Week 8; Trauma Cont. Flashcards

(142 cards)

1
Q

Burns impact bodily functions in three ways:

A

Physiologic, metabolic, and psychological

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2
Q

Patho of burn injury

A

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.

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3
Q

Types of burns

A

Heat/thermal, electrical, cold, chemical, radiation, and friction

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4
Q

Heat/Thermal Burn

A

Caused by fire, liquid, steam, grease, tar,
hot objects. Inhalation injury may occur

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5
Q

Electrical Burn

A

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).

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6
Q

Cold Burn

A

Frostbite

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7
Q

Chemical Burn–

A

Caused by powders, gases, or food (hot
pepper). Acid or base (alkali), watch for inhalation injuries

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8
Q

Radiation Burn–

A

D/t sun, cancer treatment

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9
Q

Friction Burn –

A

Abrasions, road rash

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10
Q

Extent of burn injury depends on

A

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.

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11
Q

Physical skin changes r/t burns

A

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.

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12
Q

Functional changes of skin r/t burns

A

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.

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13
Q

First degree burn

A

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.

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14
Q

Desquamation

A

Peeling of dead skin

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15
Q

Second degree burn

A

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.

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16
Q

Third degree burn

A

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.

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17
Q

Fourth degree burn

A

Deep Full Thickness; worst of all – bone, muscle, ligaments. Black and charred with eschar, pain and sensation is absent, no blisters, grafts required.

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18
Q

Vasular changes r/t burns

A

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.

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19
Q

Cardiac changes r/t burns

A

Hypovolemic shock—Common cause of
death in early phase in patients with serious
injuries and cardiac rhythm, especially in cases of
electrical burn injuries.

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20
Q

Respiratory changes r/t burns

A

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

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21
Q

GI changes r/t burns

A

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

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22
Q

Metabolic changes r/t burns

A

Increased secretions of catecholamines,
antidiuretic hormone, aldosterone, cortisol. Increased core body temperature as
response to temperature regulation by
hypothalamus.

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23
Q

Compensatory responses r/t burns

A

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.

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24
Q

Emergent management of burns

A

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

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25
Resuscitation Phase of Burn Injury
First phase after burn, continues for about 24 to 48 hours—until diuresis occurs. Injury is evaluated.
26
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
27
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.
28
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
29
Heat damage in the pharynx is often severe enough to produce __ and __ __ __ especially epiglottitis.
edema, upper airway obstruction
30
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.
31
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.
32
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.
33
Parkland Burn formula –
calculate total volume of fluid needed 24 hours after burn, 2nd degree burn or higher.
34
Potential complications of burns
Potential for decreased oxygenation, shock, pain (acute and chronic), potential for Acute Respiratory Distress Syndrome (ARDS)
35
Nursing cares include
Supporting oxygenation, preventing hypovolemic shock, preventing inadequate gas exchange, managing pain and alterations in comfort
36
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.
37
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.
38
Phases of Management 3. Rehabilitation phase –
Burns healed, pt. able to function, ADLS, PT, OT, cosmetic correction
39
Nonsurgical management of burns includes
IV fluids, monitoring patient response to fluid therapy, drug therapy
40
Electrolyte imbalances r/t burns
Potassium is leaked into intravascular system, now there is hyponatremia and hyperkalemia
41
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.
42
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
43
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.
44
Note that assessing patient for fluid overload is important. Observe for:
Dependent edema, engorged neck veins, rapid, thready pulse, lung crackles or wheezes.
45
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
46
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
47
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.
48
Nonsurgical Management: Acute Phase
Remove exudates, necrotic tissue, cleaning area to stimulate granulation and revascularization, mechanical débridement, hydrotherapy, enzymatic débridement, autolysis, collagenase, compression garments
49
Dressing the Burn Wound
Standard wound dressings - according to hospital policies, orders Biologic dressings Biosynthetic dressings Synthetic dressings
50
Escharotomy
Surgical excision - debridement
51
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
52
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
53
Shock
decrease in blood flow to body organs and tissues resulting in inadequate oxygenation, life-threatening cellular dysfunction.
54
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
55
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
56
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
57
Class III: decompensated shock
– Occurs after sustained decrease in MAP of ≥20 mmHg below normal, blood volume loss of 30–40% – Compensatory mechanisms still active but cannot maintain MAP at sufficient level for perfusion of vital organs – Vasoconstriction limits blood flow → cells become oxygen deficient ▪ Affected cells switch from aerobic to anaerobic metabolism –Sodium–potassium pump fails – Heart rate and vasoconstriction increase – Greatly diminished perfusion of skin, skeletal muscles, kidneys, GI organs – Cells in heart, brain become hypoxic – Other body cells, tissues become ischemic, anoxic – Unless treated rapidly, patient has poor chance of survival
58
Class IV: refractory (irreversible) shock
– Generalized tissue anoxia – Widespread cellular death – No treatment can reverse damage – Even if MAP is temporarily restored, too much cellular damage to maintain life – Cell death followed by tissue death → death of organs → death of body
59
Effects of shock on body systems: Cardiovascular system
–BP and heart rate normal at first –Progressive shock → damage to heart’s electrical system, contractility –Cardiac dysrhythmias may develop –Decreased blood volume, venous return → decreased CO, BP
60
Effects of shock on body systems: Respiratory system
–Blood O2 levels decrease, CO2 levels increase → acidosis –ARDS (“shock lung”) * Potentially fatal * Most common in shock caused by hemorrhage, severe allergic response, trauma, infection
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Effects of shock on body systems: Gastrointestinal system
–Arterial blood flow diverted to heart, brain –GI organs become ischemic –Gastric, intestinal motility impaired → paralytic ileus –If shock prolonged, necrosis of bowel may occur –Liver function impaired → hypoglycemia –Metabolic acidosis
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Effects of shock on body systems: Neurologic system
–Changes in mental status, LOC –Restlessness is common early symptom of cerebral hypoxia –Continued ischemia → swelling → cerebral edema, neurotransmitter failure, irreversible brain damage
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Effects of shock on body systems: Renal system
–Blood redirected to heart, brain → renal hypoperfusion * Urine output reduced, <20 mL/hr indicates progressive shock * In healthy kidneys, tubular necrosis develops after 30 minutes –If treatment restores renal perfusion, kidneys can regenerate lost epithelial cells, renal function returns to normal –Loss of renal function may be permanent in older adults, chronically ill, or sustained shock
64
Effects of shock on body systems: integumentary system
–Changes in skin color –Skin cool, moist; edematous in later stages –Body temperature decreases –May become thirsty
65
Hypovolemic shock occurs d/t
–Hemorrhage –Loss of intravascular fluid from injuries such as burns –Severe dehydration –Severe vomiting or diarrhea –Renal fluid loss –Fluid shifts to interstitial space, third spacing
66
Cardiogenic shock
▪ Occurs when heart’s pumping ability cannot maintain CO, perfusion ▪ Causes –MI (most common cause) –Cardiac tamponade –Restrictive pericarditis –Cardiac arrest –Dysrhythmias –Pathologic changes in valves, cardiomyopathies –Complications of cardiac surgery –Electrolyte imbalances –Drugs affecting cardiac muscle contractility –Head injuries causing damage to cardioregulatory center
67
Cardiogenic shock s/s
▪ Decrease in CO leads to decrease in MAP ▪ Myocardium becomes progressively deleted of oxygen → further myocardial ischemia, necrosis ▪ Typical sequence of shock unchanged ▪ Cyanosis more common ▪ Pulmonary edema may occur ▪ JVD
68
Obstructive shock
▪ Caused by obstruction in heart, great vessels –Impedes venous return or prevents effective cardiac pumping –Causes * Impaired diastolic filling * Increased right ventricular afterload * Increased left ventricular afterload –Manifestations result from decreased CO and BP → reduced tissue perfusion, cellular metabolism – Distributive shock (vasogenic shock) ▪ Several types of shock resulting from widespread vasodilation, decreased PVR ▪ Blood volume does not change → relative hypovolemia
69
Septic shock (septicemia)
▪ Leading cause of death for patient in ICUs ▪ Part of progressive syndrome: systemic inflammatory response syndrome ▪ Most often result of gram-negative bacterial infection ▪ May also follow gram-positive Staphylococcus, Streptococcus infections
70
Neurogenic shock
▪ Parasympathetic overstimulation → sustained vasodilation ▪ Dramatic reduction in systemic PVR ▪ Causes –Head injury or trauma to spinal cord –Insulin reactions, CNS drugs, anesthesia –Severe pain –Exposure to heat
71
Anaphylactic shock
▪ Result of widespread hypersensitivity reaction (anaphylaxis) ▪ Pathophysiology –Vasodilation –Pooling of blood in periphery –Hypovolemia with altered cellular metabolism ▪ Occurs when sensitized person comes into contact with allergen ▪ Allergens that can cause anaphylactic shock –Medications –Blood administration –Latex –Foods –Snake venom, insect stings
72
As body compensates for hypotension, hypovolemia, signs of shock:
– Tachycardia – Increased respiratory effort – Decreased urine output – Diaphoresis
73
If treatment not begun, shock progresses and s/s include
– Drop in systolic BP – Narrowing of pulse pressure – Reduced cerebral blood flow → decreased LOC – Progression to cardiopulmonary failure, death
74
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
75
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
76
Vasopressors include
– Norepinephrine – Phenylephrine – Epinephrine
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Inotropes include
– Dopamine – Dobutamine – Isoproterenol
78
Vasodilators include
Nitroglycerin, nitroprusside
79
Oxygen therapy for shock
All patients with shock should receive oxygen therapy, even those with adequate respirations Maintain PaO2 > 80 mmHg during first 4–6 hours of care Ventilatory assistance if cannot be maintained with unassisted respiration
80
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 – Crystalloid solutions – Colloid solutions – Blood and blood products Administered in massive amounts through two large-bore peripheral lines or a central line
81
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 ▪ Hypotension usually indicates later stage of shock than in adults – Risk factors ▪ Umbilical cord accident ▪ Fetal or neonatal hemolysis or hemorrhage ▪ Maternal infection or hypotension ▪ Asphyxia, neonatal sepsis, other complications Delayed treatment can lead to cerebral palsy, epilepsy, mental retardation
82
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
83
Shock in pregnant women
Causes ▪ Trauma ▪ Postpartum hemorrhage ▪ Septic abortion ▪ Chorioamniotic and postpartum infection ▪ Valvular disease ▪ Amniotic fluid embolism ▪ Different from shock other adults –Can affect normal changes of pregnancy: increased blood volume, heart rate, SV, CO; decreased peripheral resistance, BP –Fetal perfusion, oxygenation depend on mother’s circulation, putting fetus at risk if mother’s circulation fails
84
Shock in pregnant women cares
– Ventilate to maintain oxygen status – Avoid respiratory alkalosis, which decreases uterine blood flow – If CPR needed, place woman in left lateral tilt position – Ephedrine: first-line vasoactive drug for pregnant women in shock
85
Shock caused by postpartum hemorrhage
Administer oxytocin
86
Shock caused by sepsis in pregnant women
▪ Monitor patient for complications associated with increased chance of preterm labor and delivery, fetal infection ▪ Onset can be sudden –Patient may transition rapidly from healthy state to septic shock, multiple organ dysfunction, even death –Early detection improves outcome, survivability
87
Treatment of fetus for shock
▪ While mother is being treated for shock, fetus should undergo continuous heart rate monitoring –Fetal bradycardia may indicate hypoxia ▪ Ultrasound to assess fetal movement, reactivity, amniotic fluid volume ▪ Fetal distress may necessitate delivery
88
Older adults and shock
More likely to progress to shock and have poorer outcomes, higher risk of mortality. – Changes of aging put older adults at higher risk – Heart attack increases risk of cardiogenic shock – Chronic diuretic use, malnutrition increase risk – Hypovolemic shock treated by aggressive fluid treatment – Highly susceptible to septic shock d/t higher risk for infections such as pneumonia, UTIs especially if immunocompromised or have multiple comorbidities
89
Older adults and shock
– Assess for preshock functional status ▪ Often predictor of outcome ▪ Sudden decrease in ability to perform ADLs may be only sign of sepsis – Aggressive fluid administration may cause problems if patient has diastolic dysfunction ▪ Carefully monitor for signs of fluid overload – Common treatments such as dobutamine may have lesser effect or cause dysrhythmia – Antibiotics for sepsis based on age-related differences in pharmacokinetics – Mechanical ventilation during shock associated with increased mortality ▪ May be against patient’s wishes ▪ Talk to patient or family to determine wishes for potential end-of-life care
90
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
91
Hypovolemic shock assessment
– Recent surgery – Multiple traumatic injuries – Serious burns
92
Cardiogenic shock assessment
– Left anterior wall MI
93
Neurogenic shock assessment
– Spinal cord injuries – Spinal anesthesia
94
Anaphylactic shock assessment
– Allergies – Drug reactions
95
Septic shock assessment
– Hospitalized – Debilitated – Chronically ill – Have undergone invasive procedures
96
ED, ICU often have guidelines for nursing actions in cases of hypovolemic shock
– Assist in assessing, establishing IV access – Calculating correct amount of IV fluid, preparing it for administration – Employing IV push or pressure bag to ensure rapid fluid administration – Monitoring patient’s physiologic response to fluid bolus – 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 patient’s physiologic circulatory responses for improvement/deterioration – Notify physician immediately if any deterioration
97
Preserve cardiac output by:
– Assess, monitor cardiovascular function ▪ BP ▪ Heart rate and rhythm ▪ Pulse oximetry ▪ Peripheral pulses ▪ Hemodynamic monitoring – Conduct baseline assessment to establish stage of shock – Measure, record I&O hourly – Monitor bowel sounds, abdominal distention, abdominal pain – Monitor for sudden sharp chest pain, dyspnea, cyanosis, anxiety, restlessness – Monitor for dyspnea – Maintain bedrest, provide a calm, quiet environment
98
Primary risk factors for fracture:
Age ▪ Younger patients: sports injuries ▪ Older patients: falls, disease – Presence of bone disease ▪ Osteoporosis ▪ Osteogenesis imperfecta ▪ Bone cancer – Poor nutrition ▪ Inadequate intake of vitamin D, calcium, phosphorus – Lifestyle habits ▪ Participation in dangerous activities
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Preventing fractures
Education – Safety equipment – Good lifestyle habits * Safe living environment – Protective gates on stairs for young children – Removing rugs, clutter * Regular screenings – Osteoporosis – Fall prevention
100
s/s of fracture
Pain * Visible fracture on x-ray * Other manifestations include – Visible deformity – Swelling – Numbness – Internal or external loss of blood ▪ May lead to hypovolemic shock or ecchymosis – Crepitus
101
Compartment syndrome
Complication of fracture. Edema, swelling cause increased pressure in muscle compartment → decreased blood flow, potential muscle and nerve damage ▪ Continuous cycle: Decreased blood flow → dilation of blood vessels → more edema – If ischemia continues for significant length of time, muscles and nerves may die, limb might need to be amputated
102
Compartment syndrome s/s
▪ Severe pain and tenderness ▪ Swelling, paresthesia, pallor, numbness, decreased or absent pulses in affected limb, poikilothermia in distal part of affected limb – Most common in lower leg and forearm ▪ Can also occur in hand, foot, thigh, upper arm – Suspect if patient’s pain, swelling are disproportionate to negative x-ray findings
103
Causes of compartment syndrome
▪ Fracture ▪ Muscle bruise ▪ Crush injury ▪ Excessively tight bandage or cast – Medical emergency
104
Treatment and prevention of compartment syndrome
– Treatment ▪ Remove tight cast ▪ If symptoms caused by internal pressure, surgery (fasciotomy) to relieve pressure – Prevention ▪ Elevation, ice to reduce swelling ▪ Delaying casting
105
Complications of compartment syndrome
▪ Paralysis ▪ Amputation ▪ Volkmann contracture –Common after elbow injuries * Especially in children
106
Fracture complications include
Compartment syndrome, DVT, FES, infection
107
Fat embolism syndrome (FES)
– May occur in conjunction with closed long bone or pelvic fractures – Fat emboli released from bone marrow enter bloodstream, become trapped in pulmonary, dermal capillaries
108
FES s/s
▪ Respiratory consequences: typically first symptom –In severe cases, dyspnea → respiratory failure with tachypnea, hypoxia –Syndrome similar to acute respiratory distress syndrome (ARDS) may develop ▪ Neurologic symptoms –Confusion, restlessness, seizures, coma ▪ Transient petechial rash ▪ Purtscher retinopathy ▪ Mild fever
109
FES treatment
▪ Supportive ▪ Oxygen administration –Approx. half patients require mechanical ventilation ▪ Most symptoms resolve with adequate oxygenation ▪ Rash disappears spontaneously within a week – Prevention
110
FES treatment
Prophylactic treatment with corticosteroids Early immobilization of the injury – Rarely seen in children <10 years of age
111
Nursing role with fracture
– Maintain patient comfort – Assist with procedures – Provide patient education – Refer patient to specialists – Immobilize fracture – Prevent infection
112
Pharmacologic therapy for fracture
Analgesics for pain * Severe fractures – Opioids for pain – Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain, inflammation * Antibiotics to prevent or treat infection * Anticoagulants to prevent or treat DVT
113
Cast
– Rigid device to immobilize, support, and protect fractured bones and surrounding soft tissue ▪ Plaster or fiberglass, custom made to exactly fit injured limb ▪ Should cover, immobilize joint above and below fractured bone ▪ Functional cast allows limited movement of nearby joints
114
Nursing care of cast
▪ Frequent neurovascular assessments ▪ Palpate cast for “hot spots” indicating infection ▪ Report any drainage ▪ Assess for compartment syndrome
115
Splint
▪ Less support than cast but easily adjusted to accommodate swelling, prevent compartment syndrome
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Nonpharmacologic therapy: traction
use of weights, ropes, and pulleys to apply force to fractured bone to maintain proper alignment – Skin traction ▪ Used when only a small amount of weight is needed for traction ▪ Uses –To control muscle spasms –To maintain alignment of fracture before or after internal fixation –To provide traction if skeletal pins must be removed – Skeletal traction ▪ Used when a greater force is needed or skin traction contraindicated ▪ May be used in conjunction with skin traction ▪ Pins, wires, or screws surgically implanted into bone, weights attached to implanted hardware ▪ Monitor for infected pins
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RICE therapy
▪ Rest ▪ Ice ▪ Compression –Enough to provide support for injured area –Not so much as to decrease blood flow, causing compartment syndrome ▪ Elevation
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“Nursemaid’s elbow” (radial head subluxation)
▪ Not a fracture ▪ Partial separation of radiocapitellar joint ▪ Symptom: Child holds arm stiffly, doesn’t want to use it ▪ Prevention –Educate to avoid swinging children by hands or pulling by hands –Encourage picking children up under their arms
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Children most common fracture
Spiral fractures common because bones are porous
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Adults and older adults: fractures
– Lengthened recovery time because of slower rate of tissue growth ▪ Especially women after menopause, older adults – Older adults with osteoporosis ▪ Increased risk of hip fractures ▪ More likely to develop DVT, infections – Alterations in mental status increase risk
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5 P’s of neurovascular assessment
▪ Pain ▪ Pulses ▪ Pallor ▪ Paralysis, paresis ▪ Paresthesia
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Physical examination of fracture
– Distal pulses in injured extremity – Edema, swelling – Skin color, temperature – Deformity – Range of motion (ROM) – Sensation
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Cares for pt with fracture
Provide effective pain management – Regularly assess patient for ▪ Pain, muscle spasms, swelling ▪ Monitor vital signs – Administer pain medication – Monitor effectiveness of pain medication ▪ Advocate for stronger pain relief if needed – Elevate injured extremity – Provide ice to reduce swelling – Nonpharmacologic methods to reduce pain – Move patient gently and slowly – Support extremity above and below fracture site
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Monitor nerovascular status
– Assessments ▪ 5 P’s ▪ Assess injured limb for swelling, cramping, temperature, hematoma, movement, capillary refill, sensation to touch ▪ Every 15 minutes for first 2 hours after cast is applied ▪ Every 1–2 hours after that ▪ Report abnormal findings immediately – Have cast saw available for emergency cast removal or bivalving – If compartment syndrome suspected ▪ Assist in measuring compartment pressure – If DVT is suspected ▪ Administer anticoagulant as ordered
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Provide discharge instructions
– Cast care – Activity restrictions – When to take pain medications – Signs of complications – Injury prevention – Special instructions for using crutches on stairs – Referral for permanent or temporary ramp – Referral to home healthcare for older patients
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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
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Risk factors of hip fracture
– Old age – Osteoporosis
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Preventing hip fractures
preventing falls – Performing weight-bearing exercises – Assessing home for hazards – Education about medications that may affect balance, bone density, or muscle strength – Annual vision exam * Exercise and healthy diet * Adequate intake of calcium and vitamin D * Mobility assessment for older adults
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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 – Other fractures – Head injuries – Internal injuries
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Hip fx complications
Complications from loss of mobility – Deep venous thrombosis (DVT) – Pressure ulcers – Urinary tract infection (UTI) – Pneumonia – Muscle atrophy * Other complications – Postoperative infection – Mental deterioration – Avascular necrosis – Nonunion or malunion of bone – Loss of muscle mass, strength – Continued decline in mobility
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Treatment of hip fx
First-line treatment * Should occur as soon as possible after the fracture * Goals of surgery – Reduce pain – Stabilize fracture – Return patient to normal activity level * Three types of surgery – Repair with hardware – Partial hip replacement – Total hip replacement ▪ May require revision therapy or replacement of artificial joint after 10 years
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Pharmacologic therapy for hip fracture
Pain medications – Opioids – Patient-controlled analgesia * Antibiotics to prevent infection * Anticoagulants to prevent DVT * Anti-inflammatories for patient with well-worn prosthesis * Bone density enhancers
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Nonpharmacologic therapy for hip fracture
Bedrest * Traction – Buck – Russell * Casting – Hip spica cast * Prevention of complications – Exercise and compression stockings to prevent stiffness, DVT – 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)
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Older adults and hip fractures
– May not be able to return to independent lifestyle after hip fracture – High mortality rate if patient develops pneumonia after hip fracture – Emphasis on getting patient moving early – Nutrition, DVT prophylaxis, avoiding sensory deprivation
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Hip fracture nursing cares
– Managing pain – Promoting mobility – Preventing complications – Making referrals as necessary
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Preoperative nursing assessment includes
– Vital signs – Physical assessment – Cognitive function – Pain level – Neurovascular status: 5 P’s – Medical history ▪ History of current traumatic event ▪ Past history of osteoporosis, other conditions that affect strength, mobility, balance, coordination ▪ Medications
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Postoperative assessment
oxygenation assessment, presence of infection, ability to ambulate, urinary/bowel complications, DVT
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Nursing interventions for patients with hip fracture include
– Managing pain – Maintaining proper alignment – Promoting mobility – Monitoring patient’s neurovascular status – Monitoring for infection – Managing pre- and postoperative care – Emotional care – Instructions for home care
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Preop cares
▪ Manage pain ▪ Immobilize hip with traction or other restraints ▪ Provide information on treatment plan
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Post op cares
▪ Manage pain ▪ Promote mobility ▪ Prevent complications ▪ Assist with ambulation ▪ DVT prevention ▪ Respiratory exercises ▪ Active or passive ROM ▪ Wound care
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Provide thorough discharge instructions for hip fracture
– Proper use of abduction pillow if ordered – Proper sitting and bending techniques – Proper use of walker or cane – Explanation of weight-bearing limitations – Explanation of medications – Referrals for PT, home care agencies, medical equipment
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Patient should be evaluated for what with hip fracture?
– Return of mobility – Absence of neurologic complications – Decrease in pain – Absence of complications from fracture and surgery – Emotional state – Benefits of PT and rehabilitation programs – Adherence to discharge instructions – Patient and family/caregiver coping, functioning