Week 10: Burn Patient Management Flashcards
(87 cards)
Burn injury prevention
- Pre-emptive counseling of families essential
- Decreasewater heater temperature from 54oC to 49oC (130–>120oF) increases time for full thick-ness scald from <30 seconds to 10 minutes
- Cigarette misuse responsible for >30% of house fires
- Smoke detector installation/maintenance
Burn risks related to age
- infancy: bathing related scalds; child abuse
- toddlers: hot liquid spills
- school age children: flame injury from matches
- teenagers: volatile agents, electricity, cigarettes
- introduction of flame retardant pajamas
Causes of Burns
- Thermal burns are caused by steam, fire, hot objects or hot liquids.
- Most common burns for children and the elderly
- Electrical burns are the result of direct contact with electricity or lightning
- Chemical burns occur when the skin comes in contact with household or industrial chemicals
- Radiation burns are caused by over-exposure to the sun, tanning booths, sun lamps, X-rays or radiation from cancer treatments
- Friction burns occur when skin rubs against a hard surface, e.g. carpet, gym floor, concrete or a treadmill
Thermal Burns
**The most common burns**
*Exposure to heat
-Fire
-Friction (contact with hot objects)
-Scaling: Steam, liquids
Pathophysiology of Electrical Burns
- Small cutaneous lesions may overlie extensive areas of damaged muscle → myoglobin–>ARF.
- Monitor for at least 48 hours after injury for cardiopulmonary arrest
- May see vertebral compression fractures from tetanic contractions or other fractures from a fall.
- Visceral injury is rare but liver necrosis, GI perforation, focal pancreatic necrosis and gallbladder necrosis have been reported.
- Look for motor and sensory deficits—motor nerves are affected more than sensory nerves.
- Thrombosis of nutrient vessels of the nerve trunks or spinal cord can cause late onset deficits. Early deficits are direct neuronal injury.
- Delayed hemorrhage can occur from affected vessels
- Cataracts may form up to 3 or more years after electrical injury
- Microwave radiation damages tissues via a heating effect. Subcutaneous fatty tissue is often spared given its lower water content.
Effect of Electricity
- Effects of current depend on several factors
- Type of circuit
- Voltage
- Resistance of body
- Amperage
- Pathway of current
- Duration of contact
- High voltage (>1000V) causes underlying tissue damage.
- Deep tissues act as insulators and continue to be injured.
- • Damage more related to cross-sectional area which explains extremity injuries without trunk injuries.
Electrical Storms/Lightning
- Burns are characteristically superficial and present as a spidery or arborescent pattern.
- Cardiopulmonary arrest is common following lightning injury.
- Coma and neurologic defects are also common but usually clear in a few hours or days.
- Watch for tympanic membrane rupture
- Usually lethal in 1/3 of patients.
- World record for surviving lightning strikes is Roy C. Sullivan who was a park ranger from VA. Roy was struck 7 times from 1942-1977.
Effect of Chemicals Acids
- coagulation necrosis: denaturing proteins upon tissue contact
- area of coagulation is formed and limits extension of injury
- exception is hydrofluoric acid, which produces a liquefaction necrosis similar to alkalis.
- Acid damaged skin can look tanned and smooth; do not mistake for a suntan.
effects of chemicals alkalis
- liquefaction necrosis
- potentially more dangerous than acid burns: liquefy tissue by denaturation of proteins and saponification of fats
- In contrast to acids, whose tissue penetration is limited by the formation of a coagulum, alkalis can continue to penetrate very deeply into tissue
- Can cause severe precipitous airway edema or obstruction.
Grading of Burn Wounds
- Mild: < 5% TBSA
- Moderate: 5-15% TBSA
- Severe: > 15% (95% of burns seen)
- May require Burn Unit care because of potential for disability despite small TBSA (face, hands, feet, perineum)
Rule of 9’s for calculating percentage of body burned
- Child: 18% for head, front/back torso, head, 9% each arm, 14% each leg, subtract 1% each year over the age of 1, add 1/2% each year for each year over 1
- Adult: Front/back torso, each leg: 18%, head, each arms:9%, 1% for perineum
- Looks at body percentage
patient’s own palm is about
1% of his body surface area.
first degree burns
- burns are limited to the epidermis.
- A typical sunburn is a first-degree burn.
- Painful, but self-limiting.
- First-degree burns do not lead to scarring and require only local wound care.
second degree buns
- point of injury extends into the dermis, with some residual dermis remaining viable
- Partial thickness or Full thickness
- those requiring surgery vs those which do not
third degree burns
- full-thickness burns involve destruction of the entire dermis, leaving only subcutaneous tissue exposed.
fourth degree burn
- burn is usually associated with lethal injury.
- Extend beyond the subcutaneous tissue, involving the muscle, fascia, and bone.
- Occasionally termed transmural burns, these injuries often are associated with complete transection of an extremity
Burn Zones
- Circumferential zones radiating from primarily burned tissues, as follows:
- Zone of coagulation - A nonviable area of tissue at the epicenter of the burn
- Zone of ischemia or stasis - Surrounding tissues (both deep and peripheral) to the coagulated areas, which are not devitalized initially but, 2° microvascular insult, can progress irreversibly to necrosis over several days if not resuscitated properly
- Zone of hyperemia - Peripheral tissues that undergo vasodilatory changes due to neighboring inflammatory mediator release but are not injured thermally and remain viable
Pathophysiology of Burns
- Cell damage and death causes vasoactive mediator release:
- Histamines
- Thromboxanes: help with platelet formation
- Cytokines
- Increasing capillary permeability causes edema, third spacing and dehydration
- Possible obstruction to circulation (compartment syndrome) and/or airway
Burn Edema and Inflammation
- Generalized edema found in burns > 30% TBSA
- Heat directly damages vessels and causes increases permeability
- Heat activates complement –> histamine release and more permeability –> thrombosis and coagulation systems
Systemic Response to Burn Injury
- Accelerated fluid loss 2° leaky capillaries
- Decreases Host resistance to infection
- Multisystem Organ Failure
- Infections in burns <20% TBSA are well tolerated.
- > 40% TBSA with infection has very low survival rate
- Initially decreases CO, subsequent hypermetabolic state w/ doubling of CO in 24 – 48 hours
Inhalation Injury
- Heat dispersed in upper airways leads to edema
- Cooled smoke and toxins carried distally
- Increased blood flow to bronchial arteries causes edema
- Increased lung neutrophils – mediators of lung damage – release proteases and oxygen free radicals (ROS)
- Exudate in upper airways – formation of fibrin casts
Stages of Inhalation Injury
*Stage 1 – acute pulmonary insufficiency, Signs of pulmonary failure at presentation
*Stage 2 – 72-96 hrs after presentation (ARDS picture)
increased extravasation of water, Hypoxemia, Lobar infiltrates
Stage 3 – bronchopneumonia
-Early – Staph pneumonia (frequently PCN resistant)
-Late - Pseudomonas
inhalation injury bronchoscopy findings
- erythema
- intraglottic soot
- ulceration
Primary assessment of burn
- Cause of the burn
- Time of injury
- Place of the occurrence (closed space, presence of chemicals, noxious fumes)
- Likelihood of associated trauma (explosion,…)
- Pre-hospital interventions


