Fluid shifting and electrolyte shifting in burn injuries : emergent and later stages Fluid shift and electrolyte

imbalance The amount of plasma to interstitial fluid shift depends on the extent and severity of the injury. Occurs when at least 20 to 30% of TBSA damaged. Fluid shifting leads to hypovolemia, metabolic acidosis, hyperkalemia and hyponatremia F & E shifts in Emergent phase Generalized dehydration Reduced blood volume and hemoconcentration Decreased urine output Trauma causes release of potassium into ECF: hyperkalemia Na+ traps in edema fluid and shifts into cells as potassium is released: hyponatremia Metabolic acidosis F & E Shifts: Acute phase Fluid re-enters vascular space from the interstitial space Hemodilution Increased urinary output Sodium is lost with diuresis and due to dilation as fluid enters the vascular space: hyponatremia Potassium shifts from the ECF back into cells Metabolic acidosis Fluid Remobilization After 24 to 36 hours, fluid shifts back into circulation, electrolyte levels rebalance, increased renal blood flow, increased urine formation and diuresis. Hyponatremia increases due to increased renal sodium excretion and loss of Na+ from the wounds Hypokalemia can occur because the K+ is returning to the intracellular compartments. Vascular changesFluid Shift Vessels supplying the burned skin become occluded, blood flow in venous and arterial channels become decreased or stopped

 Damaged macrophages within tissues release chemical mediators that cause vasoconstriction Vessels adjacent to the burn injury dilate causing increased capillary hydrostatic pressure and capillary permeability. This fluid shift is known as third spacing or capillary leak syndrome Capillary leak syndrome Continuous leak of plasma from the intravascular space into the interstitial space Loss of plasma and proteins results in decreased colloidal osmotic pressure in the vascular space. Leakage of F & E from vascular space leads to significant EDEMA. Fluid Shift Occurs in the first 12 hours after injury and continues for 24 to 36 hours. Maximum edema occurs after 24 hours Starts to resolve 1 to 2 days post burn and subsides by 10 days post burn. Phase of Burn Injury Emergent or resuscitative phase: onset of injury to completion of fluid resuscitation Acute or intermediate phase: from beginning of diuresis to wound closure Rehabilitation phase: from wound closure to return to optimal physical and psychosocial adjustment Emergent phase ABCsestablish airway, administer 100% humidified 02, circulation cervical spine immobilization if electrical injury, cardiac monitoring, get large bore IV in, begin fluid resuscitation. Monitor AP and BP frequently Keep NPO, prevent asipiration N/V common due to paralytic ileus from stress response Cool the wound (Never use ice or apply very cold water or apply water longer than several minutes at a time)

 Key nursing interventions with burn victims Nursing Interventions Strict I & O q 1 hour, specific gravity, ph, Monitor electrolytes, glucose, protein and h & h C D B, Incentive Spiro Monitor vitals, temp Auscultate lungs, check pulse ox Administer 02 Mechanical vent care (intubated if Pa02 < 60) Turning & Positioning NGT Tetanus immunization Neuro assessment Eye exam if facial burns Check pain levels, anxiety levels Cardiac monitoring Nutritional assessment: severe burns require TPN Monitor for signs of infection Maintenance of Central lines Know the effects of burn injury on all of the major body systems Physiologic Changes Burns < 25% TBSA produce a local response > 25% produce local and systemic and considered major burns Systemic responses: release of cytokines and other mediators into circulation Fluid shifts and shock result in tissue hypoperfusion and organ hypofunction Cardiac Changes Due to fluid shifts and hypovolemia, decreased cardiac output results Heart rate increases to try to compensate Cardiac output increases with fluid resuscitation. Pulmonary Changes Respiratory insufficiency results from inhalation injury Occurs upper and lower airways Lining of trachea and bronchi may slough 48 to 72 hours after injury, enter the airway and cause obstruction

Increased alveolar capillary membrane permeability results in intraalveolar edema RESP DISTRESS Airway Injury Not always immediately apparent Observe all patients with possible inhalation injury for at least 24 hours Decreased lung c ompliance, decreased arterial 02 levels and respiratory acidosis may occur gradually over the first 5 days after a burn Indicators of Possible Airway Damage History of burn in enclosed area Burns on the face, neck , or chest Singed nasal hair Hoarseness, voice change, dry cough, stridor, sooty (carbonaceous sputum) Bloody sputum Complaints of headache and LOC Labored breathing, tachypnea, hypoxemia Erythema and blistering of oral mucosa Airway Injury nasal hair, drooling, difficulty swallowing, audible wheezDegree of injury dpends on the fire source, temperature, environment, and types of toxic gases Visible black particles in nose and mouth General s/s: hoarse voice, black sputum, singed es, stridor Airway edema most notable in trachea and mainstem bronchi Auscultation will reveal wheezes = obstruction If wheezing disappears, impending complete obstruction-INTUBATION Gastrointestinal Changes Blood shifts to brain, heart, and liver so GI tract has decreased perfusion. SNS increases epi and norepi which inhibits GI motility and decreases blood flow Persistalsis decreases/Paralytic ileus Curlings Ulcer: (24 hours after injury). Give Tagament, Zantac, Carafate and early enteral nutrition.

Renal changes Myoglobinuria: heat necrosis of muscle results in release of myoglobin which can precipitate in renal collecting tubules. This may result in renal failure. Treatment: IVF, mannitol diuresis, and alkalization of urine with IV bicarbonate Metabolic Changes Hypermetabolic state Increased secretion of catecholamines, ADH, Aldosterone and cortisol which all increase metabolism Stress Response Activated. Catabolism occurs (protein and fat breakdown), increased use of glucose and calories, increased loss of urinary nitrogen. Caloric requirements may double or triple normal energy needs. (Peaks 4 to 12 days after and may last for months) Immunologic Changes Loss of protective barrier: HUGE risk of INFECTION Burn injury activates inflammatory response but suppresses immune function Neutrophil function impaired, decreased lymphocytes, especially T Cells, bone marrow production impaired Sepsis leading cause of death in thermal injuries Superficial Partial Thickness
Epidermis is the portion injured, maybe a small portion of the dermis injured Basal epithelial cells and basement membrane intact: necessary for total regeneration of epithelial cells (epithelialization) S/S: mild edema, pain, increased sensitivity to heat. Desquamation occurs 2 to 3 days. Usually erythematous and moist but may also appear dry. Vesicle may form Rapid healing with NO scar in 10 to 14 days.

Deep Partial Thickness

Extend deeper into dermal layer. Epidermis and upper layers of dermis destroyed. Hair follicles remain intact S/S: red/waxy white skin without blisters. (blisters absent because dead tissues adhere to the underlying dermal collagen fibers) Moderate edema, pain not as severe because more nerve endings have been destroyed. Can progress to deeper injury from hypoxia and ischemia. Heals in 3 to 6 weeks. Scar forms

Full Thickness Burns Involves the entire epidermal and dermal layers NO living epithelial cells remain Skin grafts required in areas larger than 12 cm2 S/S: area is hard, dry, leathery, ESCHAR, (edema under the eschar) Color is waxy/white, deep red, yellow, brown, or black Thrombosed vessels, tissue is avascular. Minimal or absent sensation (nerve fibers are destroyed) Healing time depends on re-establishment of blood supply, weeks to months Deep Full Thickness Extends beyond skin into underlying fascia and tissues (Bones, tendons, muscles exposed to the surface) Wound is blackened and depressed Sensation is absent Need early excision and grafting. Amputation may be necessary

 Calculating TBSA, rule of 9s, Lund & Browder, Palm Rule of Nines: estimated % of TBSA calculated by dividing the body surface up and assigning numerical values related to 9. (Helps estimate fluid replacement needs) Lund and Browder: most accurate (chart) Relative Percentage of body surface area affected by growth Palm: 1% TBSA Use the patients palm size to represent approximately 1% of TBSA. Imagine a rectangle the width and length of the entire hand from wrist to fingertips for the size of 1 palm.

Anatomic Structure Head Anterior Torso Posterior Torso Each Leg Each Arm Genitalia/perineum

Surface Area 9% 18% 18% 18% 9% 1%

Assessing and staging burns, zones of healing Local Response from burns Zone of coagulation: point of maximum damage; irreversible tissue loss Zone of stasis: decreased tissue perfusion, potentially salvagable, want to prevent irreversible tissue loss Zone of hyperemia: outermost zone with increased tissue perfusion, good chance of tissue recovery

o Complications of burns:
scar formation Disorders of wound healing Hypertrophic scars (more common in children, dark skin, and areas of stretch and motion) Preventative measures: compression dressings, ace wraps to promote circulation Can lead to wound contractures (splinting) Keloids: mass of scar tissue Failure to heal: inadequate nutrition, DM, infection, serum albumin < 2g/dL Contracture prevention Positioning is crucial Position with minimal flexion Splints ROM exercises Encourage ambulation ASAP Finger exercises q 1 hour if hands burned Pressure dressings: wear 23 hours per day, until scar tissue mature, for 12 to24 months

infection issues Infection Prevention Common organisms: staph, proteus, psedomonas, e. coli, klebsiella Escharno blood supply Fungi loves to grow in burn wounds

 Characteristics of burn wound sepsis: 10 to the 5th power bacteria per gram of tissue, inflammation, sludging and thrombosis of dermal blood vessels Big source of infection: GI tract because intestinal mucosal barrier becomes permeable. Early enteral feeding helpful. Cultures done frequently. No prophylactic antibiotics. psychosocial issues Psychosocial Management Client grieving: loss of body parts, appearance, role identity, social identity Consult: psych, social work, pastoral care department Client and family counseling Encourage client to participate in decisions about care Encourage family to participate Calculate the Parkland Formula Fluid Resuscitation Need to replace Na+ and H20 Parkland Formula: V = %TBSA x wt in kg x 4 (use Lactated Ringers) Half of calculated fluid volume be given in the first 8 hours after injury. The other half administered over the next 16 hours for a total of 24 hours. After 24 hours, colloid solutions added Know difference with skin grafting and care of skin graft Grafting Autograft: preferred material for burn wound closure following excision. Patients own skin and not rejected. Can be split-thickness, full-thickness, pedicle flaps or epithelial flaps.

 CEAcultured epithelial autograft, keratinocytes isolated and epithelial cells are cultured and grown and then attached to the burn wound. Care of the Patient with an Autograft Occlusive dressing to immobilize the graft or may be left open with staples. First dressing change: 3 to 5 days later or earlier if foul odor/drainage If graft becomes dislodged, sterile saline compresses T & P carefully. No pressure on graft site Elevate extremity if involved to decrease edema Exercise grafted areas 5 to 7 days post Skin care, wound assessment, pressure garments Wound Care Debrided and cleaned from 1 to 3 times per day Hydrotherapy: water application, aids in debridement of necrotic tissue Topical antibiotics: silvadene, silver nitrate, and sulfamylon Acticoat Antimicrobial barrier dressing: soaked in water and left on for 5 dayssilver embedded Multiple layers of gauze covered with elastic wraps Remember to premedicate with analgesia Debridement Naturaldead tissue separates from the underlying viable tissue spontaneously Mechanicalwith dressings, scissors and forceps to separate and remove the eschar, and topical enzymatic agents Surgical debridement deep wound

Monitoring of Wounds Odor Color changes Change in texture Purulent drainage Exudate or sloughing grafts Redness at wound edges, tunneling Quantitative biopsies of eschar and granulation tissue are performed routinely Elastic Pressure Garment

Dressings Biologic: (homografts and heterografts) amniotic membrane, cultured skin. Used in large areas of burn Homografts: (allografts)skin obtained from living or recently deceased humans Heterografts: (xenografts)skin taken from animals, usually pigs Synthetic(artificial)Biobrane (commonly used), nylon adheres to wound fibrin, cells migrate into the mesh and the biobrane adheres to the wound. Stay in place for 3 to 4 weeks. Good for donor sites Many types of synthetic dressings: Integra (artificial skin), alloderm (processed from a human cadaver) Pain management in burns Pain Management Opiod and Non-opiod analgesia: morphine, demerol, nubain Emergent phase: IV analgesia CAM

 Comfort measures, promote sleep Assess pain levels frequently. Assess effectiveness of pain Medicate prior to dressing changes Compartment syndrome Edema Edema creates pressure on small blood vessels and nerves in distal extremities Causes an obstruction of blood flow which leads to ischemia Compartment syndrome: emergency and MD needs to perform an escharotomy and or fasciotomy to relieve constricting effect of burned tissue. Fasciotomy/Escharotomy Surgical Management Escharotomy Fasciotomy Tracheostomy (if long term intubation) Early surgical excision of burn wound Surgical debridement Skin grafting Reconstructive and Cosmetic Surgery Assessment and treatment for inhalation injuries Inhalation injury Carbon monoxide: most common cause CO combines with hemoglobin to form carboxyhemoglobin. The affinity of hemoglobin for CO is 200x greater than for 02 Treatment for CO injury= early intubation and mech vent with 100% 02

 CO poisoning Colorless, odorless, tasteless gas By-product of combustion Impaired 02 tissue availability, decreased 02 delivery and inability of cells to use 02 CO is a vasodilator: causes cherry red color in clients 1 TPN question