diabetic foot vinay 1
TRANSCRIPT
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Presenter: Dr. Vinay Jain
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Diabetic footIntroduction Diabetes mellitus is a group of metabolic diseases
characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both.
The chronic hyperglycemia of diabetes is associated with long-term damage, dysfunction, and failure of various organs, especially the eyes, kidneys, nerves, heart, and blood vessels.
Diabetic foot is defined as any foot pathology that results directly from diabetes or its long term complications
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Epidemiology Lesions of the feet affect ~15% of diabetics in their life
with an amputation rate 15 fold higher than non diabetics
Foot ulcerations are the commonest cause of hospital admission in diabetics
Atherosclerosis rarely seen in type I diabetics < 40 yrs while it may be present even before diagnosis in type II
Indication for lower limb amputation
Diabetes - 17.5%
PVD - 55.3%
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Epidemiology – risk factors Male sex
DM > 10 years duration
Peripheral neuropathy
Abnormal foot structure
Peripheral arterial disease
Smoking
H/O previous ulceration / amputation
Poor glycemic control (HbA1c > 7%)
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Pathophysiology Factors leading to development of diabetic foot:
Diabetic macroangiopathy – peripheral arterial occlusive disease
Diabetic microangiopathy – thickening of basement membranes
Diabetic polyneuropathy
Diabetic osteoathropathy –
abnormal foot biomechanics
Reduced resistance to infection
Delayed wound healing
Reduced rate of collateral
vessel formation
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Peripheral Neuropathy Prevalence – 20-60 %
Increases with chronic hyperglycemia, duration of diabetes and patient age
90% of cases of diabetic foot ulcer
Sensory neuropathy
Motor neuropathy
Vegetative neuropathy
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Sensory neuropathy
Predominates
Large fibers - tactile and deep sensitivity
Small fibers - pain and heat sensitivity
Motor neuropathy
Weakness and atrophy of the intrinsic muscles of the foot-clawtoe
Loss of joint mobility
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Secondarily, it contributes to loss of joint mobility, which is also due to conjunctive tissue glycosylation inducing fibrosis of the joint, soft tissue and skin
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Vegetative neuropathy Induces skin dryness with crevasses and fissures
providing entry points for infection
Hyperkeratosis in reaction to hyperpressure
Opens arteriovenous shunts and induces deregulation of capillary flow
The neuropathic foot is hot, with frequent edema and dilated dorsal veins
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ArteriopathyMacroangiopathy
Atheromatous lesions - classically
showing multi-segment and distal
involvement
distal superficial femoral,
popliteal, tibial, peroneal and
pedis arteries
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Microangiopathy
Thickening of the capillary
membrane,induce abnormal
exchange and aggravate tissue ischemia
Induces chronic ischemia, which is an aggravating factor in foot lesions
The foot is cold and the skin becomes thin and shiny
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The Lewis Triple Flare Response is
absent in diabetic patients affecting wound
healing
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Evaluation of foot deformity Foot deformity may result from motor neuropathy and
muscle imbalance, or Charcot foot
Motor neuropathy leads to the development of a cavusfoot with a mild equinus contracture at the ankle, claw toes, and increased pressure to the forefoot (metatarsal heads)
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Claw toe results from imbalance between the intrinsic muscles (lumbricals and interossei muscles that flex the MTP and extend the PIP and DIP) and
The long extensor and flexor tendons dominate (opposite) – [extensor digitorum longus & flexor digitorum longus flexes
Ulceration in three distinctive sites
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Limited dorsiflexion and Achilles tendon tension increase forefoot plantar pressure and contribute to ulcer formation
Hallux valgus deformity contributes to ulcer formation at the bunion
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Biomechanics of Ulceration Loss of pressure and pain sensitivity leads to repeated
local hyperpressure shear stress in the hyperkeratoticregion
Under which effusion develops and exteriorizes into an ulcer
Mechanical, thermal or chemical wound may also lead
to ulceration - diagnosed late due to the absence of associated pain
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At-risk feet
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Ulcer classification
Wagner Meggitt Classification
Texas Classification
Pedis Classification
King’s Classification
Amit Jain’s Classification
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Wagner Meggitt Classification
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DRAWBACKS
First of all it does not adequately address all the diabetic foot ulceration and infection
Only one of the 6 grades includes infection
Limited in its ability to identify and describe vascular disease as an independent risk factor
Superficial wounds that are infected or dysvascular are not able to be classified by this system
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Texas Classification
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PEDIS Classification
Based on five parameters
Perfusion
Extent
Depth
Infection
Sensitivity
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Each diabetic wound can be described by five elements, individualizing prognosis
The classification is thus more precise than Wagner’s
Most ulcers are induced by neuropathy, but vascular status determines prognosis
Infection is an extra severity factor for limb prognosis and patient survival
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King’s Classification
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Amit Jain’s Classification
Proposed mainly to dessiminate the knowledge of diabetic foot complications especially in developing Asian countries like India
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Type 1- Diabetic foot complications that are infective. It includes cellulitis, abscess, necrotizing fasciitis, wet gangrene, etc
Type 2-Diabetic foot complications that are non-infective. It includes diabetic charcot foot, peripheral arterial disease, neuropathy, etc. belong to this group
Type 3- Diabetic foot complications that are mixed, where both type 1 and type 2 complications can occur in combination. A common example might be a callus ulcer with underlying osteomyelitis
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Diagnosis Duration of diabetes, glycemic balance (glycemic
Hemoglobin: Hb A1C > 7% indicates poorly balanced diabetes
Associated renal and ocular complications;
History of ulcer or of minor amputation
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Neuropathy Systematically looked for as part of any foot
examination in diabetic patients
Preventive education is mandatory, as neuropathy is a factor in foot ulcer
Charcot foot is another consequence of neuropathy
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Screening• Inability to perceive the 10g
of force applied by the monofilament is associated with clinically significant large fibre neuropathy and an increased risk of ulceration (sensitivity of 66 to 91%)
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128 Hz tuning fork - The tuning fork explores vibratory sensitivity on the dorsal side of the 1st metatarsal
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Vascular Testing
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Osteo-articular imagingInfection can be assessed on
Standard X-ray
CT
MRI
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Standard X-ray Signs of osteitis
Neuro-arthropathic lesions
Comparative assessment at 1 and 2 weeks
In case of osteitis, osteolysis, which was initially absent, will be visible at 2 weeks
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CT Scan CT usefully confirms osteolysis in case of ambiguous
X-ray
USG Ultrasound diagnoses effusion and abscess, and may
guide puncture for bacteriology
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MRI It differentiates osteoarthritic from neurogenic osteo-
arthropathic lesions
Reserve it for ‘‘acute foot’’ with cellulitis
Examination of choice for diagnosing deep soft-tissue effusion and extension to tendon sheaths, and serves to guide surgical drainage
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Transcutaneous oxygenmeasurement (TcPO2)
40 mm Hg - For wound healing to occur
20 - 40 mm Hg - Impaired wound healing is noted
20 mm Hg - Failure of wound healing
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Charcot Neuropathy A chronic and progressive joint disease following loss
of protective sensation
leads to destruction of joints and surrounding bony structures
may lead to amputation if left untreated
Incidence
0.1-1.4% of patients with diabetes
7.5% of patients with diabetes and neuropathy
9-35% have bilateral disease
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No longer shows a warm and red foot, but
the edema usually persists
Rocker-bottom type deformity - cuboid becomes a
weight-bearing structure
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Ghost sign
Indicative of neuro-osteoarthropathy with superimposed osteomyelitis
Refers to poor definition of the margins of a bone on T1-weighted images, which become clear after contrast administration
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Organization of managementInternational Consensus on the Diabetic Foot,1999
Prevention and treatment of complications in diabetic foot should be organized at three levels
Level 1: GPs, nurses and podiatrists
Patient awareness of foot problems and prevention, and of early diagnosis of ulceration
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Level 2: Diabetologists, diabetology nurses, surgeons (general and/or vascular and/or orthopedic)
Management of basic preventive and curative care:
Level 3: Reference centers
Reference centers should be capable of close multidisciplinary teamwork between diabetologist, orthopedic surgeon and vascular surgeon, to manage the most difficult cases:
deep infected ulcer, severe arteriopathy, Charcot foot
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Treatment
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Prevention in at-risk feetGeneral measures
Optimal glycemic balance
Prevention of associated CVS risk
Smoking cessation
Specific measures
Podiatry
Orthoses
Adapted footwear
Patient education
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Footwear Plantar orthoses - Insoles have a
preventive and sometimes curative function
Basically, they distribute pressure, more rarely with corrective elements
Orthoplasties - Orthoplasties are little molded silicone devices that protect areas of conflict with the shoe (notably at the toes)
Shoes - Shoes are essential to prevention
They may be adapted mass-produced models, semi-therapeutic or made to measure orthopedic shoes
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Role of vascular surgery Amputation or orthopedic surgery should never be indicated
before precise assessment of lower limb vascular status
Comprises Doppler and if possible TcPO2 measurement
The main
revascularization
procedures are: distal
bridge, endovascular
techniques, stenting and
percutaneous
intentional extra-luminal
revascularization
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Foot ulcers without osteitis Managed non-surgically
Ambulatory basis in medical (diabetic podiatry) consultation (D1 and D2 on the PEDIS classification)
Non-weight-bearing for the affected foot and wound cleansing and dressing
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Foot ulcers without osteitisPostoperative shoes
BaroukTM forefoot or SanitalTM hindfoot pressure-relief shoes
Being removable to allow for dressings and avoid the hyperpressure points induced by cast immobilization, they entail a problem of strict compliance with non-weight-bearing
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Foot ulcers without osteitisOffloading casts
The Total Contact Cast (TTC)
Treatment for ulcer and acute Charcot foot
Aim - Achieve homogeneous pressure distribution in the plantar arch throughout the step: 30 to 50% of pressure is absorbed by the cast
Its non-removable 24/24 concept is fundamental to success, enabling healing in 70 to 85% of cases
Efficacy in terms of plantar pressure relief and healing is better in the fore- and mid-foot than in the hindfoot
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It should be changed weekly
The associated complications rate varies from 5 to 30%
Friction lesions liable to induce new infected wounds
Venous thrombosis
A and B. Protection of forefoot with Velband separating toes
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C. Leg and foot covered by stocking and then wadding.
D. Successive layers of plaster.
E. Resin reinforcement.
F. Device with absorbent sole to allow walking.
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G. Example of ulcer managed with Total Contact Cast
H. Result at 6 weeks
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Foot ulcers without osteitisFenestrated and/or removable casts (CROW)
(Charcot Restraint Orthotic Walker)
Enable the wound to be monitored, and reduce the risk of complications
It can also induce surrounding hyperpressure
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Foot ulcers without osteitisCommercial removable pneumatic casts (AircastTM)
They are a little less effective in offloading
removability can be countered by using resin tape
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Foot ulcers without osteitisWound cleansing
Begins with disinfection of the wound itself and the surrounding area
Polyiodine solutions are more effective than chlorhexidine and do not affect healing, while preventing the emergence of resistant bacteria (MRSA)
Limited debridement - to remove surrounding callosities
Remove any yellowish necrotic residue or fibrin
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Foot ulcers without osteitisDressing
Have a certain number of properties
Maintaining a humid microclimate,
Absorbing exudate
Protecting from bacterial contamination
Being replaceable without local trauma
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Foot ulcers without osteitisRole of surgery
In PEDIS D1 and D2 lesions, orthopedic surgery may be indicated to promote healing or avoid recurrence in resistant forefoot ulcer
Lengthening of the Achilles tendon, or sectioning the gastrocnemialaponeurotic lamina in case of ankle stiffness without dorsiflexion or even with slight equinus
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Metatarsal elevation osteotomy in case of hyperpressure caused by stasis disorder, or percutaneous distal osteotomy of the lateral metatarsals are possible, to relieve hyperpressure on a PPU
Scarf Osteotomy
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Foot ulcers with osteitis (PEDIS D3)
Requires prolonged antibiotherapy, generally beginning with a parenteral course
Multidisciplinary management may call on surgeons for revascularization, bone biopsy, bone curettage or minor amputation
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Foot ulcers with osteitisAmputation
Obtain a stump that can easily be fitted, to conserve as great a length as possible while
Enabling direct closure, and to conserve the patient’s autonomy
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Foot ulcers with osteitisPartial toe amputation
Avoid complete amputation - especially of the 2nd toe, that would induce or increase halluxvalgus
5th toe amputation - may induce 5th metatarsal head conflict and hyperpressure, as the lateral side of the foot
A ‘‘shark’s mouth’’ incision is preferable, conserving a more richly vascularized pulparflap
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Foot ulcers with osteitis
Transmetatarsal ray amputation
Alternative to complete toe amputation
Avoiding hyperpressure in the remaining head, which would induce recurrence
The 5th metatarsal should be osteotomized obliquely
Avoid hallux or even 1st ray amputation, which would impact the lateral rays, inducing claw toe
If necessary - 1st metatarsal length should be conserved as much as possible, so as to allow for possible secondary transmetatarsalamputation.
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Ray amputations
A. Aspect, cosmetic 2nd ray amputation
B. X-ray after 2nd ray amputation
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C. Ulcer with 5th toe osteitis
D. Limited cellulitis of 5th toe
E. 5th ray amputation
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Foot ulcers with osteitisTransmetatarsal amputation
Considered when it is not possible to conserve at least three metatarsals on the lateral rays or if the 1st ray is resected
It is associated to plantar extensor tenoplasty to avoid secondary equinus and conserve active motion in dorsiflexion
The level of amputation depends on the septic lesions:
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Skin incision is convex on the dorsal side, and the plantar flap needs to cover the entire resection area, as it constitutes a focus of pressure during walking and shoe-wearing
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Foot ulcers with osteitis
Mid- and hind-foot
More difficult
Amputation beyond the tarso-metatarsal Lisfranc joint line is less functionally satisfactory
Heavy antibiotherapy prolonged for several months
Surgery is complementary
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Foot ulcers with osteitisLisfranc amputation
It is important to conserve the peroneal tendon insertion (or to reinsert into the cuboid) and anterior tibial tendon
The 2nd metatarsal base, enclosed between the cuneiforms, should be conserved so as to conserve the proximal arc
Posterior tendon lengthening is often required, in order to avoid equinus
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Foot ulcers with osteitisChopart’s midtarsal amputation
results in secondary varus and equinus decompensation
There is no relative ischemia – anterior tibial and peroneus brevis tenoplasty(by anchors or transosseous reinsertion between the talar head and greater calcaneal apophysis)
With 2—3 cm resection of the Achilles tendon (avoid secondary equinus)
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Chopart’s amputation
A: Lesion secondary to emergency 2nd toe amputation in acute foot
B. 1st stage of amputation: 2 cm resection of Achilles’ tendon
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C. Amputation flaps
D. Tenoplasty of anterior tibial and peroneus brevis
tendons
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E. Immediate postoperative aspect
F. Result at 1 month
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Foot ulcers with osteitis
Partial or total calcanectomy
In case of loss of talar substance associated with calcaneal osteitis, partial or often total calcanealresection
The soft-tissue gain following bone resection often allows primary closure
A talar compensation orthosis is then required
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Foot ulcers with osteitis
Syme ankle disarticulation –
Is complex, with a risk of instability of the plantar soft tissues of the distal tibio-fibular stump
Severe infection or ischemia contraindicate this procedure
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Pirogoff-Boyd amputation -
Has the advantage of conserving sufficient limb length to avoid the need for orthoses in everyday life
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‘‘Acute’’ foot Covers ulcer associated with signs of severe
locoregional (PEDIS I3) and/or general infection (PEDIS I4)
‘‘cool’’ acute-foot lesions using parenteral empiric broad-spectrum bior tri-therapy
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Cellulitis
Amoxicilline—clavulanic acid ± aminoglycosides(gentamicin or netilmicin) or quinolones
Limb is threatened
Piperacillin—tazobactam + teicoplanin (or vancomycin or linezolid) + (quinolones)
Septic shock
Imipenem (or ertapenem) + (teicoplanin or vancomycin or linezolid) + (aminoglycosides)
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After 48—72 hours
locoregional and general infection evolution is reassessed, and indications for abscess debridement or iterative amputation are considered
Emergency gadolinium-enhanced MRI is very useful in acute foot to diagnose deep soft-tissue effusion and extension into tendon sheaths so as to guide surgical drainage
A revascularization procedure ahead of possible orthopedic surgery may be considered
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ConclusionOrthopedic surgeon plays a central role in providing a
biomechanical perspective
To avoid creating or leaving areas of hyperpressure that would induce recurrence of ulceration
In case of ulceration, scheduled surgery is preferable to emergency intervention, even in ‘‘acute’’ foot; lesions
should always be cooled by antibiotherapy, even if this has to be empiric
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Diabetic feet are high-risk neuropathic and vascular feet. Vascular assessment should always precede indication of orthopedic surgery. If vascular status is insufficient,
prior revascularization is mandatory
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