Burn Injuries Flashcards
functions of the skin
barrier (body fluids and infection) temperature elasticity appearance sensory organ
layers of skin
stratum coreneum, epidermis, dermis, subcutaneous tissue
types of burn injury
thermal (flash, flame, scald)
chemical (can progress until flushed out or neutralized)
electrical
radiological (alpha, beta, gamma radiation)
severity of burn injury and how they are classified
depth - extent of skin and tissue destruction (superficial, partial thickness, full thickness)
total body surface area involved (rule of nines)
superficial burn 1st degree
depth - destruction of epidermis
pain level - very painful
appearance - red
characteristics - dry, flaky, will heal spontaneously in 3-5 days
partial thickness burn 2nd degree
depth - superficial or deep, epidermis up to deep dermal element
pain level - very painful
appearance - bright cherry red, pink or pale ivory, usually with fluid filled blistering
characteristics - hair follicle intact, may require skin graft
full thickness burn 3rd degree
depth - all of the epidermis, dermis, down into the subcutaneous tissue
pain level - little or no pain
appearance - khaki brown, white, or charred/cherry red is pediatrics
characteristics - loss of hair follicles, will require skin graft
fourth degree
depth - full thickness extending into muscle and bone
will require skin graft or amputation
rule of 9’s for adults
head = 9 % upper extremities = 18% (each arm 9%) trunk = 36% (front = 18%, back = 18%) lower extremities = 36% (each leg 18%) genitalia = 1%
rule of 9’s for pediatrics
head = 18% upper extremities = 20% (each arm 10%) trunk = 32% (front = 16%, back = 16%) lower extremities = 28% (each leg 14%) genitalia = 1%
burns that should be transferred to burn center
full thickness burns in any age group
partial thickness >10% TBSA
burns of special areas (extreme of age, burns of face, hands, feet, perineum or major joints, inhalation, chemical, electrical burns, those burns associated with co-existing disease)
determining mortality with age and TBSA
if the age of the patient plus the TBSA is greater than 115 the mortality is greater than 80%
in a closed space thermal injury think…
airway injury
electrical injury may lead to occult
severe fracture, hematoma, visceral injury, skeletal, cardiac injury, neurologic injury
signs and symptoms of airway complications
singed facial hair, facial burns, dysphonia/hoarseness, cough/carbonaceous sputum, soot in mouth/nose, swallowing impairment, oropharynx inflammation, CXR initially normal
inhalation injury refers to
damage to the respiratory tract or lung tissue from heat, smoke, or chemical irritants carried into the airway during inspiration
upper airway inhalation injury involvement
thermal damage to soft tissues of the respiratory tract and trachea can make intubation difficult
increased risk of glottic edema with injury and fluid resuscitation
lower airway inhalation injury involvement
pulmonary edema/ARDS develops 1-5 days post burn
pneumonia and pulmonary embolism > 5 days post burn
smoke inhalation occurs in conjunction with
face/neck burns and closed space fires
chemical pneumonitis occurs after
smoke/toxic fume inhalation
honeymoon period for smoke inhalation that will show clear CXR
1st 48 hours
symptoms of smoke inhalation
increased sputum and rales/wheezing
hypoxia in the first 36 hours after inhalational injury
high risk of pulmonary edema
hypoxia in day 2-5 after inhalational injury
expect atelectasis, bronchopneumonia, airway edema maximum secondary to sloughing of airway mucosa, thick secretions, distal airway obstruction
hypoxia >5 days post inhalational injury
nosocomial pneumonia, respiratory failure, ARDS
implications of circumferential burns of chest/upper abdomen
restricted chest wall motion as eschar contracts and hardens
if inhalation injury or facial burns are suspected or known
intubate and secure the airway early!
ETT indicated in a burn patient if
pediatric, massive burn, stridor, respiratory distress, hypoxia/hypercarbia, altered level of consciousness, if deterioration likely
safest approach for intubation in burn patient
fiberoptic intubation under adequate topical anesthesia
treatment of hypoxia in burn patient with inhalational injury
PEEP, airway humidification, bronchial suctioning/lavage, bronchodilators, antibiotics, chest physiotherapy
restriction of respiratory excursion may necessitate
escharotomy
carbon monoxide is ____ times the affinity for Hgb as O2
200
CO shifts the hemoglobin dissociation curve to the ___
left impairing O2 unloading at the tissue level
CO interferes with
mitochondrial function, uncouples oxidative phosphorylation, reduces ATP production = metabolic acidosis
carbon monoxide treatment
high FiO2
hyperbaric chamber if > 30% and patient is hemodynamically and neurologically stabilized
a COHbg greater than ___ is incompatible with life
60%
CO < 15-20% symptoms
HA, dizziness, confusion
CO 20-40% symptoms
nausea, vomiting, disorientation and visual impairment
CO 40-60% symptoms
agitation, combative, hallucinations, coma, shock
blood cyanide levels of ____ confirm diagnosis of cyanide toxicity
> 0.2 mg/L
lethal blood cyanide level
1.0 mL/L
cyanide has a half life of
60 minutes
treatment for cyanide toxicity
O2, hydroxycobalamine, amyl nitrate, sodium nitrate, thiosulfate
burns and systemic effects
release of inflammatory mediators locally and systemically = edema
increase in microvascular permeability = fluid leak and loss of proteins
increased intravascular hydrostatic pressure and decreased interstitial hydrostatic pressure
increased interstitial osmotic pressure
cardiovascular stresses with burn injury
severe decrease in CO lasts 1st 24 hours
circulation tumor necrosis factor = myocardial depression
diminished response to catecholamines
increased microvascular permeability = hypovolemia
intense vasoconstriction compensation = decrease flow to tissues
decreased tissue O2 supply and coronary blood flow
after 24-48 hours of burn patients are in a ____ state
hyperdynamic state (high output CHF), CO is 2x normal
metabolism in burn patient
increased metabolic rate is proportional to TBSA burned
increased core body temp reflects increased metabolic thermostat, loss of skin = loss of vasoactivity, piloerection, insulation functions
GI complications
ileus, ulceration, cholecystitis
Renal complications
decreased GFR, RBF, loss of Ca, K, Mg with retention of Na, H2O
endocrine complications
increased corticotropin, ADH, renin, angiotensin, aldosterone, increased glucagon, insulin resistance, hyperglycemia
blood and coagulation complications
increased viscosity, increase in clotting factors including fibrinogen, V and VIII, fibrin split products at risk of DIC development, HCT usually decreases (RBCs decreased half life)
fluid resuscitation 1st 24 hours
crystalloid only
replace with 2-4 mL/kg for each 1% TBSA burned
titrate fluids to U/O 0.5 - 1 mL/kg/hr
over aggressive fluid resuscitation can lead to
airway edema, increase chest wall restriction, and contribute to abdominal compartment syndrome
fluid resuscitation after 1st 24 hours
use colloids at 0.3-0.5 mL/kg/% burn with 5% dextrose in water
Parkland formula
4 mL of LR/kg/% burn/1st 24 hours
Modified Brooke formula
2 mL of LR/kg/% burn/1st 24 hours
calculated volumes are given in the 1st 24 hours
50% first 8 hours
25% second 8 hours
25% third 8 hours
goals of resuscitation
urine output = 0.5-1 mL/kg/hr HR = 80-140 MAP = >60 in adults base deficit = < 2 normal Hct
what can we give if fluids are not enough?
low dose Dopamine 5 mcg/kg/min
anesthesia considerations/concerns
often need repeated surgeries maintain Hct coagulopathy temperature fluids and electrolytes hypermetabolic state increased risk for GI ileus
challenges for anesthesia in burn patients
burned tissue = limited access for ECG, SaO2, PNS, NIBP
need large bore IV
compensate for evaporative/exposure heat loss (room temp 28-32 C)
minimize blood loss (topical/SQ epi, only 15-20% TBSA each procedure, tourniquets)
treat complications of massive transfusion (coagulopathy, hypocalcemia)
anesthesia considerations for high voltage electrical injury
follows path of least resistance (bone most resistant)
cardiac arrhythmias
respiratory arrest
seizure
fractures
muscle damage = myoglobinurea and renal failure
muscle relaxants in 1st 24 hours
unaltered response to depolarizing and non-depolarizing muscle relaxants
muscle relaxants in 24 hours to 1 year post burn
avoid succinylcholine (massive release of K) may be due to the proliferation of acetylcholine receptors along the entire muscle membrane resistance to most NDMR if >30% TBSA burned
