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CCM > Burns > Flashcards

Burns Flashcards

1
Q

the most lethal form of trauma

A

burns

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2
Q

Pathophysiology of burns

A

tissue damage caused by enzyme malfunction and denaturation of proteins
prolonged hi temps = cell necrosis = protein coagulation
varying degrees of damage (zones of injury)

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3
Q

what should community hospitals do when receiving burn patients

A

refer to burn centers for best trt/outcomes possible

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4
Q

research advances in burns (2 primary)

A
  • fluid resuscitation
  • early excision - escharotomy (slice through edema/eschar to expand area to maintain intravascular circulation to extremities)
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5
Q

what happens to an extremity after massive edema and thick scar tissue formation from a terrible burn

A

swelling causing loss of perfusion and circulation

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6
Q

what areas of the body do commonly perform escharotomies

A

chest and abdomen

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7
Q

largest organ of human body

A

skin

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8
Q

2 major layers of the skin

A

epidermis (outermost layer of skin)
dermis (lies beneath epidermis)
subcutaneous tissue (connected to bones/organs)

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9
Q

an epidermal burn is more serious than a dermal burn, t or f

A

false - a dermal burn is more severe

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10
Q

**does the epidermis have blood supply

A

no - the dermis has blood supply

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11
Q

what type of blood supply does the dermis have

A

blood, vascular and collagen supply, sweat glands and lymph vessels

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12
Q

with damage to dermis the patient will have impaired

A

temp regulation (hypothermia) and coagulopathies (more severe burn)

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13
Q

what type of burn has more feeling epidermal or dermal

A

epidermal - comes with a lot of pain - neurons intact

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14
Q

***what does the skin actually do

A 
maintains body temp
cosmetic appearance 
Vitamin D production (metabolic activity)
immunologic protection
barrier to evaporative water loss
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15
Q

patients with injuries will be susceptible to

A 
hypothermia
massive water loss
huge metabolic deficiencies
decreased Vit D production
depleted immunologic protection
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16
Q

long term (past 36 hrs up to a year) nursing dx

A

impaired self perception/esteem

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17
Q

Patients chance of survivability estimations decrease if they fall between these two ages

A

aging (due to co-morbidities)

very young

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18
Q

mechanism of injury/causative agent of burns

A

thermal
chemical
electrical
inhalation

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19
Q

pt with this type of burn have different treatment modalities

A

inhalation and electrical burn injuries

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20
Q

why are electrical and inhalation burns trt’d differently

A

they’re having internal problems (breathing) r/t lungs/esophagus

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21
Q

the most common type of burn

A

thermal burn

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22
Q

what causes thermal burns

A

scalding hot water
fire
hot stove

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23
Q

what do we want to assess with thermal burns

A

temperature estimation

time of exposure

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24
Q

population at highest risk for thermal burns

A

*children aged 2-4

15-29 year old

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25
Q

rare type of burn mechanism

A

chemical burns

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26
Q

**which is a worse burn, acid or alkali

A

alkali, causes deeper more penetrating burns

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27
Q

alkali burns cause

A

protein denaturation

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28
Q

which acid are we concerned with

A

hydrofluoric acid or tar - very difficult to get off

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29
Q

*hydrofluoric acid or tar causes

A

severe hypocalcemia

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30
Q

where does decontamination occur

A

outside entrance to ER

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31
Q

assess this in electrical burns

A

high or low current
what is the voltage
entrance and exit site

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32
Q

what is electroporation

A 
destroys tissue along the current line 
internal damage (tissue necrosis and death)
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33
Q

inhalation burns can happen w/which mechanism/causative agent

A

thermal/chemical

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34
Q

inhalation injury has 2 types of inhalation

A

supraglottic (thermal burn)

subglottic (chemical burn)

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35
Q

what are we worried about with inhalation injury

A

airway and inflammation (airway obstruction)

in lungs as well

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36
Q

if we suspect inhalation injury

A

ET tube

intubate - don’t want to loose airway from edema

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37
Q

manifestations of supraglottic inhalation burn

A

hoarseness

dry cough

38
Q

manifestations of subglottic inhalation burn

A

wheezing
tachypnea
stridor
eventually aveoli fills with fluid causing edema - flooded aveoli causes decreased gas exchange

39
Q

*anybody with inhalation burn/injury is at risk for

A

hypoxemia

40
Q

hypoxemia vs hypoxia

A

hypoxemia - decreased oxygen in the blood

hypoxia - decreased oxygen to the tissue caused by hypoxemia

41
Q

respiratory unit of the lung is called

A

aveoli

42
Q

how do you know whose had an inhalation injury

A

clinical alert box on pg 618 in Sole
soot in nares
singed facial hair, brows
sometimes can smell it
assess nasal openings (flare in resp. distress/soot)

43
Q

hypoxemia is determined by

A 
low PaO2 (O2 levels in blood) in an arterial blood gas
low = hypoxemia
44
Q

hypoxia is caused by

A

hypoxemia

45
Q

When I become hypoxic (decreased oxygenation to tissue) what happens to my metabolism

A

goes from aerobic to anaerobic causing lactic acidosis

46
Q

what is carboxyhemoglobin

A

carbon monoxide bound to hemoglobin

happens with inhalation injuries (carbon monoxide)

47
Q

how can we determine carboxyhemoglobin

A

draw a carboxyhemoglobin level (COHgb)
suspected with singed nares, soot
table 20-2 in Sole***

48
Q

percentages of COHgb r/t signs/symptoms

A

60% - coma and death

49
Q

why are COHgb percentages important

A

pt need to be placed on high amt of O2, 100% FIO2
recovery time is faster
if s/s of inhalation injury = don’t wait for results

50
Q

what causes radiation burns

A

oncology pt/trt

51
Q

what are the zones of injury

A

zone of coagulation
zone of stasis
zone of hyperemia

52
Q

what is the zone of stasis

A

outer edge of tissue damage

53
Q

what is the zone of coagulation

A

area that met with the highest temp of heat - where most damage occurs

54
Q

what is the zone of hyperemia

A

area least damaged

55
Q

burns are classified by

A

size (to outer edges of zone of hyperemia) - total surface area AND depth (the worst at zone of coagulation) - harder time healing
type of burn (thermal, chemical) AND location
how old is the pt
do they have a past med. hx (diabetes, kidney disease)

56
Q

***what are the cardinal determinants of survival

A

patients age and the size of the burn (total body surface area - provided as a percent)

57
Q

depths of injury

A

superficial - 1st degree (1st layer/epidermis)
partial thickness burns (2 types) - second degree
full thickness - 3rd degree

58
Q

what are the 2 classifications of Partial Thickness burns (second degree burns)

A

partial thickness superficial

deep partial thickness

59
Q

its only a 1st degree burn if it ONLY says

A

superficial - sunburn (never see blisters)

60
Q

we NEVER use superficial burns in our total body surface area of a burn pt, t or f

A

true

61
Q

***manifestations of partial thickness superficial burn

A 
wet/weepy
blanch white return to color briskly
might have a blister 
painful
light red or mottled
62
Q

***manifestations of deep dermal partial thickness burn

A

not characterized by blister formation
pale mottled - patchy white
no weeping
prolonged healing - usually require grafting for better outcomes

63
Q

***manifestations of full thickness burns

A

damage all the way to the subcutaneous tissue
brown, leathery, white or charred
painless
heal by contraction - have to do skin grafting
monitor for non-infection wound healing

64
Q

when assessing a burn you want to know

A 
mechanism (thermal or chemical)
how long exposed to heat
depth
1st, 2nd, or 3rd degree
TBSA (total body surface area)
65
Q

TBSA is calculated by using the rule of

A

9’s

66
Q

circumferential burn measurements

A 
head - 9% (4.5%)
arm - 9% (4.5%)
legs - 18% (9%)
torso - 36% (18%)
perineum (1%)
67
Q

with perineum burn what intervention should be used

A

catheter - prior to edema (intra-abdominal pressure monitors attached)

68
Q

what is initial emergency burn mgmt

A

maintain body temp (high risk for hypothermia)
maintain intravascular fluid volume - massive fluid resuscitation
protect immune response (monitor for sepsis/septic shock, BURN SHOCK)
minimize disability - prevent contractures
decrease metabolic demands

69
Q

pt with massive TBSA burns of >35% have

A

increased metabolic response, provide nutrition

70
Q

burns cause

A

hyper-metabolic states

71
Q

when does the resuscitative phase begin

A

as soon as burn injury occurs

72
Q

from the time the injury occurs up to 36 hrs after injury is crucial, t or f

A

true - 1st respondents begin fluid resuscitation and intubate with inhalation injury to improve pt. outcomes

73
Q

can we put ice on a pt with a deep dermal injury

A

NEVER - causes vasoconstriction - further depleting the blood supply

74
Q

do we remove adherent tar

A

no

75
Q

do we remove clothes stuck to the skin

A

no

76
Q

why do we want to do an arterial line right away

A

edema

worried about shock - monitor BP (want MAP >60)

77
Q

TBSA is used to estimate how much fluid resuscitation is required for the burn injury, t or f

A

true

78
Q

formula we use to fluid resuscitate burns

A

parkland formula

79
Q

***what is the parkland formula

A

Lactated Ringers
4ml(kg)(TBSA burned)
divide by 2 = amt. given in first 8 hrs, second half given over next 16 hrs.

80
Q

sequencing for burns

A

start 2 Lg (18G) bore IV’s

draw labs

81
Q

***what fluids do we give for burns

A

Lactated Ringers

82
Q

***while giving fluid resuscitation accurately measure

A

urine output

83
Q

***formula for urine output

A

0.5-1.0/ml/kg/hr

84
Q

how often do we check peripheral vascular pulses

A

every 15 minutes - push through the edema

85
Q

normal basic metabolic electrolytes in burn pt due to tissue damage are

A

hyperkalemia (high potassium)
hyponatremia (low sodium)
continuous EKG monitor

86
Q

with high potassium levels what intervention should be done and why

A

continuous EKG monitor - monitor for dysrhythmias (peak T waves)

87
Q

do we give insulin and dextrose to pt in the first 36hrs.

A

no

88
Q

after the first 24-36 hrs up to 6 days anticipate electrolytes like this

A

hypokalemia - hypocalcemia - hypophosphatemia - hypomagnesemia - hypernatremia - keep on EKG monitor

89
Q

don’t replace electrolytes until after 1st 24-36 hrs

A

true

90
Q

burn shock is a combination of these types of shock

A

distributive and hypovolemic shock

CCM (13 decks)

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