BURNS Psychological Support

Epidemiology: Pathophysiology of Burn Injury

Quality of Burn Care 1. Coagulation Necrosis
Survival 2. Increased Capillary Permeability
Long-term Function 3. Hemolysis
Appearance
Surgeon’s Goal ACUTE PHASE
Well-healed, durable skin with normal •Immediate Care
function and near-normal appearance Rescue and First Aid = on scene
- remove source of heat
*Depth of Injury is directly proportional to: - CPR if necessary; O2 inhalation
Temperature applied
Duration of contact Assessment and Resuscitation = at the ER
Thickness of the skin - ABC’s take priority
- Intubation if necessary
Etiology:
1. Scald Burns Preparation for transfer to a burn facility
- usually household from hot water - for burns more than 5 – 10%
- most common among civilians TBSA
injuries
especially children •Immediate first aid measures
2. Flame Burns Cooling the burned area
- 2nd most common mechanism - application of cool water
- secondary to house fires, MVA NOT iced water
3. Flash Burns Removal of patient’s clothing
- explosion of gases & other - remove source of heat &
combustible liquids exposure of injuries
- covers larger TBSA Prevention of hypothermia
- with thermal damage to upper - wrap patient in clean blanket
airway •Admission Criteria to a Burn Facility
4. Contact Burns Partial Thickness Burns =/> 15%
- contact with hot metals, plastics, Full Thickness Burns =/> 5%
glass Burns on Face, Feet, Hands &
- common in industrial accidents Perineum
- often 4th degree All Electrical & Chemical Burns
5. Electrical Burns Presence of Smoke Inhalation Injury
- either occupational or household Associated Injuries
injuries
- severity based on voltage, duration Admission Criteria
of contact & resistance of the patient Child Abuse
6. Chemical Burns Patients <10 y.o. & >50 y.o.
- due to strong acids or alkalis Patients w/ Associated medical
- industrial accidents or assaults illness
All infected burns
PHASES OF BURN INJURY Dependent persons

•Acute Phase Patient Assessment

Fluids & Electrolytes 1. History
Pain Control Time of Injury
Burn Wound Care & Coverage Place of Injury
Septic Complications Mechanism of Injury
Nutritional Management 2. Physical Exam
•Chronic Phase Primary Survey = ABC’s
Rehabilitation 2ndary Survey = Other injuries
Reconstruction
 (2nd Degree Burns)
- form blisters, pink & wet
Estimation of Burn Injury Severity - hypersensitive to pain
Burn Size: - blanch with pressure
Rule of Nines = massive burns - spontaneously heal
Patient’s Palm = patchy burns < 3 weeks
Lund-Browder Chart = pediatrics 2. Deep Burns
a) Deep Partial-Thickness Burns
“Rule of Nines” for estimating TBSA (2nd Degree)
Anatomic Area % body surface - blisters, mottled pink and white
Head 9 - capillary refill is slow to absent
Rt. Upper extremity 9 - less sensitive to pain
Lt. Upper extremity 9 - heals in 3 to 9 weeks
Rt. Lower extremity 18
Lt. Lower extremity 18
Anterior trunk 18 b) Full Thickness Burns
Posterior trunk 18
Perineum 1 (3rd Degree)
- all layers of dermis
- leathery, dry white, firm & insensate
- develop “ESCHAR”
- heal by contracture or skin grafting

c) Fourth Degree Burns

- full thickness skin, SQ fat,fascia & muscles
- electrical, contact, immersion burns in an
unconscious patient

Assessment of Burn Depth

Methods:
1. Clinical observation – only 70% accurate
2. Detection of Dead cells or denatured collagen
- biopsy, ultrasound, use of vital dyes
3. Assessment of Change in Blood Flow
- fluorometry, laser Doppler,
thermography
4. Analysis of Wound Color
- light reflectance method
5. Evaluation of Physical Changes
Estimation of Burn Injury Severity - magnetic resonance imaging
Burn Depth is dependent on:
a. Temperature of burn source
b. Thickness of the skin Physiologic Response to Burn Injury
c. Duration of contact
d. Heat dissipating capability of skin
SYSTEMIC INFLAMMATORY RESPONSE
SYNDROME (SIRS)
Classification of Burn Depth - pathologic alterations in metabolic,
1. Shallow Burns cardiovascular, gastrointestinal and coagulation
a) Epidermal Burns systems
(1st Degree Burns) - hypermetabolism, increased cellular, endothelial
- do not blister but erythematous and epithelial permeability
- relatively painful - extensive microthrombosis
ex. Sunburn
BURN SHOCK
b) Superficial Partial-Thickness Burns - circulatory dysfunction
 - increase in vascular permeability & micro- 4. Tetanus prophylaxis
vascular hydrostatic pressure
Mediators: Compartment syndrome:
1. Histamine – release mast cells which a) Clinical Manifestations
disrupts venular endothelial junctions 6 P’s: Pulselessness Paresis/Paralysis
2. Serotonin – increase pulmonary vascular Pallor Paresthesia
resistance Pain Poikilothermia
3. Eicosanoids – increase levels of vasodilator b) Definitive Treatment: ESCHAROTOMY
PG’s FASCIOTOMY

Diagnostic Work-up
Complete Blood Count
Urinalysis, BUN & Serum Creatinine
Baseline electrolytes
Arterial blood gas determination
X-rays (Chest, other areas)
Electrocardiography

Fluid Resuscitation
Recommended Fluids:
Plain Lactated Ringer’s Solution = 1st 24
hours
Colloids or D5Water = after 24 hours

Fluid Computation & Administration Inhalation injury:

a) 1st 24 hours 1. Carbon Monoxide Poisoning
“Parkland Formula” Effects:
TFR = BW x TBSA x 4 mg/kg/%burns a) prevents reversible displacement of O2
b) decrease O2 unloading at tissue level
(1/2 given in1st 8H; 1/2 next 16H)
c) less effective intracellular respiration
b) 2nd 24 hours d) directly toxic to cardiac & skeletal
D5W replace evaporative losses muscles
Colloids maintain plasma volume Treatment: Hyperbaric Oxygen ???
c) After 48 hours
Maintenance Fluids = 30-40
cc/kg/day 2. Thermal Airway Injury
Manifestations:
- mucosal & submucosal erythema
Parameters for Monitoring Fluid Therapy - edema, hemorrhage & ulceration
1. Urine Output - potential for upper airway obstruction
Adults: 0.5 cc/kg/hour Treatment: Endotracheal Intubation
Pedia : 1 cc/kg/hour
2. Vital Signs 3. Smoke Inhalation
Blood pressure & Heart rate Factors:
Central Venous Pressure a) Type and amount of smoke inhaled
3. Sensorium b) Size of particulates
c) Duration of Toxic Exposure
Reasons for Failed Resuscitation d) Magnitude of thermal injury
1. Delayed resuscitation
2. Presence of electrical burns Clinical Manifestations:
3. Smoke inhalation injury a) dyspnea
4. Coronary artery disease b) burned vibrissae
c) carbonaceous sputum
Ancillary Management Measures
1. Gastric decompression Diagnosis: a) Chest X-ray
2. Pain control & sedation b) Bronchoscopy
3. Antibiotics
 c) Arterial blood gas
Clinical Manifestations
Management: a) Endotracheal intubation 1. Conversion from partial to full thickness
b) Mechanical ventilation 2. Dark-brown/blackish discoloration
3. Neo-eschar formation
Electrical Burns: 4. Rapid eschar separation
Classification: 5. Violaceous wound margins
Low voltage: <1,000 volts 6. Metastatic septic lesions
High voltage: >1,000 volts
Mechanisms of injury: Burn Complications
a) Direct contact
b) Conduction arc A) Distant infections
c) Secondary ignition 1. Pneumonia
2. Bacterial Endocariditis
Physiologic Alterations: 3. Urinary Tract Infection
a) Arrhythmias 4. Suppurative chondritis
b) Acute Renal Failure 5. Vascular Catheter-Related Infection
c) CNS & PNS Deficits
d) Hemorrhage & Hematomas B) Other complications
1. Curling’s ulcer
Chemical Burns: 2. Acute Acalculous Cholecystitis
3. Myocardial Infarction
Factors to consider:
a) Contact time Burn wound coverage
b) Chemical involved a) Temporary
Primary Management: 1. Biologic wound coverings
Rapid termination of burning process Allograft
Xenograft
Amnion
2. Hydrocolloid dressings
Burn Wound Care
b) Permanent
Salient Aspects: 1. Skin Grafting
Debridement of necrotic tissue a) Split-thickness
Daily dressing of burn wound b) Full-thickness
Surgical Management: 2. Skin Flaps
a) Tangential excision 3. Skin Substitutes
b) Fascial excision a) AlloDerm
b) INTEGRA
Topical Antimicrobials
4. Cultured Skin
a) Aqueous silver nitrate a) Apligraf
b) Mafenide acetate b) Epicel
c) Silver sulfadiazine
d) Povidone-iodine Chronic Phase
1. Rehabilitation:
Nutritional Support Range of motion exercises
Ambulation training
State of hypermetabolism Return to functional status
- exaggerated energy expenditure 2. Psychological Support:
- massive nitrogen loss Anxiety, Depression, Denial
Withdrawal, Regression
Formula:
3. Reconstruction:
TCR = 25 kcal/kg BW + 40 kcal/%TBSA Burn contractures
Route: Keloids
Total Enteral Nutrition (TEN) Hypertrophic scars
Adv: maintain integrity of GI tract Marjolin’s ulcer
reduce bacterial translocation & sepsis

Burn Wound Infection