Diabetic Foot Ulcer Guide

Mahnoor Rahman
Diabetic Foot and Ulcer
Department of Surgical Oncology

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Introduction
Diabetic foot disease (DFD) is a major global burden for patients and
health care systems and is one of the most serious complications of
diabetes mellitus.
It encompasses infection, ulceration, and osseous destruction of the
foot of a person with diabetes.
It is frequently accompanied with peripheral arterial disease (PAD), and
neuropathy, which play a central role in the disease.

 Approximately 12% of diabetics have foot ulcers
 Most common medical complication causing diabetics to get medical
treatment
 Foot ulcers are responsible for ~85% of lower extremity amputations

Etiology
 The three pathogenetic mechanisms involved in diabetic foot
complications are
Neuropathy Angiopathy/Ischaemia Infection

 Atherosclerosis and diabetic peripheral neuropathy are the two main
causes leading to a complication of diabetes such as ulcers.
 Atherosclerosis leads to decreased blood flow in large and medium-sized
vessels secondary to thickening of capillary basement membrane, loss of
elasticity, and deposition of lipids within the walls. Further arteriosclerosis
leads to small vessel ischemia.
 >60% of diabetic ulcers have decreased blood flow due to peripheral
vascular disease

 Peripheral neuropathy affects the sensory, motor, and autonomic nervous
system. There are multifactorial causes such as vascular disease occluding
the vasa nervorum, endothelial dysfunction, chronic hyperosmolarity, and
effects of increased sorbitol and fructose.
 Starts distally and migrates proximally in “stocking” distribution
 Large fibre loss – light touch and proprioception
 Small fibre loss – pain and temperature

• Peripheral motor neuropathy: Abnormal foot anatomy and biomechanics,
with clawing of toes, high arch, and subluxed metatarsophalangeal joints,
leading to excess pressure, callus formation, and ulcers
• Peripheral sensory neuropathy: Lack of protective sensation, leading to
unattended minor injuries caused by excess pressure or mechanical or
thermal injury
• Peripheral autonomic neuropathy: Deficient sweating leading to dry,
cracking skin

• Neuro-osteoarthropathy deformities (i.e., Charcot disease) or limited
joint mobility: Abnormal anatomy and biomechanics lead to excess
pressure, especially in the midplantar area

• Vascular (arterial) insufficiency: Impaired tissue viability, wound healing,
and delivery of neutrophils
• Hyperglycemia and other metabolic derangements: Impaired
immunological (especially neutrophil) function and wound healing and
excess collagen cross-linking

Presentation
 A diabetic foot ulcer presents as a skin sore with full thickness skin loss
often preceded by a haemorrhagic subepidermal blister. The ulcer typically
develops within a callosity on a pressure site, with a circular punched out
appearance. It is often painless, leading to a delay in presentation

 History of trauma, puncture wound, change in shoe gear,
deformity, either acquired or congenital, history of callus or blister
 Signs of infection – local and systemic signs of infection
 Symptoms of neuropathy include hypoesthesia, hyperesthesia,
paresthesia, dysesthesia, and radicular pain.
 Vascular insufficiency - most patients are asymptomatic. However,
may present with intermittent claudication, rest pain, and healing or
non-healing ulcers.

Physical exam
 Examine the skin for dryness and fissures, as well as for discrete calluses;
hemorrhagic calluses in particular are a sign of impending foot ulceration.
 Measure the size, including the depth of the wound
 Describe the wound base (granular, fibrotic, necrotic, eschar)
 Depth of ulcer
 Inspect for any undermining or tunneling of the wound
 probe for bone
 probed to look for extension into bone, sinus tract, joint and tendon sheath. Probe hitting
bone signifies possible underlying osteomyelitis.

 Presence of infection
 look for cellulitis, pus
 check for gangrene
 Describe any drainage
 Describe the periwound area (maceration, hyperkeratotic tissue)

 Assess Achilles tendon tightness
 Silverskiöld test
 improved ankle dorsiflexion with knee flexed = gastrocnemius tightness
 equivalent ankle dorsiflexion with knee flexion and extension = Achilles
tightness
 circulation
 assess dorsalis pedis , posterior tibialis pulses
 Changes of ischemia: Skin atrophy; nail atrophy, abnormal wrinkling,
diminished pedal hair - suggestive of atherosclerotic disease

Vascular assessment
 To evaluate the extent of occlusive vascular disease and in the assessment of
healing potential, especially when clinical examination suggests lower extremity
ischaemia
• Doppler segmental artery pressures
• Ankle-brachial indices (ABI) - Normal value 1.1, <0.9 abnormal
• Transcutaneous oxygen tension (TcPO2) - <10mmHg correlates with non-healing, >30mmHg correlates
with healing
 Any abnormal results of the above investigations in the presence of a non-
healing foot ulcer warrant a vascular assessment. Determination of distal run-off
and perfusion can be assessed by arteriography, digital subtraction angiography
(DSA) or magnetic resonance angiography (MRA)

Assessment of possible peripheral neuropathy
 Loss of vibratory and position sense, loss of deep tendon reflexes
(especially loss of the ankle jerk), trophic ulceration, foot drop,
muscle atrophy, and excessive callous formation, especially
overlying pressure points such as the heel.

 The nylon monofilament test helps diagnose the presence of sensory
neuropathy. A 10-gauge monofilament nylon is pressed against each specific
site of the foot just enough to bend the wire. If the patient does not feel the wire
at 4 or more of these 10 sites, the test is positive for neuropathy.
Testing sites and application. The nine plantar sites are the distal great
toe; third toe; fifth toe; first, third, and fifth metatarsal heads; medial foot,
lateral foot, and heel; and one dorsal site

Classification

Brodsky Depth-Ischemia Classification

Investigations
 CBC
 Serum Inflammatory Markers, Glycohemoglobin (HbA1C)
 X-Ray/Ultrasound: Performed for the detection of the spread of the lesion and soft
tissue involvement.
 MRI: Radiologic evaluation involves plain radiographs in two-thirds of the views
assessing for deformity.If there is suspicion of osteomyelitis, tendonitis, or joint
inflammation MRI imaging should be performed.
 Bone Scan: Can identify the involvement of deep wounds.
 Biopsy and Culture: Specimen of bone and other tissue involved and histopathological
examination is performed with the culture. This can also guide antibiotic treatment in
case of a bacterial infection.

• Venous Ulcers: It is caused by chronic elevation of venous pressure leading to
incompetent valves, varicose veins and lower limb edema. Leakage of plasma proteins
and leukocytes causing edema and free radical damage. The most common locations are
the pretibial area and above the medial malleolus. Usually, a shallow ulcer with irregular
borders and overlying fibrinous exudate is present.

 Diabetic Dermatopathy: These are purplish, round asymptomatic lesions
that usually occur in the lower extremities but can be present anywhere on
the body of diabetic patients. These lesions usually require no intervention.


 Malignancy:- Different malignancies can present as cutaneous ulcers but
systemic signs and symptoms ( fever, weight loss, malaise, etc) are also
usually present. The diagnosis can be confirmed by microscopic
examination of the biopsy specimen.
BCC SCC

 Superficial Thrombophlebitis: Characterized by pain, erythema,
tenderness overlying inflamed and thrombosed superficial veins.

 Leukocytoclastic Vasculitis: Inflammation of blood vessels and
surrounding tissues caused by the deposition of immune complexes.

• Gouty Arthritis: Monosodium urate crystal deposits in joints can result in
inflammation, usually associated with hyperuricemia.
• Infection: Primary infectious ulcer results either by direct inoculation or systemic
spread. Clinical features vary with the types of infection.
• Sickle Cell Disease: Sickle cell disease can result in painful leg ulcers commonly on
medial and lateral malleoli.
• Drugs:-Some drugs e.g, warfarin, heparin, hydroxyurea can result in ulcer formation

Management
 Precise diabetic control is in achieving resolution of the current
wound, and also in minimizing the risk of recurrence.
 Management of contributing systemic factors, such as
hypertension, hyperlipidemia, atherosclerotic heart disease, obesity,
or renal insufficiency, is crucial.
 Management of arterial insufficiency, treatment of infection with
appropriate antibiotics, offloading the area of the ulcer, and
wound care are also essential.

Offloading
 For patients with a neuropathic plantar ulcer, a nonremovable knee-high
offloading device—ie, either a total contact cast (TCC) or a removable
walker that is rendered irremovable by the provider who fits the device—is
the preferred offloading treatment
 Nonplantar foot ulcers, depending on their type and location, should be
addressed with a removable, ankle-high offloading device, footwear
modifications, toe spacers, or orthoses

Restoration of tissue perfusion
• When ankle pressure is below 50 mmHg or the ankle brachial
index (ABI) is less than 0.5, urgent vascular imaging and, in the
presence of appropriate findings, revascularization, should be
considered;
• Revascularization should also be considered if the toe pressure is
below 30 mmHg or the transcutaneous pressure of oxygen (TcpO 2)
is less than 25 mmHg; however, revascularization may be
considered at higher pressures should extensive tissue loss or
infection occur
• If optimal treatment does not result in ulcerative healing signs
within 6 weeks, revascularization should be considered,
regardless of the outcomes of these tests

 Pharmacologic treatments have not been proven to benefit perfusion
 Smoking cessation, hypertension and dyslipidemia control, and
antiplatelet drug use, as the means to reduce cardiovascular risk,
should be emphasized

Treatment of infection
 For a superficial ulcer with limited soft tissue (mild) infection –
 Debridement of all necrotic tissue and surrounding callus;
 start empiric oral antibiotic therapy directed against Staphylococcus
aureus and streptococci

 For deep or extensive (potentially limb-threatening) infection
(moderate or severe infection) –
 The need for surgical intervention to remove necrotic tissue, including
infected bone, should be urgently evaluated, and compartment pressure
should be released or abscesses drained;
 assess for peripheral artery disease (with urgent treatment, including
revascularization, to be considered if such disease is present);
 Start empiric, parenteral, broad-spectrum antibiotic therapy

Local ulcer care
 Goals of wound care and dressings
 provide moist environment
 absorb exudate
 act as a barrier
 off-load pressure at ulcer
• Foot soaking may cause skin maceration and so should not be
employed
• Negative pressure (VAC) should be considered as an aid to healing
postop (clean) wounds

• Dry wounds: Hydrocolloid dressings, such as DuoDERM or
IntraSite Hydrocolloid, are impermeable to oxygen, moisture, and
bacteria; maintain a moist environment; and support
autolytic débridement. They are a good choice for relatively
desiccated wounds.
• Exudative wounds: Absorptive dressings, such as calcium
alginates (eg, Kaltostat, Curasorb), are highly absorptive and are
appropriate for exudative wounds. Alginates are available in a rope
form, which is useful for packing deep wounds.
• Very exudative wounds: Impregnated gauze dressings (eg,
Mesalt) or hydrofiber dressings

 Wounds covered by dry eschar: In this case, simply protecting the
wound until the eschar dries and separates may be the best
management.
 Fragile periwound skin: Hydrogel sheets and nonadhesive
forms are useful for securing a wound dressing when the
surrounding skin is fragile.
 Other topical preparations: Platelet-derived growth factors
(PDGF) promote healing of diabetic foot ulcers in healthy,
granulating wounds
 Enzymatic debridement: helps remove nonviable tissue from the

Reconstructive foot and ankle surgery
 Reconstructive surgery can be considered when nonremovable
knee-high offloading devices are failing to achieve wound
healing, when the patient is unable to transition from knee-high
offloading devices to custom diabetic orthopedic shoes/insoles due
to recurring pressure, or in the setting or pre-ulcerative
lesions/calluses in the neuropathic patient.
 The goal is to rebalance the foot and create a plantigrade foot
that distributes pressure appropriately.
 Surgical options include arthroplasties, osteotomies, resection,
arthrodesis, tenotomies, tendon transfers, and tendon lengthening.

 Treatment of Charcot foot
 Neuropathic osteoarthropathy - A progressive, non infective, destructive,
lesion of bone and joints resulting from a fracture or dislocation or both in a
patient with peripheral neuropathy.
 Charcot foot is treated initially with immobilization using special shoes or
braces but eventually may require podiatric surgery such as ostectomy and
arthrodesis.

Vascular reconstruction
 The indications for vascular surgery in the presence of a
reconstructible arterial lesion include intractable pain at rest or at
night, intractable foot ulcers, and impending or existing
gangrene.
 Intermittent claudication alone is only infrequently disabling and
intractable enough to warrant bypass surgery.

Options for Soft Tissue Coverage
 Delayed primary closure for chronic, well-vascularized - clean but
nonhealing wounds
 Expedite healing by a surgical procedure.
 Surgical options include skin grafting, application of bioengineered
skin substitutes, and flap closures.
 Autologous split-thickness skin graft is the criterion standard for
viable coverage of a full-thickness granular wound.
 Principle : Clean tissues and tension-free apposition; it usually
requires undermining and mobilization of adjacent tissue planes by
creation of skin flaps, local muscle flaps, or myocutaneous flaps.

Hyperbaric Oxygen Treatment
 Hyperbaric oxygen therapy is used rarely and is certainly not a
substitute for revascularization.
 In the presence of an intractable wound and associated
noncorrectible ischemic arterial disease, hyperbaric oxygen therapy
may be beneficial in selected cases.
 Data are equivocal

 Glycemic control is imperative
 Smoking cessation, hypertension and dyslipidemia control, and
antiplatelet drug use, as the means to reduce cardiovascular risk,
must be emphasized
 Medication such as Cilostazol and Pentoxifylline may be
recommended for symptoms of intermittent claudication

 Early detection and multidisciplinary treatment can help in decreasing
complications. Timely interventions and consultations with the following
are recommended:
• Endocrinologist
• Infectious disease specialist
• Vascular surgeon
• Podiatrist
• Orthopedic surgeon
• Plastic surgeon

Long-Term Monitoring
 LOPS = Loss of protective sensation
 PAD = Peripheral arterial disease
Risk category Definition Suggested follow-up
0 No LOPS, no PAD, no deformity Annually
1 LOPS ± deformity Every 3–6 months
2 PAD ± LOPS Every 2–3 months
3 History of ulcer or amputation Every 1–2 months

Diabetic Foot Ulcer Guide

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