DIABETIC FOOT ULCER

Introduction

- The complication of long-standing diabetes mellitus

- 15% of patients with diabetes mellitus will develop a lower extremity ulcer during the course of their disease.

- They are a major source of morbidity, a leading cause of hospital bed occupancy and account for substantial health care costs and resources

- Foot complications result from a complex interplay of ischaemia, ulceration, infection and diabetic Charcot’s joint.

- They can be reduced through appropriate prevention and management.

Neuropathy

Peripheral vascular disease

Abnormal foot pressure

Hyperglycemia

Trauma

Foot deformity Limited joint mobility

Previous ulceration and amputation

Poor vision

Chronic renal disease

Old ageCondition of

diabetes

Neuropathy

Peripheral vascular disease

Abnormal foot pressure

Hyperglycemia

Trauma

Foot deformity Limited joint mobility

Previous ulceration and amputation

Poor vision

Chronic renal disease

Condition of diabetes

Pathophysiology

1. Vascular disease2. Neuropathy

• Sensory• Motor • autonomic

Vascular Disease

• Diabetics causes arthrosclerosis obliterans

• Calcification of the media

• Often increased blood flow with lack of elastic properties of the arterioles

• Not considered to be a primary cause of foot ulcers

Predisposing peripheral vascular disease

Atherosclerosis (medium-sized vessels below the knee)

Compromised blood supply

Coagulative necrosis

Dry gangreneInfection

Wet gangrene

Ischemia

Ulcer

ABPI value Interpretation Action Nature of ulcers, if present

above 1.2 AbnormalVessel hardening from PVD Refer routinely

Venous ulceruse full compression bandaging

1.0 - 1.2 Normal rangeNone

0.9 - 1.0 Acceptable

0.8 - 0.9 Some arterial disease Manage risk factors

0.5 - 0.8 Moderate arterial disease Routine specialist referralMixed ulcersuse reduced compression bandaging

under 0.5 Severe arterial disease Urgent specialist referralArterial ulcersno compression bandaging used

Neuropathy

• Changes in the vasonervorum with resulting ischemia

• cause– Increased sorbitol (in feeding vessels)– Causing block flow – Causing nerve ischemia

• Abnormalities of all three neurologic systems contribute to ulceration

Hyperglycaemia

stimulate polyol pathway

accumulation sorbitol + fructose in Schwann cellsIncrease IC osmolality

influx of water osmotic cell injury

damage schwann cell

(demyelination )

axon degeneration irreversibly

disrupt neural function

Diabetic neuropathy

Autonomic Neuropathy

• Regulates sweating and perfusion to the limb

• Loss of autonomic control inhibits thermoregulatory function and sweating

• Result is dry, scaly and stiff skin that is prone to cracking and allows a portal of entry for bacteria

Autonomic Neuropathy

Motor NeuropathyOcclusion of vaso nervorum dt AGEs > Ischaemic damage to the nerves >

Somatic motor neuropathy > muscle weakness/wasting >

plantar arch cannot maintained > exaggerated plantar arch >

abnormal distribution of pressure > ulcer on pressure point

Sensory Neuropathy• Loss of protective sensation

• Starts distally and migrates proximally in “stocking” distribution

• Large fibre loss – light touch and proprioception• Small fibre loss – pain and temperature

• Two mechanisms of Ulceration– Unacceptable stress few times (rock in shoe, glass, burn)– Acceptable or moderate stress repeatedly (inproper shoe

ware)

b) NeuropathyNeuropathy

Motor Sensory Autonomic

↓ nociception

↓ Proprioception,Unawarenessof foot position Reduced

sweating

Dry skin

Fissures andcracks

Muscle wastingFoot weakness

Postural deviation

Deformities, stressand shear pressures

Trauma

Stress on bones & jointsPlantar pressure

Callus formation

InfectionUlcer

Classification

Grade 1: Superficial Diabetic Ulcer

Grade 0: Preulcer stage

Grade 2: - Ulcer extension - To ligament/tendon/joint capsule/fascia - No abscess or osteomyelitis

Grade 3: - Deep ulcer - Involving abscess / osteomyelitis

Grade 4:- Gangrene to portion of forefoot

Grade 5:- Extensive gangrene of foot

Presentation

Ulcer - Ischaemic - NeuropathyCharcotGangreneCallus & Corn

PainlessSites of pressures (metatarsal

heads, heels)

Painful At the distal and over

bony prominencesUlceration

Warmpalpable pulses

ColdPulseless

Palpation

High arch + clawing of toesNo trophic changes

Surrounded by callus

Dependent ruborTrophic changes

Gangrenous digitsInspection

Usually painlessOr painful neuropathy

ClaudicationRest pain

Symptoms

NeuropathyIschaemia

Differentiation of Ischaemic and Neuropathy Ulcer

Charcot Joint• Any destructive arthropathy arising from loss of

pain sensibility and position sense

• Lack of the normal protective reflex against abnormal stress/injury > repetitive trauma > articular surface and bone destruction > deformity of the joint

• characterized by pathological fracture, joint dislocation and fragmentation of articular cartilage

Presentation of acute Charcot’s foot:- Swelling- Erythema- Raised skin temperature- Joint effusion - Bone resorption in an insensate foot

Charcot Foot

• Neurotraumatic– Decreased sensation + repetitive trauma = joint and bone

collapse

• Neurovascular– Increased blood flow → increased osteoclast activity →

osteopenia → Bony collapse– Glycolization of ligaments → brittle and fail →Joint collapse

Classification (Eichenholtz):

Stage 0: - Clinically, there is joint edema, but radiographs are negative.

Stage 1: -Osseous fragmentation with joint dislocation seen on radiograph ("acute Charcot").

Stage 2: -Decreased local edema-With coalescence of fragments and absorption of fine bone debris

Stage 3: -No local edema-With consolidation and remodeling (albeit deformed) of fracture fragments.

Gangrene

Dry gangrene

• no infection• little tissue liquefaction• In early stages, dull,

aching pain, extremely painful to palpate, cold, dry and wrinkled.

• In later stages, skin gradually changes in color to– dark brown, then– dark purplish-blue, then– completely black

Wet gangrene

• Bacterial infection• copious tissue

liquefaction• offensive odor• swollen, red and warm.• usually develops

rapidly due to blockage of venous and/or arterial blood flow

Gangrene is a condition that involves the death and decay of tissue, usually in the extremities due to loss of blood supply.

Callus and Corn

Callus (or callosity )- Toughened area of skin which has become relatively thick and hard- In response to repeated friction, pressure, or other irritation. - Rubbing that is too frequent or forceful will cause blisters rather than allow calluses to form

Corn (or clavus, plural clavi) - is a specially-shaped callus of dead skin - that usually occurs on thin or glabrous (hairless and smooth) skin surfaces, - especially on the dorsal surface of toes or fingers.

• X-ray– Bony destruction (Charcot or osteomyelitis)– Gas, F.B.’s

Treatment

• Debridement• Wound care• Reduction of plantar pressure (Off loading)• Treatment of infection• Vascular management of ischemia• Medical Rx of co-morbidities• Surgical management• Reduce risk of recurrence

Debridement• Surgical debridement

– Involve removal of all non-viable tissue or bone until healthy bleeding soft tissue or bone are encountered.

– Abscess: immediate I & D.– Osteomyelitic bones, joint infection, gangrene digits: require resection or

partial amputation.

• Other type of debridement: a) mechanical (surgical debridement, high pressure irrigation, wet

to dry dressing),b) Enzymaticc) Autolytic

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Wound care

• Done following debridement.

• Dressing: normal saline and others (e.g: transparent films, foam, hydrocolloids, calcium alginates, gauze pads, collagen dressings)

• Ulcer is covered to avoid contamination and trauma.

• Choice of dressings or topical agents depends on the health care provider’s experience, type and site of ulcer, costs involved and patient’s preferences

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Cast boot

Treatment of infection• Early incision and drainage• Empirical broad-spectrum antibiotic.

Vascular management of ischemia- Vascular supply should be assessed early before surgery intervention

Treat other medical co-morbidities• DM is a multi-organ systemic disease.• Multi-disciplinary approach.

Surgery

• Remove structurally deformed foot which my give rise to high pressure areas causing ulcers that do not heal with off loading technique or therapeutic foot wear

• Amputation- gangrene and ulcers with osteomyelitis

• Includes removal of infected bone or joint e.g:– metatarsal head resection, partial calcanectomy, exostectomy,

sesamoidectomy and digital arthroplasty

Indications for Amputation

Uncontrollable infection or sepsisInability to obtain a plantar grade, dry foot

that can tolerate weight bearingNon-ambulatory patient

Decision not always straightforward

3 D’s

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• Damned Nuisance - dt pain, gross malformation, recurrent sepsis, severe loss of function

• Dead - PVD, trauma, burns, frostbite

• Dangerous - malignant tumours, potentially lethal sepsis, crush injury

Complication

Early • Breakdown of skin flaps• Gas gangrene

Late• Skin- eczema, ulcer• Muscle- improper use

of prosthesis• Artery- ulcer• Nerve- pain & tender• Phantom limb