Download Musculoskeltal Disorders

What can go wrong with bones?
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They can become infected
Osteomyelitis
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They can become soft with decrease in
mineralization
Osteomalacia
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They can become porosis
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They can develop abnormal remodeling and
functioning of osteoblasts & osteoclasts
Osteoporosis
Pagets
Osteomyelitis

A severe infection of the:
 bone
 bone marrow
 surrounding connective tissue

Most common causative organism is
Staphylococcus aureus
Osteomyelitis
How does a person get an infection?
 Indirect
 Direct
Entry
Route
Development of Osteomyelitis
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Bacteria invade bone - inflammation
Edema develops and Pressure
within bone increases
Bone abscess develops under the
periosteum causing a decrease in
blood supply with ischemia and
bone necrosis. The dead bone
tissue, called sequestrum
The abscess cavity does not liquify
or drain easily.
The separated periosteum
stimulates new bone growth =
involcrum which surrounds the
sequestrum.
Infection trapped inside sequestrum
causing recurring abscesses.
Classification of Osteomyelitis
Acute
Chronic
Clinical Manifestations of
Osteomyelitis
 Systemic
 Local
Signs of Chronic Osteomyelitis

Chronic – an infection that
persists for longer than 1
month
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Signs and Symptoms
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Constant bone pain
Swelling
Tenderness
Warmth at site
Continuous Drainage
Osteomyelitis
Diagnosis
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Biopsy of bone or soft tissue
Cultures – blood and wound assessing for causative
organism
Erythrocyte sedimentation rate (ESR) – elevated
WBC - elevated
X-ray, no initial bone changes
Radionucleotidetide bone scan
MRI
What test is the best way to determine
the causative organism?
Goals of Care
Halt the Infection
Relieve Pain
Maintain Mobility
Halt the Infection
Intravenous Antibiotics

Patient will need vigorous and prolonged treatment
with antibiotics
Start out in hospital with aggressive antibiotic therapy
usually via PICC.
 Discharged to home with home health care follow up
for up to 6 months
 Patient taught care of PICC site and side effects of
antibiotics.
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Osteomyelitis
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Assorted IV antibiotics
 Penicillin, nafcillin (Nafcil)
 neomycin, vancomycin
 cephalexin (Keflex), cefazolin (Ancef)
 cefoxitin (Mefoxin)
 gentamycin (Garamycin)
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Oral Antibiotics
 ciprofloxacin (Cipro)
Nursing Care
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Toxic effects:
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Aminoglycosides - Nephrotoxic, ototoxic, optic neuritis, fluid
retention
• Renal function tests (creatinine and BUN) should be done
prior to administration and during therapy – therapy
depends on test results.
• Vestibular and auditory function are assessed prior to
therapy and again 3-4 weeks after drug discontinued.
Cephalosporins and Quinolones – jaundice, colitis,
photosensitivity, crystalluria
• C&S prior to beginning treatment
Nursing Care / Patient Teaching
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Measure peak and trough levels
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Dosages are adjusted to maintain peak levels
Preventive measures:
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Monitor I& O; Keep patient well hydrated to prevent
nephrotoxicity or crystalluria
Avoid direct sunlight, wear sunscreen
Monitor urinary function, hearing, vision
Assess for signs of yeast infections in genitourinary and
mouth
Relieve the Pain
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Immobilization of the affected limb
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Handle carefully , decreasing manipulation
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Give meds
 NSAID’S
 Opioid analgesics
 Muscle relaxants
Maintain Mobility

After the initial treatment and decrease of pain, need
to make sure that limb mobility is maintained
 ROM
 Assist to stand and ambulate
 Provide assistive devices to help with ambulation
Surgical Treatment and
Nursing Care
Debridement of the wound
 Insertion of antibiotic-impregnated
polymethylmethacrylate bead chains to combat the
infection
 Irrigation of wound with antibiotics
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Wound vac used to draw wound
together – assess wound and
drainage
Treatment and Nursing Care
Osteomyelitis
Hyperbaric oxygen therapy – stimulates circulation
and healing of infected tissue
 Bone grafts
 If all else fails – amputation
 Nursing Care – good body alignment, ROM,
dressing changes, patient teaching about antibiotics
and use of assistive devices, monitor patients response
to antibiotic therapy.
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Try This
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Which of these manifestations should cause
the nurse the MOST concern after treating a
patient with osteomyelitis for two days with
IV antibiotics?
 A. Sudden increase in temperature
 B. Complaints of pain at site of infection
 C. Drainage from wound
 D. Guarding of involved extremity
Metabolic Bone Disease
Osteomalacia
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Decalcification and softening of the bone
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Caused mainly by: vitamin D deficiency
**Vitamin D is required for the absorption of
calcium from the intestine and calcium is
responsible for mineralization of bone
Calcium
Vitamin D
Osteomalacia
 Who
is at risk for developing
osteomalacia?
Someone with:
 lack of exposure to ultraviolet rays (sun)
 GI malabsorption, extensive burns, chronic
diarrhea, pregnancy, drugs such as Dilantin.
Osteomalacia
Signs and Symptoms
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Most Common
 Bone pain
 Difficulty rising from a chair
 Difficulty walking
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Additional Signs and Symptoms
 Low back pain, muscle weakness
 Weight loss, progressive deformities
Diagnosis
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Blood work – how do each of these tests assist in
diagnosing Osteomalacia?
 serum calcium or phosphorus
 alkaline phosphatase
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X-Rays
 Show looser's transformation zone –
(ribbons of decalcification in bone)
Treatment and Nursing Care
Osteomalacia
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Medication Therapy
 Vitamin D supplements
 Calcium salts or phosphorus supplements
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What would the nurse teach the patient to eat to
increase vitamin D and calcium?
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What is the purpose of weight bearing exercises?
 What are examples of weight bearing exercises?
Osteoporosis
Characterized by low bone mass and structural deterioration
Normal homeostatic bone remodeling is altered – the rate of bone
resorption is greater than the rate of bone formation.
Osteoporosis
Osteoporosis
is more common in
women than men
because?
Diagnosis
Bone Mineral Density Test (BMD)
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Dual-energy x-ray absorptiometry (DEXA)
Treatment and Nursing Care
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Diet Therapy
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Weight bearing Exercises
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Encourage a diet high in calcium – see chart p.1636.
** Impact aerobics is NOT encouraged
Decrease Risk Factors
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Quit smoking and decrease consumption of alcohol
Medications used in Treatment of
Osteoporosis
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Estrogen Replacement Therapy
Calcium & Vitamin D supplements
Calcitonin
Bisphosphonates (Fosamax, Didronel, Actonel, Boniva,
Aredia, Bonefos, Skelid)
Selective Estrogen receptor modulator – Evista
Medications used in treatment of
Osteoporosis
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Hormone Replacement Therapy – Estrogen
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Controversy over use. Should discuss with health care
provider
Calcium
 There is a variety of calcium supplements available
(See Table 64-15, p. 1636).
• They should be taken with Vitamin D to aid in
absorption.
• Also if taking large doses i.e. 1000 mg. / day – take in
divided doses of 500mg BID for better absorption
Medications used in treatment of
Osteoporosis
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Calcitonin
 A hormone made by the thyroid gland that helps
keep calcium levels in the body from getting too
high. It does this mainly by blocking the breakdown
(absorption) of bone, which slows the release of
more calcium into the blood
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What is needed to counter that effect?
Medications used in treatment of
Osteoporosis
Bisphosphonates – (Fosamax, Boniva)
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Inhibit osteoclast-mediated bone resorption thereby
increasing BMD and total bone mass.
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Side effects – anorexia, weight loss, gastritis
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Patient Teaching
•
•
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Take on an empty stomach, in the morning, at least 30 minutes
before any food, beverages or medications.
Do not take within 2 hours of any calcium- containing food
To decrease esophageal irritation - take with a full glass of water,
and the patient must remain upright for at least 30 minutes after
taking the medication.
Medications used in treatment of
Osteoporosis
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Selective Estrogen Receptor Modulators
 Mimic effect of estrogen on bone by reducing bone
resorption without stimulating the breasts or uterus.
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Side effects
• Leg cramps
• Hot flashes
Paget’s Disease
Excessive bone resorption followed by replacement of
normal marrow by vascular, fibrous connective tissue.
 The new bone is larger, disorganized,
and weaker
 Most often affect the pelvis, long bones,
spine, ribs, sternum, and cranium
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Paget’s Disease
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Clinical Manifestations
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Bone pain
Fatigue
CV disease (vasodilation of vessels in
skin/tissues overlying affected bones)
Waddling gait; bowing of legs; Hip or knee involvement
can lead to limping, as well as pain and stiffness of the hip
or knee.
Headaches, visual deficits, loss of hearing occur as skull
becomes enlarged and thickened
Enlarged vertebrae cause spinal cord compression/ pinch of
adjacent nerves causing tingling and numbness.
Pagets Disease
skull becomes enlarged and thickened
Spinal cord
compressed
Loss of
hearing
Waddling gait
Hip or knee
involvement
can lead to limping
bowing
of legs
Paget’s Disease
 Diagnosis
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Elevated serum alkaline phosphatase
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X-ray will show increase in bone size
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Will the bone return to normal size and shape
following treatment?
Goal of Treatment
Relieve the Pain
Drug Therapy for Paget’s
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Human calcitonin (Cibacalcin) or Calcitonin-salmon (Miacalcin)
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NSAIDS
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Bisphosphonates
Paget’s Disease
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Other treatments and Nursing Care
 Back support by firm mattress
 Teaching about use of Splints or braces to support
bones and joints and help prevent weakened
bones - skin care, circulation, etc.
 Teach how to correctly use canes or walkers
 Physical Therapy
Etiology and Pathophysiology of
Rheumatoid Arthritis
Rheumatoid arthritis is an autoimmune disease. This means
that the body's immune system mistakenly attacks the tissues it
is supposed to protect.
 RF antibodies are formed in synovium against body’s IgG
antigens.
 This leads to formation of immune complexes which cause
inflammation of synovium –synovitis.
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1. Synovitis causes release of WBC and enzymes which damage
the bone and breakdown cartilage of the joint and the
surrounding tissues.
2. Vascular granulation tissue grows across the surface of the
cartilage (pannas) with loss of cartilage beneath the
expanding pannas
1
2
Etiology and Pathophysiology of
Rheumatoid Arthritis
3. Inflammatory pannus causes cartilage destruction and
bone erosion.
Loss of Bone Density
Joint Deformity
3
4. This leads to joint deformities.
Destruction of bone cartilage
Erosion o f
edges o f bone
Increased soft tissue swelling due
to Inflammation and thickening
of synovium
Rheumatoid Arthritis
Signs and Symptoms
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Fatigue
Anorexia
Weight loss
Generalized stiffness
Joints are tender, painful,
and warm to touch
Rheumatic nodules
Multi-system involvement
Rheumatoid Arthritis
Deformities
Synotenovitis
Ulnar Drift
Boutonniere
Swan neck
Rheumatoid Arthritis
Deformities
Mutlans deformity
(rapidly progressing
RA)
Hammer Toe
Hitch-hiker thumb
Genu valgus
(knee away
from midline)
Hallux valgus
(bunion)
Extraarticular
Manifestations
Nodules
See page 1652 in Lewis
Diagnostic Testing
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Blood Studies
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↑ Rheumatoid factor (RF) – 80%
↑ Erythrocyte sedimentation rate (ESR)
↑ C-reactive protein (CRP)
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Synovial fluid analysis
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X-rays
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Will not diagnosis – only show bone changes
Goals of Care
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Control disease activity
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Relieve pain
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Maintain functionality and activities of daily living
(ADLs)
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Maximize quality of life
Treatment and Nursing Care for
Rheumatoid Arthritis
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See Table 65-3 for meds used for arthritis p. 16461647.
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Salicylates
NSAIDs
Antibiotics
Topical analgesics
Corticosteroids
DMARDs
Gold compounds
Antimalarials
Immunosupressants
Biologic/Targeted therapy
Drug Therapy
Disease-Modifying Antirheumatic Drugs
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Methotrexate (Rheumatrex)is know as the
cornerstone medication in treating RA –
explain.
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What are the side effects?
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What are important nursing implications?
Drug Therapy
Antimalarials – Plaquenil and Azulfidine
 Second choice of drug treatment
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May suppress formation of antigens
Side effects:
• Ocular toxicity - changes in vision,
• Ototoxicity - changes in hearing or tinnitus,
• Peripheral neuritis - muscular weakness
Nursing Care
• Monitor CBC and hepatic function
• Tell patient to report any above changes immediately
Drug Therapy
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Gold Compounds
 Parenteral – Myochrysine, Solganal
 Oral - Ridaural
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Side effects:
• Common - Stomatitis, dermatitis, photosensitivity,
proteinuria
• Serious - Leukopenia, thrombocytopenia, anemia
Nursing Care:
• Observe for pruritis, rash, sore mouth, metallic taste
• Monitor CBC, UA
Drug Therapy
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Immunosuppressant's – Imuran, Cytoxan
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Used to decrease DNA. RNA, protein synthesis
Assess for GI irritation
Advise patient to report unusual bleeding or bruising
Avoid during pregnancy
Biologic/ targeted therapy
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Used to decrease inflammatory process and slow disease
process
Report persistent fever; it may be the only sign of an infection.
Assess for signs of CHF.
The response to a PPD may be suppressed and a false
negative may result
Giving a live vaccine could result in contracting disease
Relieve Pain
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NSAID’s
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DMARD’s
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Non-Pharmacological
 Heat or Cold applications
 Rest
 Relaxation techniques
Treatment and Nursing Care
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Diet Therapy
Rest
Heat and cold applications
Exercise
Patient and Family Teaching
Protection of joints – page 1658.
Causes of Gout
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Inflammatory response related to:
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increase in the production uric acid
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underexcretion of uric acid
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increase consumption of foods that
contain purines
Thereby causing high levels uric acid in
blood (hyperuricemia)
Causes of Gout
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Urate salts deposited in articular, periarticular
and subcutaneous tissue
Primary gout – related to heredity error of
purine metabolism in 90% of cases
Secondary gout - to increased cell turnover and
related to medications, diseases, leukemia, etc.
Clinical Manifestations of Gout
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Stage 1: asymptomatic; hyperuricemic
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Stage 2: acute gouty arthritis; affect single joint due
to trauma, stress; high level uric acid; joint hot, red
swollen; generally metatarsophalangeal joint great
toe.
Gout
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Stage 3: Chronic Tophi occur if gout untreated
>urate pool increases > develop in multiple areas
(esp. ear, bursae, toes) > compress nerves and
erode through tissues.
Diagnostic Tests
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Serum Uric acid – elevated; usually above 6 mg/dl;
not specifically diagnostic of gout
WBC- elevated as high as 20,000/mm3 during acute
attack
ESR: elevated
24 hour urine collection-determine uric acid production
and excretion (evaluate if from decreased renal excretion
or overproduction of uric acid)
Most commonly diagnosed via clinical symptoms such
as Tophi seen – indicator of chronic disease
Drug Therapy for Gout
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Colchicine
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NSAIDs
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Corticosteroids
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Uricosuric Agents
 Probenecid (Benemid)
 Sulfinprazone (anturan)
Drug Therapy
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Xanthine-oxidase inhibitors
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Decrease uric acid production
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Allopurinal (zyloprim) – can lead to agranulocytosis
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ULORIC (febuxostat)
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Force Fluids while on these medications!!
to keep urine alkaline
Treatment and Nursing Care
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Diet Therapy
 Avoid foods high in Purine
such as?
Treatment and Nursing Care
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Bedrest and position for comfort
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Joint immobilization and protect joint from pressure
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Local application of heat or cold
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Assess for complications
 Formation of kidney stones
 Hypertriglyceridemia
 Hypertension
Chronic multisystem disease involving vascular and
connective tissue
Pathophysiology of SLE
Lupus is an autoimmune disease characterized by
acute and chronic inflammation of various tissues of
the body.
 Patients with lupus produce abnormal antibodies in
their blood that target tissues within their own body
rather than foreign infectious agents.
 Because the antibodies and accompanying cells of
inflammation can affect tissues anywhere in the body,
lupus has the potential to affect a variety of areas

Causes of SLE
 The
precise reason for the abnormal
autoimmunity that causes lupus is unknown.
 Inherited
 Dozens
genes, viruses, ultraviolet light,
of medications have been reported to
trigger SLE.
Clinical Manifestations of SLE
Fatigue; Low-grade fever
 Loss of appetite
 Muscle aches; arthritis; polyarthralgia
 Ulcers of the mouth and nose
 Facial rash ("butterfly rash")
 Photosensitivity
 Pleuritis and pericarditis, tachypnea,
 Poor circulation to the fingers and toes with cold exposure
(Raynaud’s syndrome)
 Proteinuria and development of glomerulonephritis
 Focal seizures, peripheral neuropathy, organic brain syndrome

Diagnosis

Autoantibody Testing:
 Anti-DNA- specific
 Anti- smith antibody (Anti-Sm)
 Anti nuclear antibody (ANA)
ESR – elevated
 C-reactive protein – elevated
These are not diagnostic for SLE, but help in the
diagnosis
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Treatment and Nursing Care
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What is the single most important medication used in
the treatment of SLE?
Other Medications :
 Anitmalarial
 Immunosuppressive agents
Treatment and Nursing Care
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Relieve pain and discomfort and Fatigue
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Application of heat and cold
Encourage to alternate Rest and activity
Support devices – braces, splints, firm mattress
Analgesics and anti-inflammatory medications
Nursing Care
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Maintain Skin Integrity
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Apply topical anti-inflammatory
Avoid direct sunlight. Use sunscreens and protective
clothing, sun hats
Increase Mobility
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ROM
Assistive devices – walkers, canes, crutches
Treatment and Nursing Care
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Facilitate self care
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Improve body image
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Provide adaptive equipment for eating, bathing, toileting,
dressing
Allow patient extra time to complete care
Encourage patient to verbalize feelings, perceptions, and
fears
Monitor for complications
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Assess for serious adverse effects of medications used in
treatment
Avoid immunizations with live viruses