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Burns

Burns are classified based on their depth and extent of damage, and can be caused by heat, flames, chemicals, electricity, or radiation. Severe burns affecting over 30% of the body surface can lead to life-threatening shock, organ failure, and infections. Proper first aid for burns includes stopping the burning process, cooling the affected area with cool water, and seeking immediate medical attention for significant injuries.

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0% found this document useful (0 votes)
26 views31 pages

Burns

Burns are classified based on their depth and extent of damage, and can be caused by heat, flames, chemicals, electricity, or radiation. Severe burns affecting over 30% of the body surface can lead to life-threatening shock, organ failure, and infections. Proper first aid for burns includes stopping the burning process, cooling the affected area with cool water, and seeking immediate medical attention for significant injuries.

Uploaded by

Kago Ngoma
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPT, PDF, TXT or read online on Scribd
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BURNS

MS. CHRISTINE
Definition

• Burns are a result of the effects of thermal


injury on the skin and other tissues
• Human skin can tolerate temperatures up to
42-440 C (107-1110 F) but above these, the
higher the temperature the more severe the
tissue destruction
• Below 450 C (1130 F), resulting changes are
reversible but >450 C, protein damage
exceeds the capacity of the cell to repair
Classification According to Depth
• First-degree Burns (mild): epidermis
 Pain, erythema & slight swelling, no blisters
 Tissue damage usually minimal, no scarring
 Pain resolves in 48-72 hours
• Superficial Second-degree Burns: entire epidermis &
variable dermis
 Vesicles and blisters characteristic
 Extremely painful due to exposed nerve endings
 Heal in 7-14 days if without infection
• Midlevel to Deep Second-degree Burns:
 Few dermal appendages left
 There are some fluid & metabolic effects
• Full-thickness or Third-Degree: entire epidermis and
dermis, no residual epidermis
 Painless, extensive fluid & metabolic deficits
 Heal only by wound contraction, if small, or if big,
by skin grafting or coverage by a skin flap
Burn Photos
2nd degree Burn 1 day

Mild Burn

2nd degree Burn 2 days

2nd degree Burn 1 hr


Extent of Burns
Classification According to Extent

• Mild: 10% Infant Rule of Nines


(for quick assessment of
• Moderate:
total body surface area
10-30% affected by burns)
• Severe: > 30% Anatomic Surface
structure area

• Hospitalization Head 18%


for > 10% of Anterior Torso 18%
body surface area Posterior Torso 18%
Each Leg 14%
Each Arm 9%
Perineum 1%
Kinds of Burns
• Scald Burn: most frequent in home injuries; hot
water, liquids and foods are most common causes;
above 65o C, cell death
• Flame Burn: due to gasoline, kerosene, liquified
petroleum gas (LPG) or burning houses
• Chemical Burn: common in industries and
laboratories but may also occur at home; acid is
more common than alkali
• Electrical Burn: worse than the other types; with
entrance and exit wounds; may stop the heart and
depress the respiratory center; may cause
thrombosis and cataracts
• Radiation Burn: from X-ray, radioactive radiation
and nuclear bomb explosions
Burn Photos

Scald Burns Flame Burns


Burn Photos

Radiation (Flash) Burns

Chemical (Acid) Burns


Burn Photos
Severe swelling
peaks 24-72 hrs after
Electrical Burns
Exit Wounds

Electrical burns mummified


1st 2 fingers later removed

Electrical Burns
Entrance Wounds

Entrance wound of electrical


burns from an overheated tool
U.S. Statistics
• About 2.4 million people • The majority of children <4
suffer burns annually years hospitalized for burn-
• Account for an estimated related injuries suffer from
700,000 ER visits per year scald burns (65%) or
and 45,000 require contact burns (20%)
hospitalizations
• Between 8,000-12,000 burn
patients die, and
approximately one million
will sustain substantial or
permanent disabilities
• Fires kill about 500 children
<14 years annually and
injure 40,000 others
• Fire ranks 5th among
accidental injuries, after
motor accidents, poisoning,
falls and drowning
Review of PGH Cases
• Period from January 1, 2000 to February 28, 2002
revealed 205 cases of pediatric burns
• Majority of pediatric burn injuries occur at home affecting
children <5 years with mean age of 5.35 years old
• The risk of pediatric burn injury is inversely proportional to
socioeconomic status
• Less common burn forms are from fires, firecrackers,
explosions and electric shock

60.00% Flame < 2 years


33.66% 48.78% > 2-17 years
40.00% Electrical 51.22%
Scalding 13.66%
20.00%
52.68%
0.00%
Physiological Response
• Typically, biphasic response
• The initial period of hypofunction manifests as: (a)
Hypotension, (b) Low cardiac output, (c) Metabolic acidosis, (d)
Ileus, (e) Hypoventilation, (f) Hyperglycemia, (g) Low oxygen
consumption and (h) Inability to thermoregulate
• This ebb phase occurs usually in the first 24 hours and responds
to fluid resuscitation
• The flow phase, resuscitation, follows and is characterized by
gradual increases in (a) Cardiac output, (b) Heart rate, (c)
Oxygen consumption and (d) Supranormal increases of
temperature
• This hypermetabolic hyperdynamic response peaks in 10-14
days after the injury after which condition slowly recedes to
normal as the burn wounds heal naturally or surgically closed
by applying skin grafting
Pathologic Features

• Zone of coagulation (necrosis): Superficial area of coagulation


necrosis and cell death on exposure to temperatures >450
(primary injury)
• Zone of stasis (vascular thrombosis): Local capillary circulation
is sluggish, depending on the adequacy of the resuscitation, can
either remain viable or proceed to cell death (secondary injury)
• Zone of hyperemia (increased capillary permeability)
Burn Pathophysiology: Edema
• Injured tissue  Increased permeability of entire
vascular tree  loss of water, electrolytes and
proteins from the vascular compartment  severe
hemoconcentration
• Protein leakage  resultant hypoproteinemia,
increased osmotic pressure in the interstitial space
• Decreased cell membrane potential cause inward shift
of Na+ and H2O  cellular swelling
• In the injured skin, effect maximal 30 min after the
burn but capillary integrity not restored until 8-12
hours after, usually resolved by 3-5 days
• In non-injured tissues, only mild and transient leaks
even for burns >40% BSA
Burn Pathophysiology: Cardiac
• Cardiac output decreases due to:
1) Decreased preload induced by fluid shifts
2) Increased systemic vascular resistance caused by
both hypovolemia and systemic catecholamine
release
3) A myocardial depressant factor has been
described that impairs cardiac function
• Cardiac output normal within 12-18 hours, with
successful resuscitation
• After 24 hours, it may increase up to 2 ½ times
the normal and remain elevated until several
months after the burn is closed
Burn Pathophysiology: Blood
• The red-cell mass decreases due to direct losses
• Immediate, 1-2 hours after, and delayed, 2-7 days
postburn, hemolysis occurs due to damaged cells and
increased fragility
• Anemia within 4-7 days is common and expected,
typically, will persist until wound healing occur;
depressed erythropoietin levels documented
• Early mild thrombocytopenia (sequestration) followed
by thrombocytosis (2-4x normal) and elevated
fibrinogen, factor V and factor VIII levels commonly
by end of the 1st week
• A “normal” platelet or fibrinogen level may be an
early sign of disseminated intravascular coagulation
• Persistent thrombocytopenia is associated with poor
prognosis -- suspect sepsis
Burn Pathophysiology: Metabolic
• Severe catabolism with breakdown of muscle protein
for gluconeogenesis as acute response
• Prostaglandins and cytokines implicated in increased
core temperature of 1-20 C and in initiating
acceleration of nitrogen catabolism
• Plasma levels of catecholamines, glucagon and
cortisol all increase, maximal in patients with 50-60%
TBSAB, while insulin and thyroid hormone levels
decrease
• Hypermetabolic response may approach 200% of
BMR (basal metbolic rate) remaining elevated for months
after burn closed
• Early enteral feeding associated with lessening of the
hypermetabolic response
Burn Pathophysiology: Renal
• Renal blood flow and GFR decrease soon after due to
hypovolemia, decreased cardiac output, and elevated
systemic vascular  oliguria and antidiuresis
develops during 1st 12-24 hours
• Followed by a usually modest diuresis as the capillary
leaks seal, plasma volume normalizes, and cardiac
output increases after successful resuscitation and
coinciding with onset of the postburn hypermetabolic
state, and hyperdynamic circulation
Burn Pathophysiology: Immunologic
• Mechanical barrier to infection is impaired because of
skin destruction
• Immunoglobulin levels decreased as part of general
leak and leukocyte chemotaxis, phagocytosis, and
cytotoxic activity impaired
• The reticuloendothelial system's depressed bacterial
clearance is due to decreases in opsonic function
• These changes, together with a non-perfused,
bacterially-colonized eschar overlying a wound full of
proteinaceous fluid, put the patient in a significant
risk for infection
First Aid Measures in Burns
1. Extinguish flames by rolling in the ground, cover
child with blanket, coat or carpet
2. After determining airway is patent, remove
smoldering clothes and constricting accessories
during edema phase in the 1st 24-72 hours after
3. Brush off remaining chemical if powdered or solid
then wash or irrigate abundantly with water
4. Cover burn wounds with clean, dry sheet and apply
cold (not iced) wet compresses to small injuries;
significant burns (>15-20% BSA) decreases body
temperature which contraindicates use of cold
compress dressings
5. If burn caused by hot tar, mineral oil to remove it
Outpatient Management
• For 1st and 2nd degree burns less than
10% BSA
• Blisters should be left intact and
dressed with silver sulfadiazine cream
• Dressings should be changed daily
washing with lukewarm water to
remove any cream left
Recommendations for Hospitalization
1. Total burns >10% BSA or >2% full
thickness, halved for <2 or >40 yr
2. Hands, face, feet or genitalia involved
3. Evidence or suspicion of inhalation injury
4. Associated injuries present
5. Suspicion that burn inflicted
6. Burn is infected
7. Burn circumferential
8. History of prior medical illness
9. Patient is comatose
10.Patient or family unable to cope with
situation
Hospital Management
1. General assessment and cardiopulmonary
stabilization
2. Resuscitation
3. Establishment of IV lines and blood studies
4. Wound care and infection control
5. Pain relief and psychological support
6. Nutritional support
7. Physical Therapy/Occupational Therapy
Initial Procedures
• Fluid infusion must be started immediately
• NGT insertion to prevent gastric dilatation,
vomiting and aspiration
• Urinary catheter to measure urine output
• Weight important and has to be taken daily
• Local treatment delayed till respiratory
distress and shock controlled
• Hematocrit and bacterial cultures necessary
Fluid Resuscitation
• For most, Parkland formula a suitable starting guide
(4 ml Ringer’s Lactate/kg body weight/% BSA
burned), ½ to be given over 1st 8 hr from time of
onset while remaining over the next 16 hr
• During 2nd 24 hr, ½ of 1st day fluid requirement to be
infused as D5LR
• Oral supplementation may start 48 hr after as
homogenized milk or soy-based products given by
bolus or constant infusion via NGT
• Albumin 5% may be used to maintain serum albumin
levels at 2 g/dl
• Packed RBC recommended if hematocrit falls below
24% (Hgb <8 g/dl)
• Sodium supplementation may be needed if burns
greater than 20% BSA
Inhalation Injury
• Three syndromes:
1. Early CO poisoning, airway obstruction &
pulmonary edema major concerns
2. Acute Resp. Distress Syndrome usually at 24-48
hrs or much later
3. Pneumonia and pulmonary emboli as late
complications (days to weeks)
• Assessment:
1. Observation (swelling or carbonaceous material
in nasal passages
2. Laboratory determination of carboxyhemoglobin
and ABGs
• Treatment:
1. Maintain patent airway by early ET intubation,
adequate ventilation and oxygenation
2. Aggressive pulmonary toilet and chest
physiotherapy
Infection Control
• Tetanus prophylaxis: 250-500 IU TIG or 3000 units
equine ATS ANST IM; Toxoid also
• Antibiotic of choice is one that will include
Pseudomonas in its spectrum; most frequent
pathogens in burns are Staphylococcus aureus,
Pseudomonas aeruginosa and the Klebsiella-
Enterobacter species
• Topical therapy:
 0.5% Silver nitrate dressing
 Mafenide acetate or Sulfacetamide acetate cream
 Silver sulfadiazine cream
 Povidone-iodine ointment
 Gentamicin cream or ointment
Pain Relief and Adjustment
• Important to provide adequate analgesia,
anxiolytics and psychological support to:
a) Reduce early metabolic stress
b) Decrease potential for posttraumatic
stress syndrome
c) Allow future stabilization and
rehabilitation
• Family support patient through grieving
process and help accept long-term changes
in appearance
Complications of Burns
• Burn Shock
• Pulmonary complications due to inhalation
injury
• Acute Renal Failure
• Infections and Sepsis
• Curling’s ulcer in large burns over 30%
usually after 9th day
• Extensive and disabling scarring
• Psychological trauma
• Cancer called Marjolin’s ulcer, may take 21
years to develop

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