THE INCIDENCE AND RISK FACTORS OF

DIABETIC FOOT IN DIABETIC PATIENTS

INTRODUCTION

Diabetes mellitus describes a metabolic disorder of multiple aetiology

characterized by chronic hyperglycaemia with disturbances of carbohydrate,

fat and protein metabolism resulting from defects in insulin secretion,

insulin action, or both1. Diabetes mellitus may present with characteristic

symptoms such as thirst, polyuria, blurring of vision, and weight loss.2

Diabetes mellitus has been described in medical literature for almost two

millennia, however it has only been 75 years since the discovery of

insulin by Bantin and Best which transformed diabetes into a chronic

disease.

The etiology of diabetes mellitus that contributes to hyperglycemia

is reduced insulin secretion, decreased glucose utilization and increased

glucose production. This metabolic dysregulation imposes a change in

pathophysiology of multiple organs. In US, diabetes mellitus is a leading

cause of End Stage Renal Disease (ESRD), non traumatic lower limb

amputations and adult blindness.2

1
WHO Criteria for the diagnosis of diabetes mellitus2

• Symptoms of diabetes plus random blood glucose concentration

>200mg/dl.

• Fasting plasma glucose>126 mg/dl.

• Two hour plasma glucose>200mg/dl during an oral glucose

tolerance test.

Common complications of diabetes mellitus are:2 -

The effects of

diabetes mellitus include long-term damage, dysfunction and failure of

various organs. Complication are two types

Acute:

a) Diabetic ketoacidosis

b) Hyperglycemic Hyperosmolar State (HHS)

Chronic:

Vascular:

Microvascular

a) Retinopathy and macular edema

b) Neuropathy (sensory, motor and autonomic)

2
 c) Nephropathy

Macrovascular:

a) Coronary artery disease

b) Peripheral vascular disease

c) Cerebrovascular disease

Non vascular:

• Gastroparesis/diarrohea

• Uropathy/sexual dysfunction

• Fungal infection

• Cataract

• Glaucoma

• Periodontal diseases

Diabetic foot:

3
 It is one of the most important of all long term complications with

the serious repercussion of amputation of limb if not diagnosed and

treated early.

According to the World Health Organization and to the

International Working Group on the Diabetic Foot diabetic foot is

defined as the foot of diabetic patients with ulceration, infection and/or

destruction of the deep tissues, associated with neurological abnor-

malities and various degrees of peripheral vascular disease in the lower

limb.

It may vary from pre-ulcerative non infected stage to grossly

infected and ischemic condition with various grades in between as per

classification.

Diabetic foot has become in modern times what leprosy was in

ancient times.

Natural history of the diabetic foot

The natural history of the diabetic foot, which can be divided

into five stages:

Stage 1 - Normal foot;

Stage 2 - High risk foot;

4
Stage 3 - Ulcerated foot;

Stage 4 - Infected foot;

Stage 5 - Necrotic foot.

Epidemiology:

Diabetic foot incidence has increased from 0.7% (1980) to 2.7%

(1999).4 Diabetic foot is a leading cause of hospital admission among

people with diabetes mellitus. It is estimated that 15% of diabetes

mellitus patients develop foot ulcer (Most Commonly at great toe or

Metatarsel Phalangeal joint) during their life time and a significant

number of subjects(14-24% with ulcer)2 will ultimately undergo

amputation. Diabetic foot is the most frequent complication of diabetes

mellitus in developing countries.

Diabetic foot is the single most common cause of non traumatic

lower limb amputation (accounting almost 40-60% of non traumatic

amputations).5 About half the number of the amputations are performed

at the level of foot. About 30% of diabetes amputees lose the contra

lateral leg within 3 years and following amputation of leg, up to two third

die within 5 years. Up to 85% of amputations can be prevented with

5
appropriate knowledge of risk factors and subsequent application of

multidisciplinary treatment.

Risk factors:4

Following are the risk factors which increase chances of

developing diabetic foot among diabetes mellitus patients

• Sex – more common in males

• Duration - Diabetes > 10 years

• Older age

• Associated systemic disorders-

i) Peripheral neuropathy

ii) Microangiopathy

iii) Nephropathy

• Blindness/partial sight

• Structural deformity –

6
 i) Abnormal structure of foot

ii) Plantar callus and elevated foot pressure

• Limited joint mobility

• Peripheral artery disease

• History of previous ulcer- increases chance of recurrence of ulcer

• Blood sugar control- Poor hyperglycemic control

• Socio – economic status:

i) Poor social background

ii) Ethnic background – less common in Asian patients of Indian

subcontinent region.

• Others

i) Smoking

ii) Psychosocial factor (depression \ living alone)

The Aetiopathogenesis of diabetic foot4

1. Neuropathy: appears to be the most important factor not only in

developing diabetic foot but also in delaying the healing process.

About 60-70% of diabetics have neuropathy. Patients having

7
sensory loss appear to have 7 times increased risk of developing foot

ulcer. Neuropathy can be of following types.

1) Sensory

2) Motor

3) Autonomic

1) Sensory neuropathy is further divided into

a) Small fiber neuropathy

b) Large fiber neuropathy

c) Mixed neuropathy

a) Small fiber neuropathy

Small fiber loss predominate, leading to loss of pain and thermal

sensation before light or vibration sensation are blunted. Small fiber

neuropathy may produce pseudosyrinomyelic like picture with a distal

length related sensory loss mainly effecting pain and temperature

sensations.

b. Large fiber neuropathy

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 Large fiber neuropathy is late to develop than the small fiber

neuropathy presenting in form of loss of light touch and loss of

vibration sensation

c. Mixed neuropathy

Eventually mixed neuropathy develops in the diabetic patient

involving small and large sensory myelinated fiber with reduction

in touch, vibration, and proprioception as well as pain and

temperature

2) Motor

Motor fiber are also involved with slow motor conduction velocities

and reduced or absent action potentials of intrinsic muscles of the foot.

This can led to wasting and weakness of intrinsic muscle of the foot

and subsequent deformity like pesplannus, hallux valgus, clawing of

toe.

3) Autonomic

This is as the result of small fiber denervation. The evidence of

autonomic dysfunction is common before the onset of loss of tactile

sensations.

Etiopathogenesis of neuropathy

9
 Origin of neuropathy remains unclear.6 It has been postulated that

the insufficiency of instrinsic blood supply of peripheral nerves plays a

role in diffuse neuropathies. Non enzymatic glycosylation of protein in

the patient with poor hyperglycemic control can lead to structural change

in nerves but these have not been shown to contribute to physiologically

measurable dysfunction.

Recent studies have focused on the possibility of an autoimmune

basis for general and autonomic neuropathy.34 Where as another study

states that origin of endonurial microvascular ischemia caused by

accumulation of advanced glycosylated end product leads to

neuropathy.35

The combination of loss of protective sensation, motor and

autonomic neuropathy with superadded microtrauma lead to ulcer and

break down of skin under bony prominence. Ulcer becomes the most

common port of entry for bacteria leading to infection.

Classification of diabetic neuropathy (Thomas and Eliasson)6

a) Symmetrical sensory or sensorimotor polyneuropathy:

Symmetrical polyneuropathy is by far the most common initial and

10
the most troubling symptom and is invariably sensory. The autonomic

fibres although frequently involved are relatively less often affected

than the sensory fibres and with less severity and the mildest affected

are the motor fibres.

Although always bilateral and of distal onset, the symmetry of this

type of neuropathy may be disturbed by concomitant vascular

insufficiency.

The sensory symptom are positive or negative or both. Positive

symptoms include burning, itching, pin and pricks sensation, cramps

and tightness. These are peculiarly prominent at night in bed and a

common compliant is for a patient not being able to tolerate sheet or

blankets and to sleep with socks, even in warm weather.

Negative symptoms include hypoesthesia or anaesthesia.

Weakness is often mild and late complaint. Autonomic symptoms are

increasingly appreciated and may be cardiovascular, gastrointestinal,

genitourinary or cutaneous.

Electrophysiologic abnormalities affect both motor and sensory

nerves and are indicative of axonal loss. In general, clinical severity is

paralleled by the degree of electrical involvement but subclinical

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 electrical abnormalities are frequently seen in asymptomatic patient,

even thise without clinical signs of neuropathy.

b) Focal and multifocal: There can be sensory or motor or both and

can be superimposed on the symmetrical sensory polyneuropathy.

Both the cranial and the peripheral nerves are involved.

The most common cranial nerve involved is 3rd cranial nerve.

Individual Peripheral nerve dysfunction in patient with

diabetic mellitus is more common than in nondiabetic. The

question of whether an individual peripheral nerve lesion in an

individual diabetic patient is due to diabetic may be unresolvable,

but a variety of studies point to the frequent presence of such a

lesions (carpal tunnel syndrome, ulnar, peroneal or femoral

neuropathy) among diabetic. No clear cut relation was found

between the mono-neuropathies and age, gender, duration of

diabetics, diabetic control or the presence of other diabetic

complications.

Diabetic amyotrophy typically occurs in older patients with

type 2 diabetes, and in some cases, an immune-mediated epineurial

microvasculitis has been demonstrated in nerve biopsies. Clinical

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 features of amyotrophy include severe neuropathic pain and uni- or

bilateral muscle weakness and atrophy in the proximal thigh

muscles.

The diagnosis of neuropathy in young diabetic patient

population can be made on the basis of absent ankle reflex or

vibratory perception but elderly diabetic require additional deficit.

The nylon monofilament test is a simple performed office test to

diagnose patients at risk for ulcer formation due to sensory neuropathy.

This test is abnormal if the patient can not sence the touch of

monofilament when it is pressed against the foot with just enough

pressure to bend the filament.

Neuropathy is defined as the inability to sense the 10gm semmes-

Weinstein monofilament 7and vibration perception threshold > 25v.8

Other method to test sensation is neurothesiometer, which is

electrical powered device that delivers a quantitative vibratory stimulus

that can be recorded and reproduced. The tuning fork reliably detected

peripheral neuropathy in comparison with the neurothesiometer. A tuning

fork9 is a useful screening test for diabetic neuropathy

13
Flow chart: showing role of neuropathy in development of

diabetic foot ulcer4

Diabetes mellitus

Somatic moto r Autonomic

Soma tic sensory
neuropathy neuropathy
neuropathy

Decreased pain, temp, Dec reased Altered blood

Small muscle flow
and pro prioc eption sweating
wa sting

Dry skin Distende d

Foo t deformities Skin fissure & foot veins:
skin c rac k
"warm feet"

Inc reased foot Callus Prevention

Prevention
Daily feet exa ms; pressures Moisturize feet;
check inside sho es; regular po diatry;
don't wa lk barefoot well-fitting shoes
mea sure te mp with insole s; o rthoses
hand
don't use blade
At risk
neuro pathic foo t
Repetitive trauma
e.g. ill fitting shoes

Neuropathic
Prevention
foo t ulcer
Adherence to off loa ding

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2. Peripheral vascular disease (microangiopathy):

Main factor responsible for reduction in blood supply to foot is

atherosclerosis of the large vessel of the leg (often multisegmental). It is

often bilateral and distal involving tibial and peroneal vessels below the

knee and the reason for this observation is unknown. 10

The actual histopathology of large vessel wall is similar to that in

non diabetics, fatty deposits occurs in plaques with in intima. The plaques

are commonly localized at bifurcation, on the posterior wall of arteries

and where the arteries are compressed by muscle facia.

So called small vessel disease involving capillaries and

arterioles has been thought to contribute subsequently to impaired

circulation in the foot. On cellular level basement membrane thickens and

transport capabilities are impaired. Migration of polymorphonucloeocyte

slow and their chemotactic and bactericidal properties weaken.

Tissue necrosis in ischemic limb is usually associated with minor

trauma often complicated by infection. The trauma include direct

pressure from tight shoe, thermal, chemical injuries and injudicious

cutting of the nails. When external pressure on localized areas of skin

exceed capillary pressure, tissue necrosis follows. Initial incidents are

15
often trivial but are frequently neglected and rapidly lead to ulceration.

The concomitant pressure of neuropathy and ischemic foot obviously

predispose to microtrauma hence leading to ulceration and become the

portal for entry the bacteria and develop infected foot.

The presence of lower extremity ischemia is suggested by a

combination of clinical signs and symptoms plus abnormal result on non

invasive vascular tests. Signs and symptoms may include claudication,

pain in forefoot at rest or during night, absent dorsalis paedis and

posterior tibial arteries pulses, thinned or shiny skin, absent of hair on

lower leg and foot, thickened nails and dependend rubor.

Noninvasive tests include transcutaneous ankle – brachial

index(ABI) and absolute toe pressure.8 Abnormal ABI is defined as

<0.85.11

Other method of assessment of blood supply include oscillometry,

skin temperature measurement, fluorescein test, histamine wheals,

plethysmography, erometry, radionuclide scans.

In recent year the transcutaneous Doppler ultrasound flowmeter 8

has been used a sensitive tool to map the arterial tree, to assess the quality

16
of flow and to measure the systolic blood pressure at various levels in

lower limb.

3. Infection:

There are little evidence that well controlled diabetic is any way

more susceptible to infection than nondiabetic, although infection accours

it may be more serious in diabetic due to metabolic upsets.

Infection is due to neutrophil, lymphocyte and macrophage

function which are abnormal in patients with diabetes mellitus. It has

been observed that bacterial killing and phagocytic effects are improved

by lowering blood sugar level. Most common bacterial isolation is

polymicrobial. Gram positive bacteria were isolated more often than

gram negative. Most frequent bacterial isolations12 are Staphylococcus

aureus (38.4%), Pseudomonas aeruginosa (17.5%) and Proteus (14%).

Infection is secondary to ulceration and is the consequence rather than

cause of ulceration.

In addition patients with poorly controlled, diabeties has been

determined to have impaired collagen formation and diminished tensile

strength of healed wound.

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 X – ray studies are a relative insensitive method of judging

infection. Radiographic changes of osteomyelitis occur relative late

compared with the clinical courses of the patients. Bone scan are an

extremely sensitive test for bone pathology, but they are very

nonspecific.

Cellulitis will produce positive finding in the first two stage of

triple – phase scanning but so can osteomyelitis only late stage differ, i.e.

the last phase represents bone pathology.

Recent studies indicate that MRI is probably the most sensitive

measure for early bone change of osteomyelitis, even more sensitive than

bone scan.201

4. Abnormal pressure and load under foot:

In neuropathic group, most ulcers were found in the plantar surface

of toe (40.4%) and in the plantar metatarsal head region (39.1%). More

than 75% of all ulcerations were localization in toe and forefoot area,13

pointing that the ulcers are more common at pressure points.

5. Limited joint mobility

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Glycosylation of collagen in tendons and ligaments results in limited

motion of joints found in feet. Limited joint mobility contributes to the

abnormal mechanics in the diabetic foot. Diabetic patients often have

limitations in the range of motion of feet that are rigid, firm and dry.

Limited joint mobility is associated with an increased foot pressure and

greater chances of foot ulceration. In the presence of Limited joint

mobility, the foot is unable to provide its shock absorbing mechanism and

may lose its ability to maintain normal foot pressures.

Modes of Clinical Presentation

The type of foot problem presented by a diabetic depends on the

dominant role contributed by one, two or all three components of the

“diabetic triad”.

The clinical presentation developed as a complication of diabetes

includes the following:

• Cellulitis

• Abscess — superficial

— deep

• Osteomyelitis

• Septic arthritis

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• Gangrene — dry

— wet

• Ulcer

• Charcot joint disease

• Necrotising fasciitis.

Grading of diabetic foot:

It is necessary to have a thoughtful classification system for foot ulces

and grade of infection to decide an appropriate treatment. Three main

classification is used are

1. University of Texas wound classification system.

2. Wagner classification of diabetic ulcers

3. Brodsky classification of diabetic ulcers

University of Texas wound classification system14

With University of Texas wound classification system, wounds are

classified not only by depth, but also by the presence or absence of

20
infection and ischemia. Severity and risk for an amputation increase as

we move downward classification.

Grade 0: Pre or postulcerative lesion, completely epithelialized:

Stage A without infection or ischaemia

Stage B with infection

Stage C with ischaemia

Stage D with infection and ischaemia

Grade 1: Superficial wound not involving tendon, capsule or bone

Stage A without infection or ischaemia

Stage B with infection

Stage C with ischaemia

Stage D with infection and ischaemia

Grade 2: Wound penetrating to tendon or capsule

Stage A without infection or ischaemia

Stage B with infection

Stage C with ischaemia

Stage D with infection and ischaemia

Grade 3: Wound penetrating to bone or joint

21
 Stage A without infection or ischaemia

Stage B with infection

Stage C with ischaemia

Stage D with infection and ischaemia

2. The Wagner classification of diabetic ulcers is as follows:15

Grade 0—skin intact, but bony deformities produce a “foot at risk”

Grade 1—localized, superficial ulcer
Grade 2—deep ulcer to tendon, bone, ligament, or joint
Grade 3—deep abscess, osteomyelitis
Grade 4—gangrene of toes or forefoot
Grade 5—gangrene of entire foot

3. Brodsky classification of diabetic ulcers 16

a. Depth classification

Grade 0 - is intact skin, but represents a preulcerative lesion, with

erythema, callus formation, and possible intradermal

sheer hemorrhage over a bony prominence.

Grade I - is a superficial but full-thickness skin ulcer down but not

through the subcutaneous tissue.

22
 Grade II - ulceration is down to the tendon and joint capsule, but

neither the joint nor the bone is visible.

Grade III - ulceration implies exposed bone or joint and

osteomyelitis or pyarthrosis.

b. Ischaemia classification

A. Non ischaemia

B. Ischaemia without gangrene

C. Partial gangrene of foot

D. Complete gangrene of foot

Management of foot ulcer:

Foot infections in patients with diabetes cause substantial morbidity and

frequent visits to health care professionals and may lead to amputation of

a lower extremity. Diabetic foot infections require attention to local (foot)

and systemic (metabolic) management.

Diabetic foot care in all stages needs multidisciplinary

management to control mechanical, wound, microbiological, vascular,

metabolic and educational aspects. Achieving good metabolic control of

23
blood glucose, lipids and blood pressure is important in each stage, as is

education to teach proper foot care appropriate for each stage.

Blood sugar control.

Most foot ulcers have their origins in inadequate control of blood sugar,

which results in development of lower limb neuropathy. There is now

excellent evidence that improved control of diabetes can markedly

reduce the incidence of neuropathy.17 Host defenses against infection,

particularly white blood cell function, are also adversely affected in the

presence of elevated blood sugar levels but improve as blood sugar is

reduced below 14 mmol/L.18 The abnormal white blood cell response, in

combination with a reduced neuroinflammatory reaction, could explain

why up to 50% of diabetic patients with deep foot infections do not

have clinical fever or elevated white blood cell count at time of

presentation.19,20

Six modes of treatment have been established for diabetic foot

Wound.Three of these treatments are applicable to every wound; the

other three are applicable in the presence of specific criteria.21

1. Debridement

24
Frequent debridement of neuropathic wounds has been shown to enhance

and shorten the healing process.21,22 When necrotic tissue, crusted

exudate, and fibrinogen are removed, growth factors are released and

fibroblasts and keratinocytes migrate more easily into the wound. The

benefits are obtained only by sharp, surgical debridement. 21 The practices

of enzymatic and mechanical debridement such as whirlpool or

soaks in soap and water are not supported by clinical evidence

and may lead to maceration and infection.21,23

2. Off-loading

The second standard of care, referred to as ``off-loading,'' is the

avoidance of all mechanical stress on the wound.21,24 The devices to off-

load the diabetic foot wound are total contact casts, surgical shoes,

walkers, healing sandals, felted foam dressings, and bed rest. The method

of choice is determined by the location of the wound and by the patient's

level of activity.

3. Dressings

The third treatment applicable to all diabetic wounds is the dressing .21

Dressings not only protect the wound from trauma and infection but also

25
affect the wound environment.21,25 A moist but not heavily exudative

environment has been shown to enhance healing, therefore the choice of

dressing will promote or preserve this environment.

4. Control of infection

The fourth principle of treatment is aggressive management of infection.

In the infected wound, debridement of purulent debris controls the

infection and shortens the course of antibiotics.21 Attempting to cure deep

plantar space abscesses and osteomyelitis through antibiotic therapy

alone

may result in prolonged treatment or even unnecessary amputation. A

culture should be performed only after the wound has been debrided,

since superficial swabbing of an undebrided ulcer is believed to yield

results that have poor correlation to the actual pathogens.21,26

Antibiotic therapy should be instituted immediately, with selection

being based on clinical judgment. A mild infection from a superficial

wound can often be treated with an oral agent that is active against the

usual microbes in skin infections, namely the gram-positive cocci.23,26

However, infections penetrating to the level of tendon or bone should be

26
treated with broad-spectrum antibiotics that provide coverage for gram-

positive cocci, gram-negative bacilli and anaerobes.23,26 Serious limb- or

life-threatening diabetic infections are usually polymicrobial and may

often contain a pathogen that is resistant even when a regimen of broad-

spectrum antibiotics is followed. Therefore, as soon as the results of the

culture and sensitivity are available, the antibiotics should be adjusted

accordingly.

5. Revascularization

Although ischemia is rarely the most important cause of ulceration, it is

often an impediment to healing.27 Since the metabolic requirements rise

significantly when a wound or infection develops, a foot with sufficient

perfusion to sustain intact skin may not have enough perfusion to sustain

healing.27 There are no rigid indications for revascularization. 27,28 Poorly

perfused wounds will sometimes heal, while relatively well-perfused

wounds may not close until revascularization has been performed. When

a wound has failed to heal despite optimal care, and the ankle-brachial

and toe-brachial indices are less than 0.8 and 0.6 respectively, vascular

reconstruction should be considered. 28,29

6. Amputation

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Amputation is not only the most feared sequela of ulceration but also a

possible treatment. Accepted criteria for amputation are gangrene,

uncontrollable infection, and intractable ischemic pain.30 However, all too

often the impetus behind an amputation is the doctor's frustration and

impatience with treating a recalcitrant wound. Furthermore, too many

amputations are performed without any thought of biomechanical

Function.30,31 These amputations simply serve as a prelude to more

proximal amputations.

7. Adjunctive treatments

Besides the established treatments mentioned above, other adjunctive

modalities have been advocated. These include growth factors, hyperbaric

oxygen therapy, vacuum suction, maggots, living skin equivalents,

electrical stimulation, and cold laser. Of these adjunctive therapies, only

growth factors (becaplermin and platelet-derived wound growth factor)

have proven efficacious when used as supplements to good wound

care.21 Hyperbaric oxygen therapy for neuropathic, non- ischemic wounds

21
has not been supported by randomized controlled trials. This treatment

should be considered in the treatment of serious wounds that have not

28
responded to established treatments, especially when complicated by

ischemia.21 All other modalities are based on anecdotal evidence or are

still under investigation.21

The management of diabetic foot, the team approach appears

to be superior. Prevention and treatment of foot ulceration by

multidisciplinary teams decreases amputations by up to 85%.32 Medical

members of the team include an orthopaedist, diabetologist, vascular

surgeon, general surgeon, infectious disease consultant, pathologist,

psychiatrist and anaesthetist. Paramedical personnel include nurses,

medical social worker, psychologist, orthotist, prosthetist, cast technician,

vascular technician, pedorthist, occupational therapist and physical

therapist.

29
Evaluation
• Significant co-morbidities
• Glycemic control
• Systemic involvement
• Vascular evaluation
• Assessment of the ulcer
• Assessment of infection& cultures
• Evaluation of neuropathy and pain
• Evaluation of foot deformity

30
 Infection No infection

Treatment
• Abscess drainage
• Medical treatment
Treatment • Antibiotic
• External off-loading • Surgical debridement
• Wound care • Amputations
• Surgical off-loading and • Improving oxygenation
wound closure procedures • Wound care
• Off-loading &imobilization

Complete wound healing

Prevention
• Patient education
• Protective footwear & orthosis
• Prophylactic reconstructive surgery
Preventing first and recurrent ulcers:

More than 80% of ulcers should be potentially, preventable and the

first step of prevention is identification of high risk foot. Recurrent ulcer

rate reaches as high as 50% and a past history of foot ulcers is the

strongest predictor of new ulcer, efforts are also needed to prevent

recurrent ulcers.

Patient with foot ulcer risk lack knowledge and skills and consequently

are unable to provide appropriate self care33. Patients need to be informed

about risk factor and proper self foot care for prevention of diabetic foot .

31
It is believed that this single step can go a long way in preventing about

80% of the amputations.

In Singapore, all diabetics are advised to comply to the

following national guidelines which include:

• Dietary restriction

• Exercise regime

• HbA1c levels quarterly

• Capillary blood glucose monitoring regularly

• Creatinine level yearly

• Foot screening yearly

• Renal screening yearly

• Eye screening yearly

according to the Ministry of Health Guidelines for Diabetes 2006.36

Incidence

Incidence is defined as number of new cases occurring in a defined

population during a specific period of time.

Number of new case of specific disease during a given period of time

Incidence = –––––––––––––––––––––––––––––––––––––––––––––––––––––– x 1000
Population at risk during that period

32
.

33
REVIEW OF LITERATURE

41. Diabetes the global epidemic is rapidly increasing at an

alarming rate. Developing countries like India harbor the majority of

diabetic people and by the year 2030 AD India will have the largest

number of diabetic patients. Diabetic foot is one of the common

diabetic complications found in India.

42. In a study of 200 diabetic foot patients who visited the foot

clinic of Baqai Institute of Diabetology and Endocrinology (BIDE)

from January 1997 to December 2003 were reviewed it has be found

that By applying UT classification system,< 1% classified in UT grade

1 stage A, 3% classified in grade 1 stage B, 3.5% in grade 1 stage D,

29.5% in grade 2 stage B, 35% in grade 2 stage D, 10.5% in grade 3

stage B, 0.5% in grade 3 stage C, and 17.5% in grade 3 stage D

43. In a prospective study LJM and plantar pressures have

been reported to be higher in European patients than in Asian

patients.43,44 In a prospective study of 345 type 2 diabetic

patients showed that LJM and high plantar pressure appear to

be important determinants of foot ulceration irrespective of the

34
 duration of diabetes in South Indian diabetic patients.45 and perhaps

also reducing plantar pressure during walking.46

47. In a study of 654 diabetic foot Aerobic pathogens were

isolated 66.8% patients and anaerobic pathogens were isolated in

33.2%. As Wagner's grading increased, the prevalence of anaerobic

pathogens also increased. Ulcers infected with anaerobic pathogens

showed a longer healing time than ulcers infected with aerobic

pathogens. Among aerobic pathogens, Enterobacteriaceae family

(48%), Staphylococcus species (spp) (18.2%), Streptococcus spp

(16.8%) and Pseudomonas spp (17%) were seen frequently. Among

anaerobes Peptostreptococcus spp and Clostridium spp formed 69.4%.

Gram-negative anaerobes like Bacteroides spp and Fusobacterium spp

were present in 30.6%.

48. In cross-sectional hospital-based study it was found that 33.4%

presented with macrovascular complications and34.7% with

microvascular complications. The prevalence of cardiovascular and

cerebrovascular conditions, neuropathy, nephropathy, ocular lesions

and foot disease were 30.1%, 6.8%, 17.8%, 10.7%, 14.8% and 0.8%,

respectively.

35
49. In a cross sectional study, of 2067 patients with DM2 from seven

primary care units was conducted it was found that women, 65.8 %

presented the following risk factors: smoking, 24.3 %; alcoholism, 4.6

%; fasting glucose disturbance, 78 %; ulcer history, 10 %.

50. In a study it has been found that Diabetes-related lower-

extremity amputations are largely preventable. Eighty-five percent of

amputations are preceded by a foot ulcer. Effective management of

ulcers, which leads to healing, can prevent limb loss.

51. In a study it is found that the prevalence of infection was 6-11%

and prevalence of amputation was 3% in type 2 diabetic patients.

Neuropathy (15%) was found to be an important risk factor for

diabetic foot infections. Effective foot care advice should be

propagated to reduce the burden imposed by diabetic foot

complication particularly in developing countries like India.

52. In a large survey of 6,000 randomly selected patients attending

diabetic clinics it has been found that over 2% had active foot ulcers,

and 2.5% were amputees.

53.

36
54. The rate of lower limb amputation is 15 times higher in diabetic

patients compared with nondiabetic patients. Furthermore , 50% of

diabetic amputees need an amputation in the contralateral limb within

4 years after the loss of the first leg.53,54

55.

56.

57. In a cross-sectional studies it was found that Peripheral neuropathy

has been demonstrated as a strong risk factor for foot ulceration and is

present in 80% of affected patients. 55,56.57

58. In a cross sectional study was conducted during the period

from June 2009 till January 2010 in a primary care clinic at King

Khalid University hospital, Riyadh, Saudi Arabia. It has been found

that prevalence of diabetic foot among 224 diabetic patients attending

a primary care clinic, was 6.2%, and 1.3% of diabetic patients had

amputated foot. About half of the diabetic patients were 60 years and

above. Most of the patients (69.7%) were on oral hypoglycemic

agents, and 28.1% were on insulin. Only 31.7% had HBA1C less than

7, 33% followed their blood sugar levels regularly at home by gluco

37
 meter, and only 30.8% of diabetic patients examined their feet

regularly at home.

59. IN a cross-sectional study of consecutive patients with

diabetes and stage 4 or 5 chronic kidney disease (CKD) attending

clinics in Manchester (U.K) 326 patients studied with diabetes foot

ulceration was related to wearing bespoke footwear (odds ratio 5.6 )

dialysis treatment (5.1), prior foot ulceration (4.8), and years of

diabetes (1.0). In multivariate logistic regression, it was found that

only dialysis treatment and prior foot ulceration were associated with

prevalent foot ulceration.

60. In a retrospectively review of out patient department records and

diabetic foot evaluation forms of patients who visited the diabetic foot

clinic at King Chulalongkorn Memorial Hospital between 2004 and

2006. About 32% of all reported cases had lower extremity

amputation in which the toe was the most common level. Foot

problems were evaluated and categorized in four aspects,

dermatological, neurological, musculoskeletal, and vascular, which

were 67.30%, 79.3%, 74.0%, and 39.3% respectively. More than half

of the patients had skin dryness, nail problem and callus formation.

38
 Fifty six percent had the abnormal plantar pressure area, which was

presented as callus. The great toe was the most common site of callus

formation, which was correlated with gait cycle. The current ulcer

was 18.8%, which was presented mostly at heel and great toe. Three-

fourth of the patients (75.3%) had lost protective sensation, measured

by the 5.07 monofilament testing. The most common problem found in

musculoskeletal system was limited motion of the joint (44.0%).Claw

toe or hammer toe were reported as 32.0% whereas the other

deformities were bunnion (12.0%), charcot joint (6.0%) and flat feet

(5.3%)

60. Diabetic foot ulcer is the leading cause of non-traumatic lower

extremity amputation. About 80% of amputation had foot ulcer.

Contra-lateral limb amputations within 5 years were 15-50%.

60. The incidence of amputation could be decreased up to 80% by

multidisciplinary diabetic foot care including patient education (proper

foot care and foot wear), early detection and effective management of

foot problems, and scheduled follow-up.

61. IN A Cross-sectional descriptive study over five months period.

Diabetic outpatient clinic, at the Kenyatta National Hospital. The

39
 prevalence of previous foot ulceration was 16% while that of previous

amputation was 8%. Neuropathy was present in 42% of the study

subjects and was significantly associated with age, male gender,

duration of diabetes, random blood sugar, systolic blood pressure and

the presence of foot deformity. Peripheral arterial disease was present

in 12% and showed significant association with male gender.

62.

63. Foot disorders such as ulceration, infection, and gangrene are the

leading causes of hospitalization in patients with diabetes

mellitus.62,63

64. Approximately 15 to 20 percent of the estimated 16 million persons

in the United States with diabetes mellitus will be hospitalized with a

foot complication at some time during the course of their disease.

Unfortunately, many of these patients will require amputation within

the foot or above the ankle as a consequence of severe infection or

peripheral ischemia. Neuropathy is often a predisposing factor to

ulceration and amputation.

65.

66.

67.

40
68. IN A multicenter study IT is found that 63 percent of diabetic foot

ulcers is attributed to the critical triad of peripheral sensory

neuropathy, trauma, and deformity. Other factors in ulceration are

ischemia, callus formation, and edema. Although infection is rarely

implicated in the etiology of diabetic foot ulcers, the ulcers are

susceptible to infection once the wound is present. Many of the risk

factors for foot ulcer are also predisposing factors for amputation,

because ulcers are primary causes leading to amputation. 65,66,67,68

69. It has been found that a high incidence of amputation can reflect

a higher disease prevalence, late referral, limited resources, or a

particularly interventionist approach by a specialist team. Conversely,

a low incidence of amputation can indicate a lower disease prevalence

or severity, good management of diabetes in primary and secondary

care, or a particularly conservative approach by an expert team.

70. In a study new foot ulcers,it is found that 67.0% were

neuropathic, 26.3% were neuroischemic, 1.0% were ischemic, and

5.7% had no identified underlying factors. Median ulcer size at

presentation was 1.5 cm2. Lower-limb amputations were performed

for 15% of ulcers, whereas 65% healed and 16% were not healed at

study termination; 4% of patients died. Wagner grade and UT grade

41
 and stage showed positive trends with increased number of

amputations. For UT stage, the risk of amputation increased with

infection both alone and in combination with ischemia , but not

significantly with ischemia alone . Healing times were not

significantly different for each grade of the Wagner or the UT system,

but there was a significant stepwise increase in healing time with each

stage of the UT system, and stage predicted healing. Increasing stage,

regardless of grade, is associated with increased risk of amputation

and prolonged ulcer healing time. The UT system's inclusion of stage

makes it a better predictor of outcome.

71. There was an estimated 150 million people with diabetes worldwide

in the year 2000, with two-thirds of them living in developing

countries, and a twofold increase in this number is predicted over the

next two decades

71. TYPE 2 diabetes is the commonest form of diabetes constituting 90%

of the diabetic population. The global prevalence of diabetes is

estimated to increase, from 4% in 1995 to 5.4% by the year 2025. The

World Health Organization has predicted that the major burden will

occur in the developing countries. There will be a 42% increase from

51 to 72 million in the developed countries and 170% increase from

42
 84 to 228 million, in the developing countries. The countries with the

largest number of diabetic people are, and will be in the year 2025,

India, China and United States.

72. In a study by the Diabetes Research Centre prevalence of the

vascular complications observed are( in percent) Peri-neuropathy 27.5,

Retinopathy 23.7, Nephropathy 5.5, Cardiovascular disease 11.4

Peripheral vascular disease 4.0, Cerebro vascular accidents 0.9,

Hypertension 38.0.

73. In the studies it have shown that patients who have had one

amputation have a 68% risk of having another in the next 5 years and

have a 50% mortality rate in the 5 years following the initial

amputation. Thus, it is not surprising that lower extremity amputation

is considered to be one of the most serious consequences of diabetes

Diabetes mellitus is a leading cause of lower extremity amputation

and the most common cause of admission of diabetics to the hospital.

73. An observational study reported that the cumulative incidence of

developing a foot ulcer for patients with diabetes was 5-8% over 3

years and study showed that 15% of patients with diabetes will

develop a foot ulcer during their lifetime. About half of all foot ulcers

are clinically infected at the time the patient presents to a clinician

43
74. It identified 6 prospective studies and 10 comparative or

observational studies that the Semmes-Weinstein monofilament is

currently the best choice for screening for clinically significant

neuropathy because it is portable, inexpensive, painless, easy to

administer, acceptable to patients, and provides good predictive ability

for the risk of ulceration and amputation. Once the patient without

protective sensation has been identified, management with protective

footwear and patient education to prevent damage should be instituted.

75. To maximize the diagnostic value of Semmes-Weinstein

monofilament, a three site test involving the plantar aspects of the

great toe, the third metatarsal, and the fifth metatarsals should be used.

Screening is vital in identifying diabetic peripheral neuropathy ( DPN)

early, enabling earlier intervention and management to reduce the risk

of ulceration and lower extremity amputation.

76. To achieving reduction in the amputation rate in patients

with a diabetic foot syndrome, the early diagnosis and specialized

treatment of peripheral circulatory disorders is of eminent importance.

Treatment includes pressure relief, wound cleanup and stage-oriented

local wound management, measures to improve circulation, and the

appropriate treatment of bacterial infection. Useful preventive

44
 measures include the training of diabetics, regular foot care, and the

provision of appropriate footwear

77. Diabetic foot ulcers are usually caused by several factors acting in

concert, with polyneuropathy, altered biomechanics, inadequate shoes

and peripheral arterial disease (PAD) as major factors. Neuropathy is

present in most patients with diabetic foot ulcers, while PAD is

present in 30 – 50 %; infection can be diagnosed in up to 50% of

patients presenting with a foot ulcer. Because most patients have lost

the natural protective mechanism to relieve pressure from the wound,

off-loading of these ulcers is extremely important. For plantar foot

ulcers total contact casting is the current standard: with this technique

up to 90% of neuropathic ulcers can be healed.

78. Diabetes mellitus is a metabolic disease that is associated with

hyperglycemia affecting various organ systems of the body. One of

the most dreaded complications of this disease is the diabetic foot. The

diabetic foot is the end result of multiple causal pathways, which

include peripheral neuropathy and vascular disease. The problem is

compounded by the increased incidence of infection.

45
79. Neuropathy is the most common complication of diabetes. Those

patients with diabetic foot ulceration on the plantar, medial and lateral

surfaces of the foot will almost all have clinically significant

peripheral neuropathy

80. In a study with 597 newly-diagnosed diabetic

patients the prevalence of diabetic complications; 22% presented

because of symptoms of diabetes, 27% were diagnosed when

hyperglycaemia was discovered at a health screening, and 36% were

diagnosed while being treated for intercurrent illness. Neuropathy was

present in 25.1%, nephropathy in 29%, retinopathy in 15%, coronary

vascular disease in 21%, stroke in 5.6%, peripheral vascular disease in

4.8%, hypertension in 23%, obesity in 16%, central obesity in 21.3%,

hypercholesterolaemia in 11%, hypertriglyceridaemia in 14%, and low

high-density lipoprotein cholesterol in 12%.

81. In a cross-sectional study of a population-based sample of

age- and sex-matched adults with type 2 diabetes of European and

Asian descent in the U.K. Patients were assessed for neuropathic

symptoms, signs, nerve conduction, autonomic function, and

quantitative sensory testing. It is found that Asians with diabetes have

46
 substantially less large and small fiber neuropathy than Europeans,

despite comparable traditional risk factors. Independent from

smoking, the lower risk of neuropathy in Asians is due to better skin

microvascularization and may help explain the substantially reduced

Asian foot ulcer risk.

82. Since diabetes mellitus is growing at epidemic proportions

worldwide, the prevalence of diabetes-related complications is bound

to increase. Diabetic foot disorders, a major source of disability and

morbidity, are a significant burden for the community and a true

public health problem. In westernized countries, two of 100 diabetic

patients are estimated to suffer from a foot ulcer every year.

Amputation rates vary considerably: incidence ranges from 1 per

thousand in the Madrid area and in Japan to up to 20 per thousand in

some Indian tribes in North America. In metropolitan France, the

incidence of lower-limb amputation is approximately 2 per thousand

but with marked regional differences, and in French overseas

territories, the incidence rate is much higher. Nevertheless, the risk for

ulceration and amputation is much higher in diabetics compared to the

nondiabetic population: the lifetime risk of a diabetic individual

developing an ulcer is as high as 25% and it is estimated that every

47
 30s an amputation is performed for a diabetic somewhere in the world.

Peripheral neuropathy, arterial disease, and foot deformities are the

main factors accounting for this increased risk. Age and sex as well as

social and cultural status are contributing factors. Knowing these

factors is essential to classify every diabetic using a risk grading

system and to take preventive measures accordingly.

83. Diabetes is reaching epidemic proportions and with it carries the

risk of complications. Disease of the foot is among one of the most

feared complications of diabetes. The ultimate endpoint of diabetic

foot disease is amputation, which is associated with significant

morbidity and mortality, besides having immense social,

psychological and financial consequences. As the majority of

amputations are preceded by foot ulceration, it is crucial to identify

those at an increased risk. Diabetic foot ulcers may develop as a result

of neuropathy, ischaemia or both and when infection complicates a

foot ulcer, the combination can become limb and life threatening.

Structural abnormalities such as calluses, bunions, hammer toes, claw

toes, flat foot and rocker bottom foot need to be identified and

managed.

48
84. Incidence of major amputation can be reduced by implementation

of a multidisciplinary team approach.

85. In a prospective study was carried out on patients with diabetic foot

lesions to determine their clinical characteristics, the spectrum of

aerobic microbial flora Pseudomonas aeruginosa among the gram-

negative (22%) and Staphylococcus aureus among the gram-positive

(19%) were the predominantly isolated organisms, while Candida was

the most predominantly isolated fungus.

85. In a prospective study was carried out on patients with diabetic foot

lesions it is found that Neuropathy (76%) and peripheral vascular

disease (57.28%) was a common feature among the patients. Poor

glycemic control was found in 67% of the patients. Awareness about

lower limb complications of diabetes was very low (23%) among the

patients.

85. The alarming fact is that India has more people with diabetes than any

other country and the incidence of foot problems and amputations

remains very high, accounting for up to 20% of diabetes-related

hospital admissions. This can be easily attributed to several practices

prevalent in India, such as barefoot walking, inadequate facilities for

diabetes care, low socioeconomic status and illiteracy.

49
85. Among the bacterial isolates, gram-negative comprised of 76% and

gram-positive accounted for 24%. Pseudomonas aeruginosa was the

most common isolate, accounting for 21.67%; followed

byStaphylococcus aureus ,E coli and Klebsiella

pneumoniae, comprising 18.88%, 18.18% and 16.78% respectively.

86. IN a systematic review and meta-analysis the prevalence of foot

ulceration among patients with diabetes mellitus ranges from 1.3% to

4.8% in the community, to as high as 12% in hospital. This represents

considerable patient morbidity, and is associated with substantial

health-care costs. The pathophysiology of diabetic foot ulceration is

multifactorial, but peripheral neuropathy is thought to be responsible

for most cases.

86. To prevent foot ulceration and amputation, clinical guidelines

recommend early identification of risk, based on annual foot screening

of all diabetic patients, with targeting of preventive and treatment

interventions to ‘high risk’ individuals. Key to this preventive strategy

is a structured clinical assessment that incorporates diagnostic tests

alongside a thorough history and examination.

50
87. In India, diabetic foot disease is exacerbated by sociocultural factors

such as the prevalence of walking barefoot, lack of knowledge

regarding diabetic foot complications, and the socioeconomic status of

patients. Diabetic foot infection constitutes ∼10% of diabetes-related

hospital admissions.

87. In a study from Southern India, it was found that patients without

foot problems spent 9.3% of their total income towards treatment,

whereas patients with foot problems had to spend up to 32.3% of their

total income on treatment.

88. In a 1983 study it was concluded that diabetes mellitus is the

leading cause of non traumatic amputations accounting for 50-70% of

all non traumatic amputations.

89. In a study it was discovered that 3-5% of diabetics are amputees

and over 54000 new lower extremity amputations are performed in

diabetics each year. In US 80% of diabetic amputees lose contralateral

leg within 3 years and following amputation of a leg, two third die

within 5 years.

90. Approximately 16 million people in US and 15% of the population

over 65 years old have diabetes mellitus. Diabetes mellitus is sixth

51
 leading cause of death by disease and infected foot is most common

cause of admission of diabetics to the hospital.

91. In a 12 years follow up study in Nauru Australia there was a

decrease in the incidence of amputation after the commencement of

national foot care health education and prevention campaign.

92. A comprehensive program focused on foot specific patient

education, skin and nail care and protective foot wear lowers the

incidence of diabetic foot ulcers and lower extremity amputation.

93. In a study done at SZCECIN city with 4,50,000 inhabitants, it was

found that prevalence of diabetes is higher in older age group patients

with 5.03% in 51-60 years, 9.88% in 61-70 years, 14.37% in >70

years. Chronic microangiopathic diabetic complications were present

in 36.6% of type 2 diabetic patients. Retinopathy was reported in

24.8% patients, polyneuropathy in 2.4% patients, nephropathy in 1.5%

patients, diabetic foot in 0.5% and combination of different

complications in 7.4% of them.

52
4. Incidence of diabetic foot increased from 0.7% in 1980 – 1988 to

atleast 2.7% since 1999. The incidence of foot ulcer in developed

countries is approximately 2% per year in general diabetes population.

94. Diabetic foot disease is a major health problem which concerns 15%

of the 200 million patients with diabetes world wide. 60% of

amputations in western world are performed in the diabetes mellitus

population.

95. In a prospective study it was concluded that diabetic foot ulcer are

likely to occur in upto 25% of people with diabetes mellitus at some

time in their life. Overall 50% of major amputations in UK happen to

people with diabetes and within 3 years of amputation, 50% of people

will die.

96. The prevalence of diabetes is increasing globally particularly in the

developing world. The diabetic foot is one of the most devastating

chronic complication of diabetes. The step by step project was

initiated in India with participation from neighboring countries and

Tanzania to improve diabetes foot care in the developing world.

13. In a study to find the different locations of ulcer in neuropathic

group, most ulcers were found in the plantar surface of toe (40.4%)

and in the plantar metatarsal head region (39.1%). In contrast the

53
 ischaemic group had a most frequent location in the toe tips (63.6%)

while neuroischemic group had most ulcers distributed in both plantar

surface and the tips of the toes (51.8%). In a study it was found that

foot ulceration is among the most debilitating complication in diabetes

mellitus patients. The main risk factor leading to the ulcer

development is diabetes neuropathy (sensory, autonomic), limb

ischaemia (angiopathy), limited joint mobility and the plantar

pressure.

97. Debridement should be performed as often as necessary until the

wound is deemed clean and ready for reconstruction. The repair is

then dictated by how much of the foot remains post debridement and

how the foot can be closed in the most biomechanically stable

construction possible.

98. A simple step such as routine foot inspection, fitting of appropriate

shoes and orthotics combined with patient education about the

importance of self care can decrease the incidence of wound in

diabetes mellitus population.

99. Prospective, population-based cohort study of 317 type-2 diabetes

mellitus patients treated at primary care centre, show that prevalence

of complications of diabetes is increasing. Prevalence of diabetic

54
 nephropathy (12%), retinopathy (6.2%) and neuropathy (2.1%) is

increasing, and there is decrease in ischemic cardiomyopathy (6.2%),

an increase in peripheral vascular disease (5.6%).Incidence of

cerebrovascular accident and diabetes foot remain unchanged in

diabetic patients.

AIMS AND OBJECTIVES

1. To determine the incidence of diabetic foot among

diabetic patients

2. To study various forms/grades of diabetic foot at the time

of presentation.

3. To find out high risk factors for developing diabetic foot

among the patients of diabetes mellitus .

55
MATERIAL AND METHODS

A study will be conducted in diabetes mellitus population (WHO

criteria) who are admitted to Guru Nanak Dev Hospital, Govt. Medical

College, Amritsar during the period of 1st January 2009 to 31st December

2009. All the diabetic patients diagnosed using WHO criteria will be

included in study after taking consent in vernacular language. Patient will

be assessed clinically using parameters mentioned in proforma and

incidence of diabetic foot will be calculated from total diabetic patients.

Number of new case of specific disease during a given period of time

Incidence = –––––––––––––––––––––––––––––––––––––––––––––––––––––– x 1000
Population at risk during that period

They will be managed according to type and grade of diabetic

foot. Beside treatment, education regarding foot care and prevention of

first and subsequent ulcers will be discussed with patients.

56
The inclusion criteria for diabetic foot problems – as per University Of

TEXAS wound classification, all grades of diabetic foot will be included

in the proposed study .

Patient assessment – once the patient is selected for study, he/she

will be examined in relation to :

Neurological status, Vascular status and Investigations as per

proforma annexed herewith.

Radiological examination

X-ray of involved foot will be taken to see the involvement of

underlying bone and presence of osteomyelitis.

Bacteriological examination:

Deep tissue curetting will be taken for culture studies which will

help us to plan proper antibiotic therapy. Antibiotics will be stopped

for 24-48 hrs prior swab for culture and sensitivity and antibiotics will

changed accordingly. Clinically uninfected ulcers will not be cultured.

Advice to the patient at the time of discharge

The patients will be asked about their awareness about the diabetic

foot problem and the aetiopathological factors resulting in their foot

problem will be identified.

57
 Once the patient is diagnosed, graded and status of risk factors for

delayed healing (diabetes mellitus control, vascular status, bony

prominences) is assessed, the patient will be educated for proper foot

care.

58
The following instructions will be given to the patient.

1. Inspection of the foot twice a day.

2. Inspection of nails.

3. Checking of blood sugar twice weekly

4. Not to walk bare-foot.

5. Use of emollient on dry skin from toe tip upwards.

6. Not to use a rubifacient or balm.

7. Not to consume tobacco.

8. To wash feet daily with mild soap and luke warm water.

9. To keep the feet warm in stockings.

10.Not to sit cross-legged.

11.Not to use V-chappals.

12.Not to use scissors or blades to cut nails.

13.Use of special foot wear

14. Patient should report immediately if – erythma, swelling, ulcer,

trauma to foot, uncontrolled diabetes occur (alert signs).

The incidence and clinical profile of diabetic patients particularly

in relation to diabetic foot shall be determined to evaluate the

study.
59
 BIBLIOGRAPHY

1 Alberti KGMM, Zimmet PZ for the WHO Consultation.

Definition, diagnosis and classification of diabetes mellitus and

its complications. Part 1: diagnosis and classification of diabetes

mellitus. Provisional report of a WHO Consultation. Diabetic

Medicine 1998; 15: 539-553

2 Power CA. Diabetes mellitus. Chapter 338, Harrison 2007;

1: 2275-2302.

3 Edmonds M.A natural history and framework for managing

diabetic foot ulcers. Br J Nurs. 2008 Jun12-25;17(11):S20, S22,

S24-9.

4 Boulton AJM and Armstrong DG. The diabetic Foot. In:

clinical diabetes. Chapter 14, 1st edition. 2006; 179-195.

5 A pelquist J, Agarth CD. The Association between clinical

risk factor and outcome of diabetic foot ulcer. Diabetic Res Clin

Pract 1992; 18: 43-53.

6 Thomas PK: Classification, differential diagnosis, and

staging of diabetic peripheral

neuropathy. Diabetes 46(Suppl.2):S54–S57, 1997.

60
7 Nather A, Neo SB, Chionh SB, Liew SCF, Sim EY, Chew

JLL. Assessmentof sensory neuropathy in diabetic patients

without diabetic foot problems.J Diabetes Complications

2008;22:126-31.

8 Khanolkar MP, Bain SC, Stephens JW. The diabetic foot.

QJM. 2008 Sep;101(9):685-95. Epub 2008 Mar 18.

9 Kästenbauer T, Sauseng S, Brath H, Abrahamian H, Irsigler

K.The value of the Rydel-Seiffer tuning fork as a predictor of

diabetic polyneuropathy compared with a neurothesiometer.

Diabet Med. 2004 Jun;21(6):563-7.

10 Edmonds ME, Roberts VC, Watkin PJ. Blood flow in

diabetic neuropatic foot. Diabetologica 1982; 22: 9-15.

11 Weatherley BD, Nelson JJ, Heiss G, Chambless LE, Sharrett

AR, Nieto FJ, Folsom AR, Rosamond WD : The association of

the ankle-brachial index with incident coronary heart disease: the

Atherosclerosis Risk In Communities (ARIC) study, 1987–

2001. BMC Cardiovasc Disord 2007;7:3)

61
12 Sharma VK, Khadka PB, Joshi A, Sharma R. Common

pathogens isolated in diabetic foot infection in Bir hospitial;

Kathmandu Univ Med J (KUMJ) 2006; 4(3): 295-301.

13 Pithova P, Pathkova H, Golandakova I, Dolezalova L,

Kvapil M. Difference in ulcer location in diabetic foot syndrome.

Vnitr Lek 2007; 53(12): 1278-85.

14 Armstrong DG, Lavery LA, Harkless LB. Who is at risk for

diabetic foot ulceration? Clin Podiatr Med Surg 1998;15:11-19.

15 Andrew JM, Boulton, VileiKyte L. Diabetic foot problems

and their management around the world. In Levin and O’Neals

“The diabetic Foot” 6th edition. Mosby, Inc. 2001; 266.

16 Brodsky JW: The diabetic foot. In: Coughlin MJ, Mann RA,

eds. Surgery of the Foot and Ankle. St Louis, Mo: Mosby; 1999:

911.

17 The Diabetes Control and Complications Trial Research

Group. The effect of intensive treatment on the development and

progression of long-term complications in insulin-dependent

diabetes. N Engl J Med 1993;329:977-86.

62
18 Bagdade JD, Stewart M, Walters E. Impaired granulocyte

adherence: a reversible defect in host defense in patients with

poorly controlled diabetes. Diabetes 1978;27:677-81.

19 Eneroth M, Apelqvist J, Stenstrom A. Clinical characteristics

and outcome in 223 diabetic patients with deep foot infections.

Foot Ankle Int 1997;18(11):716-22.

20 48. Walmsley D, Wiles PG. Early loss of neurogenic

inflammation in the human diabetic foot. Clin Sci 1991;80:605-

10.

21 American Diabetes Association. Consensus development

conference on diabetic foot wound care. Diabetes Care

1999;22:1354-60.

22 Steed DL, Donohoe D, Webster MW, Lindsley L. Effect of

extensive debridement and treatment on the healing of diabetic

foot ulcers. J Am Coll Surg 1996;183:61-4.

23 Caputo GM, Cavanagh PR, Ulbrecht JS, Gibbons GW,

Karchmer AW. Assessment and management of foot disease in

patients with diabetes. N Engl J Med 1994;331:854-60.

63
24 Armstrong DG, Lavery LA. Evidence-based options for off-

loading diabetic wounds. Clin Podiatr Med Surg 1998;15:95-104.

25 Higgins KR, Ashry HR. Wound dressings and topical

agents. Clin Podiatr Med Surg 1995;12:31-40.

26 Joseph WS. Bone and joint infections. In: Joseph WS, ed.

Handbook of Lower Extremity Infections. New York: Churchill

Livingstone, 1990:45-63.

27 Sykes MT, Godsey JB. Vascular evaluation of the problem

diabetic foot. Clin Podiatr Med Surg 1998;15:49-83.

28 Gibbons GW. Vascular evaluation and long-term results of

distal bypass surgery in patients with diabetes. Clin Podiatr Med

Surg 1995;12:129-40.

29 Campbell DR. Diabetic vascular disease. In: Frykberg RG,

ed. The High Risk Foot in Diabetes Mellitus. New York:

Churchill Livingstone, 1991:33-47.

30 Stuck RM, Sage R, Pinzur M, Osterman H. Amputations in

the diabetic foot. Clin Podiatr Med Surg 1995;12:141-55.

64
31 Pulla RJ, Kaminsky KM. Toe amputations and ray

resections. Clin Podiatr Med Surg 1997;14:691-739.

32 Käypä hoito -suosituksen tiivistelmä. Diabetes-related foot

problems. Duodecim. 2009;125(17):1907-9

33 Mason J, O’keefe C, Mcintosh A et al. A systematic review

of foot ulcer in patients? Diabet Med 1999; 16: 245-249.

34 Guyton GT et al. Sympathetic dysfunction in diabetic foot.

Orthop Clin North Am 1997; 2: 77-86.

35 Negrine JP. Outpatient diagnosis and management of

diabetic foot orthopaedics clin north Am 1997; 2: 99-113.

36 Ministry of Health, Singapore, Clinical Practice Guidelines

for Managing Diabetes Mellitus (2006).

41. Viswanathan V. Epidemiology of diabetic foot and

management of foot problems in India. Int J Low Extrem

Wounds. 2010 Sep;9(3):122-6.

65
42. GulA, Basit A, Ali SM, Ahmadani MY, Miyan Z. Role of

wound classification in predicting the outcome of Diabetic Foot

Ulcer. JPMA 56:444;2006.

43. Toledano H, Young MJ, Veves A, Boulton AJM. Why do

Asian diabetic patients have fewer foot ulcers than Caucasians?

Diabetic. Medicine 1993;10 (Suppl.1): S38.

44. Van Schie CHM, Boulton AJM. Joint mobility and foot

pressure measurements in Asian and Europid diabetic patients:

clues for difference in foot ulcer prevalence. Diabetes

2000;Suppl.1:A197.

45. Viswanathan V, Snehalatha C, Sivagami M, Seena R,

Ramachandran A. Association of limited joint mobility and high

plantar pressure in diabetic foot ulceration in Asian Indians. Diab

Res Clin Prac 2003;60:57-61.

46. Curran F, Nikookam K, Garrett M, et al. Physiotherapy: A

novel intervention in diabetic preulceration. Proceedings of the

2nd International Symposium on the Diabetic Foot, 1995

66
47. Viswanathan V, Jasmine JJ, Snehalatha C, Ramachandran A.

Prevalence of pathogens in diabetic foot infection in South Indian

type 2 diabetic patients. J Assoc Physicians India. 2002

Aug;50:1013-6.

48. Liu Z, Fu C, Wang W, Xu B. Prevalence of chronic

complications of type 2 diabetes mellitus in outpatients - a cross-

sectional hospital based survey in urban China. Health Qual Life

Outcomes. 2010 Jun 26;8:62.

49. Bustos-Saldaña R, Prieto-Miranda S; Grupo de Estudio de

Factores de Riesgo de Ulceraciones en los Pies de los Pacientes

Diabéticos Tipo 2. Foot ulceration risk factors in type 2 diabetes

mellitus. Rev Med Inst Mex Seguro Soc. 2009 Sep-

Oct;47(5):467-76.

50. Rogers LC, Bevilacqua NJ.Organized programs to prevent

lower-extremity amputations. J Am Podiatr Med Assoc. 2010

Mar-Apr;100(2):101-4.

51. Viswanathan V, Thomas N, Tandon

N, Asirvatham A, Rajasekar S, Ramachandran

A, Senthilvasan K, Murugan VS, Muthulakshmi.Profile

67
of diabetic foot complications and its associated

complications--a multicentric study from India. J

Assoc Physicians India. 2005 Nov;53:933-6.

52. Macleod A, Williams DRR, Sonksen PH, Boulton

AJM: Risk factors for foot ulcers in hospital clinic attenders

(Abstract). D i a -b e t o l o g i a34:A39, 1991

53. Most RS, Sinnock P: The epidemiology of lower extremity

amputations in diabetic individuals. Diabetes Care6:87–91, 1983

54. Ebskov B, Josephsen P: Incidence of reamputation and

death after gangrene of the lower extremity. Prosthet Orthotics

Int 4:77–80, 1980

55. Caputo GM, Cavanagh PR, Ulbrecht JS, Gibbons GW,

Karchmer AW: Assessment and management of foot disease in

patients with d i a b e t e s . N Engl J Med331:854–860, 1994

56. P e c o r a ro PE, Reiber GE, Burgess EM: Pathways to

diabetic limb amputation: basis for prevention. Diabetes

Care13:513–521, 1990

68
57. Boulton AJM: Peripheral neuropathy and the diabetic foot.

Foot 2:67–72, 1992

58. Turki YAA. Prevalence of Diabetic foot among diabetic

patients attending a primary care clinic. at a teaching hospital,

Riyadh, Saudi Arabia April 2010 , Volume 7- Issue 2 April 2010 ,

Volume 7- Issue 2

69
 59. Mugambi-Nturibi E, Otieno CF, Kwasa TO, Oyoo GO, Acharya K. Str

diabetes into risk categories for foot ulceration. East Afr Med

60. Boulton AJ. The diabetic foot: a global view. Diabetes Metab Res Rev

61. Frykberg RG. Diabetic foot ulcers: current concepts.

J Foot Ankle Surg 1998;37:440-6

62. Reiber GE, Boyko EJ, Smith DG. Lower extremity foot ulcers and am

National Diabetes Data Group (U.S.). Diabetes in America. 2d ed.

Institutes of Health, National Institute of Diabetes and Digestive and Kid

publication no. 95-1468.

63. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputat

Diabetes Care 1990;13:513-21.

64. Boyko EJ, Ahroni JH, Stensel V, Forsberg RC, Davignon DR, Smith DG

risk factors for diabetic foot ulcer: the Seattle Diabetic Foot Study. Diabete

65. Reiber GE, Vileikyte L, Boyko EJ, del Aguila M, Smith DG, Lavery LA

for incident lower-extremity ulcers in patients with diabetes from two setti

1999;22:157-62.

66.Armstrong DG, Lavery LA. Diabetic foot ulcers: prevention, diagnosis and

Physician 1998;57:1325-32.

70
67. Jeffcoate WJ, van Houtum WH. Amputation as a marker of the quality o

diabetes.Diabetologia. 2004 Dec;47(12):2051-8. Epub 2004 Dec 11.

68. Oyibo SO, Jude EB, Tarawneh I, Nguyen HC, Harkless LB & Boulton A

diabetic foot ulcer classification systems: the Wagner and the University o

classification systems. Diabetes Care 2001; 24:84–88

69. King H, Aubert RE, Herman WH. Global burden of diabetes 1995–20

estimates and projections. DiabetesCare1998;21:1414–1431.

70. Ramachandran, A., Snehalatha, C., Satyavani, K., Latha, E., Sas

Assoc. Phys. India, 1999, 47, 1152–1156.

71.Armstrong DG, Lipsky BA. Diabetic foot infections: stepwise medical and

Wound J 2004;1:123—132.

72. Mayfield JA, Sugarman JR. The use of the Semmes-Weinstein monofil

tests for preventing foot ulceration and amputation in persons with dia

Nov;49(11 Suppl):S17-29.

71
73. Feng Y, Schlösser FJ, Sumpio BE. The Semmes Weinstein mo

a screening tool for diabetic peripheral neuropathy. J Vasc Surg. 2009

Epub 2009 Jul 30.

74. Lawall H.The diabetic foot. MMW Fortschr Med. 2006 May 25;148(

75. Schaper NC, Prompers LM, Huijberts MSP. Treatment of Diab

Endoc. & Metab. Agents in Med. Chem., 2007, 7, 95-104 95

76. Gupta SK, Panda S, Singh SK. The etiopathogenesis of the diabetic foot

Int J Low Extrem Wounds. 2010 Sep;9(3):127-31

77. Hampton S. Caring for the diabetic patient with a foot ulcer. Br J

13;15(15):S22-7.

78. Weerasuriya N, Siribaddana S, Dissanayake A, Subasinghe Z, Wariyapola

term complications in newly diagnosed Sri Lankan patients with type

Med 1998;91:439–443

72
79. Abbott CA, Chaturvedi N, Malik RA, Salgami E, Yates AP, P

AJ.Explanations for the lower rates of diabetic neuropathy in Indian

Diabetes Care. 2010 Jun;33(6):1325-30. Epub 2010 Mar 9

80. Richard JL, Schuldiner S. Epidemiology of diabetic foot problems. Rev

Suppl 2:S222-30.

81. Khanolkar MP, Bain SC, Stephens JW. The diabetic foot. QJM. 2008

2008 Mar 18.

82. Meltzer DD, Pels S, Payne WG, Mannari RJ, Ochs D, Forbes-Kearns J, et

rates in patients with diabetes mellitus. An outcome study. J Am Podiatr

28.

83. Bansal E, Garg A, Bhatia S, Attri AK, Chander J. Spectrum of micr

ulcers. Indian J Pathol Microbiol. 2008 Apr-Jun;51(2):204-8.

84. Crawford F, Inkster M, Kleijnen J, Fahey T.Predicting foot ulcers in patien

73
 systematic review and meta-analysis. QJM. 2007 Feb;100(2):65-86.

85. Viswanathan V, Madhavan S, Rajasekar S, Chamukuttan S, Ambady R. A

initiative in South India: positive impact of foot care education. Diabetes C

May;28(5):1019-21.

86. Brand PW. The diabetic foot. In: Ellen berg M Rifki

mellitus. Garden City, NY, Medical Examination Publishing C

87. Karchmer AW, Gibbons GW. Foot infection in diabe

management current topics in infections diseases 1994.

88. Diabetes statistics National diabeties clearing House,

Diabetes and Digestive and Kindney Disease. National Insti

89. Humphrey AR, Dowse GK, Thomas K, Zimmest PZ. Diabetes and non tra

amputation incidence risk factors and prevention a 12 year follow up study

1996; 19: 701-4.

90. Pinzur MS. The diabetic foot. Compr Ther 2002; 28(3

91. Fabian W, Majkowska L, Stefansri A, Moledap. Prevalence of diabetes, a

chronic diabetic complications reported by general prodicner. Przegl Lek 2

74
92. Dalla Paola L, Faglia E. Treatment of diabetic foo

stratergies for clinical approach. Curr Diabetes Rev 2006; 2

93. Bentley J, Foster A. Multidisciplinary management of diabetic foot ulcer.

2007; 12(12): s6, S8, S10¬ passim.

94. Pendsey S, Abbas ZG. The step-by-step program for r

problems: a model for the developing world. Curr Diab Rep

95. Clemens MW, Attinger CE. Biological basis of diabe

Technol Int 2008; 17: 89-95.

96. King LB. Impact of a preventive program on amput

population. J Wound Ostomy Continence Nurs, 2008; 35(5)

97. Mundet X, PouA, Piquer N, Sanmartin MI, Tarruella M, Gimbert R,

incidence of chronic complication and mortality in a cohort of type 2 d

Prim Care Diabetes 2008; 2(3): 135-140. Epub 2008 Jun. 27.

75
1. Power CA. Diabetes mellitus. Chapter 338, Harrison 2007; 1:

2275-2302.

2. Boulton AJM and Armstrong DG. The diabetic Foot. In:

clinical diabetes. Chapter 14, 1st edition. 2006; 179-195.

76
3. A pelquist J, Agarth CD. The Association between clinical risk

factor and outcome of diabetic foot ulcer. Diabetic Res Clin Pract

1992; 18: 43-53.

4. Thomas PK: Classification, differential diagnosis, and staging of diabetic

peripheral neuropathy. Diabetes 46(Suppl. 2):S54–S57, 1997.

5. Guyton GT et al. Sympathetic dysfunction in diabetic foot.

Orthop Clin North Am 1997; 2: 77-86.

6. Negrine JP. Outpatient diagnosis and management of diabetic

foot orthopaedics clin north Am 1997; 2: 99-113.

7. Edmonds ME, Roberts VC, Watkin PJ. Blood flow in diabetic

neuropatic foot. Diabetologica 1982; 22: 9-15.

8. Flynn MD, Tooke JE: Aetiology of diabetic foot ulceration. A

role for the microcireulation? Diabet Med 1992; 9: 320-329,1992.

9. Sharma VK, Khadka PB, Joshi A, Sharma R. Common

pathogens isolated in diabetic foot infection in Bir hospitial;

Kathmandu Univ Med J (KUMJ) 2006; 4(3): 295-301.

10.Pithova P, Pathkova H, Golandakova I, Dolezalova L, Kvapil

M. Difference in ulcer location in diabetic foot syndrome. Vnitr

Lek 2007; 53(12): 1278-85.

77
11. Delamaire M, Maugendre D, Moreno M et al. Impaired

leucocytes function in diabetic patients. Diabetic Med 1997; 14;

29-34.

12.Zacur H, Kirsner RS. Debridement: rationale and therapeutic

options wound 2002; 12: 2E-7F.

13.Mason J, O’keefe C, Mcintosh A et al. A systematic review of

foot ulcer in patients? Diabet Med 1999; 16: 245-249.

14.Brand PW. The diabetic foot. In: Ellen berg M Rifkin C (eds).

Diabeties mellitus. Garden City, NY, Medical Examination

Publishing Co. 1983.

15.Karchmer AW, Gibbons GW. Foot infection in diabetics:

evaluation and management current topics in infections diseases

1994.

16.Diabetes statistics National diabeties clearing House, National

Institute for Diabetes and Digestive and Kindney Disease. National

Institutes of Health 1995.

17.Humphrey AR, Dowse GK, Thomas K, Zimmest PZ. Diabetes

and non traumatic. Lower extremity amputation incidence risk

78
factors and prevention a 12 year follow up study in Nauru Diabetes

Care 1996; 19: 701-4.

18.Pinzur MS. The diabetic foot. Compr Ther 2002; 28(3): 232-37.

19.Fabian W, Majkowska L, Stefansri A, Moledap. Prevalence of

diabetes, antidiabetic treatment and chronic diabetic complications

reported by general prodicner. Przegl Lek 2005; 62(4): 201-05.

20.Dalla Paola L, Faglia E. Treatment of diabetic foot ulcer: an

overview stratergies for clinical approach. Curr Diabetes Rev 2006;

2(4): 431-47.

21. Bentley J, Foster A. Multidisciplinary management of diabetic

foot ulcer. Br J Community Nurs 2007; 12(12): s6, S8, S10 passim.

22.Pendsey S, Abbas ZG. The step-by-step program for reducing

diabetic foot problems: a model for the developing world. Curr

Diab Rep 2007; 7(6): 425-8.

23.Clemens MW, Attinger CE. Biological basis of diabetic foot

wound Surg Technol Int 2008; 17: 89-95.

24.King LB. Impact of a preventive program on amputation rate in

diabetic population. J Wound Ostomy Continence Nurs, 2008;

35(5): 483-4.

79
25.Mundet X, PouA, Piquer N, Sanmartin MI, Tarruella M,

Gimbert R, Farrus M. Prevalence and incidence of chronic

complication and mortality in a cohort of type 2 diabetes patients in

Spain. Prim Care Diabetes 2008; 2(3): 135-140. Epub 2008 Jun.

27.

//--oo00oo--//

80
 PROFORMA

Serial No.

Name Age & Sex

Address

CR. No.

Date of Admission

History

• Duration of Diabetes years

• Type of Diabetes

Personal history

• Weight and Heigtht

• H\ o smoking

• H\O alcohol intake

• Social economic status

• Ethic status

81
Family history

Drug History- oral hypoglycemics or insulin

Specific history

• H\O previous ulcer

• H\O rest pain , numbness, parashthesias

• H\O neurogenic \ vascular claudication\

• H\O nephropathy(pedal or periorbital oedma)

• H\O retinopathy or other eye ailments

General physical examination

• Anaemia

• Blood Pressure

• Peripheral pulses

• Jaundice

• Lymphadenopathy

Systemic examination

1. Neurological Examination

82
 • Sensory

a) Touch

b) Vibration

c) Joint Position

d) Pin Prick

• Motor examination

a) Reflexes

- Ankle

- Knee

- Plantar

b) Any motor deficit

2. Vascular status

• Palpation of peripheral pulses( esp. dorsalis prdis and posterior

tibial artery)

• Colour doppler study

EXAMINATION OF FOOT:

83
 • Any structural deformity of foot

• Evidence of previous scar \ pigmentation

Grade of diabetic foot (University of Texas wound classification)

Investigation:

1. Routine investigation:

• Hb

• TLC

• DLC

• ESR

• FBS

• Glycosylated haemoglobin

• Post Prandial

• Urine C/E

2. Special investigations

• Renal function tests

• Colour doppler study

• X-rays
84
 • Bacteriological examination

Prevention and rehabilitation

• Patient education of foot care for prevention of first and

subsequent foot ulcers in diabetic patients.

• Patient education regarding orthotic and prosthetic

rehabilitation if amputation becomes inevitable

85
 CONSENT OF THE PATIENT
(To be taken in vernacular from each subject)
I_________________________, w/o, d/o, s/o _____________________
_______years old, CR.No._________
Address_________________________ is under treatment in the
__________________ Department. I voluntarily agree to
participate in the thesis work titled “THE INCIDENCE AND
RISK FACTORS OF DIABETIC FOOT IN DIABETIC PATIENTS”. I
have no objection if my investigations report or any other
parameter, which are part of my treatment may be used by
the Doctor ______________ for the purpose of thesis. I have fully
understood that no special tests and extra expenditure in any
form merely for the purpose of thesis is being carried out.
Above said purpose of the study and complications (infection,
neurovascular injury, non-union, mal-union, delayed union,
shortening, screw breakage, metal work failure and others)
associated with this modality of treatment has been explained
to me in vernacular language and I give my full and informed
consent to be the part of study at my own risk and
responsibility. I have signed this consent form in the presence
of witness as a token proof.

________________________ ______________________________
Signature of the Witness Signature of the
patient

Name: Explained by the consultant/ resident

Address: Name:
Date:

86
87