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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 [24]. 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." [23].


Pathogenesis of DFS

DFS is caused not by diabetes itself, but by the interaction of polyneuropathy [10] (the generalized disease of the nervous system typical of diabetes sufferers), peripheral arterial disease (PAD)[17, 19], limited joint mobility [5, 12] and exogenic factors. Microangiopathy (microvascular disease, a condition affecting the small blood vessels) [11] has also been cited as a cause [21], but this is controversial; many experts do not see this as a co-factor [15, 20]. An exogenic factor is the wearing of improper shoes [1, 2, 3, 4, 9]. 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 [7, 8, 9, 12, 17, 22]: 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[4, 7, 12]: 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 [7]. 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 [7, 21]. 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 [5, 12]. 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 [1]. 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 [18]. This leads finally to an ulcer at the exposed location [1, 18]. Thanks to poor circulation, minor injuries cannot heal. Oedema or septic thrombosis cause a occlusion of the small blood vessels, leading to gangrene [21]. Diseases of the nails and nail beds, such as athlete's foot or bacterial infections, worsen the course of the disease [1, 13, 14, 16]. Another aggravating factor is ignorance: The sufferer has not been adequately educated about risk factors and prevention, and unwittingly worsens the condition [6]. An infected ulcer, combined with ischemia due to arterial disease, leads to the formation of gangrene and ultimately necessitates an amputation.

References

  • 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
  • 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
  • 7. Boulton AJM. The Pathogenesis of Diabetic Foot Problems: an Overview. DiabetMed 1996; 13:12-16
  • 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
  • 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
  • 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
  • 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
  • 23. Bakker, Karel: Chair of the International Working Group and IDF Consultative Section on the Diabetic Foot.www.iwgdf.org

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. [2,5,9] 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. [1,2,3,4,6] 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. [1,2] 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. [1,7] Previous callus formation, foot deformations, foot ulceration or amputation can be a risk factor for developing a diabetic foot ulcer. [1,2,9]. The gait and stance of the patient is inspected. [4,7]

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 [1,2]. 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. [4, 7] The feet examination can be split in dermatologic, musculoskeletal, footwear, vascular and neurologic examination. [1,4]

  • dermatologic examination [1,2,4,6]

Dry skin with cracks or fissures is typical for a diabetic foot [1,2,6,10]. Besides that, the nail appearance, hair growth, ulceration, gangrene, infection (giving the location, size, depth, infection status) interdigital lesions, edema, fungal infection is observed. [1,2,6,7] There are some markers of diabetes which can be helpful: diabetic dermopathy, Necrobiosis lipoidica diabeticorum (NLD), Bullosum diabeticorum, Granuloma annulare, acanthosis rigicans. [1] Further, the building of calluses and its characteristics is noticed. [1]

  • musculoskeletal examination [1,2,4,6]

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 [1,2,4,6], as they can lead to abnormal plantar foot pressure. [4] 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 [1,2,4,6]

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

  • vascular examination [1,2,4,6]

Besides the palpation of the pulses, the vascular examination involves the inspection of the foot for signs of ischaemia, symptoms of intermittent claudication [1, 2, 4, 6]. Vascular insufficiency needs a further consultation including …….. which are illuminated in the corresponding chapter.

  • neurologic examination [1,2,4,6]

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. [1,2,4,6] 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. [10]

DFS: non-invasive vascular diagnosis
  • Palpation of foot pulses [1,2,4]

The palpation of the foot pulses makes the difference between neuropathic and (neuro-) ischaemic disorders. The absence of pedal pulses suggests ischemia [1, 10].

  • 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. [1,2,4,6]

  • Pressure perception [1,2,4,6]
    • Semmes-Weinstein 10g-monofilament [1,2,4,6]

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. [2]

  • Vibration perception [1,2,4,6]
    • 128 Hz tuning fork [2,4]

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. [2]

  • Deep tendon reflexes: patella, Achilles [1,2]
  • 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. [13] 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. [13,14]

Diabetic foot infections are often polymicrobial with mixed gram-positive and gram-negative, aerob and anaerob species. [12,13,14] Some studies suggest a possible dependence and interaction among aerobes and anaerobes [12,13] which can lead to the production of virulence factors such as hemolysins, proteases, collagenases or short-chain fatty acids. [12] As the mixed flora contribute to the chronicity of the infection and can have important clinical implications, it should not be overlooked. [12, 13]

The main causative pathogen in diabetic foot ulcers are the Staphylococci, typically S. aureus. [11, 12, 14] Beta-hemolytic streptococcus are often found, too. [11] These two bacteria are the pathogens of early diabetic foot infections. [12]

Anaerobic baceteria are often present in diabetic foot ulcers. They are mostly isolated from deep tissues which are usually polymicrobial. [12,13,14] 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. [11] However, heir role in the diabetic foot ulcers is unclear. Many studies didn’t quantify the bacterial density in the infected tissues [13], the number of specimens was not representative [12] or the collection or culture of the specimen was not always carried out properly. [12] Despite that, some studies suggest that anaerobic bacteria plays a minimal role [12].


Anaerobes

Anaerobes are often present in diabetic foot ulcers but are rarely isolated from superficial samples [14] More anaerobic bacterial strains were isolated from deep tissue than from other sites cultured. [13] There is a poor concordance of results obtained from ulcer swabs with those obtained from uncontaminated deep tissue specimens [13] 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 [14]

Staph. Spp [14]

Diphteroids [14]

Streptococcus agalactiae [12, 14]

Streptococcus mitis [12]

Streptococcus milleri [12]

Enterococci [12]

Corynebacteria [12]

Eubacterium spp [14]

Peptostreptococcus spp [14]

Peptostreptococcus asaccharolyticus [14]

Finegoldia magna [12]

Gram-negative

Bacilli [13]

Clostridia [13]

Bacteroides [13]

Enterobacteriaceae [12]

Pseudomonas aeruginosa [12]

Proteus mirabilis [12]

Klebsiella [12]

Cocci [13]

Fusobacterium nucleatum [14]

Prevotella [12]

Porphyromonas [12]



Deep wounds

Deep tissue samples are more likely to reveal both aerobic and anaerobic pathogens. [14] Deeper infections are usually polymicrobial [14] Heavy growths of anaerobes were seen in the deep tissue[13]


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. [11] 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). [15] 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. [11] 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. [15]

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.
  13. 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
  14. Urbancic-Rovan V, Gubina M. Bacteria in superficial diabetic foot ulcers. Diabet. Med, 2000, 17(11), 814-15.
  15. 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



Radiologic diagnostic procedures

(The list is under construction and not yet completed)

For a image-guided diagnostic of the diabetic foot syndrome a target-oriented proceeding is recommendable. It is necessary to consider the pathogenetic factors and above all to be geared to the expected therapeutic consequences. Target-oriented diagnostic of the diabetic foot syndrome

Base diagnostic

  • conventional radiographies of the foot in 2 levels
  • strict lateral handycap absorption while the patient is staying
  • dopplersonographic measurement of the arterial terminal vascular bed


Continuative diagnostic

  • doppler duplex-examination of the arterial pelvis- and leg-vessels
  • digital subtraction angiographie of the arterial pelvis- and leg-vessels
  • magnetic resonance imaging
  • possible additional procedure of a computed tomography
  • possible additional procedure of a scintigraphy

At least the base diagnostic is to proceed at any rate und independent of the pathophysiology.

nuclear medicine

positron emission tomography
roentgen (x-ray)
DFS: deformation of bone structure in the x-ray image

magnetic resonance imaging

Therapy of DFS

DFS: severly infected foot ulcer ...

Primary Procedures

The primary treatment goal for diabetic foot ulcers is to obtain wound closure as expeditiously as possible. Resolving foot ulcers and decreasing the recurrence rate can lower the probability of lower extremity amputation in the diabetic patient [7]. Treatment of the diabetic foot ulcers should be individually tailored according to the size, depth, location and presence/absence of infection or ischemia. Location of the ulcer will give clues as to the etiology of the wound, whether it is as a result of shoe pressure, for example. Size and depth play a key role in determing the length of time required for wound healing [4].

Therapy of the internistic diseases

  • Further metabolism control
    • lipids
    • blood pressure
  • Blood glucose control

Most foot ulcers have their origins in inadequate control of blood sugar. This is an excellent evidence that blood glucose control can reduce the incidence of neuropathy [1].

  • Moisture balance

Tissue moisture balance is a term used to convey the importance of keeping wounds moist and free of excess fluids. A moist wound environment promotes granulation and autolytic processes [7].

Therapy of infection

The Treatment of infection involves debridement of all necrotic tissue and drainage of purulent collections along with antibiotic therapy [1,4,5].

  • smear test

for the test of microbes (look up to the table: Microbiological diagnosis). After this test start with the anibiotic therapy.

  • Antibiotic therapy
    • Antibiotic / (broad-spectrum) Antimicrobial therapy
      • based on the pathogens presumed to be present [3]
      • used antibiotics include: clindamycin, cephalexin, ciprofloxacin, and amoxicillin-clavulanic acid [3]
      • for treating aerobic gram-positive cocci [5]
    • (parenteral) Intravenous antibiotics
      • for more serious infections (cellulitis)
      • used antibiotics include: imipenem-cilastatin, beta-lactam/lactamase inhibitors (ampicillin-sulbactam and piperacillin-tazobactam), and broad-spectrum cephalosporins [3]
    • Aminopenicillinlactamase inhibitors [3]
  • Drainage
  • Good circulation

Debridement

Debridement can remove nonviable or deficient tissue, control infection or inflammation, reduce pressure and bacterial burden, moisture imbalance and stimulate a nonadvancing wound edge. There are several methods of wound debridement to preparate wound bed. Each method has advantages and disadvantages [2,3,4,7].

  • Autolytic

Autolytic debridement utilizing phagocytic cells and proteolytic enzymes. Acute and chronic wounds treated with occlusive dressings. The use of occlusive dressings to manage wound exudate and provide a moist wound environment. But before using occlusive dressings for debridement look for aerobe and anaerobe germs in ulcers [2,7].

Advantages of autolytic debridement
- easy to perform
- natural
- selective
- painless
- useful in wounds with minimal debris

Disadvantages of autolytic debridement
- slow process
- can not be used in infected wounds

  • Mechanical

Mechanical debridement is used for wounds with larger amounts of necrotic tissue, but also for smaller wounds by moistening necrotic eschars [2,7].
There are several methods:
- wet-to-dry dressings
A wet gauze dressing is applied to the wound bed and allowed to dry. Necrotic debris becomes embedded in the gauze and when the gauze is removed they can be mechanically stripped from the wound bed [2].
- hydrotherapy and irrigation
When the wounds are cleansed and debrided using whirlpool therapy or by irrigation saline or a cleansing agent. An other type of hydrotherapy is pulsed lavage. That utilizes a pressurized, pulsed solution to irrigate and debride wounds [2].
- dextranomers
Dextranomer is a high-molecular-weight derivative of dextran manufactured as dry. One gramm of dextranometer can absorb up to 4g of fluid [2].

Advantages of mechanical debridement
- easy to perfom
- useful in wounds with necrotic material
- moderate to large amounts of exudate

Disadvantages of mechanical debridement
- nonselective
- may remove viable tissue
- may damaga surrounding tissue

  • Chemical (proteolytic enzymes) /Enzymatical

Chemical debridement is the application to the wound of proteolytic enzymes that are able to chemically digest and remove cellular debris. Chemical debridement can be utilized in conjunction with the other methods of wound debridement. The enzymatic debridement agents are affected by the pH of the wound environment. The enzymatic debriding agents are Collagenase; Fibrinolysin/DNase; Papain/Urea; Streptokinase/Streptodornase; Trypsin [2,4,7]

Advantages of chemical / enzymatical debridement
- easy to perform
- selective
- painless
- useful in noninfected wounds

Disadvantages of chemical / enzymatical debridement
- irritation of surrounding tissue
- slow process
- enzymes may be inactivated by the wounds
- need to cross-hatch eschar, if present, prior to application of enzyme

  • Surgical (sharp)

Surgical or sharp debridement is the removal of necrotic or nonviable tissue by using sharp instruments such as scalpels, curettes or scissors. This form of debridement is recommended for the removal of thick, adherent eschars and devitalized tissue in large ulcers [2,3,7].

Advantages of surgucal debridement
- immediate results
- selective
- indicated in ulcers with large amounts of necrosis and eschars

Disadvantages of surgical debridements
- requires skilled clinician
- may cause bleeding and pain
- need for analgesia

  • Biological (maggot therapy)

The application of maggots to the wound bed. This species of maggots remove only necrotic tissue [2,7].

Advantages of biological debridement
- highly selective
- maggots produce antimicrobial factors

Disadvantages of biological debridement
- use in confined to selected cases

DFS: an earlier stage

Pressure relief / Off-loading (avoiding further trauma)

The reduction of pressure to the diabetic foot ulcer is essential to treatment. Proper off-loading and pressure reduction prevents further trauma and promotes healing. This is particularly important in the diabetic patient with decreased or absent sensation in the lower extremities [1,3,4,7].

  • Total contact cast

Total contact casting is the most effective mean of offloading diabetic foot ulcers. The total contact casting involves the use of a well-molded minimally padded plaster cast to distribute pressures evenly to the entire limb [2,4,7].

  • Advantage of total contact cast

The forced patient compliance as a result of the inability to remove the apparatus.

  • Disadvantage of total contact cast

Include the considerable skin and time required for application. The possibility of secondary skin lesions resulting from cast irritaion and the inability to assess the wound daily.

  • Boots
    • useful for neuropathic and non-ischemic ulcers
  • Therapeutical footwear
    • plastic walkers to offload plantar ulcers
    • appropriated shoes with sufficient width, depth and arch support
    • half shoes
    • short leg walkers
    • sandals
  • Orthotic
    • wheelchair
    • crutches
    • fore foot orthese
  • Horny skin elimination
  • Felted foam dressings
  • Bed rest

Dressing

Dressings promote a moist or a dry environment to assist healing. They are a focus of care for chronic wounds. Some dressings are used after or before debridement. Wound dressings can be categorized as passive, active or interactice. Passive dressings primarily provide a protective funtion. Active and interactive dressings and therapies are capable of modifying a wound's physiology by stimulating cellular activity and growth factor release. There are local and wet dressing methods [3,7].

  • felted foam dressing [3,7]
  • normal-saline dressing [7]
  • moist-to-dry dressing [7]
  • dressings with cellulose-modulating or collagen-protease-modulating framework with hyaluronan [3,7]
  • wet-to-dry dressings [2,7]
  • wet gauze dressing [2,7]
  • antimicrobial dressings [2,7]

Adjunctive treatments/ Advanced wound management

This newer technologies are expensive and they are limited by their substantial costs [1].

Growth factor therapy
  • Recombinant platelet-derived growth factor (becaplermin gel)

For the treatment of neuropathic foot ulcers. This form of therapy is useful in chronic, nonhealing neuropathic ulcers that do not respond to conventional care. It stimulate chemotaxis and mitogenesis of neutrophils, fibroblasts, monocytes and other components that form the cellular basis of wound healing [1,3].

  • Recombinant human granulocyte colony-stimulating factors (G-CSF)

This method enhance meutorphil function in vitro in patients with diabetic foot infections.
G-CSF (in addition to antibacterial therapy) does not appear to accelerate the resolution of infection but is associated with a decreased rate of lower limb amputation and other surgical procedures [5].

  • Autologous platelet-rich plasma treatment

utilize the patient's own blood to create a gel that is applied to the wound [7].

Tissue-engineered skin

Living dermis and sequentially cultured epidermis are the cellular components of which are derived from neonatal foreskin. Dermis derived from human fibroblasts. This form of treatment was associated with faster healing and lower rates of osteomylitis and lower-limb amputation [1,3].

Hyperbaric oxygen therapy (HBO)

HBO treatment involves immersing the wound in a pure oxygen atmosphere, either with steady or cyclical raised pressure, in a leg chamber or by placing the whole patient in a chamber. A number of possible mechanisms form the rationale for this treatment including improved oxygen supply promoting the proliferation of granulation tissue and antibacterial effect on anaerobic organisms. This therapy is a high technology and expensive treatment for standard lower-extremity wound care and can help salvage servely infected limbs. But this field requires furthers investigation [1,6,7].

Patient's training / foot care advice / self-care activities

  • Treatment of injuries

If your foot is hurt, do not keep walking on it. Treat blisters, cuts and scratches right away, but never use strong chemicals on your feet. Cover all injuries with clean dressings [1,8].

  • Inspection

Look every day at your feet from all sides, including the space between your toes. Look for dry patches and cracks in the skin. Check for cuts, blisters, corns, calluses, swelling, ingrown toenails or places that are red or pale [8].

  • Circulation

Stop smoke, regulary excercise and avoid using heating pads or hott water bottles [8].

  • Socks and shoes

Wear every day clean socks and they should fit well [8].
Waer shoes and socks in the house and outside at all times to protect and support your feet [8].

  • Bathing

Wash your feet daily in warm (not hot) water. Don't soak your feet and genlty dry your feet with a soft towel [8].

  • Corns and calluses

When feet are dry, genlty file away mildly callused areas with a pumice stone. Avoid do-it-yourself chemical corn or callus removers and never perform "bathroom surgery" on your feet with razor blade or similar instrument [8].

  • Toenails

Cut your toenails after bathing. Use a toenail clipper or file to shorten the nail. Don't use sharp objects to poke or dig under the toenail or around the cuticle [8].



References

  1. Bowering CK. Diabetic foot ulcers.Pathophysiology, assessment, and therapy. Canadian family physician Médecin de famille canadien, 2001, May, 47: 1007-16. Review [5]
  2. Falabella AF. Debridement and wound bed preparation. Dermatology and Cosmetic Specialists, 2006, Nov-Dec, 19(6): 317-25.[6]
  3. Haris M. Rathur, Andrew J.M. Boulton. The diabetic foot. Clinics in Dermatology, 2007, Jan-Feb, 25(1): 109-20. [7]
  4. Dinh TL, Veves A. Treatment of diabetic ulcers. Dermatologic Therapy, 2006, Nov-Dec, 19(6): 348-55. [8]
  5. Nalini Rao, Benjamin A. Lipsky. Optimising Antimicrobial Therapy in Diabetic Foot Infections. Therapy in practice. Drugs, 2007, 67(2): 195-214 [9]
  6. Robert P. Wunderlich, Edgar J.G. Peters, Lawrence A. Lavery. Systemic Hyperbaric Oxygen Therapy. Lower-extremity wound healing and the diabetic foot. Diabetes Care, 2000, Oct, 23(10): 1551-5. [10]
  7. Frykberg RG, Armstrong DG, Giurini J, Edwards A, Kravette M, Kravitz S, Ross C, Stavosky J, Stuck R, Vanore J. Diabetic foot fisorders. A clinical practice guideline (2006 revision). American College of Foot and Ankle Surgeons, 2006, Sep-Oct, 45 (5 Suppl): S1-66. [11]
  8. Deborah J. Toobert, Sarah E. Hampson, Russell E. Glasgow. The Summary of Diabetes Self-Care Activities Measure. Diabetes Care, 2000, Jul, 23(7):943-50. [12]


Internet Links

  1. Deutsche Diabetes Gesellschaft [13]. Evidenzbasierte Leitlinien; [cited on 2007 Nov]. Available from: Diagnostik, Therapie, Verlaufskontrolle und Prävention des diabetischen Fußsyndroms
  2. Deutsche Diabetes Gesellschaft [14]. Praxisleitlinien Diabetisches Fußsyndrom; [cited on 2007 Nov]. Available from: Diabetisches Fußsyndrom
  3. Diabetischer Fuß Therapie; [cited on 2007 Nov]. Available from: Netdoktor.de
  4. National Institute for Health and Clinical Excellence [15]. Clinical Guidelines for Type 2 Diabetes; [cited on 2008 Jan]. Available from: Prevention and management of foot problems

Surgical Therapy

(The list is under construction and not yet completed)
The majority of patients with diabetic foot problems can be treated nonsurgically. Here a short overview is given about the surgical procedures, which are used in the salvage of the diabetic foot.

Patient selection is a major problem in comparing studies. E.g. often the techniques may be uniform, but they are infrequently the same. Also, betimes patients with vascular diseases are included and betimes they are not. Pre- and post-operative treatment with surgical techniques and antibiotics varies. As well varies the timing of surgery. Some try long periods of conservative treatment, while others use early surgery.

Revascularization

The aim of the revascularisation procedure is ‘to provide sufficient blood flow to relieve rest pain and heal skin lesions’.
Idication and requirements:
In 564 of 902 patients, consecutively hospitalized for foot ulcer and/or rest pain, the presence of critical limb ischemia (CLI) were referred to an angiographic study. So at 62.5% of the patients a revascularization was indicated.[16] lower limb lesions preferentially located in crural arteries (74% of all lesions) [17]
Diagnostic indication:

  • Non-presence of pedal pulses
  • transcutaneous oxygen tension (TcPO2) values (<50 mmHg)
  • The posterior tibial and dorsalis pedis pulses, evaluated by palpation and a Doppler continuous wave technique
  • duplex scanning was, with haemodinamically significant stenoses [16]
  • ABI elevated >0.5 then toe blood pressure measurements or skin perfusion studies are performed [18]

see also:1.4.2.2 Vascular diagnosis

cave: too high surgical risk or lack of outflow

Procedure:

  • Angioplasty: Angioplasty is the mechanical widening of a narrowed or totally obstructed blood vessel. These obstructions are often caused by artherosclerosis. Angioplasty has come to include all manner of vascular interventions typically performed in a minimally invasive or percutaneous method. Peripheral angioplasty refers to the use of mechanical widening in opening blood vessels. It is often called percutaneous transluminal angioplasty or PTA for short. PTA is most commonly done to treat narrowings in the leg arteries, especially the common iliac, external iliac, superficial femoral and popliteal arteries. PTA can also be done to treat narrowings in veins. Angioplasty is suitable for stretching of single- or multistenosis, where appropriate for short seal.
  • Local fibrinolysis: Fibrinolysis is the process where a fibrin clot, the product of coagulation, is broken down. Its main enzyme, plasmin, cuts the fibrin mesh at various places, leading to the production of circulating fragments that are cleared by other proteinases or by the kidney and liver.
  • Endovascular prothesis-implantation: Endovascular surgery is a form of minimally invasive surgery that was designed to access many regions of the body via major blood vessels. Typically the blood vessel chosen is the femoral artery or vein found near the groin. Stents and coils are composed of fine wire materials, that can be inserted through a thin catheter and expanded into a predetermined shape once they are guided into place. A stent is a tube that is inserted into a natural conduit of the body to prevent or counteract a localized flow constriction. The term may also refer to a tube used to temporarily hold such a natural conduit open to allow access for surgery.
  • Endarterectomy: Endarterectomy is a surgical procedure to remove the atheromatous plaque material, or blockage, in the lining of an artery constricted by the buildup of fatty deposits. It is carried out by separating the plaque from the arterial wall.
  • Open bypass grafting: Arteries or veins from elsewhere in the patient's body are grafted to the lower limb vessels to bypass atherosclerotic narrowings and improve the blood supply to the footvessels supplying the foottissues.

Conclusion:
'Since foot ischaemia is one of the determinants in the development - and the most important factor preventing healing - of diabetic foot ulcers, a thorough assessment of the lower limb arterial tree should be routinely performed. The vascular surgeon is the only professional who has insight into all available revascularisation methods and can take responsibility for the vascular problems of the diabetic patient. Therefore the vascular surgeon should always be consulted without undue delay to improve leg salvage rates in diabetic patients with diabetic foot lesions.'[19] Revascoraization also is often a necessary procedure before foodsurgery, like orthopedic or graft intervention.

Complications:

  • Embolisms
  • Thrombosis
  • Venous fistula
  • perforations
  • haematomas

These complications are reatively rare.[16,17,18]


Orthopedic Surgery

Surgery at foot skeleton, to improve statics and adjust deformations. Corrective surgery in diabetic foot problems is becoming more common in the last decade. Corrective surgery in diabetes has several goals:

  • to provide a foot of good configuration that is plantigrade and that can be fitted with shoes making ambulation possible;
  • to improve the quality of life and to avoid amputation with better, more normal gait;
  • to eliminate the infectious focus;
  • to hasten the healing of ulcers by eliminating bone prominences.


Idication and requirements:
Such procedures require a sufficient blood flow, other than that a revascularization at forerun should happen.

  • The Charcot joint disease(Charcot's neuroarthropathy, or Charcot foot)
  • Osteomyelitis:
    Osteomyelitis is an infection of bone or bone marrow, usually caused by pyogenic bacteria or mycobacteria. It can be usefully subclassified on the basis of the causative organism, the route, duration and anatomic location of the infection.
  • Underlying pressure of metatarsal heads or bony

Procedure:

  • Arthrodesis:
    The most common surgery described in the treatment of diabetic foot deformity is arthrodesis. Where deformity caused chronic ulceration of deep infection. Charcot joint disease is a frequent reason for choosing arthrodesis. Because arthrodesis is an alternative to amputation, a high rate of complications is acceptable 25 to 75%. Traditionally, arthrodesis has been fixed with internal fixation (e.g. plates, screws, or a blade plate). Intramedullary nailing through the hind foot has been gaining ground in foot surgery circles, as its stability offers fast and safe mobilization. External fixation as an alternative to internal fixation allows rapid mobilization. [22]
  • Metatarsal head resection
    • Metatarsal head resection and other surgical procedures to the metatarsals in order to decrease underlying pressure increase healing of plantar ulcers have been spread for at least the last 19 years.
    • metatarsal osteotomy provide almost the same results. [23]
  • Others non standart precedures
    • Tenotomy [24]
    • Exostectomy: Removal of an exostosis. [25]
    • Achilles tendon lengthning [26]
    • Great toe amputation [27]
    • Calcanectomy [28]

Conclusion:
The surgical risk, of complication rates, for diabetic patients is almost three times that of conservatively treated patients. Also the risk of infection is four times higher in diabetic patients. Recurrence or new ulceration rates were fairly high. Despite the great rate of complications in most orthopedic surgerys, they are mostly a better alternative to amputation.


Graft Surgery

Indication and requirements:
Graft Surgery is not a standart precedure. Specialized surgeons are requiered as a well selectet subject. In most cases a revascularization is necessary. 'In patients with large tissue defects, deep space infection, osteomyelitis or exposed tendon, or bone, the limb may be lost'[29]. In these patients a free tissue transfer is recommendable.

Procedure:

  • Skin grafting: In that procedure, the affected bone is initially exposed by debridement with a scalpel, followed by partial excision with a bone scraper until fresh bleeding is observed from the exposed bone. The lesions are then immediately covered with an occlusive dressing, and finally the wound gets covered with an epidermal graft of skin harvested from suction blisters.
  • Muscle grafting: Nearly same as skin grafting, with muscle-flaps. It is often combined with skin grafting.

Conclusion:
'In certain well-selected cases, the transfer of well-vascularized tissues using microsurgical techniques can improve wound healing and may decrease hospitalization time, and may increase a patient’s chance of achieving independent ambulation.'[29] More often it is reportet, that revascurarizating procedures are per default accomplished ante free tissue graft surgery.[28,30,31]

References

Articles

Faglia E, Clerici G, Clerissi J, Gabrielli L, Losa S, Mantero M, Caminiti M, Curci V, Lupattelli T, Morabito A. Early and five-year amputation and survival rate of diabetic patients with critical limb ischemia: data of a cohort study of 564 patients. Eur J Vasc Endovasc Surg. Eur J Vasc Endovasc Surg. 2007 Apr;33(4):453-60. Epub 2006 Dec 29. [16]

Graziani L, Silvestro A, Bertone V, Manara E, Andreini R, Sigala A, Mingardi R, De Giglio R. Vascular involvement in diabetic subjects with ischemic foot ulcer: a new morphologic categorization of disease severity. [17]

Faglia E, Dalla Paola L, Clerici G. Peripheral angioplasty as the first-choice revascularization procedure in diabetic patients with critical limb ischemia: prospective study of 993 consecutive patients hospitalized and followed between 1999 and 2003. Eur J Vasc Endovasc Surg. 2005 Jun;29(6):620-7. Epub 2005 Mar 28.[18]

Lepäntalo M, Biancari F, Tukiainen E.Never amputate without consultation of a vascular surgeon. Diabetes Metab Res Rev. 2000 Sep-Oct;16 Suppl 1:S27-32. [19]


Faris I, Duncan H. Skin perfusion pressure in the prediction of healing in diabetic patients with ulcers or gangrene of the foot. J Vasc Surg 1985;2:536–540. [20]

Sanders LJ. The Charcot foot: historical perspective 1827-2003. Diabetes Metab Res Rev. 2004 May-Jun;20 Suppl 1:S4-8. [21]

Resch S. Corrective surgery in diabetic foot deformity. Diabetes Metab Res Rev. 2004 May-Jun;20 Suppl 1:S34-6. [22]

Tillo TH, Giurini MJ, Habershaw GM, Chrzan JS, Rowbotham JL. Review of metatarsal osteotomies for the treatment of neuropathic ulcerations. J Am Podiatr Med Assoc 1990; 80(4): 211–217. [23]

Kile TA, Donnelly PA, Gehrke JC, Werner ME, Johnson KA. Tibiotalocalcaneal arthrodesis with an intramedullary devise. Foot Ankle Int 1994; 15: 669±673. [24]

Ruth Chaytor E. Surgical treatment of the diabetic foot. Diabetes Metab Res Rev. 2000 Sep-Oct;16 Suppl 1:S66-9. [25]

Maluf KS, Mueller MJ, Strube MJ, Engsberg JR, Johnson JE. Tendon Achilles lengthening for the treatment of neuropathic ulcers causes a temporary reduction in forefoot pressure associated with changes in plantar flexor power rather than ankle motion during gait. J Biomech. 2004 Jun;37(6):897-906. [26]

Quebedeaux TL, Lavery LA, Lavery DC. The development of foot deformities and ulcers after great toe amputation in diabetes. Diabetes Care 1996; 19(2): 165–167 [27]

Bollinger M, Thordarson DB. Partial calcanectomy: an alternative to below knee amputation. Foot Ankle Int 2002; 23(10): 927–932. [28]


Sunar H, Aygit CA, Afsar Y, Halici U, Duran E. Arterial and venous reconstruction for free tissue transfer in diabetic ischemic foot ulcers. Eur J Vasc Endovasc Surg. 2004 Feb;27(2):210-5. [29]

Ozkan O, Coşkunfirat OK, Ozgentaş HE. Reliability of free-flap coverage in diabetic foot ulcers. Microsurgery. 2005;25(2):107-12. [30]

Vermassen FE, van Landuyt K. Combined vascular reconstruction and free flap transfer in diabetic arterial disease. Diabetes Metab Res Rev. 2000 Sep-Oct;16 Suppl 1:S33-6. [31]

Shenaq SM, Dinh TA. Foot salvage in arteriolosclerotic and diabetic patients by free flaps after vascular bypass: report of two cases. Microsurgery. 1989;10(4):310-4. [32]

The British journal of dermatology, Rapid healing of intractable diabetic foot ulcers with exposed bones following a novel therapy of exposing bone marrow cells and then grafting epidermal sheets. [33]


Diabetischer Fuss Manual [34]

Internet

Wikipedia [35]

Diabetic Nephropathy

What is Diabetic Nephropathy?

Besides Diabetic Foot Syndrom (DFS), Neuropathy and cardiovascular diseases, Diabetic Nephropathy is one of the most important and most expensive long-term consequences of diabetes mellitus. It is associated with a significant reduction of both life expectancy and quality of life (Brändle & Herman 2004). The course of disease is similar for type 1 and type 2 diabetes (Hasslacher et al. 1989). Initially the enduring high level of blood sugar causes a saccharification of the small blood vessels in the kidney and consequently coarsing the renal filters. In a first step this results in a selective expulsion of micromolecular proteins in the urine. According to Mogensen this state is called Microalbuminuria (MAU) or incipient nephropathy (Mogensen, Christensen & Vittinghus 1983) and is considered as the most important early symptom fo diabetic nephropathy. As the diseases progresses the albumin expulsion increases and is becomes increasingly less selective. It is then refered to as Macroalbuminura (MA), apparent nephropathy or clinical proteinuria.

Risc factors and therapy

The most important risc factors for the development and progression of diabetic nephropathy are hyperglycemia, hypertonia and smoking.

References

Articles