Diabetic Foot

Two main Complications of Hyperglycemia

Predisposing peripheral vascular diseaseAtherosclerosis (medium-sized vessels below the knee)Compromised blood supplyCoagulative necrosisDry gangreneInfectionWet gangreneIschemiaUlcer

NeuropathyNeuropathyMotorSensoryAutonomic nociception Proprioception,Unawarenessof foot positionReduced sweatingDry skinFissures andcracksMuscle wastingFoot weaknessPostural deviationDeformities, stressand shear pressuresTraumaStress on bones & jointsPlantar pressure

Callus formation

InfectionUlcer

Activation of Protein Kinase CIntracellular hyperglycaemiaStimulates de novo synthesis for diacylglycerol (DAG)Activates PKC Downstream effects:Production of vascular endothelial growth factor Increased vasoconstrictionincreased deposition of extracellular matrix and basement membrane materialProduction of plasminogen activator inhibitor Production of proinflammatory cytokines

Disturbance in polyol pathwayHyperglycemiaincrease IC glucose(eg: nerves, lens, kidney, blood vessels)metabolize by aldose reductasesorbitol (polyol)Fructose

Accumulated sorbitol & fructoseIncrease IC osmolarityInflux of waterOsmotic cell injury NADPH used up during polyol pathwayDecreased GSH (Reduced glutathione)Cells susceptible to oxidative stressOxidative cell injuryNerve Damage

Diffentiation of Ischaemic and Neuropathy Ulcer

Claw toeSevere atrophy of the intrinsic foot muscles (lumbrical & interossei)d/t motor neuropathy resulted in imbalance of foot muscles & cocked-up toes.

Neuropathic foot ulcerCallus formation on its surrounding ulcer lesion.

InfectionIndividuals with DM have a greater frequency and severity of infection. Reasons: abnormalities in cell-mediated immunity and phagocyte function diminished vascularizationHyperglycaemia 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 JointDiabetic neuropathy is the most common cause.

An acute Charcots foot will have swelling, erythema, raised skin temperature, joint effusion and bone resorption in an insensate foot

Charcot JointRocker bottom charcot foot

Gangrene Dry gangreneno infectionlittle tissue liquefactionIn early stages, dull, aching pain, extremely painful to palpate, cold, dry and wrinkled.In later stages, skin gradually changes in color todark brown, thendark purplish-blue, thencompletely black

Wet gangreneBacterial infectioncopious tissue liquefactionoffensive odorswollen, red and warm.usually develops rapidly due to blockage of venous and/or arterial blood flowGangrene is a condition that involves the death and decay of tissue, usually in the extremities due to loss of blood supply.Treatment is surgical debridement and amputation.

****Firm evidence was set forth that proinflammatory cytokines, especially the receptor activator of the nuclear factor-B (RANK) ligand (RANKL) system is responsible for abnormally intense osteoclastogenesis (4). Increased osteoclastic activity is indicated for the excessive and unsupported bone turnover

Furthermore, the neurovascular theory relates to the increase in peripheral blood flow that is responsible for the weakening and the osteopenia found in the Charcot foot, causes bone resorption and demineralization. This increased perfusion is due to the loss of vascular sympathetic tone associated with the autonomic neuropathy.

It is the result of a combination of motor, autonomic, and sensory neuropathies in which there is muscle and joint laxity that lead to changes in the arches of the foot. Further, the autonomic denervation leads to bone demineralization via the impairment of vascular smooth muscle, which leads to an increase in blood flow to the bone with a consequential osteolysis. An illustration of some commonly described abnormalities*A prospective study conducted in Singapore with 202 diabetic patients revealed that 42.1% of the patients had sensory neuropathy and 2% of them had Charcot arthropathy (29). The incidences of Charcot foot in type 1 and type 2 diabetes do not differ, although osteopenia, as a predisposing factor, appears to be more prevalent in type 1

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3733015/**