This document outlines an overview of pressure ulcers including their definition, risk factors, classification, diagnosis, treatment and prevention. Pressure ulcers are localized injuries to the skin and underlying tissue that are usually over bony prominences due to pressure or pressure in combination with shear and friction. They are caused by both extrinsic factors like pressure, friction and shear as well as intrinsic factors like advanced age, malnutrition and altered mental status. Treatment involves controlling risk factors, dressing wounds, and sometimes surgery for advanced cases. Prevention focuses on proper positioning, pressure dispersion and skin care.
NILOFAR LOLADIYA
MSN: OBGY
Pressure ulcers (also known as pressure sores or bedsores) are injuries to the skin and underlying tissue, primarily caused by prolonged pressure on the skin. They can happen to anyone, but usually affect people confined to bed or who sit in a chair or wheelchair for long periods of time.
t is widely believed that other factors can influence the tolerance of skin for pressure and shear, thereby increasing the risk of pressure ulcer development. These factors are protein-calorie malnutrition, microclimate (skin wetness caused by sweating or incontinence), diseases that reduce blood flow to the skin, such as arteriosclerosis, or diseases that reduce the sensation in the skin, such as paralysis or neuropathy. The healing of pressure ulcers may be slowed by the age of the person, medical conditions (such as arteriosclerosis, diabetes or infection), smoking or medications such as anti-inflammatory drugs.
NILOFAR LOLADIYA
MSN: OBGY
Pressure ulcers (also known as pressure sores or bedsores) are injuries to the skin and underlying tissue, primarily caused by prolonged pressure on the skin. They can happen to anyone, but usually affect people confined to bed or who sit in a chair or wheelchair for long periods of time.
t is widely believed that other factors can influence the tolerance of skin for pressure and shear, thereby increasing the risk of pressure ulcer development. These factors are protein-calorie malnutrition, microclimate (skin wetness caused by sweating or incontinence), diseases that reduce blood flow to the skin, such as arteriosclerosis, or diseases that reduce the sensation in the skin, such as paralysis or neuropathy. The healing of pressure ulcers may be slowed by the age of the person, medical conditions (such as arteriosclerosis, diabetes or infection), smoking or medications such as anti-inflammatory drugs.
Diabetic foot and Foot care
Dr Joel Arudchelvam
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Lymphoedema is an abnormal swelling of limb due to the collection of excessive amount of high protein fluid secondary to defective lymphatic drainage in the presence of normal capillary filteration.It is very disabiling condition to the patient. In this ppp I have discussed its clinical picture and management in a simple way
Diabetic foot and Foot care
Dr Joel Arudchelvam
Definition
Prevalence
Teaching Hospital Anuradhapura [THA]
High risk foot
Neuropathy
Pathogenesis of neuropathy
Charcot foot
Testing for neuropathy
Local Ulcer care
wound management briefing training course including wounds, wound healing & wound types, wound closure, wound covers, wound dressings and marketing plan for new product launch, wound assessment types and measures.
for HCP , wound care specialists, nursing, and wound care and health associations
Include infections of skin, subcutaneous tissue, fascia, and muscle, encompass a wide spectrum of clinical presentations, ranging from simple cellulitis to rapidly progressive necrotizing fasciitis.
Diagnosing the exact extent of the disease is critical for successful management of a patient of soft tissue infection
Lymphoedema is an abnormal swelling of limb due to the collection of excessive amount of high protein fluid secondary to defective lymphatic drainage in the presence of normal capillary filteration.It is very disabiling condition to the patient. In this ppp I have discussed its clinical picture and management in a simple way
Esophagoscopy continues to be a reliable diagnostic and therapeutic tool with a wide variety of applications, including biopsy, dilatation of strictures, repair of Zenker's diverticulum, placement of stents, and retrieval of foreign bodies.
Management Of Malignant Salivary Gland Tumors Take note of the peculiarities
Management Of Malignant Salivary Gland Tumors Take note of the peculiarities
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
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ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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
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
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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.
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
5. Introduction
Definition:
• National Pressure Ulcer Advisory Panel (NPUAP) and European
Pressure Ulcer Advisory Panel (EPUAP) defined pressure ulcers as
“localized injury to the skin and/or underlying tissue usually over a
bony prominence as a result of pressure, or pressure in combination
with shear and/or friction”
6. Historical perspective
• Pressure ulcers are an ancient problem, observed in bodies found preserved by
mummification in Egypt
• Ambrose Pare in 16th century enlisted ; nutrition, pain relief and debridement as
key factors for pressure ulcers to heal
• Sir James Paget in 1873 recognized the effect of eternal pressure on the
cutaneous circulation and the skin necrosis that ensued if the pressure was not
relieved
• John Staige Davies was the first to suggest replacing unstable scar with flap tissue
in 1938
• Lamon described the first closure of open pressure sore in 1945
• Kostrubala and Greenley recommended excision of bony prominences and
padding the exposed bone with local fascia or muscle flap in 1947
7. Epidemiology
• Highest incidences
-Elderly patients with femoral neck fractures (66%)
-Quadriplegic patients (60%)
-Neurologically impaired young (spinal cord injury [SCI] and
veterans)
-Chronic hospitalization and on palliative care
8. Epidemiology cont’d
• Prevalence
• General acute care setting: 10%-18% (15%)
• Long-term care facilities: 2.3%-28% (15%)
• Home care setting: 0%-29% (15%)
• Incidence
• General acute setting: 0.4%-38%
• Long-term care facilities: 2.2%-23.9%
• Home care setting: 0%-17%
• Over 60,000 death per year
9. Epidemiology cont’d
• Constitute about 25% of total cost of whole patient care
Susceptible areas
Majority of pressure sores
Developed over the bony
Prominence in the lower part
Of the body
Bony prominences
Ischial tuberosity (28%)
Trochanter (19%)
Sacrum (17%)
Heel (9%)
Scalp
10. • Statement of surgical importance
• A major cause of patient morbidity, prolonged hospital stay,
depression, representing a major health burden and drain on
resources
• IT’S PREVENTABLE
12. Risk assessment
• The first step in prevention of pressure ulcers is evaluation of risk
• Several scales have been devised but the Braden scale is widely used
A composite of 6 subscales
1. Sensory perception
-Ability to respond meaningfully to pressure-related discomfort
- Scored 1-4
2. Skin moisture
- Degree to which skin is exposed to moisture
- Scored 1-4
13. Risk assessment
3. Activity
- Degree of physical activity
- Scored 1-4
4. Mobility
- Ability to change and control body position
- Scored 1-4
5. Friction and shear- scored 1-3
6. Nutritional status
- Usual food intake
- Scored 1-4
14. Risk assessment
• Minimum value of 6 and maximum of 23
• Lower scores- increase risk of pressure ulcer development
• Higher scores- decrease risk of development
• Threshold score
- 16 tertiary care facilities
- 19 in veterans hospital
- 18 in skilled nursing care facilities
• Norton scale- used in geriatrics ( 5 greatest risk, 20 least risk)
• General physical condition, mental status, activity, mobility, incontinence
• Nutritional status- Gosnell scale ( modified Norton)
16. Pathology
• Pathogenesis
• Extrinsic and intrinsic factors work together
1. Extrinsic factors
a. Pressure
• Mechanical force/ unit area perpendicular to plane
• Tissue deformation, mechanical damage, blockage of vessels- deep
necrosis
• Pressure of twice the arterial capillary pressure (32mmHg) for 2 hours
produce irreversible ischemia
17.
18. Pathology
b. Friction
• Resistance to movement between two surfaces
• Outermost skin layer lost, resulting in increased water loss ->
increased coefficient of friction
• Most often during patient transfer
c. Shear
• Mechanical stress parallel to tissue plane
• Stretches or compresses muscles perforators to the skin resulting in
ischaemia
19. Pathology
2. Intrinsic factors
• Local ischaemia or fibrosis -> decrease tissue perfusion
• Infection/sepsis -> decrease tissue perfusion
• Decrease autonomic control -> excess perspiration, spasms, and lack
of bladder or bowel control
20. Pathology
• Increased age- decreased skin moisture, tensile strength, increased
skin friability
• Anaemia- decrease wound healing capability and weakness or fatigue
-> prolonged immobilization
• Altered level of consciousness- loss of protective reflexes or voluntary
movement to off-load pressure
• Sensory loss- absent feeling of discomfort from prolonged pressure
• Malnutrition- decrease ability to heal wound
• Vascular disease- PVD, diabetes, smoking
21. Pathology
• Pathophysiology
• High degree of pressure can be tolerated when evenly distributed
• Soft tissue compression (> 32mmHg ) results in ischaemia -> necrosis
-> ulceration
• Accelerated by infection/inflammation, oedema
• Muscles necrosis occur after 4 hours whereas skin after 12 hours
22. Pathology
• Natural history
1. Hyperemia is observed within less than 30 minutes of pressure
• Disappears within an hour after pressure relieve
2. Ischaemia – continuous pressure for 2-6 hours
• Redness requires at least 36 hours to completely disappear after
relieve of pressure
3. Necrosis-unrelieved pressure within 6 hours
• Skin becomes bluish and indurated areas can be felt
23. Pathology
4. Ulceration- within 2 weeks following development of necrosis
typically in bony prominences
• However, other factors (friction, shear) may influence this sequence
• Grade 1 & 2- typically friction and shear
• Grade 3 & 4 may be primarily pressure-time component
24. Classification
Different classification systems exist
• National Pressure Ulcer Advisory Panel developed a four stage
classification
• Modifications- Shea’s and Yarkony-Kirk
• Shea’s- presence of large cavities accessible only through small
sinuses
• Yarkony-Kirk- subclassifies grade 1 and identifies the tissue at the
base of the wound in grade 2 through 6
25. National Pressure Ulcer Advisory Panel Shea classification Yarkony-Kirk classification
Stage I: Non-blanchable erythema
of intact skin; the heralding lesion of
skin ulceration
1 Limited to epidermis, exposing the
dermis
Includes red areas
1 Red area
A Present longer than 30 minutes
but less than 24 hours
B Present longer than 24 hours
Stage II: Partial thickness skin loss
involving epidermis and or dermis. The
ulcer is superficial and present clinically
as abrasion, blister, or crater
2 Full thickness of dermis to the
junction of subcutaneous fat
2 Epidermis and or dermis ulcerated
with no subcutaneous fat observed
Stage III: Full thickness skin loss
involving damage or necrosis of
subcutaneous tissue which may extend
down to, but not through underlying
fascia. The ulcer present clinically as
deep crater with or without
undermining of adjacent tissue
3 Fat obliterated, limited by the deep
fascia undermining skin
3 Subcutaneous fat observed, no
muscle observed
Stage IV: Full thickness skin loss with
extensive destruction, tissue necrosis or
damage to muscle, bone or supporting
structures e.g tendon, joint, capsule
4 Bone at the base of ulceration
5 Close large cavity through a sinus
4 Muscle fascia is observed but no
bone observed
5 Bone is observed but no
involvement of joint space
6 Involvement of the joint space
26.
27. Diagnosis
• Diagnosis of pressure ulcers is clinical
• History and physical examination is focused on:
Determining the etiologic factors
Associated factors that influence wound healing-
31. Treatment
• Surgical
• Goals:
• Prevent progressive osteomyelitis and sepsis
• Reduce protein loss through the wound
• Improve quality of life
• Lower rehabilitation cost
• Improve patient hygiene and appearance
32. • In general, grade 1 & 2 can be managed non-surgically
• Grade 3 & 4 usually is protracted, culminating in non-healing or early
recurrence
34. Treatment
Post-operative care
• Pressure relief bed for 3-6 weeks
• Antispasmodics
• Nutrition optimization
• Active or passive range of motion of the uninvolved extremity
• Culture-directed antibiotics with infectious disease consultation
• Sitting protocol
• Education
36. Follow up
• Prevention begins the management of pressure ulcers
1. Skin care
• Consistent cleaning and bathing of patient and keeping the body dry
• Clean and neatly stretched out powdered bed sheet
• Proper bowel/ bladder program to keep skin clean and dry
2. Control of spasticity
• Proper patient positioning
• Medications- diazepam, baclofen, dantrolene sodium, mephenesin
carbonate
37. 3. Pressure dispersion
• Padding of pressure point-
• Pressure relieve behavior or alternate weight bearing surface
• Seated patient must be lifted for up to 10 seconds every 10 minutes
• Supine patients must be turned every 2 hours
• Support surface
• At least 4 inches of ring foam
• Water bed
38. Prevention
• Alternating air cell mattress (AAC)
• Air cells oriented perpendicular to patient
• Inflates and deflates
• Dispersal of accumulated metabolites via vascular and lymphatic drainages
• Head of bed elevation not > 45 degrees
• Low air loss mattress(LAL)
• Controlled loss of air within the mattress
• Facilitates drying of the skin
• Exerts <25mmHg pressure on any one part of the body
• As bed overlay or multiple pinholes that act to periodically redistribute
pressure
39. Prevention
• Air fluidized beds
• Patient floats on ceramic beads while warm, regulated air is forced through
• Eliminates excessive moisture from skin
• Keeps surface interface pressure at <20mmHg
• May cause dehydration
• Turning and repositioning in bed difficult- large and heavy
• Expensive
• Cushions for wheelchair filled with gel, foam, air, or water for pressure
relieve
• Rigid-based cushion provide lumbar support and decrease ischial pressure
• Optimization of underlying medical conditions
40. Peculiarities of our environment
• Poverty
• Ignorance
• Lack of modern pressure dispersal equipment
41. Conclusion
• Pressure ulcers are here to stay despite all the advances in prevention
and management.
• Management requires a multidisciplinary approach.
• One has to keep abreast with the etio-pathogenesis, risk factors and
staging in detail so as to improve upon the understanding of this
preventable condition.
42. References
1. Karen LP, Linda GP. In: Charles HT. Pressure Sores. Grabb and Smith’s Plastic Surgery.
7th edition. China. Lippincott Williams & Wilkins. 2014: 989- 997
2. Jeffrey EJ, Jeffrey MK. Pressure sores. Selected Reading in Plastic Surgery vol. 9(39).
Dallas. The University of Texas Southwestern Medical Centre2003: 1-43
3. Jeffrey EJ, Eamon BO. In: Jeffrey EJ. Pressure sores. Essentials of Plastic Surgery. 2nd
edition. Columbus, Ohio. CRC Press Taylor & Francis Group. 2014: 641- 649
4. Waterlow J. Pressure sores: A risk assessment card. Nurs Times. 1985;81:49–55.
5. Braden B, Bergstrom N. A conceptual schema for the study of the etiology of pressure
sores. Rehabil Nurs. 1987;12:8–12.
6. Gosnell DJ. Pressure sore risk assessment. Part II. Analysis of risk factors. Decubitus.
1989;2:40–3
7. Defloor T. The risk of pressure sore: A conceptual scheme. J Clin Nurs. 1999;8:206–16.
8. Pressure ulcer prevention: Clinical guideline No. 7. London: NICE; 2003. National
Institute for Clinical Excellence.