Burn Injuries and Anasthesia Flashcards
(45 cards)
what are pediatric burn injuries most often d/t?
scalding
what are the main causes of early death (less than 48 hrs.)?
- shock
- inhalation injury
after 48 hrs., what are the main causes of death?
multi-organ failure and sepsis
describe superficial thickness burns
- 1st degree burns
- depth: epidermis involvement
- clinical findings: erythema, minor pain, lack of blisters
describe partial thickness-superficial burns
- 2nd degree burn
- depth: superficial (papillary) dermis
- clinical findings: blisters, clear fluid, pain
describe partial thickness-deep burns
- 2nd degree burns
- depth: deep (reticular) dermis
- clinical findings: whiter appearance, decreased pain
- difficult to distinguish from full thickness
describe full thickness burns
- 3rd or 4th degree burns
- depth: dermis and underlying tissue, possibly fascia, bone, and muscle
- clinical findings: hard, leather like eschar; purple fluid; no sensation (insensate)
describe the rule of nines values for an adult
- head 9% (front and back)
- back 18%
- chest 18%
- r. arm 9%
- l. arm 9%
- r. leg 18%
- l. leg 18%
- peritoneum 1%
describe rule of nine values for a child
- head 18% (front and back)
- back 18%
- chest 18%
- r. arm 9%
- l. arm 9%
- r. leg 13.5 %
- l. leg 13.5 %
- peritoneum 1%
what does the ABA Severity Grading System consider as major burns?
- 2nd degree: greater than 20% TBSA (adult) or greater than 10 % at age extremes (very young or old)
- 3rd degree: greater than 10% TBSA (adult)
- electrical burn
- any burn w/ inhalation injury
According to the National Burn Registry, how can mortality risk be determined w/ burns?
- patient age plus TBSA%
- if greater than 115, there is a greater than 80% mortality risk
- ex: 70 y/o w/ 50% TBSA burn equal 120, so risk over 80%
- older the patient, and greater the % of burn, increases risk
- mortality doubles with inhalation injury
what are the four types of burn injury?
- chemical
- electrical
- thermal (flame, scald)
- inhalation
describe electrical burn injury
- damage concentrated at entry and exit wounds
- major internal tissue damage not seen (heart conduction?)
- significant electrical burn leads to myoglobin release from tissue damage which leads to renal failure
describe inhalation burn injury
- suspect until ruled out
- classified as upper airway, lower airway, or metabolic asphyxiation (carbon monoxide or cyanide)
- brief exposure to hot, dry air or steam causes rapid airway tissue destruction and edema
- interesting phenomenon: heat in upper airway is dissipated but causes reflex laryngospasm, so lower airway damage uncommon
- most lower airway damage d/t toxins (carbon monoxide, cyanide)
what are warning signs of inhalation burn injury?
- hoarseness
- sore throat
- dysphagia
- hemoptysis
- tachypnea
- respiratory distress
- elevated carbon monoxide levels
what is burn treatment for airway burns?
- airway exam: direct visualization via laryngoscopy or fiberoptic bronchoscopy (gold standard)
- if upper airway damage present, EARLY intubation, even when asymptomatic
- avoid Succs if over 24 hrs.
why should Succs be avoided after 24 hrs.?
- burns lead to receptor up regulation (increase) of extrajunctional ACh receptors
- causes massive hyperkalemia since these receptors keep potassium channel open longer than normal
- hyperkalemia leads to cardiac arrest/death
- significant up regulation occurs after 1st 24 hrs.
if swelling/obstruction is present upon airway assessment, hour should the pt. be intubated?
- awake intubation
- topicals, incremental ketamine, or dexmedetomidine
- no relaxants
- fiberoptic, LMA assisted, blind nasal, retrograde wiring, light wand, GlideScope, surgical tracheostomy
what is an indication that airway swelling is subsiding?
progressive air leak around the ETT
*in ICU may have to change out tube since smaller size may have been initially used d/t swelling
describe treatment for burns d/t carbon monoxide?
- suspect CO poisoning if victim rescued from enclosed space (house fires)
- CO bind to Hgb 200x the affinity of O2 (left shift)
- decreased SaO2
- metabolic acidosis
- behavior of CO poisoning looks like a drunk
- pulse oximetry does not detect CoHgb and shows falsely high O2 sat
- arterial CoHgb must be analyzed to obtain accurate measurement
- treatment: 100% O2
describe treatment for burns d/t cyanide
- burned plastic, paint, some fabrics lead to hydrogen cyanide (HCN)
- HCN causes blocked intracellular O2 use leading to metabolic acidosis
- symptoms: changes in LOC, seizures, dilated pupils, hypotension, apnea, high lactate levels
- tx: hydroxocabalamin (B12a)
- 2-3 min lead to resp depression and arrest
- 6-8 min lead to cardiac arrest
how is shock r/t burn treated?
- after securing airway, aggressive fluid resuscitation begins
- burn lead to loss of circulating plasma causing: hemoconcentration, massive edema, decreased urine output, CV depression/collapse
- fluid resuscitation required to prevent hypovolemic shock but also increases edema formation
- *beware of compartment syndrome (tissue tightened d/t edema; but DONT restrict fluids to prevent)
when is the greatest fluid loss d/t burns?
- 1st 12 hrs.
- begins to stabilize after 24 hrs.
describe fluid resuscitation w/ burn injury
- heavy isotonic crystalloid (NO colloid or blood during resuscitation period unless other traumatic injury present)
- Parkland guideline
- caution fluid management w/ children; fluid management must be precise
- need large bore IV access