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DIABETIC FOOT byDr. Li Wei Hao
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Diabetic foot characteristicsSensory neuropathie.Motor neuropathie.
Autonomic neuropathies: maylead to islands of cutaneousischaemia,
caused by alterations in bloodflow
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Foot deformities.Alteration of pressure distribution.
Ulcerations & Infections.Classical "mal perforans" ulcer.
Caused by loss of sensation & painless
trauma.Can occur in absence of ischaemia.Frequently heals with conservative
measures.Aggressive wound management.
Unweighting
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Diabetes mellitus importantrisk factor
Diabetic vasculopathy:
sustained by macroangiopathy ,sustained by impairment inflow in small vessels,
sustained by innervation ofvascular bed.
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Basic mechanism of problem woundsTissue hypoperuIision, ischaemia & infection ,
Ischaemia caused by hypoperfusion.Defective cellular immunity.
Defective humoral immunity.Synergistic effect of ischaemia & impairedimmune response .
Atherosclerosis.
Decreased chemotaxis.Decreased phagocytosis.Decreased chemotactic response.Reduced inflammatory reaction.Abnormal lymphocytic function
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Areas of low flow & hypoxiaEven possible in presence of palpable arterial pulses.
Feet & ankles.Contributing factors:
increased blood viscosity,decreased red blood cell deformability,
platelet aggregation,accelerated capillary endothelial growth,hypoperfusion possible mechanism of injury to
subendothelial area of vessels,
capillary wall hyalinization leading to capillary obstruction.Even restored circulation can fail wound healing.Non-diabetics respond to local tissue stress with
inflammation .Diabetics respond to local tissue stress with thrombosis &
necrosis
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Hyperbaric oxygen in woundhealing
Fundamental role of oxygenin physiology of wound
healing .Hypoxia impairs woundhealing.
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Hypoxia impairs leucocyte bacterial
killing functionDiabetic wounds are polymicrobial.High incidence of anaerobic organisms.
HBO:Increases killing ability of leucocytesLethal to certain anaerobic bacteria.Inhibits toxin formation by certain
anaerobes
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Oxygen tension determinant of wound healingTcpO2 in non-healing diabetic wounds:
Far below wound healing level.Breathing 100 % O2 not enough.
HBO:TcpO2 elevation .
TcpO2 levels stay above baseline next 3 - 4hours.Generation of oxygen free radicals.
No increase tissue damage .
No vasoconstrictive effect in ischemic or hypoxic tissue
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Perfusion delivery ofoxygen to wound area
Many factors causeimpaired oxygenation indiabetic foot
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HBO:Oxygen delivery along partial pressure
gradient.Increases flexibility of red blood cells.Acts synergistically on blood flow with
pentoxifylline .Reduces tissue edema .
Preserves intracellular adenosinetriphosphate .
Maintains tissue oxygenation in absence of
hemoglobin .Stimulates fibroblast growth.Increases collagen formation & deposition.Promotes more rapid growth of capillaries
Terminates lipid peroxidation
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HBO can not:Substitute surgicalrevascularization inadvanced arterial
insufficiency.Reverse an inadequatemicrovascular circulation
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PathophysiologyHBO is application of physical
laws in a knownpathophysiologic process.
Indication is pathophysiology
of local & focal hypoxia.HBO is able to reverse hypoxia
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When to consider HBO indiabetic foot ulcers?Foot & ankle ulcers with
Wagner grading 3, 4 or 5.Amputation seems
unavoidable
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Classification of problem wounds
Wagner grading system .later adapted by Boulton .0 obvious ulcer in a foot at risk.
5 gangrene of whole foot.Ulcers grades 1 - 3 tend to beneuropathic.
Ulcer grades 4 & 5 are mainlyvascular
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Wounds unsuccessfully treated for weeks
or months:Local wound care.Surgical d bridements.
Antibiotics.Reconstructive vascular surgery.
Adequate metabolic control of diabetesmellitus.
Control of infection.Non-invasive vascular evaluation.Angiographic vascular evaluation.
Judge peripheral perfusion.
If possible arterial reconstructive surgery
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Transcutaneous oxygen mappingPatient selection by oxygenchallenge test:
Measure TcpO2 while breathingnormoxic air.100 % normobaric O2 advocated.100 % hyperbaric O2 advocated
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Successful wound healing afteramputation .
TcpO2 > 40 mm Hg required.TcpO2 > 100 mm Hg all wounds healed.
Wound aggravation .TcpO2 < 100 mm Hg no improvement.
Great likelihood healing .TcpO2 > 400 mm Hg
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Healing chances :TcpO2 < 5 mm Hg healingchances 0% amputation.
TcpO2 > 20 mm Hg healingchances 20 %.
TcpO2 > 35 mm Hg healingchances
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Indication for HBOtreatment .
Lille Consensus meeting 1994100 % O2 breathing at 2,5ATA.
Toe TcpO2 > 30 mm Hg.Ankle TcpO2 > 75 mm Hg
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HBO selection criteria ( 8).Jefferson C. Davis Wound Care & Hyperbaric Medicine Center.
San Antonio, Texas.Normoxic air breathing.IF TcpO2 > 40 mm Hg.
THEN no HBO.Normoxic air breathing.
IF TcpO2 10 - 40 mm HgTHEN test 100 % O2 breathing at 1 ATA.IF TcpO2 rise > 50 %
THEN HBO.Normoxic air breathing.
IF TcpO2 < 20 mm HgTHEN test 100 % O2 breathing at 1 ATA.IF TcpO2 rise = 0%.
THEN no HBO amputation unavoidable
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TcpO2 value predicts wound healing .
Literature review by Matos and Nu ez. 350 patients.
161 healthy volunteers.Objective criterium.Reliable method to predict wound
healing.Determine level of amputation in
advance.
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