440 Final-BURNS

• -Depth of burn
• -Extent of burn calculated in % of TBSA
• -Location of burn
• -Pt risk factors

• Partial Thickness skin destruction:
• Superficial (1st degree): erythema, blanching on pressure, pain and mild swelling, no vesicles or blisters [structures: superficial epidermal damage with hyperemia, tactile and pain sensation intact]
• -Deep (2nd degree): Fluid filled vesicles that are red, shiny, wet (if vesicles ruptured); severe pain caused by nerve injury; mild to mod edema [structures: epidermis and dermis involved]

• Full-Thickness Skin Destruction
• Third & Fourth degree: dry-waxy white-leathery or hard skin; visible thrombosed vessels; insensitivity to pain bc of nerve destruction; possible involvement of muscles/tendons/bones [structures: ALL skin elements and local nerve endings destroyed]

-Hypovolemic shock (caused by massive fluid shifts out of blood vessels as a result of increased capillary permeability and can begin early..like 20 min after)

• -As capillary walls become more permeable, water-sodium-and later plasma proteins (albumin) moves into intersitial space and surrounding tissue
• -Even more fluid shifts out of vascular space into interstitial spaces (second spacing) bc colloidal osmotic pressure decreases with progressive loss of protein from vascular space

• Intravascular volume depletion.
• S+S: decreased BP, increased pulse rate, manifestations of hypovolemic shock
• -Also...insensible loss by evaporation from large denuded body surfaces

• HEMOLYSIS of RBCs
• -This happens by a circulating factor released at time of burn. Elevated hct is caused by hemoconcentration resulting from fluid loss.
• -Na rapidly shifts to interstitial spaces and remains there until edema ceases. K shift initially develops bc injured cells and hemolyzed RBCs release K into circulation

• -Loss of skin integrity
• -Fluid shifts
• -Electrolyte loss
• -Eschar formation
• -Infection
• -Complication of circumferential injuries

• Coagulation necrosis--tissue and vessels damaged/destroyed
• Neutrophils and monocytes accumulate at the site of injury. Fibroblasts and newly formed collagen fibrils appear and begin wound repair within first 6-12 hrs after injury

• Skin barrier destroyed, resulting in bone marrow depression and decreasing circulating levels of immunoglobulins
• Inflammatory cytokine cascade triggered by tissue damage impairs function of lymphocytes, monocytes, & neutrophils-which put pt at greater risk for INFECTION!

• -Infection, circulatory compromise distal to burn with subsequent neuro impairment of affected extremity
• -compartment syndrome: increase pressure in compartment which compromises nerve function of tissue

• Pathogens invade through destroyed skin layer. May progress to transient bacteremia as a result of burn wound manipulation (debridement)
• Pt may develop sepsis (hypo/hyperthermia, increase pulse & RR, decrease BP, decrease urine output)
• *Begin with antibiotics and maybe topical ointment

• Dysrhythmia's and hypovolemic shock
• Impaired circulation-edema, ischemia from occlusion of blood supply.
• Escharatomy performed to restore circulation

• Upper respiratory tract injury--from direct heat injury and edema leading to mechanical airway obstruction and asphyxia.
• Inhalation injury--direct insult at alveolar level secondary to inhalation. Result is interstitial edema that prevents diffusion of oxygen from the alveoli into circulatory system

• NO physical symptoms but..
• can become extremely disorientated, combative, hallucinations. Delirium at night with older pt (can be from electrolyte imbalance, stress, cerebral edema, sepsis, drugs)

• As burn injuries begin to heal and scar tissue forms, the skin is less supple and pliant.
• Limited ROM and contractures occur.
• Bc of pain, pt will prefer to assume flexed position for comfort
• Splinting is beneficial to reduce contracture formation

• Paralytic ileus results from sepsis
• Diarrhea may be caused by antibiotics or tpn...even constipation from opioids
• Curling's Ulcer (diffuse superficial lesions) is caused by generalized stress response resulting in decrease mucus and increased gastric acid secretion--
• this is d/t decrease blood flow to GI tract during hypovolemic shock. Use antacids and ranitidine to help prevent this

• Increase blood glucose levels bc of stress-mediated cortisol and catecholamine release, resulting in increased mobilization of glycogen stores
• Also increase in insulin production and release. later, hyperglycemia can be caused by increased caloric intake (but give IV insulin drip, DO NOT limit calories)

• 1. Wound care
• 2. Excision and grafting
• 3. Pain managment
• 4. Physical & Occupational therapy
• 5. Nutritional Therapy
• 6. Psychosocial Care

• Goals--cleanse and debride area of necrotic tissue and debris that would promote bacterial growth and promote wound re-epithelialization and/or successful skin grafting
• Enzymatic debridement speeds up removal of dead tissue from healthy wound bed

• Eschar removed, graft placed on clean viable tissue
• Hemostasis achieved by pressure and application of topical thrombin/epi and wound covered with pt's own skin
• -Cultured Epithelial Autografts:obtain permanant skin from a person to harvest for a person with not enough viable skin
• -Artificial Skin:replaces all functions of skin and consist of both dermal and epidermal elements

• 2 types: continuous-background pain all day/night & treatment induced pain
• -Continuous IV morphine allows for steady therapeutic level of medication.
• -MUST have breakthrough meds!
• -Premedicate before treatments
• -Fentanyl (short acting) is good.

• Rigorous therapy to maintain optimal joint function.
• -Good time for exercise if during and after wound cleansing when skin is softer and bulky dressings are removed
• Passive and active ROM, custom fitted splints are great!

• Goal--provide adequate calories and protein to promote wound healing
• Burn pt is hypermetabolic with highly catabolic state. Work with dietician and readjust diet as needed
• May need feeding tube or tpn
• Increase in protein and carbs! WEight loss should NOT be more than 10% of preburn weight

• First 24-48 hrs:
• *Hyperkalemia bc K leaves cell and Na enters. Water, Na, & Albumin leave capillary and move into extracellular space =edema!!
• After 48 hrs:
• *Hypokalemia bc K moves back into cell and Na leaves. Water and sodium move back into capillary but albumin stays in extracellular space.

• MINOR:
• *1st & 2nd degree <10% TBS
• *3rd degree burns <2% TBSA
• *NO burns on face/feet/hands/genitalia
• MODERATE:
• *2nd degree=10-20% TBSA
• *3rd degree <10% TBSA
• *Burns on face/feet/hands/genitalia
• SEVERE:
• *2nd degree >20% TBSA
• *3rd degree >10% TBSA

• ABC's=100% oxygen
• -Meds (cautious use of narcotics, hydroxocobolamin for cyanide)
• -Hyperbaric therapy?