Week 8; Trauma Cont. Flashcards
Burns impact bodily functions in three ways:
Physiologic, metabolic, and psychological
Patho of burn injury
Tissue destruction caused by a burn injury
leads to local and systemic problems that
affect fluid and electrolyte imbalance leading
to protein losses, sepsis, changes in metabolic, endocrine, respiratory, cardiac, hematologic, and
immune functioning.
Types of burns
Heat/thermal, electrical, cold, chemical, radiation, and friction
Heat/Thermal Burn
Caused by fire, liquid, steam, grease, tar,
hot objects. Inhalation injury may occur
Electrical Burn
From electrical current, damages
skin and other structures under skin. Iceberg effect (worse underneath), causes heart muscle and dysrhythmias, muscle damage, and release myoglobin into blood and lead to kidney
damage (acute tubular necrosis).
Cold Burn
Frostbite
Chemical Burn–
Caused by powders, gases, or food (hot
pepper). Acid or base (alkali), watch for inhalation injuries
Radiation Burn–
D/t sun, cancer treatment
Friction Burn –
Abrasions, road rash
Extent of burn injury depends on
Age, general health (diabetes, compromised
circulation, heart failure where heart muscle is
weak), depth and extent of injury, specific body area injured – face/head/neck can
cause respiratory issues, torso can restrict
breathing, perineum can be related to infection, as well as inhalation injury.
Physical skin changes r/t burns
Epidermis can grow back after a burn, sweat
and oil glands and hair follicles extend into the
dermal tissue and regrow to heal partial
thickness wounds. Skin can regrow as long as parts of dermis are left. When entire dermal layer is burned, skin can no longer restore itself.
Functional changes of skin r/t burns
Skin maintains fluid and electrolyte balance. Massive fluid loss occurs through excessive evaporation proportionate to the total body surface area. Full thickness burns destroy sweat glands reducing this ability.
First degree burn
Superficial thickness, least damage; epidermis is only part of skin that is injured. Red, pink and painful, but all nerve endings still there. Warm to touch. Desquamation (peeling of dead skin) occurs
2 to 3 days after burn.
Desquamation
Peeling of dead skin
Second degree burn
Partial Thickness; superficial partial thickness or deep partial thickness. Involves entire epidermis and dermis (varying depths). Shiny and moist, red and pink, blisters, scars can result, very painful.
Third degree burn
Full Thickness; black, yellow, brown, white, or red. Severe and extends into hypodermis, no blisters. Eschar present – hard, leathery. Grafts required. Not as painful, nerve layers destroyed. Destruction of entire epidermis and dermis; skin does NOT regrow.
Fourth degree burn
Deep Full Thickness; worst of all – bone, muscle, ligaments. Black and charred with eschar, pain and sensation is absent, no blisters, grafts required.
Vasular changes r/t burns
Fluid shift after initial vasoconstriction. Blood vessels near the burn dilate and leak fluids into interstitial space. Also called “third spacing” or capillary leak syndrome. Profound imbalance of fluid, electrolyte, acid-base; hyperkalemia and hyponatremia. Fluid remobilization after 24 hour, diuretic stage begins 48 to 72 hour after injury, hyponatremia and hypokalemia occur as potassium moves back into cells.
Cardiac changes r/t burns
Hypovolemic shock—Common cause of
death in early phase in patients with serious
injuries and cardiac rhythm, especially in cases of
electrical burn injuries.
Respiratory changes r/t burns
Occurs even when lung tissues have not
been damaged directly; Burns on nose and mouth
Torso burns – restrictive to chest, impeding
respirations
Histamine, other inflammatory mediators
cause capillaries to leak fluid into pulmonary
tissue space
GI changes r/t burns
Decreased blood flow and sympathetic
stimulation during early phase cause reduced
GI motility, paralytic ileus
GI bleeding – gross and occult
Curling’s ulcer – acute gastroduodenal ulcer
from stress injury, not as common because of
use of H2 histamine blockers and proton
pump inhibitors
Metabolic changes r/t burns
Increased secretions of catecholamines,
antidiuretic hormone, aldosterone, cortisol. Increased core body temperature as
response to temperature regulation by
hypothalamus.
Compensatory responses r/t burns
Inflammatory compensation – triggers healing
bur is also responsible for the fluid shift and
edema and hypovolemic shock.
Sympathetic nervous system compensation –
increased heart rate, increased BP, widen
bronchial passages, slow intestines.
Emergent management of burns
Assess airway (A)
Administer Oxygen (B) Breathing
Maintain Circulation (C) – loosen clothing
Disability (D) - All patients should be assessed for
responsiveness with the Glasgow coma scale; they may be confused because of hypoxia or hypovolemia.
Exposure (E) Cover with linens, blanket – maintain
warm, prevent nerve endings from air currents, security and calm.
Make NPO, start IVs, head to toe
Resuscitation Phase of Burn Injury
First phase after burn, continues for about 24
to 48 hours—until diuresis occurs. Injury is evaluated.
Goals of management during Resuscitation Phase of Burn Injury
Secure airway, support circulation—fluid replacement, keep comfortable with analgesics, prevent infection through careful wound care, maintain body temperature, provide emotional support
Carbon monoxide poisoning –
when a pt breathes CO, it is rapidly transported across lung membrane and binds tightly to hemoglobin, impairs oxygen unloading at tissue level. Assess for cCOHb level, neuro changes – nausea, headache, drowsiness, bright cherry color. Treatment is 100% oxygen on non-rebreather mask to replenish oxygen.
Inhalation injury assessment
Where and how suffered injury, where are burns noted, abnormal sputum, carbonaceous (black soot), charred or singed hair, soot around nose and
mouth, bright red lips, cherry red skin, voice hoarse, brassy cough, anxiety
Heat damage in the pharynx is often
severe enough to produce __ and __ __ __ especially epiglottitis.
edema, upper airway obstruction
During fluid resuscitation
Tissues rehydrate and can swell, intubation ma be performed as an early intervention to prevent obstruction. Continually assess for recognition of edema and obstruction. If signs of pulmonary edema, elevate head of bed to 45 degrees, apply oxygen, contact Rapid Response Team.
Cardiovascular Assessment: Noticing
Changes in the cardiovascular system begin
immediately after the burn injury and include
shock as a result of disrupted FLUID AND
ELECTROLYTE BALANCE. Hypovolemic shock is a common cause of death in the resuscitation phase in patients with serious injuries.
Skin assessment for burns
Size and depth of injury, percentage of total body surface affected (TBSA). “Rule of nines” using multiples of 9% of total BSA, used to calculate surface area. Body fluid shifting and risk for hypovolemia and death. Parkland Burn formula – calculate total volume of fluid needed 24 hours after burn, 2nd degree burn or higher.
Parkland Burn formula –
calculate total volume of fluid needed 24 hours after burn, 2nd degree burn or higher.
Potential complications of burns
Potential for decreased oxygenation, shock, pain (acute and chronic), potential for Acute Respiratory Distress Syndrome (ARDS)
Nursing cares include
Supporting oxygenation, preventing hypovolemic shock, preventing inadequate gas exchange, managing pain and alterations in comfort
Phases of Management
1.Emergent –
Resuscitative, onset with burn, ends with
restoration of capillary permeability, depends on severity. Respiratory Management, hypovolemic shock, swelling, compartment syndrome may occur.
Phases of Management
2. Acute –
Capillary permeability has stabilized, diuresis,
preventing infection, alleviating pain, proper nutrition and wound care, ends at closure of wound and wound heals.
Phases of Management
3. Rehabilitation phase –
Burns healed, pt. able to function, ADLS, PT, OT, cosmetic correction
Nonsurgical management of burns includes
IV fluids, monitoring patient response to fluid therapy, drug therapy
Electrolyte imbalances r/t burns
Potassium is leaked into intravascular system, now there is hyponatremia and hyperkalemia
Hypovolemic shock review
Abnormally decreased volume of circulating fluid causing peripheral circulatory failure. Endangers vital organs. Brain, heart, kidneys are particularly vulnerable. Tachycardia is an early sign of compensation for excessive blood loss. Tachycardia, tachypnea, BP normal initially, decrease or narrowing in pulse pressure (difference between systolic and
diastolic). Elevated BP can occur initially until compensatory mechanisms
fail. Acidosis with vasodilation and decreased BP, increased bleeding, decreased circulating volume, and subsequent organ death.
Emergent phase nursing cares
Monitor for oliguria and renal failure
Monitor for ARDS
Elevate extremities to decrease edema
Assess GI – ulcers can develop due to stress reaction related to loss of perfusion, cells that decrease acid and release bicarb can be affected and contribute to ulcer formation. Bleeding – gross or occult
Ileus – decreased or absent bowel sounds, vomiting lime green, food stagnant
NG tube – when bowel sounds return and pt. moves into acute phase, they can eat and are removed from NPO status. High protein and High carb. May have hyperglycemia
Stress response: can cause liver to release glycogen that increases blood sugar
Managing pain and alterations in Comfort
Opiates, non-opioid analgesics IV route or PCA. IM not recommended due to fluid shifts. NPO and problems with absorption. Other therapeutic measures: relaxation, acupuncture. Environmental – quiet environment, sleep and rest, change positions every 2 hours, warm room to prevent shivering.
Note that assessing patient for fluid overload is
important. Observe for:
Dependent edema, engorged neck veins, rapid, thready pulse, lung crackles or wheezes.
Fluid replacement for burns
Need 2 IVs or central venous catheter so
massive fluid loads can be given in first 24 hours. Parkland Burn Formula based on TBSA
Lactated Ringers – expand intravascular
compartment
Colloid solutions – albumin replaced, pulls fluid
back into vascular system
Acute Phase of Burn Injury
Begins 36-48 hours after injury, when fluid shift
resolves and lasts until wound closure is complete. Burn wound care – pre-medicate, sterile procedure, covering
Prevent infection – Protective isolation, protect from others (hair covering, shoe covering, full PPE), tetanus shot if none in 5-10 years
Temperature regulation – room temp 85 degrees
plus
Pain control – become painful when wound care,
give IV
Indications of Infection and Sepsis
Swelling inflammation of intact skin surrounding
the wound, change in the color, odor or amount of exudate, increased pain, loss of previously healed skin grafts.
Nonsurgical Management:
Acute Phase
Remove exudates, necrotic tissue, cleaning
area to stimulate granulation and
revascularization, mechanical débridement, hydrotherapy, enzymatic débridement, autolysis, collagenase, compression garments
Dressing the Burn Wound
Standard wound dressings - according to
hospital policies, orders
Biologic dressings
Biosynthetic dressings
Synthetic dressings
Escharotomy
Surgical excision - debridement
Psychosocial Aspects
The goals include:
Willingness to touch affected body part, adjustment to changes in body function, willingness to use strategies to enhance appearance
and function, successful progression through the grieving process, use of support systems
Rehabilitative Phase of Burn Injury
Begins with wound closure, ends when patient
returns to highest possible level of functioning. Focus on Comfort
No burned area touching other burn area –
webbing can occur
Avoid pillows for burns to ears or neck. Ear
circulation is compromised. Can cause
contractures.
Emphasis on psychosocial adjustment,
prevention of scars and contractures, resumption
of preburn activity
This phase may last years or even a lifetime if
patient needs to adjust to permanent limitations
Shock
decrease in blood flow to body organs and tissues resulting in inadequate oxygenation, life-threatening cellular dysfunction.
Patho of shock
One or more cardiovascular components malfunction → altered hemodynamic
properties → inadequate tissue perfusion → shock Manifestations result from body’s attempts to maintain vital organs
▪ Especially heart, brain
– Triggered by sustained drop in MAP
▪ Decrease in cardiac output
▪ Decrease in circulating blood volume
▪ Increase in size of vascular bed from peripheral vasodilation
– Death if injury or condition severe enough, prolonged enough, physiologic events
not stopped
Class I: early shock
– Begins when baroreceptors in aortic arch, carotid sinus detect sustained drop in
MAP of <10 mmHg from normal
– Circulating blood volume may decrease
▪ Not enough to cause serious effects in adult
– SNS increases heart rate, force of cardiac contraction
▪ Increases CO
– Peripheral vasoconstriction
▪ Increased SVR, arterial pressure
– Perfusion maintained
– Symptoms almost imperceptible
▪ Pulse slightly elevated
Class II: compensatory shock
Class II: compensatory shock
– Begins after MAP falls 10–15 mmHg below normal
– Circulating blood volume reduced 15–30%
– Compensatory mechanisms maintain BP, tissue perfusion to vital organs
▪ Stimulation of SNS → increased CO, oxygenation
▪ Renin-angiotensin response
▪ Hypothalamus releases adrenocorticotropin hormone
▪ Posterior pituitary gland releases ADH
▪ As MAP falls, decreased capillary hydrostatic pressure causes fluid shift
from interstitial space to capillaries, raising blood volume
– MAP can be maintained for only short time
– If effective treatment provided, process stops with no permanent damage
– Unless underlying cause is reversed, compensatory mechanisms become
harmful, perpetuating shock
