nursing management of burn wounds.. [Autosaved].pptx

this powerpoint presentation gives an indepth insight on care of burn wpunds.

1. BURNS.

2. OBJECTIVES. By the end of this lesson, the learner should; Define burns. Explain the types and classification of burns. Explain the pathophysiology of burns Explain complications of burns. Demonstrate an understanding of nursing management of burn patients.

3. Introduction. Burns- are injuries caused by direct tissue damage from exposure to high intensity sun rays, chemicals, thermal or electricity.

4. Types of burns. 1. Heat/thermal burn. M ost common type. Sources: May come from hot steam, fire, hot liquid getting on the surface of the skin.e.t.c Patients with these types of burn injuries suffer from inhalation injury to the airway structures .

5. 2. Electrical burns. May be from some type of electrical source. It damages the skin and other structures including muscles and bones of the burn victim.( iceberg effect). Damage to muscles may lead to release of myoglobin, and damaged cells release Hemoglobin . This results to too much myoglobin and hemoglobin in circulation which may clog in the kidneys resulting to Acute Tubular Necrosis .

6. 3. C hemical burns. This is a type of burn where a toxic substance has come into contact with the skin. Examples: acidic sources. Alkaline burns.

7. 4. Radiation burns. Examples; sunburns, chemotherapy 5. Friction burns. This may be as a result of abrasion to skin. Examples; car accidents.

8. Factors that determine burn severity in patients. 1.Burn depth. 2. Percentage of total body surface area burned. 3. Age( the elderly and children) 4. Location of burn.(face, hands and feet, joints, genitals)

9. Skin layers.

10. The epidermis Top skin layer that offers protection from external environment and infections. The dermis. Contain blood vessels. Nerve endings, sweat/oil glands, and cells that create new skin.

11. The hypodermis. This is the subcutaneous tissue containing fatty tissue, veins, arteries and nerves. It insulates the underlying structures.

12. ASSESSMENT OF BURN WOUNDS.

13. Classification of burns according to depth. 1. First degree burns( superficial burns) 2. Second degree burns( partial thickness) Superficial partial thickness Deep partial thickness. 3.Third degree burns.(full thickness burns) 4. Fourth degree burns(deep full thickness)

14. 1.First Degree Burns: Superficial Burns . Affects the top layer of the skin only. Signs and symptoms: Appears very red or pink,. Painful and warm to touch. no blisters or scars left behind. Brisk capillary refill.

15. 2. Second degree burns . Affects the epidermis and the dermis. Clinical manifestations. Very painful, shiny and moist( red/pink) painful blisters. A blister is a red,moist shiny fliud -filled vescicle . Rapture of the blister causes a Scars are formed.

16. a.) Superficial 2 nd degree burns Involves the epidermis and superficial portion of the dermis Often seen with scalding injuries Presents with blister formation and typically blanches with pressure Sensitive to light touch or pinprick Commonly treated on outpatient basis; heal in 1-3 wks

17. b.) Deep 2 nd degree burns Involves the epidermis and most of the dermis Appears white or poorly vascularized; may not blister Less sensitivity to light touch and pinprick than superficial form Extensive time to heal (3-4 wks ) Patients often require excision of the wound and skin grafting .

18. 3. Third degree burns.( full-thickness burns.) The epidermis and dermis are destroyed along with the hair follicles, sweat glands and nerves. Involves epidermis, and all layers of dermis, extending down to the hypodermis.. Appears dry, leathery, and numb, often without blisters

19. Clinical manifestations . decreased pain. Dry waxy white,leathery or charred black color Non – blanchable and inelastic. Skin does not heal( requires skin grafting)

20. Formation of eschar. eschar- is a burned leathery dead tissue. It may obstruct breathing or circulation depending on the location of the burn. It must be removed for healing to occur.

21. 4. Fourth degree burns. This is a full-thickness burn extending to the muscles or bones. It is the most severe of the types. Common result of high-voltage electric injury or severe thermal burns . All the skin layers are severely destroyed and skin sensation is lost( hypoesthesia). Requires hospital admission during management.

22. Classification according to total body surface area burned. 1. The rule of nine/Wallace Rule Of Nine It is used for early assessments. It is a quick way to calculate the extent of burns. It assigns percentages in multiples of nine to major body surfaces.

23. Note: Superficial burns are not included in the assessment of TBSA burnt.

24. 2. Lund and Browder chart. A more precise method for assessing the burns wound. It recognizes that the percentage of total TBSA of various anatomic parts, especially the head and legs, changes with growth. Here each part of the body is individually assessed.

25. Age in years 1 5 10 15 Adult Head (back or front) 9½ 8½ 6½ 5½ 4½ 3½ 1 thigh (back or front) 2¾ 3¼ 4 4¼ 4½ 4¾ 1 leg (back or Front ) 2½ 2½ 2¾ 3 3¼ 3½

26. 4. Rule Of Palm. The patients entire palm is approximately 1%. A clean piece of paper may be cut to the size of the hand, and through that a percentage of burns is calculated. It is useful for small scattered burns.

27. Pathophysiology of burn injuries.

28. Jackson Thermal Wound Theory. Zone of coagulation. It is the centre area of wound where all tissues are damaged It is the point of maximum damage. There is irreversible tissue loss. Coagulative necrosis occurs. .

29. b) Zone of stasis surrounds the coagulation area. It is characterized by decreased tissue perfusion and characterized by ischemia. It is potentially salvageable.

30. c) Zone of hyperemia. unburned area that surrounds the zone of stasis. it is red due to inflammation. It is characterized by increased perfusion.

31. Pathophysiology of burns . Heat causes damage to the epidermal layer of the skin. Damage to the keratinocytes in the epidermal layer, initiates immune response by activating immune cells in the skin layer including mast cells and macrophages. The damaged keratinocytes secrete pro-inflammatory cytokines triggering an immune response.

32. These pro-inflammatory cytokines stimulate nerve endings around the dermis hence pain. Some cytokines will cause increased vascular permeability resulting to fluid leakage leading to interstitial oedema . This may result to hypotension .

33. Altered capillary permeability leads to loss of fluids- hypovolemia . Severe hypovolemia leads to decreased cardiac output, decreased myocardial function . Cytokines also cause vasodilation leading to further hypotension in severe cases.

34. Vasodilation also contributes to warmth in burnt surfaces, blanching, and erythema . Decreased cardiac output may also result to altered pulmonary resistance causing pulmonary edema.

35. Pulmonary edema may result to infection hence Systemic Inflammatory Response Syndrome ( SIRS) and Multi-organ Dysfunction Syndrome

36. Hemodynamic changes in burn injuries. Decreased cardiac output. Increased systemic vascular resistance. Increased pulmonary vascular resistance. These hemodynamic changes results to hypovolemic shock . Hypovolemic shock- Hypovolemia is a condition that occurs when your body loses fluid, like blood or water

37. Microvascular changes in burn injuries. 1 . Increased vascular permeability 2. Increased microvascular hydrostatic pressure. These changes results to increased extracellular fluid hence edema .

38. Systemic effects of Burn Injuries. 1. digestive system. Decreased perfusion to the digestive system results to increased acid production due to stress response on the body. This causes Curling Ulcers . Curling ulcers are characterized by nausea and vomiting, epigastric pain and hematemesis( blood stained vomitus) and blood in stool.

39. Decreased perfusion to the digestive system also leads to decreased GI motility -ileus . Ileus is characterized by lime-green vomitus.( always assess for the presence of bowel sounds in burn patients .)

40. 2. Respiratory system. Inflammatory mediators cause bronchoconstriction , and in severe burns respiratory distress syndrome can occur. Gross edema of the throat causing airway obstruction. May have an increased respiratory rate as a result of pulmonary edema and as an attempt to compensate the increased metabolic rate.

41. 3. The Immune system. The humoral immunity is altered as seen by decreased levels of immunoglobulins, and formation of membrane-attacking complexes leading to inflammation and cytolysis . The skin is exposed to the external environment predisposing the patient to infections.

42. Infection preventive measures undertaken include: Protective isolation Hand hygiene. Wearing masks. Sterile linen and covers. Tetanus injections administration. Temperature regulation-ensuring the room is warm.

43. 4 . The cardiovascular system. Capillary permeability is increased , leading to the loss of intravascular proteins and fluids into the interstitial compartment . Decreased intravascular fluid means there is not enough blood for the heart to pump, therefore there is decreased cardiac output. The heart rate increases as the heart tries to pump faster to perfuse body tissues. Myocardial contractility is decreased but the rate increases causing reduced cardiac output.

44. Increased vascular permeability also results in decreased sodium blood levels and albumin levels This is because, as the fluids escape from the intravascular space into the interstitial space, sodium and albumin moves along resulting to decreased levels within the intravascular space. Within the intravascular space, there is increased levels of potassium due to cell injury.

45. Phases of Burn Management.

46. There are three phases of burn management. These include 1. Emergent phase. 2. Acute phase 3 .Rehabilitative phase.

47. Emergent phase. This is the initial phase of a burn injury. Refers to the onset of burn injury to restoration of capillary permeability. It occurs in the first 24-48 hours .

48. In this phase, the patient is at risk of; Hypovolemic shock. Respiratory distress. Compartment syndrome- Compartment syndrome is an increase in pressure inside a muscle, which restricts blood flow and causes pain.

49. Signs and symptoms of compartment syndrome . Pain Paresthesia( numbness) Pallor. Paralysis( weakening with movement) pulselessness The main focus of interventions in the emergent phase is to correct hypovolemia through fluid replacement therapy..

50. Acute phase. In this phase, the capillary permeability has stabilized and wound healing process is ongoing. starts at 48-72hours , until the wound heals. Here, the patient is at risk of circulatory overload.

51. The patient experiences diuresis . The main objectives of interventions in Acute phase is Prevention of infection. Relieving pain. Proper nutrition( increased calorie intake) Wound care

52. Rehabilitative phase. Occurs from when the burn is healed to when the patient is able to function again mentally and physically. interventions in this phase include; Psychosocial ADLs Occupational therapy. Cosmetic corrections.

53. Complications of Burns. Early/immediate complications. Airway obstruction. Hypothermia. Fluid and electrolyte imbalance. Anemia Paralytic ileus. Compartment syndrome.

54. Late complications. wound complications. Curling ulcers. Depression. Keloids. Multi-organ failure Contractures-A permanent tightening of the muscles, tendons, skin, and nearby tissues that causes the joints to shorten and become very stiff. This prevents normal movement of a joint or other body part.

55. Parklands Formula. This formula is used to calculate the initial fliud requirements in burn patients. 4ml *body weight (KG) *TBSA(%) =TOTAL CRYSTALLOID FLIUDS IN FIRST 24HOURS. Half of the total volume is given in the first 8hours Half of the total volume is given over the next 16 hours.

56. NOTE: THE FIRST 8HOURS IS FROM THE TIME OF THE BURN INJURY, IT IS NOT FROM THE TIME OF EVALUATION OR CALCULATION. ONLY PARTIAL THICKNESS AND FULL THICKNESS BURNS ARE INCLUDED IN THE CALCULATION.

57. CONTRACTURES. Correct Answer: A. Applying knee splints. Applying knee splints prevents leg contractures by holding the joints in a position of function. Maintain proper body alignment with supports or splints, especially for burns over joints. Promotes functional positioning of extremities and prevents contractures, which are more likely over joints. Option B:  Elevating the foot of the bed can’t prevent contractures because this action doesn’t hold the joints in a position of function. Medicate for pain before activity or exercise. Reduces muscle and tissue stiffness and tension, enabling the patient to be more active and facilitating participation. Option C:  Hyperextending a body part for an extended time is inappropriate because it can cause contractures. Incorporate ADLs with physical therapy, hydrotherapy, and nursing care. Combining activities produces improved results by enhancing the effects of each. Option D:  Performing shoulder range-of-motion exercises can prevent contractures in the shoulders, but not in the legs. Perform ROM exercises consistently, initially passive, then active. Prevents progressively tightening scar tissue and contractures; enhances maintenance of muscle and joint functioning and reduces loss of calcium from the bone.