Burns (Trauma) Powerpoint - Medical School

medical burns ppt

1. BURNS (LI)

2. MICROANATOMY OF SKIN
Layers of the Epidermis
Reference: Gray’s Anatomy: The Anatomical Basis of
Clinical Practice, 41st Edition (2016)

3. PATHOLOGY OF TISSUE INJURY

4. PATHOLOGY OF TISSUE INJURY
Reversible Cell Injury

5. PATHOLOGY OF
TISSUE INJURY
Irreversible Cell Injury

6. MECHANISM OF REPAIR
Tissue Regeneration

7. MECHANISM OF REPAIR
Scar Formation

8. MECHANISM OF
REPAIR
Healing of Skin Wounds

9. DEGREE OF BURNS
Tintinalli, Judith , et al. “Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e | AccessMedicine | McGraw Hill Medical.” Mhmedical.com, 2020,
accessmedicine.mhmedical.com/book.aspx?bookid=2353.

10. DEGREE OF BURNS
First Degree
superficial burn
involves only the epidermal layer of skin.
burned skin is red, painful, and tender without blister formation
heal in about 7 days without scarring
require only symptomatic treatment

11. DEGREE OF BURNS
Second Degree - Superficial
superficial partial-thickness burns, the epidermis and the superficial dermis (papillary layer
which is the top layer of your dermis) are injured
deeper layers of the dermis, hair follicles, and sweat and sebaceous glands are spared
skin is blistered, and the exposed dermis is red and moist.
exceedingly painful to touch
dermis is well-perfused with intact capillary refill
Healing typically occurs in 14 to 21 days, scarring is usually minimal, and there is full return of
function.

12. DEGREE OF BURNS
Second Degree - Deep
Deep partial-thickness burns extend into the deep dermis (reticular layer)
Hair follicles and sweat and sebaceous glands are damaged, but their deeper portions usually
survive.
The skin may be blistered, and the exposed dermis is pale white to yellow in color.
The burned area does not blanch; it has absent capillary refill and absent pain sensation.
Healing takes 3 weeks to 2 months; scarring is common and related to the depth of the injury.
Surgical debridement and skin grafting may be necessary to obtain maximum function.

13. DEGREE OF BURNS
Third Degree
Full-thickness burns involve the entire thickness of the skin
All epidermal and dermal structures are destroyed.
The skin is charred, pale, painless, and leathery
Because all dermal elements are destroyed, these injuries do not heal
spontaneously. Surgical repair and skin grafting are necessary;
significant scarring is the norm

14. DEGREE OF BURNS
Fourth Degree Burn
Fourth-degree burns are those that extend through the skin to the subcutaneous fat, muscle, and
even bone.
These are devastating, life-threatening injuries.
Amputation or extensive reconstruction is sometimes required.

16. HEMODYNAMIC
CHANGES IN
BURN INJURY

21. Rule of Nines1.
Back of Hand = 1%2.
Lund-Browder burn diagram3.
ESTIMATION OF BURN EXTENT: SIZE
Source: Tintinalli’s 9e

22. ESTIMATION OF BURN EXTENT:
RULE OF NINES
Source: Tintinalli’s 9e

23. ESTIMATION OF BURN EXTENT:
BACK OF HAND = 1% TBSA
Source: Tintinalli’s 9e

24. ESTIMATION OF BURN EXTENT:
LUND-BROWDER BURN DIAGRAM
Source: Tintinalli’s 9e

25. ESTIMATION OF BURN EXTENT: DEPTH
Source: Tintinalli’s 9e

26. ESTIMATION OF BURN EXTENT: DEPTH
Source: Tintinalli’s 9e

27. ESTIMATION OF BURN EXTENT: DEPTH
Source: Tintinalli’s 9e

28. PHYSIOLOGY OF PAIN
“Pain occurs whenever tissues are being damaged and
causes the individual to react to remove the pain stimulus.”
Source: Guyton & Hall 14e
Fast pain is “sharp”, “pricking”, “acute”, “electric” (~0.1 seconds)1.
Slow pain is “slow burning”, “aching”, “throbbing”, “naseous”,
“chronic” (>=1 second)
2.

29. Pain receptors are free nerve endings
Mechanical, thermal, chemical stimuli excite receptors
Nonadapting nature, hyperalgesia
Rate of tissue damage as a stimulus for pain
pain assoc. with heat is correlated with damage rate
Chemical, tissue ischemia, muscle spasm also causes
Source: Guyton & Hall 14e
PHYSIOLOGY OF PAIN

30. Fast pain pathway (remove stimulus)
small type Aδ fibers, 6-30 m/s
Slow pain pathway (seek relief)
type C fibers, 0.5-2 m/s
Double sensation possible
Source: Guyton & Hall 14e
PHYSIOLOGY OF PAIN

31. Source: Guyton & Hall 14e
Enters spinal cord via dorsal spinal roots, terminate on relay neurons in dorsal horns
neospinalthalamic tract for fast pain, paleospinothalamic tract for slow pain
PHYSIOLOGY OF PAIN

32. Source: Guyton & Hall 14e
Neospinothalamic tract
A few terminate in the reticular areas of the brain stem
Most pass without interruption to thalamus
From thalamic areas, signals pass to other basal areas
and somatosensory cortex
Localization can be nearly exact with tactile receptors
~< 10cm with only pain receptor stimulation
Glutamate (believed) neurotransmitter at Aδ ending
PHYSIOLOGY OF PAIN

33. Source: Guyton & Hall 14e
Paleospinothalamic tract
Older system, mostly C fibers, sometimes Aδ fibers
Neurotransmitters glutamate and Substance P (slow
build up of concentration)
Terminates widely in the brain stem, “suffering” pain
reticular nuclei of medulla and mesencephalona.
tectal area of the mesencephalon, orb.
periaqueductal gray region surrounding Aq. of Sylviusc.
Only 10-25% pass to thalamus
Poor localization
PHYSIOLOGY OF PAIN

34. Source: Guyton & Hall 14e
Analgesia system
neurons signal from periaqueductal and
periventricular area to
1.
nuclei (raphe magnus nucleus & nucleus
reticularus paragigantocellularis in
medulla), sends secondary order signals to
2.
pain inhibitory complex in the dorsal horns3.
analgesia signals can block here
Electrical stimulation in 1 or 2 can also block
Main xmtrs: enkephalin (pre & post synaptic) &
serotonin
PHYSIOLOGY OF PAIN

35. Source: Guyton & Hall 14e
PHYSIOLOGY OF PAIN
“activation of the analgesia
system by nervous signals
entering the periaqueductal gray
and periventricular areas, or
inactivation of pain pathways by
morphine-like drugs, can almost
totally suppress many
pain signals entering through the
peripheral nerves.”
~12 opiate-like substances
almost all from breakdown of three
protein molecules
pro-opiomelanocortin
proenkephalin
prodynorphin
most important opiate-like
substances
β-endorphin,
met-enkephalin,
leu-enkephalin,
and dynorphin.

36. Source: Guyton & Hall 14e
PHYSIOLOGY OF PAIN
Referred Pain can be used
as a clinical sign

37. Source: Tintinalli’s 9e, Schwartz 11e
ESCHAROTOMY
eschara (burnt crust, scab) tome (cutting or incision)
Identification: palpation or doppler ultrasound
5P’s: pain, pallor, paraesthesia, paresis, pulselessness
Indication: vascular compromise / inadequate perfusion
example: deteriorating pulse, loss of pulse
Particularly in patients with circumferential deep burns
Can be performed at bedside, not usually needed in first 8 hours
Tools: electrocautery or scalpel under local anesthesia or
intravenous sedation
Technique: proceed as distally as necessary using lateral and
medial aspects, depth to the level of the fat tissue
Digital escharotomies not recommended, usually no meaningful
salvage of functional tissues (Schwartz)

38. ESCHAROTOMY

39. Source: Tintinalli’s 9e, Schwartz 11e
FASCIOTOMY
fascia (band, bundle) tome (cutting or incision)
Inadequate perfusion despite proper escharotomies may
indicate the need for fasciotomy, but this procedure should not
be routinely performed as part of the eschar release.” (Schwartz)
Predictive factors: within 24 hours, 1. myglobinuria, burns >20%
TBSA, full-thickness burn >12% TBSA (Tintinalli)
compartment syndrome from edematous or dead fascia
Most often needed in high-voltage power line electrocutions that
lead to deep muscle necrosis
If necrotizing fasciitis -> fasciotomy, wide local debridement,
broad-spectrum IV antibiotics
Contraindication: missed timely diagnosis of compartment
syndrome as elevated pressured tissues of 24 to 48 hours may
have already caused permanent dysfunction

40. FASCIOTOMY
Emergency decompression
of the tissue compartment

41. BODY FLUID COMPARTMENTS
1. Total Body Fluid Distribution:
- Primarily divided into extracellular fluid (ECF) and intracellular fluid (ICF).
- ECF further divided into interstitial fluid and blood plasma.
- Additionally, there's a small compartment called transcellular fluid, which
includes synovial, peritoneal, pericardial, and cerebrospinal fluids.
2. Quantitative Aspects:
- For women approximately 55%, for men approximately 60%
- This percentage varies based on factors like age, sex, and body
composition.
- With age, the percentage of total body water tends to decrease due to
increased fat mass.
- Women generally have a lower percentage of total body water compared to
men due to higher body fat composition.
- In newborns, total body water is higher, ranging from 70-75% of body
weight.
Hall, John, and Michael Hall. “Guyton and Hall Textbook of Medical Physiology - 14th Edition.”
Shop.elsevier.com, 2020, shop.elsevier.com/books/guyton-and-hall-textbook-of-medical-
physiology/hall/978-0-323-59712-8.
division in terms of how portions of the body's water,
solutes, and suspended elements are segregated

42. BODY FLUID COMPARTMENTS
Fluid compartments
Homeostasis
- Maintaining stable body fluid volume and composition is crucial for homeostasis.
- Abnormalities in fluid control systems can lead to significant clinical issues.
2. Fluid Intake and Output
- Balance between intake and output crucial for stability.
- Despite continuous exchange with the environment, body fluid volume remains relatively constant.
3. Daily Intake of Water
- Sources: Ingested liquids/foods (about 2100 ml/day) and synthesis from carbohydrate oxidation (about 200 ml/day).
- Total intake around 2300 ml/day, subject to variation based on factors like climate and activity level.
4. Daily Loss of Body Water
- Insensible Water Loss:
- Continuous loss via evaporation from respiratory tract and diffusion through skin (about 700 ml/day).
- Factors like burns or cold weather can affect rates.
- Sweat (100ml), Feces (100ml), Kidneys highly variable

43. BODY FLUID COMPARTMENTS
Fluid Homeostasis
6. Body Fluid Compartments
1. Intracellular Fluid: About 40% of total body weight; located within
cells.
2. Extracellular Fluid:
- Includes interstitial fluid and plasma.
- About 20% of body weight; distributed outside cells.
- Transcellular Fluid: Small compartment (1-2 liters) in various body
spaces.
Blood contains extracellular and intracellular but considered
separate compartment because contained in a chamber of its
own (circulatory system)

44. BODY FLUID COMPARTMENTS
During Burns ↑ Fluid loss
-Replacing fluid in the intravascular compartment is crucial to maintain tissue perfusion of vital organs.
-Hypovolemia reduces tissue perfusion, depriving cells of oxygen and nutrients essential for their function and survival.
Additionally, hypovolemia can result in systemic hypoperfusion and organ dysfunction, leading to complications such as shock,
organ failure, and even death if not promptly addressed.
burn → inflammatory response → histamines and cytokines → increased capillary
permeability → fluid shifts from intravasc. to interstitial space → fluid loss (risk for
hypovolemia)
Evaporation - skin barrier damaged leading to loss of
moisture
Increased metabolic demand - increased fluid
requirements for tissue repair, thermoregulation and
other metabolic processes for healing
Inflammatory response - i

45. Associated with closed-space fire and
conditions that decrease mentation
(overdose, alcohol intoxication, drug
abuse, head injury)
exposure to smoke --> exposure to heat,
particulate matter, toxic gases
INHALATION INJURY

46. SMOKE INHALATION
Causes injury in two ways:
direct heat injury to the upper airways1.
inhalation of combustion products into the lower
airways
2.
Direct heat injury-> airway swelling-> maximal
edema
endotracheal intubation necessary
Combustion products in smoke-> lower airway
injury
toxic inhalants (3): tissue asphyxiants,
pulmonary irritants, systemic toxins

49. SMOKE INHALATION
Combustion products in smoke:
two major tissue asphyxiants:
carbon monoxide
hydrogen cyanide
irritants cause direct mucosal injury:
mucosal sloughing, edema, reactive
bronchoconstriction, obstruction of
lower airways

52. humidified oxygen (100%) by facemask
obtain ABG (carboxyhemoglobin levels)
Endotracheal intubation
indications: full thickness burns of face or perioral
region, circumferential neck burns, acute respiratory
distress, progressive hoarseness or air hunger,
respiratory depression or altered mental status,
supraglottic edema and inflammation on
bronchoscopy
routine use of nebulized bronchodilators (albuterol)
recommended
nebulized N-acetylcysteine, aerosolized heparin,
intrabronchial surfactant (severe burns with
inhalation injury), last effort - inhaled nitric oxide
TREATMENT

53. HEAT
REGULATION
IN BURN
PATIENTS

54. Skin performs thermal regulation
Loss of skin surface from burn leads to direct
loss of its functions —> resulting in alteration in
thermoregulation, sweat regulation and
alteration of regulation of blood flow (heat
losses by radiation and convection)
Burn patients needs to maintain higher body
temperature due to increased energy
expenditure
High ambient temperature —> decreases hyper-
metabolic response and therefore energy
consumption
HEAT REGULATION

55. in burn patients, overall metabolism is
increased and skin and body temp is higher
than normal
hypermetabolic response, hypothalamic
reprogramming causes increase in basal
temperature in burn patients to 37-38.5
degrees Celsius
Burn patients are at increased risk for
hypothermia due to unprotected and
prolonged body surface exposure and loss of
protective thermoregulation provided by
normally intact skin
HEAT REGULATION

56. high body temperature is a systemic response
to burn injury
hypermetabolic processes --> increase in core
+ skin temperature (2 degrees C above normal)
mild hyperthermia upon first 24 hours following
burn injury normal due to release of pyrogens
72 hours- systemic inflammatory response
syndrome
reference:
https://www.sciencedirect.com/science/article/pii/S2468912217300159#:~:text=Hyperthe
rmia%20which%20has%20been%20defined,in%20such%20patients%20%5B1%5D.
HEAT REGULATION

57. METABOLIC
ABNORMALITIES
IN BURNS

62. TNF

64. BURN SHOCK

67. RAAS SYSTEM

69. PATHOPHYSIOLOGY OF BURN
THE INITIAL RESPONSE TO A BURN INVOLVES
THREE DISTINCT ZONES: ZONE OF
COAGULATION, ZONE OF STASIS, AND ZONE
OF HYPEREMIA.

70. TYPES OF BURN
1. THERMAL BURNS
THESE ARE CAUSED BY HEAT
SOURCES SUCH AS HOT
METALS, SCALDING LIQUIDS,
STEAM, AND FLAMES, WHICH
RAISE THE TEMPERATURE OF
THE SKIN AND TISSUES,
LEADING TO TISSUE CELL
DEATH. THEY ARE CLASSIFIED
AS FIRST-, SECOND-, OR
THIRD-DEGREE BURNS,
DEPENDING ON THE DEPTH OF
PENETRATION INTO THE
SKIN'S SURFACE
2. ELECTRICAL BURNS:
CAUSED BY ELECTRIC
CURRENT TRAVELING
THROUGH THE BODY,
RESULTING IN TISSUE
DAMAGE. THEY CAN LEAD
TO A SYSTEMIC
INFLAMMATORY
RESPONSE AND AFFECT
MULTIPLE ORGAN
SYSTEMS.

71. 3. CHEMICAL BURNS
RESULT FROM EXPOSURE TO
CORROSIVE SUBSTANCES,
CAUSING TISSUE DAMAGE
THROUGH A CHEMICAL
REACTION. THESE BURNS ARE
DUE TO STRONG ACIDS,
ALKALIES, DETERGENTS, OR
SOLVENTS COMING INTO
CONTACT WITH THE SKIN OR
EYES. THE SEVERITY DEPENDS
ON THE TYPE AND
CONCENTRATION OF THE
CHEMICAL
4. RADIATION BURNS
CAUSED BY EXPOSURE TO
NUCLEAR RADIATION OR
ULTRAVIOLET LIGHT,
LEADING TO TISSUE
DAMAGE AND CELL DEATH.
THE SEVERITY DEPENDS ON
THE DURATION AND
INTENSITY OF EXPOSURE

72. PHARMACOLOGY OF
ANALGESICS

73. PATHWAY

74. PATHWAY

75. PATHWAY

76. PATHWAY

77. PATHWAY

78. PATHWAY

79. PATHWAY

80. PATHWAY

81. PATHWAY

82. PATHWAY

83. PATHWAY

84. high body temperature is a systemic response
to burn injury
hypermetabolic processes --> increase in core
+ skin temperature (2 degrees C above normal)
mild hyperthermia upon first 24 hours following
burn injury normal due to release of pyrogens
72 hours- systemic inflammatory response
syndrome
reference:
https://www.sciencedirect.com/science/article/pii/S2468912217300159#:~:text=Hyperthe
rmia%20which%20has%20been%20defined,in%20such%20patients%20%5B1%5D.
HEAT REGULATION

85. REHABILITATION
OF BURN
PATIENT

87. PHYSICAL THERAPY
focuses on improving the
patient's ability to move their
body
OCCUPATIONAL THERAPY
FOCUSES ON IMPROVING THE PATIENT'S
ABILITY TO PERFORM ACTIVITIES OF DAILY
LIVING(ADL).
A STUDY ON BURN
PATIENTS FOUND THAT
EARLY INTERVENTION
WITH OCCUPATIONAL
THERAPY LED TO
IMPROVED HAND
FUNCTIONALITY AND
QUALITY OF LIFE!!!

89. IT IS ESSENTIAL THAT
PHYSICAL
REHABILITATION IS
COMMENCED AT DAY 1
OF ADMISSION
WHETHER THE PATIENT
IS AMBULANT AND
WELL OR ON BED REST
AND IMMOBILE.

91. THIS AXILLARY CONTRACTURE CAN BE PREVENTED BY LYING
AND SITTING WITH ARMS ABDUCTED AT 90 DEGREES
SUPPORTED BY PILLOWS OR FOAM BLOCKS BETWEEN
CHEST AND ARMS AND FIGURE OF EIGHT BANDAGING OR
STRAPPING TO PROVIDE STRETCH ACROSS CHEST.
CLAWING OF FINGERS CAN BE AVOIDED BY
KEEPING THE MP JOINTS IN FLEXION, IP JOINTS IN
EXTENSION, THUMB MID PALMAR RADIAL
ABDUCTION.

92. THIS GROSS MANDIBULAR DEFORMITY, MALOCCLUSION
AND NECK CONTRACTURE CAN BE PREVENTED BY
PROPER NURSING AND SPLINTAGE. A WELL PADDED
TUBE CAN BE INSERTED INTO THE MOUTH TO COMBAT
MOUTH CONTRACTURE.

94. Infection in burns is defined as the presence of high concentrations (>10^5
organisms/g of tissue) of bacteria in the burn wound and scab.
Invasive infection is the leading cause of death and morbidity in burn patients,
accounting for 51% of deaths.
Invasive infection of burn wounds constitutes a surgical emergency due to high
bacterial concentrations and necrosis, often accompanied by sepsis signs and
burn wound discoloration. Urgent resuscitation, broad-spectrum
antimicrobials, antifungals, and surgical debridement are imperative.
WHAT ARE POSSIBLE MICROORGANISMS
THAT AFFECT PATIENT?
NORBURY, W., HERNDON, D. N., TANKSLEY, J., JESCHKE, M. G., & FINNERTY, C. C. (2016).
INFECTION IN BURNS. SURGICAL INFECTIONS, 17(2), 250–255.
HTTPS://DOI.ORG/10.1089/SUR.2013.134

95. Staphylococcus aureus remains a prominent cause of burn wound infections, with methicillin-resistant
strains becoming predominant due to broad-spectrum antibiotic use. Staphylococci produce toxins
facilitating tissue invasion and systemic spread, contributing to high infection rates and graft loss.
Pseudomonas aeruginosa is pervasive in burn wounds and can lead to severe infections and sepsis,
requiring careful management with antibiotics
Streptococci, once common, are now easily treated with penicillin's, with Group A (S. pyogenes) posing
occasional challenges, particularly in graft failure.
Enterococcus infections have declined but are significant due to emerging vancomycin-resistant
strains, emphasizing the need for vigilance and alternative treatments like linezolid.
WHAT ARE POSSIBLE MICROORGANISMS
THAT AFFECT PATIENT?
NORBURY, W., HERNDON, D. N., TANKSLEY, J., JESCHKE, M. G., & FINNERTY, C. C. (2016).
INFECTION IN BURNS. SURGICAL INFECTIONS, 17(2), 250–255.
HTTPS://DOI.ORG/10.1089/SUR.2013.134

96. Acinetobacter infections are increasing, often requiring carbapenems or colistin due to resistance.
Enterobacteriaceae, while less problematic, can cause pneumonia and urinary tract infections, with
evolving resistance patterns.
Anaerobes are rare causes of infection, typically seen in specific scenarios like myonecrosis.
Fungal infections are increasing due to antimicrobial use, with Candida albicans and molds like
Aspergillus posing significant risks, necessitating antifungal agents like caspofungin or voriconazole.
Viral infections can occur secondary to burn wounds, requiring prompt antiviral treatment.
WHAT ARE POSSIBLE MICROORGANISMS
THAT AFFECT PATIENT?
NORBURY, W., HERNDON, D. N., TANKSLEY, J., JESCHKE, M. G., & FINNERTY, C. C. (2016).
INFECTION IN BURNS. SURGICAL INFECTIONS, 17(2), 250–255.
HTTPS://DOI.ORG/10.1089/SUR.2013.134

97. COMPUTATION
OF TOTAL FLUID
REPLACEMENT

98. Used to calculate the ideal amount of fluid
required for fluid resuscitation in burn patients.
rehydrate and prevent further damage to burn
patients.
Severe burns can trigger an inflammatory
response system, increasing capillary
permeability.
intravascular fluid, plasma proteins, and
electrolytes move to the interstitial space.
hypoperfusion, decreased cardiac output, and
potentially cardiogenic shock and tissue
damage.
Hypoperfusion can progress to end organ
ischemia if left untreated.
The Parkland formula is particularly crucial
within the first 24 hours after a burn injury when
fluid resuscitation is critical.
PARKLAND FORMULA

99. Prevent VOLUME OVERLOAD

100. 4.5% anterior head
9% chest with neck
9%abdomen
4.5%left
forearm
4.5%right
forearm
1% groin
4.5%left
thigh
4.5%right
thigh
2.25% left
forearm
2.25%right
forearm
9%left
thigh
9%right
thigh
ANTERIOR PART
50.5% BSA 37% BSA

101. Volume of lactated ringers =
4ml x 50.5% x assuming 40kg

102. 4ml x 50.5% x assuming 40kg
= 8080 ml / 1000ml/L = 8.08L
8.08L / 2 = 4.04L 8.08L / 2 = 4.04L

103. Volume of lactated ringers =
4ml x 37% x wt in kg

104. 4ml x 37% x assuming 40kg
= 5920 ml / 1000ml/L = 5.92L
5.92L / 2 = 2.96L 5.92L / 2 = 2.96L

105. The Parkland formula is used only as a guide for resuscitation. The patient is
continually reassessed with frequent vital signs.
A Foley catheter is mandatory, as urine output is the single best indicator of
adequacy of resuscitation.
The resuscitation is adjusted to keep a urine output between 0.5 and 1 mL/kg per
hour (30 to 50 mL/hour in adults).
Maintenance fluids are replaced with D5½NS. (D51/2NS, 0.9 NaCl. Volume
expanders. Are solutions used to increase the blood volume after a severe blood
loss, or loss of plasma.)
NOTES

106. The Parkland formula consists of 4 mL/kg per %TBSA burn of lactated Ringer's (LR) for
the first 24 hours. Colloid and D5½NS maintenance fluid are given beginning at 24
hours post-burn as described below:
a. 2 mL x kg x %TBSA given over first 8 hours post-burn
2ml x 40kg x 50.5% = 4040ml/4.04L
b. 1 mL x kg x %TBSA given over second 8 hours post-burn
1 mL x 40kg x 50.5% = 2020ml/2.02L
c. 1 mL x kg x %TBSA given over third 8 hours post-burn
1 mL x 40kg x 50.5% = 2020ml/2.02L
MAINTENANCE

107. The Parkland formula consists of 4 mL/kg per %TBSA burn of lactated Ringer's (LR) for
the first 24 hours. Colloid and D5½NS maintenance fluid are given beginning at 24
hours post-burn as described below:
d. 0.1 mL x kg x %TBSA of 25% albumin given over the first 4 hours of the second day
to correct hypoalbuminemia.
0.1 x 40kg x 50.5% = 202ml/0.202L
e. 1 mL x kg x %TBSA D5½NS given per day of maintenance fluid (D51/2NS, 0.9 NaCl.
Volume expanders. Are solutions used to increase the blood volume after a severe
blood loss, or loss of plasma.)
1 mL x 40kg x 50.5% = 2020ml/2.02L

MAINTENANCE

108. The Parkland formula consists of 4 mL/kg per %TBSA burn of lactated Ringer's (LR) for
the first 24 hours. Colloid and D5½NS maintenance fluid are given beginning at 24
hours post-burn as described below:
a. 2 mL x kg x %TBSA given over first 8 hours post-burn
2ml x 40kg x 37% = 3040ml/3.04L
b. 1 mL x kg x %TBSA given over second 8 hours post-burn
1 mL x 40kg x 37% = 1480ml/1.48L
c. 1 mL x kg x %TBSA given over third 8 hours post-burn
1 mL x 40kg x 37% = 1480ml/1.48L
MAINTENANCE

109. The Parkland formula consists of 4 mL/kg per %TBSA burn of lactated Ringer's (LR) for
the first 24 hours. Colloid and D5½NS maintenance fluid are given beginning at 24
hours post-burn as described below:
d. 0.1 mL x kg x %TBSA of 25% albumin given over the first 4 hours of the second day
to correct hypoalbuminemia.
0.1 x 40kg x 37% = 148ml/.148L
e. 1 mL x kg x %TBSA D5½NS given per day of maintenance fluid (D51/2NS, 0.9 NaCl.
Volume expanders. Are solutions used to increase the blood volume after a severe
blood loss, or loss of plasma.)
1 mL x 40kg x 37% = 1480ml/1.48L

MAINTENANCE

110. “Clostridium tetani spores are ubiquitous
in the environment and enter the body
through nonintact skin”
- Kretsinger, K., et al., CDC, 2006
IMPORTANCE OF
ANTI-TETANUS SERUM
“The spores are ubiquitous in soil and
animal feces and can survive on
environmental surfaces for years. In
agricultural areas, adults may harbor the
organism; spores are found in many
places, including on the skin...”
- Tintinalli’s Emergency Medicine: A Comprehensive
Guide, 9th Edition

111. TYPES OF TISSUE
TRANSPLANT

112. TYPES OF TISSUE
TRANSPLANT

113. Occurs when a burn scar matures, thickens, and
tightens.
a long term complication of burn injury that
can result in significant morbidity.
result from both contracture and scar
contracture and prevents range of motion of a
particular joint.
CONTRACTURES

114. burn depth
activation of dermal fibroblasts,
microfibroblasts, fibricytes,
and Helper T Cells.
FACTORS INFLUENCING
CONTRACTURES
DEVELOPMENT

115. surgical and non surgical options ranging
from oressure garments and splints to laser
therapy and contracture excision.
TREATMENT

116. WHAT ABOUT SPORTS
AND EXERCISE?
Explain how exercise can
help manage diabetes.

117. WHAT TYPES OF
MEDICATION WILL
YOU NEED?
Explain the type medications for people with
diabetes.

118. THANK YOU!
Thank you so much for watching our
presentation! Do you have any questions,
comments, or suggestions?

119. GET IN TOUCH
SOCIAL MEDIA:
@reallygreatsite
CONTACT NUMBER:
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WEBSITE:
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EMAIL ADDRESS:
[email protected]

121. IMMEDIATE
CONCERNS
FOR
DROWNING

122. Children under
5 years old
EPIDEMIOLOGY
3 VULNERABLE GROUPS
Elderly
individuals
Adolescents and
young adults (15-
24 years old)

123. PRE HOSPITAL
IMMEDIATE
CONCERNS FOR DROWNING
HOSPITAL

124. Initial management involves coordinated
prehospital care following ABCs (airway,
breathing, circulation).
SAFETY!
CPR at the scene is imperative
Focus on rapidly restoring oxygenation,
ventilation, and circulation.
IMMEDIATE CONCERNS FOR DROWNING

125. Focus on rapidly restoring oxygenation, ventilation, and
circulation.
A-AIRWAY
Clear airway of vomitus and foreign material.
Protect cervical spine if traumatic neck injury is
suspected.
B-Breathing
Initiate ventilatory support immediately for ineffective
respiration or apnea.
Administer supplemental oxygen as soon as available.
IMMEDIATE CONCERNS FOR DROWNING

126. C-CIRCULATION
Evaluate and treat cardiovascular status
urgently.
Consider hypothermia and its effects on
myocardial function; rewarming may be
necessary.
IV fluids and vasoactive medications may be
required to improve circulation.
Consider intraosseous catheter placement for
rapid vascular access.
PRE HOSPITAL
IMMEDIATE CONCERNS FOR DROWNING

130. SPEECH DISORDER
CAUSED BY ANOXIC
BRAIN INJURIES

131. Oxygen and Brain Function:
Oxygen is crucial for the brain to utilize
glucose, its primary energy source.
Consciousness can be lost within 15 seconds
without oxygen, and brain damage can occur
after about four minutes.
Types of Oxygen Deprivation:
Cerebral Anoxia: Complete interruption of
oxygen supply to the brain.
Cerebral Hypoxia: Partial oxygen supply
inadequate for normal brain function.
SPEECH DISORDER CAUSED BY ANOXIC BRAIN INJURIES
Hypoxic and anoxic brain injury

132. Cardiac or respiratory arrest
Irregular heart rhythm resulting in inefficient
supply of blood to the brain
Very low blood pressure (shock), resulting from
blood loss (haemorrhage) or disturbed heart
function
Suffocation, Choking, Strangulation
Very severe asthma attack
Near drowning
Smoke inhalation
Carbon monoxide inhalation
Poisoning
etc.
SPEECH DISORDER CAUSED BY ANOXIC BRAIN INJURIES
CAUSES

133. Hypoxic/Anoxic Brain Injury:
Mild:
Concentration, attention, coordination, and short-term memory issues.
Symptoms: headache, dizziness, increased breathing, sweating, restricted vision.
Severe:
Confusion, agitation, drowsiness.
Cyanosis (bluish skin), myoclonus (limb jerks), seizures.
Loss of consciousness and coma.
Vulnerable Areas:
Cerebral cortex (parietal and occipital lobes).
Hippocampus (memory).
Basal ganglia and cerebellum (movement control).
SPEECH DISORDER CAUSED BY ANOXIC BRAIN INJURIES
INITIAL effects of hypoxic/anoxic brain injury

134. SPEECH DISORDER CAUSED BY ANOXIC BRAIN INJURIES
LONGTERM effects of hypoxic/anoxic brain injury

135. SPEECH DISORDER CAUSED BY ANOXIC BRAIN INJURIES
LONGTERM effects of hypoxic/anoxic brain injury
Physical effects
Visual disorders
Visual disorders
Speech and language
Executive dysfunction
Emotional and behavioural
changes
Hormonal imbalances

136. SPEECH DISORDER CAUSED BY ANOXIC BRAIN INJURIES
LONGTERM effects of hypoxic/anoxic brain injury
Damage to Speech Centers
(Broca’s area, etc.)
Neurological Impairments
Cognitive and Language
Psychological Factors
Secondary Muscle Effects

137. SPEECH DISORDER CAUSED BY ANOXIC BRAIN INJURIES
Articulation Disorders:
Substituting "wabbit" for "rabbit"
Omitting "s" in "spoon" (saying "poon" instead)
Phonological Disorders:
Simplifying words by saying "tat" for "cat" or "gog" for "dog"
Difficulty with consonant clusters, saying "poon" for "spoon" consistently
Fluency Disorders (Stuttering):
Repetitions: "I-I-I want..."
Prolongations: "Sssssssstop"
Blocks: Silent pauses or hesitation before starting a word

138. SPEECH DISORDER CAUSED BY ANOXIC BRAIN INJURIES
Voice Disorders:
Hoarse voice quality
Breathy voice quality
Strained or effortful voice production
Resonance Disorders:
Hypernasality: Excessive nasal sound in speech due to conditions like cleft
palate
Hyponasality: Insufficient nasal resonance, often heard in individuals with
nasal congestion

139. SPEECH DISORDER CAUSED BY ANOXIC BRAIN INJURIES
Apraxia of Speech:
Difficulty sequencing sounds and syllables, resulting in speech
errors like saying "banana" instead of "panama"
Inconsistent speech sound errors, where the same word may be
pronounced differently each time
Dysarthria:
Slurred speech due to weakness or incoordination of speech
muscles
Imprecise articulation and reduced speech intelligibility
Difficulty controlling pitch, loudness, and voice quality

140. SPEECH DISORDER CAUSED BY ANOXIC BRAIN INJURIES