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SM P.Surg 1
SM P.Surg 1
Introduction
The burn is depicted as a traumatic lesion provoked by several possible agents (thermal, chemical,
mechanical, or electrical) involving different skin layers to a certain degree.
Burns are one of the most devastating conditions encountered in medicine. The injury represents
an assault on all aspects of the patient, from the physical to the psychological. It affects all ages,
from babies to elderly people, and is a problem in both the developed and developing world. Most
of us have experienced the severe pain that even a small burn can bring. However the pain and
distress caused by a large burn are not limited to the immediate event. The visible physical and the
invisible psychological scars are long lasting and often lead to chronic disability.
Skin surface area is about 0.2–0.3m2 in the newborn and about 1.5–2.0m2 in the adult. Thickness
of epidermis from 0.05mm (eyelids) to 1mm (sole of the foot). Dermis is approximately 10×
thicker than epidermis site for site.
2-Chemical burn :
Alkalis (cause a liquefactive necrosis)
*more severe, liquefactive continuous deeply
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Acids (cause a coagulative necrosis)
Organic compounds
Phosphorus
3-Electrical burn :
Low voltage <1,000 V
High voltage >1,000 V
4-Radiation injury
A. Thermal injury causes coagulation necrosis of the skin and underlying tissues to a variable
depth. Burn injury also exerts deleterious effects on all other organ systems.
B. Hemodynamic—The first 24-h postburn are characterized by decreased blood volume,
increased blood viscosity, and depressed cardiac output. Microvascular permeability is increased
directly by heat and indirectly by endogenous mediators. The diminished blood volume and
cardiac output cause oliguria, which may progress to acute renal failure. Numerous factors have
been reported to increase vascular permeability and leukocyte infiltration:
• Histamine
• Arachidonic acid metabolites (principally thromboxane A2 and the leukotrienes)
• Substance P
• Fibrin degradation product D
• Activated proteases
• Platelet-activating factor (PAF)
• Cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF)
C. Immune system—Humoral and cell-mediated immunity are both impaired and are manifested
as depressed levels of immunoglobulin, reduced activation of complement, and diminished
stimulation of lymphocyte proliferation and response.
D. Hematologic—There is immediate red blood cell destruction in direct proportion to the extent
of the burn, particularly third-degree burns. Endothelial injury may lead to release of
thromboplastins and to collagen exposure; the latter then initiates platelet adhesion, aggregation,
and contact activation of factor XII. Severe full-thickness burns induce consumption of
coagulation factors at the burn site, which contributes to the development of disseminated
intravascular coagulation (DIC).
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E. Gastrointestinal—Ileus is universal in patients with burns of more than 25% total body surface
area (TBSA). Gastric and duodenal mucosal damage, secondary to focal ischemia, can be observed
as early as 3–5 h postburn. If the mucosa is unprotected, the early erosions may progress to frank
ulceration.
F. Endocrine—In the early postburn period, a catabolic endocrine pattern develops that is
characterized by elevated glucagon, cortisol, and catecholamine levels with depressed insulin and
triiodothyronine levels. These effect an increase in metabolic rate, glucose flow, and a negative
nitrogen balance. Their magnitude correlates with the size of the burn area.
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Evaluation of burn involves:
• Extent of burns (surface area): Although the classic “Wallace Rule of 9” is still followed in
many centers
The Wallace rule of nines
• Adult body surface area (BSA):
∘ 9% head and neck
∘ 9% each arm
∘ 18% anterior trunk
∘ 18% posterior trunk
∘ 18% each leg
∘ 1% perineum.
• BSA of children up to 1 year old is distributed differently:
∘ 18% head and neck
∘ 9% each arm
∘ 18% anterior trunk
∘ 18% posterior trunk
∘ 13.5% each leg
∘ 1% perineum.
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– For each additional year of age up to age 10, 1% should be subtracted from the head and neck
and 0.5% added to each leg.
• Depth of burn injury is generally difficult to assess initially. It is sufficient to distinguish
between erythema and actual skin damage at the initial examination.
• First-degree burn—superficial burn that involves only the epidermis. The area is erythematous,
tender, and usually heals in less than 7 days.
• Second-degree burn—destruction of the epidermis and upper dermal layer. The skin is red,
blistered, and sensory nerve damage causes extreme pain.
• Third-degree burn—destruction of the epidermis and dermis. The area is white, leathery,
charred, and pain is absent due to destruction of sensory nerves
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• Fourth-degree burn—destruction of skin, muscle, and bone.
Fluid resuscitation :
Fluid resuscitation is required for:
∘ Adults with burns >15% TBSA.
∘ Children with burns >10% TBSA.
Parkland formula
• 4 ml/kg/% burn of Hartmann’s solution in the first 24 hours after the burn.
∘ Half the fluid is given in the first 8 hours after injury.
∘ The second half is given in the next 16 hours.
• Hartmann’s solution contains:
Na+ 131 mmol/l
Cl− 111 mmol/l
Lactate 29 mmol/l
K+ 5 mmol/l
Ca2+ 2 mmol/l.
The rate of infusion is modified to meet specific end points of resuscitation:
∘ Urine output is the best indicator of tissue perfusion
– Aim for 0.5–1 ml/kg/h in adults; 1–1.5 ml/kg/h in children
– Double this after high-voltage electrical injuries.
∘ Other parameters to be monitored:
– Pulse, blood pressure, capillary refill
– Core–peripheral temperature gradient
– Respiratory rate
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– Urine osmolality.
• Serial measures of arterial blood lactate and base excess also indicate adequacy of resuscitation.
Factors specific to children resuscitation
• Proportionately greater surface area than adults.
• Reduced physiological reserves.
∘ Because of this, children require additional maintenance fluid containing dextrose.
• Daily maintenance fluid requirement:
∘ 100 ml/kg for the first 10 kg body weight
∘ 50 ml/kg for the next 10 kg body weight
∘ 20 ml/kg for the remainder of the body weight
• Maintenance fluid is given enterally whenever possible.
Inhalation Injury
Inhalation injury—a chemical tracheobronchitis and acute pneumonitis—is caused by the
inhalation of smoke and other irritative products. In severe cases, it progresses to development of
adult respiratory distress syndrome (ARDS).
Typical Signs of Significant inhalational Injury
1. Singeing of nasal hair
2. Significant facial burns
3. Carbonaceous sputum
4. Hoarseness
5. Stridor swelling of upper airway
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Treatment of inhalational injury
is mainly supportive with oxygen therapy Immediate treatment involves administering 100% oxygen.
Endotracheal intubation is necessary in some cases. Hyperbaric oxygen has been used in some units.
Surgical decompression
• Deep dermal and full thickness burns are inelastic.
∘ Can cause distal limb ischemia if circumferential .
• Similarly, extensive involvement of the chest (or abdomen in a child) can impair ventilation.
• Constriction becomes worse once fluid resuscitation is begun.
• Escharotomy relieves this constriction.
∘ Usually done with electrocautery, because they tend to bleed.
• Fasciotomies usually required only for burns involving muscle, or high-voltage electrical
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injuries.
• Escharotomies begin and end in unburnt or superficially burnt skin.
• Limb escharotomies are generally made in midaxial lines.
∘ Avoid the ulnar nerve at the elbow and common peroneal nerve at the knee.
• Chest escharotomies are made along the mid-axillary lines to the subcostal region.
∘ They are joined across the upper abdomen by a chevron incision parallel to the costal margin.
∘ This creates a mobile breastplate that moves with ventilation.
∘ The anesthetist can advise on the adequacy of chest escharotomy by a drop in ventilator airway
pressures.
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نفس سجينة ال
skin graft
Water jet-powered VersaJet: useful for excision of concave surfaces of the hand and feet, as well
as for excision of the eyelids, ear, and nose
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Pain control in burnt patients:
Background pain :Best treated with longer acting agents :MORPHIN
Procedural pain occurs during daily wound care and therapy. shorter acting agents are probably
best. use of short-acting benzodiazepines is favorable.
Avoid NSAID
Topical Agents used in local wound care of burn
• Silver sulfadiazine (1% Silvadene)—most commonly used agent. Active against most Gram-
positive and Gram-negative organisms. The “pseudoeschar” that forms over the burn can confuse
the inexperienced observer. Leukopenia can occur.
• Sulfamylon (Mafenide acetate)—has superior eschar penetration. Excellent choice for ears,
noses, and some electrical burns. It has the disadvantage of causing intense pain on application
and is associated with metabolic acidosis.
1%, twice daily
• Silver nitrate (0.5%)—effective as a prophylactic against Pseudomonas colonization.
Disadvantages include production of black stains, hyponatremia, and methemoglobinemia.
• Povidone iodine—not effective, inactivated by wound exudate
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References
1-Handbook of plastic surgery , Arvind N.Padubidri, and Maria Siemionow, chapter 25; burn
pp :176-180.
2-Key Notes In Plastic Surgery ,2nd edition, Adrian Richards and Hywel Dafydd,chapter 8,
burn ,pp 490-516.
3-Stone's Plastic Surgery Facts and Figures ,3rd edition, chapter2 burn, pp 25-29.
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Slides
Acute burn
By : Dr.Muhammed Naeem
PLASTIC & RECONSTRUCTIVE SUEGERY
Learning objectives
• 2-Chemical burn :
*more severe, liquefactive continuous deeply
• Alkalis (cause a liquefactive necrosis)
• Acids (cause a coagulative necrosis)
• Organic compounds
• Phosphorus
• 3-Electrical burn :
• Low voltage <1,000 V
• High voltage >1,000 V
• 4-Radiation injury
Flame burn
Flash burn
Contact burn
Scald burn
Chemical burn
Radiation burn
Pathophysiology of burn injury
• A. Thermal injury causes coagulation necrosis of the skin and underlying
tissues to a variable depth. Burn injury also exerts deleterious effects on all
other organ systems.
• B. Hemodynamic—The first 24-h postburn are characterized by decreased
blood volume, increased blood viscosity, and depressed cardiac output.
Microvascular permeability is increased directly by heat and indirectly by
endogenous mediators. The diminished blood volume and cardiac output
cause oliguria, which may progress to acute renal failure
• C. Immune system—Humoral and cell-mediated immunity are both
impaired and are manifested as depressed levels of immunoglobulin,
reduced activation of complement, and diminished stimulation of
lymphocyte proliferation and response
Zone of burn injury
more than 20%
(Hypovolemic shock)