nr203 test5 musculoskeletal 7 Final Questions

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meds for osteoporosis: Bisphosphanates
Alendronate (Fosamax)
Risendronate (Actonel)

HRT

Selective Estrogen Receptor Modulator (SERMs)
Raloxifene (Evista)

Teriparatide (Forteo)

Calcitonin (Miacalcin)
gout is characterized by: deposits of urates in the connective tissues of the body
Peak age onset is between 40-50 years; rare in women before menopause
Primary Gout
Results from an inborn error of purine metabolism leading to decrease in renal uric acid secretion
men>women
Secondary gout
Occurs as a result of another disorder or treatment with certain medications
Stages of gout: Asymptomatic hyperuricemia
Asymptomatic hypouricemia, serum levels average 9-10 mg/dL
Acute gouty arthritis
Usually affecting a single joint, occuring unexpectedly
Tophaceous or chronic gout
Occurs when hyperuricemia is not treated.
Acute gout: Gout has an acute onset and the joint most often affected is the first MP joint (big toe)
Acute attacks are characterized by severe pain, swelling, and erythema of the joint.
Gouty arthritis results from deposits in the synovial fluids causing acute inflammation of the joint.
Chronic gout: Chronic gout occurs when hyperuricemia is not treated. This leads to urate crystal deposits (tophi) to develop in cartilage, synovial membranes, tendons, and soft tissues. Such tophi can destroy the joint and adjacent bone.
Gout diagnostic tests: serum uric acid is nearly always elevated >7.5 mg/dL indicating hyperuricemia
regular levels men: 3.4-7.0
women 2.4-6.0
WBC-significant elevation in gout 20,000
ESR (sed rate)-elevated during an acute attack from the acute inflammatory process
24 hour UA-analyzed to determine uric acid production and excretion
Analysis of fluid from inflamed joint
Gout-Collaborative care: Directed toward ending acute attack and preventing recurrent attacks
Medications-acute attack
NSAIDS (Indocin most frequent)
Colchicine
Corticosteroids
Analgesics
Prophylactic therapy
Colchicine
Uricosuric drugs

Bed rest
Affected joint elevated/hot or cold compresses applied
Fluid intake to maintain daily urinary output of 2000 mL
Osteoarthritis: Conservative Treatment
a) Physical therapy
b) Rest of involved joint
c) Using ambulation devices
d) Weight loss
Osteoarthritis common problem for many people_____: a common problem for many people after middle age. In ideopathic OA 90% of individuals affected by age 40, but manifestations don't occur until after age 50 or 60.
Osteoarthritis diagnosis: The diagnosis can usually be made on the basis of the initial history and physical examination and x-rays. Affected joints initially slow irregular goint space narrowing. Progressive changes include increased density of subchondral (under cartilage) bone.
Interventions for osteoarthritis: Aimed at relief of pain and maintaining client's function and mobility.

So, reduce pain and inflammation, preserve function, and prevent deformity.
Systemic Lupus Erythematosis: A chronic inflammatory immune complex, connective tissue disease affecting multiple body systems.
systemic scleroderma: uncommon, chronic disease
excess fibrous connective tissue and fibrosis of the skin and internal organs.
Women 3:1 over men
Onset 30-50 years of age.
Increased incidence in coal and gold miners and with chemical exposure.
Scleroderma Pathophysiology: abnormality in cellular immune function
fibrous connective tissue occurs in tissue involving skin, blood vessels, lungs, kidneys, and other organs
Can be localized (skin only) or systemic (skin and organs).
Scleroderma manifestations: Skin thickining non-pitting edema, atrophy of skin, taut, shiny, hyperpigmentation
Facial tightening, less of skin lines
Arthralgia, arthritis
CREST: Calcinosis of Scleroderma
Raynaud's Phenomenon
Esophageal hardening of scleroderma
Sclerodactyly of scleroderma
Telangiactasis of Scleroderma
Scleroderma visceral organ involvement: Pulmonary
exertional dyspnea, pulmonary hypertension
Heart
pericarditis, dysrhythmias
GI
diarrhea, constipation, malabsorption
Renal
Proteinuria, hematuria, HTN, renal failure
Scleroderma Nursing care: care of clients may be quite varied, depending on the effects of the disease
Skin Care
Nutrition
Pulmonary/Renal
Emotional
Raynaud's care
Physical Therapy
Lyme disease: Most frequent time of onset is summer months
Certain geographical areas at highest risk
Northeast
Mid-Atlantic
Northcentral
Most common tick borne disease in US
Deer ticks transmit it (weeds/bushy areas)
Bacteria (spirochete)
Borrellia Burgdorferi
Lyme disease initial manifestations: Erythema Migrans (Bulls eye rash), malaise, fatigue, fever, chills
Lym disease secondary manifestations: Secondary skin lesions develop if disease progresses
Musculoskeletal symptoms
Persistent fatigue
Neuro symptoms
Late manifestations (can develop months to years later)
chronic recurrent arthritis (affecting large joints) inflammatory joint changes resemble rheumatoid arthritis
Key to prevention lyme disease complications: the Key to prevention of disability and complications secondary to Lyme disease is prevention, recognition of manifestations, and seeking appropriate treatment.
Osteomyelitis: Infection of the bone
Can occur over age 50 are more commonly affected
Usually bacterial in nature
Nursing care for individuals with Amputations: Goals of nursing care
to relieve pain
Promote healing
Prevent complications
Support client and family during the process of grieving and adaptations to alterations in body image
Restore mobility
LE amputation, exercises for UE to increase ability to ambulate using assistive devices
Osteoporosis ( â€œPorous bonesâ€) 1. Definition: a) Systemic Metabolic Disorder characterized by loss of bone mass, increased bone fragility, increased risk for fractures
b) Imbalance of processes that influence bone growth and maintenance (estrogen deficiency, parathyroid gland abnormalities, vitamin deficiency, malabsorption, physical inactivity) associated with aging, but may result from endocrine disorder or malignancy
Osteoporosis Risk Factors unmodifiable: Unmodifiable risk factors
(1) Aging: decrease in osteoblastic (form new bone) and osteoclastic activity related to decreasing levels of hormones (estrogen in females; testosterone in males)
(2) Gender: women have 10 â€“ 15% less peak bone mass than men; bone loss begins earlier (30â€™s) and proceeds more rapidly.
(3) European Americans and Asians have less bone density than African Americans (small frame)
(4) Endocrine disorders affecting metabolism: hyperthyroidism, hyperparathyroidism, Cushingâ€™s syndrome, diabetes mellitus
Osteoporosis Risk Factors modifiable: c) Modifiable risk factors (nutrition, estrogen, physical activity influence bone mass)
(1) Calcium deficiency: insufficient calcium in diet results in body removing calcium from bones.
(2) Menopause, decreasing estrogen levels: estrogen replacement therapy can reverse bone changes but may increase risk for other diseases. (estrogen stimulates osteoblast activity, decreases osteoclast activity)
(3) Cigarette smoking: decreased blood supply to bones: (smokers have 2:1 times the risk of fxs)
(4) Excessive alcohol intake: toxic effect on osteoblastic activity (high alcohol intake frequently associated with nutritional deficiencies and increase risk of falls)
(5) Sedentary life style: weight-bearing exercise such as walking positively influences bone metabolism; (physical activity stimulates bone growth from tension of weight bearing and pull of muscles on bone)
(6) Use of specific medications: aluminum-containing antacids, corticosteroids, anticonvulsants
Osteoporosis Pathophysiology: Pathophysiology
(1) Normal bone continually undergoes remodeling, the process by which old bone is replace by new (1. Replaces old bone with new so biochemical properties of the skeleton are not compromised by continous use. 2. Plays a role in mineral homeostasis by transferring calcium and other ions into and out of the skeletal reservoir)
(2) The exact cause is unclear; but it is known to involve an imbalance of the activity of osteoblasts (form new bone) and osteoclasts (resorb bone). After peak bone mass is achieved, bone formation does not keep up with resorbtion resulting in a bone loss of ~0.3 â€“ 0.5% per year.
Osteoporosis Manifestations: Often called the â€œsilent diseaseâ€ because bone loss occurs without symptoms.
(1) Loss of height
(2) Progressive curvature of spine (dorsal kyphosis, cervical lordosis, accounting for â€œdowagerâ€™s humpâ€)
(3) Low back pain
(4) Fractures of forearm, spine or hip
Osteoporosis Complications: Complications include
(1) Fractures (> 1.5 million fractures yearly)
(2) Persistent pain
(3) Associated posture changes
(4) Restricted client activities and ability to perform ADL
Osteoporosis Lab & diagnostic tests: Lab & diagnostic tests
a) Xrays: picture of skeletal structures but osteoporotic changes not seen until > 30% of bone mass lost
b) Dual-energy Xray absorptiometry (DEXA): measures bone density in lumbar spine or hip; highly accurate gold standard (0 calcium supplements for 24 hours before ; wait 7 days after barium study, contrast dye, CT or MRI)
c) Bone Mineral Density (BMD) tests. Bone density tests can:
(1) Detect low bone density before a fracture occurs
(2) Confirm a diagnosis of osteoporosis if you have already fractured
(3) Predict your chances of fracturing in the future
(4) Determine your risk of bone loss and/or monitor the effects of treatment if the test is conducted at intervals of a year or more.
d) Alkaline phosphatase (AST): rises in proportion to new bone cell production resulting from osteoblastic activity and the deposit of calcium in the bones
Osteoporosis Collaborative Care: Collaborative Care
a) Directed at stopping or slowing bone loss, alleviating symptoms and preventing complications such as fracture.
Osteoporosis Pharmacology: Pharmacology
(a) Bisphosphonates: potent inhibitors of bone resorption used to prevent and treat osteoporosis. (bone gain instead of loss; research shows a decrease in fxâ€™s by 30-50%) see nursing implications on handout)
(i) Alendronate (Fosamax)
(ii) Risedronate (Actonel)
(b) Estrogen or hormone replacement therapy (HRT) reduces bone loss, increases in bone density in spine and hip, reducing risk of fractures in postmenopausal women. Benefits must be weighed against risks.(some combinations of estrogen/progesterone were found to increase risk of CHD, stroke, breast CA, thromoembolitic disorders)
(c) Raloxifene (Evista): selective estrogen receptor modulator (SERM) that prevents bone loss by mimicking estrogen effects on bone density; side effects are hot flashes and blood clots
(d) Teriparatide (Forteo): a (synthetic form of PTH)parathyroid hormone; is an anabolic (bone-building agent) administered daily SQ (up to 24 mo.); stimulates osteoblast activity; use with caution in patients who take digoxin as it may cause hypercalcemia and increase risk of digoxin toxicity
(e) Calcitonin (Miacalcin & Calcimar): hormone increases bone formation and decreases bone resorption; available as nasal spray or parenteral.(less effective than Fosamax, Actonel; SQ)
Osteoporosis Nursing Diagnosis: Nursing Diagnosis
Health Seeking Behaviors
Risk for Injury
Pain
Osteoporosis Health Seeking Behaviors: Health Seeking Behaviors
(1) Calcium intake
(a) Optimal intake before age 30-35 increases peak bone mass
(b) Foods high in calcium milk, milk products, salmon, sardines, clams, oysters, dark green leafy vegetables
(c) Supplementation in divided doses; calcium combined with Vitamin D for older adults; Vitamin D needed for absorption of Ca/ or sunlight (Vitamin D is synthesized in the skin thru exposure to sunlight; elderly donâ€™t absorb or process vitamin D form the sun as efficiently as younger adults
(i) Age 19 â€“ 50: 1000 mg
(ii) Age 51-64: 1200 mg
(iii) Age 65 up: 1500 mg
(2) Exercise
(a) Weight-bearing physical activity
(b) Walking 20 minutes, 4 or more times per week; resistance training; strengthening the skeletal muscles by using resistance
(3) Health-related behaviors
(a) No smoking
(b) Avoid excessive alcohol
(c) Screening
(i) All postmenopausal women under age 65 with one or more additional risk factors (fx, estrogen deficient women, vertebral abnormalities, steroid therapy, hyperthyroidism, those being monitored on osteoporosis drug therapy)
(ii) All women over age 65
Osteoporosis Risk for Injury Pain: Risk for Injury
(1) Preventing falls
(a) Outdoors
(i) Cane or walker for stability
(ii) Rubber soles for traction
(iii) Carry salt or kitty litter to sprinkle on sidewalks
(b) Indoors
(i) Rooms free of clutter
(ii) Avoid walking in socks or stockings
(iii) Area rugs with skid proof backing or just get rid of them
(iv) Stairwells well lit
(v) Grab bars
(vi) Flashlight by bedside
(2) Hip protectors

Pain
Gout Definition: Definition
a) Metabolic disorder characterized by deposits of urate crystals in connective tissue of the body. Occurs from inflammatory response to excess production or decreased excretion of uric acid resulting in high levels of uric acid.(in blood and other body fluids such as synovial fluid)(also myocardium, kidneys and ears)
Gout Primary gout Secondary gout: Primary gout: genetic disturbance in purine (end product of protein metabolism) metabolism. Uric acid production is greater than renal excretion. Urate crystals precipitate in the tissues, especially synovial tissue. 85% of gout is primary; of those 95% are men

Secondary gout: hyperuricemia occurs as a result of other disorders or treatments.
(1) Malignancies (leukemia)
(2) Chronic renal failure
(3) Certain medications (aspirin)and some diuretics (thiazide)
Gout Pathophysiology: Pathophysiology
a) Uric acid is a breakdown product of purine metabolism and is normally excreted through urine and feces.
b) Levels > 7.0 mg/dL (normal: 3.4 â€“ 7.0 mg/dL in males; 2.4 â€“ 6.0 mg/dL in females) lead to formation of urate crystals (tophi) in peripheral tissues (synovial membranes, cartilage, heart, earlobe, kidneys) and perpetuate inflammation. (Because crystals are deposited in connective tissue, gout is classified as a form of arthritis)
Gout Manifestations: Manifestations
a) Asymptomatic Hyperuricemia stage 1
(1) Serum levels 9 â€“ 10 mg/dL
(2) Many persons do not progress beyond this level
b) Acute Gouty Arthritis stage 2
(1) Acute attack usually affecting a single joint, usually the big toe
(2) Pain, severe in affected joint
(3) Redness and swelling of affected joint
(4) Fever, chills, malaise, elevated WBC and ESR
(5) May be triggered by trauma, alcohol ingestion, dietary excess, stressors such as surgery or hospitalization
c) Chronic Gout stage 3
(1) Occurs when hyperuricemia not treated
(2) Tophi evident (deposits of uric acid)
(3) Joint stiffness, limited ROM
(4) Leads to joint deformities and nerve compression (limited ROM, severe pain, crutches needed)
(5) May lead to acute renal failure and cardiac disorders
Gout Lab & diagnostic tests: Lab & diagnostic tests
a) Serum uric acid is nearly always elevated
b) Analysis of synovial fluid reveals intracellular crystals
c) WBC: elevated during acute attack
d) Erythrocyte sedimentation rate (ESR): elevated from acute inflammation process
e) 24 hour urine collection to determine uric acid production and excretion
Gout Collaborative Care: Directed toward ending acute attack and preventing recurrent attacks and complications. Pharmacology:: a) Pharmacology
(1) Acute attack
(a) NSAIDs treatment of choice for an acute attack (Indocin or Naproxen)
(b) Colchicine: interrupts cycle of urate crystal deposits and inflammation. (one source said this is the drug of choice for acute attacks
(i) Anti-inflammatory use limited to gout: reduces migration of leukocytes to the synovial fluid; therapeutic dose close to toxic dose)
(ii) Use limited by significant side effects: with oral administrant abdominal cramping, diarrhea, nausea, vomiting
(c) Corticosteroids
(d) Analgesia, including narcotics
(2) Prophylactic Therapy: Clients who do not eliminate uric acid adequately are treated with colchicine and uricosuric (drugs that increase urinary excretion of uric acid) drugs, such as probenecid (Benemid) and sulfinpyrazone (Anturane). Clients who produce excessive amounts of uric acid are treated with allopurinol (Zyloprim), which lowers serum uric acid levels. If more than two attacks per year, long term medication)
Gout Other Treatments: Other Treatments
(1) Bed rest
(2) Affected joint elevated and hot/cold compresses applied for comfort
(3) Fluid intake to maintain a daily urinary output of 2000 ml or more (to increase urate excretion and reduce risk of urinary stone formation) (intake 3-4,000)
Gout Nursing Dx / Interventions: Nursing Dx / Interventions
a) Acute Pain
b) Impaired Physical Mobility
c) Health Seeking Behaviors
(1) Education regarding prescribed medications
(2) Education on maintaining high intake of fluid and avoiding alcohol (interferes with removal of uric acid)
(3) Avoid high purine foods: meat, legumes, mushrooms, oatmeal and the alcohol
Degenerative Bone Disease: Osteoarthritis Definition: Degenerative Bone Disease: Osteoarthritis (OA)/Degenerative Joint Disease (DJD)
Definition: A degenerative joint disease characterized by degeneration and loss of articular (involving a joint) cartilage in articulating joints.
1. Idiopathic: no history of joint injury, joint disease or systemic illness associated with development of arthritis
a) Most common articular disease in adults >65 by 2030, # of people > 65 with arthritis will be > 41 million) (chronic and incurable)
b) Substantial disability in lower extremities
2. Secondary: Results from trauma or other inflammatory joint disease
Osteoarthritis Risk Factors: Risk Factors
1. Age
2. Strong familial disposition: may be inherited as autosomal recessive trait
3. Gender
a) Idiopathic: more common in women than men
b) Secondary: more common in men
4. Excessive weight especially in hip and knee
5. Inactivity
6. Strenuous, repetitive exercise as with sports participants increased risk for secondary OA
7. Hormonal factors such as decreased estrogen in menopausal women
Osteoarthritis Pathophysiology: Pathophysiology
1. Cartilage lines the joints and serves 2 purposes.
a) It provides a smooth surface for bones to glide over one another without friction
b) It distributes the load from one bone to the next decreasing mechanical stress.
2. In osteoarthritis, over time large areas of cartilage are lost and underlying bone is exposed.
3. Osteophytes (bony outgrowths) form and change the anatomy of the joint
Osteoarthritis Manifestations: Manifestations
1. Onset is gradual, insidious, slowly progressive
2. Joint stiffness/chronic pain; deep, aching; worse in the morning and with exercise and weather changes
3. Decreased ROM and crepitus with motion
4. Pain relieved by rest but may become persistent with time
5. Periods of immobility are followed by stiffness
6. Joint spurs/deformity (Heberdenâ€™s and Bouchardâ€™s nodes)(bony overgrowth causes joint enlargement)
7. Flexion contractures occur with joint instability
Osteoarthritis Lab & diagnostic tests: Lab & diagnostic tests
1. Characteristic changes seen on x-ray of joints
2. Some lab tests done to rule out other conditions (rheumatoid factor, serum uric acid)
3. Arthrocentesis: removal of fluid for testing
Osteoarthritis Pharmacology: Pharmacology
a) Pain management with acetaminophen first choice (inhibit prostaglandin synthesis by CNS), then NSAIDâ€™s Naproxyn, Ibuprofen)(research is showing that NSAIDs disrupt articular cartilage metabolism
b) Capsaicin cream topically to reduce joint pain and tenderness
c) COX-2 inhibitors-Celecoxib (Celebrex), Meloxicam (Mobic) and valdecoxib (Bextra)
d)Corticosteroids
e)Viscosupplementation (Hyaluronan)
Osteoarthritis Pharmacology COX-2 inhibitors: COX-2 inhibitors
(1) Fewer GI side effects than conventional NSAIDs
(a) NSAIDs work by interfering with the cyclooxygnase (COX) pathway, ultimately inhibiting prostaglandin synthesis. Prostaglandin causes vasodilation, which allows more blood flow to an affected area and results in the heat and redness of inflammation prostaglandin also prolongs pain. By inhibiting prostaglandin synthesis, NSAIDs can decrease inflammation and pain associated with arthritis. The COX-1 enzyme in the stomach wall continuously produces prostaglandins that stimulate mucous formation and protect the stomach lining. Traditional NSAIDs such as ibuprofen and naproxen interfere with the COX-1 enzyme pathway, leading to increased risk of gastrointestinal side effects for clients taking these drugs. In contrast, production of the COX-2 enzyme is induced bay macrophages a s a part of the inflammatory process. Newer NSAIDs are selective for the COX-2 enzyme pathway, decreasing inflammation while potentially having fewer gastrointestinal effects.
(2) Celecoxib (Celebrex), Meloxicam (Mobic) and valdecoxib (Bextra)
Osteoarthritis Pharmacology Corticosteroids Viscosupplementation: Corticosteroids may be injected into the joint space for relief of severe pain, but this may hasten rate of cartilage breakdown
e) Viscosupplementation (Hyaluronan) a polysaccharide that is a major component of synovial fluid, can be administered by intraarticular injection into the knee (FDA approves as a medical device rather than as a drug)
Osteoarthritis Alternative therapies: Alternative therapies
(1) Oral glucosamine sulfate: is considered a dietary supplement; the FDA doesnâ€™t regulate it. Is said to slow or even halt the progression of osteoarthritis; has a weak anti-inflammatory effect; reduces pain and improves ROM. Instruct patients that research findings are promising but still inconclusive. Follow recommended daily dosage, inform health provider of use. 1500mg/day
(2) Acupuncture
Osteoarthritis Surgery Arthroscopy: Arthroscopy
(1) Arthroscopic debridement and lavage of involved joints
(2) Unclear about effectiveness long term
Osteoarthritis Surgery Joint arthroplasty: Joint arthroplasty
(1) Reconstruction or replacement of joint indicated when client has severely restricted joint mobility and pain at rest.
(2) Total joint replacement is procedure done for most OA clients (replaces both surfaces of affected joint)
(3) Most prosthetic joints are uncemented; made of porous ceramic and metal components inserted to fit tightly into existing bone; implant secured by new bone growth in about 6 weeks; requires longer non-weight-bearing period but implant has longer useful life span for use in younger, more active individuals
(4) Cemented joint replacement uses polymethyl methacrylate (PMMA) to secure prosthesis to existing bone; client able to resume normal activities sooner but inflammation eventually loosens joint Has been around a long time
Osteoarthritis Surgery Specific joint replacements: Specific joint replacements
(a) Total hip replacement (THR) or Total hip Arthroplasty (THA) (L&B p. 1243-1244 for pre- and post op care) About 600,000 American have joint replacements each year
(i) Articular surfaces of acetabulum and femoral head are replaced
(ii) Success rate > 90% 95% last 10 years; 85-90% last 15 years
(b) Total knee replacement
(i) > 80% clients obtain significant or total relief
(ii) Vigorous rehabilitation program required
(iii) Joint failure rate higher than with THR: due to loosened joint components on tibial side
(c) Total shoulder replacement
(i) Indicated for unremitting pain and limited ROM
(ii) Joint immobilized in sling of abduction splint for 2 â€“ 3 weeks post arthroplasty
(d) Total elbow replacement
Osteoarthritis Nursing Dx: Health Seeking Behaviors (health promotion)
Pain management
Deficient Knowledge
Acute Pain and Chronic Pain
Impaired Physical Mobility
Risk for Peripheral Neurovascular Dysfunction
Risk for Fluid Volume Deficit
Risk for Injury
Risk for Infection
Risk for Impaired Skin Integrity
Risk for Altered Tissue Perfusion related to decreased circulation secondary to Deep Vein Thrombosis:
Risk for Impaired Gas Exchange
Self Care Deficit
Risk for Constipation
Osteoarthritis Nursing Dx / Interventions Deficient Knowledge: 3. Deficient Knowledge related to prior inexperience with total hip replacement (pre-op THR)
a) Group class â€œtotal joint campâ€
(1) Transfer training
(2) Post-op positioning
(3) Walker training
(4) Incentive spirometer use
(5) Home modifications
(6) Pain control
b) Regarding pharmacological and other forms of pain relief
Osteoarthritis Nursing Dx / Interventions Acute Pain and Chronic Pain: Acute Pain and Chronic Pain
a) Related to local tissue trauma from surgical incision
b) Related to inflammatory process in remaining joints
Osteoarthritis Nursing Dx / Interventions Impaired Physical Mobility: Impaired Physical Mobility related to pain or fear of movement
a) Know weight bearing limitations
b) Have enough help: IV lines, catheters, wound drains, O2 tubing, etc; move away from operative side; use brakes, slippers; gait belt
c) Remind patient to keep knee slightly lower than the hip (avoid flexion of hip to avoid dislocation)
d) Support therapist in bed exercises
Osteoarthritis Nursing Dx / Interventions Risk for Peripheral Neurovascular Dysfunction: Risk for Peripheral Neurovascular Dysfunction related to lower extremity edema or positioning (compartment syndrome and nerve injury)
a) Assess CSM at least q 4 h or as directed by surgeon (q hour x 4 then q 4 hrs)
b) Assess CSM (Circulation, Sensation, Movement) at least q 4 h or as directed by surgeon; five Pâ€™s
(1) Pain
(2) Pallor
(3) Pulselessness
(4) Paresthesia
(5) Paralysis
Osteoarthritis Nursing Dx / Interventions Risk for Fluid Volume Deficit: Risk for Fluid Volume Deficit secondary to blood loss
a) THA 1,000-2,000 mL loss
b) TKA 500 â€“ 1,000 mL loss
c) Take good I&O. If > 250 cc in first 24 hours, or if drainage remains bright red after 24 hoursâ€¦
Osteoarthritis Nursing Dx / Interventions Risk for Injury: Risk for Injury related to prosthesis dislocation
a) Reposition q 2 hrs using precautions (if posterolateral approach, do not flex hip beyond 90-dgree angle)
b) Elevated toilet seat
c) Abduction pillow
d) S/S of dislocation: acute groin pain, sudden pain or increase in pain, shortening of involved leg, sever rotation (external or internal), patient may have heard a â€œpopâ€
Osteoarthritis Nursing Dx / Interventions Risk for Infection: Risk for Infection
a) Impaired skin integrity and decreased blood supply may lead to osteomyelitis; organisms include Pseudomonas, Staphylococcus or Clostridium
b) Prophylactic IV antibiotics before incision is made and continued for 2 â€“ 3 days post-op
c) Empty drains using aseptic technique
d) Assess surgical site
e) Dressing changes using strict aseptic technique
f) Tips on assessing Temperature
(1) Likely location of a post-op infection can be predicted by timing of fever. Classic sources of post-op fever can be listed as the 5 Wâ€™s
(a) Wind â€“ likely pulmonary source if fever occurs 1-2 days after surgery
(b) Water â€“ urinary source if occurring 2 â€“ 4 days post-op
(c) Wound â€“ likely surgical site source of fever if occurring 5 days after surgery (+ or -)
(d) Walking â€“ likely DVT in leg if occurring 7 days after surgery (+ or -)
(e) Wonder drugs â€“ likely abnormal response to antibiotic medication
(f) Example: fever 101.8 first day post-op, more likely suspect post-op altelectasis vs wound infection
Osteoarthritis Nursing Dx / Interventions Risk for Impaired Skin Integrity: Risk for Impaired Skin Integrity
a) Related to decreased physical mobility intra-operatively and post-operatively
b) Related to shearing forces, tape
Osteoarthritis Nursing Dx / Interventions Risk for Altered Tissue Perfusion: Risk for Altered Tissue Perfusion related to decreased circulation secondary to Deep Vein Thrombosis: most common complication after a THA
a) Assess for excessive pain, unilateral edema, red vein track
b) Early mobilization
c) Pneumatic compression devices/elastic stockings
d) Pharmacologic agents[low molecular weight heparin such as Lovenox}
e) Frequently assess respiratory status, can lead to pulmonary embolism [sudden dyspnea, chest pain, diaphoresis, tachycardia, tachypnea]
Osteoarthritis Nursing Dx / Interventions Risk for Impaired Gas Exchange: Variations in nursing care for TKA vs THA
a) Emphasis on knee exercise is greater
b) Elevate operative extremity when up in chair
Osteoarthritis Newer procedure: Minimally invasive procedure:: Newer procedure: Minimally invasive procedure:
1. 1-2 small incisions 4â€ or less
2. One for acetabular component and one for femoral component
3. Less traumatic; promotes better healing; joint stability; lose less blood and go home sooner
4. Canâ€™t use for someone morbidly obese or severe femoral deformities
Autoimmune and inflammatory disorders Rheumatoid Arthritis (RA) Definition: Definition
a) Chronic systemic autoimmune disease causing inflammation of connective tissue primarily in the synovial tissue of the joints
(1) Three times more likely to affect females than males
(2) Onset occurs more frequently between 20 â€“ 40 years
b) Course and severity are variable; periods of remission and exacerbation; clients exhibit pattern of symmetrical multiple peripheral joint involvement
c) Cause is unknown; combination of genetic, environmental, hormonal, reproductive factors, infectious agents esp. Epstein-Barr thought to play a role
Rheumatoid Arthritis Risk Factors Pathophysiology: Risk Factors
a) Genetic factors
b) Presence of RF (rheumatoid factor)
3. Pathophysiology
a) Normal antibodies become autoantibodies (rheumatoid factors - RF) and attack host tissues, which bind with target antigens in blood and with synovial membranes forming immune complexes
b) Synovial membrane damaged from inflammatory and immune processes; leads to erosion of articular cartilage and inflammation of ligaments and tendons
c) Granulation tissue (pannus) forms over denuded areas of synovial membrane and this leads to scar tissue formation immobilizing the joint.
d) The normal joint (the place where two bones meet) is surrounded by a joint capsule that protects and supports it. Cartilage covers and cushions the ends of the two bones. The joint capsule is lined with a type of tissue called synovium, which produces synovial fluid. This clear fluid lubricates and nourishes the cartilage and bones inside the joint capsule. In RA, the immune system, for unknown reasons, attacks a personâ€™s own cells inside the joint capsule. White blood cells that are part of the normal immune system travel to the synovium and cause a reaction. This a reaction, or inflammation, is called synovitis, and it results in the warmth, redness, swelling and pain that ar typical symptoms of RA. During the inflammation process, the cells of the synovium grow and divide abnormally, making the normally thin synovium thick and resulting in a joint that is swollen and puffy to the touch. As RA progresses, these abnormal synovial cells begin to invade and destroy the cartilage and bone within the joint.
Rheumatoid Arthritis Manifestations Joint manifestations: Joint manifestations
(1) Onset typically insidious but may be acute after stressor, such as infection
(2) Preceded by systemic manifestations of inflammation fatigue, anorexia, weight loss and non-specific aching and stiffness precedes joint involvement
(3) Joint swelling with stiffness, warmth, tenderness and pain; joint involvement is typically polyarticular and symmetric involvement
(4) Stiffness most pronounced in the morning
(5) ROM limited in joints affected and weakness may be evident
(6) Joint deformity
(a) Proximal interphalangeal and metacarpophalangeal joints of fingers, wrists, knees, ankles, and toes are frequently involved; weakening or destruction of supporting structure result in deformity
(b) Joint deformity of fingers include swan-neck deformity and boutonnier deformity; writs deformity leads to carpel tunnel syndrome; knee deformity leads to disability and feet and toes develop typical deformities
Rheumatoid Arthritis Manifestations Extra-articular manifestations systemic: Extra-articular manifestations systemic
(1) Fatigue, weakness, anorexia, weight loss, low grade fever while disease is active
(2) Skeletal muscle atrophy and anemia
(3) Rheumatoid nodules may develop in subcutaneous tissue in areas subject to pressure on forearm, olecranon bursa, over metacarpophalangeal joints
(4) Pleural effusion, pericarditis, splenomegaly may occur
Rheumatoid Arthritis Diagnostic Criteria for RA (Box 39-3 pg. 1250 L&B): Diagnostic Criteria
Rheumatoid Arthritis Diagnostic Tests: a) Rheumatoid factors (RFs) are present in approximately 75% of people with RA Supports a tentative dx of RA
b) Erythrocyte sedimentation rate (ESR) is typically elevated and is often used as an indicator of disease and inflammatory activity
c) Examination of synovial fluid; signs associated with inflammation
d) X-rays of affected joints are taken; shows diagnostic changes
e) CBC â€“ shows moderate anemia with elevated platelet count
Rheumatoid Arthritis Collaborative Care: Aimed at pain relief and reduction of inflammation; slow or stop joint damage; improve function Irreversible damage takes place in the first two years of RA Pharmacology: Aspirin and other NSAIDs
Selective NSAIDs such as Cox-2 inhibitors
Disease Modifying Rheumatic Agents (DMARDs)
Biologic Response Modifiers (BMRs)
Corticosteroids
Rheumatoid Arthritis Pharmacology Aspirin and other NSAIDs Corticosteroids: Aspirin and other NSAIDs (relieve inflammation, but have little effect on disease progression; GI side effects) Often prescribed in high does just under toxic does, which produces tinnitus and hearing loss

Corticosteroids
(a) Low dose oral to reduce pain and inflammation and to slow development and progression of disease dramatic improvements in a very short time; but long-term use results in multiple side effects
(b) Intra-articular corticosteroids

Recent research shows combining Enbrel with Methotrexate can induce clinical remission and stop joint damage in some patient with RA
Rheumatoid Arthritis Pharmacology Disease Modifying Rheumatic Agents (DMARDs): Disease Modifying Rheumatic Agents (DMARDs)
(a) Antimalarial drug Hydroxychloroquine (Plaquenil): clients need vision exam every 6 months since can cause pigmentary retinitis and vision loss
(b) Immunosupressive drug Methotrexate (Rheumatrex): treatment of choice for early aggressive RA; best if given in combination with cyclosporine (anti-rejection) Used to restrain the overly active immune system, which is key to the disease process; side effects include upset stomach, potential liver problems, low WBCâ€™s; monitor regular blood tests, including liver function test, baseline chest x-ray; youâ€™ve had this medication before, so not on MS drug handout
(c) Other DMARDs: Gold compounds, IM injection,skin rash, mouth sores, upset stomach, kidney problems low blood count D-penicillinamine,potential for severe toxic reactions (bone marrow suppression, preteinuri, nephrosis) azathioprine, cyclophosphamide, leflunomide (Arava) slows progressive destruction of joint tissues, Azulfidine EN Tabs (sulfasalizine, antiinflammataory)
Rheumatoid Arthritis Pharmacology Biologic Response Modifiers (BMRs): Enbrel (Etanercept) Etanercept binds specifically to tumor necrosis factor (TNF) and blocks its interaction with cell surcvade TNF receptors. TNF is a naturally occurring cytokine that is involved in normal inflammatory and immune responses. Etanercept is genetically engineered (TNF) receptors from Chinese hamster ovary cells that keep the inflammatory response to autoimmune disease in check by reacting with and deactivating free-floating TNF released by active leucocytes. Twice weekly SQ injection fo 25 mg.
(b) Remicade (infliximab) is a monoclonal antibody to TNF-alphs. Intravenous infusion of 3mg/kg over 2 hours at initrially, at 2 weeks, 6 wks and then every 8 wks
Autoimmune and inflammatory disorders Rheumatoid Arthritis Pharmacology Corticosteroids Enbrel and Methotrexate: Corticosteroids
(a) Low dose oral to reduce pain and inflammation and to slow development and progression of disease dramatic improvements in a very short time; but long-term use results in multiple side effects
(b) Intra-articular corticosteroids

Recent research shows combining Enbrel with Methotrexate can induce clinical remission and stop joint damage in some patient with RA
Autoimmune and inflammatory disorders Rheumatoid Arthritis Treatments: (1) Balanced program of rest and exercise
(a) Rest with exacerbation and may utilize splinting
(b) Exercise to maintain ROM, muscle strength when disease is under control
(c) Low impact exercise such as swimming or walking
(2) Physical and occupational therapy
(3) Heat and cold: analgesia and muscle-relaxation
(4) Assistive devices and splints which help rest joints and prevent contractures
(5) Diet: well-balanced; some benefit from omega-3 fatty acids found in fish oils
(6) Surgery: variety of procedures may be done: synovectomy, arthrodesis, joint fusion, arthroplasty or total joint replacement
Autoimmune and inflammatory disorders Rheumatoid Arthritis Nursing Dx / Interventions: Nursing Dx / Interventions
a) Chronic Pain
b) Fatigue/Sleep Deprivation
c) Impaired Physical Mobility
d) Chronic Low Self Esteem, Disturbed Body Image, Hopelessness, Ineffective Role Performance, Powerlessness
e) Risk for Ineffective Therapeutic Regimen Management
Autoimmune and inflammatory disorders Ankylosing Spondylitis: Chronic inflammatory arthritis primarily affecting the axial skeleton leading to pain, progressive stiffening and fusion of the spine. Cause unknown. Ankylosis (fusion) spondylitis (inflamed vertebrae)
Autoimmune and inflammatory disorders Ankylosing Spondylitis Risk factors Pathophysiology: Risk factors
a) Gender more often in males with more sever disease 3:1 or 4:1
b) Age
c) Genetics

Pathophysiology
a) As joint cartilage erodes, joint margins ossify and are replaced by scar tissue.
b) Inflammatory joint changes often are first noted in the sacroiliac joints.
c) Joints of the spine are also affected, with inflammation of the cartilaginous joints, and gradual calcification and ossification that leads to ankylosis, or joint consolidation and immobility.
Ankylosing Spondylitis Manifestations: Manifestations
a) Onset usually gradual and insidious
b) Persistent or intermittent back pain
c) As disease progresses, back motion becomes limited, the lumbar curve is lost, and the thoracic curvature is accentuated and entire spine becomes fused
d) For most clients the disease is intermittent with mild to moderate acute episodes
e) Systemic manifestations: anorexia, weight loss, fever, fatigue
Ankylosing Spondylitis Lab & diagnostic tests: Lab & diagnostic tests
a) Usually confirmed with x-ray examination of the SI sacro iliac joints and spine
b) ESR â€“ elevated during active disease
c) 90% of people with Ankylosing Spondylitis have the HLA-B27 antigen; ~8% of the general population has this antigen
Ankylosing Spondylitis Collaborative Care: Collaborative Care: Provide support and education
a) Pharmacology
(1) NSAIDs (Indocin is the most commonly use)
(2) Azulfidine and topical or intra-articular corticosteroids
b) Other treatment
(1) Physical Therapy and daily exercise
Connective Tissue Disorder: Systemic Lupus Erythematosus (SLE) Definition Pathophysiology:: Definition
a) SLE is chronic inflammatory immune complex connective tissue disease affecting multiple body systems (pg. 1262 L&B); can range from mild episodic disorder to rapidly fatal disease process
b) Most clients have mild chronic case with periods of remissions and exacerbations

Pathophysiology: Production of large variety of autoantibodies against the normal components of body especially the nucleic acids; leads to development of immune complexes which leads to tissue damage in multiple organs misguided immune cells attack the bodyâ€™s DNA
Connective Tissue Disorder: Systemic Lupus Erythematosus (SLE) Risk factors: Risk factors
a) Gender⬦hormonal changes, affects mostly females in childbearing age; 9:1 female/male ratio
b) Race - more common in African Americans, Hispanics, Asians
c) Genetics
d) Some Drugs Reaction to some medications (procainamide, hydralazine, isoniasid, chlorpromazine) causes a syndrome similar to lupus, which usually resolves when medication is discontinued
Connective Tissue Disorder: Systemic Lupus Erythematosus (SLE) Manifestations: Manifestations
a) Early manifestations: fever, anorexia, malaise, weight loss, multiple arthralgias and symmetric non-deforming polyarthritis early symptoms mimic RA
b) Neurologic organic brain syndrome, psychosis, seizures; secondary to vasculitis/cranial or peripheral
c) Opthalmologic conjunctivitis, photophobia, retinal vasculitis; due to impact on retinal capillaries
d) Dermatologic:: red butterfly rash across the cheeks and bridge of the nose; accompanied by photosensitivity (maculopapular rash upon sun exposure); alopecia is common
e) Hematologic manifestations hemolytic anemia, leukopenia, thrombocytopenia
f) Cardiovascular system pericarditis, vasculitis, Raynaudâ€™s phenomenon, endocarditis
g) Pulmonary system pleurisy, pleural effusion
h) Renal: 50% of persons have renal involvement, proteinuria, cellular casts, nephritic syndrome; 10% develop renal failure
i) GI symptoms hepatomegaly, anorexia, nausea, abdominal pain, diarrhea; may be related to med use
j) Musculoskeletal Fatigue is a universal complaint
Connective Tissue Disorder: Systemic Lupus Erythematosus (SLE) Diagnosis:: Diagnosis: Often difficult due to the diversity of manifestations in individual clients. Differentiated by presence or development of glomerulonephritis, photosensitivity, characteristic skin rashes, CNS disease and various cytopenias such as the Coombsâ€™ positive hemolytic anemia, leucopenia, and thrombocytopenia
Connective Tissue Disorder: Systemic Lupus Erythematosus (SLE) Diagnostic Tests: Diagnostic Tests
a) Most specific: Anti-DNA: of various antibodies, this antibody is more specific for SLE; rarely found in any other disorder
b) Most sensitive: ANA assay
c) ESR: typically elevated, especially during exacerbations
d) Serum complement levels: levels are low (used in development of antigen-antibody complexes)
e) CBC abnormalities
f) Urinalysis: mild proteinuria, hematuria, blood cell casts
g) BUN and creatinine: determine renal function
h) Kidney biopsy: obtain accurate diagnosis of kidney lesion and plan definitive treatment with renal insufficiency
i) C-reactive protein useful to distinguish from infection (where itâ€™s elevated)
Connective Tissue Disorder: Systemic Lupus Erythematosus (SLE) Collaborative Care:: Collaborative Care: based on system involved. Goals based on maintaining skin integrity, promoting a healthy lifestyle, reducing stress, maintaining proper nutrition, promoting comfort, increasing independence, and maintaining emotional well-being
a) Medications
(1) Mild cases of SLE may be treated with supportive care and possible aspirin and NSAIDs
(2) Skin and arthritic manifestations are treated with anti-malarial drugs such as Plaquenil (can cause retinal toxicity, so eye exams q 6 mo)
(3) Severe cases are often treated with high-dose corticosteroid therapy tapered as clientâ€™s disease allows; treatment may also include immunosuppressive agents (cyclophosphamide or azathioprine) alone or with the steroids
Connective Tissue Disorder: Systemic Lupus Erythematosus (SLE) Nursing Dx / Interventions: Nursing Dx / Interventions
a) Varies according to organ systems involved
b) See http://www.niams.nih.gov/hi/topics/lupus/lupusguide/chp4.htm for nursing care of SLE
c) Thorough nursing history: fever, weight loss, fatigue, energy level changes, medication history, changes in skin, photosensitivity, nails, loss of hair, mouth or nasal sores, seizure activity, visual disturbances, vertigo, headaches, emotional status, cognition
d) Thorough assessment: integumentary and musculoskeletal systems, including butterfly rash, discoid lesions, digital gangrene, loss of scalp hair, vascular lesions (petechiae, purpuric lesions, Raynaudâ€™s phenomenon), joint manifestations, ROM; for infectious complications of skin, respiratory tract and urinary tract, neurological system for auras or triggers
e) Deficient Knowledge about effective coping
f) Self Care Deficits
g) Impaired thought processes related to inflammation of the CNS and high doses of steroids
h) Fluid volume excess
i) Risk for Infection: SLE affects immune system, decreased body ability to fight infection
j) Some stem cell research being done
Connective Tissue Disorder: Systemic sclerosis (scleroderma): Definition Etiology Pathophysiology: Greek â€œsclerosisâ€ â€“ hard; â€œdermaâ€ â€“ skin Chronic disease (connective tissue disorder) characterized by formation of excess fibrous connective tissue and diffuse fibrosis of skin and internal organs; multisystem inflammatory disease
1. Etiology and Risks: Cause is unknown but higher incidence in females, persons exposed to certain chemicals (plastics, coal, silica dust), high ETOH intake; onset between 30 â€“ 50
2. Pathophysiology
a) Abnormalities in cellular immune function; fibrosis occurs in tissue involving skin, blood vessels, lungs, kidneys
b) May be localized (skin only) or generalized with both skin and organ involvement
Connective Tissue Disorder: Systemic sclerosis (scleroderma): Manifestations: Manifestations
a) Initially marked thickening of skin, diffuse non-pitting swelling
b) Eventually skin atrophies, becoming taut and hyperpigmented
c) CREST syndrome poor prognosis, 10 yr survival 65%
(1) Calcinosis (abnormal calcium salt deposits in the tissue)
(2) Raynaudâ€™s phenomenon Spasms of small arteries in digits limit blood flow, on occasion the toes, blue first (decreased circulation) the white (more sever) then red (as spasms resolve)
(3) Esophageal dysfunction mobility is affected
(4) Sclerodactyly (scleroderma of the fingers)
(5) Telangiectasia (dilated, superficial blood vessels)
d) Visceral organ involvement
(1) Pulmonary hypertension
(2) Pericardidtis, cardiac dysrhythmias
(3) GI problems including malabsorption
(4) Renal effects - proteinuria, HTN, renal failure
Connective Tissue Disorder: Systemic sclerosis (scleroderma): Diagnostic Tests: Diagnostic Tests
a) ESR is elevated due to chronic inflammatory process
b) CBC: anemia
c) Gammaglobulin levels are high; may be low levels of antinuclear antibodies
d) Skin biopsy helps confirm diagnosis
Connective Tissue Disorder: Systemic sclerosis (scleroderma): Collaborative Care:: Collaborative Care: Treatment is aimed at symptomatic treatment and prevention of complications
a) Pharmacology
(1) Immunosuppressive therapy and corticosteroids used with pulmonary fibrosis and/or significant joint and muscle involvement
(2) Calcium channel blockers and alpha-adrenergic blocking agents to treat Raynaudâ€™s phenomenon visodilation
(3) H2 receptor blockers to treat esophagitis blocks gastric secretions Zantec, pepcid
(4) Antibiotics for intestinal malabsorption
(5) ACE-inhibitors to treat HTN and renal involvement
Treatment
(1) Physical Therapy: treatment to maintain mobility of affected tissues especially in hands and face pertaining to ability to eat.
Lyme disease Manifestations: Lyme disease: Inflammatory connective tissue disorder caused by a spirochete Borrelia burgdorferi and transmitted by ticks carried by deer and mice deer tick/blacklegged tick; prevalent in mid-Atlantic, northeastern and north central areas of USA
1. Manifestations
a) Initial manifestations
(1) Flu-like symptoms and skin rash
(2) â€œBullâ€™s eyeâ€ skin lesion at site of tick bite
(3) Followed by fatigue, malaise, fever, chills, myalgia
b) Secondary manifestations
(1) As the disease progresses secondary skin lesions develop
(2) Musculoskeletal symptoms
(3) Persistent fatigue
(4) Neuro symptoms - headache and neck stiffness
c) Late manifestations (months to years later)
(1) Chronic recurrent arthritis often affecting the knee
d) Progression is highly individualized; may result in permanent disability with neurologic and cardiac involvement
Lyme disease Diagnostic Tests:: Diagnostic Tests: Manifestations and laboratory studies
a) Antibodies to B. burgdorferi detected by ELISA or Western blot methods within 2 â€“ 4 weeks of initial skin lesion
b) Organism is difficult and slow to culture from tissues or body fluids
Lyme disease Treatment: Treatment is important to prevent development of complications
a) Antibiotics such as doxycycline, tetracycline, amoxicillin, cefuroxime axetil, or erythromycin for up to a month
b) Arthritic manifestations are treated with aspirin or NSAIDs
Lyme disease Nursing Interventions: Nursing Interventions: Focus on the prevention of the disease
a) Avoid tick-infested areas
b) If going out doors in areas with ticks, dress appropriately and use insect repellents containing DEET
c) Inspect skin afterward, remove ticks
d) Seek specific treatment for Lyme disease, if manifestations of disease occur (especially site of tick bite
Osteomyelitis: Pathophysiology: Osteomyelitis: Infection of the bone. The cause is usually bacterial, however, fungi, parasites, and viruses can also cause bone infection.
A. Pathophysiology
1. Usually bacterial in nature: most commonly Staphylococcus aureus
2. Sources of infection
a) Direct contamination of bone from open wounds (trauma)
b) Complication of surgery
c) Extension of chronic ulcers including venous, arterial, diabetic
3. Infection develops in bone, which may interfere with vascular supply to the bone, and necrosis occurs; difficult for antibiotics to reach the bacteria within the bone
Specific incidents of osteomyelitis: Specific incidents of osteomyelitis
1. Hematogenous osteomyelitis
a) Pathogens carried by blood from infections elsewhere in the body. primarily occur in older adults, persons with sickle cell anemia, intravenous drug users
b) Site of the infection is usually the spine, commonly lumbar
2. Osteomyelitis from a contiguous infection
a) Infection results from deep penetrating wounds, decubitus ulcers, surgery, total joint replacement
b) Diagnosis often not made until infection has become chronic because acute signs are masked by chronic inflammation; non-healing wound or fracture
3. Osteomyelitis associated with vascular insufficiency
a) Clients with PVD and diabetic neuropathy at risk
b) Infection often diagnosed when client seeks treatment for nonhealing wound, swollen toe, acute cellulites
Manifestations of osteomyelitis: Manifestations of osteomyelitis
1. Local
a) Pain in infection site
b) Redness of skin over infection site
c) Decreased ROM in nearest joint
2. Systemic
a) Fever/malaise
b) Nausea
c) Tachycardia
Osteomyelitis Diagnostic Tests: Diagnostic Tests
1. MRI and CT scans: show abscesses and soft tissue changes
2. Radionucleotides bone scans: determine whether infectious or inflammatory changes in bone
3. CBC and ESR: WBC and ESR are elevated
4. Blood and tissue cultures: identify infectious organism and determine appropriate antibiotic therapy
Collaborative Care Pharmacology: Collaborative Care

Pharmacology
a) Antibiotics mandatory to prevent acute case from becoming chronic osteomyelitis
b) Initially treated as staph infection until results of culture are obtained
c) Definitive antibiotics prescribed according to culture results
d) Continued at least 4 â€“ 6 weeks with intravenous or oral antibiotics
Osteomyelitis Collaborative Care: Treatment
a) Pain relief
b) Infection elimination or prevention
c) Early diagnosis to prevent bone necrosis by early antibiotic therapy
d) Often requires bone debridement and long course of antibiotics
Musculoskeletal Trauma: Musculoskeletal Trauma: Hip Fractures: One of the leading causes of morbidity and mortality among the older population incidence increasing due to aging population, 250,000 hip fx each year; 90% occur from falls
1. 4% die during initial hospitalization
2. 24% dies in the first year following injury
3. 50% remain unable to walk without an assistive device
4. 25% of previously independent clients remain in institutions for more than a year after a hip fracture
5. LOS was 6.5 days in 2000
Musculoskeletal Trauma: Hip Fractures Risk factors Pathophysiology: Risk factors
1. Bone loss due to hormonal changes (post menopausal women), low body weight, physical inactivity, low dietary calcium, inadequate levels of serum vitamin D, cigarette smoking and consumption of alcohol
2. Falling due to interaction between intrinsic risk factors and physical environment

Pathophysiology
1. Relationship to joint capsule
a) Intracapsular Sub-capital or mid-neck; fractures of the head or neck of femur; greater risk of nonunion and avascular necrosis; does not normally have large blood supply
b) Extracapsular
2. By anatomic area of proximal hip
a) Femoral neck
b) Intertrochanteric
c) Subtrochanteric
Musculoskeletal Trauma: Hip Fractures Manifestations: Manifestations: pain, shortening of affected leg, external rotation
1. Emergency Dept Care
a) Vitals and PA, why they fell (underlying cardiac/neuro problem?)
b) Current living status
c) If displace hip fx may see classic positioning of shortening and external rotation
d) Stabilize and get x-rays/lab work
Musculoskeletal Trauma: Hip Fractures Collaborative care: Collaborative care
1. Skin traction (Buckâ€™s) to decrease muscle spasms
2. Surgery: ORIF (open reduction and internal fixation) using hardware to secure femur
3. Fractures of femoral neck often disrupts blood supply to head of femur; surgery may be hemiarthroplasty (replacement of either femoral head or acetabulum with prosthesis)
Nursing Diagnoses/Interventions Musculoskeletal Trauma: Hip Fractures: Nursing Diagnoses/Interventions
1. Same as any post-surgical
2. Same as post total hip arthroplasty except: Non-weight-bearing orders are usual
3. Health Seeking Behaviors
a) Trauma prevention
b) Maintain good bone health
Musculoskeletal Trauma: Amputations Partial or total: Musculoskeletal Trauma: Amputations Partial or total removal of body part resulting from traumatic event or chronic condition
Musculoskeletal Trauma: Amputations Partial or total Risk Factors: A. Risk Factors
1. PVD is major cause
2. Trauma is major cause of upper extremity amputation
3. Other traumatic events resulting in amputation include frostbite, burns, electrocution
4. Underlying cause of amputation is interruption in blood flow either acute or chronic
Musculoskeletal Trauma: Amputations Partial or total Goals: C. Goals
1. Alleviate symptoms
2. Maintain healthy tissue
3. Increase functional outcome: joints are preserved whenever possible to allow for greater function
4. Meet client directives: ethical issues can arise related to amputations
Musculoskeletal Trauma: Amputations Partial or total Levels of amputation Types of amputation: Levels of amputation Determined by local (ischemia and gangrene) and system factors (cardiovascular status, renal function, severity of diabetes mellitus)

Types of amputation
1. Open (guillotine) performed when infection is present and remains open to drain
2. Closed (flap) wound is closed with flap of skin sutured in place over stump

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