1. 1

2. Burn

3. Introduction

4. Definition:
Burn is a coagulation necrosis due to heat.
Hydrofluoric acid is somewhat different from other
acids in that it produces a liquefaction necrosis.

5. Causes (Types(:
)1(Thermal burn (Flame , scald &hot gases(
)2(Electric burn
)3(Chemical burn
)4(Friction burn
)5(Radiation ( Sun rays & X-ray(

6. DEGREE:
Superficial partial thickness burns:
the damage goes no deeper than the papillary dermis.
Deep partial thickness burns:
burn involved damage to the deeper parts of the
reticular dermis.
Full thickness burns:
the whole of the dermis is destroyed

8. Partial thickness Full thickness
Appearance Blisters-erythema-
wet-moist-red
White-black-dry.
Pain painful Painless
Pain prick
test&hair follicle
test.
+ve -ve

9. First-degree
Second-degree
Third-degree
Fourth-degree
Fifth-degree
Sixth-degree
Erythema from vasodilatation
Vesication filled with serum
coagulation of the epidermis
but the deeper sebaceous and
sweat glands escape.
Destruction of the whole skin,
so that, the subcutaneous fat
is exposed.
Muscle is involved in the
coagulation process.
Bone is burnt.

10. 10
2nd
degree burns with…..blisters,( vesicals)

11. 11
Full thickness 3rd
. degree burns

12. 12
2ND
DEGREE BURN RIGHT ARM

13. Flame injury showing all burn depths

14. Rule of nine.
Rule of hand.
Chart.
EXTENT:

15. The Lund and Browder chart
used to assess total body surface area
of burns. Pediatric patients require a
special chart (not shown).

17. 17Extent of burn surface…

Determined by rule of 9 in adults
 Head and neck =9%
 Right arm =9%
 Left arm =9%
 Chest& abdomen front =18%
 Chest & abdomen back =18%
 Right lower limb =18%
 Left lower limb =18%
• Total =99%
Different formula for children and infants.

18. Severity:
Burns are classified according to extent into:
Minor---------<15%
Intermediat --------15—30%
Major --------------->30%
Fatal -------->60%

19. Mechanisms of injury

20. Thermal injuries
Scalds—About 70% of burns in children are caused by
scalds. Scalds tend to cause superficial to superficial
dermal burns
Flame—Flame burns comprise 50% of adult burns. They
are often associated with inhalational injury and other
concomitant trauma. Flame burns tend to be deep
dermal or full thickness.
Contact—These types of burns are commonly seen in
people with epilepsy or those who misuse alcohol or
drugs. Contact burns tend to be deep dermal or full
thickness.

21. Major burn in elderly patient

22. Top: Deep dermal
injury from bath scald.
Bottom: Six weeks after
tangential excision and
grafting with 3:1 mesh
and cultured epithelial
autograft in suspension.
Note biopsy site for cell
culture on buttock

23. Large blister on
thenar eminence
restricting movement
of hand (top). Blister
is de-roofed using
aseptic technique
(bottom)

24. Contact burns in an elderly patient after
a collapse and
prolonged contact with a radiator.
Treatment required excision
and split skin grafting as well as
investigation into the cause of
the collapse

25. Contact burn
In order to get a burn from direct contact, the object
touched must either have been extremely hot or the
contact was abnormally long.
These types of burns are commonly seen in people with
epilepsy or those who misuse alcohol or drugs. They
are also seen in elderly people after a loss of
consciousness; .
Contact burns tend to be deep dermal or full thickness.

26. a contact burn from a hot iron

27. Electrical injuries
Electricity exerts its tissue-damaging effects by conversion to
thermal energy
An electric current takes the path of least resistance and there
is destruction of tissue at the point of entry of the current
and at the point of exit of the current to earth.
Tissue resistance to electrical current increases from nerve
(least resistant) to vessel to muscle to skin to tendon to fat
to bone (most resistant(.
The amount of heat generated, and hence the level of tissue
damage, is equal to 0.24×(voltage)2×resistance. The
voltage is therefore the main determinant of the degree of
tissue damage

28. Tissue damage occurs in tissues with the least resistance to
electrical current, although the high heat generated by the
high resistance in bone will cause
secondary thermal damage to the adjacent musculature.
Muscles that are closest to bone sustain a higher degree of
secondary thermal damage than more superficial muscles.
As a result, the full extent of the underlying tissue damage
is not always evident by inspection.
Blood vessels offer little resistance to electric
current,therefore vascular damage can be sever and gives
rise to prolonged healing time and even gangrene of limb.

29. The voltage is the main determinant of the degree of tissue
damage,and it is logical to divide electrocution injuries into
those caused by
@Low voltage, domestic current.
@High voltage injuries can be further divided into
“*true” high tension injuries, caused by high voltage current
passing through the body
“*flash” injuries, caused by tangential exposure to a high voltage
current arc where no current actually flows through the body.

30. Differences between true high tension burn
and flash burn

31. Tend to cause small, deep contact burns at the exit and
entry sites.
The alternating nature of domestic current caninterfere
with the cardiac cycle, giving rise to arrhythmias.
Domestic electricity—Low voltages

32. “True” high tension injuries
Occur when the voltage is 1000 V or greater.
There is extensive tissue damage and often limb loss.
There is usually a large amount of soft and bony tissue necrosis.
Muscle damage gives rise to rhabdomyolysis, and renal failure
may occur with these injuries.
This injury pattern needs more aggressive resuscitation and
debridement than other burns.
Contact with voltage greater than 70 000 V is invariably fatal.

33. Can occur when there has been an arc of current from
a high tension voltage source. The heat from this
arc can cause superficial flash burns to exposed body
parts,
No current actually passes through the victim’s body.
A particular concern after an electrical injury is the
need for cardiac monitoring.
Flash” injury

34. Fluid resuscitation is the keystone to prevent acute renal failure. Mannitol 25 g IV
is given to increase renal perfusion.
Sodium bicarbonate is administered to alkalinize the urine to keep hemoglobin and
myoglobin in a more soluble state.
Sulfamylon (with high eschar penetrability) is used for local burn care.
Technetium 99m muscle scans may be useful to evaluate muscle damage.
Electrical burns involving the extremities are observed closely for compartment
syndrome.
Early excision and skin grafting are advocated.
Oral commissure burns are managed conservatively and monitored for bleeding
from the labial artery, which is seen in about 10% of cases.
Electric burn is usually underestimated due to underlying tissue destruction.

35. CHEMICAL BURNS
These burns tend to be deep, as the corrosive agent continues to
cause coagulative necrosis until completely removed.
Most acids produce a coagulation necrosis by denaturing
proteins, forming a coagulum (eg, eschar) that limits the
penetration of the acid.
Hydrofluoric acid is somewhat different from other acids in that
it produces a liquefaction necrosis.
Bases typically produce a more severe injury known as
liquefaction necrosis. This involves denaturing of proteins as
well as saponification of fats, which does not limit tissue
penetration.

36. The severity of the burn is related to a number of factors,
the pH of the agent,
the concentration
the length of the contact time,
the volume of the offending agent,
the physical form of the agent.
Concentrated forms of some acids and bases generate
significant heat when diluted or neutralized, resulting in
thermal and caustic injury.

37. The initial treatment is lavage with copious amounts of water or saline.
A. Hydrofluoric acid burns are treated with the application of 10%
calcium gluconate paste over the affected area.
B. Phenol burns are treated with application of propylethylene glycol.
C. Phosphorus burns require continuous application of saline Topical
copper sulfate (1%) stains the phosphorus particles dark, which
facilitates debridement.
D. Tar burns respond well to application of bacitracin or neomycin
ointment.

38. Chemical burn due to spillage of
sulphuric acid

39. Bitumen burns to face in work related
incident

40. INHALATION INJURY
A chemical tracheobronchitis and acute
pneumonitis caused by the inhalation of smoke
and other irritative products.
In severe cases, it progresses to development of adult
respiratory distress syndrome (ARDS(.

41. Mechanism:
Three forms of inhalation injury
1(Systemic toxicity (CO,Hydrogen cyanid(
2(Thermal Injury
Inhalation of superheated air or water vapor can
cause a thermal burn to the airway mucosa.
3(Chemical irritation
Transudation of fluids can induce bronchconstriction.

42. A. Typical Signs of Significant Injury
1.Singeing of nasal hair
2.Significant facial burns
3.Carbonaceous sputum
4.Hoarseness
5.Stridor
6.Carboxyhemoglobin level of more than 15%
at 3 h postexposure is strong evidence of
smoke inhalation
7.Soot over face or in sputum
8.Tachypnea

43. Chest x-ray
Arterial blood gases.
Fiberoptic bronchoscopy.
Xenon ventilation/perfusion scanning
Pulse oximetry
B. Evaluation

44. Endoscopic findings with inhalation injury
Erythema
Edema
Soot
Bronchorrhea
Mucosal disruption
Blistering
Sloughing
Ulceration
Exudates
Hemorrhage

45. C. Treatment
100%oxygen. Ventilator management goals:
Maximize oxygenation while avoiding oxygen
toxicity (keep FiO2 <0.7) and barotrauma
Endotracheal intubation.
Hyperbaric oxygen
Bronchodilators:.
Nebulize 500 units of heparin with 3 ml normal saline
every 4 h for 7 days
Nebulize bronchodilators every 4 h for 7 days
Nasotracheal suctioning as needed

46. Coexisting thermal injury &inhalation
injury increase fluid requirements by
40%compared to thermal injury alone

47. Carbonaceous particles
staining a patient’s face after
a burn in an enclosed space.
This suggests there is
inhalational injury

49. Bronchoscopy image showing mucosal
inflammation

50. Carbon monoxide (CO) poisoning
CO is generated by fire. When inhaled and absorbed, it
preferentially binds with hemoglobin, displacing
oxygen and blocking oxygen binding sites, causing a
substantial reduction in oxygen delivery.
Signs and symptoms
a. Pulse oximetry is unreliable.
b. Cherry red skin.
c. Hypoxemia.
d. Mental status changes or a history of a loss of
consciousness.
e. Persistent acidosis in the presence of normovolemia.

51. CO level
a. May be normal or minimally elevated, even with
significant exposure.
b. 20% to 40%: Associated with severe neurologic
symptoms.
c. Greater than 60%: Commonly fatal.
Treatment
a. 100% oxygen administration: Displaces CO from
hemoglobin.
b. Hyperbaric therapy: Consider if the patient has mental
status changes.

52. PATHOPHYSIOLOGIC
CHANGES IN BURN
PATIENTS

53. Thermal injury causes coagulation necrosis of the skin
and underlying tissues to avariable depth.
Burn injury also exerts deleterious effects on all other
organ systems.
Burn injuries result in both:
Local response
Systemic response.

54. Local response
The three zones of a burn were described by Jackson in
1947.
Zone of coagulation.
Zone of stasis.
Zone of hyperaemia.

55. Zone of coagulation
At the point of maximum damage.
Irreversible tissue loss due to
coagulation of the constituent proteins.

56. Zone of stasis
Decreased tissue perfusion.
The tissue is potentially salvageable.
The main aim of burns resuscitation is to
increase tissue perfusion here and
prevent any damage becoming irreversible.
Additional insults—such as prolonged hypotension,
infection, or oedema—can convert this zone into an area
of complete tissue loss

57. Zone of hyperaemia
In this outermost zone tissue perfusion is increased.
The tissue here will recover unless there is severe
sepsis or
prolonged hypoperfusion.

58. Jackson's burns zones and the effects
of adequate and inadequate
resuscitation
These three zones of a burn are three
dimensional, and loss of tissue in the
zone of stasis will lead to the wound
deepening as well as widening

59. Clinical image of burn zones. There is
central necrosis,
surrounded by the zones of stasis and
of hyperaemia

60. Systemic response
Thermal injuries of greater than 30% have been
demonstrated to initiate a cascade of inflammatory
mediators leading to capillary leak that leads to the
anasarca in unburned areas and pulmonary edema.
These mediators include histamine,bradykinin, and
serotonin but the exact mechanism to initiate the
cascade has not been elucidated.
.

61. Systemic changes that occur after a burn
injury

62. Cardiovascular changes
Capillary permeability is increased,leading to loss of intravascular
proteins and fluids into the interstitial compartment.
Peripheral and splanchnic vasoconstriction occurs.
Myocardial contractility is decreased, possibly due to release of tumour
necrosis factor.
Hypovolemia Because vessels in burned tissue exhibit increased vascular
permeability, an extravasation of fluids into the burned tissues occurs.
Hypovolemia is the immediate consequence of this fluid loss, which
accounts for decreased perfusion and oxygen delivery.
Systemic hypotension and end organ hypoperfusion. These changes,
coupled with fluid loss from the burn wound, result in systemic
hypotension and end organ hypoperfusion.

63. Hemodynamic
Decreased blood volume,
Increased blood viscosity
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.

64. Respiratory changes
Bronchoconstriction, and in severe burns adult respiratory
distress syndrome caused by inflammatory mediators
(histamine, serotonin, and thromboxane A2( .
A decrease in pulmonary function can occur in severely
burned patients without evidence of inhalation injury
from the bronchoconstriction
A decrease in lung and tissue compliance is a manifestation
of this reduction in pulmonary function.

65. ARDS is defined as an acute condition characterized by
bilateral pulmonary infiltrates and
severe hypoxemia
in the absence of evidence for cardiogenic pulmonary edema.
It is associated with diffuse alveolar damage (DAD) and lung capillary endothelial
injury.
Early ARDS is characterized by an increase in the permeability of the alveolar-
capillary barrier leading to an influx of fluid into the alveoli. The alveolar-
capillary barrier is formed by the microvascular endothelium and the epithelial
lining of the alveoli.
The main site of injury may be focused on either the vascular endothelium (eg,
sepsis) or the alveolar epithelium (eg, aspiration of gastric contents(.
Acute respiratory distress syndrome (ARDS)

66. The severity of hypoxemia necessary to make the diagnosis
of ARDS is defined by
the PaO2/FiO2 the ratio of the partial pressure of oxygen in
the patient's arterial blood to the fraction of oxygen in the
inspired air.
In ARDS, this ratio is less than 200, and in
acute lung injury (ALI), this ratio is less than 300.

67. Metabolic changes
The basal metabolic rate increases up to three times.
This, coupled with splanchnic hypoperfusion,
necessitates early and aggressive enteral feeding to
decrease catabolism and maintain gut integrity.
Burned skin exhibits an increased evaporative water
loss associated with an obligatory concurrent heat
loss, which can cause hypothermia
.

68. Nonpharmacologic approaches include early excision
and wound closure, aggressive management of sepsis,
elevation of the environmental temperature, continuous
high carbohydrate/high protein enteral feeding, and
early institution of resistive exercise programs.
Pharmacologic modulation of the postburn
hypermetabolic response has been achieved through
administration of recombinant human growth hormone,
low-dose insulin infusion, use of synthetic testosterone
analog (oxandrolone), and beta blockade with
propranolol.
strategies are being used to reverse the
catabolic effect of thermal injury.

69. Humoral and cell-mediated immunity are both
impaired and are manifested as
Depressed levels of immunoglobulin,
Reduced activation of complement,
Diminished stimulation of lymphocyte proliferation
and response.
Immunological changes

70. 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(.
Hematologic

71. Ileus is universal in patients with burns of more than 25%.
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 (Curling’s ulcer(.
In patients with serious burns, release of catecholamines,
vasopressin, and angiotensin causes peripheral and
splanchnic bed vasoconstriction that can compromise in-
organ perfusion.
.
Gastrointestinal

72. .Acalculous cholecystitis
.Pancreatitis
.Acute dilatation of the colon (Ogilvie’s syndrome)
may occur in burn patients who develop sepsis.
.The use of early enteral feeding:
improves mucosal blood flow,
and reduces mucosal atrophy
and subsequent bacterial translocation.

73. In the early postburn period, a catabolic endocrine
pattern develops that is characterized by
elevated glucagon, cortisol, and catecholamine levels
with depressed insulin levels.
These effect an increase in metabolic rate, glucose
flow, and a negative nitrogen balance.
Endocrine

74. Multiple Organ Failure

75. Development of multiple organ failure is often
associated with infectious sepsis , which in severe
burns is
The massive skin injury or from
Lung infections (pneumonias).

76. As organisms proliferate out of control,
Endotoxins are liberated from gram-negative
bacterial walls and
Exotoxins from gram-positive and gram negative
bacteria are released.
Their release causes the initiation of a cascade of
inflammatory mediators that can result, in
organ damage and failure if secreted in
excessive amounts.

77. Endotoxin, It also stimulates monocytes, the
predominant source of cytokines, to produce
and secrete excessive amounts of cytokines
Arachidonic acid metabolites, endogenous
immunosuppressant &pulmonary dysfunction
Cytokines, associated with sepsis and multiple
organ failure.
Nitric oxide, one of the major mediators of the
hypotensive response to sepsis
Oxygen free radicals oxidize membrane
lipids, resulting in cellular dysfunction
Among these mediators are

78. ENDOTOXIN
Endotoxin, a component of the wall of gram-negative
bacteria, is released upon lysis of bacteria
Endotoxemia causes fever, hypotension, and activation
of liver cells to release acute phase proteins.
It also stimulates monocytes, the predominant
source of cytokines, to produce and secrete
excessive amounts of cytokines.

79. CYTOKINES
Cytokines are a group of proteins produced by a variety of
cells that are thought to be important for host defense,
and wound healing .
Although cytokines in low physiologic concentrations
preserve homeostasis, excessive production may lead to
widespread tissue injury and organ dysfunction.
Four of these cytokines, tumor necrosis factor alpha (TNF-
α), interleukin 1 beta (IL-1β), interleukin 6 (IL-6) and
interleukin 8 (IL-8) have been most strongly associated
with sepsis and multiple organ failure.

80. OXYGEN FREE RADICALS
Tissues that initially were in shock and are then reperfused
produce oxygen free radicals that are known to damage a
number of cellular metabolism processes.
This process occurs throughout the body during burn
resuscitation,
Oxygen free radicals oxidize membrane lipids,
resulting in cellular dysfunction.
Endogenous natural antioxidants, such as vitamins C and E, are
low in patients with burns, suggesting that therapeutic
interventions may be beneficial..
.

81. Nitric oxide
, a metabolite of the amino acid arginine, is one of the
major mediators of the hypotensive response to
sepsis.
Inhaled nitric oxide will improve oxygenation and lower
pulmonary artery pressures during ARDS, by selectively
dilating those pulmonary vessels that flow past open
alveoli.
This results in an increase in flow to the open airways,
allowing for better air exchange and a decrease in
pulmonary shunting

82. ARACHIDONIC ACID METABOLITES
Arachidonic acid is the precursor for prostaglandins ,
thromboxanes and leukotrienes .
Prostaglandins (PGE), especially PGE2, is a powerful
endogenous immunosuppressant.
Thromboxane A2 are potent vasoconstrictors in
both the splanchnic and pulmonary
microvasculature.
Leukotrienes affect vascular tone and increase
vascular permeability,contributing to edema
formation and pulmonary dysfunction

83. PREVENTION
Since different cascade systems are involved in the
pathogenesis, it is so far impossible to pinpoint a single
mediator that initiates the event.
Thus, since the mechanisms of progression are not well known,
specific intervention to treat the cause is not possible.
Therefore, prevention is likely to be the best solution.
The great reduction of mortality from large burns was seen
with early excision and an aggressive surgical approach to deep
wounds

84. Prevention Measures
Aggressive Resuscitation
Early and Complete Burn Wound Excision
Routine Central Line Changes
Directed Antimicrobial Therapy
Pulmonary Toilet
Continued Infection Surveillance
Enteral Feedings
Immunomodulation

85. We recommend
@ Complete early excision of clearly full-thickness wounds
within 48 h of the injury.
@Oxidative damage from reperfusion after low flow states
make early aggressive fluid resuscitation imperative.
@Furthermore,the volume of fluid may not be as important
as the timeliness with which it is given.
@Pneumonia, which contributes significantly to mortality in
burned patients, should be anticipated and aggressively
treated

86. ORGAN FAILURE
The general development begins either in the renal or
pulmonary systems and can progress through the liver,
gut, hematologic system, and central nervous system

87. RENAL FAILURE
Renal failure is hallmarked by:
 decreasing urine output,
 fluid overload,
 electrolyte abnormalities including
metabolic acidosis
hyperkalemia,
azotemia,
increased serum creatinine.

88. Causes of renal failure:
)1(Fluid shifts and hypovolemia.
)2(Myocardial depression(due to tumor necrosis factor.
)3(Stress-related hormones(catecholamines(.
)4(Inflammatory mediators(TNF-leading to fluid shift(
)5(Denaturated proteins)
)6(Nephrotoxic drugs
(

89. Treatment :Urine output of 1 cc/kg/h is sufficient.
When the output falls below this level,initial efforts should be
concentrated on the status of the intravascular volume.
Initial fluid boluses should be given and if these go without
response,atrial filling and pulmonary artery pressures should
be measured with a Swan-Ganz catheter.
If it appears to be primary renal dysfunction with an adequate
intravascular volume and cardiac output, loop diuretics should
be given to maintainurine output (up to 1 mg/kg of lasix
every 4 h).

90. Oftentimes in primary renal insufficiency, these measures
will fail requiring other treatments( dialysis may be
necessary)
The indications for dialysis are fluid overload
or electrolyte abnormalities not amenable to other
treatments.
Severely burned patients require exogenous potassium
because of the heightened aldosterone response
which results in potassium wasting, therefore
hyperkalemia is rare evenwith some renal insufficiency.

91. PULMONARY FAILURE
Many of these patients require mechanical ventilation
to protect the airway in the initial phases of their
injury.
The first sign of impending pulmonary failure is a
decline in oxygenation.
This is best followed by continuous oximetry, and a
fall in saturation below 92% is indicative of failure.
Increasing concentrations of inspired oxygen will be
necessary,

92. HEPATIC FAILURE
When the liver begins to fail, protein concentrations of the
coagulation cascade will fall to critical levels and these
patients will become coagulopathic.
Toxins will not be cleared from the bloodstream, and
concentrations of bilirubin will increase.
With the development of coagulopathies, treatment should
be directed at replacement of factors II, VII, IX, and
X until the liver recovers.
Albumin replacement may also be required.

93. HEMATOLOGIC FAILURE
Burn patients may become coagulopathic via two
mechanisms, either:
 Through depletion/impaired synthesis of
coagulation factors( through disseminated
intravascular coagulation (DIC) associated with
sepsis).or
Through thrombocytopenia.
Treatment of DIC should include infusion of fresh
frozen plasma and cryoprecipitate to maintain
plasma levels of coagulation factors.

94. Thrombocytopenia is common in severe burns from
depletion during burn wound excision.
Platelet counts of below 50,000 are common and do
not require treatment.
Only when the bleeding is diffuse and is also noted
from the IV sites exogenous platelets be given.

95. CENTRAL NERVOUS SYSTEM FAILURE
The new onset of mental status changes not
attributed to sedative medicationsin a severely
burned patient should incite a search for a septic
source.
Treatment is supportive

96. Burn Infections

97. Burn Infections
Suppurative thrombophlebitis
Acute endocarditis
Suppurative sinusitis
Pneumonia
Burn wound infections.

98. 1.Burn wound infections
Burn wound sepsis is defined as >10(5) organisms per
gram of tissue.
Histologic examination of the biopsy specimen, is the
only reliable means of differentiating wound
colonization from invasive infection.
Fungal wound infections have become an important
cause of burn-associated morbidity and mortality.

99. The clinical signs of burn wound sepsis are:
•Conversion of second-degree burn to fullthickness
•Focal dark brown discoloration of wound
•Degeneration of wound with formation of new eschar
•Hemorrhagic discoloration of subeschar fat
•Erythematous and edematous wound margin

100. Clinical criteria for diagnosis of sepsis
include the presence of at least five of the following:
1.Tachypnea ( 40 breaths/min in adults(
2.Prolonged paralytic ileus
3.Hyper- or hypothermia ( 36.5C or 38.5C(
4.Altered mental status
5.Thrombocytopenia (50,000 platelets/mm3(
6.Leukocytosis or leukopenia (15,000 or 3500 cells/
mm3(
7.Unexplained acidosis
8.Hyperglycemia

101. Cardinal signs of gram-positive sepsis
1.Symptoms develop gradually
2.Increased temperature to 40°C or higher
3.Leukocytosis 20,000/l
4.Anorexia
5.Decreased bowel sounds
6.Decreased blood pressure and urinary output

102. Gram-negative sepsis
1.Rapid onset (8–12 h(
2.Increased temperature 38–39°C (may be normal(
3.Normal or high white cell count
4.If not controlled, patient become hypothermic (34–
35°C) plus leukopenia
5.Decreased bowel sounds
6.Decreased blood pressure and urinary output
7.Wounds develop focal gangrene
8.Mental obtundation

103. The most common site of infection in the burn patient is the lungs.
Pneumonia is considered to be the primary cause of death in over half
of fatal burns.
Bronchopneumonia is commonly caused by Staphylococcus aureus
and Gram negative opportunistic bacteria.
Hematogenous pneumonia commonly begins relatively late in the
postburn course. An infected wound or a vein harboring a focus
of intraluminal suppuration is the source of infection in the majority of
cases.
2. Pneumonia

104. Can occur in any previously cannulated peripheral or
even central vein.
Strict limitation of cannula residence to 3 days or less in
burn patients has been associated with a reduction in the
incidence of this complication from 4.3% to 2.5%.
Treatment involves surgical excision of the entire length of
vein involved & the systemic administration of antibiotics.
3. Suppurative thrombophlebitis

105. Identification of characteristic murmurs is difficult in burn
patients because of their hyperdynamic circulation.
Two-dimensional echocardiographic examination may
detect valvular lesions.
Staphylococcus aureus is the most common causative
agent.
Systemic maximum-dose antibiotic therapy is prescribed
for at least 3 weeks.
4. Acute endocarditis

106. Most likely to occur in patients who require long-term
transnasal intubation, particularly those with tubes in
both the airway and the gastrointestinal tract.
CT scan is useful as a diagnostic test.
Therapy is initiated with broad-spectrum antibiotics, but
surgical drainage of the sinuses may be necessary.
5. Suppurative sinusitis

107. COMPLICATIONS

108. General Complications
1(Respiratory.
2(Shocks
3(Acute renal failure.
4(Gastro intestinal
5(Hypoprotinemia.
6(Multiple organ failure.
7(DEATH ;(Respiratory ,Renal. ,Shock. ,Sepsis ,Catabolism(.

109. Bronchopneumonia 2%
Sepsis 0.7%
Inadequate fluid resuscitation 1%
Inhalation injury 1%
G I T hemorrhage 0.1%
The most common cause of death

110. Local Complications:
)1(Sepsis.
)2(Scar and its complications:
Keliods.
Marjolin ulcer.
Functional deformity.
Lymphedema

111. Hypertrophic Scars/Keloids
1.These scars are red, thick, hard, pruritic, and dry.
2.Treatment begins conservatively with massage,
moisturizers, antihistamines, pressure
garments, and silicone sheet therapy.
3.Intralesional injections of triamcinolone are also
used.
4.Scar revision with Z-plasty, V-Y plasty, or W-
plasty may be required

112. Example of hypertrophic scarring

113. Contractures
1.Every effort is made in the initial care of a burn
patient to prevent contractures.
When contractures develop, they are released and
reconstructed with skin grafts or flaps
2.Tissue expanders may be used to provide tissue
with the closest match.
3.Occasionally, free tissue transfers have been used
to resurface large defects.

114. Marjolin’s s Ulcer
1.Squamous cell carcinoma arises in the chronic
burn scar after a latency period of approximately
35 years.
2.These tumors are highly invasive, and regional
node metastases are present in 35% of
cases.