Burn Flashcards
functions of skin
barrier to body fluids and infection temperature elasticity appearance sensory organ
types of burn injury
thermal (flash, flame, scald)
chemical
electrical (entry and exit wound)
radiological (alpha, gamma, delta)
severity of burn injury: depth (4 categories)
superficial, partial thickness, deep partial thickness, full thickness
partial thickness burn 2nd degree
epidermis to deep dermal element
very painful
bright cherry red, pink or pale ivory, usually blisters**
hair follicle intact, may require skin graft
5-21 days healing superficial, 21-35 days deep
minimal to no scarring, may have discoloration
full thickness (3rd degree)
all of epidemics, dermis, down to SQ tissue
little or no pain because nerve endings destroyed
khaki brown, white, or charred/cherry red (pedes)
loss of hair follicles, will require skin graft
still will “feel pain”-psychological
small areas-months to heal. large areas-need grafting
scarring present
4th degree
full thickness to muscle and bone, will require skin graft and possible amputation
rule of nines
head 9% upper extremities: 9% each, 18% total trunk 36% (front 18%, back 18%) lower extremities 36% (18% each leg) perineal 1%
burns that should be transferred to burn center
full thickness burns in any age group
partial thickness >10% TBSA
burns of special areas (at extreme of age, burns of face hands feet perineum or major joints, inhalation/chemical/electrical burns, those burns associated with co existing disease)
national burn registry mortality >80% correlates with
if age of patient plus TBSA is greater than 115
burns: resuscitative phase involves
ABC’s + coexisting trauma
closed space thermal injury equates to
airway injury
source of injury consideration: closed space thermal injury equates to
airway injury- anytime they’re in a closed/close contact space consider this ex) house fire.
source of injury consideration: open space “accidental” injury means
multiple co existing injury ex) campfire, motor vehicle crash
source of injury consideration: electrical injury may lead to occult (6)
severe fracture hematoma visceral injury skeletal (contraction) cardiac injury (arrhythmias) neurologic injury (seizures) -electrical current will follow path of least resistance -entrance AND exit wound
airway management of the burn patient
aggressively r/o upper airway injury (soot in nose and face, singed nasal hairs or eyebrows, hoarse, having trouble swallowing, coughing up carbonaceous sputum)
dx made by hx/physical (DVL or fiberoptic)
-singed nasal hairs/facial burns-intubate
phases of burns
resuscitative, debridement and grafting, and ____
initial CXR for AW
normal until pedema or infiltration develops
inhalation injury
refers to damage to respiratory tract or lung tissue from heat, smoke, or chemical irritants carried into AW during inspiration
upper airway inhalation injiry
thermal damage to soft tissues of respiratory tract and trachea can make intubation difficult. thermal injury plus fluid resuscitation=worse pedema. increases risk of glottic edema
lower airway inhalation injury
pedema/ards develops 1-5 days post burn
pna/pembolism >5days post burn
high risk of pedema is in
first 36 hours
days 2-5 after inhalation injury, expect
atelectasis, bronchopneumonia, AW edema maximum secondary to sloughing of aw mucosa, thick secretions, distal aw obstruction
> 5d post burn inhalation injury, expect
nosocomial PNA, resp failure, ARDS
chest/upper abdomen circumferential burns considerations
restricted chest wall motion as eschar contracts and hardens. will need to do chest escharotomies
AW management in burn patient includes
patent aw=max FiO2 via face mask
serial larygoscopic/bronchoscopic exams** (tube loaded on scope so you could slip in if needed. 8.0 tube usually the move), CXR, ABG’s, PFT’s in suspected inhalation AW injury
ETT indicated if massive burn, stridor, resp distress, hypoxia/hypercarbia, altered LOC
prophylactic intubation if deterioration likely
intubation technique depends on patient factors, extent of aw damage, age, co existing disease
adults fiberoptic intubation under adequate topical anesthesia is safest approach
pedes patients small diameter airways and low threshold for intubations
AW management in burn patient includes
patent aw=max FiO2 via face mask
serial larygoscopic/bronchoscopic exams** (tube loaded on scope so you could slip in if needed. 8.0 tube usually the move), CXR, ABG’s, PFT’s in suspected inhalation AW injury
ETT indicated if massive burn, stridor, resp distress, hypoxia/hypercarbia, altered LOC
prophylactic intubation if deterioration likely
intubation technique depends on patient factors, extent of aw damage, age, co existing disease
adults fiberoptic intubation under adequate topical anesthesia is safest approach
pedes patients small diameter airways and low threshold for intubations**
tx of hypoxia in burn patient with inhalation injuy
PEEP aw humidification bronchial suctioning/lavage bronchodilators abx (when PNA develops) CPT N2O can be administered as short term vasodilator
CO has ______ the affinity as compared to O2
200x
CO shifts HGB dissociation curve to the
LEFT
Co interferes with
mitochondrial function
uncouples oxidative phosphorylation
reduces ATP production
resulting in metabolic acidosis
CO and cardiac
may act as myocardial toxin and prevent survival of cardiac arrest
CO and sx
SaO2 may be normal
resp effort may appear normal
“cherry red” blood color may not be present if CO <40% and/or patient is cyanotic and hypoxic
measure with ABG and carboxyHGB concentrations
CO toxicity management
high FiO2 on all burn patients until CO toxicity ruled out
hyperbaric chamber if COHgb is >30% and patient is hemodynamically and neurologically stabilized
-can get rid of it in about an hour if at 100% FiO2
COHbg >___ is incompatible with life
60%
CO-assume it is possible if
facial burns
Carbon monoxide toxicity: <15-20%
HA, dizziness, confusion
Carbon monoxide toxicity: 20-40%
n/v, DO, visual impairment
Carbon monoxide toxicity: 40-60%
agitation, combative, hallucinations, coma, shock
cyanide toxicity
produced as synthetic materials burn. victims inhale and absorb through mucous membranes
ex) phones, wool, silk, plastic
metabolic acidosis results with elevated ______
lactate levels
cyanide toxicity s/sx
altered LOC, agitation, confusion, coma, CV depression/arrhythmia risk
half life of cyanide
1 hour
blood cyanide levels
> .2mg/L confirms diagnosis
1mg/L is lethal
tx of cyanide toxicity
oxygen**
hydroxycobalamine, amyl nitrate, sodium nitrate, thiosulfate
burn injury and systemic effects
release of inflammatory mediators locally at burned tissue and systemically contribute to edema associated with burn injury
increase in microvascular permeability-fluid leak/loss of proteins, increased intravascular hydrostatic pressure/decreased interstitial hydrostatic pressure
interstitial osmotic pressure increases
-leaking of proteins from intravascular space creates increased colloidal pull in extravascular space
-migrates to unburned tissues (generalized edema)
surgery and infections can perpetuate this mediator induced systemic inflammatory response that may lead to multiple organ failure
cardiovascular stresses with burn injury
severe decrease in CO in first 24h
circulating tumor necrosis factor creates myocardial depression
diminished response to catecholamines
increased microvascular permeability-hypovolemia
intense vasoconstriction compensation (decreased flow to tissues extends/worsens burn wound)
decreased tissue O2 supply and coronary blood flow
hemolysis of erythrocytes (patients usually anemic throughout their stay)
-after 24h capillary leak “heals”
hyper dynamic state after
24-48h. (increased BP, HR, CO 2x normal)
overall systemic results from burns
immune suppression (depressed leukocyte activity)
activation of hypothalami-adrenal axis and RAAS
hyper-metabolism
protein catabolism (breakdown products of skin itself)
sepsis
MSOF
electrical injury-myoglobinurea
metabolism in burn patient
increased metabolic rate is proportional to TBSA burned (can double in 50% TBSA)
increased core body temp reflects increased metabolic thermostat
loss of skin=loss of vasoactivity, piloerection, insulation functions
caloric consumption increased (nutrition after resuscitative feeds, high carb to conserve protein)
daily evaporative fluid loss is
4000ml/m^2
end organ complications: GI
ileus, ulceration, cholecystitis
end organ complications: renal
decreased GFR, RBF, loss of Ca, K, Mg with retention of Na, H2O
end organ complications: endocrine
increased corticotropin, ADH, renin, angiotensin, aldosterone, increased glucagon, insulin resistance, hyperglycemia (at risk nonketotic hyperosmolar coma esp TPN)
end organ complications: blood and coagulation
increased viscosity, increase in clotting factors including fibrinogen, V, and VII, fibrin split products at risk of DIC development, HCT usually decreases (RBC’s decreased half life)
fluid resuscitation: 1st 24h
replace with 2-4ml/kg for each 1% TBSA burned. crystalloid only
fluid resuscitation and UOP
titrate to .5-1ml/kg/h. try not to overdo it because you can worsen aw edema.
-really titrate based on UOP. if decreased in 1st 24h, replete at necessary. this UOP maintenance is on top of resuscitation calculation
fluid resuscitation: >24h
colloids at .3-.5ml/kg/% burn, with 5% dextrose in water
fluid resuscitation: parkland formula
4ml/kg LR per % burn in 1st 24h
fluid resuscitation: modified brooke formula
2ml/kg LR per % burn in 1st 24h
fluid resuscitation: calculated volumes administration over 24h
50% in 1st 8h
25% in 2nd 8h
25% in 3rd 8h
(given over 24h)
can you give albumin in first 24h
no because it increases extravascular pull
fluid resuscitation: albumin 5%
after 1st 24h, .3-.5ml/kg dose
fluid resuscitation: goals
UOP .5-1ml/kg/h HR 80-140 (consider age) MAP=adults >60mmHg base deficit <2 normal Hct
when to consider low dose dopa or vasopressor
if perfusion/UOP is inadequate despite >6ml/kg/%TBSA burn or
normal/high CVP
dopamine gtt dose
5mcg/kg/min
anesthesia considerations for the burn patient includes
maintain HCT (multiple transfusions)
coagulopathy
temperature (room temp 28-32c, compensate for evaporative/exposure heat loss)
fluids/lytes
need large bore IV access (CVC may be poop access)
hyper metabolic state (increase O2, ventilation, nutrition)
increased risk for GI ileum, aspiration/hyperalimentation
duodenal tube feeds->dont have to stop preop but ensure its in duodenum
anesthesia: monitors considerations
burned tissue=limited access for ECG, SaO2, PNS, NIBP
ECG on sylvadine works well because conducts well
silvadine for burn dressings
can cause hypernatremia and leukopenia
anesthesia and blood loss consideration
topical/SQ epinephrine can help decrease this
200-400mL blood loss for each % body surface area excised (ex 10%, 2-4L blood)
only do 15-20% TBSA per procedure
tourniquets (hard to see when you get to healthy tissue aka tissue that bleeds)
thrombin soaked sponges also an option
preop eval includes
airway phase of resuscitation monitoring (aline probs good idea) intravascular access equipment (pumps, pressors, bair hugger, fluid warmer, infuser in room if you think you'd need)
anesthesia considerations for high voltage electrical injury
follows past of least resistance, bone most resistant
cardiac arrhythmias/arrest
respiratory arrest
seizure
fractures
muscle damage->myoglobinurea->renal failure
anesthesia in burn patient: pharmacology and opioids
high opioid requirement
anesthesia in burn patient: ideal anesthetic choice
isoflurane and large dose opioid
anesthesia in burn patient: serial debridements
ketamine in incremental doses, regional anesthesia
remi good for dressing changes as well in OR
anesthesia in burn patient: muscle relaxant in 1st 24h
unaltered response to depolarizing and non depolarizing paralytics
anesthesia in burn patient: muscle relaxant 24h-1y post burn
avoid succ r/t proliferation of Ach receptors, can also develop extrajunctional Ach receptors
resistance to most NDMR if >30% TBSA burned r/t increase in Ach receptors
burns and regional
usually not option, cant give regional through burn tissue ma’am
anesthesia in burn patient: drug binding
altered catabolism, decreased albumin, decrease in protein and therefore altered drug binding
