DIABETIC FOOT

• The diabetic foot, is one of the most feared complications of

diabetes.
• Diabetic foot is characterized by a classical triad of
neuropathy, ischemia, and infection.
• Preventing the diabetic foot should be the first priority.
• This can be achieved by identifying the high-risk individuals,
like those with peripheral neuropathy, peripheral vascular
disease, foot deformities, and presence of callus.
• Diabetic foot: infection, ulceration or destruction of tissues of
the foot associated with neuropathy and/or peripheral artery
disease in the lower extremity of a person with (a history of)
diabetes mellitus.
Pathogenesis
• Multi-factorial and Complex
1. Neuropathy
2. Vasculopathy
3. Immune dysfunction

Prolonged hyperglycemia contributes to all the above factors

through different mechanisms
neuropathy
• Sensory neuropathy
-Loss of pain sensation – Unnoticed trauma (thermal,
chemical, mechanical) – progression of lesion unchecked –
callous formation – tissue necrosis & damage beneath callus –
development of cavities filled with serous fluid – erupt into
surface – results in ulcer formation
• Motor neuropathy
-weakness and wasting of intrinsic foot muscles – foot
deformities – abnormal gait - ulceration
• Foot deformities predisposing to ulceration
- Clawed toes; bunions; nail deformities; deformities from
previous trauma or surgery; ankle equinus; Pes cavus; pes
planus; charcot foot; hallux rigidus; hallux varus / hallux
Valgus; hammer toe
• Autonomic neuropathy
- Decreased sweating – dry & brittle skin – fissures/cracks –
secondary infection - ulceration
Factors contributing to foot ulceration
1. Intrinsic factors
- Bony prominences, limited joint mobility, deformities, callus
formation, previous foot ulcer, neuropathy (charcot)
2. Extrinsic factors
- Walking barefoot, inappropriate foot ware, falls and
accidents, objects inside shoes, thermal trauma, activity level
Vasculopathy
• There is macro and microangiopathy
1. Macroangiopathy
-Atherosclerosis of large arteries – occlusive narrowing - ischemia
2. Microangiopathy
-increased thickness of basement membrane of capillaries – functional
AV shunting

Decreased local blood flow - ischemia - poor antibiotic penetration, -

poor wound healing – in the end amputation
Immune dysfunction
• Impaired defences against infection
-decreased polymorphonuclear leukocyte migration
-decreased phagocytosis
-decreased intracellular killing
-decreased chemotaxis
Clinical Presentation
• HISTORY
• PHYSICAL EXAMINATION
History
• The history should focus on the signs and symptoms of a
diabetic foot ulcer or pre-ulcerative lesion.
• Symptoms indicative of possible peripheral neuropathy or
peripheral arterial insufficiency should also be investigated.
In the diagnosis of diabetic foot ulcers or pre-ulcerative
lesions, the following should be taken into account:
• History of trauma
• History of puncture wound (with or without shoe gear)
• History of change in shoe gear
• History of deformity, either acquired or congenital
• History of callus or blister
• History of wound care management
• History of offloading – (a non-removable knee-high offloading device OR a
removable knee-high or ankle-high offloading device.
• Local signs of infection
• Systemic signs of infection
Symptoms of peripheral neuropathy
• Hypoesthesia
• Hyperesthesia
• Paresthesia
• Dysesthesia
• Radicular pain
• Anhidrosis
Symptoms of peripheral arterial
insufficiency
• Most patients are asymptomatic; others develop ischemic
symptoms.
- intermittent claudication, ischemic pain at rest, nonhealing
ulceration of the foot, or frank ischemia of the foot.
- In some cases, a fissure, ulcer, or other break in the integrity
of the skin envelope is the first sign that loss of perfusion has
occurred.
Features of Diabetic foot infection
• Fever, chills, rigors, tachycardia, swelling, discharge, loss or
decreased function, inter-digital web (fungal infection),
cellulitis, tissue necrosis, abscess, osteomyelitis, gangrene
Physical Examination
• Physical examination of the extremity that has a diabetic ulcer can be
divided into different categories:
-Examination of ulceration
-Examination of the feet
-Assessment of the possibility of vascular insufficiency
-Assessment for the possibility of peripheral neuropathy

• Remember that diabetes is a systemic disease. Hence, a

comprehensive physical examination of the entire patient is also vital.
Examination of ulceration

• Determine the location of the ulceration

• Measure the size, including the depth of the wound
• Describe the wound base (granular, fibrotic, necrotic, eschar)
• Inspect for probing to bone
• Inspect for any undermining or tunneling of the wound
• Describe any drainage
• Describe the periwound area (maceration, hyperkeratotic tissue)
Examination of feet

• Inspect the static posture of the feet on the examination table, as well
as when weight-bearing.
• ​Assess for gross deformities and determine if they are reducible or
rigid
• Assess ankle range of motion using the Silfverskiöld test - If there is
limited ankle dorsiflexion (cannot pass neutral) with the knee both
flexed and extended, it is considered gastrocsoleal tightness; if there is
increased dorsiflexion with the knee flexed, however limited with the
knee in extension, it is considered gastrocnemius equinus
• Assess range of motion at the interphalangeal joints,
metatarsophalangeal joints, midtarsal joints, and subtalar
joints
• Evaluate muscle power of dorsiflexors, plantar flexors,
invertors, and evertors to identify any muscular imbalances
• Examine the skin for dryness and fissures, as well as for
discrete calluses; hemorrhagic calluses in particular are a sign
of impending foot ulceration.
Assessment of possible peripheral arterial
insufficiency
• Physical examination discloses absent or diminished peripheral pulses
below a certain level.
• Diminished common femoral artery pulsation is characteristic of
aortoiliac disease
• loss of the femoral pulse just below the inguinal ligament occurs with
a proximal superficial femoral artery occlusion.
• Loss of the popliteal artery pulse suggests superficial femoral artery
occlusion, typically in the adductor canal.
• Loss of pedal pulses is characteristic of disease of the distal popliteal
artery or its trifurcation.
• Other findings suggestive of atherosclerotic disease include a
bruit heard overlying the iliac or femoral arteries, skin
atrophy, loss of pedal hair growth, cyanosis of the toes,
ulceration or ischemic necrosis, and pallor of the involved
foot followed by dependent rubor after 1-2 minutes of
elevation above heart level.
Assessment of possible peripheral
neuropathy
• Signs of peripheral neuropathy include 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 (10g Semmes-Weinstein
monofilament) test helps diagnose the presence of sensory
neuropathy.
• A turning fork (128 Hz, detects loss of vibratory sensation).
• Light touch test (Ipswich touch test can be used to screen for
loss of protective sensations.
• 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.
Diagnostic Considerations/DIFFERENTIAL
Diagnosis
• The classic diabetic trophic ulcer must be distinguished from various other
problems that tend to occur in persons with diabetes, such as diabetic
dermopathy, bullosis diabeticorum, eruptive xanthoma, necrobiosis lipoidica,
and granuloma annulare.
• The leg pain of peripheral arterial disease must be distinguished from other
causes of leg pain, such as arthritis, muscle pain, radicular pain, spinal cord
compression, thrombophlebitis, anemia, and myxedema.
• Diabetic neuropathy should be distinguished from other forms of neuropathy,
including vasculitic neuropathies, metabolic neuropathies, autonomic
neuropathy, radiculopathy, and many others.
• Should be differentiated from skin and soft tissue infections like: Gas gangrene,
Cellulitis.
• Inflammatory disorders like: pyoderma gangrnosum, necrobiosis lipoidica
• Bone infections like osteomyelitis
• Sickle cell disease: can result in painful leg ulcers commonly on medial and lateral
malleoli
• Drugs: eg warfarin, heparin, hydroxyurea can result in ulcer formation.
• Malignancy: can present as cutaneous ulcers but systemic signs and symptoms (fever,
weight loss, malaise, etc) are also usually present. Eg Kaposi Sarcoma,
Basal Cell Carcinoma, Cutaneous B-Cell Lymphoma, Cutaneous T-Cell Lymphoma
• Pressure sores
• Chronic venous insufficiency: causing varicose veins and limb edema and with ulcer
formation
• Bone tumour
•JESUS CHRIST IS LORD OF ALL
•ACTS 10:36