diabetic foot

DIABETIC FOOT
Dr Jitendra Dalai
2nd yr PG
Dept Of General Surgery
Mkcg mch ,Berhampur ,odisha

Contents
• Introduction
• Anatomy
• Pathogenesis
• Assesment
• Investigation
• Treatment

Introduction
A diabetic ulcer is a condition in, which an open sore or
wound occurs on the foot of a diabetic patient. Around
15% of the patients with diabetes develop this disease.
Uncontrolled diabetes leads to the breaking down of skin
tissue and revealing the layers underneath the foot. The
diabetic foot ulcer can be very deep and may affect bones,
tendons, and foot muscles.
source:sabiston textbook of surgery 21st edition

If a diabetic foot ulcer is left untreated,
it can result in:
• Accumulation of fluids (pus) in the foot
• Infection in the bone
• Infection that can spread to other parts
• Gangrene, due to poor blood flow
source :sabiston textbook of surgery 21st edition

Risks factors for Diabetic foot ulcers
Every diabetic patient is at risk of developing a foot ulcer.
Some other factors that can increase the risk of diabetic foot
are:
• High glucose levels
• Excessive alcohol consumption
• Cardiovascular disease
• Obesity
• Smoking or any other form of tobacco intake
• Kidney disease

Symptoms
One of the most common symptoms of the diabetic foot is a
development of ulcer on the bottom or the other side of the foot.
This ulcer may drain some abnormal fluid leaving spots on your
socks and shoes. The critical symptom of diabetic foot is the
formation of an eschar (dead tissue) around the ulcer. Lack of
blood flow to the foot often results in the death of tissue in the
foot.

The other symptoms of diabetic foot may include:
• Excessive swelling
• Bleeding
• Irritation
• Redness
• Pain around the foot ulcer
• Unpleasant smell from the feet

PLANTAR APONEUROSIS
• Condensation of deep fascia Triangular
shaped
• Apex- attached to medial tubercle of
calcaneum
• Base- divided into 5 processes near heads of
the metatarsal
• Digital nerve and vessels pass through the
interval between
source :Gray’s anatomy 41st edition

INTRINSIC MUSCLES OF 1ST LAYER OF
THE SOLE
• Flexor digitorum brevis
• Abductor hallucis
• Abductor digiti minimi

INTRINSIC MUSCLE OF 2ND
LAYER OF SOLE
• Flexor digitorum longus
• Flexor digitorum accessorius
• Lumbricals
• Flexor hallucis longus

MUSCLES OF 3RD LAYER OF THE SOLE
• flexor hallucis brevis
• Adductor hallucis
• Flexor digiti minimi brevis

MUSCLES OF 4TH LAYER OF THE SOLE
• Dorsal interossei
• Plantar interossei

ARCHES OF THE FOOT
• Medial longitudinal arch
• Lateral longitudinal arch
• Anterior transverse arch
• Posterior transverse arch

NERVE OF THE SOLE
Medial plantar nerve
it supplies: flexor hallucis brevis
Abductor hallucis
Flexor digitorum brevis
1st lumbricals
Cutaneous branch- supplies medial part
of sole medial three and a half toes

Lateral plantar nerve
Terminal branch of tibial nerve
Supply-remaining short muscle of the sole
Cutaneous branch- skin over the lateral side of the foot
lateral one and a half toes

CUTANEOUS NERVE SUPPLY OF FOOT

Pathogenesis
• Multi-factorial, Complex and still poorly understood
• Neuropathy
• Vasculopathy
• Immune dysfunction
• Infection
• Prolonged Hyperglycemia contributes to all the above
factors through different mechanisms

Pathophysiology

Peripheral Neuropathy
• Main Issue
• Nerve Death due to
• Metabolic Changes
• Vascular
• Histological
source :Harrison’s internal medicine 20th edition

Metabolic Mechanisms of neuropathy
• Buildup of sorbitol + fructose with decrease in myo-inositol +
Na+/K+ ATPase
• Increase tissue glucose metabolised by alternative pathway due
to decrease in insulin
• Decreased nerve function + disruption of membrane associated
Na+ pump
• Demyelination/nerve injury = Death due to failure to
maintain normal polarised state)

Metabolic mechanism of neuropathy
• Loss of small sensory fibers
– Decrease in pain + Temp
• Loss of Large sensory fibers
– Decrease in Light touch + Proprioception

Effects of Peripheral Neuropathy
• Affects
– Sensory
– Motor
– Autonomic

Sensory
• Decreased sensation
 Unable to detect trauma / discomfort = repeated insult to
tissue + bone
• Wounds go unnoticed
• Areas of pressure progressively deteriorate
 Loss of protective sense in joints = excessive force applied to
ligaments + cartilage
• Joint erosion / Dislocation / #s & Charcot joints

Motor
• Motor nerves to intrinsic muscle affected
– Imbalance between flexion / extension
• Foot deformity – abnormal pressure areas
hence skin breakdown + ulcerations
– E.g. Claw toe deformity
• Common Peroneal nerve also affected
– Foot drop due to loss of tibialis anterior motor function

Limited Joint Mobility Syndrome
• Can affect the hand/joints/foot
• Due to loss of foot sensation/proprioception &
intrinsic muscle function,
• Leads to wide based gait for balance that progresses to
claw toes / midfoot valgus & calcaneoequinovalgus +
decreased subtalar/ankle movement
– Hence flat/stiff/insensate foot prone to injury & ulcerformation

Autonomic
• Decreased function of sebaceous glands of foot
–decreased sweat and oil secretion
– Dryness of skin = cracks and infection
• Local blood flow regulation
– Abnormal dilatation of the Arteriovenous shunts
(Mostly in the skin of soles & not dorsum)
• Abnormal dilatation = bypass of blood from the skin
– Decrease in integrity of skin = dryness + Breakdown

Peripheral Vascular Disease
• 2 mechanisms
– Atherosclerosis
– Monkenberg’s Medial Sclerosis
• Calcification of media of artery = rigid vessels without narrowing
of lumen
• Interferes with measurements of doppler pressures –false high
readings
Source : bailey and love’s short practice of surgery27th edition

• 20-40% of DM patients have Peripheral vascular disease
• Level of glycemic control plays a part
– 26% increase in risk of PVD for every 1% increase in HbA1c
• Usual symptoms (ischemic rest pain etc) may be
absent due to peripheral neuropathy.

Pattern of atherosclerosis in DM as compared to non DM pts
– Affects younger patients
– More Aggressive
– Progression is faster
– Affects distal vessels > prox
• Rapid progression overcomes rate of distal collateral
revascularization

Infections and Diabetic Foot
Immunology
– Poor response to infection seen because
• Polymorphonuclear leukocyte migration
• Phagocytosis
• Intracellular killing
• Chemotaxis
– Antibiotics may be subtherapeutic in ischemic tissues
• Decreased blood flow in swollen and infected tissues =
large necrotic dead spaces

Organism for infection
• During acute infection– Staph aureus commonest
• Chronic infection
 Polymicrobial (>75% of pts)
 Gram-ve isolates (51.2%), Gram+ve (32%)
 Spectrum moves from gram +ve to Gram-ve, anaerobics as
the wagner classification progresses

• Osteomyelitis
Bone infected in at least 20% of foot ulcers
Majority – contiguous spread from adjacent soft
tissue infection (not conventional)
Frequently missed or under diagnosed = Amputations
Risk of amputation increases 4X
Presence of Osteomyelitis requires longer duration of
antibiotic therapy

• Commonest site
 Forefoot (90%)
 Midfoot & Hind foot – 5% each
• Commonest bone affected
Tripod of foot
 1st metatarsal
 5th metatarsal
 Calcaneus

Infections and Diabetic foot
Clinical testing with Probe to bone test
– Controversial
– Some studies – sensitivity 98%, Specificity 79%
• Plain Radiography
– 30-50% bone destruction to show visible
changes(2-3 wks to manifest)
• Bone biopsy is gold standard

Prevention of diabetic foot ulcer
• Diabetic foot ulcer (DFU) is not only a patient
problem but also a major health care concern
throughout the world.
• Diabetic foot ulcer is one of the common and serious
complications in diabetic patients.

• Treatment of infection in diabetic ulcer is difficult
and expensive.
• Patients usually need to take long-term medications
or become hospitalized for an extended period of
time.
• It is estimated that usually 15-25% of diabetic
patients develop DFU during their life-time.

Preventive measures
• Life style modification
• Blood pressure control
• Lipid management
• Glycemic control
• Smoking cessation.

Foot Specific History
Daily activity
Foot wear
Chemical exposure
Callus formation
Deformity
Previous foot surgery
Neuropathic / ischemic symptoms

Wound/Ulcer History
• Location
• Duration
• Inciting event / trauma
• Infection
• Wound care/ off loading methods
• Compliance on wound care
• Previous foot surgery / trauma
• Edema unilateral vs bilateral

Examination
1. General
2. Vascular examination
Palpation of pulses
• Dorsalis pedis, posterior tibial, popliteal, femoral
Venous filling time
Colour changes
• Cyanosis , erythema
Presence of edema
Skin changes consistent with ischemia
Skin atrophy
• Nail atrophy
• Abnormal wrinkling
• Decreased pedal hair

Vascular
• Assessment of peripheral pulses of paramount
importance
• If any concern, vascular assessment
– ABI (n>0.45)
• Sclerotic vessels
– Toe pressures (n>40-50mmHg)
– Transcutaneous oxygen tension(TcO2 ) >30 mmHg
• Expensive but helpful in amputation level

3. Neurological examination
Vibration perception
-Tuning fork 128 Hz
Light pressure : Simmes –Weinstein 10
gram monofilament
Light touch
Two point discrimination
Pain – pinprick
Temperature perception: hot and
Cold,

Musculo-skeletal Examination
Orthopaedic deformities: Hammer toes,
claw toes
hallux valgus
pes cavus
charcots joints
Gait abnormalities
Muscle group atrophy

Charcots joint
• Neuropathic destruction of joints
• Hot ,swollen ,red extrimities
• Oftenly mistaken with gout, fracture, DVT, Cellulitis
• CROW ( Charcots retaining orthotic walker ) is used
to prevent ulcer formation and deformity

Dermatological Examination
Skin appearance: colour, texture,
dry
Calluses
Fissures
Nail appearance
+ Hair
Tinea pedis

Foot Wear Examination
Type of shoe
Fit
Lining of shoe
Foreign bodies in the shoe.

Investigation
• CBC
• Glycosylated hemoglobin (HbA1C)
• FBS / 2HR PPBS
• Serum profile
• Wound and Blood culture sensitivity
• Urinalysis

Imaging
Plain X-rays
- Osteomyelitis, fractures
- Soft tissue gas
- Dislocations in neuropathic arthropathy
Duplex scan of arterial system in b/l limb
CT Scan
MRI

Classification
• Commonest
– Meggit - Wagners
– University of Texas

Meggit - Wagners Classification
0 - Intact Skin (Impending ulcer/foot at risk)
1 - Superficial Ulcer
2 - Deep ulcer to bone/tendon/ligaments
3 - Osteomyelitis
4 - Localised Gangrene – toes/ forefoot
5 - Extensive Gangrene

• Advantages
– Simple
– Higher grades related to increased risk of
amputation
– Provides a guide to planning treatment
• Disadvantages
– Location and size of ulcer not evaluated
– Neuropathy status not evaluated
– Doesn’t take into account ischaemia & infection

University of Texas Classification
• Used in many clinical trials & Diabetic foot
centres
• Uses 4 grades each of which is modified
-No infection Stage A
– Infection Stage B
– Ischemia Stage C
– Both Stage D

UNIVERSITY OF TEXAS DIABETIC WOUND CLASSIFICATION SYSTEM
STAGE GRADE
0 I II III
A
( no
infection/ischemia)
Pre or post
ulcerative lesion
Completely
epithelialized
Superficial wound
not inviloving
tendon, capsule or
bone
Wound
penetrating to
tendon or
capsule
Wound
penetrating bone
or joint
B Infection Infection Infection Infection
C Ischemia Ischemia Ischemia Ischemia
D Infection
And Ischemia
Infection
And Ischemia
Infection
And Ischemia
Infection
And Ischemia

• Advantages
– Shows greater association with outcome of an
ulcer/healing/amputation compared to Wagners
– Provides a guide to treatment
• Disadvantages
– Location and size of ulcer not evaluated
– Neuropathy status not evaluated

Treatment
• Multidisciplinary Approach
• Careful Evaluation of Diabetic foot
• Patient Education & Good Glycemic Control
• Wound Care – Obtain closure ASAP

Ulcers
Extend of ulcer need to be recorded
– Location / Size / Color of wound / wound margin
Exudate
• Type / Amount / color / consistency / adherance to
ulcer bed

• Deeper ulcers may need debridement
-debridement should be done 1 to 2 stages maximum
• Treatment with IV antibiotics based on swab culture
• Non operative method
– Shoe modification
• To prevent formation of ulcer – custom
insoles /wide shoes
– Relief of pressure by distributing stresses
over large area –total contact cast
Offloading

Dressing of the wound
Operative
– Debridement
• Surgical
• Chemical
• Enzymatic-Collagenase, papain, fibrolysin
– medicated dressing
Source: schwartz’s principle of surgery 11th edition

Wound care
• – Goals to Provide moist environment , absorb
exudate, act as a barrier & offload pressure at
ulcer
RECOMMENDED WOUND DRESSING
dressing indication
Alginate Exudative wound
Polyurethane films Dry wounds
Polyurethane foams Exudative wound
hydrocolloid Exudative wound
hydrogel Dry and necrotic wounds
Saline gauze Dry and necrotic wound

Mechanical dressing
• VAC (vaccum assisted closure) dressing
-pressure =125mmHg
-remove exudate and reduce edema
-contraindicated in avascular wound, untreated osteomyelitis
• Hyperbaric oxygen therapy(HBOT)
-improve hypoxia, enhance perfusion,
Fibroblast proliferation,collagen production

SOURCE ;INTERNET VAC DRESSING, HBOT

– Endogenous growth factors such as platelet derived
GF, transforming GF B, Epidermal growth
factors now being used to accelerate wound
healing
– Recombinant Human Platelet derived growth factor

Skin replacement
Skin grafts and tissue replacements can be used to
reconstruct skin defects for people with diabetic foot
ulcers in addition to providing them with standard care.
• Autografts
• Allografts and xenografts
• Bioengineered or artificial skin
• Source : bailey and love’s short practice of surgery27th edition

Amputation
Indication
• Unsalvagable foot
• Fulminant sepsis
• Hemodynamic instability
• Severe acid base and electrolyte abnormalities
• Source : bailey and love’s short practice of surgery27th edition

Amputation
• Amputations need proper investigation and patient counselling
• Avoid distal amputations if non invasive vascular studies show poor
vasculature
• Ankle brachial index (>0.5) –
• Absolute toe pressure (>45mmhg)
• Transcutaneous partial pressure of O2 (>30mmHg)
• Pts nutritional status needs evaluation
– Albumin > 2.5g/dl
– Total Protein >6g/dl
– Good lymphocyte count
• Wound closure depends on infection and adequacy of
bleeding.

• Attempt minor amputation at 1st sitting (if
possible)
• When major amputation done, mortality rate
increases
–Complications.
• 80% of minor amputees alive after 2yrs,
73% of them preserving the limb,
64% fully ambulant
• In the Below knee amputation group – 52% died within 2yrs, 64%
ambulant on prosthesis
• Difference in mortality being 1.6 times more in major amputees compared
to ray amputations

REVASCULARISATION
• Peripheral vascular disease is an important risk factor for
lower extremity amputation in diabetic patients with chronic
foot ulcers.
• Successful revascularization reduces the major amputation
rate in diabetic patients.
• This can be achieved either by peripheral bypass or by
percutaneous transluminal angioplasty.
• Percutaneous transluminal angioplasty (PTA) is today
considered the first choice revascularization procedure in
many cases. It is feasible, safe and cost affective for limb
salvage in a high percentage of diabetic patients.

REVASCULARISATION
• According to TransAtlantic inter society consensus
(TASC), there are 4 types of lesion i.e A,B,C and D in
aortoiliac and 4 types in femoropopliteal lesion
• Aortoiliac lesion
TASC A and B- endovascular therapy is the
treatment of choice
TASC Cand D-surgery is the preferred treatment

SURGICAL MANAGEMENT
• Aortoiliac disease: aortobifemoral bypass
• Lower extremity occlusive :femoropopliteal bypass,
infrapopliteal bypass
source :sabiston textbook of surgery 21stedition

Endovascular management
1. Subintimal angioplasty
2. Balloon angioplasty
3. Stenting
4. Stent graft
5. Cutting balloon
6. Atherecotmy

Take home message
• Patient counselling and education
• Daily washing of foot and moisturizer
• Daily inspection of foot for any cuts or sores
• Avoid walking bare foot
• Well fitting shoes( mcr/ mcp slipper)
• Avoid using counter irritant for foot care

References
1. Sabiston textbook of surgery 21st edition
2. Harrison’s internal medicine 20th edition
3. Bailey and love’s short practice of surgery27th edition
4. Gray’s anatomy 41st edition
5. Schwartz’s principle of surgery 11th edition

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