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BURNS Flashcards

1
Q

increased moratlity for burns

A
  1. older age (>60y/o)
  2. >40%TBSA burned
  3. +Inhalational Injury
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2
Q

age of pt + %TBSA =

A

>115 then >80% moratality from burn

* mortality doubled with inhalational injuries

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3
Q

1st degree burns

A
  • epidermis involved
  • erythema
  • heal spontaneously
  • painful, tender, sore
  • 2-5 days healing, peeling
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4
Q

second degree burns - partial (superficial dermal)

A
  • very painful
  • epidermis + superficial layer of dermis
  • healing 5 - 21 days
  • no grafiting/excision needed
  • spontaneous regeneration
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5
Q

2nd degree burns - deep dermal

A
  • very painful
  • requires excision and grafting
  • epiderms + deep dermal layer - basement membrane not intact
  • healing: 21 - 35 days
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6
Q

3rd degree burns

A
  • not painful because of all of dermis is burned
  • leathery, dry, no elasticity, charred appearance,
  • small areas may tak months to heal, large areas require grafting
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7
Q

criteria for major burns

A
  1. 2nd degree burns >20% of TBSA in adults
  2. 2nd degree burns >10% of TBSA at extremes of age
  3. 3rd degree burn involving 10% of TBSA in adults
  4. 3rd degree burn involving any electrical burn
  5. 3rd degree burn associated with smoke inhalation
  6. 3rd degree burn associated with burns of face, airway, or genitalia (any%)
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8
Q

in minutes to hours after burns:

burned tissue releases ->

A

Inflammatory and vasoactive mediators

  1. histamine
  2. prostaglandins
  3. kinins
  4. leukotrienes
  5. thromboxane
  6. nitric oxide

all these mediators lead to increased capillary permeability and cause localized burn wound edema

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9
Q

Reperfusion Injury

A

reperfusion of the tissue later will lead to perferusion injry and formation of:

  • ROS
  • toxic metabolites

these cause further cellular membrane dysfunction and additional propagationof the immune response.

Becomes a viscious cycle.

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10
Q

Electrical Burn Considerations

A
  • tissue damage based on VOLTAGE, DURATION
  • exit and entry wounds suffer highest degree of damage
  • 10-46% of electrical burns have concurrent cardiac arrthymias - may damage myocardium
  • massive muscle damage! muscle break down - RHABDOMYOLYSIS
  • myoglobinemia -> from rhabdo
  • end up with AKI
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11
Q

inhalational injuries are most commonly associated with

A

THERMAL burns

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12
Q

inhalational injury symptoms:

A
  1. hoarseness
  2. sore throat
  3. dysphagia
  4. hemoptysis
  5. tachypnea
  6. accessory muscle usage
  7. wheezing
  8. carbonaceous sputum
  9. increase CO levels
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13
Q

pathophys of inhalational injury:

A
  1. Heat of burn denatures protein
  2. This in turn activates complement
  3. complement activates release of histamine
  4. Histamine causes the formation of xanthine oxidase
  5. xanthine oxidase is the enzyme involved in breakdown of purines to uric acid
  6. breakdown of purines to uric acid results in creation of ROS
  7. ROS combine with NO and these form reactive nitrogen species (RNS)
  8. RNS leads to edema in the burned area by increases the microvascular pressure and permability to proteins
  9. Neutrophils than migrate to site but are stiff and non-derformable bc they are injured
  10. injured neutrophils propogate the creation of ROS and injury
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14
Q

inhalational injuries evolve

A

evolve and get wrose as the process continues (inflammatory process)

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15
Q

With smoke damage: (Inhalational injury)

A
  • will see increased pulmonary trans vasculature fluid flux
  • all the fluid shifts - proportional to the duration of smoke exposure
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16
Q

parenchymal lung damage occurs

A
  • over 1 -5 days after [inhalational] injury
  • resembles ARDS
  • after 5 days, can also see pneumonia and PEs
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17
Q

elimination of COHgb

A
  • giving 100% FIO2 can reduce 1/2 life of CO from 4 hours to 60-90 minutes
18
Q

Affinity of Hgb for CO

A

is 200x higher than the affinity of Hgb for O2

affinity for myoglobin is even higher -> binding to cardiac myoglobin = myocardial depression

19
Q

CO binds to myoglobin

A
  • with higher affinity than it binds to Hgb (very high)
  • leads to myocardial depression
  • Hypotension
  • arrthymias
  • Metabolic acidosis at the cellular level
20
Q

cyanide poisoning leads to tissue hypoxia by

A

blocking the intracellular use of O2

  • binds to the terminal cytochrome of the electron transport chain
  • result = hypoxia, lactic acidosis, increased mixed venous saturation bc unable to use O2.
  • S/sx: loss of conscioussness, mydriasis, seizures, HoTN, Tachypnea than apnea, increased lactate levels.
  • tx with B12
21
Q

S/SX of Cyanide Poisoning

A
  1. loss of consciousness
  2. mydriasis (dilated pupils)
  3. seizures
  4. hypotension
  5. tachypnea then apnea
  6. increased lactate levels
22
Q

Antitode to Cyanide poisoning

A
  • cyanide has a very short half life
  • hydroxocobalami (VITB12) - actively binds to cyanide and will for cyanocobalamin
  • also amyl nitrate, sodium nitrite, sodiumthiosulfate
23
Q

substances that can release CO:

A
  1. polyvinyl chloride
  2. cellulose
  3. uphostlery
  4. wire/pipe coating
  5. walls
  6. flooring
  7. clothing/fabric
  8. wood
  9. paper
  10. cotton
24
Q

substances that release cyanide:

A
  1. wool
  2. silk
  3. cotton
  4. paper
  5. plastic
  6. polymer
  7. polyurethane
  8. polycrylonitrile
  9. polyamide
  10. malamine resins
  11. clothing/fabric
  12. blankets/furniture
  13. insulation
  14. upholstery
  15. applicances
  16. engineering
  17. plastics
  18. carpeting
  19. household and kitchen goods
25
Q

Pharmokinetic changes during burn shock/early phase:

A
  1. generally decreased requirements of your drugs
  2. decrease in renal and hepatic blood flow
  3. prolonged rate of drug distribution
  4. prolonged onset of clinical effects
26
Q

Non-depolarizing drugs in the late/hyperdynamic phase:

A
  • increase dose frequency and requirements by 2-5x
  • decreases sensitivity overall to non-depolarizing NMB
27
Q

burn shock is a combination of

A
  1. hypovolemic
  2. distributive
  3. cardiogenic
28
Q

burn shock occurs

A
  • 6-8 hrs after injury
29
Q

leading cause of death in burns =

A
  • infection
30
Q

first priority on all burn patients:

A

Airway exam

31
Q

all pts with face/neck/upper chest burns are considered

A
  • potential difficult airways r/t to facial and a/w edema, inability to move neck appropriately.
  • mask ventilation may be challenging and DL may be impossible.
32
Q

fluid losses are greatest

A

within first 12 hours

33
Q

fluid losses stablizes around

A

24 hours

34
Q

in early phase, large volume of fluid resuscitation is needed and

A

tissue edema and hypoproteinemia are inevitable

35
Q

Complications of OVER fluid resuscitation

A
  • “fluid creep”
  • intra abdominal HTN = IAP >12
  • intrabdominal compartment syndrome = IAP >20
  • pleural and pericardial effusions
  • pulmonary edema
  • fasciotomies
  • conversion of partial thickness to full thickness
36
Q

PARKLAND FORMULA

A

4 ml/kg/%TBSA over first 24 hours

  • first 50% in first 8 hrs
  • next 25% in following 8 hrs
  • next 25% in last 8 hours

next 24 hours

  • 20-60% of estimated plasma volume in crystalloid
  • enough colloid to maintain UO of 30 mL/hr
37
Q

dextrose containing MIVF fluids are sometimes given to

A

pediatric patients r/t depletion of glycogen stores

38
Q

factors indicating adequate resucitation:

markers of end organ perfusion (8)

A
  1. normal blood pressure
  2. urine output between 1 - 2 mL/kg per hour
  3. Blood lactate <2
  4. Base Defecit <-5
  5. Gastric intramucosal > 7.32
  6. Normal CVP
  7. CI 4.5 L/min
  8. Oxygen Delivery DO2I 600min/m2
39
Q

Pre-Op Evaluation of Burn Patient

A

Pre-Op Evaluation of Burn Patient

  1. patient age/body weight
  2. pre-existing comorbid conditions
  3. review labs, acid/base
  4. airway assessment, vent settings
  5. TBSA% burned, note inhalational injury, co-existing traumas
  6. mechanism of injury (flame, explosion, chemical, etc)
  7. time elapsed since injury
  8. vascular access, adequace of resucitation (pressors, fluid status, UO)
  9. Surgical Plan
  10. Review previousanesthesia records
40
Q

Ileus common in burns when

A

TBSA% burned is >20%

41
Q

Art line required for

A

burns with TBSA >20-30%

42
Q

Protective lung ventilation strategies

A
  1. 4-8 mL/kg
  2. plateau pressure <30 cm H2O
  3. permissive hypercapniea up to pH of 7.2

Advanced Principles (8 decks)

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