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ADV Prin Test 3 > Burns > Flashcards

Burns Flashcards

1
Q

Incidence statistics for burns?

A
  • 1.25 million burns annually worldwide
  • 486,000/year in US required ER visits
  • 40,000 hospitalized
  • 30,000 admitted to specialized burn center
  • incidence of burns has decreased secondary to education on prevention and safety regulations
  • survival rate 96.8%

Where they occur

  • 73% home
  • 8% occupational
  • 5% traffic accidence
  • 5% recreational sport
  • 9% other causes
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2
Q

Etiology of burns?

A
  • Electricla burn 4%
  • Chemical burn 3%
  • Inhalational burn (burn in a closed space is suspicious for inhalational)
    • no percent on chart
  • Thermal burn 43%
    • (same as flame/fire on pie chart provided)
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3
Q

Mortality of burns?

A
  • INCREASED MORTALITY
    • ​Older age >60 yo
    • >40% TBSA
    • inhalational injury
  • age of patient + %TBSA burned if > 115, then mortality of patient >80%
  • mortality doubled if burn + inhalational injury
  • Burn size with LD 50 *lethal dose 50%* >90% TBSA (total body surface area)
  • Approx. 3240 die from fire/smoke inhalation injury
  • 2855 from residential fires
  • 300 motor vehicle/aircraft
  • 75% dies at scene or during transport
  • 35% burn victims <17 yo
  • Decreased mortality in burns due to:
    • increased access emergenyc care
    • better airway mgmt
    • better infection contorl
    • better nutritional support
    • early burn excision/grafting
    • treatment of hypermetabolic response with EBP
      *
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4
Q

Anatomy of integumentary system

A
  • Largest organ
  • layers
    • epidermis- protective outer surface
      • ​avascular. nourished by dermis
    • dermis
      • vascular
      • heavily innervated
      • collagen and elastic fibers
      • deep layer dermis- hair follicles, sebaceous gland. afferent nerve endings
      • most nerve terminals at dermis and a few penetrate the epidermis
      • deep fascia- deepest layer, dense organized connective tissue layer, seats skin into sq tissue
    • subcutaneous

Function

  • protection
    • immune function
    • fluid/electrolyte homeostasis
  • containment
  • heat regulation
    • sweating/vasomotor regulation of superficial blood flow
      • blood vessels dilate in heat, constrict in cold
  • sensation
  • vitamin D
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5
Q

Burn categorization?

A
  • Basis: depth and body surface area
  • 1st degree- epidermis
    • heals spontaneously
  • 2nd degree- important to know if basement membrane is intact/not intact
    • superficial partial thickness (basement membrane intact)
      • if basement membrane intact- skin will generate and grafting not needed
    • deep dermal burn (basement membrane not intact)
      • need grafting
  • 3rd degree- full thickness burns
    • subcutaneous extension
    • will need grafting
  • 4th degree
    • muscle, fascia, bone
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6
Q

What is a first degree burn?

depth? how the wound looks? causes? levelof pain? healing time? scarring?

A
  • Depth- epithelium
  • How the wound looks- no blisters; dry, pink
  • Causes- sunburn, scald, flash flame
  • Level of pain- painful, tender and sore
  • Healing time- two to five days; peeling
    • Scarring- no scarring, may have discoloration
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7
Q

What is a second degree burn?

depth? how the wound looks? causes? level of pain? healing time? scarring?

A
  • Depth- epithelium and top aspect of dermis
  • How it looks- moist, oozing, blisters,
    • moist, white, pink to red
  • Causes
    • scalds
    • flash burns
    • chemicals
  • Level of pain
    • very painful
  • Healing time
    • superficial- five to 21 days- no grafting needed
    • deep 21-35 days- needs grafting
  • Scarring
    • minimal to no scarring
    • may have discoloration
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8
Q

Characteristics of third degree burn?

depth? how the wound looks? causes? level of pain? healing time? scarring?

A

aka full thickness

  • Depth- epithelium and dermis
  • how it looks-
    • leathery, dry
    • no elasticity
    • charred
  • Causes
    • contact with flame, hot surface
    • hot liquids
    • chemical
    • electrical
  • Level fo pain
    • very little pain or no pain
  • Healing time
    • small areas may take months to heal
    • large areas to be grafted
  • Scarring present
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9
Q

Summary of burns?

A
  • 1st degree
    • involves epidermis
    • erythema
    • spontaneous healing
  • 2nd degree
    • superficial burn
      • spontaneous healing 7-10 days
      • painful
    • deep dermal
      • requires excision/grafting
      • 2-8 weeks to heal
      • scarring
  • 3rd degree- complete dermal loss
    • no pain d/t nerve damage
  • 4th degree- expect to lose limb
    • muscle/bone/tnedon involved
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10
Q

What is the rule of nines?

A
  • How we estimate burns
  • Head and neck 9% (total)
    • Ant 4.5%
    • Post 4.5%
  • RUE 9%
    • Ant 4.5%
    • Post 4.5%
  • LUE 9%
    • Ant 4.5%
    • Post 4.5%
  • RLE 18%
    • Ant- 9%
    • Post 9%
  • LLE 18%
    • Ant- 9%
    • Post 9%
  • Anterior tunk 18%
  • Post trunk 18%
  • Perineum 1%
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11
Q

Criteria of major burn?

A

2nd degree burn >20% TBSA in adult, or 10% in extremes of age

or

3rd degree burn >10% TBSA in adult

or

any electrical burn

or

any burn associated with smoke inhalational

or

any burn involving face, airway, or genitals of any percent

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12
Q

What determines initial resuscitation in burn

A

TBSA

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13
Q

How is TBSA estimated in children?

A
  • Lund and Browder chart
    • not expected to memorize
  • Rules of nine inaccurate in children
    • head and trunk proportionally larger in children
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14
Q

Pathophysiology of burns?

A
  • 2 distinct phases
    • burn/shock phase
    • hypermetabolic phase
  • SIRS response
  • every system affected
  • necrotic and ischemic area
    • potential viability of ischemic area with adequate resuscitation
    • no potential for viability with necrotic area
  • Minutes to hours: burned tissues release inflammatory and vasocative mediators
    • All lead to increased capillary permeability,
      • histamine
      • prostaglandin
      • kinin
      • leukotrienese
      • thomboxane
      • nitric oxide
  • Later
    • reperfusion injury
      • tissue produces ROS and toxic cell metabolites
      • leads to further cell membrane dysfunction
      • worsening of immune response, cascade of responses
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15
Q

What should we keep in mind in regards to burn zones?

A
  • Burn
    • zone of coagulation- area dead
    • zone of stasis
    • zone of hyperemia
  • with adequate resuscitation, zone of stasis and zone of hyperemia blood flow can be restored and maintain viabiilty
  • without adequate resus, the zone of coagulation will grow and zone of stasis will become infarcted and won’t be able to regenerate
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16
Q

Electrical burns?

A
  • Devastating injury to bones, BV, muscle, and nerves
  • tissue damage based on voltage and duration
    • entry and exit are where most energy (damage) are concentrated
    • 10-46% with concurrent cardiac arrhythmias; may have damage to the myocardium
    • massive muscle damage leads to renal failure secondary to myoglobinemia (from rhabdo)
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17
Q

Chemical burns?

A
  • Occupational injury
  • reaction with tissue proteins and cellular components leads to tissue destruction
  • chemical burn: must neutralize; copious irrigation
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18
Q

Thermal burns?

A
  • Scaled inuries account for 70% burns in <4 yo
  • >5 yo: flame associated
  • burns in young children 15-20% is non-acciedental burn (d/t abuse/neglect)
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19
Q

Symptoms Inhalational injury?

A
  • hoarseness
  • sore throat
  • dysphagia
  • hemoptysis
  • tachypnea
  • accessory muscle usage
  • wheezing
  • carbonaceous sputum
  • increased CO levles
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20
Q

Types of inhalational burns?

A
  • Most commonly associated with thermal burns
  • likely in closed space burn; suspect in pt unconscious at scene

3 types

  • 1) Upper airway injuries- inhalation of superheated air/steam
    • may spare lower airway d/t reflexive VC closure
  • 2) Lower airway/parenchymal
    • soot particle/chemical inhalation
    • acute phase will have significant bronchopasms
      • bronchodilator therapy always required
        • may need epi b/c refractory to other treatment
  • 3) metabolic asphyxiation- carbon monoxide, etc.
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21
Q

Pathophys of inhalational injury?

A
  • microvascular changes
  • heat denatures proteins, activates complements
    • causes release of histamine
  • histamine causes release of xanthin oxidase
    • enzyme involved in breakdown of purine–> uric acid
  • ROS released
    • ROS combine with NO–> reactive nitrogen species formed
      • causes edema in burned area
      • increases microvascular pressure and permeability to protein
  • release proinflammatory cytokine and oxygen free radical/interleukin
    • attract polymorphonuclear cells to area and neutrophils applify release of oxygen radicals, proteases and other materials
    • becomes vicious cycle
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22
Q

Consequence of inhalational injury?

A
  • Coagulopathy
  • Bronchospasm
  • mucus secretion–> airway obstruction
  • airway epithelial exfoliation because of neutrophil migration
  • increased airway blood flow
    • causes airway wall edema
    • upregulation of adhesion molecules, ROS, superoxide
      • end up with lots of cellular dysfunction, pulmonary edema, V/Q mismatch, loss of hypoxic vasoconstriction

All major burns are going to have change in pulmonary physio even with no direct inhalational injury

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23
Q

Indications for ealy trahceal intubaiton after inhalation injury

A
  • Extensive burn over face/neck
  • over s/s of airway obstruction by edema
  • inability to protect the airway
  • sig toxicity from CO or cyanide
  • Respiratory failure
  • hemodynamic instability
24
Q

What is carbon monoxide poisoning?

A
  • Suspect with inhalational injuries; detected by measurement of arterial COHgb levels
  • the severity of symptoms correlates with COHgb level
    • >30% requires high FIo2 to reduce half-life
      • 4hours on RA down to 60-90 minutes with 100% Fio2
      • Hyperbaric O2 considered if >25% COHgb levels
      • need to go ahead and intubate patient
    • 200 times greater affinity for Hgb than oxygen
  • Oxygen-Hgb dissociation curve of the remaining oxyhemoglobin shifts to the left, reducing oxygen release
  • Affinity of CO for myoglobin is even greater than for hemoglobin
    • binding cardiac myoglobin leads to myocardial depression, hypotension, and arrhythmias
  • Metabolic acidosis at cellular level
    • because oxygen delivery impated
  • FALSELY ELEVATED pulse ox reading
25
Q

Symptoms associated w/ specific COHgb levels?

A
  • Symptoms noted at >20%
26
Q

What is cyanide poisoning?

Symptoms?

A
  • cyanide poisoning leads to tissue hypoxia by blocking the intracellular use of O2
  • Binds to terminal cytochrome on the electron transport chain
    • result is hypoxia, lactic acidosis, elevated mixed venous oxygen saturation
  • Symptoms:
    • loss of consciousness
    • mydriasis
    • seizures
    • hypotension
    • tachypnea then apnea
    • increased lactate levels
27
Q

Treatment of cyanide poisoning?

A
  • Antidote: Hydroxocobalamin (vitamin B12)
    • Actively binds cyanide by forming cyanocobalamin
    • directly excreted by kidney
  • other treatment amyl nitrate, sodium nitrite, sodium thiosulfate
28
Q

When should we suspect carbon monoxide or cyanide poisoning?

A
  • CO- burning of upholstery, walll, floor, furniture coverings, clothing, fabric, wood,paper, cotton
  • Cyanide- clothing, fabric, blankets, furniture, insulation, appliances, plastics, carpeting, clothing

Good rule of thumb in house fire will probably need to manage CO/cyanide poisoning as well

29
Q

What are pharmacokinetic changes involved in the burn shock phase? hypermetabolic phase?

A

Burn shock phase: generally decreased requirements

  • reduction in hepatic and renal blood flow
  • prolonged rate of drug distribution
  • prolonged onset of clinical effects

Hypermetabolic: phase: generally increased requirements

  • Decreased albumin
  • increased alpha 1-acid glycoprotein
  • denervation phenomenon with spreading of acetylcholine receptors
  • increased nicotinic acetylcholine receptors and decreased function
30
Q

Anesthetic considerations for patients with burn injuries?

A
  • Fluids
    • crystalloid mainstay for early phase
    • colloid considered after 24 hours
  • Succinylcholine
    • succ okay <24 hours
    • avoid if >24 hours and up to 18 months after burn injury
  • Nondepolarizing muscle relaxants
    • increase dose frequency and requirements (2-5 fold)during hyperdynamic phase
    • no change in reversal requirements
    • Consider rocuronium > 24 hours after burn injury for RSI
  • IV anesthetics
    • decrease dose early phase
    • increase dose hyperdynamic phase
    • use multimodal therapy
  • Inhalation agents
    • Decrease MAC early phase
    • Increase MAC hyperdynamic phase
    • may be beneficial for inhalation injury (bronchodilator)
  • Beta blocker
    • attenuate hyperdynamic phase
  • Insulin
    • attenuate hyperdynamic phase burn injury
31
Q

Approach to burn managmeent?

A
  • Biphasic response to injury
    • Burn shock developed 6-8 hours after injury
    • hypermetabolic phase develops in several days to weeks after
  • Burn treatment occurs in 3 phases
    1. resuscitative
    2. debridement and grafting)
    3. reconstructive
32
Q

CV changes in early vs late phase?

A
  • Early:
    • hypovlemia
    • decrease cardiac output
    • increase SVR
  • Late
    • increase cardiac output
    • tachycardia
    • systemic HTN -Depleted catecholamine
33
Q

Pulmonary changes in burn early vs late phase?

A

Early:

  • Airway obstruction and edema
  • pulmonary edema
  • carbon monoxide poisoning

Late:

  • chest wall restriction due to scar formation
  • tracheal stenosis due to repeat/prolonged intubation
34
Q

Renal changes in burn injury early vs late phase?

A
  • Early
    • decrease GFR
    • myoglobinuria
  • Late
    • increase GFR
    • Increase tubular dysfunction
35
Q

Endocrine and metabolic early vs late?

A
  • Early
    • no changes
  • Late
    • increase metabolic rate
    • increase core body temperature
    • increase muscle catabolism
    • increase insulin resistance
    • increase lipolysis
    • increase glucolysis
    • decrease thyroid and PTH hormone
36
Q

Hepatic changes early vs late?

A
  • Early
    • decrease perfusion
  • Late
    • increase perfusion
    • increase metabolism
37
Q

Hematologic changes early vs late

A
  • Early
    • hemoconcentration
    • hemolysis
    • thrombocytopenia
  • Late
    • anemia
38
Q

GI changes in early vs late phase?

A
  • Early
    • decrease perfusion with mucosal damage
  • late
    • stress ulcers
    • adynamic ileus
39
Q

Neuro changes early and late phase?

A
  • early
    • increase cerebral edema
    • increase ICP
  • Late
    • hallucination
    • personality change
    • delirium
    • seizure
    • coma
40
Q

Initial airway assessment?

A
  • Consider inhalation injury likelihood
  • inspect neck &oral cavity for overt issues
  • gold standard airway assessment: fiberoptic bronchoscopy
  • cxr is usually normal in early phase
  • early intubation when upper airway injury suspected- do not wait for decompensation
41
Q

Leading cause of death in burn patients?

A
  • infection
    • eschar is ideal bacteria medium
  • largest complication is renal failure
    • many placed on CRRT
42
Q

Initial airway assessment in burn patients?

A
  • consider inhalational injury likelihood
    • facial burn
    • hoarseness
    • evidence smoke exposure
  • insepct neck and oral cavity
  • gold standard airway assessment: fiberoptic bronch
  • CXR is usually normal in early phase
  • Early intubation when upper airway injury suspected- do not wait for decompensation
43
Q

Airway mgmt in burn patients?

A
  • intubation will be easier if not delayed
    • always cuffed ETT
  • awake, spontaneously breathing fiberoptic intubation if any airway abnormality suspected
    • topical anesthesia plus hypnotic that preserves spontaneous ventialtion
      • ketamine
      • dexmedetomidine
      • opioids/sedatives judiciously
  • If no airway abnormality, rapid sequence techniques can be used however NO SUCCINYLCHOLINE permitted beyond 1st 24 hours after injury
  • severe airway burns may require immediate surgical airway/trach
  • Potential difficult airway
    • face
    • neck
    • upper chest burn
44
Q

Initial managmeent in burn shock phase?

When is fluid loss the greatest?

What contributes to volume loss and edema?

What complications can over-resuscitation cause?

A
  • Combination of distributive, hypovolemic, and cardiogneic shock
  • priorities
    • airway managmenet
    • fluid resus
      • crystalloid only in first 24 hours
  • fluid loss greatest in first 12 hours; stabilizes at 24 hours
  • volume loss and edema
    • transudation of plasma proteins directly from wound bed
    • interstitial fluid shifts in unburned tissue secondary to capillary leak
  • over-resus can lead to complications
    • intraabd HTN ( intra abd > 12 ,mHg)
    • Abd compartment syndrome (intra-abd pressure >20 mmHg)
      • see organ damage and death at this point
    • pericardial effusion/pleural effusion
    • pulmonary edema
    • conversion of partial thickness to full thickness lesion
  • crystalloid fluid of choice in 1st 24 hours
45
Q

Fluid resuscitation formula in burns?

targets for fluid resus?

A
  • All based on pt weight and % TBSA burned
  • parkland formula most widely used foruma in world
    • recommended fluid is LR
    • 4mL/kg per percentage of TBSA in 1st 24 hours
      • 1/2 of calculated volume in first 8 hours
      • remained of fluid over next 16 hours
  • may need dextrose containing fluid for children in early phase d/t depletion of glycogen stores
  • target fluid resus
    • normal BP
    • UOP 1-2mL /kg/hr
    • blood lactate
    • base deficit
    • gastric intramucosal pH >7.32
    • normal CVP/CI/O2 delivery index
46
Q

Physio behind of hypermetabolic phase of burns?

Symptoms?

A
  • Develops over several days to weeks; changes persist long term
  • Caused by an immense surge in catecholamines and corticosteroids (10-50x baseline)
    • ​increase myocardial O2 consumption and cardiac work
    • cardiac output/HR increase 150% above non-burn patient
      • can stay elevated 2 years post burn
  • S/S
    • Persistent tachycardia
    • systemic HTN
    • Tachypnea
    • increased muscle protein degradation
    • insulin resistance
    • elevated core temp
    • liver dysfunction
    • increased risk of infection
  • can lead to physical exhaustion and death without treatmnt
47
Q

Treatment for hypermetabolic phase of burns?

A
  • Early excision and grafting
  • warming strateigies
  • nutritional support
  • insulin
  • beta blockers
48
Q

What are escharotomies and grafting considerations?

A
  • Early debridement is preferred with closure/grafting
    • decreases rate of sepsis
  • surgeries often staged
    • usually started on 2nd day to 2nd week after injury
      • burn has to establish itself
  • indications to suspend surgery and return later:
    1. 20% BSA excised (may extend to larger area if stable)
    2. time of 2-3 hours
    3. temperature drop to 35C
    4. blood los requiring 10 units or more of PRBC
  • Surgery done every 2-3 days
  • blood loss can be significant
    • up to 2L in 15-20 min
    • anticipate need for massive transfusion
    • manage fluid/electrolyte abnormalities
49
Q

Preop eval of burn patients?

A
  • Patient age, body weight
  • pre-existing co-morbidities
  • review labs including acid-base
  • airway assessment, vent settings
  • TBSA burned, note inhalation injury, note co-existing trauma
  • mechanism of inury
    • flame, explosion, chemical, electrical, scald
    • time lapse since injury
  • vascular access and adequacy of resus (current fluid requirements, urine output, vasopressor requirement)
  • surgical plan
  • review previous anesthetic records and mgmt
50
Q

NPO status in burn patients?

A
  • Adequate caloric intake is critical in ongoing mgmt
  • NPO after MN NOT appropriate
  • enteral feeds
    • intubated pt ;no need to D/C enteral feeds before sx
    • Unintubated pt: feeds stay on up to 4 hours before sx
    • once in OR: decompress NG tube
      • check gastric residuals
  • Parenteral feeds: continue intraop and do not use the line for lipids and hyperalimentation
51
Q

Preop setup for burn patients?

A
  • Warm the OR ahead of time
    • should not exceed 95 degree
  • Check availability of blood products and order more if needed
    • based on preop Hgb, size of burn, extent of planned debridement
  • have blood products immediately available in OR as surgical debridement is initiated. critical for ped patient
  • have at least one blood warmer primed, plugged in, and turned on
    • if burn large, have two
  • make sure you have adequate IV access before srugoen begins debriding burn
  • have adequate supply of narcs/MR
  • know and plan ahead of time if invasive lines needed
  • plan for airway mgmt and ventilation both intraop/postop as needed
  • have a plan but be willing to modify it if necessary
52
Q

Induction for burn patient?

A
  • All standard monitors
    • challenges: ECG lead, NIBP, SPo2 placement
      • suture/staple ECG leads in
      • may need invasive BP
  • Rare to see pt in OR in 1st 24 hours
    • urgent surgery needed at outset you must reduce dosage of inducitona gents secondary to shock
  • NO SUCCINYLCHOLINE after 1st 24 hours
  • Expect resistance to NDNMB- higher/more frequent dosing
  • if unable to take off ICU vent, consider TIVA
  • consider benefits of VA
    • helpful with bronchospasm
  • no ideal anesthetic mgmt but ketamine helpful
    • increase SVR
    • maintain airway reflex preservation
    • analgesic
    • use anticholinergic along with ketamine
53
Q

Intraop considerations for burn patient?

A
  • ABP required if >20-30% TBSA involved
  • Accurate temp monitoring essential/avoid hypothermia/actively warm
    • HME
    • Low flows
    • OR 28-33 degree celsius
    • plastic to retain heat
  • continue ICU infusions (including narcs) and O2 during transport
  • ensure ETT securement is infalliable
    • ​may not be able to secure tube to face as usual
  • blood loss can be rapid and tremendous- need adequate product immediately available and checked in room
    • start unit immediately after induction or even prior
    • don’t only look at suction, look at drape too
  • anticipate use of epi-soaked gauze, may see systemic effects
  • pain control
  • may need co-oximeter to look at metHgb and CarboxyHgb concentration
54
Q

Ways to secure tube in burn patient?

A
  • ties
  • suture to teeth
  • tie circumferential behind patient’s head
  • loop NG tube through nostril and hard palate
  • suture mandible, septum., nares
    • probably have surgery sew in the tube if difficult airway
55
Q

Burns and NMB considerations?

A
  • Proliferation of extrajunctional nicotinic Ach receptors
    • increased resistance to NDNMB
    • Increased sensitivity to depolarizing MR
  • succinylcholine >24 hours postburn injury is prohibited
    • potentially lethal hyperkalemic response
    • may persis for 18 months p injury
  • resistance to NDNMB may develop within week of burn injury
    • persist for up to a year
    • 2-5 fold dose increase
    • roc in large doses up to 1.2 mg/kg can be used RSI
    • Resistane does not prolong recovery times or alter efficcy of reversal agnets
56
Q

Ventilator management for burn patients?

A
  • Anticipate pulmonary compromise
    • RAD
    • Laryngospasm
    • bronchospasm
    • V/Q mismatch
    • decrease pulm compliance
    • PNA
    • ALI
    • ARDS
  • HIgh fio2 and frequent sucitoning needed (thick/copious secretion)
  • Lung protective ventilation
    • target TV 4-8 mL/kg
    • plateau pressure <30 cm H2o
    • permissive hypercapnia up to pH 7,2
  • HFOV (if needed) may require TIVA

ADV Prin Test 3 (3 decks)

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