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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
rare type of burn mechanism
chemical burns
26
**which is a worse burn, acid or alkali
alkali, causes deeper more penetrating burns
27
alkali burns cause
protein denaturation
28
which acid are we concerned with
hydrofluoric acid or tar - very difficult to get off
29
*hydrofluoric acid or tar causes
severe hypocalcemia
30
where does decontamination occur
outside entrance to ER
31
assess this in electrical burns
high or low current what is the voltage entrance and exit site
32
what is electroporation
``` destroys tissue along the current line internal damage (tissue necrosis and death) ```
33
inhalation burns can happen w/which mechanism/causative agent
thermal/chemical
34
inhalation injury has 2 types of inhalation
supraglottic (thermal burn) | subglottic (chemical burn)
35
what are we worried about with inhalation injury
airway and inflammation (airway obstruction) | in lungs as well
36
if we suspect inhalation injury
ET tube | intubate - don't want to loose airway from edema
37
manifestations of supraglottic inhalation burn
hoarseness | dry cough
38
manifestations of subglottic inhalation burn
wheezing tachypnea stridor eventually aveoli fills with fluid causing edema - flooded aveoli causes decreased gas exchange
39
*anybody with inhalation burn/injury is at risk for
hypoxemia
40
hypoxemia vs hypoxia
hypoxemia - decreased oxygen in the blood | hypoxia - decreased oxygen to the tissue caused by hypoxemia
41
respiratory unit of the lung is called
aveoli
42
how do you know whose had an inhalation injury
***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
hypoxemia is determined by
``` low PaO2 (O2 levels in blood) in an arterial blood gas low = hypoxemia ```
44
hypoxia is caused by
hypoxemia
45
When I become hypoxic (decreased oxygenation to tissue) what happens to my metabolism
goes from aerobic to anaerobic causing lactic acidosis
46
what is carboxyhemoglobin
carbon monoxide bound to hemoglobin | happens with inhalation injuries (carbon monoxide)
47
how can we determine carboxyhemoglobin
draw a carboxyhemoglobin level (COHgb) suspected with singed nares, soot table 20-2 in Sole***
48
percentages of COHgb r/t signs/symptoms
60% - coma and death
49
why are COHgb percentages important
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
what causes radiation burns
oncology pt/trt
51
what are the zones of injury
zone of coagulation zone of stasis zone of hyperemia
52
what is the zone of stasis
outer edge of tissue damage
53
what is the zone of coagulation
area that met with the highest temp of heat - where most damage occurs
54
what is the zone of hyperemia
area least damaged
55
burns are classified by
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
***what are the cardinal determinants of survival
patients age and the size of the burn (total body surface area - provided as a percent)
57
depths of injury
superficial - 1st degree (1st layer/epidermis) partial thickness burns (2 types) - second degree full thickness - 3rd degree
58
what are the 2 classifications of Partial Thickness burns (second degree burns)
partial thickness superficial | deep partial thickness
59
its only a 1st degree burn if it ONLY says
superficial - sunburn (never see blisters)
60
we NEVER use superficial burns in our total body surface area of a burn pt, t or f
true
61
***manifestations of partial thickness superficial burn
``` wet/weepy blanch white return to color briskly might have a blister painful light red or mottled ```
62
***manifestations of deep dermal partial thickness burn
not characterized by blister formation pale mottled - patchy white no weeping prolonged healing - usually require grafting for better outcomes
63
***manifestations of full thickness burns
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
when assessing a burn you want to know
``` mechanism (thermal or chemical) how long exposed to heat depth 1st, 2nd, or 3rd degree TBSA (total body surface area) ```
65
TBSA is calculated by using the rule of
9's
66
circumferential burn measurements
``` head - 9% (4.5%) arm - 9% (4.5%) legs - 18% (9%) torso - 36% (18%) perineum (1%) ```
67
with perineum burn what intervention should be used
catheter - prior to edema (intra-abdominal pressure monitors attached)
68
what is initial emergency burn mgmt
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
pt with massive TBSA burns of >35% have
increased metabolic response, provide nutrition
70
burns cause
hyper-metabolic states
71
when does the resuscitative phase begin
as soon as burn injury occurs
72
from the time the injury occurs up to 36 hrs after injury is crucial, t or f
true - 1st respondents begin fluid resuscitation and intubate with inhalation injury to improve pt. outcomes
73
can we put ice on a pt with a deep dermal injury
NEVER - causes vasoconstriction - further depleting the blood supply
74
do we remove adherent tar
no
75
do we remove clothes stuck to the skin
no
76
why do we want to do an arterial line right away
edema | worried about shock - monitor BP (want MAP >60)
77
TBSA is used to estimate how much fluid resuscitation is required for the burn injury, t or f
true
78
formula we use to fluid resuscitate burns
parkland formula
79
***what is the parkland formula
Lactated Ringers 4ml(kg)(TBSA burned) divide by 2 = amt. given in first 8 hrs, second half given over next 16 hrs.
80
sequencing for burns
start 2 Lg (18G) bore IV's | draw labs
81
***what fluids do we give for burns
Lactated Ringers
82
***while giving fluid resuscitation accurately measure
urine output
83
***formula for urine output
0.5-1.0/ml/kg/hr
84
how often do we check peripheral vascular pulses
every 15 minutes - push through the edema
85
normal basic metabolic electrolytes in burn pt due to tissue damage are
hyperkalemia (high potassium) hyponatremia (low sodium) continuous EKG monitor
86
with high potassium levels what intervention should be done and why
continuous EKG monitor - monitor for dysrhythmias (peak T waves)
87
do we give insulin and dextrose to pt in the first 36hrs.
no
88
after the first 24-36 hrs up to 6 days anticipate electrolytes like this
hypokalemia - hypocalcemia - hypophosphatemia - hypomagnesemia - hypernatremia - keep on EKG monitor
89
don't replace electrolytes until after 1st 24-36 hrs
true
90
burn shock is a combination of these types of shock
distributive and hypovolemic shock

CCM (13 decks)

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