Burn Injuries and Anasthesia Flashcards
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
describe the Parkland formula
4 mL x kg x % TBSA burned
ex: 70 kg pt w/ 30% TBSA burn = 8,400 mL over 1 st 24 hrs. (350 ml/hr)
what do children require along with resuscitation fluids?
- maintenance glucose infusion (on a pump)
* or will become hypoglycemic
describe hypermetabolism d/t burns
- highest stress response 1st 3 days of injury
- plasma catecholamines 10-50x higher than usual
- if not managed, physiologic exhaustion (death)
- around 48 hrs. post injury, pronounced hypermetabolic phase sets in
- hypermetabolic phase for up to 2 yrs. after 40% TBSA burn
- multi drugs and treatment can be used for prevention of sepsis, temp. maintenance, etc.)
what are drugs seen in therapy of hypermetabolism d/t burns?
- rhGH (improved inflammation and body composition)
- insulin like growth factor1 (improved inflammation, body comp., net protein balance, and insulin resistance)
- oxandrolone (improved inflammation, body comp., net protein balance)
- insulin (inflammation, body comp., protein balance, insulin resistance)
- fenofibrate (insulin resistance)
- glucagon like peptide 1 (indirect improvement of insulin resistance; effects on other symptoms unknown)
- propranolol (inflammation, stress hormones, other sx. unknown)
- ketoconazole (stress hormones, body comp., protein, insulin resistance, hyperdynamic circulation)
- rhGH and propranolol (all 6 sx improved)
- oxandrolone and propranolol (all 6 sx improved)
describe CV changes d/t burn injury
- loss of plasma proteins leading to hypovolemia, hypotension (“burn shock”)
- decreased CO initially compensated by catecholamines (increased HR, vasoconstriction)
- in children, HTN persists for weeks after injury
- treating hyperdynamic response may improve long-term outcomes
describe pulmonary changes d/t burn injury
- decreased function even w/ no inhalation injury
- decreased FRC and decreased compliance d/t circumferential burns, edema, eschar
- may require escharotomy
- increased capillary permeability plus fluid resuscitation lead to risk of pulmonary edema that can lead to ARDS (caused by plasma proteins seeping out and stuff leaking into alveoli)
- *current trend: low Vt, low PiPs to minimize barotrauma (may need to increase d/t decreased compliance causing issues)
describe renal changes d/t burn injury
-function decreased d/t myo and hemoglobinuria
-“RIFLE” criteria used to categorize acute kidney injury
Risk, Injury, Failure, Loss, End stage kidney disease
describe immune changes d/t burn injury
- high risk of sepsis and pneumonia
- sepsis is leading cause of death in children (up to 100%) and adults (up to 75%)
describe GI/Nutrition changes d/t burn injury
- metabolic rate 2x normal
- failure to meet nutritional requirements leads to poor healing, sepsis, multi-organ dysfunction, death
- insulin resistance (glucose/insulin protocols common)
- if intubated, do not stop enteral feedings pre-op (if not sure of tube placement may not want to risk aspiration)
- continue TPN intra-op
- monitor glucose peri-op
- use infusion pumps for pediatrics
- ileus common with greater than 20% TBSA burn
describe debridement and grafting for burns
- multiple procedures frequently required (debridements, grafting, amputation)
- standard: early debridement w/ rapid coverage
- debridement/grafting done every 2-3 days until grafting complete
- autologous skin (best), cultured skin (small sample of skin taken and grown in lab), skin substitutes (porcine; chance of not healing well or rejection)
what are common guidelines for burn procedures?
- no more than 20% of body surface at a time
- stop surgery if core temp cannot be maintained at greater than 35 degrees C (rewarming is impossible; OR kept really warm)
- stop when 10 units of PRBCs given (less in children)
- increased risk of coagulopathy
describe pre-op for burn pts.
- thorough airway (neck mobility, oral opening) and pulmonary assessment (PiPs, MV)
- prepare for difficult airway techniques
- minimally safe NPO orders
- evaluate IV access (2 large bore PIVs or CVLs)
- check labs and blood availability (have blood in OR before debridement begins, esp. w/ pediatrics)
- plan for heavy use of narcotics, muscle relaxants (hypermetabolic state)
- warm OR, fluids, bed, surgeon
- plan for post-op ventilation, ICU bed
describe monitoring during burn cases
- may require needle electrodes for EKG
- arterial line if all extremities affected or being used as donor graft sites
- pulse ox: ear lobes, nose, toes, cheek
- esophageal or bladder temp probe for accurate temp
- extreme caution when transporting and moving (losing airway could be lethal; watch invasive lines ; monitor VS while transporting)
describe airway management for burn pts.
if not intubated and no airway injury, induction and intubation done as usual, but NO SUCCS
describe temp regulation during burn cases
- heat everything to a very hot level
* *staying warm is much easier than rewarming
describe fluid/blood replacement during burn cases
- keep up and stay ahead
- debridement causes heavy, rapid blood loss
- may be at transfusion trigger on arrival; start blood as soon as blood loss begins
- EBL is difficult; look for “hidden blood loss”
- transfuse based on hemodynamics (hypotensive?, tachycardia?, pale?), urine output, labs (hgb, hct)
describe induction and maintenance for burn pts.
- volatiles and opioids ok to use
- anesthetic effects may be exaggerated if hypovolemic
- propofol ok if stable; ketamine if unstable
- TIVAs for ICU pts. on specialized ventilators (will not use our machines)
- NO SUCCS
- receptor up regulation requires increased amounts of NMB
what are concerns with regional anesthesia w/ burn pts.?
- never pass a needle through burned tissue
- associated vasodilation may lead to hemodynamic instability
- may have burn-related coagulopathy
- regional is a poor choice if areas of debridement and grafting cannot be anesthetized
- caudals may be good choice for children w/ lower extremity burns (hips down)
- if unsure of coagulation status, don’t do regional
describe emergence after burn cases
-caution w/ intra-op narcotics if extubation planned, esp. w/ possible airway compromise
describe pain management w/ burn cases
- post-op PCA pumps are good choice if pt. stable
- donor graft sites more painful than grafted sites
- opioids best when hemodynamically labile
- caution w/ NSAIDS (can interfere w/ hemostasis)
- repeated painful procedures leads to analgesic tolerance (need more)
what happens long term from burns and frequent surgeries?
- scarring and contractures of mouth and neck (if burned in that area)
- be prepared for difficult intubation
- children w/ repeated procedures probably need pre-op sedation (procedure is associated w/ pain!)
