burns Flashcards
3 layers of the skin
epidermis, dermis, hypodermis/subcutaneous
any wound alters and disrupts ______ and ______ of the skin but is dependent on the individual wound
anatomic and physiologic function
wounds heal by ______ or ________ formation depending on extent of tissue involvement
regeneration or scar formation
wounds can be ________, ________ ________, or _______ _________
superficial, partial thickness, or full thickness
phases of wound healing
- inflammatory phase
- proliferation phase
- remodeling/maturation
the inflammatory phase is also the
lag or exudative phase
duration of the inflammatory phase
1-4 days
what happens during the inflammatory process
blood clot forms; wound becomes edematous; debris of damaged tissue and blood clot are phagocytosed
proliferation phase is also known as the
fibrolastic or connective tissue phase
duration of proliferative phase
5 - 20 days
what happens during the proliferation phase
collagen produced; granulation tissue forms; wound tensile strength increases
remodeling phase is also known as the
maturation phase
duration of remodeling phase
21 days to months or even years
what happens during the remodeling phase
fibroblasts leave wound; tensile strength increases; collagen fibres reorganize and tighten to reduce scar size
burn injuries usually result from
energy transfer from a heat source to the body in which the agent exceeds the threshold for resistance
most burn injuries occur in
the home
2 most common burn etiologies are
flame and cold
gerontologic considerations
- 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
3 types of energy that cause burn injuries
- thermal
- chemical
- electrical
thermal injuries
- the most common type of burn injury
- varies according to severity
- better prognosis
most common type of burn injuries
- flame source
- scald burns from steam
- contact with a hot object
3 distinct zones that appear in a bull’s eye pattern
- zone of coagulation
- zone of stasis
- zone of hyperemia
zone of coagulation
tissue is completely destroyed -> cellular death
zone of stasis
- surrounds non-viable tissue
- compromised blood supply, inflammation and tissue injury -> potentially viable
zone o f hyperemia
- blood flow secondary to the natural inflammatory response
- sustains least amount of damage
electrical injuries
electricity travels the path of least resistance; therefore tissue, nerves, and muscle are easily damaged, bone is not
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
chemical injuries
result from contact, ingestion, inhalation or injection of acids, alkalis or vesicants - blistering agents
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
_______ ________ is a critical element in determining the severity of the injury
contact time
pathophysiology of burns
- cell damage
- increase vascular permeability
- fluids, electrolytes, proteins move from the intravascular to interstitial space
- decrease tissue perfusion
decrease tissue perfusion in burns can lead to
- edema formation
- hypovolemic shock - BURN SHOCK
burn shock (hypovolemic) from burns can cause
vasoconstriction
Phases of burn management
- emergent / resuscitative
- acute / intermediate
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
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
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
signs of cerebral hypoxia
- restlessness
- confusion
- difficulty responding to questions
- decrease LOC
when does the acute/intermediate phase of burn management occur
begins 48-72 hrs post burn injury
what are focused assessments in the acute / intermediate phase
- maintenance of respiratory and circulatory status
- fluid and electrolyte balance
- GI function
priorities of care in acute/intermediate phase
- infection prevention
- burn wound care
- pain management
- nutritional support
other important assessments for burn pts
- determine the depth of burn damage
- ABG - hypoxemia, metabolic acidosis
- carboxyhemoglobin level
- CBC, creatinine and myoglobin levels
- electrolytes
what is the carboxyhemoglobin level
extent of smoke inhalation
what would you expect the creatinine and myoglobin levels to be in a burn pt and why
increased due to muscle damage
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
classification of burn injuries
- depth
- considerations in determining depth
- superficial burns
- superficial partial thickness
- deep partial thickness burns
- full thickness burn
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
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
superficial burns
- damages only the dermis
- pink or red
- dry
- slight swelling; no blister formation
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
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
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
what is TBSA
estimated % of total body surface area
- rule of nines
what is rule of nines
anatomic body parts are counted as multiples of 9%
deep partial thickness burns TBSA
<15% TBSA in adults or <10% in children
full thickness burns TBSA
<2% TBSA not involving special care areas
moderate, uncomplicated burn injury
- deep partial thickness burns of 15-25% TBSA in adults or 10-20% in children
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
parkland baxter formula for fluid restriction
- first 24 hrs crystalloids
- 24 hrs colloids
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
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
hemodynamic instability
fluid lost from the vascular, interstitial, and cellular compartments
- hypovolemic shock - BURN shock
hemodynamic instability begins
almost immediately with injury to capillaries in the burned area and surrounding tissue
what to expect in hemodynamic instability
decrease CO
increase PVR
decrease perfusion of vital organs
respiratory system dysfunction
smoke inhalation and post burn lung injury
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
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
carbon monoxide
colorless, odorless, tasteless, nonirritating gas produced from incomplete combustion of carbon-containing materials
carbon monoxide poisoning
affinity of hemoglobin for CO is 200x greater than for oxygen
hypermetabolic response
stress of burn injury increased metabolic and nutritional requirements
what is increased during hypermetabolic response
catecholamines and cortisol increased in an attempt to maintain homeostasis; heat production increase to balance heat losses
hyper metabolism and stress peaks includes
glycolysis, proteolysis, lypolysis
hypermetabolism and stress peaks at
7-17 days post burn
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
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
how can the GI tract be affected in burn pts
- gastric dilation and decreased peristalsis
- acute ulceration of the stomach and duodenum
neurological changes that can occur in burn pts
- neurological damage; head injuries, carbon monoxide poisoning, fluid volume deficit, hypovolemia
- d/t periods of hypoxia
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
_______ is a significant complication of the acute phase of burn injury
sepsis
