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ONE MORE TIME. BURN INJURY. NPN 205 Medical Surgical II. PATHOPHYSIOLOGY. Tissue destruction = local and systemic problems r/t age, general health, extent of injury, and area of body injured injury made compounded d/t scarring and contractures

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  1. ONE MORE TIME

  2. BURN INJURY NPN 205 Medical Surgical II

  3. PATHOPHYSIOLOGY • Tissue destruction = local and systemic problems • r/t age, general health, extent of injury, and area of body injured • injury made compounded d/t scarring and contractures • skin can regenerate if a portion of the dermis remains after the burn injury • sweat glands are lost and secretory function is gone in the area of the burn • very painful if partial thickness burns occur d/t the exposed nerve endings • if full thickness burn occurs the area is free of pain, but may feel pressure • partial thickness burns reduce the ability of skin to absorb Vit D ( which converts cholesterol )

  4. PATHO, CONT. • the skin helps regulate the body temperature-so when skin lost-body temp drops internal environment of body is 84.2 to 109.4 degrees body can dissipate heat as soon as it occurs unless above 104 degree then damage begins to occur at 158 degrees injury occurs and skin cell are destroyed • the amount of damage to the skin depends on the cause, and duration of the burn • some tissue is thicker than others and can tolerate more heat (eyes, ears, nose, genitalia hands, feet, toes, can burn rapidly)

  5. CLASSIFICATION OF BURNS • American Burn Association classes by minor, moderate, or major and by depth, extent, location • major=partial thickness burns greater than 25% of body full thickness >10% with other criterion on pg 1558 • moderate=deep partial thickness burns 15-25% full thickness burns 2-10% • minor=deep partial thickness burns <15% full thickness burns <2%

  6. DEPTH OF BURNS • Superficial thickness wounds-least destruction, epidermis only area burned, ex. sunburn area may become red and peeling of dead skin will occur for 2-5 days and heals in 3-5da

  7. Partial thickness burns- 2 divisions-involves the epidermis and dermis in various depths 1. superficial partial thickness – result from prolonged duration or intensity of exposure blister forms, erythremic and moist- blister forms sterile area which protects the wound from infection/fluid loss-may be increased pain, and sensitivity to touch-heal in 10-14 days Deep partial thicknesswounds—deeper in the dermis-red, waxy white without blisters less pain but still there and some edema noted, no blisters, decreased blood supply d/t vasoconstriction-deeper injury can occur d/t hypoxia and ischemia- can become full thickness if infection and hypoxia continues-heal in 3-6 wks with large amount of scarring BURN INJURY, CONT.

  8. BURN INJURY, CONT. • Full thickness wounds-entire epidermis and dermis-no viable tissue remains- • skin grafts are necessary-or secondary wound closure may help-tissue is hard, dry leathery eschar ) which is dead tissue. • Eschar must be taken off to allow the wound to heal. • area may be edematous under the dead tissue. if burns surrounds the entire extremity or the thorax-may impair circulation/ventilation escharotomies/fasciotomies may need to be performed to relieve pressure • color-white, red, waxy, yellow or black/brown • thrombosed blood vessels may be visible due to burning vessels and is without blood supply • minimal to no pain d/t the destruction of the nerve endings

  9. BURN INJURY, CONT. • Deep full thickness wounds/4th degree burn • involve skin and fascia as well as muscles, bone, and tendons • are burns from flame, chemical or electrical • wound is black • no pain • need early skin grafts • may need amputation

  10. BURN PHASES • Fluid Accumulation Phase: • lasts for 36-48 hrs • skin maintains fluid and electrolyte balance • after a burn massive fluid loss occurs 4x the rate of normal tissue • evaporation from denuded body surfaces (may be as much as 400ml/hr) • during this phase the fluid shifts from the intravascular space to the interstitial space • which leads to edema ( which if severe may lead to problems with circulation) HYPOVOLEMIC SHOCK • THIRD SPACING==HYPOVOLEMIA==DECREASE CARDIAC OUTPUT TACHYCARDIA==HYPOTENSION==SHOCK==CARDIAC ARRYTHEMIAS

  11. PHASES, CONT. Fluid Accumulation • Blood more concentrated due to fluid loss • H2O loss can amount to 8L/day • Decrease UOP from kidneys • In response to a burn the body produces aldosterone and antidiuretic hormone which causes retention of NA and H2O • breathing may be effected in this stage • Hypovolemia may cause decrease in GI motility (ileus) ulcers are common, metabolic needs increase due to tissue destruction • Hyperkalemia d/t massive cellular trama, metabolic acidosis, or renal failure • Hyponatremia d/t loss of water and NA from the cells (NA trapped in the fluid) • Hypernatremia d/t use of hypertonic sodium solution with fluid replacements • Hypocalcemia when CA goes to damaged tissue at burn site • Metabolic acidosis can occur as well as respiratory acidosis

  12. PHASES, CONT • Fluid Mobilization Phase: -diuresis phase-occurs about 48hrs after burn -fluid shifts back into the intravascular space -edema decreases -blood flow to kidneys increases-UOP increases -NA is lost and K+ moves back into the cell or is lost in the urine -hypokalemia may develop when K+ shifts back into the cell -hypervolemia may occur d/t the shift of fluid into the vascular compartment and with the additional IV’s given -hyponatremia may occur with the loss of NA in the urine

  13. BURN PHASES, CONT. • Convalescent Phase: -time when focus is placed on the healing of the burn injury -may have some anemia and fluid and E-lyte changes based on intake etc.

  14. SYSTEMIC EFFECTS OF BURNS • Metabolic - client is in a hypermetabolic stage • Endocrine -increased catecholamines, ADH, aldosterone, and cortisol increase metabolism -O2 and calorie needs are increased -the body is under stress response=catabolism increases calorie requirements may be double or triple the usual amount needed

  15. SYSTEMIC, CONT. • Respiratory Major cause of morbidity/ mortality -inhalation injury r/t contact to steam, toxic fumes, or smoke -may be r/t treatment===large amount of fluid volume infused may cause edema -increase in alveolar capillary permeability -constriction of chest r/t circumferential burn -injury can occur from edema from irritants which cause edema and blockage of trachea -decreased movement of the normal cilia in the trachea may allow foreign bacteria and particles to enter into the lungs -lining of the trachea may slough off and become lodged in the bronchus -damage to the alveoli and the capillary membrane may lead to infection and respiratory failure

  16. SYSTEMIC,CONT. • Cardiac -cardiac output is the most effected by the loss of fluid -early the rate increases to compensate for the loss of volume -cardiac output remains decreased in spite of the increase rate -may be decreased for 36 hrs -when fluid is replaced goes back to normal function

  17. SYSTEMIC, CONT. • GASTROINTESTIONAL • Effects occur due to the shift of blood volume to vital organs • Epinephrine and nor-epi inhibit gastric motility and decrease blood flow to the GI tract • Decreased periostalis occurs • H+ ion production increases • Develop ulcers (Curling’s ulcer within 24 hours) • Use H2 blockers

  18. IMMUNE RESPONSE • Widespread impairment of the immune system • Skin is barrier to invading organisms • Changes in the WBC’s occur, • Susceptibility to infection increases

  19. RENAL RESPONSE • Blood flow to the kidneys is decreased and renal ischemia occurs • Unless flow is improved renal failure occurs • With full thickness electrical burns myoglobin and hemoglobin are released in the blood and can occlude the renal tubles • With adequate diuretics and fluid the problem can be corrected

  20. COMPENSATORY RESPONSES • Inflammatory response -blood flow increases to the area in response to injury -oncotic pressure increases forcing fluid and plasma proteins into the injured area -extent of response depends upon the amount of the injury -this response is supposed to be short term if lasts may be tissue damaging • Sympathetic nervous system autonomic and endocrine system responses respiratory/cardiac and GI

  21. ETIOLOGY OF BURN INJURY • Many causes==cause affects the outcome Dry heat-open flame=house fire and explosionsŸ Moist heat=scald==older adults most common=spills and splatters Contact burns==hot metal/tar/grease (industrial, home and restaurants) usually deep because liquid is extremely hot Chemical injury occurs in home and industry (drain cleaner, acids used in industry or chemicals in industry ) Severity depends on the length of contact and amount of tissue exposed

  22. TYPES OF BURNS • Electrical Injury • Damage goes from inside out==coagulation necrosis with tissue damage and death • When current passes thru heart, brain and kidneys have major effects • Current may also cause cloths to ignite and causes internal and external effects • Current enters body and has an exit site • Involves organs and limbs • Damage depends on amps, volts, resistance, type of current, duration and path through body • Body has different resistance ( bone, soft tissue, nerves, muscle )

  23. TYPES, CONT. • Wet skin has less resistance • “The higher the resistance the greater the heat generated by the current flow and the greater the potential for soft tissue injury” • The longer the contact the greater the damage • Titanic contractions of the muscles sometimes causes a longer exposure ( some have factured spine) • Route taken thru the body may be difficult to determine

  24. WAYS ELECTRICAL BURNS OCCUR • 3 ways electrical burns occur 1.Thermal ==cloths ignite 2.Flash==current arcs between 2 surfaces 3.True electrical==body has direct contact with an electrical source

  25. RADIATION INJURY • Occurs in health care but usually minor • Most serious in industry when large amounts of radioactive material is involved • Severity is determined by the type, duration and amount

  26. PHASES OF BURN INJURY • Emergency=early intervention improves survival • Burns-Clinical Manifestations -First 48 hours is most critical -Must do assessment quickly- - ---Obtain info from client if possible or family about cause, time of injury, any other health problems -Weigh( used to calculate fluids, and drug dosages), etc.

  27. AIRWAY/RESPIRATORY ASSESSMENT • 2 Types of Respiratory Injuries 1. Upper airway injuries that cause edema and obstruction 2. Inhalation injuries

  28. UPPER AIRWAY INJURIES • Maintain an open airway, ensure adequate breathing/circulation • assess for stridor,hoarceness, cough, dysphagia, wheezes, crowing • if gets worse may indicate emergency!!! • look for edema by looking at the mouth, nose and pharynx • assess for facial burns-eyelids, ears, neck, singed nasal hairs, black carbon particles

  29. INHALATION INJURIES • Carbon monoxyde poisoning accounts for the major deaths at the scene of the fire • CO2 is major gas produced by the combustion of burning materials • odorless, tasteless, and colorless • displaces O2 in the hemoglobin molecule causing hypoxia and carboxyhemoglobinemia and death • usually found in clients in closed areas • causes vasodilating = cherry red skin color • effects dependent on amt inhaled 11-20% mild-H/A, breathlessness 21-40%=H/A, tinnitus, nausea, vertigo, confusion, stupor, decrease B/P, ^ HR, 41-60%= coma, convulsions 61-80% =death

  30. THERMAL ( HEAT ) INJURY • Inhalation of superheated air or steam • Effects entire respiratory tract/H2O holds heat and lungs moist • Ulcers, edema, and possible airway obstruction may occur • Indicated by signs of obstruction • ( stridor, hoarseness, etc.)

  31. SMOKE POISONING • Most common injury • Cyanide is produced when plastics burn • Will see atelectasis, pulmonary edema, and tissue anoxia • Amount of injury is R/T length of exposure • May not be seen until 12-24 hrs after injury • May lead to ARDS

  32. PULMONARY FLUID OVERLOAD • Pulmonary edema can occur when other tissues are injured and capillary permeability is increased • Fluid overload, from needed hydration, may cause left sided heart failure

  33. EXTERNAL FACTORS • External factors-constriction by eschar may cause difficult expansion of lungs

  34. INTERVENTIONS FOR RESPIRATORY PROBLEMS • May require Vent O2 < 60% is indicator • Suctioning frequent to remove sloughing tissue • Chest x-rays, PAWP, CVP • DRUGS • antibiotics, Norcuron, (sedation, analgesia and antianxiety ) • Chest physiotherapy • Chest tubes • Trach • Help prevent ARDS by application of PEEP

  35. CARDIOVASCULAR • Begin immediately after injury • Hypovolemic shock is common cause of death in immediate postburn • Arrhythmias also are problem with electrical burns • Circulation to extremities may impede flow

  36. CV ASSESSMENT • Pulses, B/p, pulse ox, capillary refill (may be decreased in early stages) • Look for edema and weight gain • EKG changes may be evident

  37. RENAL/URINARY • Acute Tubular Necrosis is the most common complication d/t hypovolemia • Debris from destroyed RBC’s, and uric acid, may block the filtration of kidneys ASSESSMENT -Strict I/O, maintain output at 30-50 ml/hr -BUN, Creatine, and NA levels -Observe urine for color, character, odor, and particles

  38. INTREGUMENTARY • ASSESS SEVERITY BY: • Depth of burn (1st, 2nd or 3rd degree) • Extent or size of burn ( estimated by % of total body surface area ) • Location

  39. Size= Rule of Nines- most rapid method Divides the body into areas which are multiples of nine Head and neck = 9% Arms = 9 % Anterior trunk = 18 % Posterior trunk = 18 % Legs = 18 % Perineum = 1 % Lund-Browder and Berkow method is more specific. Uses changes of the body according to growth and development SEVERITY, CONT.

  40. LOCATION • location also impt. • face, neck and hands=breathing, eating , emotional • feet, joints, and eyes are impt for ability of self care • ears and nose susceptible to infections due to poor blood supply • buttocks and genitals are prone to infections

  41. GI TRACT • Not directly injured • Decreased blood flow d/t decreased blood volume • Ileus and motility • Assess -bowel sounds =may be decreased -may have n/v and distention -may need NG -stress ulcer=observe for fecal blood

  42. OTHER ASSESSMENTS • Labs -H and H may be ^ d/t hypovolemia, -E-Lytes – K+ increases -ABG changes -protein – low -BUN and Creatinine – elevated -WBC - ^ early but drops rapidly d/t immune system failure—sepsis may decrease further • Other Cat scan/eye consults bronch when needed—if other organs are involved

  43. NURSING DIAGNOSIS • Decreased cardiac output • Deficient fluid volume • Ineffective tissue perfusion (multiple) • Ineffective breathing pattern • Pain • Excess fluid volume • Risk for ineffective thermoregulation • Sensory/perceptual alterations

  44. INTERVENTIONS • IV Therapy • Must replace loss and prevent shock • Given per formula = ml/kg/% of TBSA • ½ given first 8 hours and ½ given next 16 hours May be combination of L/R, albumin, crystalloids

  45. IV FLUID FORMULA • Amount given is based on keeping UOP 30 ml/hr • Example • Parkland/Baxter = 4 ml LR per Kg of body weight per % of TBSA • 70 kg patient with 50 % TBSA = 4 x 70 x 50 % = 14,000 ml in 24 hours

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