DIABETIC ULCERS OF THE LOWER EXTREMITY. Scott Silver, MD Department of Vascular Surgery. William Beaumont Hospitals

Transcription

1 DIABETIC ULCERS OF THE LOWER EXTREMITY By Scott Silver, MD Department of Vascular Surgery William Beaumont Hospitals

2 Introduction Scott M. Silver MD General Surgery Resident at University of South Carolina Vascular Fellowship at Detroit Medical Center Practice Vascular and Endovascular Associates at WBH

3 Practice Make-up What I thought I would be doing... What I am actually doing Really cool stuff...5% Open Arterial Surgery...15% Dialysis Access...10% Venous disease...15% Endovascular Surgery...30% Limb Salvage...25%, this is increasing

4 Age Adjusted Rate of Diabetics

5 Objectives Emphasize the growing problem of diabetic foot disease Introduce the pathophysiology of the diabetic foot wound Outline a comprehensive approach to limb salvage in the diabetic patient Promote early recognition of diabetic wounds

6 Scope of the Diabetic Problem Increased from 3% to 11% of population over 30 years...approximately 33 million people 20% of diabetic patients will be admitted to the hospital for a foot infection/wound Diabetic foot infections and wounds are always limb threatening

7 Pathophysiology of the Diabetic Foot Multifactoral- To many to cover in ½ hour Neuropathy Ischemia Infection Discussed separately, occur simultaneously

8 Diabetic Neuropathy Affects Autonomic and Somatic Nervous System Autonomic: peripheral nervous system that controls involuntary functions Somatic: peripheral nervous system that controls voluntary functions

9 Mechanism of Nerve Injury Vascular Theory Observational data demonstrates thickening of nutrient vessels of the nerves Metabolic Component Sorbitol Pathway: Increased metabolism results in increased production of toxic metabolites yielding demyelination Neurotrophic Factors Observed decrease in the diabetic patient

10 Mechanism of Nerve Injury Increased Protein glycosylation observed with blood sugars greater than 140

11 Diabetic Neuropathy: Autonomic Sweat gland stimuli is diminished Decreased antibacterial Dry cracked skin due to diminished oil and moisture

12 Diabetic Neuropathy: Autonomic Arterial Venous Shunting of Micro-circulation Decreased regulation of vasodilatation and constriction yielding ischemia due to shunting Diminished response to areas of increased metabolic need. Minor injury, pressure and infection. Relative local ischemia in the absence of PVOD

13 Diabetic Neuropathy: Autonomic Nocioceptive Reflex: afferent activity produced in the peripheral and central nervous system to noxious stimuli Diabetics have diminished Nocioceptive reflex

14 Diabetic Neuropathy:Nocioceptive Reflex Reflex: Sensory fibers>central Nerve Cell body(spinal cord)>axon Branches >Substance P >Mast Cells to release histamine> Vasoactive >Initiates wound/injury response

15 Diabetic Neuropathy: Somatic Decreased tonic neural stimulation of the intrinsic muscles of the foot Leads to atrophy of muscles Long flexors of calf relatively increased tone Affects digital stability at MTP joint

16 Diabetic Neuropathy: Somatic Toes are drawn upward MTP pushed downward Abnormal pressure points at MTP, dorsum and tips of toes

17 Diabetic Neuropathy: Sensory Diminished sensation to pain High pressure: Penetrating injury such as pebbles in shoe, needles. Low pressure: Repetitive stress at pressure points due to walking and standing Thermal injury Unrecognized fractures Diminished Proprioception Foot deformity resulting in abnormal pressure points

18 Diabetic Neuropathy Classic hammering of the toes Abnormal weight bearing on tips of toes Diminished sensation

19 Diabetic Neuropathy: Summary Clawed/Hammer toes Pronounced arch Dry/cracked skin Atrophy of intrinsic muscles of foot

20 Diabetic Neuropathy: Summary Abnormal pressure points and pressure relief yielding callus Diminished pain sensation Diminished response to injury

21 Diabetic Infection: Rapid Tissue Loss Intact skin is the bodies first and best defense against infection Diabetic neuropathy leaves skin prone to injury Skin breakdown is an open portal for entry of bacteria

22 Diabetic Infection: Rapid Tissue Loss Hyperglycemia is immunosuppressive Diabetics have diminished response to infection and injury Reduce neurogenic inflammatory response Inability to direct blood to areas of increased metabolic demand Skin is more resistant to ischemia and infection than underlying structures. This results in loss of subcutaneous tissue with minimal visible skin defect

23 Diabetic Infection: Rapid Tissue Loss

24 Diabetic Infection: Classification Minimally limb threatening All diabetic foot wounds can be limb threatening Superficial ulcer with partial thickness skin defect and underlying dermis intact i.e. blistering or abrasion No bone, tendon or subcutaneous tissue exposure No signs of systemic infection: Hyperglycemia, tachycardia, fever, lymphangitis, purulent drainage, necrotic tissue, crepitus

25 Diabetic Infection: Classification Minimally limb threatening No evidence of severe ischemia Cultures demonstrate aerobic gram-positive cocci i.e. staph or strep

26 Diabetic infection: Classification Limb threatening Deep ulcer involving subcutaneous fat, joint, tendon or bone Presence of necrotic skin or subcutaneous tissue

27 Diabetic Infection: Limb Threatening Wound associated with significant or severe ischemia Signs of systemic infection Cellulitis Lymphangitis Fever Hyperglycemia Rigors

28 Diabetic Infection: Classification Limb threatening Cultures demonstrate polymicrobial infection Gram-positive staph and strep not uncommon Gram-negative: Escherichia coli, Proteus Anaerobes: Peptostreptococcus, Bacteroides and clostridium Chronic ulcers: Enterobacter and Pseudomonas

29 Diabetic Ulcer: Ischemic Most ischemia is due to the macro vascular occlusion Microvascular small vessel disease False Concept Originated from microscopic evaluation of amputated limbs of diabetic patients. Periodic acid shift positive material found occluding arterioles...arterioloslerosis. Goldberg et al

30 Diabetic Ulcer: Ischemia Microvascular small vessel disease Strandness et al. Prospective study comparing diabetic and nondiabetic patient's demonstrated no diabetic associated arteriole occlusive disease Supported by years of equivalent patency of lower extremity bypass graft and limb salvage in a diabetic patient

31 Diabetic Ischemia Diabetic occlusive disease is most commonly present in the proximal tibial and peroneal arteries The foot vessels are usually spared

32 Diabetic Ulcer: Management Wound inspection Determine severity of ulcer i.e. inpatient versus outpatient management Palpate the entire foot for fluctuance and crepitus Unroofing probe all wounds and calluses

33 Diabetic Ulcer: Management Infection control Excisional debridement of non-viable skin and subcutaneous tissue Send tissue for cultures Empiric treatment with antibiotics Foot x-rays

34 Diabetic Ulcer: Management Local wound care Never used wet to dry dressings Silvadene SoloSite Santyl Dakin solution Acetic acid solution

35 Diabetic Ulcer: Management Nonweightbearing and pressure relief

36 Diabetic Ulcer: Offload

37 Diabetic Ulcer: Offload Wound

38 Diabetic Ulcer: Management Smoking cessation Diabetic control with a goal of a hemoglobin A1c less than 7.0 Foot and skin hygiene: Daily inspection, moisturizer, Dove or Ivory Soap Edema control Leg elevation above the level of heart Compression stockings versus compressor grip

39 Diabetic Ulcer: Management Arterial reconstruction Angioplasty Bypass graft Hyperbaric oxygen therapy Wagner grade 3 wound Chronic refractory osteomyelitis