the duration of diabetes. Multiple factors such as blood glucose concentration, blood lipids, structure of myelin sheath and its permeability, axonal flow and micro and macroangiopathy of the peripheral nerves contribute to the production of diabetic neuropathy [9]. Longitudinal data from the Rochester Study [10] supported the contention that the duration and severity of exposure to hyperglycemia influenced the severity of the neuropathy. Current research on diabetic neuropathy is focused on oxidative stress, advanced glycation-end products, protein kinase C and the polyol pathway [11]. 2.2. Blood flow in diabetic neuropathic foot Recent studies have shown that the blood flow is increased in diabetic foot. The latter is due to the arterio-venous shunting and dilated and stiff peripheral arteries [12]. The pulsatility index which is inversely proportional to the quantity of the blood flow is markedly reduced in diabetic foot. The normal Doppler flow pattern is triphasic: a forward flow in systole followed by a reverse flow and a further short forward flow in diastole. In diabetics there is an increased forward flow with the absence of reverse flow. 2.3. Skeletal changes in diabetic foot Due to increased blood flow to the lower limb there in enhanced blood supply to the bones of the diabetic foot. 2.4. Stiffening of arterial wall The medial wall calcification in the peripheral vessels in the lower limb raises ankle brachial systolic pressure and shortens transit times of pulse wave. In Charcot's diabetic neuroarthropathy vascular calcification is found in about 90% [13]. Ward et al. have shown that rapid increase in flow of blood bypasses small vessels and the capillary nutrient circulation and results in a relative distal ischaemia [14]. The enhanced blood flow, vasodilatation and arteriovenous shunting, all arising out of sympathetic denervation leads to abnormal venous pooling and oedema. Atherosclerosis of the large vessels of the leg in a diabetic is often multisegmental, distal and bilateral. Diabetic angiopathy is reported to be the most frequent cause of
morbidity and mortality in diabetic patients [15]. Macroangiopathy manifests as a diffuse multisegmental involvement typically involving the infrapopliteal vessels, and is also associated with compromised collateral circulation. Parving and Resmusen have demonstrated functional abnormality in the form of leakage of albumin from the capillaries to the interstitium; however an occlusive microvascular disease in the diabetic foot has not been clearly demonstrated [16]. The presence of neuropathy makes the feet insensitive and the diabetic patient is often not aware of even a severe mechanical trauma and gross infection. 3. Presentation Patients present with a variety of complaints ranging from local to systemic signs of infections. Local signs of infection may include pain/tenderness, erythema, oedema, purulent drainage and newonset malodor. Systemic signs of infection include anorexia, nausea, vomiting, fever, chills, night sweats, change in mental status and a recent worsening of glycaemic control. Wagner's classification is one of the most widely used and universally accepted grading systems for DFU, consisting of six simplistic wound grades used to assess ulcer depth (grades 0e5) [17]. This classification is limited by the inability to recognize ischaemia and infection as independent risk factors in all classification grades [18] (Table 1). Q3 A more recently proposed and popularized DFU classification is the University of Texas Health Science Center San Antonio (UT) classification system [18]. This system incorporates a matrix structure of four grades of wound depth with subgroups to denote the presence of infection, ischaemia or both (Table 2). Wounds with frank purulence and/or two or more local signs of inflammation such as warmth, erythema, lymphangitis, lymphadenopathy, oedema, pain and loss of function may be classified as ‘infected.’ Lower extremity vascular insufficiency is made by a combination of one or more clinical signs or symptoms of claudication, restpain, absent pulses, dependent rubor, atrophic integument, absence of pedal hair or pallor on elevation. From the practical point of view the diabetic foot can be divided into two major types: (1) Ischaemic diabetic foot and (2) Non Ischaemic neuropathic diabetic foot [8]. 4. Investigations Assessment of peripheral neuropathy and evaluation of peripheral arterial status are the two important investigations in a diabetic foot. Accurate sensory testing in diabetic neuropathy is of paramount importance in the diagnosis, objective quantification and monitoring natural evolution or effects of therapy. These involve testing for (1) Vibration perception Threshold (VPT) {assessed by a Biothesiometer}, (2) Thermal Discrimination Threshold (TDT) {assessed by using 1. Marstock stimulator 2. Automated thermal
Table 1 Wagner classification system. Grade
Wound depth
0 1 2 3 4 5
Pre-ulcerative area without open lesion Superficial ulcer (partial/full thickness) Ulcer deep to tendon, capsule, bone Stage 2 with abscess, osteomyelitis or joint sepsis Localized gangrene Global foot gangrene
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P.D. Sinwar / International Journal of Surgery xxx (2015) 1e4 Table 2 The University of Texas Health Science Center San Antonio (UT) classification system.
A B C D
0
1
2
3
No open lesion With infection Ischaemic Infection/ Ischaemia
Superficial wound With infection Ischaemic Infection/ Ischemia
Tendon/Capsule With infection Ischaemic Infection/ Ischemia
Bone/Joint With infection Ischaemic Infection/ Ischemia
3
line agent for the treatment of painful neuropathy [32]. Duloxetine is an inhibitor of the re-uptake of 5-hydroxytryptamine and norepinephrine and has recently been approved by the Food and Drug Administration for the treatment of neuropathic pain. 5.3. Management of diabetic ischaemic foot
5. Treatment
1. Medical Management. 2. Surgical Management. 3. Percutaneous Transluminal Angioplasty of stenosed and occluded lower extremity arteries. Medical management: It is indicated when ulcer is small, recent and also in those patients unfit for reconstructive surgery. Surgical management: This comprises of arterial reconstruction, sympathectomy and amputation. Arterial reconstruction e Indications for reconstructive surgery are intractable rest pain and claudication, nonhealing ulcers even after good medical management. Lumbar sympathectomy e For relief of ischaemic rest pain this has an important role to play. Percutaneous transluminal angioplasty: Angioplasty is particularly useful in high risk patients where surgery is contraindicated. The lesions most amenable for angioplasty include stenoses less 4 cm long and occlusions shorter than 10 cm.
5.1. Management of diabetic neuropathic ulcer
6. Dressing
The three cardinal principles of management are [8]: 1. Appropriate and timely removal of callus. 2. Control of infection. 3. Reduction of weight bearing forces. Delbridge and Lequesne et al. [23] have shown that the formation of callus is central to the development of neuropathic ulcer in a diabetic. After removing the callus a bacterial swab may be taken from the floor of the ulcer and appropriate antibiotic instituted. Dressing materials can include natural, modified and synthetic polymers, as well as their mixtures or combinations, processed in the form of films, foams, hydrocolloids and hydrogels. Moreover, wound dressings may be employed as medicated systems, through the delivery of healing enhancers and therapeutic substances (drugs, growth factors, peptides, stem cells and/or other bioactive substances). The most important aspect of promoting healing is to remove weight bearing force from the site of ulcer and ensure a redistribution of the shearing forces [24]. A recent systematic review by Patton et al. [25] demonstrated that insoles may prevent diabetic foot ulceration, but most of the evidence is poor and inconclusive. The current state of the art in insole design primarily addresses vertical forces with the aim of reducing foot pressures [26e28]. 1. Special foots. 2. Polyethylene foam insoles (Plastozole). 3. Micro cell rubber insole (Tovey's insole) [29]. 4. “Cork cradle” shoe. 5. Special windows cut out in the shoes to accommodate the deformed foot. 6. Total contact plast cast with minimum padding [29].
Wound dressing material can be of various categories like antimicrobials, silver impregnated dressings, enzymatic debridement, negative pressure device, advanced wound dressing, skin substitute, growth factors and biologic wound product, hyperbaric oxygen etc.
threshold tester [19e21]}. Although angiography and visualisation of the vascular tree is taken as the gold standard for evaluation of peripheral arterial disease, currently, non-invasive vascular laboratory has assumed an important role in the evaluation of peripheral ischemia and the diabetic foot [22]. The various tests used consist of: 1. Doppler ultrasound (for estimation of ankle brachial ratio). 2. Photo-plethysmography. 3. Transcutaneous oximetry. 4. Laser doppler flowmetry. 5. Television microscopy.
5.2. Tricyclic drugs Several randomised clinical trials have supported the use of these agents in the management of neuropathic pain. Selective serotonin-re-uptake inhibitors e These inhibit presynaptic reuptake of serotonin. Studies suggest that treatment with paroxetine [30], but not fluoxetine [31], is associated with considerable relief from pain. Similarly, citalopram was confirmed to be efficacious in relieving neuropathic pain, but was less effective than imipramine [32]. Anticonvulsants e These have been used in the management of neuropathic pain for many years [33,34]. Gabapentin is an adjuvant anticonvulsant which is emerging as a first-
6.1. Sugar management The importance of choosing one type of long acting insulin, becoming familiar with it and sticking with it is recommended. In view of recent information from the UGDP study, oral agents should be employed with more caution. Emphasis on foot care is stressed [35]. In our institution we experience good results of diabetic foot management with proper sugar level management, proper wound care in form of daily dressing and debridement of slough, skin grafting for large chronic red granulating tissue wound. 7. Conclusion Diabetic sensorimotor polyneuropathy is common (20%e30% of diabetics). Multiple factors such as blood glucose concentration, blood lipids, structure of myelin sheath and its permeability, axonal flow and micro and macroangiopathy of the peripheral nerves contribute to the production of diabetic neuropathy. Half of patients with diabetic sensorimotor polyneuropathy are asymptomatic. It cannot be diagnosed by history alone. It is essential to examine the feet carefully and regularly. The presence of unilateral heat and swelling in a neuropathic diabetic patient should be presumed to be due to acute Charcot neuropathy until proven otherwise. Ethical approval Its review study based on the previous research work. Funding None.
Please cite this article in press as: P.D. Sinwar, The diabetic foot management e Recent advance, International Journal of Surgery (2015), http:// dx.doi.org/10.1016/j.ijsu.2015.01.023
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Author contribution All work done by the corresponding author.
[15] [16]
Conflicts of interest [17]
None. [18]
Guarantor Prabhu Dayal Sinwar. Acknowledgement No source of funding present.
[19]
[20]
[21]
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