RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,

BANGALORE, KARNATAKA,

ANEXURE – II

PROFORMA FOR REGISTRATION OF SUBJECT FOR DESSERTATION

NAME OF THE CANDIDATE : Dr NITHIN HUMAYOON

ADDRESS : DEPARTMENT OF GENERAL SURGERY

Dr B R AMBEDKAR MEDICAL COLLEGE

BANGALORE – 560045.

NAME OF THE INSTITUTION : DR B R AMBEDKAR MEDICAL COLLEGE

BANGALORE.

COURSE OF STUDY & SUBJECT : MS GENERAL SURGERY.

DATE OF ADMISSION : 31st MAY 2013.

TITLE OF THE TOPIC : SURGICAL MANAGEMENT OF DIABETIC FOOT AND FACTORS INFLUENCING THE MANAGEMENT OF DIABETIC FOOT

BRIEF RESUME OF THE INTENDED WORK:

7.1 NEED FOR STUDY:

Over the past few decades there has been an alarming rise in the prevalence of diabetis. According to the International Diabetes Foundation, there are more than 300 million people living with diabetes worldwide.1 The CPR (Crude prevalence rate) in the urban areas of India is thought to be 9 per cent.In rural areas, the prevalence is approximately 3 per cent of the total population.2.

Close to one-fifth of all adults with diabetes in the world live in the South-East Asia Region. Current estimates indicate that 8.3% of the adult population, or 71.4 million people, have diabetes in 2011, 61.3 million of whom are in India. The number of people with diabetes in the region will increase to 120.9 million by 2030, or 10.2% of the adult population.3

IGT (Impaired Glucose Tolerance) is also a mounting problem in India. The prevalence of IGT is thought to be around 8.7 per cent in urban areas and 7.9 per cent in rural areas, although this estimate may be too high. It is thought that around 35 per cent of IGT sufferers go on to develop type 2 diabetes, so India is genuinely facing a healthcare crisis.

Diabetes is also beginning to appear much earlier in life in India, meaning that chronic long-term complications are becoming more common. The implications for the Indian healthcare system are enormous.

One of the most important and disabling complications of diabetes mellitus (DM) is the diabetic foot ulcers (DFU). Development of DFU is traditionally believed to result from a combination of oxygen deficiency caused by peripheral vascular disease, peripheral neuropathy, minor foot traumas, foot deformities, and infection.4,5,6 DFU, with a lifetime development risk of 15% , incidence of 1–4%, and prevalence of 5.3% to 10.5% in all diabetic patients, accounts for more than half of the non-traumatic lower-extremity amputations in the world . Globally, one lower limb is lost every 30 seconds because of DFU 7. The range of mortality following diabetic foot amputation is 39–80% after 5 years, which is worse than the mortality rate for most malignancies.8 Approximately, 20% of hospital admissions among diabetic patients are in consequence of foot problems.9 Furthermore, DFU is among the most prevalent causes of hospitalization and morbidity and is responsible for more days of hospital stay than any other chronic complication of DM .

DFU lesions are significant health and socioeconomic problem as they exert adverse effects on patients’ quality of life and impose heavy economic burden on the patient and the state due to rising the need for rehabilitative and home care service. Given the DFU’s high prevalence, heavy burden, and severe impact on patients’ life quality, it is advisable that sufficient heed be paid to prevention of this particular complication of DM. Hence this study has been taken up to understand the clinical presentation, risk factors of diabetic foot and the various treatment modalities including surgical treatment and newer techniques for the management of diabetic foot and the factors influencing the management of diabetic foot.

7.2 REVIEW OF LITERATURE:

 A diabetic foot is a foot that exhibits any pathology that results directly from diabetes mellitus or any long-term (or "chronic") complication of diabetes mellitus.10 Presence of several characteristic diabetic foot pathologies is called diabetic foot syndrome.  The most serious foot complications in diabetes are:11,12

Diabetic foot ulceration. -It occurs in 15% of all patients with diabetes and

precedes 84% of all diabetes-related lower leg amputations.13

Diabetic foot infections

Neuropathic osteoarthropathy of the foot

 Several factors predispose diabetic patients to developing a Diabetic foot, including neuropathy, vasculopathy and immunopathy. Peripheral neuropathy occurs early in the pathogenesis of diabetic foot complications and is considered the most prominent risk factor for diabetic foot ulcers 14.

 Diabetic patients with impaired protective sensation and altered pain response are vulnerable to trauma and extrinsic forces from ill-fitting shoewear. Motor neuropathy causes muscle weakness and intrinsic muscle imbalance leading to digital deformities such as hammered or clawed toes. This results in elevated plantar pressure due to metatarsophalangeal joint instability. Autonomic dysfunction leads to changes in microvascular blood flow and arteriolar-venous shunting, diminishing the effectiveness of perfusion and elevating skin temperatures. With the loss of sweat and oil gland function, the diabetic foot becomes dry and keratinized which cracks and fissures more easily, leading to a portal for infection. The most commonly utilized clinical method of objectively diagnosing sensory neuropathy in the foot and ankle setting involves the use of a Semmes-Weinstein 10-g monofilament to assess for protective sensation and a 128 Hz tuning fork for loss of vibratory sensation 15.

 Impaired host defenses secondary to hyperglycemia include defects in leukocyte function and morphologic changes to macrophages. Decreased chemotaxis of growth factors and cytokines, coupled with excess of metalloproteinases, impede normal wound healing by creating a prolonged inflammatory state. Fasting hyperglycemia and the presence of an open wound create a catabolic state. Negative nitrogen balance ensues secondary to insulin deprivation, caused by gluconeogenesis from protein breakdown. This metabolic dysfunction impairs the synthesis of proteins, fibroblasts and collagen, and further systemic deficiencies are propagated which lead to nutritional compromise. Research indicates impairment of the immune system with serum glucose levels ≥150 ml/dl16. Patients with diabetes tolerate infection poorly and infection adversely affects diabetic control. This repetitive cycle leads to uncontrolled hyperglycemia, further affecting the host's response to infection.

 In a large prospective study 17, significant independent risk factors for Diabetic foot included wounds that penetrated to bone, wounds with a duration >30 days, recurrent wounds, wounds with a traumatic etiology and the presence of PAD.

 The diagnosis of a Diabetic Foot Infection is made on the basis of clinical findings. According to the Infectious Disease Society of America (IDSA) guidelines, infection is present if there is obvious purulent drainage and/or the presence of two or more signs of inflammation (erythema, pain, tenderness, warmth, or induration) 18

 Objective physical examination should begin by acquiring vital signs, BMI and assessment of patient's general well-being. Hypothermia (<36°C) or fever (38°C), hypotension, tachycardia, and tachypnea are considered signs of severe infection and sepsis18. However, patients with DM may have an impaired neuroinflammatory response and not manifest typical signs of infection. It has been documented in a study 19 that 82% of patients admitted for osteomyelitis (OM) were afebrile on admission often failing to mount a physiological response to infection. Therefore, secondary signs of infection must be assessed such as exudate production, delayed wound healing and wound breakdown  Wagner's classification is one of the most widely used and universally accepted grading systems for Diabetic foot ulcer, consisting of six simplistic wound grades used to assess ulcer depth (grades 0–5) 20

Wagner classification system

0 Pre-ulcerative area without open lesion 1 Superficial ulcer (partial/full thickness) 2 Ulcer deep to tendon, capsule, bone 3 Stage 2 with abscess, osteomyelitis or joint sepsis 4 Localized gangrene 5 Global foot gangrene

 A more recently proposed and popularized Diabetic foot ulcer classification is the University of Texas Health Science Center San Antonio (UT) classification system .21 This system incorporates a matrix structure of four grades of wound depth with subgroups to denote the presence of infection, ischemia or both. Wounds with frank purulence and/or two or more local signs of inflammation such as warmth, erythema, lymphangitis, lymphadenopathy, edema, 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, rest-pain, absent pulses, dependent rubor, atrophic integument, absence of pedal hair or pallor on elevation coupled with one of more non- invasive values such as a TCPO2 <40 mmHg, ABI <0.8 or absolute toe systolic pressure <45 mmHg.

University of Texas Health Science Center San Antonio classification system 0 1 2 3 A No open lesion Superficial Wound Tendon/Capsule Bone/Joint B With infection With infection With infection With infection C Ischemic Ischemic Ischemic Ischemic D Infection/Ischemia Infection/Ischemia Infection/Ischemia Infection/Ischemia

 Diabetic foot infection classification schemes22

Diabetic foot infection classification schemes: Infectious Diseases Society of America (IDSA) Infectious International Diseases Clinical description Working Group on Society of the Diabetic Foot America Wound without purulence or any manifestations of Uninfected 1 inflammation ≥2 Manifestations of inflammation (purulence or Mild 2 erythema, pain, tenderness, warmth, or induration); any cellulitis or erythema extends ≤2 cm around ulcer, and infection is limited to skin or superficial subcutaneous tissues; no local complications or systemic illness Infection in a patient who is systemically well and Moderate 3 metabolically stable but has ≥2 cm; lymphangitis; spread beneath fascia; deep tissue abscess; gangrene; muscle, tendon, joint, or bone involvement Infection in a patient with systemic toxicity or Severe 4 metabolic instability (e.g., fever, chills, tachycardia, hypotension, confusion, vomiting, leukocytosis, acidosis, hyperglycemia, or azotemia)

 The IDSA formulated guidelines and key recommendations for treatment of Diabetic foot stating that an empirical antibiotic regimen should be implemented primarily on the basis of infection severity and likely pathologic agents 18. Optimally, definitive therapy should be based upon culture and susceptibility analysis. The antibiotic regimen should always include an agent active against gram positive cocci with special attention for MRSA in high risk patients. Previously treated or severe Diabetic foot should include extended coverage for gram-negative bacilli and enteroccocus species. Gangrenous and foul smelling wounds may require anti-anaerobic therapy.

 Surgical management of moderate to severe Diabetic foot infection(DFI) is often required and includes aggressive incision, drainage and debridement of non-viable soft tissue and bone. Multiple debridements are often necessary to provide adequate drainage and control of infection. One study reported amputation rates of 2.8, 46.2 and 77.7% in mild, moderate and severe infections respectively 22. The need for both minor (removal of a portion of foot distal to the ankle joint) and major amputations (proximal to the ankle joint) increased as the severity of infection increased. Foot infections can extend proximally into the leg through the tarsal tunnel, resulting in rapidly ascending limb and life threatening infection. Early surgical treatment of DFI may reduce the need for major amputations.

 Another study 23 retrospectively evaluated two groups of patients treated for DFI. Patients in group 1 were treated with only IV antibiotic therapy, while patients in Group 2 received IV antibiotic therapy in addition to surgical management within the first 3 days of hospital admission. Patients in Group 2 were found to have fewer above ankle amputations and a 6-day shorter hospital course than Group 1.

 With severe life threatening DFI, open amputation or guillotine procedures may take precedence to limb salvage regardless of vascular status 24. It is preferable to preserve as much distal viable soft tissue and bone as possible when performing an amputation, potentially allowing for delayed closure and functional weight bearing.

7.3 OBJECTIVES OF STUDY:

 To study the clinical presentation in diabetic foot patients admitted in Department of General Surgery in Dr B R Ambedkar Medical College  To study the risk factors for diabetic foot ulceration in patients admitted in Department of General Surgery in Dr B R Ambedkar Medical College

 To study the factors influencing the management of diabetic foot in according to glycemic control presence of vascular abnormality presence of neuropathy

 To study the multidisciplinary treatment modalities in the management of diabetic foot and its complication.

 To observe and record the various surgical treatments and newer techniques in the wound care of diabetic foot ulcer in consultation with the operating surgeon

8. MATERIALS AND METHODS:

8.1 SOURCE OF DATA:

The study will be obtained from 80 patients admitted with diabetic foot in the Department of Gereral Surgery at Dr B R Ambedkar Medical College from period of October 2013 to November 2015.

8.2 METHOD OF COLLECTION OF DATA:

Patients admitted with diabetic foot during October 2013 to November 2015 at Dr B R Ambedkar Medical College will be taken up for study with the help of relevant history, clinical examination, appropriate investigations, details of treatment given and outcome.

INCLUSION CRITERIA: Patients with diabetis mellitus presenting with lesions of foot i.e ulcer, blister, abscess, gangrene admitted in the Department of General Surgery at Dr B R Ambedkar Medical College.

EXCLUSION CRITERIA:

Patients with chronic foot, leg ulcers due to etiologies other than diabetis.

Patients with blisters, cellulitis, abscess, gangrene of foot without Diabetis

Patients above 80 yrs of age.

PROFORMA:

Name:

Age:

Sex: M/F

Occupation:

Address:

In patient number:

Date of admission:

Date of discharge:

Socio-economic status

History: Chief Complaints :

History of present illness :

Ulceration Gangrene Neuropathy Delayed wound healing Recurrent infection Polyuria Polydipsia Polyphagia Burning sensation of palm/ soles Tingling / numbness Loss of appetite Loss of weight Fever Claudication Duration Distance Intermittent Rest pain

Diabetic history : Duration of diabetis Type of diabetis- NIDDM / IDDM Controlled/ uncontrolled Duration of control Method of treatment Diet Oral hypoglycemic : dose Insulin : dose Past history Visual disturbance Septic lesions- ulcerations/ gangrene/ carbuncle/ furunculous/ abscess CVS- i) angina ii) myocardial infarction CNS- TIA/ peripheral neuropathy Recurrent systemic infection H/o hypertension Previous hospital admissions Number Duration Treatment Cured / not cured

Family history Family members suffering from diabetis mellitus- Y/N

Personal history Diet- veg / non veg Appetite- normal/ decreased / increased Micturition- normal/ polyuria Bowel -regular/ irregular Smoker - Y/ N Alcoholic consumption- Y/ N History of prolong drug intake- Y/N – duration

Menstrual history in females

General physical examination:

Built – well/ moderate/ poor Nourishment – well/ moderate/ poor Pallor/icterus/clubbing/cyanosis/odema/lymphadenopathy Temperature Pulse Blood pressure Respiratory rate Systemic examination: Nervous system Central Peripheral Motor Sensory Reflexes Respiratory system Cardio vascular system Per abdomen examination

Local examination 1) Site Toe Sole Heel Web space Other foot lesions- dorsum/ lateral borders 2) Mode of presentation Ulcer Inspection-size, shape ,number ,position, edge, floor, Discharge, Surrounding area. Palpation-tenderness ,edge, base, bleeding, relation with deeper structure.-.mobile/ fixed Cellulitis Blister Abscess Gangrene Extend and colour, type- wet/ dry, line of demarcation, Crepitus, limb above gangrene area 3) Local temperature 4) Tenderness- Y/ N 5) Peripheral neuropathy- Y/N 6) Sensation- touch/ vibration/ joint 7) Skin/ nail changes Presence or absence of callosities 8) Peripheral pulses Dorsalis pedis artery- present/ weak/absent Posterior tibial artery- present/ weak/ absent Popiliteal artery- present/ weak/ absent Femoral artery-- present/ weak/ absent 9) Examination of regional lymph nodes 10) Examination of other limb

Investigations:

Urine – albumin/ sugar/ microscopy/ ketone bodies Blood- Hb/ total count/ differential count/ FBS/PPBS/ blood urea/ Serum creatinine/ lipid profile/ HbA1c ECG X ray – foot Wound swab for culture/ sensitivity Special investigation( if any) Doppler study Angiography

Treatment

Diet Oral hypoglycemic agents- dose Insulin – dose Antibiotics according to culture & sensitivity Dressing Glycerine magsulf Soframycin Betadine Hyrocolloid Supplimentary treatment Pre operative treatment Anesthesia used Surgical Incision & Drainage Wound debribement Fasciotomy Disarticulation Amputation Ray’s amputation Transmetatarsal Tarsometatarsal Midtarsal At the level of ankle joint Below knee Transcondylar Above knee Split skin graft Post operative treatment Discharge notes Condition of patient Nature of operation Advice given Diet Strict diabetic control Treatment Change of occupation

Follow up General condition/ diabetic condition/ local condition/ complication/ recurrence or fresh lesion Once in 1 month/ once in 3 month/ once in 6 month/ once in 1 year.

9 REFERENCES:

1. www.idf.org/millions-unite-diabetes-awareness-world-diabetes-day-2010

2. Diabetes.co.uk © 2013 Diabetes Digital Media Ltd

3. International Diabetes Federation Diabetes Atlas- fifth edition

4. Boulton AJ: The pathogenesis of diabetic foot problems: an overview. Diabetes Med 1996, 13:12-16. 5. Wieman TJ: Principles of management: the diabetic foot. Am J Surg 2005, 190:215-229. 6. Reiber GE, Vileikyte L, Boyko EJ, Del Aguila M, Smith DG, Lavery LA, Boulton AIM: Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings. Diabetes Care 1999, 22:157-162 7. Bakker K, Riley PH: The year of the diabetic foot. Diabetes Voice 2005, 50:11- 14. 8. Reiber GE: The epidemiology of foot ulcers and amputations in the diabetic foot. In Levin and o’Neal’s The Diabetic Foot. 6th edition. Edited by Bowker JH, Pfeiter MA. St Louis: Mosby; 2001::13-32

9. Levin ME: Pathophisiology of diabetic foot lesions. In Clinical Diabetes Medicine. Edited by Davidson JK. St Louis: Mosby; 1991::504-520.

10. Boulton in Diabetes, 30;36 2002

11. Frykberg RG, Armstrong DG, Giurini J, et al. (2000). "Diabetic foot disorders: a clinical practice guideline. American College of Foot and Ankle Surgeons". J Foot Ankle Surg 39 (5 Suppl): S1–60.PMID 11280471. 12. "Diabetic Foot". North Yorkshire Orthopaedic Specialists. Retrieved 4 February 2013.

13. Brem Harold, Tomic-Canic Marjana (2007). "Cellular and Molecular basis of wound healing in diabetes". JCI 117 (5): 1219– 1222. doi:10.1172/JCI32169. PMC 1857239. PMID 17476353. 14. -Reiber GE, Vileikyte L, Boyko EJ, del Aguila M, Smith DG, Lavery LA, et al. Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings. Diabetes Care 1999; 22: 157–62.

15. Snyder RJ, Kirsner RS, Warriner RA, III, Lavery LA, Hanft JR, Sheehan P. Consensus recommendations on advancing the standard of care for treating neuropathic foot ulcers in patients with diabetes. Ostomy Wound Manage 2010; 56: S1–24.

16. Inzucchi SE. Clinical practice. Management of hyperglycemia in the hospital setting. N Engl J Med 2006; 355: 1903–11.

17. Lavery LA, Armstrong DG, Wunderlich RP, Mohler MJ, Wendel CS, Lipsky BA. Risk factors for foot infections in individuals with diabetes. Diabetes Care 2006; 29: 1288–93.

18. Lipsky BA, Berendt AR, Deery HG, Embil JM, Joseph WS, Karchmer AW, et al. Infectious Diseases Society of America. Diagnosis and treatment of diabetic foot infections. Clin Infect Dis 2004; 39: 885–910.

19. Armstrong DG, Lavery LA, Sariaya M, Ashry H. Leukocytosis is a poor indicator of acute osteomyelitis of the foot in diabetes mellitus. J Foot Ankle Surg 1996; 35: 280–3. 20. Wagner FW, Jr. The dysvascular foot: a system for diagnosis and treatment. Foot Ankle 1981; 2: 64–122.

21. Oyibo SO, Jude EB, Tarawneh I, Nguyen HC, Harkless LB, Boulton AJ. A comparison of two diabetic foot ulcer classification systems: the Wagner and the University of Texas wound classification systems. Diabetes Care 2001; 24: 84–8.

22. Lavery LA, Armstrong DG, Murdoch DP, Peters EJ, Lipsky BA. Validation of the Infectious Diseases Society of America's diabetic foot infection classification system. Clin Infect Dis 2007; 44: 562–5.

23. Tan JS, Friedman NM, Hazelton-Miller C, Flanagan JP, File TM, Jr. Can aggressive treatment of diabetic foot infections reduce the need for above-ankle amputation?. Clin Infect Dis 1996; 23: 286–91.

24. Krause FG, deVries G, Meakin C, Kalla TP, Younger AS. Outcome of transmetatarsal amputations in diabetics using antibiotic beads. Foot Ankle Int 2009; 30: 486–93

HAS ETHICAL CLEARANCE BEEN OBTAINED FROM THE INSTITUTION: SIGNATURE OF THE CANDIDATE:

REMARKS OF THE GUIDE:

NAME AND DESIGNATION OF THE GUIDE:

Dr V KRISHNA RAO

PROFESSOR AND HEAD OF DEPARTMENT

DEPARTMENT OF GENERAL SURGERY

Dr B R AMBEDKAR MEDICAL COLLEGE

BANGALORE

SIGNATURE OF THE GUIDE:

CO-GUIDE IF ANY:

HEAD OF DEPARTMENT: Dr V KRISHNA RAO

PROFESSOR AND HEAD OF DEPARTMENT

DEPARTMENT OF GENERAL SURGERY

Dr B R AMBEDKAR MEDICAL COLLEGE

BANGALORE

SIGNATURE: