BURN CME.pptx

BURN
PRESENTER : NAJMI SHAFIZ BIN ROZMAN

Definition
A burn is by definition is thermal injury caused by biological , chemical, electrical and
physical agents with local and systemic reprecussions

Types and Causes
Thermal burns are burns due to external heat sources that raises skin and tissue temperature causing
tissue cell death or charring. Flame is the most common type of burn. Inhalation injury is found in 30%
of victims of major flame burns.
Chemical burns are due to strong acids, alkalis, detergents or solvents coming into contact with the skin.
Tissues are damaged by protein coagulation or liquefaction rather than hyperthermic activity.
Electrical burns are due to electrical current or lightning coming in contact with the body.
Cold injury - frostbite
Ionising radiation- sunburn

Degree of burns
First degree burns or superficial burns appears similar to sunburn that is
painful, dry, swollen, erythematous without blisters and involves only the
epidermis. It causes redness, mild pain, but there is no blistering. A sun-burn is a good
example of a 1st degree burn
Second degree burns or partial-thickness burns has appearance of moist blebs,
formation of vesicle and blister; underlying tissue is mottled pink and white with good
capillary refill; this involves the entire epidermis and a variable portion of the dermal
layer. Blister formation with fluid accumulation are classic signs. Blisters are formed
when the epidermis seperates from the dermis because of fluid accumulation between
these layers. Accessory structures such as hair follicles, and sebacious and sudoriferous
glands are usually not damaged. These burns may take 3-4 weeks to heal.
Third degree burns or full-thickness burns appears dry, leathery eschar, mixed white
waxy, khaki, mahogany and soot stained. It involves the entire epidermis and dermis,
leaving no residual epidermis cells, may include fat, subcutaneous tissue, fascia,
muscle and bone. Because sensory nerves have been destroyed, the area is numb with
marked edema.

First-Degree Burns or Superficial Burns
Appearance: Similar to sunburn – painful, dry, swollen, erythematous
without blisters & involves only the epidermis
Not included in estimates for fluid resuscitation
Hospitalization not required; pain resolves in 48-72 hours, peels off
without residual scarring in 2-5 days
Second-Degree Burns or Partial-Thickness Burns
Appearance: Moist blebs, formation of vesicle & blister; underlying tissue
is mottled pink & white with good capillary refill; this involves the entire
epidermis & a variable portion of the dermal layer
Considered significant burns & are counted in burn size estimates
Subclassification
Superficial:
Extreme pain attributed to a large number of remaining viable nerve
endings exposed
Re-epithelialize in 7-14 days in the absence of infection
Deep
Pain is less because fewer nerve endings remain viable; fluid losses &
metabolic effects are similar to those of third-degree burn
Heals in 21-35 days if without infection; converts to full thickness
burns if with wound infection, some may require grafting
Third-Degree Burns or Full-Thickness Burns
Appearance: Dry, leathery eschar, mixed white waxy, khaki, mahogany,
soot-stained
Involves the entire epidermis & dermis, leaving no residual epidermis
cells, may include fat, subcutaneous tissue, fascia, muscle & bone
No pain sensation & capillary filling
Wound cannot epithelialize, heals only by wound contracture or skin
grafting
The difference in the growth rate of the head & extremities throughout
childhood makes it necessary to use surface area charts
The “rule of nines” used in adults is applicable only to children >14 year
or as a very rough estimate to initiate therapy before transfer to a burn
unit
In small burns <10%, the “rule of palm” (area from the wrist crease to
finger crease in the child) may be used
This equals 1% of the child’s body surface area (BSA)
Calculation of the fluid for resuscitation depends on the total BSA
involved in the burn injury

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 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 >45 degree celcius (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:
Decreased preload induced by fluid shifts
Increased systemic vascular resistance caused by both hypovolemia and systemic
catecholamine release
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 1-2 degree
celcius 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 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

History
Find out the exact mechanism, including temperature of flame or water,duration of
contact, concentration of chemical, voltage etc
Record factors suggesting inhalation injury, e.g. burns in a confined space,flash burns.
Enquire about other injuries.
Document first aid given so far.
Document timings of injury, first aid, and resuscitation

Physical Examination
Estimate area of burn(TBSAB) Do not include areas of unblistered erythema.
Rule of nines
Rule of palm Patient’s hand is approximately 1% total body surface area (TBSA).
Lund and Browder chart is the most accurate method
Minor <15% tbsa
Moderate 20-25% tbsa
Severe >25 % tbsa
Rule of nine
-Adult : head 9 % back 18% chest 18% r arm 9% perineum 1 % r leg 18% l leg 18%
-children : head 18% back 18% chest 18% r arm 9 % l arm % perineum 1 % r leg 13.5 % l leg 3.5 %

Burns- Initial management
Immediate first aid
Stop the burning process (do not endanger yourself ).
Cool the wound. Douse with running water at 2–15 degree celcius for 20min
(beware risk of hypothermia in infants, young children, and adults with 25% TBSA).

Resuscitation
A. Airway maintenance with C-spine control. Intubate if suspected inhalation injury;
airway edema can be rapidly fatal.
B. Breathing and ventilation.
C. Circulation with haemorrhage control.
D. Disability and neurological status.
E. Exposure and environmental control.
F. Fluid resuscitation: child, >10% TBSA; adult, >15% TBSA burned.

Two large peripheral IV lines, preferably through unburned skin.
Send blood for FBC, UE, clotting, amylase, carboxyhaemoglobin.
Give 3–4mL Hartmann’s solution/kg/% TBSA burned. Half of this is given over the first 8h following injury, half over the
next 16h.
Children need maintenance fluid in addition.
Monitor resuscitation with urinary catheter (aim for urine output 0.5–1mL/kg/h in adults and 1–1.5mL/kg/h in children).
Consider ECG, pulse, BP, respiratory rate, pulse oximetry, ABGs.
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

Infection Control
Tetanus prophylaxis
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

Fluid Resuscitation
Modifications
Bicarbonate - one ampule of sodium bicarbonate may be added to each liter of fluid
if a significant metabolic acidosis is present.
Colloid (FFP/albumin): Added after initial 12 hours in burns greater than 40% (30% if
age < 5) or if fluid requirement at 12 hours is > 20% above that estimated initially.

Monitoring
The Parkland Formula is an estimate and IV rates must be adjusted.
Under-resuscitation results in hypoperfusion of organs and the burn wound;
hypoperfusion of the wound increases cellular death and may convert partial
thickness burns to full thickness injury
Over-resuscitation exacerbates any co-existing pulmonary injury and increases edema.
Increased edema results in hypoperfusion of the wound and conversion of partial
thickness burn to full thickness injury.
Both under- and over-resuscitation are detrimental to the wound. Determining the
adequacy of resuscitation remains one of the most difficult aspects of burn care.

Goal is urine output of 0.5 ml/kg/hr (1.0 ml/kg/hr in infants)
Urine outputs greater than 1.0 ml/kg/hr are to be avoided.
The initial metabolic acidosis should be improving after 12 hours.
Lactic acid levels are unreliable indicators of resuscitation in the burn patient. Full thickness
skin death results in release of lactic acid that will not resolve until the burn is excised.
Young, healthy patients may be adequately resuscitated with CVPs < 8.
Myocardial depression occurs in patients with burns > 20% and persists for 24 - 36 hours.
Low urine outputs may occur despite adequate fluid resuscitation in patients with pre-
existing myocardial dysfunction that is exacerbated by this response to the burn injury.

Wound Care
Immediate transfer:
clean, dry, or lubricated dressing
tetanus
no systemic antibiotics
Transfer delay > 6 hours: topical agents
Systemic antibiotics do not penetrate the dead
surface tissue of the burn wound and cannot
prevent infection of the necrotic tissue. There is no
role for prophylactic antibiotic use in burn patients
Topical antibiotics decrease surface colonization
and decrease the incidence of invasive infections.
The ideal topical antibiotic would have a broad
spectrum of coverage, penetrate necrotic burned
tissue, and have minimal systemic toxicitie

Topical Agents
Silver Nitrate:
poor penetration electrolyte disorder
stains skin, sclera, nurses, patient’s room, lab coat, etc.
advantage - no known resistance
rarely used
Mafenide Acetate:
extremely painful to second degree burns metabolic
acidosis (carbonic anhydrase inhibitor)
advantage - excellent penetration no known resistance
Silver Sulfadiazine:
poor penetration
allergies - Sulfa drug
transient neutropenia - WBC of <1,500 are not
uncommon
resistant Pseudomonas strains exist
inhibits epithelial healing - should not be used in
superficial
second degree burns which have minimal risks of
infection
advantage - soothing
overall excellent coverage

Pain Relief and Adjustment
Important to provide adequate analgesia, anxiolytics and psychological support to:
Reduce early metabolic stress
Decrease potential for posttraumatic stress syndrome
Allow future stabilization and rehabilitation
Family support patient through grieving process and help accept long-term changes
in appearance

Inhalation Injury
Three syndromes:
1. Early CO poisoning, airway obstruction & pulmonary edema major concerns
2. ARDS 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

Signs of inhalation injury
Singed nasal hair.
Burns to face or oropharynx. Look for blistered palate.
Sooty sputum.
Drowsiness or confusion due to carbon monoxide inhalation.
Respiratory effort, breathlessness, stridor, or hoarseness are signs of impending
airway obstruction and require immediate intubation

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

Criteria for referral to a burns unit
>15% TBSA burn in adult; >10% TBSA in child.
Burns to face, hands, feet, perineum, genitalia, major joints.
Full thickness burns >5% TBSA.
Electrical or chemical burns.
Associated inhalation injury—always intubate before transfer.
Circumferential burns of limbs or chest.
Burns in very young or old, pregnant women, and patients with significant
comorbidities.
Any burn associated with major trauma.

BURN CME.pptx

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