Fluid shifting and electrolyte shifting in burn injuries : emergent and later stagesFluid 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 changes—Fluid 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 vasoconstrictionVessels 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 resuscitationAcute or intermediate phase: from beginning of diuresis to wound closureRehabilitation phase: from wound closure to return to optimal physical

and psychosocial adjustment Emergent phase

ABCs—establish 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 obstructionIncreased alveolar capillary membrane permeability results in intra-alveolar 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

Curling’s 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 patient’s 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 Surface AreaHead 9%Anterior Torso 18%Posterior Torso 18%Each Leg 18%Each Arm 9%Genitalia/perineum 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 formationDisorders 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 issuesInfection Prevention

Common organisms: staph, proteus, psedomonas, e. coli, klebsiella

Eschar—no 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 issuesPsychosocial 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 Ringer’s)

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. Patient’s own skin and not rejected. Can be split-thickness,

full-thickness, pedicle flaps or epithelial flaps.

CEA—cultured 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 days—silver embedded

Multiple layers of gauze covered with elastic wraps

Remember to premedicate with analgesia

Debridement

Natural —dead tissue separates from the underlying viable tissue

spontaneously

Mechanical —with 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

routinelyElastic 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