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Classification of Burns:
- -Depth of burn
- -Extent of burn calculated in % of TBSA
- -Location of burn
- -Pt risk factors
Degree of burn based on depth of injury
- 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]
Fluid and Electrolyte Shifts: what to watch for
-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)
Synopsis of electrolyte shifts:
- -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
Net result of fluid shift:
- Intravascular volume depletion.
- S+S: decreased BP, increased pulse rate, manifestations of hypovolemic shock
- -Also...insensible loss by evaporation from large denuded body surfaces
Impaired circulatory status bc of _____?
- 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
Pathophysiology of burn injuries:
- -Loss of skin integrity
- -Fluid shifts
- -Electrolyte loss
- -Eschar formation
- -Complication of circumferential injuries
Inflammation & Healing:
- 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!
Complications of Circumferential Burns
- -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
Complications during acute phase of burn injury: INFECTION
- 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
Complications during acute phase of burn injury: CARDIOVASCULAR
- Dysrhythmia's and hypovolemic shock
- Impaired circulation-edema, ischemia from occlusion of blood supply.
- Escharatomy performed to restore circulation
Complications during acute phase of burn injury: RESPIRATORY
- 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
Complications during acute phase of burn injury: NEUROLOGICAL
- 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)
Complications during acute phase of burn injury: MUSCULOSKELETAL
- 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
Complications during acute phase of burn injury: GASTROINTESTINAL
- 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
Complications during acute phase of burn injury: ENDOCRINE
- 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)
Nursing care during Acute phase of burn injury (6)
- 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
Excision and Grafting:
- 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.
Phsyical and occupational therapy:
- 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, Moderate, & Severe classifications of burn injuries:
- *1st & 2nd degree <10% TBS
- *3rd degree burns <2% TBSA
- *NO burns on face/feet/hands/genitalia
- *2nd degree=10-20% TBSA
- *3rd degree <10% TBSA
- *Burns on face/feet/hands/genitalia
- *2nd degree >20% TBSA
- *3rd degree >10% TBSA
Management of Inhalation injuries
- ABC's=100% oxygen
- -Meds (cautious use of narcotics, hydroxocobolamin for cyanide)
- -Hyperbaric therapy?