WARNING: VERY VISUAL PRESENTATION. My first presentation on burns and their various medical, surgical and nursing interventions. It's a total crash course. Pardon me for forgetting the references. PS: All images are from Google.
Brief description about what are burns, structure of skin, how we can classify burns based upon mechanism and differential diagnosis ,pathophysiology of burn, rule of 9, general and systemic response to burns, complications, fluid resuscitation, parkland formula, monitoring of resuscitation
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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
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.
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.
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
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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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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
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
- 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
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
3. Learning objectives
Type of burn injury
Classification of burns
Pathophysiology of burn
Treatment
Complications of burn
4. 10/22/2016 4
INTRODUCTION
Majorty of burns in children are SCALDS caused
by accidents with kettles,pans,hot drinks and
bath water
In young males burn caused by experimenting
With mathes and inflamable liquides
Electrical and chemical injuries occur in adults with
Associated conditions such as mental disease,
Epilepsy Alcohal and drug abuse
6. 10/22/2016 6
CLASSIFICATION OF BURNS
1.Depending on the percentage of burns
MILD
o Partial thickness burns <15% in adults and <10%
In children
or
o Full thickness <2%
o Can be treated on outpatient department
8. 10/22/2016 8
CLASSIFICATION (CONT……)
SEVERE
oSecond degree burns more then 25% in adults
and More then 20% in children
oAll third degree burns more then 10%
oAll electrical burns and inhalation burns
oBurns with fracture
oBurns involving eyes,ears,feet,hands and
perineum
9. Classification(cont…..)
2.Depending on thickness of skin involved
First degree
Second degree
Third degree
Fourth degree
Partial thickness burns
I. Superficial
II. Deep
Full thickness
7
19. Extent of surface area burned
Rule of nines-An estimated
of the TBSA involved as a
result of a burn.
The rule of nines measures
the percentage of the body
burned by dividing the body
into multiples of nine.
The initial evaluation is
made upon arrival at the
hospital.
1
9
20. 10/22/2016 20
Pathophysiology of burn injury
Most common organ affected is the skin
Burn can also damage airways and lungs with life
Threatening consequenses
Respiratory system injuries occure if person trapped
In a burning vehicle,house,car and is forced to inhale
The hot and poisonous gases
Hot gases burn the lining of airway above the larynx
And lining start to swell later on block the airway
Steam causes damage to the lower airways,respiratory
Epithelium swells and detach from bronchial tree
22. Pathophysiology(cont……)
Metabolic poisoning
Carbon monoxide is a product of incomplete combustion
That is often produced by fires in a closed space is one of
Many poisonous gases
Co binds to hb with an affinity of 240> O2 so block
Transport Of O2
Level of carboxyhaemoglobin in blood can be measure
Conc >10% dangerous and need treatment with pure
Oxygen for more then 24hours
Hydrogen cynide causes metabolic acidosis by interefering
1W0/22i/t20h16 mitochondrial respiration 13
23. Pathophysiology(cont……)
Inhalational injury
caused by mainute particles within thick smoke because
Of their small size and are not filtered by the upper
Airwayand are carried down to
lung parenchyma
Stick to moist lining causes
intense reaction in alveoli
Causes chemical pneumonitis
followed by oedema within
Alveolar sac and dec gaseous
exchange
14
24. Pathophysiology(cont……)
Inflamtion and circulatory changes
Burn skin release of neuropeptides activation of
Complement are intiated by stimulation of pain fibers and
Alteration of proteins by heat
Activation of hageman factor alter archidonic acid
Thrombin and kallikrein pathways
24
25. Pathophysiology(cont……)
At cellular level
Complement causes degranulation of mast cells
Attracts neutrophils which also degranulate and releases
Large amount of free radicals and proteases
Mast cells also releases TNF@ which act as chemotactic
Agent to inflamatory cells
These inflamatory factors alter permeability of bld vessels
Large protein molecules can also escape with ease
Damaged collagen and extravasated proteins oncotic
Pressure further increase flow of water from intravascular
Toextravascular space
25
26. Pathophysiology
Heat causes coagulation necrosis of skin and
subcutaneous tissue.
↓
Release of vasoactive peptides
↓
Altered capillary permeability
↓
Loss of fluid → Severe hypovolaemia
↓
Decreased cardiac → Decreased myocardial
output function
↓
Decreased renal blood → Oliguria
flow (Renal failure)
↓
Altered pulmonary resistance causing pulmonary
Oedema infection
Systemic Inflammatory Response Syndrome (SIRS)
↓
Multi Organ Dysfunction Syndrome (MODS).
26
27. ASSESSMENT OF BURNS
1.ASSESSING SIZE
Burn size should be assessed in a controlled environment
Toavoid hypothermia
In smaller burns just cut a piece a clean paper the size of
patient ,s whole hand (digit and palm)which present 1% TBSA
And match this to the area
Another accurate way of measuring the size of burns is to draw
The burn on a LUND AND BROWDER CHART
Age in
yrs
0 1 5 10 15 adult
A head 9 8 6 5 4 3
B thigh 2 3 4 4 4 4
01C6leg 2 2 3 3 3 3 18
28. 28
ASSESSMENT(CONT…..)
RULE OF 9 (wallace,s rule of 9
Each upper limb is 9% TBSA
Each lower limb is 18% TBSA
Torso 18% each side
Head and neck 9%
Perineum 1%
In children head and neck is 18% and
Lower limb is 13.5% each=13.5*2=27%
33. 33
ASSESSMENT(CONT…..)
2.Assessing depth from the history
Burning of human skin is temperature and time dependent
It takes 6 hours for skin maintained at 44c* for irreversible changes
A surface teperature of 70c* for 1 second produce epidermal
destruction
example of exposure t o hot water at 65c*
45 second exposure produce full thickness burn
15 second exposure produce deep partial thickness burn
7 second exposure produce superficial partial thikness burn
34. 34
ASSESSMENT(CONT…..)
a) Superficial partial thickness burns
No deeper then papillary dermis
Blister formation
Loss of epidermis
Capillary return visible
When blanched
Dermis is pink and moist
Pin prick sensation normal
Heal without scarring
In 2 weeks
Treatment is non surgical
37. 37
ASSESSMENT(CONT…..)
b)Deep partial thickness burn
Damage to deeper parts of dermis
Epidermis is usually lost
Fixed capillary staining
Colour does not blanch with pressure
Sensation is reduced
Pt is unable to distinguish sharp from blunt pressure
Takes 3 or more weeks to heal without surgery
Leads to hypertrophic scarring
38. 38
ASSESSMENT(CONT…..)
c)Full thicknessburns
Whole of the dermis destroyed
Hard and leathery feel
No capillary return
Often thrombosed vessels can be seen under
The skin
These are completely anesthetised
No pain and no bleeding
39. 39
Causes of death in burns
a. Hypovolaemia and shock
b. Renal failure
c. Pulmonary oedema and ARDS
d. Septicaemia
e. Multiorgan failure
44. Management of burns
Prehospital care
Stop the burning process
Stop,drop and roll is a good method of extinguishing
Fire
Cool the burn wound
This provide analgesia and slow the delayed micro-
-vascular damage which occure after a burn injury
Cooling should be for minimum 10 mintues and up to
One hour to avoid hypothermia
Give oxygen
Give oxygen especialy if there is altered level concious_
10/22/20-1n6 ess level 32
45. 10/22/2016 45
Management of burns
Elevate
Sitting a patient up with a burned airway may prove life
Saving
Elevation of burned limbs reduce swelling and discomfort
Check for other injuries
A standard ABC check followed by a secondary survey
Patients burned in explosions may have head and spine injuries
And other life threatening problems
46. 10/22/2016 46
Management of burns
Indications for admission in burns
Susected airway or inhalational injury
Any burn require fluide resusciation
Any burn in extreme of ages
All electrical and chemical burns
Any burn which require surgery
Burn of any significance to hands,face,feet or perineum
Suspicious of non accidental injury
47. 10/22/2016 47
Management of burns
Hospital care
Admit the patient
Airway control
Breathing and ventilation
Circulation
Disability
Exposure with environment control
Fluid resuscitation
Assess the %age,degree and type of burn
Keep the patient in clean environment
Sedation and proper analgesia
48. 10/22/2016 48
Management of burns
A.AIRWAY CONTROL
Burned airway creates problems by swelling and can completely
Occlude the airway
Secure airway with an endotracheal tube until
swelling subsided which is Usually 48 hours
Delayed diagnosis of airway burn make difficult to intubate the
Patient in presence of lyrangeal oedema so cricothyroidectomy
Should be done
Early intubation of suspected airway burn is the treatment of
Choice in such patients
49. 10/22/2016 49
Management of burns
B.BREATHING
A progressive increase in respiratory rate and effort ,anxiety
Rising pulse and confusion with decreasing o2 saturation
These symptoms take 24 hours to 5 days to appear
Treatment starts as soon as possible including
Physiotherapy
Nebulisers
Warm humidified oxygen
50. 10/22/2016 50
Management of burns
Fluide resuscitation
Iv volume must be maintained following a burn in order to
provide sufficient circulation to perfuse not only the organs but
also the peripheral tissues,especially damaged skin
Iv resuscitation is appropriate for any child with a burn greater
Then 10% and 15%for TBSA for adults
If oral resuscitation is to be commenced then water is given
Should not be salt free
It is appropriate to give oral rehydration with a solution such as
DIORALYTE*
Most common fluid used is ringer lactate
51. Management of burns
Fluid volume is relatively constant in proportion to the area
Of body burned therefore there are formulate that calculate
The approximate volume of fluid needed for the pt of a given
Body weight with a given %age of the body burned
Formulas to calculate the fluid replacement
1.parkland regime (commonly used)
4ML/%burn/kg body weight/24 hours
4*50*60=12000ml in 24 hours
Half this volume is given in the frist 8 hours
Second half is given in the subsequent 16 hours
Others
1. Evan,s formula
2. Muir and barclay
10/223/2.016Modified brook formula 39
52. 10/22/2016 52
Management (cont…)
Fluids used
Crystalloid resuscitation
Ringer lactate is the most commonly used crystalloid
These are as effective as colloids for maintaining intra-
-vascular volume
Less expensive
In children
Dextrose saline given for maintanaince
100ml/kg for 24 hours for frist 10kg
50ml/kg for 24 hours for next 10kg
20ml/kg for 24 hours for each kg above 20kg body weight
53. 10/22/2016 53
Management (cont…)
hypertonic saline
it produces hyperosmolarity and hypernatremia
Reduces shift of intracellular water to extracellular space
Advantages
Include less tissue oedema and a resultant decrease in
Escharotomies and intubations
54. 10/22/2016 54
Management (cont…)
Colloid resuscitation
Plasma proteins are responsible for the inward oncotic
Pressure that counteracts the outward capillary hydrostatic
Pressure.
Without proteins there will be oedema
Proteins should be given after frist 12 hours of burn before
This time proteins will leak out of cells
Given through muir and barclay formula
0.5*%agebsa burn*weight=one portion
Periods of 4/4/4, 6/6, 12 hours respectively
One portion to b given in each period
55. 10/22/2016 55
Management (cont…)
Monitoring of resuscitation
The key to monitoring of resuscitation is urinary output
Output should be between 0.5ml and 1.0ml/kg/hour
If urine output is below this infusion rate should increase
By 50%
If still output is inadequate then a bolus of 10ml/kg given
2ml/kg/hr urinary output signals decrease in the rate of
Perfusion
Haematocrit measurement is a usefull tool in confirming
Suspected under or overhydration
56. 10/22/2016 44
As an absorbent
Management (cont…)
Treating the burn wound
Dressings
Paraffine guaze
Hydrocolloids (duoderm)
Biological dressings
synthetic (biobrane)
natural (amniotic membrane)
Full-thickness and deep dermal burns need antibacterial
dressings to delay colonisation prior to surgery
Open method
Silver sulfadiazine application without dressings commonly
Used in burns of face,head and neck.
Closed method
Dressing done to soothen and to protect the wound
Toreduce the pain
57. Management (cont…)
Treating the burn wound (cont……
Tangential excision
Can be done within 48 hours with skin grafting in patients with less
Then 25% burn
Usually done in deep
dermal burns
Dead dermis is removed
layer by layer Untill fresh
bleeding occurs
Later skin grafting done
10/22/2016 45
58. Treating the burn wound
(cont……
Treating the burn wound (cont……
escharotomy
Circumferential full-thickness burns to the limbs require emergency
Surgery
The tourniquet effect of this injury
is easily treated by incising the whole length of full-thickness
burns.
This should be done in the mid-axial line, avoiding major
Nerves
The burn needs to be cleaned and the size and depth need to be
Full thickness burns and deep partial-thickness burns that will
requireoperative treatment will need to be dressed with an
antibacterialdressing to delay the onset of colonisation of the
wo10
u/22
n/2
d016 46
59. A full-thickness burn to the upper limb with a mid-axial
escharotomy.
The soot and debris have been washed off.
10/22/2016 59
60. 10/22/2016 60
Topical agent advantages problems
Silver sulfadiazine 1 -Antiseptic (G +ve -Neutropenia,
% and G –ve pseudoeschar
-Soothening, good -- Causes wound
penetration maceration
- Hydration and
softening of eschar
occurs
Sulfamylon – 5% - Antipseudomonal, Very irritant,painful
(Mafenide acetate) anticlostridial Causes acidosis
- Penetrates very
well in to tissues
Silver nitrate – 0.5% - Antiseptic Stains burn area
Povidone iodine Irritant
(5%) - Used on Painfull
granulation tissue - Not used in partial
after eschar burns
separation
Silver sulphadiazine - Boosts cell
and cerium nitrate mediated immunity
and forms sterile
eschar
61. 10/22/2016 61
Additional aspects of treating burn
patient
Analgesia
Oral form of paracetamol and nsaids in superficial burns
Iv opiates for large burns
Im should not be given in over 10% of TBSA as absorption is
Unpredictable
Short acting analgesia given before dressing
Energy balance
Feeding should start within 6 hrs of injury to reduce gut mucosal damag
Burns patients need extra feeding
A nasogastric tube should be used in all patients with burns over 15%
of TBSA and 10% in case of children
Burn injuries are catabolic in the acute episode.
Removing the burn and achieving healing stops the catabolic drive
62. Additional aspects of treating burn
patient
control of infection
Patients with major burns are immunocompromised,
pathogenic and opportunistic bacteria and fungi enter via the burn
wound,cathetars and iv lines
They have compromised local defences in the lungs and gut due to
oedema
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
Nursing care
Physiotherapy
Psy10c/2h2/2o016logical support 50
63. 10/22/2016 63
SURGERY FOR THE ACUTE BURN
Any deep partial-thickness and full-thickness burns except
those that are less than about 4 cm2, need surgery
A topical solution of 1:500 000 adrenaline also helps to reduce
bleeding,
deep dermal burns, the top layer of dead dermis is shaved
off until punctate bleeding is observed and the dermis can be
seen to be free of any small thrombosed vessels
Full-thickness burns require full-thickness excision of the
Skin
Postoperative management of these patients obviously
requires careful evaluation of fluid balance and levels of haemoglobin.
64. 10/22/2016 64
Delayed reconstruction and scar
management
is common for large Full thickness burns
Eyelids must be treated before exposure keratitis arises
Transposition flaps and Z-plasties with or without tissue
expansion are useful
Full-thickness grafts and free flaps may be needed for large
or difficult areas
Hypertrophy is treated with pressure garments to be worn
for 6-18 months
Smaller areas of hypertrophy, silicone patches will speed
scar maturation,as will intralesional injection of steroid.
Pharmacological treatment of itch is important
65. 10/22/2016 65
Effects of burn
Shock due to hypovolaemia
Renal failure(toxins from burn&myoglobin)
Pulmonary oedema,resp infections,ARDS,resp failure
Infection by staph aureus,pseudomonas,klebsella leads to
Septicemia
Fungal and viral infections of dangerous type can occure
GIT: Hypovolaemia, ischaemia of mucosa, erosive
gastritis—Curling’s ulcer (seen in burns > 35%).
Fluid and electrolyte imbalance.
immunosuppression predisposes to severe opportunistic infection.
Eschar formation and its problems like defective
circulation, ischaemia when it is circumferential.
Electrical injuries often cause fractures, major
internal organ injury, convulsions.
66. 10/22/2016
.
66
Effects of burn(cont…..)
Inhalation burn causes pulmonary oedema,
respiratory arrest, ARDS.
Chemical injury causes severe GIT disturbances like
erosions, perforation, stricture oesophagus (alkali),
pyloric stenosis (acid), mediastinal injury.
Other problems
DVT, pulmonary embolism
bed-sores,
severe malnutrition with catabolic status,
Toxic shock syndrome:
It is a life-threatening exotoxin mediated disease caused by
Staphylococcusaureus. It is common in children, presents with
rashes, myalgia, diarrhoea, vomiting, and multiorgan
failure with high mortality
67. 10/22/2016 67
Effects of burn(cont…..)
Development of contracture is a late problem. It
leads to ectropion, microstomia, disability of
different joints, defective hand functions, growth
retardation causing shortening
COMPLICATIONS OF BURNS CONTRACTURE
Ectropion of eyelid causing keratitis and corneal
ulcer.
Disfigurement in face.
Narrowing of mouth microstomia.
Contracture in the neck causing restricted neck movements.
Disability and nonfunctioning of joints due to contracture
Hypertrophic scar and keloid formation.
68. COMPLICATIONS OF BURNS CONTRACTURE
Marjolin’s ulcer
It is a very well-differentiated squamous cell carcinoma
occurring in a scar ulcer due to repeated breakdown (unstable
scar of long duration).
• It is locally malignant.
•As there are no lymphatics in the scar, so there
is no spread to lymph nodes.
• As there are no nerves in the scar it is painless.
• It has raised and everted edge with induration.
• Biopsy confirms the diagnosis.
Treatment
Radiotherapy is not given for Marjolin’s ulcer.
Treatment is either wide excision or amputation. It is curable.
Once it spreads out of the scar tissue it behaves like
any other squamous cell carcinoma and so can spread to
10/22/20r1e6gional lymph nodes 56
73. 10/22/2016 73
Treatment of burn contracture
• Release of contracture surgically and use of skin graft
or “Z” plasty or different flaps.
• Proper physiotherapy and rehabilitation is essential.
• Pressure garments to prevent hypertrophic scars.
• Management of itching in the scar using aloe vera,
antihistamines and moisturizing creams.
74. 74
Prevention of development of
contracture
•Joint exercise in full range during recovery period of
burns
• Pressure garments for a long period
• Topical silicon sheeting
• Saline expanders for scars
76. 76
Non thermal(cont……)
Electrical burns 1000v
Low tension injuries
Low tension injuries do not have enough energy to cause
Significant destruction
Entry and exit points normally in the fingers suffers small
Deep burns may damage underlying nerves and vessels
Accreates a tetany within muscles so patient unable to
Release the device untill the power was turned off
May interfere with normal cardiac pacing and can cause
Cardiac arrest
77. Electrical burns(cont…..)
high tension injuries
3 sources of damage
1) The flash
2) The flame
3) The current
When a high tension line is earthed it can arc over the pt
And causes a flash burn
Extremely rapid heating of the air causes an explosion
That propel the victim backward
It is always a major burn
There is a wound of entry and wound of exit
Major internal organ injuries occures
Convulsions can develope 65
78. Electrical burns(cont…..)
Management
Depending on injury it is managed accordingly
Patient should always be admitted and should be assessed by
i. ECG
ii. u/s abdomen
iii. Chest x-ray
iv. Ct scan head sometimes
v. Cardiac enzyme analysis
Acidosis is common so bicarbonate infusion needed
Fractures and dislocations common so managed accordingly
Release of myoglobin can cause renal tubular damage and renal
Failure so manitol is used to prevent myoglobin induced renal
failure (compartment syndrome)
66
80. Electrical burns(cont…..)
An exit wound of a high-tension
injury,
Amputation and cover with the
lateral portion of the second toe.
80
81. 81
Chemical burns
There are 70000 different chemicals in regular use within industry
Occasionally these cause burns
There are two aspects to a chemical injury
1. Physical destruction to the skin
2. Systemic absorption
The initial management of any chemical injury is copious lavage
With water but some need to be remove physically eg.phosphorus
A component of millitary devices
The more common injuries are caused by either
1. Alkalis
2. acids
82. 10/22/2016 82
Chemical burns(cont…)
Alkalis
alkalis are more destructive and especially when come in contact
With eyes
Commonly used alkalis are sodium hydroxide,lime,bleach
They cause fat sponification,fluide loss,release of alkali proteinase
Alkali burns occur in oral cavity and oesophagus
which leads to multiple oesophageal strictures.
After copious lavage, the next step in themanagement of any
chemical injury is to identify the chemical
and its concentration and to elucidate whether there is any
underlying threat to the patient’s life if absorbed systemically
83. Acidaemia should be corrected by IV sodium bicarbonate.
83
Chemical burns(cont…)
Acids
Acid burn occurs in skin, soft tissues and GIT. In GIT,
Burns affecting the fingers and caused by dilute acid are relatively
common.
The initial management is with calcium gluconate gel topically
severe burns or burns to large areas of the hand can be
subsequently treated with Bier’s blocks containing calcium
gluconate 10 per cent gel
it is common in stomach either due to nitric acid or sulphuric acid
which may lead to severe gastritis or pyloric stenosis.
Other acids are formic acid, hydrofluoric acid.
They cause metabolic acidosis, renal failure, ARDS, haemolysis.
84. Cold injuries
Cold injuries are principally divided into two types
1. Acute cold injuries from industries
2. Frost bite
inflammatory reaction is not as marked.
The tissue is more resistant to cold injury than to heat injury
The assessment of depth of injury is more difficult,
Frostbite
injuries affect the peripheries in cold climates
cold injury produces delayed microvascular damage similar to
that of cardiac reperfusion injury.
The initial treatment is with rapid rewarming in a bath at 42°C.
The level of damage is difficult to assess
10/
s2
u2/2
r0
g16
eryusually does not play a role in its management 72
85. 10/22/2016 85
Ionising radiation
These injuries can be divided into
1. Localised
2. Whole body exposure
The management of localised radiation damage is usually
Conservative until the true extent of the tissue injury is apparent.
If damage have caused an ulcer, then excision and coverage with
vascularised tissue is required.
A patient who has suffered whole-body irradiation and is suffering
From acute desquamation of the skin has received a lethal dose of
Radiation which can cause a particularly slow and unpleasant death
Dose may be lethal and may not be lethal
Giving iodine tablets, the management of these injuries is supportive
86. References.
1. Bailey & Love’s Short Practise of surgery 25th edition.
2. ACS Surgery: Principles & Practice, 2007 Edition
3. Heffner, Hess.Clinics in Chest Medicine 22 , 2001.
4. Cummings: Otolaryngology: Head & Neck Surgery, 4th ed.2005.
5. SRB’s Manual of Surgery Paperback – 1 January 2016
6. SCHWARTZ'S PRINCIPLES OF SURGERY 2-volume set 11th
edition
21 October 202086