DIABETIC FOOT

I. INTRODUCTION

Diabetes mellitus (DM) refers to a group of common metabolic disorders

that share the phenotype of hyperglycemia. Several distinct types of DM are

caused by a complex interaction of genetics and environmental factors. Depending

on the etiology of the DM, factors contributing to hyperglycemia include reduced

insulin secretion, decreased glucose utilization, and increased glucose production.

The metabolic deregulations associated with DM causes secondary

pathophysiologic changes in multiple organ systems that impose a tremendous

burden on the individual with diabetes and on the health care system.1

In the United States, DM is the leading cause of end-stage renal disease

(ESRD), non traumatic lower extremity amputations, and adult blindness. It also

predisposes to cardiovascular diseases. With an increasing incidence worldwide,

DM will be a leading cause of morbidity and mortality for the foreseeable future.1

Two features of the current classification of DM diverge from previous

classifications. First, the terms insulin-dependent diabetes mellitus (IDDM) and

non-insulin-dependent diabetes mellitus (NIDDM) are obsolete. 1

The complications of longstanding diabetes mellitus often appear in the

foot, causing chronic disability. Factors affecting the foot are: (1) a predisposition

to peripheral vascular disease; (2) damage to periph- eral nerves; (3) reduced

resistance to infection.2

II. EPIDEMIOLOGY

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The prevalence of foot ulceration in the general diabetic population is 4–

10%, being lower (1.5–3.5%) in young and highest (5–10%) in older patients. The

lifetime risk for foot ulcers in diabetic patients is about 15%. The major adverse

outcome of foot ulceration is amputation. Data from several studies have

documented that foot ulcers precede approximately 85% of all amputations

performed in patients with diabetes. Risk of ulceration and amputation increases

2- to 4-fold with both age and duration of diabetes.3

More than 30 per cent of patients attending diabetic clinics have evidence

of peripheral neuropathy or vascular disease and about 40 per cent of non-

traumarelated amputations in British hospitals are for complications of diabetes. 2

‘Charcot joints’ occur in less than 1 per cent of diabetic patients, yet

diabetes is the commonest cause of a neuropathic joint in Europe and America

(leprosy and tertiary syphilis being the other common causes worldwide). The

mid-tarsal joints are the most commonly affected, followed by the MTP and ankle

joints. There is usually a provocative incident, such as a twisting injury or a

fracture, following which the joint collapses relatively painlessly.2

III. ANATOMY

Dorsum pedis4

2

Plantar pedis4

Compartement4

3

Arteries

Blood supply to the foot is by branches of the posterior tibial and dorsalis

pedis (dorsal artery of the foot) arteries.

The posterior tibial artery enters the sole and bifurcates into lateral and

medial plantar arteries. The lateral plantar artery joins with the terminal end of the

dorsalis pedis artery (the deep plantar artery) to form the deep plantar arch.

Branches from this arch supply the toes

The dorsalis pedis artery is the continuation of the anterior tibial artery,

passes on the dorsal aspect of the foot and then inferiorly, as the deep plantar

artery, between metatarsals I and II to enter the sole of the foot.5

Posterior tibial artery and plantar arch

The posterior tibial artery enters the foot through the tarsal tunnel on the

medial side of the ankle and posterior to the medial malleolus. Midway between

the medial malleolus and the heel, the pulse of the posterior tibial artery is

palpable because here the artery is covered only by a thin layer of retinaculum, by

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superficial connective tissue, and by skin. Near this location, the posterior tibial

artery bifurcates into a small medial plantar artery and a much larger lateral

plantar artery.5

Lateral plantar artery

The lateral plantar artery passes anterolaterally into the sole of the foot,

first deep to the proximal end of the abductor hallucis muscle and then between

the quadratus plantae and flexor digitorum brevis muscles. It reaches the base of

metatarsal V where it lies in the groove between flexor digitorum brevis and

abductor digiti minimi muscles. From here, the lateral plantar artery curves

medially to form the deep plantar arch, which crosses the deep plane of the sole

on the metatarsal bases and the interossei muscles.

Between the bases of the metatarsals I and II, the deep plantar arch joins

with the terminal branch (deep plantar artery) of the dorsalis pedis artery, which

enters the sole from the dorsal side of the foot.5

Major branches of the deep plantar arch include:

a digital branch to the lateral side of the little toe;

four plantar metatarsal arteries, which supply digital branches to adjacent

sides of toes I to V and the medial side of the great toe;

three perforating arteries, which pass between the bases of metatarsals II to

V to anastomose with vessels on the dorsal aspect of the foot.5

Medial plantar artery

The medial plantar artery passes into the sole of the foot by passing deep

to the proximal end of the abductor hallucis muscle. It supplies a deep branch to

adjacent muscles and then passes forward in the groove between the abductor

hallucis and the flexor digitorum brevis muscles. It ends by joining the digital

branch of the deep plantar arch, which supplies the medial side of the great toe.

Near the base of metatarsal I, the medial plantar artery gives rise to a

superficial branch, which divides into three vessels that pass superficial to the

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flexor digitorum brevis muscle to join the plantar metatarsal arteries from the deep

plantar arch.

Dorsalis pedis artery

The dorsalis pedis artery is the continuation of the anterior tibial artery

and begins as the anterior tibial artery crosses the ankle joint. It passes anteriorly

over the dorsal aspect of the talus, navicular, and intermediate cuneiform bones,

and then passes inferiorly, as the deep plantar artery, between the two heads of the

first dorsal interosseous muscle to join the deep plantar arch in the sole of the foot.

The pulse of the dorsalis pedis artery on the dorsal surface of the foot can be felt

by gently palpating the vessel against the underlying tarsal bones between the

tendons of extensor hallucis longus and the tendon of extensor digitorum longus

to the second toe.

Branches of the dorsalis pedis artery include lateral and medial tarsal

branches, an arcuate artery, and a first dorsal metatarsal artery:

the tarsal arteries pass medially and laterally over the tarsal bones,

supplying adjacent structures and anastomosing with a network of vessels

formed around the ankle;

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the arcuate artery passes laterally over the dorsal aspect of the

metatarsals near their bases and gives rise to three dorsal metatarsal

arteries, which supply dorsal digital arteries to adjacent sides of digits II

to V, and to a dorsal digital artery that supplies the lateral side of the digit

V;

the first dorsal metatarsal artery (the last branch of the dorsalis pedis

artery before the dorsalis pedis artery continues as the deep plantar artery

into the sole of the foot) supplies digital branches to adjacent sides of the

great and second toes.

The dorsal metatarsal arteries connect with perforating branches from the deep

plantar arch and similar branches from the plantar metatarsal arteries.5

Veins

There are interconnected networks of deep and superficial veins in the

foot. The deep veins follow the arteries. Superficial veins drain into a dorsal

venous arch on the dorsal surface of the foot over the metatarsals

the great saphenous vein originates from the medial side of the arch and

passes anterior to the medial malleolus and onto the medial side of the leg;

the small saphenous vein originates from the lateral side of the arch and

passes posterior to the lateral malleolus and onto the back of the leg. 5

Nerves

The foot is supplied by the tibial, deep fibular, superficial fibular, sural, and

saphenous nerves.

all five nerves contribute to cutaneous or general sensory innervation;

the tibial nerve innervates all intrinsic muscles of the foot except for

extensor digitorum brevis, which is innervated by the deep fibular nerve;

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the deep fibular nerve often also contributes to the innervation of the first

and second dorsal interossei.5

Tibial nerve5

The tibial nerve enters the foot through the tarsal tunnel posterior to the

medial malleolus. In the tunnel, the nerve is lateral to the posterior tibial artery,

and gives origin to medial calcaneal branches, which penetrate the flexor

retinaculum to supply the heel. Midway between the medial malleolus and the

heel, the tibial nerve bifurcates with the posterior tibial artery into:

a large medial plantar nerve;

a smaller lateral plantar nerve

The medial and lateral plantar nerves lie together between their corresponding

arteries.

Medial plantar nerve

The medial plantar nerve is the major sensory nerve in the sole of the

foot. It innervates skin on most of the anterior two-thirds of the sole and adjacent

surfaces of the medial three and one-half toes, which includes the great toe. In

addition to this large area of plantar skin, the nerve also innervates four intrinsic

muscles-abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, and the

first lumbrical.

The medial plantar nerve passes into the sole of the foot deep to the

abductor hallucis muscle and forward in the groove between abductor hallucis and

flexor digitorum brevis, supplying branches to both these muscles

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The medial plantar nerve supplies a digital branch (proper plantar digital

nerve) to the medial side of the great toe and then divides into three nerves

(common plantar digital nerves) on the plantar surface of flexor digitorum

brevis, which continue forward to supply proper plantar digital branches to

adjacent surfaces of toes I to IV. The nerve to the first lumbrical originates from

the first common plantar digital nerve.5

Lateral plantar nerve

The lateral plantar nerve is an important motor nerve in the foot because

it innervates all intrinsic muscles in the sole, except for the muscles (abductor

hallucis, flexor digitorum brevis, flexor hallucis brevis, and first lumbrical)

supplied by the medial plantar nerve. It also innervates a strip of skin on the

lateral side of the anterior two-thirds of the sole and the adjacent plantar surfaces

of the lateral one and one-half digits.5

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The lateral plantar nerve enters the sole of the foot by passing deep to the

proximal attachment of the abductor hallucis muscle. It continues laterally and

anteriorly across the sole between the flexor digitorum brevis and quadratus

plantae muscles, supplying branches to both these muscles, and then divides near

the head of metatarsal V into a deep and superficial branch.

The superficial branch of the lateral plantar nerve gives rise to a proper

plantar digital nerve, which supplies skin on the lateral side of the little toe and

to a common plantar digital nerve, which divides to supply proper plantar

digital nerves to skin on the adjacent sides of toes IV and V.

The proper plantar digital nerve to the lateral side of the little toe also

innervates flexor digiti minimi brevis and the dorsal and plantar interossei

muscles between metatarsals IV and V.

The deep branch of the lateral plantar nerve is motor and accompanies the

lateral plantar artery deep to the long flexor tendons and the adductor hallucis

muscle. It supplies branches to the second to fourth lumbrical muscles, the

adductor hallucis muscle, and all interossei except those between metatarsals IV

and V, which are innervated by the superficial branch.5

Deep fibular nerve

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The deep fibular nerve innervates extensor digitorum brevis, contributes

to the innervation of the first two dorsal interossei muscles, and supplies general

sensory branches to the skin on the adjacent dorsal sides of the first and second

toes and to the web space between them.

The deep fibular nerve enters the dorsal aspect of the foot on the lateral

side of the dorsalis pedis artery, and is parallel with and lateral to the tendon of

the extensor hallucis longus muscle. Just distal to the ankle joint, the nerve gives

origin to a lateral branch, which innervates extensor digitorum brevis from its

deep surface.

The deep fibular nerve continues forward on the dorsal surface of the foot,

penetrates deep fascia between metatarsals I and II near the metatarsophalangeal

joints, and then divides into two dorsal digital nerves, which supply skin over

adjacent surfaces of toes I and II.

Small motor branches, which contribute to the supply of the first two dorsal

interossei muscles, originate from the deep fibular nerve before it penetrates deep

fascia.5

Superficial fibular nerve

The superficial fibular nerve is sensory to most skin on the dorsal aspect

of the foot and toes except for skin on adjacent sides of toes I and II (which is

innervated by the deep fibular nerve) and skin on the lateral side of the foot and

little toe (which is innervated by the sural nerve;).

The superficial fibular nerve penetrates deep fascia on the anterolateral

side of the lower leg and enters the dorsal aspect of the foot in superficial fascia. It

gives rise to cutaneous branches and dorsal digital nerves along its course.5

Sural nerve

The sural nerve is a cutaneous branch of the tibial nerve that originates

high in the leg. It enters the foot in superficial fascia posterior to the lateral

malleolus close to the short saphenous vein. Terminal branches innervate skin on

the lateral side of the foot and dorsolateral surface of the little toe.5

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Saphenous nerve

The saphenous nerve is a cutaneous branch of the femoral nerve that

originates in the thigh. Terminal branches enter the foot in superficial fascia on

the medial side of the ankle and supply skin on the medial side of the proximal

foot.

IV. ETIOLOGY

Peripheral neuropathy. Peripheral neuropathy is usually present in patients with

diabetic foot infections. Although peripheral vascular disease can contribute to the

severity of peripheral neuropathy, it is not the primary factor. Distal

polyneuropathy is present in approximately 60% of diabetics and can be seen in

any age group regardless of whether they require insulin or not. Nerve death in the

diabetic is a result of metabolic, vascular, and histologic changes.6,7

Peripheral vascular disease. Blood vessels in the diabetic are subject to

accelerated atherosclerosis, and blood is characterized by increased viscosity,

clotting, and thrombosis formation . This causes nerve death, ischemia, and

embolization. The concept that diabetic ischemia is due to small vessel disease has

been challenged. It appears that there is minimal collateral vessel formation in the

foot due to the rapid onset of diabetic arteriosclerosis and lack of angiogenesis.

Although neuropathy is the cause of most ulcerations, vascular disease, either

alone or superimposed on neuropathy, can cause diabetic foot infection.6,7

Infection. Diabetics have a poor response to infection. Decreased phagocytosis of

bacteria and impaired cell-mediated immunity are noted and are worse when the

serum glucose is poorly managed. Diabetic foot infections are polymicrobial and

usually involve both aerobic and anaerobic species . Skin flora can cause deep

infections in diabetics, occasionally making it difficult to determine the

correlation between cultures taken from superficial ulcers or sinus tracts and the

true pathogens causing deep infection . Therefore, the most meaningful cultures

are those that are taken in the operating room from deep tissue underneath the

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ulcers or open wounds. Many of the acute soft tissue infections are caused by

streptococci or Staphylococcus aureus, which may be found as the single

pathogenic species. With an a monomicrobic anaerobic infection.6,7

V. PATHOPHYSIOLOGY

Pathway to foot ulceration in diabetic patients.3

Diabetic neuropathy 3,6,7

1. The diagnosis of foot ulcerations results in the greatest rate of hospital

admissions in diabetic patients, as well as lower extremity amputations.

2. The combination of neuropathy and excess pressure on the plantar foot leads to

ulceration.

3. Sensation

Polyneuropathic loss of sensation begins in a stocking distribution of the

feet and progresses proximally.

Diagnosed by the inability to perceive the 5.07 Semmes-Weinstein

monofilament

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90% of patients who cannot feel the 5.07 monofilament have lost

protective sensation to their feet and are at risk for ulceration.

With the Therapeutic Shoe Bill, money is allocated for neuropathic

patients to purchase extradepth shoes and total contact inserts (three per

year) for ulcer prevention.

4. Autonomic neuropathy

An abnormal sweating mechanism leads to a dry foot.

Vulnerable to fissuring cracks, which then become portals for infection.

5. Motor neuropathy

Most commonly involves the common peroneal nerve

Resultant loss of tibialis anterior motor function and a footdrop

Small intrinsic musculature of the foot also commonly affected, resulting

in claw toes and subsequent toe-tip ulcerations due to excessive pressure

Hypomobility syndrome3,6,7

1. Result of excessive glycosylation of the soft tissues of the extremities.

2. Leads to decreased joint ROM

Peripheral vascular disease3,6,7

1. Occurs in 60% to 70% of patients who have had diabetes for over 10 years,

involving both large and small vessels

2. Noninvasive vascular examination should be performed when pulses are not

palpable.

Waveforms (normal is triphasic)

Ankle-brachial indices (minimum for healing, 0.45; normal, 1.0)

Calcifications in the artery can falsely elevate the ankle-brachial index.

Greater than 1.3 is nonphysiologic and consistent with calcification of the

vessels.

Absolute toe pressures (minimum for healing, 40 mm Hg; normal, 100

mm Hg)

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3. Transcutaneous oxygen pressure of the toes greater than 40 mm Hg have been

found to be predictive of healing.

Immune system impairment3,6,7

1. Poor cellular defenses such as abnormal phagocytosis, altered chemotaxis of the

WBCs, and a poor cytotoxic environment (due to hyperglycemia) to fight off

bacteria lead to difficulty in fighting off infection once it has developed.

E. Metabolic deficiency

1. Reduced total protein less than 6.0 g/dL, WBC count less than 1500, and

albumin levels less than 2.5 g/dL result in poor healing potential.

VI. CLINICAL PRESENTATION

Neuropathic3

Neuropathy is present in about 85–90%

of foot ulcers in patients with diabetes.

Develop at areas of high plantar

pressures

Are painless, unless they are

complicated by infection.

There is callus formation at the borders

of the ulcer.

Its base is red, with a healthy granular

appearance.

On examination evidence of peripheral

neuropathy (hypoesthesia or complete

loss of sensation of light touch, pain,

temperature, and vibration, absence of

Achilles tendon reflexes, abnormal vibration perception threshold, often

above 25 V, loss of sensation in response to 5.07 monofilaments, atrophy

of the small muscles of the feet, dry skin and dis- tended dorsal foot veins)

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is present. However, the pattern of sensory loss may vary considerably

from patient to patient.

The foot has normal temperature or may be warm.

Peripheral pulses are present and the ankle brachial pressure index is

normal or above

Ischemic3

Ischemia is a major factor in 38–52% of cases of foot ulcers

Develop on the borders or the dorsal aspect of the feet and toes or between

toes.

They are usually painful

There is usually redness at the borders of the ulcer.

Its base is yellowish or necrotic (black).

There is a history of intermittent claudication.

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On examination indications of peripheral vascular disease (skin is cool,

pale or cyanosed, shiny and thin, with loss of hair, and onychodystrophy;

peripheral pulses are absent or weak; the ankle brachial index is <0.9) are

present.

Non-invasive vascular testing (duplex or triplex ultrasound examination,

segmental pressures measurement, plethysmography), and angiography

confirm peripheral vascular disease.

There are no findings of peripheral neuropathy.

Neuro-Ischemic Ulcers3

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Neuro-ischemic ulcers have a mixed etiology, i.e. neuropathy and ischemia, and a

mixed appearance

VII. CLASSIFICATION

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The Meggitt–Wagner classification is the most well-known and validated system for foot ulcers.1

Grade Interpretation

Grade O 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 fore

Grade 5 Gangrene of entire foot

VIII. DIAGNOSIS

Anamnesis 3

Questioning the patient to ascertain whether symptoms of peripheral

neuropathy, as described above, are present. Typically neuropathic symptoms are

worse during the night and may wake the patient, who finds relief on walking.

Some of important history for patient with diabetic foot are :

- History of previous foot ulceration or Amputation

- Peripheral neuropathy

- Peripheral vascular disease

- Trauma (poor footwear, walking barefoot, objects inside the shoes)

- Foot deformities (prominent metatarsal heads, claw tow, hammer toe, pes

cavus, nail deformities, deformities related to previous trauma and surgery,

bony prominences, etc.)

- Callus formation

- Neuro-osteoarthropathy

- Limited joint mobility

- Long duration of diabetes

- Poor diabetes control

Physical examination 3

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All patients with diabetes should be examined annually for peripheral

neuropathy, so that those at risk for ulceration can be identified. The tests for

peripheral neuropathy are many and some of them are quite sophisticated, and are

undertaken only in specialist centers. However, the tests that are used to

characterize the patient with loss of protective sensation are simple, fast and easily

carried out at the outpatient clinic. These tests are as follows : Loss of sensation of

(a) pain (using a disposable pin; this test is carried out only when the skin is

intact), (b) light touch (using a cotton wisp), and (c) temperature (using two metal

rods, one at a temperature of 4 ◦C and the other at 40 ◦C) on the dorsum of the

feet.

Typically, in diabetic peripheral neuropathy the sensory deficit is

pronounced at the periphery of the extremities (in a ‘glove and stocking

distribution’). A zone of hypoesthesia is found between the area of loss of

sensation and a more central area of normal sensation. Achilles tendon reflexes

may be reduced or absent. Wasting of small muscles of the feet results in toe

deformities (claw, hammer, curly toes) and prominent metatarsal heads. Vibration

perception is tested using a 128-Hz tuning fork on the dorsal side of the distal

phalanx of the great toes. A tuning fork should be placed perpendicular to the foot

at a constant pressure. During examination the patient is revented from seeing

where the examiner has placed the tuning fork. Examination is sepeated twice

and there is at least one ‘sham’ application in which the tuning fork is not

vibrating. The patient has normal sensation when his reactions are correct in two

out of three tests, but is at risk for ulceration when they are incorrectin two out of

the three tests.

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Pressure perception is tested with Semmes–Weinstein monofilaments. Many

studies have shown that inability to perceive pressure is related to a several-fold

increase in the risk for foot ulceration. The filaments are available in large

setswith varying levels of force required tobend them. Diabetic neuropathy can

bedetected using the 5.07 monofilament(this filament bends with the application

of a 10-g force). Monofilament should be applied perpendicular to the skin

surface and with sufficient force so that it bends or buckles. Total duration of skin

contact of the filament should be approximately 2 s. During examination the

patient is prevented from seeing if and where the examiner applies the filament.

The patient is asked to say whether he can feel the pressure applied (yes/no) and

in which foot (right/left foot). 3

Examination is repeated twice at the same site and there is at least one ‘sham’

application, in which no filament is applied (a total of three questions per site).

The patient has normal protective sensation when the correct answer is given for

two out of the three tests and is at risk for ulceration when they are not. The

International Consensuson the Diabetic Foot suggested three sites to be tested on

both feet: the plantaraspect of the great toe, the first and the fifth metatarsal heads.

The filament must be applied at the perimeter and not at an ulcer site, callus, scar

or site of necrotic tissue. 3

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Semmes–Weinstein (5.07) monofilament

Examination of vibration perception by the usefork of tuning examination

Determination of vibration perception thresholds using a biothesiometer or a

neurothesiometer. Vibration perception threshold is measured at the tip of the

great toes with the vibrating head of the device balanced under its own weight.

(The vibrating stimulus is increased until the patient feels it, the stimulus is then

withdrawn and the test repeated. This test is usually carried out three times at each

site and the mean value is calculated. Several studies have shown that a vibration

perception threshold over 25 V is associated with a 4- to 7-fold increase in risk for

foot ulceration. 3

Additional Examination

X-Ray 3

The clinical presentation and findings on physical examination determine

the need for imaging studies. Imaging studies are often overused. Plain

radiographs suffice in the vast majority of DFI cases. In all patients presenting

with DFI, high-quality radiographs of the feet include anteroposterior (AP),

lateral, and oblique views. Look for loss of soft-tissue planes, lucencies indicating

gas, foreign bodies that may have precipitated the infection, and bony changes

such as erosion and periosteal new bone formation that may indicate

osteomyelitis. The osseous radiographic changes of neuroarthropathy can simulate

osteomyelitis and the differential diagnosis can sometimes be difficult. Lytic

changes in bone without overlying skin ulceration is usually not due to

osteomyelitis but rather due to neuroarthropathy.

X-ray images should be obtained in patients with diabetic foot ulcers to

evaluate for the presence of osteomyelitisand gas in the soft tissues. Osteomyelitis

was noted in this case; however, the soft tissue gas is much more prominent

(Figure 3). The presence of gas on xray of the affected area should prompt the

clinician to obtain images up to the next proximal joint in order to ascertain the

extent of the infection [10]. In cases where gas is not seen, but deep space soft

tissue infection is suspected, computed tomography (CT) or magnetic resonance

imaging (MRI) may be appropriate.

Medial calcification, which is very common in diabetes (Figure 3), renders

the underlying arteries incompressible, resulting in spuriously high ABI values

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(more than 1.2). In these cases, the severity of arterial occlusive disease can be

assessed by toe pressure measurements. Other causes of inaccurately high ABI

values include too high positioning of the upper body, chronic venous

insufficiency and significant ankle edema. Spurious low ABI values can result

from the rapid deflation of the cuff, excessive probe pressure, and an insufficient

rest period.

Culture 3

Swab cultures from the surface of an ulcer or from sinus drainage have

been shown to be poor indicators of the bacterial species below. Therefore,

clinicians should curet and culture an ulcer from the base for aerobic and

anaerobic organisms. Start with empirical antibiotics if infection is suspected, and

modify them, if necessary, when the culture results and antibiotic sensitivities are

available. The bacterial species seen in DFIs are often multiple and range from

streptococcus or staphylococcus species (the two most common) to gram-negative

organisms and anaerobic organisms. Treatment with intravenous antibiotics based

on a swab culture, or preferably, a deep culture, is helpful if significant cellulitis is

present.

Arteriography 3

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Extensive calcification of the posterior tibial artery

X-ray reveals soft-tissue gas consistent with gangrene

Arteriography remains the definitive diagnostic procedure before any form

of surgical intervention. It should not be used as a diagnostic procedure to

establish the presence of arterial disease. Contrast material may exaggerate any

preexisting renal disease and for this reason the contrast material used should be

limited as much as possible. In addition, the International Meeting on the

Assessment of Peripheral Vascular Disease in Diabetes strongly recommended

that in diabetic patients arteriography should be carried out before any decision

regarding an amputation is made, in order to assess the exact status of the vascular

tree, particularly when the ankle brachial index and toe systolic pressure indicate

that arterial disease is present.

IX. TREATMENT

Basic principles of wound healing apply equally to diabetic foot ulcers as

to wounds in any other site or condition. Basically, a diabetic foot ulcer will heal

if the following three conditions are satisfied:

Arterial inflow is adequate.

Infection is treated appropriately.

Pressure is removed from the wound and the immediate surrounding area.

Ulcer location (forefoot, midfoot, and heel) and the presence or absence of

arterial disease influence healing rates.7,8

Classification and treatment8,9

Depth-ischemia classification (modification of Wagner- Meggitt classification)

1. Ulcer

Grade Description Treatment

Grade 0 Skin intact with bony

deformity - at risk

Extradepth shoe and pressure-relief

insoles

Grade 1 Localized superficial ulcer

without tendon or bone

involvement

- In-office ulcer debridement

- Total-contact cast

Grade 2 Deep ulcer with exposed - Formal operative debridement of all

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tendon or joint capsule exposed tendon and nonviable tissue

- Followed by dressing changes and

total-contact casting once wound bed

is healthy

Grade 3 Extensive ulcer with exposed

bone/osteomyelitis or abscess

- Surgical debridement of exposed

bone/ osteomyelitis and nonviable

tissue

- Followed by dressing changes and

total contact casting once wound bed

is healthy

2. Ischemia8

Grade Description Treatment

Grade A Normal vascularity

Grade B Ischemia without gangrene Noninvasive vascular studies and

surgical revascularization if indicated

Grade C Partial (forefoot) gangrene - Noninvasive vascular studies and

surgical revascularization if indicated

- Metabolic assessment

- Delay surgery if albumin is less than

2.5 g/dL or total protein is less than 6

g/dL, and improve nutritional status of

the patient.

- Operative intervention—partial foot

amputation

Grade D complete foot gangrene - Same as with grade C

- Operative intervention : below-the-

knee or above- the-knee amputation

Additional treatment8

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i. Midfoot collapse may require ostectomy of bony prominence or midfoot

fusion if instability of the midfoot is present.

ii. Equinus contracture is very common, and tendo- Achilles lengthening will

offload the midfoot/forefoot.

Achilles lengthening required

a. Recurrent forefoot/midfoot ulceration

b. Ulceration with equinus deformity

iii. Toe deformities often require joint resection or amputation.

The ultimate goal is an ulcer-free, functional, plantigrade foot that can fit within a

brace or shoe.

Diabetic foot infections8

i. Treat with initial broad-spectrum antibiotic coverage once surgical

cultures are obtained, and adjust once sensitivity results return.

ii. Abscesses require surgical drainage and antibiotics.

iii. Osteomyelitis is treated with antibiotics and usually surgical débridement.

iv. Culture-specific antibiotics from a bone biopsy have proven to be an

effective tool in treating osteomyelitis without the need for bone resection.

Resection of all nonviable or infected soft tissue should also be performed.

v. If culture-specific antibiotic therapy fails, then surgical resection of

infected bone and débridement of surrounding tissue is required in

addition to antibiotic therapy.

vi. Often results in more extensive debridement, including ray resection,

partial calcanectomy (calcaneal involvement), and partial or complete foot

amputation

Amputation level8

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i. Transmetatarsal

Lowest energy expenditure

No tendon transfer needed

ii. Lisfranc

Must transfer peroneal tendons to the cuboid to prevent varus

Achilles lengthening to prevent equinus

iii. Chopart

Transfer anterior tibialis to talus to prevent equinus.

Achilles lengthening to prevent equinus

iv. Syme

Amputation level with the next lowest energy expenditure after a

transmetatarsal amputation. Superior to both a Lisfranc and Chopart

amputation with regard to the amount of energy required to ambulate

v. Transtibial

Superior results with postoperative casting for 3 to 5 days with conversion to

rigid removal dressing

Pressure Off- loading

The mainstay in the management of an active plantar foot ulcer is the

effective offloading of the ulcer area. Once an ulcer is present, it will not heal

unless the mechanical load on it is removed. In patients with peripheral

neuropathy, it is important to offload at-risk areas of the foot in order to

redistribute pressures evenly. Inadequate offloading leads to tissue damage and

ulceration. The gold standard is the total contact cast (TCC). This is a

wellmoulded, minimally padded foot and lower leg cast that distributes pressures

evenly over the entire plantar surface of the foot. It ensures compliance because it

is not easy for the patient to remove. Using a TCC in patients with a unilateral

uncomplicated plantar ulcer can reduce healing time by

around six weeks.7,8,10

TCCs are contraindicated in patients with ischaemia because of the risk of

inducing further DFUs. They are also not appropriate for patients with infected

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DFUs or osteomyelitis because, unlike removable devices, they do not allow

wound inspection. Removable devices (such as removable cast walkers,

Scotchcast boots ( healing sandals and crutches, walkers and wheelchairs) should

be selected in these patients. 9,10

Gambar. a) Total Contact Cast (TCC), b) removable Scotch Cast Boots3,9

X. PREVENTION Early detection of potential risk factors for ulceration can decrease the

frequency of wound development. It is recommended that all patients with diabetes undergo foot examinations at least annually to determine predisposing conditions to ulceration.

Patients should be educated regarding the importance of maintaining good glycemic control, wearing appropriate footwear, avoiding trauma, and performingfrequent self-examinations.10

XI. COMPLICATIONS

Charcot joint 2

Neuropathic joint disease ‘Charcot joints’ occur in less than 1 per cent of

diabetic patients, yet diabetes is the commonest cause of a neuropathic joint in

Europe and America (leprosy and tertiary syphilis being the other common causes

worldwide). The mid-tarsal joints are the most commonly affected, followed by

28

a

b

the MTP and ankle joints. There is usually a provoca- tive incident, such as a

twisting injury or a fracture, following which the joint collapses relatively pain-

lessly. X-rays show marked and fairly rapid destruction of the articular surfaces.

These changes are easily mis- taken for infection but the simultaneous

involvement of several small joints and the lack of systemic signs point to a

neuropathic disorder. Joint aspiration and microbiological investigation will also

help to exclude infection.

/

Picture A and B, Note collapse at Lisfranc joints, valgus posturing of forefoot,

and shortening of first ray. Prominence medially is medial cuneiform. C, Same

foot with subluxations at tarsometatarsal joints, fragmentation of bone, shortening

and angulation of first ray, and new bone formation.

Osteomyelitis.3,11

Diagnosis can be a difficult problem in diabetic patients with foot infections;

some physicians will make the dianosis of osteomyelitis if they can palpate bone

thru the skin lesion; this method is quick, inexpensive, and generally accurate;if

there is not a lesion over the area of question, then it is more likely that the lesion

has resulted from Charcot changes;neuropathic osteoarthropathy often appears

29

indistinguishable from osteomyelitis, with multiple and widespread abnormalities

that can appear hot on all three phases of a bone scan; peripheral vascular disease

will also affect the uptake; In-WBC may be most accurate for detection of OM in

the diabetic foot; cellulitis is frequently present and can be confused with OM,

especially if osteoarthritis or neuropathic disease is also present.

Patient usually complain of numbness and a sensation of pins and needles in

her feet at night.

On examination, the patient will have findings of severe neuropathy (no

feeling of light touch, pain, temperature, vibration or a 5.08 monofilament;

Achilles tendon reflexes were absent; the vibration perception threshold was >50

V in both feet). Peripheral pulses were weak and the ankle brachial index was 0.7.

Dry skin and nail dystrophies were present. A superficial ulcer with a slough base

was seen on the dorsum which was red, swollen and painful, having a sausage-

like appearance.

The sausage-like appearance of a toe usually denotes osteomyelitis. Bone

infection was confirmed on X-ray, showing osteolysis of the first and second

phalanges.

/

30

Picture shows a large irregular , soaked and infected neuropathic ulcer with

slough bed and surrounding cellulitis of 3 cm in diameter is shown here. A minor

trauma reported to have occurred 2 years earlier was the cause of this ulcer.

/

Picture shows osteolysis of the first metatarsal head and the base of proximal

phalanx of the hallux with periosteal reaction due to osteomyelitis are shown on

this plain radiograph of the foot illustrated in picture before.

31

a