Ch.

57 Burn Injury
Burn Injuries
 Approximately 486,000 people require medical attention of burns every year
 Most burns occur in the home
 Gerontologic Consideration: Burn Injury in Older Adults
o Greater mortality associated with burns
o Skin – thinner and less elastic, affects depth of injury and ability to heal
o Complications -
 Pneumonia, UTI, respiratory failure, septicemia, cellulitis, wound infection kidney injury, arrythmias, and other
hospital-acquired infections
o Assessment for older patients –
 Safely perform ADLs
 Modify environment
 Instrumental Activities of Daily Living (IADLs) – ability to carry out complex tasks
 Prevention of burn injuries
o Education regarding prevention concepts and promoting safety legislation
o Matches/lighters kept out of reach of children
o Never leave children unattended around fire or in bathroom
o Educate installation/maintenance of smoke and CO detectors
o Recommend practice of home exit fire drill with household
o Water heater temperature no higher than 48.9° C (120° F)
o Recommend having fire extinguisher in home and how to use it

Goals of Burn Care

 Prevention
 Institution of lifesaving measures for the severely burned person
 Prevention of disability and disfigurement through early specialized and individualized care
 Rehabilitation through reconstructive surgery and rehabilitation programs

Classifications of Burns
First-degree burns: negative Nikolsky’s sign Third-degree burns: Full Thickness
 Epidermis  Epidermis, dermis, and underlying tissue
 Cause: Sunburn or superficial scald burn  Lack of sensations
 Recovery: few days  Cause: flame, prolonged exposure to hot liquids, electric
 Treatment: current, chemical, contact
o PO Pain meds  Recovery: Eschar may slough, scarring and loss of contour
o Cool compress and function
o Skin lubricants – ointment, emollients  Treatment: Grafting
Second-degree burns: Partial Thickness Fourth-degree burns: Deep burn necrosis
 Epidermis, portion of dermis  Deep tissue, muscle, and/or bone
 Painful with blisters  Cause: prolonged exposure or high-voltage electrical injury
 Cause: Scalds, flash flame, contact  Treatment:
 Recovery: 2- 3 weeks, possible scarring and depigmentation o Amputation
 Treatment: Grafting o Grafting

Factors to Consider in Determining Burn Depth

 How the injury occurred
 Causative agent (flame or scalding liquid)
 Temperature of agent
 Duration of contact with the agent
 Thickness of the skin at the injury
Methods to Estimate Total Body Surface Area (TBSA) Burned

 Rule of Nines
 Most common, estimated percentage of TBSA calculated by anatomic region

Lund and Browder method

 More precise method
 Recognizes % of TBSA of various anatomic parts
 Relates to age of patient
 Initial evaluation revised within first 72 hours – demarcation and depth more clear by this time

Palmer method
 Used to estimate extent of scattered burns
 Size of patient’s hand, including fingers is 1% TBSA

Pathophysiology of Burns
 Burns are caused by:
o Chemical exposure injury
o Heat transfer from one site to another
 Tissue destruction through
coagulation
 Protein denaturation
 Ionization of cellular contents
 Thermal (includes electrical)
o Skin and mucosa of upper airway most common site
 Radiation
o Thermal Effect - cutaneous burn injuries
o Damage to cellular DNA – localized or whole body
Zones of Burn Injury
 Zone of Coagulation: central area of the wound; coagulation necrosis of cells
occur; cellular death
 Zone of Stasis: surrounding zone, injured cells that remain viable but, with
persistent ischemia, undergoes necrosis within 24 – 48 hours; compromised blood
supply
 Zone of Hyperemia: outermost zone that sustains minimal injury/least damage and may fully recover
Depth of Burn Injury:
 54° C (130° F) – exposure for 30 seconds result in burn injury
 60° C (140° F) – tissue destruction in 5 seconds
 71° C (160° F) or higher – full-thickness burn

Major Burn Injury

 Severe Burns: > 30% may produce a local and systemic response
o Systemic response: proinflammatory and anti-inflammatory release of cytokines and other mediators into systemic
circulation
 Fluid shifts and shock result in tissue hypoperfusion and organ hypofunction
Pathophysiological Changes with Severe Burns
Body System Physiologic Changes
Cardiovascular  Cardiac depression – decrease in cardiac output
 Loss of plasma volume – release of free O2 radicals that increase capillary permeability
 Edema – water migrates to the interstitium
  Vasoconstriction – response to intravascular fluid loss that releases catecholamines
o Workload of heart and oxygen demand increases
 Hypovolemia – decreased perfusion and oxygen delivery to organs and tissues
o Burn Shock: Capillary leakage – decrease in vascular volume, CO, and BP
 Intravascular Fluid Leak: 24 – 36 hrs after burn injury; peak: 6 – 8 hours after initial injury
 Intrinsic Diuresis: several days to 2 weeks
Pulmonary  Cause: Inhalation Injuries
 Diagnosis: Bronchoscopy and x-rays
 Vasoconstriction
 Edema
 Upper airway: Above the glottis
o Edema – direct thermal injury or secondary to face or neck burns
o Interventions – protective intubation to maintain patency of airway
 Lower airway: Below the glottis
o Inhaling products of incomplete combustion or noxious gases:
 Carbon monoxide poisoning
 Treatment: 100% O2
 Hydrogen cyanide:
 S/S: SOB, headache, vertigo, confusion, mucous membrane irritation
o Smoke inhalation: loss of ciliary action, triggers an inflammatory response causing
hypersecretion.
o Expectoration of carbon particles in the sputum
o Bronchoconstriction:
 Hypoxia
 Treatment: Administration of supplemental oxygen
o Restrictive defects: occur with full-thickness burns encircling the thorax

Gastrointestinal  Impaired motility and absorption

 Vasoconstriction
 Inadequate tissue perfusion
 Loss of mucosal barrier function with bacterial translocation
 Increased pH
 Most common GI Alterations:
o Paralytic ileus (Absence of intestinal peristalsis
o Curling’s ulcer
o Translocation of bacteria
 Indicators of GI ischemia:
o Increased bladder pressure
o Increased serum lactate
o Feeding intolerance
 Medication: vasopressors
 Treatment: Surgery
Kidney  Decreased blood volume post burn injury due to compensatory response to intravascular volume
loss
 Free hemoglobin in urine due to destruction of RBCs at the injury site
o Red urine – myoglobin released from muscle cells and excreted by kidneys
 Vasoconstriction
 Acute tubular necrosis and AKI
o Inadequate blood flow through kidneys – hgb and myoglobin occlude renal tubules
 Kidney Ischemia
o Increased abdominal pressure from injury
 Treatment:
o Adequate fluid volume replacement
 Restores renal blood flow
 Increase glomerular filtration rate
 Increase urine volume

Thermoregulations  Integumentary loss: inability to regulate body temperature

  Low body temperatures in burn injuries
 Treatment: cooling of wounds, IV resuscitation fluids, and exposure resulting in increased
evaporative heat loss
Fluid and Electrolyte  Edema
Shifts o Forms after burn injury
o Superficial burn: localized edema formed within 4 hours
o Deeper burns: form continued edema up to 18 hours post injury
o Treatment of Edema :
 Elevation of extremity
 Eschar removal – escharotomy
 Decompression – fasciotomy (surgical incision through fascia to relieve
constricted muscle to restore tissue perfusion)
 Fluid increases edema
 Hyperkalemia (Excessive Potassium)
o Cause: massive cell destruction
 Hypokalemia (Potassium depletion)
o Cause: Occurs later with fluid shifts and inadequate potassium replacement
 Hyponatremia (serum sodium depletion)
o Cause: from plasma loss or during first week of acute phase
 Thrombocytopenia (decrease in platelets)
 Prolonged clotting and prothrombin times
Immunologic  Immunological defense altered by burn injury
 Burn injury produces systemic release of cytokines and other substances that cause
leukocyte and endothelial cell dysfunction
 Intervention: Infection controlled environment to protect patient and minimize exposure to
potential harmful organisms

 Renal and GI alterations

Phases of Burn Injury
 Emergent or resuscitative phase
o Onset of injury to completion of fluid resuscitation
 Acute or intermediate phase
o From beginning of diuresis to wound closure
 Rehabilitation phase
o From wound closure to return to optimal physical and psychosocial adjustment
Emergent/Resuscitative Phase-On-the-Scene Care
 Prevent injury to rescuer
 Stop injury: extinguish flames, cool the burn, irrigate chemical burns
 ABCs: establish airway, breathing, and circulation
 Start oxygen and large-bore IVs
 Remove restrictive objects and cover the wound
 Do assessment surveying all body systems and obtain a history of the incident and pertinent patient history
 Note: Treat patient with falls and electrical injuries as for potential cervical spine injury
Emergent/Resuscitative Phase
 Patient is transported to emergency department
 Fluid resuscitation is begun
 Foley catheter is inserted
 Patient with burns exceeding 20% to 25% should have an NG tube inserted and placed to suction
 Patient is stabilized and condition is continually monitored
 Patients with electrical burns should have ECG
 Address pain; only IV medication should be administered
 Psychosocial consideration and emotional support should be given to patient and family
Nursing Management of the Patient during the Emergent/Resuscitative Phase of Burn Injury
 ABC
 Vital signs and hemodynamic status
 Monitor for fluid volume deficit
 Assess extent of the burn
 Refer to Chart 57-5
Potential Complications during the Emergent/Resuscitative Phase of Burn Injury
 Acute respiratory failure
 Distributive shock
 Acute kidney injury
 Compartment syndrome
 Paralytic ileus
 Curling’s ulcer
Acute/Intermediate Phase
 48 to 72 hours after injury
 Continue assessment and maintain respiratory and circulatory support, fluid and electrolyte balance, GI and renal function
 Prevention of infection, burn wound care, pain management, modulation of the hypermetabolic response, and early
positioning/mobility
Nursing Management during the Acute/Intermediate Phase of Burn Injury
 Restoring fluid balance
 Preventing infection
 Modulating hypermetabolism
 Promoting skin integrity
 Relieving pain and discomfort
 Promoting mobility
 Strengthening coping strategies
 Supporting patient and family processes
 Monitoring and managing complications
Collaborative Problems and Potential Complications during the Acute/Intermediate Phase of Burn Injury
 Acute respiratory failure and acute respiratory distress syndrome
 Heart failure and pulmonary edema
 Sepsis
 Delirium
 Visceral damage (electrical burns)
Rehabilitation Phase
 Rehabilitation is begun as early as possible in the emergent phase and extends for a long period after the injury
 Focus is on wound healing, psychosocial support, self-image, lifestyle, and restoring maximal functional abilities so that the
patient can have the best quality life, both personally and socially
 The patient may need reconstructive surgery to improve function and appearance
 Vocational counseling and support groups may assist the patient
Management of Shock – Fluid Resuscitation
 Maintain blood pressure of greater than 100 mm Hg systolic and urine output of 30 to 50 mL/hr; maintain serum sodium at near-
normal levels
 Consensus formula
 Evans formula
 Brooke Army formula
 Parkland Baxter formula
 Hypertonic saline formula
 Note: Adjust formulas to reflect initiation of fluids at the time of injury
Fluid and Electrotype Shifts – Emergent/Resuscitative Phase
 Generalized dehydration
 Reduced blood volume and hemoconcentration
 Decreased urine output
 Trauma causes release of potassium into extracellular fluid: hyperkalemia
 Sodium traps in edema fluid and shifts into cells as potassium is released: hyponatremia
 Metabolic acidosis
Fluid and Electrolyte Shifts – Acute/Intermediate Phase
 Fluid reenters the vascular space from the interstitial space
 Hemodilution
 Increased urinary output
 Sodium is lost with diuresis and due to dilution as fluid enters vascular space: hyponatremia
 Potassium shifts from extracellular fluid into cells: potential hypokalemia
 Metabolic acidosis
Burn Wound Care
 Wound cleaning
 o Hydrotherapy
 Use of topical agents: refer to Table 57-4
 Wound debridement
o Natural debridement
o Mechanical debridement
o Surgical debridement
 Wound dressing, dressing changes, and skin grafting
Psychosocial Support
 Patient’s outlook, motivation, and support system are important to overall well-being and ability to progress
 Psychological support of patient and family
 Early consultation with mental health professionals
 Discharge planning for reintegration
 Support groups
 Organizations
Burn Pain
 Burn pain has been described as one of the most severe forms of acute pain
 Pain accompanies care and treatments such as wound cleaning and dressing changes
 Types of burn pain
o Background or resting
o Procedural
o Breakthrough
Pain Management
 Analgesics
o IV use during emergent and acute phases
o Morphine
o Fentanyl
o Other
 Role of anxiety in pain
 Effect of sleep derivation on pain
 Nonpharmacologic measures
Nutritional Support
 Burn injuries produce profound metabolic abnormalities, and patient with burns have great nutritional needs related to stress
response, hypermetabolism, and requirement for wound healing
 Goal of nutritional support is to promote a state of nitrogen balance and match nutrient utilization
 Nutritional support is based on patient preburn status and % of TBSA burned
 Enteral route is preferred. Jejunal feedings are frequently used to maintain nutritional status with a lower risk of aspiration in a
patient with poor appetite, weakness, or other problems
Home Care Instruction
 Mental health
 Skin and wound care
 Exercise and activity
 Nutrition
 Pain management
 Thermoregulation and clothing
 Sexual issues
 Refer to Chart 57-7