DIABETIC FOOT

Dr. Li Wei Hao

by

Diabetic foot characteristics Sensory neuropathie. Motor neuropathie. Autonomic neuropathies: may lead to islands of cutaneous ischaemia, caused by alterations in blood flow

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

Diabetes mellitus important risk factor Diabetic vasculopathy: sustained by macroangiopathy , sustained by impairment in flow in small vessels, sustained by innervation of vascular bed.

Basic mechanism of problem wounds Tissue hypoperuIision, ischaemia & infection , Ischaemia caused by hypoperfusion. Defective cellular immunity. Defective humoral immunity. Synergistic effect of ischaemia & impaired immune response . Atherosclerosis. Decreased chemotaxis. Decreased phagocytosis. Decreased chemotactic response. Reduced inflammatory reaction. Abnormal lymphocytic function

Areas of low flow & hypoxia Even 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

Hyperbaric oxygen in wound healing Fundamental role of oxygen in physiology of wound healing . Hypoxia impairs wound healing.

Hypoxia impairs leucocyte bacterial killing function Diabetic wounds are polymicrobial. High incidence of anaerobic organisms. HBO: Increases killing ability of leucocytes Lethal to certain anaerobic bacteria. Inhibits toxin formation by certain

anaerobes

Oxygen tension determinant of wound healing TcpO2 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 - 4 hours. Generation of oxygen free radicals. No increase tissue damage . No vasoconstrictive effect in ischemic or hypoxic tissue

Perfusion delivery of oxygen to wound area Many factors cause impaired oxygenation in diabetic foot

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 adenosine triphosphate . Maintains tissue oxygenation in absence of hemoglobin . Stimulates fibroblast growth. Increases collagen formation & deposition. Promotes more rapid growth of capillaries Terminates lipid peroxidation

HBO can not: Substitute surgical revascularization in advanced arterial insufficiency. Reverse an inadequate microvascular circulation

Pathophysiology HBO is application of physical laws in a known pathophysiologic process. Indication is pathophysiology of local & focal hypoxia. HBO is able to reverse hypoxia

When to consider HBO in diabetic foot ulcers? Foot & ankle ulcers with Wagner grading 3, 4 or 5. Amputation seems unavoidable

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 be neuropathic. Ulcer grades 4 & 5 are mainly vascular

Wounds unsuccessfully treated for weeks or months: Local wound care. Surgical dbridements. Antibiotics. Reconstructive vascular surgery. Adequate metabolic control of diabetes mellitus. Control of infection. Non-invasive vascular evaluation. Angiographic vascular evaluation. Judge peripheral perfusion. If possible arterial reconstructive surgery

Transcutaneous oxygen mapping Patient selection by oxygen challenge test: Measure TcpO2 while breathing normoxic air. 100 % normobaric O2 advocated. 100 % hyperbaric O2 advocated

TcpO2 predictive value for HBO outcome 188 patients with diabetic leg or foot ulcers . TcpO2 < 20 mm Hg. Significantly more ulcers. Significantly more amputations

Successful wound healing after amputation . 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

Healing chances : TcpO2 < 5 mm Hg healing chances 0% amputation. TcpO2 > 20 mm Hg healing chances 20 %. TcpO2 > 35 mm Hg healing chances

Indication for HBO treatment . Lille Consensus meeting 1994 100 % O2 breathing at 2,5 ATA. Toe TcpO2 > 30 mm Hg. Ankle TcpO2 > 75 mm Hg

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 Hg THEN test 100 % O2 breathing at 1 ATA. IF TcpO2 rise > 50 % THEN HBO. Normoxic air breathing. IF TcpO2 < 20 mm Hg THEN test 100 % O2 breathing at 1 ATA. IF TcpO2 rise = 0%. THEN no HBO amputation unavoidable

TcpO2 value predicts wound healing .

Literature review by Matos and Nuez. 350 patients. 161 healthy volunteers. Objective criterium. Reliable method to predict wound healing. Determine level of amputation in

advance.

ALL WORK and NO PLAY; MAKES a dull DOCTOR