Two main Complications of Hyperglycemia Ischemia Neuropathy
Predisposing peripheral vascular disease Atherosclerosis (medium-sized vessels below the knee)
Compromised blood supply
Ischemia
Coagulative necrosis
Ulcer Ischaemic toes due to artherosclerosis
Infection
Dry gangrene
Wet gangrene
Neuropathy Neuropathy
Sensory
Motor
Muscle wasting Foot weakness Postural deviation
↓ nociception
Deformities, stress and shear pressures
Trauma
↓ Proprioception, Unawareness of foot position
Stress on bones & joints Plantar pressure
Callus formation
Ulcer
Autonomic
Reduced sweating
Dry skin
Fissures and cracks
Infection
Activation of Protein Kinase C Intracellular hyperglycaemia
Stimulates de novo synthesis for diacylglycerol (DAG)
Activates PKC
Downstream effects: •Production of vascular endothelial growth factor •Increased vasoconstriction •increased deposition of extracellular matrix and basement membrane material •Production of plasminogen activator inhibitor •Production of proinflammatory cytokines
Disturbance in polyol pathway Hyperglycemia
increase IC glucose (eg: nerves, lens, kidney, blood vessels)
metabolize by aldose reductase
sorbitol (polyol)
Fructose Accumulated sorbitol & fructose
NADPH used up during polyol pathway
Increase IC osmolarity
Decreased GSH (Reduced glutathione)
Influx of water
Cells susceptible to oxidative stress
Osmotic cell injury
Oxidative cell injury
Nerve Da
Diffentiation of Ischaemic and Neuropathy Ulcer
Symptoms
Inspection
Palpation Ulceration
Ischaemia
Neuropathy
Claudication
Usually painless
Rest pain
Or painful neuropathy
Dependent rubor
High arch + clawing of toes
Trophic changes
No trophic changes
Gangrenous digits
Surrounded by callus
Cold
Warm
Pulseless
palpable pulses
Painful
Painless
At the distal and over
Sites of pressures
Claw toe
Severe atrophy of the intrinsic foot muscles (lumbrical & interossei) d/t motor neuropathy resulted in imbalance of foot muscles & cocked-up toes.
Neuropathic foot ulcer
Callus formation on its surrounding ulcer lesion.
Infection • Individuals with DM have a greater frequency and severity of infection. • Reasons: – abnormalities in cell-mediated immunity and phagocyte
•
function – diminished vascularization – Hyperglycaemia aids the colonization and growth of a variety of organisms (Candida and other fungal species). Common pathogens:
• Combined with local ischemia, insensitivity to skin injury and localized pressure d/t deformity, more susceptible to infection
Clinical presentation of diabetic foot
Ischemic foot ulcer
Foot ulcers
Charcot Joint • Diabetic neuropathy is the most common cause.
• An acute Charcot’s foot will have swelling, erythema, raised skin temperature, joint effusion and bone resorption in an insensate foot
Charcot Joint
Rocker bottom charcot foot
Dry Gangrene
Wet Gangrene
Gangrene • Gangrene is a condition that involves the death and decay of tissue, usually in the extremities due to loss of blood supply. Dry gangrene
Wet 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
• Bacterial infection
– dark brown, then – dark purplish-blue, then – completely black
• copious tissue liquefaction • offensive odor • swollen, red and warm. • usually develops rapidly due to blockage of venous and/or arterial blood flow
• Treatment is surgical debridement and amputation.
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