Approach to the Patient with (suspected) Arterial Insufficiency Related Ulceration Elisa C. Taffe, MD, CWSP Vascular Medicine Medical Director Allegheny General Advanced Wound Healing and Lymphedema Center
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Name that wound!!
Case 1
Case 2
Case 3
Case 4
Case 5
Arterial Anatomy
Angiosomes
Blood Vessel Anatomy
Definition of Atherosclerosis A form of arteriosclerosis in which plaques develop on the inner walls (intima/endothelium) of the arteries Athere from the Greek- gruel Skleros from the Greek- hard So hard gruel-filled arteries
Pathophysiology of Atherosclerosis
Epidemiology Atherosclerosis begins in childhood Autopsy studies of young adults All had atherosclerotic plaques
Epidemiology of Atherosclerosis Leading cause of mortality worldwide Over 400,000 admissions to the hospital per year in the US $10.4 billion per year in hospital costs
Relative 5-year Mortality Rates 100 86 80 Patients (%) 60 40 20 8 18 23 32 39 0 Prostate Cancer* Hodgkin's Disease * Breast Cancer* PAD Colorectal Cancer* Lung Cancer* *American Cancer Society. Cancer Facts and Figures, 2000. Criqui MH et al. N Engl J Med. 1992;326:381-6.
The heart matters in diabetes: 10-Year outcomes of peripheral artery disease Mueller, TM,. 2017 PMID: 29163948
5-Year PAD Outcomes 100 80 73 PAD Patients (%) 60 40 20 16 7 4 0 Stable Claudication Worsening Claudication Leg Bypass Surgery Major Amputation Adapted from Weitz Jl. Circulation. 1996;94:3026-49.
Histology Fatty streak Thickening of the intima, accumulation of lipid-rich macrophages, smooth muscle cells Fibrous cap atheromas Lipid core, overlying acellular cap Vasa vasorum fragile blood vessels Advanced lesions Calcified Plaque rupture
Fatty Streak
Advanced Lesions
Pathogenesis of Atherosclerosis Endothelial Dysfunction Infection Atheromatous plaque Inflammation Flow characteristics of vessels Dyslipidemia
Endothelial Dysfunction Primarily the result of oxidized low density lipoproteins (LDL) Results in increased expression of adhesion molecules which lead to increased monocyte/macrophage adhesion Increased levels of LDL result in increased O 2 free radicals which inactivate NO leading to vasoconstriction Other risk factors have similar effect
Inflammation Macrophages (scavenger white blood cells) take up oxidized LDL Results in the release of cytokines, MMPs, growth factors, interleukins, etc
LDL in Atherosclerosis Direct endothelial damage Alteration in vascular tone Recruitment of monocytes/macrophages Foam cell formation Induction of growth factors Increased platelet aggregation Formation of autoantibodies to oxidized LDL
Flow Characteristics Within Vessels Loss of laminar flow at bends, branches and bifurcations Decreased shear stress leads to altered endothelial function Increased adhesion of monocytes
Infection Total number of pathogen exposures vs. specific pathogen exposures HOPE study odds ratio of 1.62 of cardiovascular event occurring for those evidence of infection with 4 pathogens vs those with 0 Organisms capable of causing chronic infections Chlamydia, CMV, HIV, H. pylori, Periodontal disease (multiple additional organisms)
Risk Factors Age Gender Dyslipidemia Tobacco abuse Diabetes Hypertension Family history
Symptoms Asymptomatic +/- ulceration Claudication +/- ulceration Latin: claudicatio to limp Rest pain +/- ulceration
Physical Exam Pulse exam Femoral Inguinal crease, 2-3 cm lateral to the pubic tubercle Popliteal Slight passive knee flexion, use both hands Dorsalis pedis Palpate simultaneously Use all fingers Posterior tibial Palpate simultaneously, Posterior and inferior to medial malleolus
Physical Exam Temperature Color Dependent rubor Skin changes Loss of hair, thin, shiny, atrophic skin
Physical exam Dependent Rubor
Arterial Ulcerations
Acute Arterial Occlusion Pain Pallor Pulselessness Paresthesia Paralysis
Diagnostic Testing
Diagnostic Testing Non Invasive Vascular Testing Indirect Physiologic Testing Duplex Evaluation
Indirect Physiologic Evaluation Plethysmography (air, photo) Pulse Volume Recording Detection of limb volume change Segmental Limb Pressures 5 cuff, 3 cuff method Always consider the presence bypass grafts and stents!!
Normal Segmental Pressures
Normal Pulse Volume Recordings
Abnormal Segmental Pressures
Abnormal Segmental Pressures
Indirect Physiologic Testing >1.4 Noncompressible 1-1.4 Normal 0.91-0.99 Borderline 0.8-0.9 Mild 0.5-0.79 Moderate <0.5 Severe
Duplex Evaluation Direct imaging Duplex B-Mode Doppler Sensitivity for detection of hemodynamically significant lesions 70-90% Use for patients with bypass grafts, trauma, dissections, stents
Normal Duplex
Abnormal Duplex with Stenosis
Abnormal Duplex with Limited Flow
Abnormal Duplex
Additional Imaging Techniques Non-Invasive CTA MRA Invasive Angiography
Case 1
Case 1 64 yo female with PMHx of PAD, Hep C, tobacco abuse Exquisitely painful lower abdominal, left medial thigh and gluteal cleft wounds 15 years prior right iliac stent Admitted recently with difficulty ambulating, urinary incontinence, numbness in a saddle distribution Extensive inpatient work up
Case 1 ABI 0.4 on the right, 0.3 on the left CTA occlusion of the abdominal aorta and iliac vessels with collaterals reconstituting the internal and external iliac arteries Ultimately underwent bilateral axillaryfemoral bypass
Case 2
Case 2 84 yo without PMHx, very active Left lateral distal calf/ankle wound Developed after scratching the area Present for a year, told she might have a blockage Diminished pedal pulses on exam, surrounding hemosiderin staining, no claudication
Case 2
Case 2 Angiogram severe tibial disease with occlusion of the anterior and posterior tibial arteries. Stenosis of the proximal peroneal angioplasty Venous reflux testing reflux of GSV and SSV Anomalous anatomy with the GSV originating laterally in the area of the wound Ablation and phlebectomy
Case 3
Case 3 91 yo with PMHx of osteoarthritis,??ra, ITP Developed a right shoulder injury and compression fractures Unable to sleep in bed, legs dependent all day, edema developed, then wounds. Superficial macerated wounds bilaterally Moderate to severe edema Absent pulses
Case 3
Case 3 Angiogram demonstrated severe tibial occlusive disease with occlusion of the anterior and posterior tibial arteries
Case 4
Case 4 53 year old referred from her podiatrist with a non-healing right ankle wound with unknown etiology PMHx of poorly controlled DM, hyperlipidemia, CVA,PAD Exam: normal pulses Wound closed, reopened 2 months later, loss of pedal pulse Non-invasive testing: ABI: 0.67, DBI: 0.29
Case 4 Angiography: PTA of right SFA, popliteal and anterior tibial arteries Pedal pulse exam normal, pain improved, wound improving again
Case 5
Case 5 74 yo female with a history of remote left lower extremity DVT Presented with a heavily draining left leg wound Normal pulse exam, hemosiderin staining
Case 5 Venous leg ulcer!!!!!!!!
Thank you! Questions??