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Knowledge Base

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Diabetic Foot Syndrom (DFS)

Team of the Knowledge Base

What is DFS?

More than 10% of patients with diabetes suffer from foot ulcer at one point in their life. It is the most dreaded complication of diabetes worldwide. The ulcers lead to immobility and discomfort, some never heal. Every year one of 200 patients loses a leg . Therefore the intention of this knowledgebase is to describe the pathogenesis of the DFS, the treatment and the prevention.

Karel Bakker, Chair of the International Working Group and IDF Consultative Section on the Diabetic Foot wrote: "Diabetes is a serious chronic disease. In 2003 the global prevalence of diabetes was estimated at 194 million. This figure is predicted to reach 333 million by 2025 as a consequence of longer life expectancy, sedentary lifestyle and changing dietary patterns. Although many serious complications, such as kidney failure or blindness, can affect individuals with diabetes, it is the complications of the foot that take the greatest toll. Of all lower extremity amputations, 40-70% are related to diabetes. In most studies the incidence of lower leg amputation is estimated to be 5-25/100,000 inhabitants/year: among people with diabetes the figure is 6-8/1,000.

Lower extremity amputations are usually preceded by a foot ulcer in people with diabetes. The most important factors related to the development of these ulcers are peripheral neuropathy, foot deformities, minor foot trauma and peripheral vascular disease. The spectrum of foot lesions varies in different regions of the world due to differences in socio-economic conditions, standards of foot care and quality of footwear.

Foot complications are one of the most serious and costly complications of diabetes. However, through a care strategy that combines: prevention; the multi-disciplinary treatment of foot ulcers; appropriate organization; close monitoring, and the education of people with diabetes and healthcare professionals, it is possible to reduce amputation rates by between 49% and 85%. It is this objective that should motivate the advocacy work of those fighting to make a difference for those living with diabetes around the world." .

Pathogenesis of DFS

DFS is caused not by diabetes itself, but by the interaction of polyneuropathy (the generalized disease of the nervous system typical of diabetes sufferers), peripheral arterial disease (PAD), limited joint mobility and exogenic factors. Microangiopathy (microvascular disease, a condition affecting the small blood vessels) has also been cited as a cause , but this is controversial; many experts do not see this as a co-factor . An exogenic factor is the wearing of improper shoes . With adequate prevention, a range of problems, from the development of ulcers to amputation, can be avoided. Only an appropriate treatment enables healing.

Polyneuropathy as a cause of DFS

Diabetes causes polyneuropathy. The latter can be seen as the leading factor in the development of DFS. Polyneuropathy can be divided into three functional parts: sensory, motor and autonomous neuropathy. Each of these can lead to ulcers. Because these dysfunctions usually appear more or less at the same time, ulcers are extremely likely to develop. Unfortunately the more advanced the polyneuropathy is, the less the patient feels, and the less likely he or she is to take adequate preventive steps. To explain the development of ulcers each part of the neuropathy has to be seen seperately.

DFS: neuropathy of the skin as a promoter of ulcer and wounds

Sensory neuropathy

The reduction or lack of sensory function causes the sufferer not to notice damage or trauma to his or her foot (so actually "sufferer" is a misnomer!), which can lead to the development of ulcers : As accidental traumas to the foot are not associated with pain, the patient pays less and less attention to foot care. Small lesions are not treated, and instead of healing, become ulcerous.

Motor neuropathy

Motor neuropathy causes a flexion deformity of the toes and an abnormal gait  : The deformities cause areas of increased pressure, such as the region under the head of the metatarsal bones and the toes. The skin in these regions cannot withstand the pressure and develops more and more calluses and eventually ulcers. Calluses themselves increase pressure in the tissues, impairing circulation and thus leading the skin to die off.

Autonomous neuropathy

Autonomous neuropathy causes a cessation of perspiration, leading to dry, cracked skin. The increase in blood flow through opened arteriovenous shunts results in a warm, often oedemous foot with dilated dorsal veins . While on the one hand the toughness of the skin is reduced, the cracks are an invitation for fungal and bacterial infection.

Peripheral arterial disease as a cause of DFS

The impaired circulation is a direct cause of the development of ulcers, disturbing the healing process and ultimately leading to gangrene . The foot is not adequately supplied with the nutrients required for healing; at the same time, the immune defence is reduced, causing inflammation.

DFS: ischemic and non-ischemic foot

Limited joint mobility as a cause of DFS

A glycosylation of proteins in the joints, tendons and soft tissue, in combination with a disturbance of gait and deformations of the foot, leads to an abnormal load in the plantar pressure distribution . This effect is similar to the effect of motor neuropathy and compounds the problem.

Interaction of the deficits

DFS is the result of the interaction of all the above risk factors, whereas improper footwear is the most important trigger . Repeated traumas that are not recognized as such and pressure from improper posture lead to thickened, callused skin. This layer causes its own pressure and promotes the formation of lesions, namely subkeratotic hematomas . This leads finally to an ulcer at the exposed location . Thanks to poor circulation, minor injuries cannot heal. Oedema or septic thrombosis cause a occlusion of the small blood vessels, leading to gangrene . Diseases of the nails and nail beds, such as athlete's foot or bacterial infections, worsen the course of the disease . Another aggravating factor is ignorance: The sufferer has not been adequately educated about risk factors and prevention, and unwittingly worsens the condition . An infected ulcer, combined with ischemia due to arterial disease, leads to the formation of gangrene and ultimately necessitates an amputation.

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For Backup purposes only

• 1. Apelqvist J, Castenfors J, Larsson J, Stenstrom A, Agardh CD. Wound classification is more important than site of ulceration in the outcome of diabetic foot ulcers. Diabet Med 1989;6(6):526-530

• 2. Armstrong DG, Lavery LA, Bushman TR.Peak foot pressures influence the healing time of diabetic foot ulcers treated with total contact casts. J Rehabil Res Dev 1998;35(1):1-5
• 3. Armstrong DG, Lavery LA, Harkless LB.Validation of a diabetic wound classification system. The contribution of depth, infection, and ischemia to risk of amputation. Diabetes Care 1998;21(5):855-859

• 4. Armstrong DG, Lavery LA, Harkless LB. Who is at risk for diabetic foot ulceration? Clinics in Podiatric Medicine and Surgery 1998;15:11-19

• 5. Barnett SJ, Shield JPH, Potter MJ, Baum JD.Foot Pathology in Insulin Dependent Diabetes. Archives of Disease in Childhood 1995;73:151-153

• 6. Birke JA, Rolfsen RJ.Evaluation of a Self-Administered Sensory Testing tool to Identify Patients at Risk of Diabetes Related Foot Problems. Diabetes Care 1998;21:23-25

• 7. Boulton AJM. The Pathogenesis of Diabetic Foot Problems: an Overview. DiabetMed 1996; 13:12-16

• 8. Boyko E.J., Ahroni JH, Stensel V.A Prospective Study of Risk Factors for Diabetic Foot Ulcer. The Seattle Diabetic Foot Study. Diabetes Care 1999;22:1036-1042

• 9. Cavanagh PR, Ulbrecht JS, Caputo, GM. The Non-Healing Diabetic Foot Wound: Fact or Fiction? Ostomy/Wound Management 1998;44 (3A)Suppl:6-12

• 10. Haslbeck M, Redaelli M, Parandeh-Shab F, Neundörfer B, Stracke H, Ziegler D. Diagnostik, Therapie und Verlaufskontrolle der sensomotorischen diabetischen Neuropathien. Evidenzbasierte Diabetes-Leitlinien DDG. Scherbaum WA, Lauterbach KW, Renner R (Hrsg.). 1. Auflage. Deutsche Diabetes-Gesellschaft 2004

• 11. Jörneskog G, Brismar K, Fagrell B. Skin Capillary Circulation is More Impaired in the Toes of Diabetic than Non-Diabetic Patients with Vascular Disease. Diabetic Medicine 1995, 12:36-41

• 12. Laing P. The development and complications of diabetic foot ulcers. Am J Surg 1998;176(2A Suppl):11-19.

• 13. Litzelman DK, Marriot DJM, Vinicor F. Independent physiological predictors of foot lesions in patients with NIDDM. Diabetes Care 1997;20(8):1273-1278

• 14. Litzelman DK, Marriot DJM, Vinicor F. The role of footwear in the prevention of foot lesions in patients with NIDDM. Diabetes Care 1997;20:156-162

• 15. LoGerfo FW, Coffman JD. Vascular and microvascular disease of the foot in diabetes. Implications for foot care. New Engl J Med 1984;311:1615-1619

• 16. Macfarlane RM, Jeffcoate WJ. Factors contributing to the presentation of diabetic foot ulcers. Diabetic Med 1997;14:867-870

• 17. McNeely MJ, Boyko EJ, Ahroni JH. The independent contributions of diabetic neuropathy and vasculopathy in foot ulceration. Diabetes Care 1995;18: 216-219

• 18. Murray HJ, Young MJ, Hollis S, Boulton AJM. The Association Between Callus Formation, High Pressure and Neuropathy in Diabetic Foot Ulceration. DiabetMed 1996;13:979-982

• 19. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation: basis for prevention. Diabetes Care 1990;113:516-521

• 20. Rayman G, Malik RA, Sharma AK, Day JL. Microvascular response to tissue injury and capillary ultrastructure in the foot of type 1 diabetic patients. Clin Sc (Colch) 1995;89(5):467-474

• 21. Tooke JE, Brash PD. Microvascular Aspects of Diabetic Foot Disease. Diabet Med 1996, 13:26- 29

• 22. Young MJ, Breddy JL, Veves A, Boulton AJM. The prediction of neuropathic foot ulceration using vibration perception thresholds. Diabetes Care 1994,17:557-561

• 23. Bakker, Karel: Chair of the International Working Group and IDF Consultative Section on the Diabetic Foot.www.iwgdf.org

• 24. Morbach, Stephan: Diagnosis, Treatment and Prevention of the Diabetic Foot Syndrome

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Diagnostic Procedures

Non radiologic diagnostic procedures

(The list is under construction and not yet completed)
Foot injuries are the most common chronic complication of diabetes mellitus that can lead to lower extremity amputation in the worst case. The two major risk factors for diabetic foot ulceration and amputation are peripheral neuropathy and peripheral vascular disease. Fundamental foot care and systematically examination in people with diabetes can prevent or delay these problems.

Anamnesis

General medical assessment

Besides a general medical assessment, the social situation of the patient has to be evaluated. The reduced capacity for self care, social isolation, poor access to health care, previous foot education are social factors that can have an impact on the development of a diabetic foot. The poor eyesight or reduced mobility of many patients makes the self care difficult. The patient’s habits like bare-foot walking, his daily activities, his work, his footwear, his nutritional status or use of alcohol, tobacco or drugs play a role, too. The medical history of the patient and his foot may reveal important details which can be the issue to further examinations: diabetes duration, glycemic management, cardiovascular, renal and ophthalmic evaluations, current medications, allergies. Previous callus formation, foot deformations, foot ulceration or amputation can be a risk factor for developing a diabetic foot ulcer. . The gait and stance of the patient is inspected.

Foot inspection

All diabetic patients should get a meticulous feet examination at least once a year, more often if they have confirmed risk factors for foot injuries . The medical practitioner inspects the dorsal, plantar and posterior surfaces of the feet, but it’s important not to forget to look between the toes. The feet examination can be split in dermatologic, musculoskeletal, footwear, vascular and neurologic examination.

• dermatologic examination

Dry skin with cracks or fissures is typical for a diabetic foot . Besides that, the nail appearance, hair growth, ulceration, gangrene, infection (giving the location, size, depth, infection status) interdigital lesions, edema, fungal infection is observed. There are some markers of diabetes which can be helpful: diabetic dermopathy, Necrobiosis lipoidica diabeticorum (NLD), Bullosum diabeticorum, Granuloma annulare, acanthosis rigicans. Further, the building of calluses and its characteristics is noticed.

• musculoskeletal examination

In addition to the analysis of gait and stance, the medical practitioner has to pay attention about any bone or joint deformity like claw toes, hammer toes or callus , as they can lead to abnormal plantar foot pressure. A dramatic complication of the diabetic neuropathy is the diabetic neuropathic osteoarthropathy (DNOAP) or Charcot’s foot [7] which is a complication due to the diabetic polyneuropathy and musculoskeletal changes which results in osseous fragmentation. [1,7] Risk factors for a DNOAP are: neuropathy, rubor, hyperthermia, turgor, pain and foot deformities. [7]

• footwear examination

The footwear is assessed both inside and outside: type of shoe, fit, depth of toe box, shoewear, etc. is noticed. [1, 2]

• vascular examination

Besides the palpation of the pulses, the vascular examination involves the inspection of the foot for signs of ischaemia, symptoms of intermittent claudication . Vascular insufficiency needs a further consultation including …….. which are illuminated in the corresponding chapter.

• neurologic examination

The diabetic polyneuropathy manifests in the reduced vibration, temperature and pain perception. Typical pain is pinprick or tingling. The symptoms can be checked with light pressure and light touch, two point discrimination, deep tendon reflexes (patella, Achilles), but the two most important methods are the examination of vibration perception with the Rydel-Seiffer tuning fork and the testing of the pressure perception with the 10 g-Semmes-Weinstein monofilament. which are explained further.

Vascular diagnosis

As ischaemia of the affected foot following occlusive disease is a very significant risk of amputation for diabetic patients, the diagnosis of circulatory diseases is essential to avoid it. Diabetics often have arterial circulatory disorders caused by arteriosclerotic vessel processes which reduce the elasticity of the vessel.

The first thing to do in assessing the vascular status of the diabetic patients is to make a differentiation of neuropathic and (neuro-) ischaemic findings with the palpation of the foot pulses.

DFS: non-invasive vascular diagnosis

• Palpation of foot pulses

The palpation of the foot pulses makes the difference between neuropathic and (neuro-) ischaemic disorders. The absence of pedal pulses suggests ischemia .

• Ankle brachial index (ABI)
• Measurement of the arterial wedge pressure
• Doppler sonography

Functional diagnosis

• Pedography

Neurologic diagnosis

The diabetic neuropathy manifests in the reduced vibration, temperature and pain perception. It can be checked with light pressure and light touch, two point discrimination, deep tendon reflexes (patella, Achilles), but the two most important methods are the examination of vibration perception with the Rydel-Seiffer tuning fork and the testing of the pressure perception with the 10 g-Semmes-Weinstein monofilament.

• Pressure perception
  • Semmes-Weinstein 10g-monofilament

The patient should not be able to see the examiner applying the monofilament, as well as where he applies it. The monofilament should be firstly applied on an other site (hand, elbow, forehead) “damit” the patient knows how it feels. After that, the examiner has to apply the monofilament perpendicularly to the skin and with enough force: the monofilament should bend or buckle. Further, he has to take care not to repeate the contact of the filament on the test site. While the filament is pressed to the skin, the patient has to say if he feels the pressure applied and where he feels it. This application has to be repeated twice at the same site and has to be alternated with at least one test in which no filament is applied. If the patient answers two out of three applications correctly, protective sensation is present. It he does not, the patient is at risk of ulceration.

• Vibration perception
  • 128 Hz tuning fork

The patient should not be able to see the examiner applying the tuning fork, as well as where he applies it. The tuning fork should be firstly applied on an other site (wrist, elbow, clavicula) “damit” the patient knows how it feels. After that, the examiner has to apply the tuning fork perpendicularly on a bony part on the dorsal side ot the distal phalanx of the first toe, with a constant pressure. This application has to be repeated twice and has to be alternated with at least one test in which the tuning fork is not vibrating. If the patient answers two out of three applications correctly, the test is positive. If he does not, the test is negative and the patient is at risk of ulceration. The test has to be repeated more proximally (malleolus, tibial tuberositas) if the patient is unable to sense the vibration of the tuning fork at the big toe.

• Deep tendon reflexes: patella, Achilles
• Neuropathy symptom score (NSS)
• Neuropathy deficit score (NDS)

Microbiological diagnosis

The methods of obtaining cultures from diabetic foot ulcers are various and can lead to a poor concordance of results obtained. They have to take into account in the interpretation of the results. Cultures from diabetic foot ulcers may contain as well clinically significant pathogens as non pathogenic bacteria from the surrounding skin, especially when the specimens are collected with a swab.

Diabetic foot infections are often polymicrobial with mixed gram-positive and gram-negative, aerob and anaerob species. Some studies suggest a possible dependence and interaction among aerobes and anaerobes which can lead to the production of virulence factors such as hemolysins, proteases, collagenases or short-chain fatty acids. As the mixed flora contribute to the chronicity of the infection and can have important clinical implications, it should not be overlooked.

The main causative pathogen in diabetic foot ulcers are the Staphylococci, typically S. aureus. Beta-hemolytic streptococcus are often found, too. These two bacteria are the pathogens of early diabetic foot infections.

Anaerobic baceteria are often present in diabetic foot ulcers. They are mostly isolated from deep tissues which are usually polymicrobial. The gram-positive strict anaerobic bacteria are generally present in little deep wounds whereas the gram-negative strict anaerobic bacteria are associated to ischemic necrosis or a deep wound. However, heir role in the diabetic foot ulcers is unclear. Many studies didn’t quantify the bacterial density in the infected tissues , the number of specimens was not representative or the collection or culture of the specimen was not always carried out properly. Despite that, some studies suggest that anaerobic bacteria plays a minimal role .

Anaerobes

Anaerobes are often present in diabetic foot ulcers but are rarely isolated from superficial samples More anaerobic bacterial strains were isolated from deep tissue than from other sites cultured. There is a poor concordance of results obtained from ulcer swabs with those obtained from uncontaminated deep tissue specimens Sligthly better concordance with deep tissue results was obtained from currattage specimens and needle aspirates.

The following table shows the most important bacteria in diabetic foot syndrome:

	Aerob	Anaerob
Gram-positive	S. aureus Staph. Spp Diphteroids Streptococcus agalactiae Streptococcus mitis Streptococcus milleri Enterococci Corynebacteria	Eubacterium spp Peptostreptococcus spp Peptostreptococcus asaccharolyticus Finegoldia magna
Gram-negative	Bacilli Clostridia Bacteroides Enterobacteriaceae Pseudomonas aeruginosa Proteus mirabilis Klebsiella	Cocci Fusobacterium nucleatum Prevotella Porphyromonas

Deep wounds

Deep tissue samples are more likely to reveal both aerobic and anaerobic pathogens. Deeper infections are usually polymicrobial Heavy growths of anaerobes were seen in the deep tissue

Multiresistent bacteria

The multiresistant bacteria play a important role, too. Especially Methicillin-resistant S. aureus (MRSA) constitutes a very serious problem, although their isolation is not obligatory associated with increased virulence. In patients with recurrent diabetic ulcers, more S. aureus are MRSA than in patients with ulcers that presented at a first time, as the patients with recurrent ulcers are likely to have been previously hospitalized and treated with antibiotics (which are risk factors for MRSA). Other bacteria must also be taken into accout: Vancomycin-resistant Enterococci (VRE), Glycopeptide-resistand S. aureus (GRSA), Enterobacteriaceae resitant to third-generation cephalosporins, Pseudomonas aeruginosa and other environmental bacteria. In clinically infected wounds, the bacteria has genes for both virulence and resistance factors. Lipsky suggests that virulence factors are markers for infected wound, as they were found in 98% of infected patients, especially in S. aureus and that the clinical severity of infection is greater by he presence of antibiotic resistance genes.

References

The sources have to be completed.

1. Frykberg RG, Zgonis T, Armstrong DG, Driver VR, Kravitz SR, Landsman AS et al. American College of Foot and Ankle Surgeons. Diabetic foot disorders - a clinical practice guideline. J Foot Ankle Surgery, 2006, Sept-Oct, 45(5): 1-60
2. Apelqvist J, Bakker K, van Houtum WH, Nabuurs-Franssen MH, Schaper NC, on behalf of the International Working Group on the Diabetic Foot. International consensus and practical guidelines on the management and the prevention of the diabetic foot. Diabetes Metab Res Rev, 2000, 16 (Suppl 1): 84-92
3. Lipsky BA, Berendt AR, Deery HG, Embil JM, Joseph WS, Karchmer AW et al. Diagnosis and Treatment of Diabetic Foot Infections. Clinical Infectious Diseases, 2004, 39: 885-910
4. National Institute of Clinical Evidence (NICE), UK. Clinical guidelines for type 2 diabetes – Prevention and management of foot problems. 2004, Jun [cited 2007 Nov 18]. Available from: http://www.nice.org.uk/guidance/index.jsp?action=download&o=29242
5. National Institute of Clinical Evidence (NICE), UK. Type 2 diabetes – Prevention and management of foot problems. 2004, Jan [cited 2007 Nov 18]. Available from: http://www.nice.org.uk/guidance/index.jsp?action=download&o=29241
6. Foot In Diabetes UK. The The National Minimum Skills Framework for Commissioning of Foot Care Services for People with Diabetes. 2006, Nov [cited 2007 Nov 18]. Available from: http://www.footindiabetes.org/guidelines
7. Eckhardt A, Lobmann R. Der diabetische Fuß. Springer Verlag Berlin Heidelberg, ISBN 978-3-540-22719-9 (Print), 978-3-540-27609-8 (Online), 2005, chap 3-5, p. 25-178. [cited 2007 Nov 18].
8. Andrew J.M. Boulton. Management of Diabetic Peripheral Neuropathy. Clin. Diabetes, 2005, 23: 9-15
9. Pham H, Armstrong DG, Harvey C, Harkless LB, Giurini JM, Veves A. Screening techniques to identify people at high risk for diabetic foot ulceration: a prospective multicenter trial. Diabetes Care, 2000, 23: 606-611
10. Morbach S. Diagnosis, Treatment and Prevention of the Diabetic Foot Syndrome. Hartmann medical edition, 2004, Mar, ISBN 3-929870-29-0. [cited 2007 Dec 02] Available from: http://en.hartmann.info/images/banner/ME_Diab_Fuss_Inhalt_engl_30.pdf
11. Société de Pathologie Infectieuse de Langue Française. Recommandations pour la pratique clinique, prise en charge du pied diabétique infecté. Texte long. [Management of diabetic foot infections. Long text]. Med Mal Infect, 2007, Jan, 37(1), 26-50. [cited 2007 Dec 09]
12. Citron DM, Goldstein EJ, Merriam CV, Lipsky BA, Abramson MA.

Bacteriology of moderate-to-severe diabetic foot infections and in vitro activity of antimicrobial agents. J Clin Microbiol, 2007, Sep, 45(9), 2819-28.

1. Sapico FL, Canawati HN, Witte JL, Montgomerie JZ, Wagner FW Jr., Bessman AN. Quantitative aerobic and anaerobic bacteriology of infected diabetic feet. J Clin Microbiol, 1980;12:413–20
2. Urbancic-Rovan V, Gubina M. Bacteria in superficial diabetic foot ulcers. Diabet. Med, 2000, 17(11), 814-15.
3. Lipsky BA. Diabetic foot infections: microbiology made modern? Array of hope. Diab Care, 2007, Aug, 30(8), 2171-72.

Internet links

1. Deutsche Diabetes Gesellschaft. [1]. Evidenzbasierte Leitlinien: Diagnostik, Therapie, Verlaufskontrolle und Prävention des diabetischen Fußsyndroms. 2006. [cited 2007 Dec 02]. Available from: http://www.deutsche-diabetes-gesellschaft.de/redaktion/mitteilungen/leitlinien/EBL_Fusssyndrom_2004.pdf
2. Deutsche Diabetes Gesellschaft. [2]. Evidenzbasierte Leitlinien: Diagnostik, Therapie und Verlaufskontrolle der Neuropathie bei Diabetes mellitus Typ 1 und Typ 2. 2006. [cited 2007 Dec 02]. Available from: http://www.deutsche-diabetes-gesellschaft.de/redaktion/mitteilungen/leitlinien/EBL_Neuropathie_Update_2004.pdf
3. Deutsche Diabetes Gesellschaft. [3]. Praxisleitlinien: Diabetisches Fußsyndroms. 2006. [cited 2007 Dec 02]. Available from: http://www.deutsche-diabetes-gesellschaft.de/redaktion/mitteilungen/leitlinien/PL_DDG2007_Fusssyndrom
4. Deutsche Diabetes Gesellschaft. [4]. Praxisleitlinien: Diabetische Neuropathie. 2006. [cited 2007 Dec 02]. Available from: http://www.deutsche-diabetes-gesellschaft.de/redaktion/mitteilungen/leitlinien/PL_DDG2007_Neuropathie
5. Arbeitsgemeinschaft Diabetischer Fuß. Leitlinien & Links, Offizieller Untersuchungsbogen. [cited on 2007 Dec 02]. Available from: http://www.ag-fuss-ddg.de