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b. princip. exam 2 (w13) > anesthesia for burns > Flashcards

anesthesia for burns Flashcards

1
Q

1.

what are three methods of being burned (and the problems each one causes)?

A
  1. thermal injury- destroys skin, affects bodies barrier, thermoregulation, fluid and electrolyte balance, infection defenses
  2. electrical - current passes thru body, creates thermal injury that destroys tissue (especially skin and bone). Inability to track path makes assessing damage difficult.
  3. chemical- depends on agent, concentration and duration of contact (systematic absorption may be life threatening).
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2
Q

2.

what are the depths of burn injury:

A

first, second, third, fourth degree

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3
Q

3.

first degree burn:

A

first degree: affects epidermis ONLY; redness, pain, minimal edema, no blisters (sunburn).

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4
Q

4.

second degree burn

A

second degree: partial thickness burn, affects epidermis an dermis, some blood vessel involvement; skin will be pink, mottled, wet, edematous, painful, sensitive. Basement membrane intact (scald or flash fire).

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5
Q

5.

third degree burn:

A

third degree-full thickness burn, reaches large arteries and veins, possible confluent thrombosis or coagulation of vessels; white/charred (avascular) skin, no pain d/t destruction of nerve endings (immersion scald, electrical flame).

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6
Q

6.

fourth degree burn:

A

deep thermal injury involving muscle, tendon and bone

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7
Q 
7.
what is the rule of nines?
name the % for each body part:
1. face?
2. genitalia?
3. front of leg?
4. front of arm?
5. whole arm?
6. whole head?
7. upper and lower posterior trunk?
A

an algorithm that assigns a % score to regions of the body that are burned.

  1. face=4.5%
  2. genitalia= 1%
  3. front of leg=9%
  4. front of arm=4.5%
  5. whole arm=9% (4.5% front and 4.5%back)
  6. whole head=9% (4.5% front and 4.5% back)
  7. upper and lower posterior trunk=18% (9% upper,9% lower)
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8
Q

8.

  1. what are major burns?
  2. what does this constitute as far as degrees and %? (5 criteria)
A
  1. burns that require hospitalization
  2. a)second degree to 25% of body
    b) third degree to 10% of body
    c) third degree to face & hands or face and feet
    d) electrical burns (d/t potential organ involvement)
    e) smoke inhalation injury (respiratory issues)
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9
Q

9.

pathology of burns; what are the 9 things that burns affect (or cause)?

A
  1. disrupt skin integrity
  2. have cardiovascular effects
  3. respiratory effects
  4. metabolic effects
  5. renal effects
  6. gastrointestinal effects
  7. neurological effects
  8. hematological effects
  9. infection/ sepsis
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10
Q

10.

  1. disrupted skin integrity & its basic effects
  2. what is dead skin succeptable to? what are the medications? side effects of medicines B & C?
  3. when are IV antibiotics warranted
A
  1. Loss of fluid, nutrients and heat
  2. avascular tissue is succeptible to microbe colonization which is unresponsive to IV antibiotics (no blood to get it there). must use topical abx:
    a-silvadene
    b-silver nitrate (causes deficet in Na+, K+ & Cl-; causes methemoglobinemia, stains skin and equipment
    c-mafenide acetate (sulfamylon) (painful and causes acidosis by inhibiting carbonic anhydrase
  3. iv antibiotics only given when infection goes systemic or is in blood
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11
Q
  2. what treatment is essential for disrupted skin integrity:
  3. name the 4 different types or ways to cover skin:
A
  1. early debridment with application of temporary or permanent cover
  2. –autograft: patient’s own skin from donor site (permanent)
    • allograft: from cadaver skin (temporary)
    • xenograft: donated from “xeno”-somthing different; i.e. porcine skin (temporary)
    • artificial skin: manufactured from collagen and cultured epidermis (must be grown in vitro from patient’s own cells-takes 6 weeks) (permanent).
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12
Q 
12.
cardiovascular effects (#1-3) and the treatment (#4)in first 24-48 hours after burn:
A
  1. vascular permeability increases (loss of fluid)
  2. plasma volume is subsequently reduced
  3. cardiac output decreases (initially)
  4. fluid resusitation
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13
Q 
13. 
cardiovascular effects (#5-7) in next 12 hours (day 2, 3 or 4):
A
  1. hyperdynamic state (bp/hr increase post 24 hours (fight/flight))
  2. decreased RBC survival time (down to 40 days)
  3. potential for cardiac arrest (d/t lyte imbalances or damage to conduction system of heart-electric burns).
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14
Q 
14
cardiovascular effects:
increased vascular permeability:
1. if burn is greater than 30% TBSA?
2. if burn is less than 30% TBSA?
3. what happens intravascularly if fluid loss (d/t increased vascular permeability)continues?
4. why dont we give colloids?
5. what decreases (d/t volume loss)
6. what happens to cell membranes; what does it cause? where? what is the treatment (preferably in ER)?
A
  1. if >30% causes generalized loss of microvascular integrity
  2. if < 30% causes localized loss of microvascular integrity
  3. there is a loss of intravascular proteins which pulls more fluid out with it
  4. if colloids are given, it would leak out pulling even more fluid (give LR/NS)
  5. preload is decreased
  6. altered cell membranes allow swelling (especially of tongue and oropharynx= airway edema/ obstruction..intubate in ER).
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15
Q

what are the 3 stages of a burn patient treatment

A
  1. resucitative phase
  2. debridment and grafting
  3. reconstructive phase
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16
Q 
15.
cardiovascular effects:
reduced plasma volume:
1. fluid sequestration (isolation or loss)causes:
2. reduced plasma causes:
A
  1. hemoconcentration, reduced plasma volumes
  2. decrease circulating blood volume and increased blood viscosity causing increased HCT (viscosity also d/t myoglobin release from damaged tissues & denatured RBCs)
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17
Q 
16. 
cardiovascular effects:
cardiac output initially decreases:
1.why (2 reasons)?
2. what is the treatment?
A
  1. a)decreased blood volume d/t loss of plasma
    b) decreased myocardial contraction d/t MDF (myocardial depressing factor) which is released in response to tissue damage
  2. give fluids to:
    a) flush blood stream
    b) maintain volume and increase C.O.
    c) maintain perfusion
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18
Q

17.
fluid resucitation:
1. fluids key in decreasing what?
2. especially administered to patients with >__ to __% TBSA burns
3. what is the parkland formula?
4. ex: 90 kg person burned over 60% of body; what is the total fluid for 24 hours and what is the first 8 hours dose?

A
  1. M&M (morbidity and mortality)
  2. 15-20% TBSA burns
  3. first 24 hours: 4 ml LR x % burned x kg:
    a) give first 1/2 in first 8 hours
    b) give second 1/2 over last 16 hours
  4. ex: 4* 60% * 90kg=21,600 ml (1/2=10,800ml over first 8 hours)
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20
Q

18
hyperdynamic state: (24-36 hours post burn):
1. what happens to vascular system?
2. what begins to rise? why?

A
  1. after 24-36 hours the microvascular integrity is reestablished.
  2. C.O. begins to rise, becomes heightened (supra-normal) d/t catecholamine release
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21
Q

19
decreased CBC survival time (24-36 hours post burn)
1. what is normal RBC life span
2. it decreases to what?

A
  1. 120 days

2. 40 days

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22
Q

20
cardiac arrest (24-36 hours post burn):
1. what type burn is high risk for cardiac arrest?
2. why?

A
  1. electrical/ high voltage burn

2. damage to myocardial conduction system

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23
Q

21
Respiratory effects: Carbon monoxide poisoning-
1. how is it measured?
2. what does it come from?
3. what is COs affinity to Hgb? what does this cause?

A
  1. measured by carboxyhgb levels (normal is <1%/ smokers are approx 10%).
  2. odorless, non irritating comes form incomplete combustion of carbon products
  3. CO affinity is 200x greater than O2; causes shift to the left (oxygen is left on-cant release).
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24
Q

22

  1. what does CO poisoning cause?
  2. what is the treatment?
  3. what is the half life of CO
    a) without treatment?
    b) with 100% oxygen?
    c) with hyperbaricc chamber?
A
  1. leads to anemic hypoxia (causes seizures, MI).
  2. 100% oxygen by mask or hyperbaric chamber
  3. a) 4 hours
    b) 1 hour
    c) 0.5 hour (at 2-3 atmospheres)
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25
Q 
23
carbon monoxide poisoning symptoms:
1. less than 15-20=
2. 20-40=
3. 40-60=
4. >60=
A
  1. headache, dizziness, confusion
  2. n/v, disorientation, visual disturbance
  3. agitation, combativeness, hallucinations, coma, shock
  4. death
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26
Q

24
inhalation injury:
2 types:

A
  1. direct thermal inury

2. parenchymal injury

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27
Q 
25
inhalation injury:
direct thermal injury:
1. cause?
2. side effects?
A
  1. from inhaling super heated air, flames
  2. leads to:
    • edema of upper airway;
    • obstruction (may take 48 hours to progress)
    • 70-80% obstructed causes stridor (which may be an impending total airway obstruction).
28
Q

26
inhalation injury: Parenchymal lung injury:
1. what causes it?
2. what does it cause (5 things)?
3. what does this lead to regarding patient ventilation issues?

A
  1. inhalation of steam, smoke, toxic fumes containing aldehydes, H2SO4 (sulferic acid), soot, particulate matter causes degeneration of lung tissue.
  2. mucosal edema, decreased cilliary cells, decreased surfactant (type II) cells, tracheobronchitis, V/Q mismatch.
  3. increased airway resistance and decreassssed lung comppliance equals increased work of breathing.
29
Q

27
inhalation injury
1. why do these patients need a higher minute ventilation from a metabolic standpoint?
2. what else might be going on with the lung that would speed up rate?

A
  1. to increase o2 utilization and co2 clearance
    (rate may be 26 just to clear all the extra co2 from being hypermetabolic).
  2. lung may be ineffecient at oxygen exchange d/t damage.
30
Q

28
metabolic effects:
1. what is the “state” burn patients go into?
2. what is this “state”? How much greater will BMR be above normal?
3. what does this state cause in regards to co2 and o2?
3.

A
  1. “Hypercatabolic” state
  2. BMR increases linearly with burn size and will begin to catabolize own tissues for fuel; greater than 2x the norm with
  3. increase in O2 consumption and increased CO2 production
31
Q

29

  1. what is catabolic?
  2. in a hypercatabolic, what is being mobilized?
A
  1. breaking down of one’s own muscle and tissue for food (opposite of anabolic).
  2. neuro-humoral mechanisms mobilize substrates for wound healing i.e.
    a-increased catecholamine release
    b-increased catabolic hormones
    -increased cortisol releases aminos for building
    -increased GH increases serum lipids as energy source
    -increased glucagon leads to hyperglycemia
    2.
32
Q

30

  1. what are side effects of hypermetabloic state if not treated properly?
  2. what type of diet is best for this patient? why?
A
  • Protein, fat and carbohydrate metabolism are increased. Inadequate nutrition leads to body wasting, decreased immunity and altered wound healing.
    2. high calorie, high protein diet, increase O2 to maximize ventilation (this helps to decrease BMR).
33
Q 
31
hypercatabloic state:
body temp:
1. what happens to body temp after a burn?
2. what should you do?  why?
A
  1. body resets thermostat to higher temp which increases BMR

2. keep the room warm so that the patient doesnt waste more energy trying to maintain his/her body temp

34
Q

32

s/s of stress response?

A

tachycardia, autonomic changes, (acidosis in high voltage injury).

35
Q

33
renal effects of burns:
1. what happens to the kidneys (a,b,c)?
2. what will the body/brain do in response?
3. what will inadequate fluid resuscitation cause?
4. what is the most sensitive indicator of volume status and peripheral perfusion?
5. what is the minimal urine output for:
a) adults?
b) children under age ___?
c) adults with high voltage burns?

A
  1. due to fluid loss,
    - -a)the kidneys are hypoperfused
    - -b)toxins and cellular debris clog kidneys (myoglobin causes ATN
    - -c)metabolic acidosis decreases kidney function
  2. body releases ADH to conserve H2O
  3. oliguria
  4. urine output
  5. a)0.5 ml/kg
    b) 1.0 ml/kg
    c) 1-1.5 ml/kg
36
Q 
34
GI effects:
1. how much of TBSA must be burned in order to have paralytic ileus?
2. how long does it last?
3. what does it cause?
4. what is the treatment?
A
  1. 15%
  2. 3-5 days
  3. increased risk of aspiration
  4. (NGT to decompress)
37
Q 
35
GI effects:
1. what is the name of the stress ulcer of the duodenum associated with burns?
2. what is the incidence and tx?
3. what other ulcers may occur?
A
  1. Curling’s ulcer
  2. 86% without treatment; treatment is prophylactic antacids and H2 blockers
  3. gastric ulcers
38
Q 
36
GI effects:
liver hypoperfusion:
1. what does it lead to?
2. what does this do to certain meds?
3. what is late jaundice associated with?
A
  1. decreased function (less detoxification capacity, decreased levels of albumin, increased levels of AAG (alpha-1-acid-glycoprotein)
  2. decreased albumin causes higher FREE fraction of albumin bound drugs such as benzos and dilantin;
    increased levels of AAG cause increased binding of drugs such as MRs, lidocaine and propanolol.
  3. late jaundice is associated with high mortality
39
Q

37
Neurological effects:
1. what things associated with burns affect the cns?

A

1.

a) carbon monoxide poisoning
b) anoxia and hypovolemia decrease LOC
c) high voltage injury short circuit CNS, cause paralysis, respiratory arrest and MI

40
Q

38
hematological effects:
1. infection does what to coagulation (2 disorders)?
2. what happens to platelets?
3. rbcs are altered how?
4. what immunological responses are activated by tissue damage? what does this cause cardiovascularly, resp, hematologically, integ (4 things)?

A
  1. activates coag pathway, may lead to DIC or coagulopathy (by using up all of the clotting factors)
  2. platelet function is qualitatively and quantitatively depressed (thrombocytopenia with less function)
  3. rbc live decreases to 40 days
  4. inflammatory responses are initiated causing tachycardia, hyperthermia, hyperventilation and leukocytosis
41
Q

39
Infection/ sepsis
1. what can you do to limit infection?
2. what organism/bacterial biproduct leads to septic shock?
3. besides loss of barrier and burned skin being a good medium, why are they at risk for infection?
4. what other actions (besides mentioned in #1) can help prevent infection?

A
  1. isolation and strict aseptic technique
  2. enterococci (endotoxins)
  3. phagocytic and chemotactic properties of WBCs are altered (altered/depressed immune system)
  4. debridment and covering of viable skin (either enzymatically or by excision and grafting), antibiotics
42
Q

40

Initial preop assessment should consist of chart review: what are you looking at/for?

A
  1. check initial H&P (see what happened, when etc to devise plan of care).
  2. review old anesthesia records: see what meds and methods have been used for previous surgeries
  3. make sure there is a surgical and anesthesia consent
  4. chart summary: check for current meds, urine output over last 24 hours, recent labs, ekg, cxr
  5. review progress notes from last operation
43
Q

41
preop assessment: patient assessment
1. what should you check in order to plan your case?

A
  1. extent and location of injury
  2. vital signs (& method of measurement (art line, cvp)
  3. venous access/ location and guage (should be large bore or central line)
44
Q 
42
pre-op assesment: patient physcal assessment
1. Airway 
2. CNS
3. renal status
4. nutrition
A
  1. Airway: is the patient intubated, trach, on vent, what settings. if not intubated, can they be- rom of neck, strictures from burnt skin, may need FOB (fiber optic bronchoscope) to intubate, assess for stridor, hoarseness, can they open their mouth?
  2. mental status, peripheral nerve function
  3. bun, creat, urine output
  4. NGT, feeding tube -dobhoff/peg(if not held, will need to stop the feed- treat as a full stomach), tpn (take it with you-keep it going)
45
Q

43
perianesthesia considerations
1. what questions should you be asking?

A
  1. what is the procedure, what % tbsa will they be working on, is it grafting & from where will the donor site be(will the patient need to be flipped), how will they be positioned, length of procedure
46
Q

44
peri anesthetic considerations:
iv access, how is blood pressure checked?

A
  1. you NEED 2 large bore (preferably 18g) or 1 central line with CVP
  2. blood pressure from where (art line, arm cuff - placed where? etc).
47
Q

45
peri-anesthetic considerations:
1. what should you have in the room before the case?
2. if large amounts of grafting, what might you do?

A
  1. 2-4 units of blood

2. start the blood before the procedure or you may get behind

48
Q

46
OR room prep
1. think ahead means what (14 things)?

A
  • have a plan A & B
  • make sure the room is warm
  • ANESTHESIA MACHINE CHECK!!!
  • table top is set up (NO sux)
  • make sure you have all of your monitoring equipment,
  • suction,
  • leads (or use needle leads),
  • blood warmers (x2),
  • esophageal stethoscope,
  • make sure you can take a temperature,
  • make sure you can take a BP,
  • make sure there is some place to take a pulse ox,
  • make sure there is a foley,
  • how will you work your PNS (will the leads stick or do you need needles?).
49
Q

47
anesthetic management:
1. what should you consider and find out where your patient is in…
2. why

A
  1. 3 phases of burn recovery

2. dictates your fluid management and what urine outputs you will have

50
Q

48

  1. what are the phases of burn recovery?
  2. what happens in the first phase?
A
  1. resuscitation phase, post-resuscitation phase, rehabilitation phase
  2. initial resuscitation (fluids etc.)- first 36-48 hours post burn; patients are extremely unstable cardiovascularly
51
Q 
49
post resuscitation phase
1. Starts...
2. Lasts...
3. What happens?
4. When does it end?
A
  • starts after 36-48 hrs. lasts 3-6 days,
  • patients become hypermetabolic,
  • go thru inflammation stage,
  • develop multi-organ failure,
  • wound closures are initiated in this phase,
  • lasts until wound closure is complete
52
Q

50

rehabilitation phase

A

chronic sequale of the patients burns are addressed

53
Q

51

preopertive medication: what should you know as far as current meds, and future meds?

A
  1. what meds the patient is already on (ativan gtt, morphine gtt etc.)
  2. will patient need fentanyl for transfer to OR bed
  3. will the patient be an awake FOB, you will need airway prep
54
Q

52
induction options:
regional, mask, other options to consider

A
  1. regional- is it possible (only if small area)
  2. mask case-can it be done- burns to face? unstable airway?
  3. is patient already intubated?
  4. will it be a difficult intubation d/t airway burns, neck and face scars and/or contractures; positioning concerns? awake vs. asleep?
55
Q

53

awake vs. asleep intubation: options with both

A
  1. direct oral or nasal ETT
  2. indirect NET (endotrol)
  3. indirect OET (intubating LMA)
  4. FOB
56
Q

54

best induction agents: 5 best:

A
  1. etomidate if really sick (hypotensive)
  2. decreased doses of pentothal or propofol (watch BP)
  3. fentanyl to blunt response of catecholamines
  4. ketamine is good
  5. versed or valium
57
Q

55

  1. muscle relaxants: sux?should I use it?
  2. what can happen?
  3. what if only slight burns, can I use it?
  4. how long after burn should sux not be given?
A
  1. do not use SUX-
  2. burn patients have heightened response which releases high amounts of K+ causing cardiac arrest
  3. No. K+reaction happens with patients with as little as 8% TBSA burn
  4. avoid sux from 24 hours to 2 years after burn.
58
Q

56
what NDMR should be used:
1. how do I choose?
2. what about burns changes the potency and duration of MRs?

A
  1. base on duration of case and presence of co-existing disease that might affect metabolism of drug
  2. may be more resistant to MRs d/t:
    a) increased BMR,
    b) increased AAG (which binds MRs-less free fraction to get to target),
    c) altered receptor affinity
    d) up regulation= more EJRs to share drug
59
Q

58

  1. how much blood loss from grafting 1% of TBSA?
  2. what else should be given after multiple blood tx?
A
  1. 200-400 ml of blood

2. give calcium to prevent arrhythmias (also 1 gm for every 3 units of blood d/t preservatives in blood).

59
Q

57
anesthesia maintainance:
what agents and vent modes?

A
  1. TIVA if using floor ventilator for special modes (unable to administer gas)
  2. O2, N2O, MR, narcotic, low dose VAs
  3. due to increased co2 production and o2 demand, may need high minute volumes
60
Q 
59
rules of thumb:
1. blood?
2. resp?
3. cv/volumes
4.temp?
A
  1. start early, replace based on formula, may need FFP etc.
  2. remember monitors, plan for airway- induction, maintainance, emergence, bronchodilators etc. abg, pulse ox, humidifie o2
  3. are we doing colloids, crystaloids (where is patient at in phases of burn), electrolytes for arrhythmias
  4. keep them warm (fluids warmer, forced air, room warm).
61
Q 
60
emergence
questions to ask re:
1. reversal
2. pain
3. where is the patient going? should I extubate?
A
  1. reverse MRs (or are they going to aicu)
  2. do they need more narcotic
  3. return patient in same condition as they were when they went (if possible…if not on vent prior, extubate etc.).
62
Q

61

post op complications (the 4 hypos)

A
  1. hypotension
  2. hypothermia
  3. hypocalcemia
  4. hypoxemia
63
Q 
62
grades of grafting: what is involved (ebl, duraton, anesthesia)
1. grade I
2. grade II
3. grade III
A
  1. I-10% tbsa, 30-90 min
  2. II-10-30%, 60-240 min, 500-2500 EBL; narcotic, N2o, MR, VA
  3. III->30%, >120 min, >3000 ebl, high dose narcotic + MR
64
Q 
If patient has smoke inhalation, burns causing inability to flex neck, & needs intubation which is best choice?
A. Awake glidescope
B. Blind Nasal intubation
C. trach
D. Standard intubation?
A

A. Awake glidescope

b. princip. exam 2 (w13) (5 decks)

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