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  • 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
  • 7. Partial thickness Full thickness Appearance Blisters-erythema- wet-moist-red White-black-dry. Pain painful Painless Pain prick test&hair follicle test. +ve -ve
  • 8. 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.
  • 9. 10 2nd degree burns with…..blisters,( vesicals)
  • 10. 11 Full thickness 3rd . degree burns
  • 11. 12 2ND DEGREE BURN RIGHT ARM
  • 12. Flame injury showing all burn depths
  • 13. Rule of nine. Rule of hand. Chart. EXTENT:
  • 14. The Lund and Browder chart used to assess total body surface area of burns. Pediatric patients require a special chart (not shown).
  • 15. 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.
  • 16. Severity: Burns are classified according to extent into: Minor---------<15% Intermediat --------15—30% Major --------------->30% Fatal -------->60%
  • 17. Mechanisms of injury
  • 18. 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.
  • 19. Major burn in elderly patient
  • 20. 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
  • 21. Large blister on thenar eminence restricting movement of hand (top). Blister is de-roofed using aseptic technique (bottom)
  • 22. 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
  • 23. 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.
  • 24. a contact burn from a hot iron
  • 25. 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
  • 26. 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.
  • 27. 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.
  • 28. Differences between true high tension burn and flash burn
  • 29. 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
  • 30. “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.
  • 31. 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
  • 32. 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.
  • 33. 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.
  • 34. 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.
  • 35. 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.
  • 36. Chemical burn due to spillage of sulphuric acid
  • 37. Bitumen burns to face in work related incident
  • 38. 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(.
  • 39. 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.
  • 40. 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
  • 41. Chest x-ray Arterial blood gases. Fiberoptic bronchoscopy. Xenon ventilation/perfusion scanning Pulse oximetry B. Evaluation
  • 42. Endoscopic findings with inhalation injury Erythema Edema Soot Bronchorrhea Mucosal disruption Blistering Sloughing Ulceration Exudates Hemorrhage
  • 43. 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
  • 44. Coexisting thermal injury &inhalation injury increase fluid requirements by 40%compared to thermal injury alone
  • 45. Carbonaceous particles staining a patient’s face after a burn in an enclosed space. This suggests there is inhalational injury
  • 46. Bronchoscopy image showing mucosal inflammation
  • 47. 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.
  • 48. 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.
  • 49. PATHOPHYSIOLOGIC CHANGES IN BURN PATIENTS
  • 50. 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.
  • 51. Local response The three zones of a burn were described by Jackson in 1947. Zone of coagulation. Zone of stasis. Zone of hyperaemia.
  • 52. Zone of coagulation At the point of maximum damage. Irreversible tissue loss due to coagulation of the constituent proteins.
  • 53. 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
  • 54. Zone of hyperaemia In this outermost zone tissue perfusion is increased. The tissue here will recover unless there is severe sepsis or prolonged hypoperfusion.
  • 55. 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
  • 56. Clinical image of burn zones. There is central necrosis, surrounded by the zones of stasis and of hyperaemia
  • 57. 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. .
  • 58. Systemic changes that occur after a burn injury
  • 59. 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.
  • 60. 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.
  • 61. 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.
  • 62. 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)
  • 63. 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.
  • 64. 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 .
  • 65. 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.
  • 66. 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
  • 67. 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
  • 68. 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
  • 69. .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.
  • 70. 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
  • 71. Multiple Organ Failure
  • 72. 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).
  • 73. 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.
  • 74. 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
  • 75. 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.
  • 76. 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.
  • 77. 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.. .
  • 78. 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
  • 79. 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
  • 80. 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
  • 81. 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
  • 82. 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
  • 83. 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
  • 84. RENAL FAILURE Renal failure is hallmarked by:  decreasing urine output,  fluid overload,  electrolyte abnormalities including metabolic acidosis hyperkalemia, azotemia, increased serum creatinine.
  • 85. 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 (
  • 86. 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).
  • 87. 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.
  • 88. 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,
  • 89. 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.
  • 90. 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.
  • 91. 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.
  • 92. 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
  • 93. Burn Infections
  • 94. Burn Infections Suppurative thrombophlebitis Acute endocarditis Suppurative sinusitis Pneumonia Burn wound infections.
  • 95. 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.
  • 96. 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
  • 97. 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
  • 98. 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
  • 99. 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
  • 100. 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
  • 101. 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
  • 102. 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
  • 103. 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
  • 104. COMPLICATIONS
  • 105. 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(.
  • 106. Bronchopneumonia 2% Sepsis 0.7% Inadequate fluid resuscitation 1% Inhalation injury 1% G I T hemorrhage 0.1% The most common cause of death
  • 107. Local Complications: )1(Sepsis. )2(Scar and its complications: Keliods. Marjolin ulcer. Functional deformity. Lymphedema
  • 108. 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
  • 109. Example of hypertrophic scarring
  • 110. 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.
  • 111. 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.

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