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 Burnβ
Caused by powders, gases, or food (hot
pepper). Acid or base (alkali), watch for inhalation injuries
Radiation Burnβ
D/t sun, cancer treatment
Friction Burn β
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 β 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 β 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 β 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 βthird spacingβ 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 shockβCommon 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 β 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 β gross and occult
Curlingβs ulcer β 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 β triggers healing
bur is also responsible for the fluid shift and
edema and hypovolemic shock.
Sympathetic nervous system compensation β
increased heart rate, increased BP, widen
bronchial passages, slow intestines.
Emergent management of burns
Assess airway (A)
Administer Oxygen (B) Breathing
Maintain Circulation (C) β 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 β 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 hoursβuntil diuresis occurs. Injury is evaluated.
Goals of management during Resuscitation Phase of Burn Injury
Secure airway, support circulationβfluid replacement, keep comfortable with analgesics, prevent infection through careful wound care, maintain body temperature, provide emotional support
Carbon monoxide poisoning β
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 β 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). βRule of ninesβ using multiples of 9% of total BSA, used to calculate surface area. Body fluid shifting and risk for hypovolemia and death. Parkland Burn formula β calculate total volume of fluid needed 24 hours after burn, 2nd degree burn or higher.
Parkland Burn formula β
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 β
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 β
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 β
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 β 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 β gross or occult
Ileus β decreased or absent bowel sounds, vomiting lime green, food stagnant
NG tube β 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 β 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 β expand intravascular
compartment
Colloid solutions β 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 β pre-medicate, sterile procedure, covering
Prevent infection β Protective isolation, protect from others (hair covering, shoe covering, full PPE), tetanus shot if none in 5-10 years
Temperature regulation β room temp 85 degrees
plus
Pain control β 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 dΓ©bridement, hydrotherapy, enzymatic dΓ©bridement, 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 β
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 β altered hemodynamic
properties β inadequate tissue perfusion β shock Manifestations result from bodyβs attempts to maintain vital organs
βͺ Especially heart, brain
β Triggered by sustained drop in MAP
βͺ Decrease in cardiac output
βͺ Decrease in circulating blood volume
βͺ Increase in size of vascular bed from peripheral vasodilation
β Death if injury or condition severe enough, prolonged enough, physiologic events
not stopped
Class I: early shock
β Begins when baroreceptors in aortic arch, carotid sinus detect sustained drop in
MAP of <10 mmHg from normal
β Circulating blood volume may decrease
βͺ Not enough to cause serious effects in adult
β SNS increases heart rate, force of cardiac contraction
βͺ Increases CO
β Peripheral vasoconstriction
βͺ Increased SVR, arterial pressure
β Perfusion maintained
β Symptoms almost imperceptible
βͺ Pulse slightly elevated
Class II: compensatory shock
Class II: compensatory shock
β Begins after MAP falls 10β15 mmHg below normal
β Circulating blood volume reduced 15β30%
β Compensatory mechanisms maintain BP, tissue perfusion to vital organs
βͺ Stimulation of SNS β increased CO, oxygenation
βͺ Renin-angiotensin response
βͺ Hypothalamus releases adrenocorticotropin hormone
βͺ Posterior pituitary gland releases ADH
βͺ As MAP falls, decreased capillary hydrostatic pressure causes fluid shift
from interstitial space to capillaries, raising blood volume
β MAP can be maintained for only short time
β If effective treatment provided, process stops with no permanent damage
β Unless underlying cause is reversed, compensatory mechanisms become
harmful, perpetuating shock
Class III: decompensated shock
β Occurs after sustained decrease in MAP of β₯20 mmHg below normal, blood
volume loss of 30β40%
β Compensatory mechanisms still active but cannot maintain MAP at sufficient
level for perfusion of vital organs
β Vasoconstriction limits blood flow β cells become oxygen deficient
βͺ Affected cells switch from aerobic to anaerobic metabolism
βSodiumβpotassium pump fails
β Heart rate and vasoconstriction increase
β Greatly diminished perfusion of skin, skeletal muscles, kidneys, GI organs
β Cells in heart, brain become hypoxic
β Other body cells, tissues become ischemic, anoxic
β Unless treated rapidly, patient has poor chance of survival
Class IV: refractory (irreversible) shock
β Generalized tissue anoxia
β Widespread cellular death
β No treatment can reverse damage
β Even if MAP is temporarily restored, too much cellular damage to maintain life
β Cell death followed by tissue death β death of organs β death of body
Effects of shock on body systems: Cardiovascular system
βBP and heart rate normal at first
βProgressive shock β damage to heartβs electrical system, contractility
βCardiac dysrhythmias may develop
βDecreased blood volume, venous return β decreased CO, BP
Effects of shock on body systems: Respiratory system
βBlood O2 levels decrease, CO2 levels increase β acidosis
βARDS (βshock lungβ)
* Potentially fatal
* Most common in shock caused by hemorrhage, severe allergic
response, trauma, infection
Effects of shock on body systems: Gastrointestinal system
βArterial blood flow diverted to heart, brain
βGI organs become ischemic
βGastric, intestinal motility impaired β paralytic ileus
βIf shock prolonged, necrosis of bowel may occur
βLiver function impaired β hypoglycemia
βMetabolic acidosis
Effects of shock on body systems: Neurologic system
βChanges in mental status, LOC
βRestlessness is common early symptom of cerebral hypoxia
βContinued ischemia β swelling β cerebral edema, neurotransmitter
failure, irreversible brain damage
Effects of shock on body systems: Renal system
βBlood redirected to heart, brain β renal hypoperfusion
* Urine output reduced, <20 mL/hr indicates progressive shock
* In healthy kidneys, tubular necrosis develops after 30 minutes
βIf treatment restores renal perfusion, kidneys can regenerate lost
epithelial cells, renal function returns to normal
βLoss of renal function may be permanent in older adults, chronically ill,
or sustained shock
Effects of shock on body systems: integumentary system
βChanges in skin color
βSkin cool, moist; edematous in later stages
βBody temperature decreases
βMay become thirsty
Hypovolemic shock occurs d/t
βHemorrhage
βLoss of intravascular fluid from injuries such as burns
βSevere dehydration
βSevere vomiting or diarrhea
βRenal fluid loss
βFluid shifts to interstitial space, third spacing
Cardiogenic shock
βͺ Occurs when heartβs pumping ability cannot maintain CO, perfusion
βͺ Causes
βMI (most common cause)
βCardiac tamponade
βRestrictive pericarditis
βCardiac arrest
βDysrhythmias
βPathologic changes in valves, cardiomyopathies
βComplications of cardiac surgery
βElectrolyte imbalances
βDrugs affecting cardiac muscle contractility
βHead injuries causing damage to cardioregulatory center
Cardiogenic shock s/s
βͺ Decrease in CO leads to decrease in MAP
βͺ Myocardium becomes progressively deleted of oxygen β further myocardial ischemia, necrosis
βͺ Typical sequence of shock unchanged
βͺ Cyanosis more common
βͺ Pulmonary edema may occur
βͺ JVD
Obstructive shock
βͺ Caused by obstruction in heart, great vessels
βImpedes venous return or prevents effective cardiac pumping
βCauses
* Impaired diastolic filling
* Increased right ventricular afterload
* Increased left ventricular afterload
βManifestations result from decreased CO and BP β reduced tissue
perfusion, cellular metabolism
β Distributive shock (vasogenic shock)
βͺ Several types of shock resulting from widespread vasodilation, decreased
PVR
βͺ Blood volume does not change β relative hypovolemia
Septic shock (septicemia)
βͺ Leading cause of death for patient in ICUs
βͺ Part of progressive syndrome: systemic inflammatory response syndrome
βͺ Most often result of gram-negative bacterial infection
βͺ May also follow gram-positive Staphylococcus, Streptococcus infections
Neurogenic shock
βͺ Parasympathetic overstimulation β sustained vasodilation
βͺ Dramatic reduction in systemic PVR
βͺ Causes
βHead injury or trauma to spinal cord
βInsulin reactions, CNS drugs, anesthesia
βSevere pain
βExposure to heat
Anaphylactic shock
βͺ Result of widespread hypersensitivity reaction (anaphylaxis)
βͺ Pathophysiology
βVasodilation
βPooling of blood in periphery
βHypovolemia with altered cellular metabolism
βͺ Occurs when sensitized person comes into contact with allergen
βͺ Allergens that can cause anaphylactic shock
βMedications
βBlood administration
βLatex
βFoods
βSnake venom, insect stings
As body compensates for hypotension, hypovolemia, signs of shock:
β Tachycardia
β Increased respiratory effort
β Decreased urine output
β Diaphoresis
If treatment not begun, shock progresses and s/s include
β Drop in systolic BP
β Narrowing of pulse pressure
β Reduced cerebral blood flow β decreased LOC
β Progression to cardiopulmonary failure, death
Dx of shock
H&H, ABGs, electrolytes, BUN, creatinine, urine specific gravity, osmolality, blood cultures, WBC and differential, serum cardiac enzymes, central venous catheterization, X-rays, CT scan, MRI, endoscopic examination, echocardiogram, gastric tonometry, sublingual PaCO2 measurement
Pharmacologic therapy for shock
Vasoconstrictors (vasopressors), Inotropes, and vasodilators, colloid solutions, albumin, diuretics, sodium bicarbonate, calcium, antidysrhythmic agents, broad-spectrum antibiotics, ephinephrine, antihistamines, inhaled beta2-agonists, morphine
Vasopressors include
β Norepinephrine
β Phenylephrine
β Epinephrine
Inotropes include
β Dopamine
β Dobutamine
β Isoproterenol
Vasodilators include
Nitroglycerin, nitroprusside
Oxygen therapy for shock
All patients with shock should receive oxygen therapy, even those with adequate respirations
Maintain PaO2 > 80 mmHg during first 4β6 hours of care
Ventilatory assistance if cannot be maintained with unassisted respiration
Fluid replacement therapy for shock
IV fluids or blood: most effective treatment for hypovolemic shock
Fluids also used to treat septic, neurogenic, anaphylactic shock
Fluids administered alone or in combination
β Crystalloid solutions
β Colloid solutions
β Blood and blood products
Administered in massive amounts through two large-bore peripheral lines or a central
line
Shock in neonates and infants
Even a small amount of blood loss can be devastating, especially low-birthweight, very-low-birthweight neonates. Prolonged very high or very low heart rate can compromise CO, contributing to
shock
βͺ Hypotension usually indicates later stage of shock than in adults
β Risk factors
βͺ Umbilical cord accident
βͺ Fetal or neonatal hemolysis or hemorrhage
βͺ Maternal infection or hypotension
βͺ Asphyxia, neonatal sepsis, other complications
Delayed treatment can lead to cerebral palsy, epilepsy, mental retardation
Shock in children
Septic shock definition slightly different from that for adults. Involves sepsis plus cardiovascular dysfunction but not necessarily
hypotension. Signs of cardiovascular dysfunction will depend on age-specific values for
vital signs, WBC counts. S/S include altered mental status, tachypnea, tachycardia, reduced urine output, delayed capillary refill, temperature instability, metabolic acidosis, hypotension is a late sign in children, correlated with poor prognosis
Shock in pregnant women
Causes
βͺ Trauma
βͺ Postpartum hemorrhage
βͺ Septic abortion
βͺ Chorioamniotic and postpartum infection
βͺ Valvular disease
βͺ Amniotic fluid embolism
βͺ Different from shock other adults
βCan affect normal changes of pregnancy: increased blood volume,
heart rate, SV, CO; decreased peripheral resistance, BP
βFetal perfusion, oxygenation depend on motherβs circulation, putting
fetus at risk if motherβs circulation fails
Shock in pregnant women cares
β Ventilate to maintain oxygen status
β Avoid respiratory alkalosis, which decreases uterine blood flow
β If CPR needed, place woman in left lateral tilt position
β Ephedrine: first-line vasoactive drug for pregnant women in shock
Shock caused by postpartum hemorrhage
Administer oxytocin
Shock caused by sepsis in pregnant women
βͺ Monitor patient for complications associated with increased chance of
preterm labor and delivery, fetal infection
βͺ Onset can be sudden
βPatient may transition rapidly from healthy state to septic shock,
multiple organ dysfunction, even death
βEarly detection improves outcome, survivability
Treatment of fetus for shock
βͺ While mother is being treated for shock, fetus should undergo continuous
heart rate monitoring
βFetal bradycardia may indicate hypoxia
βͺ Ultrasound to assess fetal movement, reactivity, amniotic fluid volume
βͺ Fetal distress may necessitate delivery
Older adults and shock
More likely to progress to shock and have poorer outcomes, higher risk of mortality.
β Changes of aging put older adults at higher risk
β Heart attack increases risk of cardiogenic shock
β Chronic diuretic use, malnutrition increase risk
β Hypovolemic shock treated by aggressive fluid treatment
β Highly susceptible to septic shock d/t higher risk for infections such as pneumonia, UTIs especially if immunocompromised or have multiple comorbidities
Older adults and shock
β Assess for preshock functional status
βͺ Often predictor of outcome
βͺ Sudden decrease in ability to perform ADLs may be only sign of sepsis
β Aggressive fluid administration may cause problems if patient has diastolic
dysfunction
βͺ Carefully monitor for signs of fluid overload
β Common treatments such as dobutamine may have lesser effect or cause
dysrhythmia
β Antibiotics for sepsis based on age-related differences in pharmacokinetics
β Mechanical ventilation during shock associated with increased mortality
βͺ May be against patientβs wishes
βͺ Talk to patient or family to determine wishes for potential end-of-life care
Nursing process r/t shock
Rapid assessment
Reaction to subtle symptoms to prevent downward cascade of events
Anticipating potential for shock can promote rapid intervention
Hypovolemic shock assessment
β Recent surgery
β Multiple traumatic injuries
β Serious burns
Cardiogenic shock assessment
β Left anterior wall MI
Neurogenic shock assessment
β Spinal cord injuries
β Spinal anesthesia
Anaphylactic shock assessment
β Allergies
β Drug reactions
Septic shock assessment
β Hospitalized
β Debilitated
β Chronically ill
β Have undergone invasive procedures
ED, ICU often have guidelines for nursing actions in cases of hypovolemic shock
β Assist in assessing, establishing IV access
β Calculating correct amount of IV fluid, preparing it for administration
β Employing IV push or pressure bag to ensure rapid fluid administration
β Monitoring patientβs physiologic response to fluid bolus
β Preparing second and third fluid bolus
* Use warmed fluids for resuscitation
* Verify correct blood when administering packed RBCs
* Change IV fluid to normal saline during blood administration
* Carefully assess patient for transfusion reaction
* Monitor patientβs physiologic circulatory responses for improvement/deterioration
β Notify physician immediately if any deterioration
Preserve cardiac output by:
β Assess, monitor cardiovascular function
βͺ BP
βͺ Heart rate and rhythm
βͺ Pulse oximetry
βͺ Peripheral pulses
βͺ Hemodynamic monitoring
β Conduct baseline assessment to establish stage of shock
β Measure, record I&O hourly
β Monitor bowel sounds, abdominal distention, abdominal pain
β Monitor for sudden sharp chest pain, dyspnea, cyanosis, anxiety, restlessness
β Monitor for dyspnea
β Maintain bedrest, provide a calm, quiet environment
Primary risk factors for fracture:
Age
βͺ Younger patients: sports injuries
βͺ Older patients: falls, disease
β Presence of bone disease
βͺ Osteoporosis
βͺ Osteogenesis imperfecta
βͺ Bone cancer
β Poor nutrition
βͺ Inadequate intake of vitamin D, calcium, phosphorus
β Lifestyle habits
βͺ Participation in dangerous activities
Preventing fractures
Education
β Safety equipment
β Good lifestyle habits
* Safe living environment
β Protective gates on stairs for young children
β Removing rugs, clutter
* Regular screenings
β Osteoporosis
β Fall prevention
s/s of fracture
Pain
* Visible fracture on x-ray
* Other manifestations include
β Visible deformity
β Swelling
β Numbness
β Internal or external loss of blood
βͺ May lead to hypovolemic shock or ecchymosis
β Crepitus
Compartment syndrome
Complication of fracture. Edema, swelling cause increased pressure in muscle compartment β decreased blood flow, potential muscle and nerve damage
βͺ Continuous cycle: Decreased blood flow β dilation of blood vessels β more
edema
β If ischemia continues for significant length of time, muscles and nerves may die,
limb might need to be amputated
Compartment syndrome s/s
βͺ Severe pain and tenderness
βͺ Swelling, paresthesia, pallor, numbness, decreased or absent pulses in
affected limb, poikilothermia in distal part of affected limb
β Most common in lower leg and forearm
βͺ Can also occur in hand, foot, thigh, upper arm
β Suspect if patientβs pain, swelling are disproportionate to negative x-ray findings
Causes of compartment syndrome
βͺ Fracture
βͺ Muscle bruise
βͺ Crush injury
βͺ Excessively tight bandage or cast
β Medical emergency
Treatment and prevention of compartment syndrome
β Treatment
βͺ Remove tight cast
βͺ If symptoms caused by internal pressure, surgery (fasciotomy) to relieve
pressure
β Prevention
βͺ Elevation, ice to reduce swelling
βͺ Delaying casting
Complications of compartment syndrome
βͺ Paralysis
βͺ Amputation
βͺ Volkmann contracture
βCommon after elbow injuries
* Especially in children
Fracture complications include
Compartment syndrome, DVT, FES, infection
Fat embolism syndrome (FES)
β May occur in conjunction with closed long bone or pelvic fractures
β Fat emboli released from bone marrow enter bloodstream, become trapped in
pulmonary, dermal capillaries
FES s/s
βͺ Respiratory consequences: typically first symptom
βIn severe cases, dyspnea β respiratory failure with tachypnea, hypoxia
βSyndrome similar to acute respiratory distress syndrome (ARDS) may
develop
βͺ Neurologic symptoms
βConfusion, restlessness, seizures, coma
βͺ Transient petechial rash
βͺ Purtscher retinopathy
βͺ Mild fever
FES treatment
βͺ Supportive
βͺ Oxygen administration
βApprox. half patients require mechanical ventilation
βͺ Most symptoms resolve with adequate oxygenation
βͺ Rash disappears spontaneously within a week
β Prevention
FES treatment
Prophylactic treatment with corticosteroids
Early immobilization of the injury
β Rarely seen in children <10 years of age
Nursing role with fracture
β Maintain patient comfort
β Assist with procedures
β Provide patient education
β Refer patient to specialists
β Immobilize fracture
β Prevent infection
Pharmacologic therapy for fracture
Analgesics for pain
* Severe fractures
β Opioids for pain
β Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain, inflammation
* Antibiotics to prevent or treat infection
* Anticoagulants to prevent or treat DVT
Cast
β Rigid device to immobilize, support, and protect fractured bones and surrounding
soft tissue
βͺ Plaster or fiberglass, custom made to exactly fit injured limb
βͺ Should cover, immobilize joint above and below fractured bone
βͺ Functional cast allows limited movement of nearby joints
Nursing care of cast
βͺ Frequent neurovascular assessments
βͺ Palpate cast for βhot spotsβ indicating infection
βͺ Report any drainage
βͺ Assess for compartment syndrome
Splint
βͺ Less support than cast but easily adjusted to accommodate swelling, prevent compartment syndrome
Nonpharmacologic therapy: traction
use of weights, ropes, and pulleys to apply force to fractured bone to
maintain proper alignment
β Skin traction
βͺ Used when only a small amount of weight is needed for traction
βͺ Uses
βTo control muscle spasms
βTo maintain alignment of fracture before or after internal fixation
βTo provide traction if skeletal pins must be removed
β Skeletal traction
βͺ Used when a greater force is needed or skin traction contraindicated
βͺ May be used in conjunction with skin traction
βͺ Pins, wires, or screws surgically implanted into bone, weights attached to
implanted hardware
βͺ Monitor for infected pins
RICE therapy
βͺ Rest
βͺ Ice
βͺ Compression
βEnough to provide support for injured area
βNot so much as to decrease blood flow, causing compartment
syndrome
βͺ Elevation
βNursemaidβs elbowβ (radial head subluxation)
βͺ Not a fracture
βͺ Partial separation of radiocapitellar joint
βͺ Symptom: Child holds arm stiffly, doesnβt want to use it
βͺ Prevention
βEducate to avoid swinging children by hands or pulling by hands
βEncourage picking children up under their arms
Children most common fracture
Spiral fractures common because bones are porous
Adults and older adults: fractures
β Lengthened recovery time because of slower rate of tissue growth
βͺ Especially women after menopause, older adults
β Older adults with osteoporosis
βͺ Increased risk of hip fractures
βͺ More likely to develop DVT, infections
β Alterations in mental status increase risk
5 Pβs of neurovascular assessment
βͺ Pain
βͺ Pulses
βͺ Pallor
βͺ Paralysis, paresis
βͺ Paresthesia
Physical examination of fracture
β Distal pulses in injured extremity
β Edema, swelling
β Skin color, temperature
β Deformity
β Range of motion (ROM)
β Sensation
Cares for pt with fracture
Provide effective pain management
β Regularly assess patient for
βͺ Pain, muscle spasms, swelling
βͺ Monitor vital signs
β Administer pain medication
β Monitor effectiveness of pain medication
βͺ Advocate for stronger pain relief if needed
β Elevate injured extremity
β Provide ice to reduce swelling
β Nonpharmacologic methods to reduce pain
β Move patient gently and slowly
β Support extremity above and below fracture site
Monitor nerovascular status
β Assessments
βͺ 5 Pβs
βͺ Assess injured limb for swelling, cramping, temperature, hematoma,
movement, capillary refill, sensation to touch
βͺ Every 15 minutes for first 2 hours after cast is applied
βͺ Every 1β2 hours after that
βͺ Report abnormal findings immediately
β Have cast saw available for emergency cast removal or bivalving
β If compartment syndrome suspected
βͺ Assist in measuring compartment pressure
β If DVT is suspected
βͺ Administer anticoagulant as ordered
Provide discharge instructions
β Cast care
β Activity restrictions
β When to take pain medications
β Signs of complications
β Injury prevention
β Special instructions for using crutches on stairs
β Referral for permanent or temporary ramp
β Referral to home healthcare for older patients
Hip fracture:
a break in the neck, head, or trochanter region of upper femur
* Associated with older adults but can occur at any age due to trauma
* Often results in long-term functional impairment in older adults
Risk factors of hip fracture
β Old age
β Osteoporosis
Preventing hip fractures
preventing falls
β Performing weight-bearing exercises
β Assessing home for hazards
β Education about medications that may affect balance, bone density, or muscle
strength
β Annual vision exam
* Exercise and healthy diet
* Adequate intake of calcium and vitamin D
* Mobility assessment for older adults
s/s of hip fracture
Severe pain in hip, upper thigh, groin, lower back
* May be unable to move, stand, or walk
* May have stiffness, bruising, swelling in hip area
* Bone may be visible through skin
* Because they result from trauma, other injuries may also be present
β Other fractures
β Head injuries
β Internal injuries
Hip fx complications
Complications from loss of mobility
β Deep venous thrombosis (DVT)
β Pressure ulcers
β Urinary tract infection (UTI)
β Pneumonia
β Muscle atrophy
* Other complications
β Postoperative infection
β Mental deterioration
β Avascular necrosis
β Nonunion or malunion of bone
β Loss of muscle mass, strength
β Continued decline in mobility
Treatment of hip fx
First-line treatment
* Should occur as soon as possible after the fracture
* Goals of surgery
β Reduce pain
β Stabilize fracture
β Return patient to normal activity level
* Three types of surgery
β Repair with hardware
β Partial hip replacement
β Total hip replacement
βͺ May require revision therapy or replacement of artificial joint after 10 years
Pharmacologic therapy for hip fracture
Pain medications
β Opioids
β Patient-controlled analgesia
* Antibiotics to prevent infection
* Anticoagulants to prevent DVT
* Anti-inflammatories for patient with well-worn prosthesis
* Bone density enhancers
Nonpharmacologic therapy for hip fracture
Bedrest
* Traction
β Buck
β Russell
* Casting
β Hip spica cast
* Prevention of complications
β Exercise and compression stockings to prevent stiffness, DVT
β Respiratory exercises to prevent pneumonia
* Postoperative physical therapy (PT): range of motion (ROM), strengthening exercises
* Postoperative occupational therapy (OT): to gain independence in activities of daily
living (ADLs)
Older adults and hip fractures
β May not be able to return to independent lifestyle after hip fracture
β High mortality rate if patient develops pneumonia after hip fracture
β Emphasis on getting patient moving early
β Nutrition, DVT prophylaxis, avoiding sensory deprivation
Hip fracture nursing cares
β Managing pain
β Promoting mobility
β Preventing complications
β Making referrals as necessary
Preoperative nursing assessment includes
β Vital signs
β Physical assessment
β Cognitive function
β Pain level
β Neurovascular status: 5 Pβs
β Medical history
βͺ History of current traumatic event
βͺ Past history of osteoporosis, other conditions that affect strength, mobility,
balance, coordination
βͺ Medications
Postoperative assessment
oxygenation assessment, presence of infection, ability to ambulate,
urinary/bowel complications, DVT
Nursing interventions for patients with hip fracture include
β Managing pain
β Maintaining proper alignment
β Promoting mobility
β Monitoring patientβs neurovascular status
β Monitoring for infection
β Managing pre- and postoperative care
β Emotional care
β Instructions for home care
Preop cares
βͺ Manage pain
βͺ Immobilize hip with traction or other restraints
βͺ Provide information on treatment plan
Post op cares
βͺ Manage pain
βͺ Promote mobility
βͺ Prevent complications
βͺ Assist with ambulation
βͺ DVT prevention
βͺ Respiratory exercises
βͺ Active or passive ROM
βͺ Wound care
Provide thorough discharge instructions for hip fracture
β Proper use of abduction pillow if ordered
β Proper sitting and bending techniques
β Proper use of walker or cane
β Explanation of weight-bearing limitations
β Explanation of medications
β Referrals for PT, home care agencies, medical equipment
Patient should be evaluated for what with hip fracture?
β Return of mobility
β Absence of neurologic complications
β Decrease in pain
β Absence of complications from fracture and surgery
β Emotional state
β Benefits of PT and rehabilitation programs
β Adherence to discharge instructions
β Patient and family/caregiver coping, functioning