This document provides an overview of burns, including definitions, causes, pathophysiology, assessment, and management. It defines burns as tissue damage caused by thermal, electrical, chemical or radiation sources. The depth and extent of burns are assessed using tools like the Rule of Nines. Major burns are those over 25% Total Body Surface Area and can cause local and systemic effects like fluid shifts, metabolic changes and increased risk of infection. Burn management involves three phases - emergent, acute, and rehabilitation - and priorities include wound care, infection prevention and rehabilitation.
Burns are one of the most common household injuries, especially among children. The term “burn” means more than the burning sensation associated with this injury. Burns are characterized by severe skin damage that causes the affected skin cells to die.
Most people can recover from burns without serious health consequences, depending on the cause and degree of injury. More serious burns require immediate emergency medical care to prevent complications and death
With growing industrialization and mechanization of every household electrical injuries are becoming quite common. Electrical injuries are quite intricate with the damage caused. They cause not only external burns injury but a wide spectrum of visceral injuries which in many cases is difficult to diagnose and manage. Therefore, a sound understanding of the engineering aspects is pivotal in diagnosing and managing these cases. A brief review of the pathophysiology and management of electrical injuries is presented.
Burns are one of the most common household injuries, especially among children. The term “burn” means more than the burning sensation associated with this injury. Burns are characterized by severe skin damage that causes the affected skin cells to die.
Most people can recover from burns without serious health consequences, depending on the cause and degree of injury. More serious burns require immediate emergency medical care to prevent complications and death
With growing industrialization and mechanization of every household electrical injuries are becoming quite common. Electrical injuries are quite intricate with the damage caused. They cause not only external burns injury but a wide spectrum of visceral injuries which in many cases is difficult to diagnose and manage. Therefore, a sound understanding of the engineering aspects is pivotal in diagnosing and managing these cases. A brief review of the pathophysiology and management of electrical injuries is presented.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
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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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
Triangles of Neck and Clinical Correlation by Dr. RIG.pptx
Burns.pptx
1. Burns
Dr Janai A. M. Ondieki
For Clinical Medicine Diploma Class
yr 2
2. Definitions
• Burns are caused by transfer of energy from a
heat source to the body. Heat may be transferred
through conduction or electromagnetic radiation.
• Burns are defined as a wound caused by
exogenous agent leading to coagulative necrosis
of tissue
• Tissue destruction results from coagulation,
protein denaturation, or ionization of cellular
contents.
4. Thermal Burns
– Heat changes the molecular structure of tissue causing
denaturing of proteins
– The extent of burn damage depends on
• Temperature
• Amount of heat
• Duration of contact
For example, in the case of scald burns in adults, 1 second of contact
with hot tap water at 68.9°C (156°F) may result in a burn that
destroys both the epidermis and the dermis, causing a fullthickness
(third-degree) injury.
Fifteen seconds of exposure to hot water at 56.1°C (133°F) results in a
similar full-thickness injury.
5. • The effects of thermal burns are influenced by
– Intensity of the energy
– the duration of exposure
– the type of tissue injured
6. Pathophysiology of burns
•Burns that do not exceed 25% TBSA produce a primarily local
response.
•Burns that exceed 25% TBSA may produce both a local and a
systemic response and are considered major burn injuries.
•The incidence, magnitude, and duration of pathophysiologic
changes in burns are proportional to the extent of burn injury,
with a maximal response seen in burns covering 60% or more
TBSA
•These systemic responses are due to the release of cytokines
and other mediators into the systemic circulation
7. • Fluid shift
– period of inflammatory response
– Vessels adjacent to burn injury dilate, increased
capillary hydrostatic pressure and permeability
– Continous leak of plasma from intravascular space
into interstitial space
– associated imbalences in fluids, electrolytes and
acid-base occur
– Haemoconcentration
– Lasts 24-36 hours
8. • Fluid mobilization
– capillary leak ceases and fluid shifts back into the
circulation
– Restores fluid balance and renal perfusion
• increased urine formation and diuresis
– continued electrolyte imbalances
• hypokalaemia
• Hyponatremia
– Haemodilution
9. • Systemic Changes
• Cardiac
– decreased cardiac output
• Pulmonary
– Respiratory insufficiency as a secondary process
– can lead to respiratory failure
• Gastrointestinal
– Decreased or absent motility
– Stress Ulcer formation ( Curlings Ulcer)
10. • Metabollic
– Hypermetabolic state
– increased oxygen and calorie requirements
– increased in core body temperature
• Immunological
– loss of protective barrier
– increased risk of infection
– suppression of humoral and cell-mediated immune responses
11. Acute Phase
• Clinical issues
• External loss of Plasma
• Loss ofd circulating red cells
• Burn oedema
12. Sub Aute Phase
• Diuresis
• Clinical Anaemia
• Accelerated metabolic rate
• Nitrogen Disequilibrium
• Bone and joint changes
• Endocrine disturbances
• Electrolyte and chemical imbalance
• circulatiry derangements
• loss of function of skin as an organ
13. Body's response to Burns
• Emergent Phase (stage 1)
– Pain response
– Catecholamine release
– tachycardia, tachypnoea, mild Hypertension, mild anxiety
• Fluid Shift Phase (stage 2)
– Length 8-24 hours
– Begins after emergent phase
• reaches peak in 6-8 hours
– damaged cells initiate inflammatory response
• increased blood flow to cells
• Shift of fluid from intravascular to extra vascular space
– MASSIVE OEDEMA
14. • Hypermetabolic Phase (stage 3)
– Lasts for days to weeks
– Large increase in the body's need for nutrients as
it repairs itself
• Resolution phase(stage 4)
– scar formation
– general rehabilitation and progression to normal
function
15. Jackson's theory of Thermal Burns
• Zone of coagulation
– Area nearest to the heat
source that suffers the most
damage as evidenced by
clotted blood and
thrombosed blood vessels
• Zone of Stasis
– Area surrounding zone of
coagulation characterized by
decreased blood flow
• Zone of Hyperemia
– Peripheral area around burn
that has increased blood flow
16.
17. • Severity of burns is determined by
– depth of the burn
– Extent of the burn/total Burn Surface A (TBSA)
– Location of the burn
– Patient risk factors
18. Grading of burn according to depth
• First Degree - Injury to the
Epidermis
• Superficial Second Degree -
injury to epidermis and
Superficial Papillary dermis
• Deep secondary Degree -
Injury from epidemis to
reticular dermis
• Third degree -full thickness
burn through epidermis and all
layers of dermis
• Fourth degree - injury trhough
skin, subcutaneous fat into
underlying muscle or bone
19. • Burn Depth
• Burn depth determines whether epithelialization will occur.
• Determining burn depth can be difficult even for the
experienced burn care provider.
• The following factors are considered in determining the
depth of the burn:
– How the injury occurred
– Causative agent, such as flame or scalding liquid
– Temperature of the burning agent
– Duration of contact with the agent
– Thickness of the skin
20. 1st Degree Burn
• Involves only the epidermis
• Reddening/Darkening of the
skin
• Pain at burn site
• Blanch to touch
• Have an intact epidermal
barrier
• Do not result in scarring
• Examples: Sun Burn, Minor
Scald from Kitchen accident
• Treatment aimed at comfort
21. 2nd degree Superficial
Burn
• Involves the epidermis
and papillary dermis
• Intense pain
• Blisters
• reddening/darkening
• Spares hair follicles ,
sweeat glands etc
• erythematous & blanch
to touch
• Very painful/sensitive
• No/Minimal Sacrring
• Spontaneously re-
epithelialize from
retained epidermal
structures in 7-14 days
22. 2nd degree deep burn
• Involves the epidermis and
reticular dermis
• less pain, remain painful to
pin prick
• Appears pale and mottled
• do not blanch to touch
• capillary return sluggish or
absent
• takes 14-35 days to heal by
epithelialisation from hair
follicles & sweat glands
often with severe scaring
• Contractures possible
• may require excision & skin
grafting
23. 3rd degree burns
• dry, leathery skin(white,
dark, brown or charred)
• Loss of sensation
• All dermal layers are
invovled
• will require surgery
26. Assessing Total Burn Surface Area
• Rule of Nines
– best used for large surface areas
– Expedient tool to measure extent of burn
– Modified to Rule of Sevens for pediatric age group
• Rule of palms
– best used for burns< 10% BSA
• Lund and Browder Chart
31. Criteria for Classifying the Extent of Burn
Injury(American Burn Association)
Minor Burn Injury
• Second-degree burn of less than 15% total body
surface area(TBSA) in adults or less than 10%
TBSA in children
• Third-degree burn of less than 2% TBSA not
involving special care areas (eyes, ears, face,
hands, feet, perineum, joints)
• Excludes electrical injury, inhalation injury,
concurrent trauma, all poor-risk patients (eg,
extremes of age, concurrent disease) 31
32. Criteria for Classifying the Extent of Burn
Injury(American Burn Association)
Moderate, Uncomplicated Burn Injury
• Second-degree burns of 15%–25% TBSA in
adults or10%–20% in children
• Third-degree burns of less than 10% TBSA not
involving special care areas
• Excludes electrical injury, inhalation injury,
concurrent trauma, all poor-risk patients (eg,
extremes of age, concurrent disease) 32
33. Criteria for Classifying the Extent of Burn
Injury(American Burn Association)
Major Burn Injury
• Second-degree burns exceeding 25% TBSA in adults
or 20% in children
• All third-degree burns exceeding 10% TBSA
• All burns involving eyes, ears, face, hands, feet,
perineum, joints
• All inhalation injury, electrical injury, concurrent
trauma, all poor-risk patients 33
34. Pre Hospital care for burn victims
• Ensure rescuer safety
• Stop the burning process: Stop, drop and roll
• Check for other injuries
– Standard ABC (airway, breathing, circulation)followed by a rapid
secondary survey
• Cool the burn wound
– Analgesia
– Slows the delayed microvascular damage
– minimum of 10 min
– effective up to 1 hour after the burn injury
• give oxygen
• elevate
35. Management of the Patient With a
Burn Injury
35
• Burn care must be planned according to the burn
depth and local response, the extent of the injury,
and the presence of a systemic response.
• Burn care then proceeds through three phases:
– Emergent/resuscitative phase (on-the-scene care),
– Acute/intermediate phase, and
– Rehabilitation phase.
• Although priorities exist for each of the phases, the
phases overlap, and assessment and management
of specific problems and complications are not
limited to these phases but take place throughout
burn care.
36. Table: phases of burn care
36
Phase Duration Priorities
Emergent or
immediate
resuscitative
From onset of injury to
completion
of fluid resuscitation
First aid
Prevention of shock
Prevention of respiratory distress
Detection and treatment of concomitant
injuries
Wound assessment and initial care
Acute From beginning of diuresis
to near
completion of wound
closure
Wound care and closure
Prevention or treatment of
complications, including infection
Nutritional support
Rehabilitatio
n
From major wound closure
to return
to individual’s optimal level
of physical
and psychosocial
adjustment
Prevention of scars and contractures
Physical, occupational, and vocational
rehabilitation
Functional and cosmetic reconstruction
Psychosocial counseling
37. • Criteria for admission to hospital/Burns Unit
• suspected airway/inhalational injury
• any burn requiring fluid resuscitation (>15% in adults and 10% in
children)
• any burn requiring surgery
• burns to special areas; face, hands, feet perineum
• pts with psychiatric or social circumstance making it inadvisable to
send them home
• any suspicion of non-accidental Injury
• Any burn in a patient at extremes of age
• any burn associated with potentially serious sequelae
• high tension electrical burns
• Chemical burns
38. Emergent/resuscitative phase mgt
• Emergency Medical Management
• A: Airway Control
• B: Breathing and ventilation
• C: Circulation
• D: Disability - neurological status
• E: Exposure with environmental control
• F: Fluid resuscitation
38
39. • Airway Recognition of the
potentially burned airway
– A history of being trapped in
the presence of smoke or hot
Gases
– Burns on the palate or nasal
mucosa, or loss of all the
hairs in the nose
– burns around the mouth and
neck
40. Burned airway
• Early elective intubation is
safest
• Delay can make intubation
very difficult because of
Swelling
• Be ready to perform an
emergency cricothyroidotomy
if intubation is delayed
41. Upper Airway Injury
• Injury above the glottis
• Results from direct heat (hot air) or edema
• Manifested by mechanical obstruction of the
upper airway, including the pharynx and the
larynx
• Assess patients for facial burns, erythema,
swelling, tachypnea, dyspnea, hoarsness, and
singed nasal hairs.
• Treatment: early endotracheal or nasotracheal
intubation
42. Lower Airway Injury
• Injury below the glottis
• Results from inhaling toxic gases and chemical
contained in inhaled smoke
• When these substances come in contact with
pulmonary mucosa, irritation and inflammation
reaction occurs, resulting in hypersecretion, severe
mucosal edema, ciliary action , and possibly
bronchospasm
• Pulmonary surfactant is reduced, causing atelectasis
• Assess patient for expectoration of sputum with
carbon particles
43. Carbon Monoxide (CO) Poisoning
• CO is a colorless, odorless
gas that is a by-product of
the combustion of organic
materials.
• The affinity of hemoglobin
for CO is 200X greater than
that for O₂
• CO combines with
hemoglobin to form
carboxyhemoglobin and
blocks the uptake of O₂ and
causing tissue hypoxia
• Treatment: early intubation
and mechanical ventilation
with 100% O₂
44. Fluids for resuscitation
• In children with burns over 10% TBSA and adults with burns
over 15% TBSA, consider the need for intravenous fluid
resuscitation
• Fluids needed can be calculated from a standard formula
• Parkland Formula: Total percentage body surface area ×
weight(kg) × 4 = volume (ml)
– Half this volume is given in the first 8 hours, and
– the second half is given in the subsequent 16hours.
45. • Crystalloid : Ringer’s lactate
• Hypertonic saline
• Human albumin solution
• Colloid resuscitation
Not Routinely
Used in Our set
up !!
46. Management of fluid loss and shock
Fluid Replacement Therapy:
• The total volume and rate of intravenous fluid
replacement are gauged by the patient’s
response.
• The adequacy of fluid resuscitation is determined
by:
– urine Output totals of 30 to 50 mL/hour
–systolic blood pressure exceeding 100 mm Hg
and/or
– pulse rate less than 110/minute. 46
48. Acute Phase management
• Hemodynamically stable through diuresis
• Capillary permeability is restored
• 48-72 hours after injury
• Goal is restorative therapy
• Focus on infection control, wound care and
closure, nutritional support, pain management,
PT
• Concluded when the burned area is completely
covered by skin grafts or when the wounds are
healed 48
49. Full to deep partial
thickness HWB
Skin graft
Day 1
3 weeks
Day 12
50. Acute Phase management
Pathophysiology
• Diuresis from fluid mobilization occurs, and the
patient is no longer grossly edematous
• Bowel sounds return
• Healing begins
• Formation of granulation tissue
• A partial-thickness burn wound will heal from
the edges
• Full-thickness burns must be covered by skin
grafts 50
51. Acute Phase management
• Wound Care
• Daily observation
• Assessment
• Cleansing
• Debridement
• Appropriate coverage of the burn
51
52. TREATING THE BURN WOUND
• Escharotomy Circumferential
full-thickness burns to the limbs
require emergency surgery.
• The tourniquet effect of this
injury is easilytreated by incising
the whole length of full-
thickness burns..
• Escharotomy•
– Incise along medialand/or
lateral surfaces.
– Avoid bonyprominences.
– Avoid tendons, nerves,major
vessels.
53. • Debridement•
• Types of debridement:
– 1. Auto debridement.
– 2. Tangential excision (at the
end of 1st week)
– 3. Staged primary
debridement (1-3 days
postburn).
• This early debridement of
dead tissue interrupts and
attenuates the systemic
inflammatory response and
normalize immune function
– .4. For deep circumferential
burn, urgent escharotomy is
done
54. • Superficial burns expected to heal by
epitheliaization are managed by either
Exposure Method or by Closed Dressing
55. Acute Phase management
Excision and Grafting
• Eschar is removed down to the subcutaneous
tissue or fascia and skin grafts done
55
59. Acute Phase management
Pain Management
• Opioids
• Several drugs in combination ( MULTIMODAL
ANALGESIA)
• Non pharmacologic strategies
• Relaxation tapes
• Visualization, guided imagery
• Meditation
59
60. Acute Phase management
• Nutrition
– Burns patients need extra feeding
– A nasogastric tube should be used in allpatients with
burns over 15% of TBSA
– Removing the burn and achieving healing stops the
catabolic drive.
• Nutrition Sutherland formula
– Children: 60 kcal/ kg + 35 kcal% TBSA
– Adults: 20 kcal /kg + 70 kcal% TBSA
– Protein20% of energy1.5 to 2 g/kg protein/day
61. Acute Phase management
Infection Prevention
• Tetanus prophylaxis
– Tetanus toxoid, 0.5 mL intramuscularly, if thelast booster dose was
more than 5 years beforethe injury.
– If immunization status is unknown,human tetanus immunoglobulin
250 to 500units, I.M. plus tetanus toxoid in opposite side
• Monitoring and control of infection
– Burns patients are immunocompromised
– They are susceptible to infection from manyroutes
– Sterile precautions must be rigorous
– Swabs should be taken regularly
– A rise in white blood cell count,thrombocytosis and increased
catabolism are warnings of infection
62. • Topical treatment of deep burns
– 1% silver sulphadiazine cream
– • 0.5% silver nitrate solution
– Mafenide acetate cream•
– Serum nitrate, silver sulphadiazine and
ceriumnitrate
63. Rehabilitation Phase
• The rehabilitation phase is defined as
beginning when the patient’s burn wounds
are covered with skin or healed and the
patient is able to resume a level of self-care
activity
• Complications
– Skin and joint contractures
– Hypertrophic scarring
63
64. Rehabilitation Phase
• Both patient and family actively learn how to
care for healing wounds
• Cosmetic surgery is often needed following
major burns
• Role of exercise (physiotherapy) cannot be
overemphasized
• Constant encouragement and reassurance
• Address spiritual and cultural needs
• Maintain a high-calorie, high-protein diet
• Occupational therapy 64
65. Complications of Burns
• Emergent phase
– Shock and multi organ failure
• Renal failure
– Respiratory failure (inhalational Injury)
– Hypothermia
70. Chemical Burns
Chemical Burns
Acids
• Protein injury by hydrolysis.
• Thermal injury is made with skin contact.
Alkali
• Saponification of fat
• Hygroscopic effect- dehydrates cells
• Dissolves proteins by creation of alkaline
proteinates (hydroxide ions)
71. Electrical Burns
• Greatest heat occurs at the points
of resistance
• –Entrance and Exit wounds
• –Dry skin = Greater resistance
• – Wet Skin = Less resistance
• Longer the contact, the greater the
potential of injury
– Increased damage inside body
• Smaller the point of contact, the
more concentrated the energy, the
greater the injury.
72. • Electrical Current Flow
• –Tissue of Less Resistance
• • Blood vessels
• • Nerve
– –Tissue of Greater Resistance
• • Muscle
• • Bone
• Results in………..
• –Serious vascular and nervous injury
• –Immobilization of muscles
• –Flash burns
• Late complications: cataracts, progressive
demyelinating neurologic loss
73.
74. • Assess patient
• Entrance & Exit wounds
• Remove clothing, jewelry, and leather items
• Treat any visible injuries– Thermal burns
• ECG monitoring– Bradycardia, Tachycardia, VF or
Asystole– Treat cardiac & respiratory arrest– Aggressive
airway, ventilation, and circulatory management.
• Consider Fluid bolus for serious burns– 20 ml/kg
• Look out for compartment syndrome – prohylactic
fasciotomy
• Myoglobinuria – leads to renal failure
Editor's Notes
CO poisoning is the most common cause of inhalation injury because it is a byproduct of the combustion of organic materials and therefore present in smoke
The pathophysiologic effects of CO poisoning is hypoxemia
100% O₂ is essential to accelerate the removal of CO from hemoglobin molecules