1
Q
3 layers of the skin
A
epidermis, dermis, hypodermis/subcutaneous
2
Q
any wound alters and disrupts ______ and ______ of the skin but is dependent on the individual wound
A
anatomic and physiologic function
3
Q
wounds heal by ______ or ________ formation depending on extent of tissue involvement
A
regeneration or scar formation
4
Q
wounds can be ________, ________ ________, or _______ _________
A
superficial, partial thickness, or full thickness
5
Q
phases of wound healing
A
- inflammatory phase
- proliferation phase
- remodeling/maturation
6
Q
the inflammatory phase is also the
A
lag or exudative phase
7
Q
duration of the inflammatory phase
A
1-4 days
8
Q
what happens during the inflammatory process
A
blood clot forms; wound becomes edematous; debris of damaged tissue and blood clot are phagocytosed
9
Q
proliferation phase is also known as the
A
fibrolastic or connective tissue phase
10
Q
duration of proliferative phase
A
5 - 20 days
11
Q
what happens during the proliferation phase
A
collagen produced; granulation tissue forms; wound tensile strength increases
12
Q
remodeling phase is also known as the
A
maturation phase
13
Q
duration of remodeling phase
A
21 days to months or even years
14
Q
what happens during the remodeling phase
A
fibroblasts leave wound; tensile strength increases; collagen fibres reorganize and tighten to reduce scar size
15
Q
burn injuries usually result from
A
energy transfer from a heat source to the body in which the agent exceeds the threshold for resistance
16
Q
most burn injuries occur in
A
the home
17
Q
2 most common burn etiologies are
A
flame and cold
18
Q
gerontologic considerations
A
- impaired senses and reaction times
- tend to incorrectly assess risk
- thinner skin, with decreased microcirculation and increased susceptibility to infection
- morbidity and mortality rates associated with burns are greater than in the older adult
- chronic illness decreases the older adult’s ability to withstand the multisystem stresses resulting from a major burn
19
Q
3 types of energy that cause burn injuries
A
- thermal
- chemical
- electrical
20
Q
thermal injuries
A
- the most common type of burn injury
- varies according to severity
- better prognosis
21
Q
most common type of burn injuries
A
- flame source
- scald burns from steam
- contact with a hot object
22
Q
3 distinct zones that appear in a bull’s eye pattern
A
- zone of coagulation
- zone of stasis
- zone of hyperemia
23
Q
zone of coagulation
A
tissue is completely destroyed -> cellular death
24
Q
zone of stasis
A
- surrounds non-viable tissue
- compromised blood supply, inflammation and tissue injury -> potentially viable
25
zone o f hyperemia
- blood flow secondary to the natural inflammatory response
- sustains least amount of damage
26
electrical injuries
electricity travels the path of least resistance; therefore tissue, nerves, and muscle are easily damaged, bone is not
27
effects of electricity on the body
- type of current (alternating or direct)
- pathway of the current
- duration of contact
- resistance of the body tissue
- amount of voltage
28
chemical injuries
result from contact, ingestion, inhalation or injection of acids, alkalis or vesicants - blistering agents
29
alkaline substances
- not neutralized by tissue fluids as readily as acids
- adhere to tissue causing protein; hydrolysis and liquefaction
- damage occurs rapidly and continues until the pH returns to a normal physiologic level
30
_______ ________ is a critical element in determining the severity of the injury
contact time
31
pathophysiology of burns
- cell damage
- increase vascular permeability
- fluids, electrolytes, proteins move from the intravascular to interstitial space
- decrease tissue perfusion
32
decrease tissue perfusion in burns can lead to
- edema formation
- hypovolemic shock - BURN SHOCK
33
burn shock (hypovolemic) from burns can cause
vasoconstriction
34
Phases of burn management
- emergent / resuscitative
- acute / intermediate
35
emergent / resuscitative management phase
- from onset of injury to completion of fluid resuscitation
- first aid, prevention of shock, prevention of respiratory distress, detection and treatment of concomitant injuries, wound assessment and initial care
36
acute / intermediate management phase
- from beginning of diuresis to near completion of wound closure
- wound care and closure, prevention and treatment of complications including infection, nutritional support
37
what do you assess in immediate care
A- support the airway and protect the cervical spine
B- assesses and promotes breathing
C - apical pulse and BP
neurological status - indications of cerebral hypoxia
38
signs of cerebral hypoxia
- restlessness
- confusion
- difficulty responding to questions
- decrease LOC
39
when does the acute/intermediate phase of burn management occur
begins 48-72 hrs post burn injury
40
what are focused assessments in the acute / intermediate phase
- maintenance of respiratory and circulatory status
- fluid and electrolyte balance
- GI function
41
priorities of care in acute/intermediate phase
- infection prevention
- burn wound care
- pain management
- nutritional support
42
other important assessments for burn pts
- determine the depth of burn damage
- ABG - hypoxemia, metabolic acidosis
- carboxyhemoglobin level
- CBC, creatinine and myoglobin levels
- electrolytes
43
what is the carboxyhemoglobin level
extent of smoke inhalation
44
what would you expect the creatinine and myoglobin levels to be in a burn pt and why
increased due to muscle damage
45
what can you expect electrolytes to look like in a burn pt
- hyponatremia - massive fluid shifts
- hyperkalemia - fluid shifts and cell lysis
- BUN - fluid loss or increase protein breakdown
46
classification of burn injuries
- depth
- considerations in determining depth
- superficial burns
- superficial partial thickness
- deep partial thickness burns
- full thickness burn
47
depth of burn injuries
- depth of tissue destruction
- depth depends on how much the skins dermis is affected
- burn depth determines whether spontaneous healing will occur and helps determine the plan of care
48
considerations in determining depth
- how the injury occurred
- causative agent
- temperature of the burning agent
- duration of contact with the burning agent
- thickness of the skin in area burned
49
superficial burns
- damages only the dermis
- pink or red
- dry
- slight swelling; no blister formation
50
superficial partial thickness
epidermis is destroyed and a small portion of the underlying dermis is injured
- painful, pink and moist
- hair follicles intact; often presents as blisters
- heals in 5 to 10 days without scarring
51
deep partial thickness burns
- extends into the reticular layers of the dermis
- difficult to distinguish from a full-thickness burn
- red or white
- mottled
- moist or fairly dry
- severe pain
- takes up to 14 days to heal with variable amounts of scarring
52
full thickness burn
- involves the total destruction of the dermis and extends into the subcutaneous fat; can also involve muscle and bone
- heals by contraction or epithelial migration; requires skin grafting
- wound color ranges widely from mottled white to red, brown, or black
- wound appears leathery
- hair follicles and sweat glands are destroyed
53
what is TBSA
estimated % of total body surface area
- rule of nines
54
what is rule of nines
anatomic body parts are counted as multiples of 9%
55
deep partial thickness burns TBSA
<15% TBSA in adults or <10% in children
56
full thickness burns TBSA
<2% TBSA not involving special care areas
57
moderate, uncomplicated burn injury
- deep partial thickness burns of 15-25% TBSA in adults or 10-20% in children
58
major burn injury
- deep partial thickness burns >25% TBSA in adults or >20% in children
- all full thickness burns >/= 10% TBSA
- all burns involving special care (eyes, ears, face, hands, feet, perineum, joints)
- all pts with inhalation injury, electrical injury, or concurrent trauma
59
parkland baxter formula for fluid restriction
- first 24 hrs crystalloids
- 24 hrs colloids
60
parkland baxter formula for fluid restriction first 24 hr crystalloids
lactated ringers solution: 4ml/kg per percentage of TBSA burned; 50% given during first in 8 hrs; 25% given during the following 8hrs
61
parkland baxter formula for fluid restriction 24 hrs colloids
- 0.3-0.5 ml/kg per percentage of TBSA burned
- capillary membrane has returned to normal/near normal and plasma remains in the vascular space and expands the circulating volume
- glucose in water; amount to replace estimated evaporative losses
62
hemodynamic instability
fluid lost from the vascular, interstitial, and cellular compartments
- hypovolemic shock - BURN shock
63
hemodynamic instability begins
almost immediately with injury to capillaries in the burned area and surrounding tissue
64
what to expect in hemodynamic instability
decrease CO
increase PVR
decrease perfusion of vital organs
65
respiratory system dysfunction
smoke inhalation and post burn lung injury
66
smoke inhalation and post burn lung injury is injury caused by . . .
- injury caused by toxic gas exposure
- injury above the level of the vocal cords d/t direct heat or chemicals
- injury below the level of the vocal cords causing pulmonary edema, pneumonia and later signs of inflammation
67
manifestations of inhalation injury
- hoarseness, hacking cough, soot in mouth or nose, singed nose hairs
- drooling; inability to handle secretions), darkened sputum, mucosal burns
- laboured and shallow breathing
68
carbon monoxide
colorless, odorless, tasteless, nonirritating gas produced from incomplete combustion of carbon-containing materials
69
carbon monoxide poisoning
affinity of hemoglobin for CO is 200x greater than for oxygen
70
hypermetabolic response
stress of burn injury increased metabolic and nutritional requirements
71
what is increased during hypermetabolic response
catecholamines and cortisol increased in an attempt to maintain homeostasis; heat production increase to balance heat losses
72
hyper metabolism and stress peaks includes
glycolysis, proteolysis, lypolysis
73
hypermetabolism and stress peaks at
7-17 days post burn
74
when pt experiences hypermetabolism + stress what to expect
- tissue breakdown decrease as the wounds heal
- increase O2 consumption
- increase glucose use
- protein and fat wasting
75
why can renal insufficiency occur in burn pts
d/t hypovolemic state, damage to the kidneys at the time of the burn, or administered drugs
76
how can the GI tract be affected in burn pts
- gastric dilation and decreased peristalsis
- acute ulceration of the stomach and duodenum
77
neurological changes that can occur in burn pts
- neurological damage; head injuries, carbon monoxide poisoning, fluid volume deficit, hypovolemia
- d/t periods of hypoxia
78
how can the musculoskeletal system be affected in burn pts
- fractures that occur at the time of the accident
- deep burns extending to the muscles and bones
- hypertrophic scarring and contractures
- increases tissue catabolism = severe protein and fat wasting
79
_______ is a significant complication of the acute phase of burn injury
sepsis
Med-Surg
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