This document discusses wound diagnosis and treatment by etiology, focusing on arterial and venous wounds. It provides 3 key points:
1. Arterial wounds are caused by ischemia due to macrovascular or microvascular disease. They typically occur on the extremities and are evaluated using pulses, capillary refill time, ABI, and other vascular tests. Treatment involves revascularization or wound care to address ischemia.
2. Venous wounds account for about 70% of lower extremity wounds and are caused by venous insufficiency and hypertension. They usually occur in the gaiter area. Risk factors include DVT history, surgery, prolonged standing, and obesity.
3. Both arterial and venous wounds are evaluated based
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VenoStrong
The unique formula of a natural veinotonic VenoStrong is specifically created to ensure a broad-spectrum effect on the venous system and addresses all causes and manifestations of the venous insufficiency.
toskovicgoca@gmail.com
Does All Saphenous Reflux Need Ablation?Vein Global
By: Paul M. McNeill, MD, FACS
Visit VeinGlobal at http://www.veinglobal.com/ for more presentations and videos on this topic, or for more information on venous disease news, education and research.
Does All Saphenous Reflux Need Ablation?Vein Global
By: Paul M. McNeill, MD, FACS
Visit VeinGlobal at http://www.veinglobal.com/ for more presentations and videos on this topic, or for more information on venous disease news, education and research.
PHYSIOTHERAPY IN COMMON VASCULAR CONDITIONS.pptxKunjalPardeshi1
Vascular disease includes any condition that affects your circulatory system, or system of blood vessels. This ranges from diseases of your arteries, veins and lymph vessels to blood disorders that affect circulation.
Blood vessels are elastic-like tubes that carry blood to every part of your body. Blood vessels include:
Arteries that carry blood away from your heart.
Veins that return blood back to your heart.
Capillaries, your tiniest blood vessels, which link your small veins and arteries, deliver oxygen and nutrients to your tissues and take away their waste.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
3er Curso Latino Americano de Cicatrización Avanzada en Heridas (II)
1. 3 ER CURSO LATINO AMERICANO DE
CICATRIZACIÓN AVANZADA EN HERIDAS
2. WOUND DIAGNOSIS AND
TREATMENT BY ETIOLOGY
ARTERIAL, VENOUS, NEUROPATHIC/DIABETIC
Tammy Luttrell MSPT, PhD, CWS , FACCWS
Profesora Adjunto
Colorado Univerisity, Anschutz Medical Campus
National Jewish Health
3. WOUND HEALING PHASES
• Acute wounds heal by predictable and timely
course of events
• Hemostasis
• Inflammation
• Proliferation
• Granulation
• Epithelialization
• Remodeling
4. CHRONIC WOUNDS
“those wounds that fail to progress through a normal,
orderly, and timely sequence of repair or wounds
that pass through the repair process without
restoring anatomic and functional results”
Lazarus, GS, et al. (1994) Definitions and guidelines for assessment for
wounds and evaluation of healing. Arch of Derm. 130, 489-493.
5. CHRONIC WOUNDS
• Characteristics
• Necrotic tissue
• Bioburden
• Chronic inflammation
• Impaired hemodynamics
• Senescent fibroblasts and keratinocytes
• Chronic wound fluid with growth inhibiting proteases
• Overgrowth of epithelium with lack of underlying
connective tissue => rolled edges
6. DIAGNOSING WOUNDS
• By tissue involvement (to determine local
care)
• Superficial
• Partial thickness
• Full thickness
• By etiology (to determine systemic care)
• Arterial
• Venous insufficiency
• Neuropathic
• Pressure
• Atypical
8. ARTERIAL WOUNDS
• Caused by ischemia
• Usually located at the peripheral extremities
• Caused by macro- or microvascular disease
• Macro – obstruction of the larger named arteries by
PVD, embolus, thrombus, trauma
• Micro – disease of the small unnamed arterioles and
capillaries, usually with diabetes or small emboli after
some type of vascular surgery
9. PERIPHERAL VASCULAR DISEASE
• Arteriosclerosis
• abnormal thickening and hardening of the artery walls
• Smooth muscle cells and collagen fibers migrate into
the inner arterial wall and cause it to harden
• Atherosclerosis
• Arteriosclerosis in which fat and fibrin deposit on the
inner walls of the arteries
• Begins with a fatty streak and then becomes a fibrous
plaque
12. PVD – CRITICAL PHASES
1. Collateral circulation insufficient for metabolic needs =>
shunting of blood to muscles where there is less resistance
=> delayed healing of traumatic wounds
2. Claudication - pain with activity – most effectively
treated with exercise
a. thigh and buttock claudication = aortoiliac or
iliac involvement
b. calf claudication = femoral or popliteal
involvement
3. Rest pain – requires revascularization surgery
• May have “dependent leg syndrome”
• May be accompanied by signs of ischemia at distal digits
13. MICROVASCULAR DISEASE
• Occlusion of the small arteries too small to be
named (<0.5mm)
• Most frequently seen in patients with diabetes
• Cannot be treated with vascular surgery
• May result in non-healing wounds even after
revascularization
14. ARTERIAL WOUNDS
• Evaluation
• Pulses
• Capillary refill time
• Rubor of dependency
• Skin appearance – shiny, thin, pale, NO hair growth
• Condition of nails and hair
• Location – distal toes or fingers
• Edges – even, punched out appearance
• Tissue – dry, necrotic, little or no granulation
15. ARTERIAL SCREENING
• Pulses • Grading
• Upper extremity • 0 = no pulse
• Brachial • 1+ = barely felt
• Radial • 2+ = diminished
• Ulnar • 3+ = normal
• 4+ = bounding
• Lower extremity (indicative of
• Femoral aneurysm)
• Popliteal
• Dorsalis pedis Doppler signal is NOT
• Posterior tibialis equal to a palpable
pulse!!!
16. ARTERIAL SCREENING
• Rubor of dependency
• Elevate the lower extremity 45 , note slight blanching of
plant surface
• Place in dependent position, redness or rubor that takes 30
secs or more to occur
• Indicative of arterial disease, usually advanced
17. ARTERIAL SCREENING
• Capillary refill
• Detects microvascular disease
• Press the end of any toe for 2-3 seconds and observe for
blanching
• Normal refill is less than 3 seconds
21. BUERGER DISEASE
• Also known as thromboangiitis obliterans
• Disease of macrovascular circulation
• Occurs in feet and/or hands
• More common in men, especially heavy
smokers
• Pathology
• Inflammation of the peripheral arteries with thrombi
and vasospasm
22. BUERGER DISEASE
• Symptoms
• Pain and tenderness
• Redness
• Cyanotic skin
• Thin shiny skin
• Thick malformed nails
• Gangrene or ulcers (advanced cases)
Age may assist in diagnosis – usually younger than
typical patient with arterial wounds.
Arterial wounds in younger patients indicative of
some other pathology.
23.
24. INVASIVE TESTS FOR PVD
• Arteriogram
• Radiographs of
vascular system after
injection of
radiopaque dye
• Used to determine
specific site of lesion
prior to by-pass
surgery
25. NON-INVASIVE TESTS FOR
MACROVASCULAR DISEASE
• Ankle-brachial index
• Doppler arterial waveforms
• Ultrasound duplex scanning
• Ultrasound
• Doppler
• Color flow doppler scanning
• Great toe pressure
• Plethysmography (measures volume)
• Segmental blood pressure recordings
• Exercise stress test
26. ABI ---ANKLE BRACHIAL INDEX
(ABPI-ANKLE BRACHIAL PRESSURE INDEX)
• Where PLeg is the systolic blood pressure of dorsalis
pedis or posterior tibial arteries and
• PArm is the highest of the left and right arm brachial
systolic blood pressure
27. ANKLE-BRACHIAL INDEX
• Ratio of ankle systolic pressure to brachial systolic pressure
• Indicates the severity of PVD
• Interpretations
• 1.0– 1.2 – normal
• 0.8-1.0 – minimal peripheral arterial disease.
Compression for edema control is safe to use.
• 0.5-0.8 – moderate peripheral arterial disease, often
accompanied by intermittent claudication. Referral to
a vascular specialist is advised. Compression therapy is
contraindicated if <0.6; modified compression is
indicated if 0.6-0.8.
• <0.5 – severe ischemia with resting pain. Compression
therapy is always contraindicated.
• <0.2 – tissue death will occur.
28. Presión máxima tobillo
Indice
Presión en el tobillo-brazo = derechoPresión máxima
brazo derecho derecho brazo (mm Hg)
e izquierdo
Presión máxima
tobillo 92 mm Hg Obstrucción
= = 0.56= moderada
Presión braquial 164 mm Hg
máxima
Presión en la arteria Interpretación del índice
tibial posterior y calculado
pedia del tobillo Por encima de 0.90 – normal
derecho e izquierdo 0.71 – 0.90 – obstrucción leve
0.41 – 0.70 – obstrucción moderada
0.00 – 0.40 – obstrucción severa
N Engl J Med 355; august 3, 2006
29. ANKLE-BRACHIAL INDEX
• ABI > 1.3 is not reliable
• Frequently seen in diabetics
• Caused by calcification of the arteries resulting in
artificially high systolic pressure
• Great toe pressure and toe/brachial index used
instead of ABI
• Normal > 55 mmHg pressure
• Normal TBI – 0.8-0.99
• < 30 mmHg – pt will need revascularization
31. PREVENTION OF ARTERIAL WOUNDS
• No smoking
• Control blood sugars
• Control hypertension, hyperlipidemia,
hypercholesterolemia
• Provide proper foot care (Goodman, p454)
• Exercise (Goodman, p 455)
32. Cuidado Pre-Operatorio
No haga desbridamiento.
Mantenga el área seca; proteja los dedos con
algodón o gaza estéril entre ellos.
Use una cuna para los piés
Descargue los talones con
almohadas
Eschar management – Dry and intact, paint with
Betadine, use of dry topical silver. Eschar is the
“barrier” substitute.
Do not debride
Keep area dry; protect toes with
cotton or sterile gauze between toes
Use foot cradle
Off-load heels with pillows
33. Cuidado Pre-Operatorio
No haga desbridamiento.
Mantenga el área seca; proteja los dedos con
algodón o gaza estéril entre ellos.
Use una cuna para los piés
Descargue los talones con
almohadas
Disminuya elevación de la extremidad
Eleve la cabecera de la cama 5-7 grados
Mantenga la extremidad caliente
Evite ejercicio en exceso
34. TRATAMIENTO DESPUÉS DE CIRUGÍA
Desbride la herida con tejido necrótico
cuando haya tejido de granulación visible en
sus bordes. (D. Armstrong)
Provea un medio ambiente húmedo con el
apósito avanzado apropiado.
Proteja los piés con almohadas debajo de las
pantorrillas.
• Debride wound of necrotic tissue when granulation tissue is visible
at the edges (D. Armstrong)
• Provide moist wound environment with the appropriate advanced
dressing
• Protect foot with pillows under calves
38. TRATAMIENTO DESPUÉS DE CIRUGÍA
Descargue la herida con ortóticos, zapatos
especiales, dispositivos.
Controle el edema post-operatorio para
prevenir dehiscencia de sutura.
Cubra la incisión con gaza estéril seca
Aplique vendaje de corta elasticidad en forma de
espiral
• Off-load wound with orthotic, special shoes, assistive device
• Control post-op edema to prevent incisional dehiscence
• Cover incision with dry sterile gauze
• Apply short stretch elastic bandage in spiral wrap
39.
40.
41.
42. GIVE AND TAKE OF ARTERIAL
WOUNDS
• GIVE
• Blood supply
• Protection
• TAKE
• Any cause of trauma
• Necrotic tissue if signs of infection are
present
43. VENOUS WOUNDS
• Relate to ≈70% of LE wounds
• 500,000-1,000,000 in US
• 40% occur before the age of 50
• Recurrence rate is as high as 72%
• Estimated cost of care $40,000/case
44. VENOUS SYSTEM
• Superficial veins
• Great saphenous
• Small saphenous
• Deep veins
• Femoral
• popliteal
• Perforator veins
• Lymphatic system
45. CHRONIC VENOUS INSUFFICIENCY
• Causes
• Reflux as a result of incompetent valves in the perforator,
superficial, or deep veins
• Obstruction – e.g. chronic deep vein thrombosis
• Lack of venous pump activation during the gait cycle
• Dorsiflexion – calf muscles compress deep veins with up to 250
mmHg pressure
• Plantarflexion – deep vein pressure falls and allows blood to flow
from superficial veins to deep veins, through perforators
• Does not occur with ankle hypomobility or gastrocsoleus
weakness/paralysis
• Results in venous hypertension and excessive moisture in
the interstitial tissue
• Prevents adequate oxygen and nutrients from reaching the
skin
46. VENOUS PUMP
James, R et.al.: Incompetent venous valves: ultrasound imaging and exo-
stent repair
Phlebolymphology N°56
47. PATHOPHYSIOLOGICAL CHANGES
• Vessel dilatation and elongation
• Increased collagen deposition in both vein walls
and skin
• Plasma protein leaks into interstitial space with
resulting fibrin cuff around arterioles
• Increased leukocytes with decreased immune
function
• Increased inflammatory cells resulting in tissue
remodeling and dermal fibrosis
48. RISK FACTORS
• Hx of DVT (37%)
• Hx of hip/knee/calf surgery
• Ankle hypomobility/fusion
• Employment involving prolonged standing
• Morbid obesity
• Pregnancy
• Congestive heart failure
Systemic disorders will cause bilateral
edema; extremity dysfunctions will
cause unilateral edema.
49. PROGRESSION OF VENOUS DISEASE
• Heavy, aching
feeling in legs
• Telegentsia or
reticular veins
• Varicose veins
• Edema without
ulceration
• Skin changes
without ulceration
• Skin changes with
ulceration
50. COMMON SKIN CHANGES – CRITICAL IN
DIAGNOSING CVI
• Hyperpigmentation (hemosiderin)
• Lipodermatosclerosis
• Dilated long saphenous vein
• Atrophie blanche
• Unlateral or bilateral edema
• Dermatitis
• Thickened skin
• Cellulitis
56. VENOUS WOUND EVALUATION
• Girth of arch, malleoulus, calf
• Type and amount of drainage
• Edges (uneven) and location (gaiter,
above the ankle)
• Pulse exam/ABI in case of absent pulses,
severe pain, failure to heal with
standard care
• Other components of any wound
evaluation
57.
58.
59. VASCULAR TESTS - SCREENING
• Approximation of central venous pressure
• Screens for cardiac incompetence as cause of
edema
• Jugular distention
• Indicates right ventricular failure
• Valve competency with Doppler
• Percussion test for saphenous vein
competency
• Homan’s sign – not reliable
• Ankle-brachial index – r/o arterial component
60. VASCULAR TESTS/VALVE
COMPETENCY
• Place probe over
distended vein
• Compress vein 10-15 cm
proximally
• Audible sound (reflux)
means valves between
compression and probe
are incompetent
• Compress vein distal to
probe
• NO audible sounds
indicates venous
obstruction
61. TREATMENT - PREVENTION
• Compression hosiery
• Elevation (higher than heart)
• Exercise to activate venous pump
• Avoid prolonged sitting or standing
• Avoid crossing the legs
• Skin lubrication
62. COMPRESSION HOSE
• Class I
• 20-30 mmHg pressure
• Used for venous disease with skin changes
• Class II
• 30-40 mmHg pressure
• Used for history of ulceration or severe skin changes
• Class III
• 40-50 mmHg pressure
• Used for lymphedema, pts who reulcerate with Class II, pts who work
standing (e.g. dentists)
• Class IV
• > 60 mmHg pressure
TED hose used for DVT prophylaxis are NOT sufficient for
treatment of Chronic Venous Ulcers I!!!
68. LAPLACE EQUATION
• P = (TN x 4630) / CW
• P = pressure in mmHg
• T = bandage tension (in kgf)
• N = number of layers applied
• C = circumference of the limb (in cm)
• W = bandage width(in cm)
The pressure gradient between the ankle and calf makes the
compression effective in managing the edema.
74. INTERMITTENT COMPRESSION THERAPY
• Used as adjunct for wounds that do not
respond to other compression methods or for
maintenance in severe lymphedema
• Applies compression in sequence, distal to
proximal
• Pressure must be less than the diastolic BP
(usually ≈50 mmHg)
• Recommend 1-2 hours daily or bid, depending
on severity
75.
76. GIVE AND TAKE OF VENOUS
WOUNDS
• GIVE
• Protection
• Compression
• Exercise
• TAKE
• Edema
• Bacteria
• Devitalized tissue
77. DIABETIC / NEUROPATHIC WOUNDS
• Occur on the foot, usually plantar surface or toes
• Caused by mechanical forces or minor trauma
• Occur in patients with diabetes, PVD, or Hansen’s
disease because of peripheral neuropathies
78. INCIDENCE IN DIABETICS
• 18.2 million people in US have DM (6.3% of the total
population)
• In certain ethnic groups, % is as high as 14.5%
• 15% of people with DM will have neuropathic ulcer
• 14-24% of those with ulcer will have amputation
79. NEUROPATHIES
• Motor – muscle weakness => changes in the
shape of the foot => high peak pressures during
weight bearing activities
• Caused by damage to large nerve fibers
• Sensory – diminished sensation => lack of
protective sensation
• Caused by damage to small nerve fibers
• Autonomic – decreases sweat and oil
production => dry, inelastic skin
• Caused by damage to the large nerve fibers and the
sympathetic ganglion
80. COMMON FOOT DEFORMITIES
• Pes aquinas – short Achilles tendon
• Hallux limitus/rigidus
• Hallux valgus
• Hammer toes
• Cock-up deformity
• Varus deformities of toes
• Tailors bunion on 5th metatarsal head
• Charcot foot – collapse of arch
81. NEUROPATHIC WOUND
CLASSIFICATION
Wagner scale
• 0 – at risk due to skin and foot changes
• 1 – full thickness skin loss, no infection
• 2 – subcutaneous tissue loss, infection
• 3 – deep ulceration, infection, osteomyelitis or abscess
• 4 – partial foot gangrene or necrosis
• 5 – full foot gangrene
88. EVALUATION
• Risk factors
• Recent trauma, diet, footwear, poor foot hygiene, medications,
comobidities
• Subjective history
• Skin inspection
• Dry skin with fissures
• Calluses
• Discoloration in dermal layer (RBCs from deep injury)
• Lack of toe and dorsal hair
• Heel inspection
• Toe inspection
• Nail condition
• Interdigital spaces
• Foot deformities
• Shoe assessment
89.
90. EVALUATION
• Sensory assessment
• Vibration test
• Pressure assessment with Semmes-Weinstein
monofilaments
• Skin temperature - 3 discrepancy is significant
• Reflexes
• Musculoskeletal assessment, especially ROM
• Dorsiflexion - 10
• Hallux extension – 50-60
91. PREDICTORS OF COMPLICATIONS
• Semmes-weinstein monofilaments
• 3.61 (0.4g) = normal
• 5.07 (10g) = loss of protective sensation
• 6.10 (100g) = total loss of sensation
• Vibration
• 128 Hz tuning fork
• Measures only yes/no response
• Test end of great toe, medial malleolus, tibial
tuberosity
• Reflexes
• Diminished due to large motor nerve involvement
• Predictable pattern (LE>UE, distal>prox,
symmetrical pattern)
92. NON-INVASIVE VASCULAR ASSESSMENT
• Pulses
• Capillary refill time
• Ankle brachial index
• May be unreliable in diabetic if >1.3
• Great toe pressure
• Normal is 60-90% of the brachial pressure
• Normal TBI is 0.8-0.99
• Exercise stress test
• Transcutaneous oxygen tension
• Color flow Doppler imaging
93. TREATMENT - PREVENTION
• Patient education
• Blood glucose control
• Properly fitting shoes
• Nail and callus care
• Skin care
• Diabetic or molded shoes if foot
deformities are severe
95. PROPER FOOT CARE
• Properly fitting shoes
• Daily foot inspection
• Check for red spots, blisters, calluses
• Use mirror or family member if necessary
• Proper foot care
• Never walk barefoot
• Avoid soaking and hot surfaces
• Lubricate skin well
• Do not use adhesives on skin
• Wear thick white cotton socks
• Cut nails straight across
96. TREATMENT OF WOUNDS
• Treat infection (systemic vs topical)
• Revascularize if needed
• Control blood sugars
• Debride wound
• Provide moist wound environment
• OFF-LOAD
• Pressure redistribution
• Special shoes, total contact casting, assistive devices
4 categories are largely a division of convenience: Treatment algorithms, reimbursement, research/literature, and statistical data are organized accordingly.