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Chapter 57

Chapter 57. Management of Patients With Burn Injury. Burn Prevention. Keep matches and lighters out of the reach of children. Emphasize the importance of never leaving children unattended around fire. Develop and practice a home exit fire drill.

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Chapter 57

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  1. Chapter 57 Management of Patients With Burn Injury

  2. Burn Prevention • Keep matches and lighters out of the reach of children. • Emphasize the importance of never leaving children unattended around fire. • Develop and practice a home exit fire drill. • Set the water heater temperature no higher than 70°C. • Don’t smoke in bed, and caution against falling asleep while smoking. • Caution against throwing flammable liquids onto an already burning fire.

  3. Burn Prevention • Caution against using flammable liquids to start fires. • Caution against removing the radiator cap from a hot engine. • Watch for overhead electrical wires and underground wires when working outside. • Keep hot irons out of reach of children. • Caution against running electric cords under carpets or rugs. • Avoid storing flammable liquids near a fire source. • Caution when cooking. • Keep a working fire extinguisher in the home, and to know how to use it.

  4. BURNS • Results in ??? deaths annually • Survival best at ages 15-45 • Children, elderly, and diabetics are at higher risk • Survival best when burns cover less than 20% of TBA

  5. TYPES OF BURNS • Thermal Exposure to flame or a hot object (i.e. hot water) • Chemical Exposure to acid, alkali or organic substances • Electrical Result from the conversion of electrical energy into heat. Extent of injury depends on the type of current, the pathway of flow, local tissue resistance, and duration of contact • Radiation Result from radiant energy being transferred to the body resulting in production of cellular toxins

  6. Chemical Burn

  7. Electrical Burn

  8. BURN WOUND ASSESSMENT • Classified according to depth of injury and extent of body surface area involved • Burn wounds differentiated depending on the level of dermis and subcutaneous tissue involved 1. Superficial (first-degree) 2. Deep (second-degree) 3. Full thickness (third and fourth degree)

  9. SUPERFICIAL BURNS (FIRST DEGREE) • Epidermal tissue only affected • Tingling, Hyperesthesia, pain that is soothed by cooling • Wound: Reddened; blanches with pressure; dry, minimal or no edema, Possible blisters • Complete recovery within a week; no scarring, Peeling • i.e. sunburn

  10. DEEP (SECOND DEGREE) • Involves the epidermis and deep layer of dermis • Pain, hyperesthesia, sensitive to cold air. • Blistered, mottled red base; weeping surface;edema • Recovery in 2 to 4 weeks, some scarring and depigmentation, contractures • Infection may convert it to full thickness • Hospitalization required if over than 25% of body surface involved • i.e. scald burn, flame

  11. FULL THICKNESS (THIRD/FOURTH DEGREE) • Destruction of all skin layers • Requires immediate hospitalization • Dry, waxy white (or charred), leathery, or hard skin, no pain, edema • Exposure to flames, electricity or chemicals can cause 3rd degree burns • Grafting necessary, scarring and loss of contour and function; contractures,loss of digits or extremity possible

  12. Calculation of Burned Body Surface Area • Calculation of Burned Body Surface Area

  13. TOTAL BODY SURFACE AREA (TBSA) • Superficial burns are not involved in the calculation • Lund and Browder Chart is the most accurate because it adjusts for age • Rule of nines divides the body – adequate for initial assessment for adult burns • Palm rule

  14. Lund Browder Chart used for determining BSA Evans, 18.1, 2007)

  15. RULES OF NINES • Head & Neck = 9% • Each upper extremity (Arms) = 9% • Each lower extremity (Legs) = 18% • Anterior trunk= 18% • Posterior trunk = 18% • Genitalia (perineum) = 1%

  16. Pathophysiology • Tissue destruction results from coagulation, protein denaturation, or ionization of cellular contents. • skin and the mucosa of the upper airways are the sites of tissue destruction • Disruption of the skin can lead to increased fluid loss, infection, hypothermia, scarring, compromised immunity, and changes in function, appearance, and body image. • Burns that do not exceed 25% TBSA produce a primarily local response. Burns that exceed 25% TBSA may produce both a local and a systemic response

  17. Cardiovascular Alterations • Hypovolemia is the immediate consequence of fluid loss and results in decreased perfusion and oxygen delivery. • Cardiac output decreases and BP decrease. • SNS releases adrenaline, resulting in peripheral vasoconstriction and increase in HR. • Patient needs immediate fluid replacement. • Most of fluid (in first 24-36 hr) leaks out of blood vessels.

  18. Cardiovascular Alterations • As the capillaries begin to regain their integrity, burn shock resolves and fluid returns to the vascular compartment. • As fluid is reabsorbed from the interstitial tissue into the vascular compartment, blood volume increases. • If renal and cardiac function is adequate, urinary output increases. • Diuresis continues for several days to 2 weeks.

  19. Fluid shift • Local edema occurs if burn area is less that 25% TBSA • Generalized edema if burn area is more than 25% TBSA • Maximal edema is after 24 hours. • Begins to resolve 1 to 2 days after the burn and usually is completely resolved within 7 to 10 days. • As edema increases, pressure on small blood vessels and nerves in the distal extremities causes an obstruction of blood flow and consequent ischemia. • This complication is similar to a compartment syndrome. • The physician may need to perform an escharotomy, a surgical incision into the eschar (devitalized tissue resulting from a burn), to relieve the constricting effect of the burned tissue

  20. Circulating blood volume decreases during burn shock. • Evaporative fluid loss through the burn wound may reach 3 to 5 L or more over a 24-hour period until the burn surfaces are covered. • Usually, hyponatremia is present. • Immediately after burn injury, hyperkalemia results from massive cell destruction. Hypokalemia (potassium depletion) may occur later with fluid shifts and inadequate potassium replacement.

  21. FLUID REMOBILIZATION • Occurs after 24 hours • Capillary leak stops • See diuretic stage where edema fluid shifts from the interstitial spaces into the vascular space • Blood volume increases leading to increased renal blood flow and diuresis • Body weight returns to normal • ? Hypokalemia if no potassium replacement

  22. Effects on blood volume • At the time of burn injury, some red blood cells may be destroyed and other damaged, resulting in anemia • Despite this the hematocrit may be elevated due to plasma loss • Blood loss during surgical procedures, wound care, diagnostic studies and ongoing hemolysis further contribute to anemia • Blood transfusions are required periodically to maintain adequate hemoglobin levels for oxygen delivery

  23. Effects on blood volume • Abnormalities in coagulation, including a decrease in platelets (thrombocytopenia) and prolonged clotting and prothrombin times occur with burn injury

  24. Pulmonary Alterations • Inhalation injury is the leading cause of death in fire victims • Half of these deaths could have been prevented with use of a smoke detector • Burn victims make it out of a burning home safely • Once they are outside they may realize that loved ones or valuable items are still inside the burning home • They then reenter the burning home and are overcome with toxic smoke and fumes and become disoriented or unconcious

  25. Pulmonary response • Pulmonary imjuries fall into several categories, upper airway injury, inhalational injury, including carbon monoxide poisining, and restrictive defects • Upper air way injury results from direct heat or edema • It is manifested by mechanical obstruction of the upper airway, including the pharynx and larynx • Upper airway injury is treated by early nasotracheal or endotracheal intubation

  26. Pulmonary response • Inhalation injury below the glottis results from inhaling products of incomplete combustion (Burning) or noxious gases: carbon monoxide, sulfer oxide, nitrogen oxide, & benzene • The injury results directly from chemical irritation of the pulmonary tisues at the alveolar level • Inhalation injuries below glottis cause loss of ciliary action, hypersecretion, severe mucosal edema and bronchospasm • The pulmonary surfactant is reduced, resulting in atelectasis (collapse of alveoli)

  27. Pulmonary response • Expectoration of carbon particles in the sputum is the cardinal sign of this injury • The pathophysiology effects are due to tissue hypoxia a result of carbon monoxide combining with hemoglobin to form carboxyhemoglobin which competes with oxygen for available hemoglobin sites • The effinity of hemoglobin for carbon monoxide is 200 times greater than that for oxygen • Treatment usually consists of ealy intubation and mechnical ventilation with 100% oxygen • Administering 100% O2 is essential to accelerate the removal of carbon monoxide from the hemoglobin molecule

  28. Pulmonary response • restrictive defects arise when edema develops under full-thickness burns encircling the neck and thorax • Chest expansion may be greatly restricted resulting in decreased tidal volume • In such situation escharotomy is necessary • More than half of all burn victims with pulmonary involvement do not intially demonstrate pulmonary signs and symptoms • Any pat with possible inhalation injury must be observed for at least 24 h for respiratory complications

  29. Pulmonary response • Airway obstruction may occur very rapidly in hours • Decreased lung compliance, decreased arterial oxygen levels and respiratory acidosis may occur gradually over the first 5 days after a burn

  30. Indication of possible pulmonary damages include • History indicating that the burn occured in an enclosed area • Burns of the face and neck • Hoarseness , voice change, dry cough, stridor. • Bloody sputum • Labored breathing or tachypnea (rapid breathing) and other signs of reduced oxygen levels • Erythema and blistering of the oral or pharyngeal mucosa

  31. Pulmonary response • The immediate intervention is intubation and mechanical ventilation • If ventilation is impaired by restricted chest excursion, immediate chest escharotomy is needed • ARDS may develop in the first few days after the burn injury secondary to systemic and pulmonary responses to the burn and inhalation injury

  32. Renal alteration • Renal function may be altered as a result of decreased blood volume • Destruction of red blood cells at the injury site frees hemoglobin in the urine • If muscle damage occurs (from electric burns e..) myoglobin is released from the muscle cells and excreted by the kidney • Adequate fluid volume replacement restores renal blood flow, increasing the glomerular filtration rate and urine volume • If there is inadequate blood flow through the kidneys, the hemoglobin and myoglobin occlude the renal tubules, resultinh in acute tubular necrosis and renal failure

  33. Immunologic Alterations • The immunologic defences of the body are greatly altered by burn injury • Serious burn injury diminishes resistance to the infection • As a result, sepsis remains the leading cause of death in thermally injured patients • The loss of skin integrity is compounded by the release of abnormal inflammatory factors, altered levels of immunglobulins, impared neutrophil function and a reduction in lymphocytes (lymphocytopeni) • Research suggest that burn injury results in loss of T-helper.cell lymphocytes

  34. Thermoregulatory Alterations • Loss of skin results in an inability to regulate body temperature • Burn patients may therefore exhibit low body temperature in the early hours after injury • As of hypermetabolism, core temperature increase. • Burn patients become hyperthermic for much of the postburn period, even in the abscence of infection

  35. GI responses • Paralytic ileus (absence of intestinal peristalsis): • decreased peristalsis and bowel sounds are manifestations of paralytic ileus resulting from burn traumaand • Gastric distention and nausea may lead to vomiting unless gastric decompression is intiated • Curling´s ulcer (gastric or deuodenal erosion) • Gastric bleeding secondary to massive physiologic stress may be signaled by occult blood in the stool, regurgitation of coffee ground material from the stomach or bloody vomitus

  36. PHASES OF BURN INJURIES Emergent Phase: From onset of injury to completion of fluid resuscitation Acute Phase: From beginning of diuresis to near completion of wound closure Rehabilitative Phase: From major wound closure to return to individual's optimal level of physical and psychosocial adjustment

  37. EMERGENT PHASE • Immediate problem is fluid loss, edema, reduced blood flow (fluid and electrolyte shifts) • Goals: • First aid (A, B, C) • Intubation if needed • Prevention of shock • Prevention of respiratory distress • Detection and treatment of concomitant injuries • Wound assessment and initial care

  38. Emergent phase/ at fire sceine • Extinguish the flames , switch off power source, remove chemical soaked clothes, etc… • Assess and maintain an open airway • Cool the burn • Remove restrictive objects. • Cover the wound • Irrigate chemical burns

  39. First Aid Scene • Cool burn wound: - reduce direct thermal trauma & stabilize mast cells, reducing release of histamine and other inflammatory mediators, and will reduce edema - pain relief - running water (15 degree C.) - worth considering for up to 2 hours

  40. Intubation : • Suspicion of inhalational injury • Severe facial & neck burn “ easy early intubation will become difficult and impossible later on”

  41. Inhalational injury • Fires • Closed space • Carbonaceous material in nose & mouth

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