Presentation 070512
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Transcript of Presentation 070512
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DIABETIC FOOT ULCER
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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.
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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
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Pathophysiology
1. Vascular disease2. Neuropathy
• Sensory• Motor • autonomic
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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
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Predisposing peripheral vascular disease
Atherosclerosis (medium-sized vessels below the knee)
Compromised blood supply
Coagulative necrosis
Dry gangreneInfection
Wet gangrene
Ischemia
Ulcer
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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
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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
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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
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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
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Autonomic Neuropathy
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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
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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)
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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
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Classification
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Grade 1: Superficial Diabetic Ulcer
Grade 0: Preulcer stage
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Grade 2: - Ulcer extension - To ligament/tendon/joint capsule/fascia - No abscess or osteomyelitis
Grade 3: - Deep ulcer - Involving abscess / osteomyelitis
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Grade 4:- Gangrene to portion of forefoot
Grade 5:- Extensive gangrene of foot
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Presentation
Ulcer - Ischaemic - NeuropathyCharcotGangreneCallus & Corn
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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
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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
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Presentation of acute Charcot’s foot:- Swelling- Erythema- Raised skin temperature- Joint effusion - Bone resorption in an insensate foot
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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
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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.
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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.
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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.
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• X-ray– Bony destruction (Charcot or osteomyelitis)– Gas, F.B.’s
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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
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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
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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.
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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
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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
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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
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Complication
Early • Breakdown of skin flaps• Gas gangrene
Late• Skin- eczema, ulcer• Muscle- improper use
of prosthesis• Artery- ulcer• Nerve- pain & tender• Phantom limb
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