Musculoskeletal disorders pdf

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By: Getenet D(BScN, MSc in MSN, MSc student in
Epidemiology at BDRU )
LECTURER at
BDU-CHS, DEP’T OF NURSING
Musculo skeletal system

MANAGEMENT OF PATIENT WITH
MUSCULOSKELETAL SYSTEM
 The musculoskeletal system includes:
 bones,
 joints,
muscles,
tendons,
ligaments, and
 bursae of the body.

Degenerative Joint Disease
(Osteoarthritis)
 joint disease that damages the articular cartilage
leading to reactive new bone formation.
 Osteoarthrites (OA) is described as progressive joint
failure where all structures involved in joint function
undergo pathologic changes.
 Weight bearing joints (hips, knees), cervical and lumbar
spine and the metacarpophalangeal and distal
interphalangeal joints of the hands are commonly
affected.

(Osteoarthritis)
 the most common and frequently disabling of the joint
disorders.
 The wrist, elbow and ankle joints are chacterstically
spared or very raely involved.
 It is more common in females than males.
 OA is both over diagnosed and trivialized; it is frequently
over treated or undertreated.

Degenerative Joint Disease (Osteoarthritis)
 OA can be categorized into localized or generalized
forms.
 Generalized OA consists of involvement of three or
more joint sites.
 OA is generally a non inflammatory type of arthritis
but some patients can have predominantly inflammatory
arthritis characterized history of swelling, night pain,
morning stiffness greater than 30 minutes, warm and
tender joints on physical examination.

Degenerative Joint Disease (Osteoarthritis)
 The functional impact of OA on quality of life,
especially for elderly patients, is often ignored.
 OA has been classified as primary (idiopathic), with no
prior event or disease related to the OA, and
secondary, resulting from previous joint injury or
inflammatory disease.
 The distinction between primary and secondary OA is
not always clear.

(Osteoarthritis)
 Increasing age directly relates to the degenerative
process in the joint, as the ability of the articular cartilage
to resist micro fracture with repetitive low loads
diminishes.
 OA often begins in the third decade of life and peaks
between the fifth and sixth decades.
 By age 75 years, 85% of the population has either x-ray
or clinical evidence of OA, but only 15% to 25% of these
people experience significant symptoms.

(Osteoarthritis)
Risk Factors for Osteoarthritis
 Increased age
 Obesity
 Previous joint damage
 Repetitive use (occupational and
recreational)
 Anatomic deformity
 Genetic susceptibility

(Osteoarthritis)
Clinical Manifestations
 Pain at initiation of exercise (walking)
 Morning stiffness which improves with exercise
 Diminution of joint movement
 Crepitus on moving affected joint(s)
 Heberden's nodes and deformed joints in the hands
 Joint swelling, warmth and effusions (knee especially)
 If cervical and lumbar spine involved; muscle weakness
in hands and legs respectively (myelopathy)

(Osteoarthritis)
 Characteristic bony nodes may be present; on
inspection and palpation, these are usually painless,
unless inflammation is present.
 Tender and enlarged joints are common.
 Investigations
– CBC : high greater than 11,000
– ESR :usually >50 mm/h
– X-ray of affected joints: osteophyte formation, joint
space narrowing, subchondral sclerosis and cysts

Medical Management
Osteoarthritis
 Objectives
– Relieve pain
– Prevent and manage deformities
– Educate patient
 Although no treatment halts the degenerative
process, certain preventive measures can slow the
progress if undertaken early enough.
 These include weight reduction, prevention of
injuries, perinatal screening for congenital hip
disease, and ergonomic modifications.

(Osteoarthritis)
 Conservative treatment measures include:
 the use of heat,
 weight reduction,
 joint rest and avoidance of joint overuse,
 orthotic devices to support inflamed joints (splints,
braces),
 isometric and postural exercises, and
 aerobic exercise.
 Occupational and physical therapy can help the patient
adopt self-management strategies.

(Osteoarthritis)
PHARMACOLOGIC THERAPY
 Pharmacologic management of OA is directed
toward symptom management and pain control.
 Medications are used in conjunction with non
pharmacologic strategies;
 Acetaminophen.
 nonselective NSAIDs,
 COX-2 inhibitors (cyclo-oxygenase-
inflamatory enzyme).
 opioids and
 intra-articular corticosteroids

Pharmacologic mgt of osteoarthritis)
 Pain management
 Inflammatory osteoarthritis
 First line-Ibuprofen, 200-400mg P.O., TID
 Diclofenac, 50-75mg P.O., BID or rectal suppository
100mg/daily
 Indomethacin, 25-50mg, P.O., 2-3 times/day;
maximum dose is 200mg/day or rectal suppository
100mg/daily. Avoid indomethacin in hip OA.
 Piroxicam, 10-20mg, P.O., once per day. Maximum
dose is 20mg/day Dosage forms:

(Osteoarthritis)
 PLUS GI protection for high risk individuals
 Omeprazole, 20mg, P.O., once daily or BID.
 Esomeprazole, 20-40mg, P.O., once daily
 Pantoprazole, 40mg, P.O., once daily
 Alternative-H2 blockers,
 Cimetidine, 400mg P.O., BID
 Ranitidine, 150mg, P.O, BID 2.

(Osteoarthritis)
 Non inflammatory osteoarthritis
 First line Paracetamol, 1g 4–6 hourly P.O., when
required to a maximum of 4 doses per 24 hours
 If ineffective: start NSAIDS as above Additional
pain management –for both inflammatory and non
infla mmmatory OA.
 Third option
 First line Tramadol, 50mg to 100mg, P.O., once to
twice per day.
 Alternative Codeine phosphate 30mg P.O., QID. USE
CODEINE FOR SHORT DURATION ONLY.

(Osteoarthritis)
 Intra-articular steroids
 osteoarthritis of the knee and shoulder that is refractory
to NSAIDS
 Not more than 2–3 injections per year per joint are
recommended.
 First line Methylprednisolone acetate, 20–80mg
depending on joint size OR
 Triamcinolone acetonide: Initial: Smaller joints: 2.5-5mg,
larger joints: 5-15mg, up to 40mg for large joints.
 methylprednisolone above Dosage forms: Injection,
10mg/ml, 40mg/ml in vial

(Osteoarthritis)
SURGICAL MANAGEMENT
 In moderate to severe OA, when pain is severe or
because of loss of function, surgical intervention
may be used.
 Procedures most commonly used are:
 Osteotomy- to alter the force distribution in the
joint and
 Arthroplasty- diseased joint components are
replaced with artificial products.

(Osteoarthritis)
SURGICAL MANAGEMENT
 Viscosupplimentation- the reconstitution of
synovial fluid viscosity.
 Hyaluronic acid, that acts as a lubricant and
shock absorbing fluid in the joint, may be used in
this procedure.
 Tidal irrigation/ (lavage) of the knee-
introduction and then removal of a large volume
of saline into the joint through cannulas.

Pyogenic Osteomyelitis
 Pyogenic Osteomyelitis is an acute infection of the bone
and its structures caused by bacteria.
 Osteomyelitis occurs as a result of hematogenous
spread, contiguous spread from adjacent soft tissues or
direct infection from trauma or surgery.
 Hematogenous osteomyelitis is usually monomicrobial,
while osteomyelitis due to contiguous spread or direct
inoculation is usually polymicrobial.
 Staphylococcus aureus is the most common causative
organism. Coagulase-negative staphylococci and
aerobic gram-negative bacilli are also common causes.

 Clinical features Gradual onset varying from few days
to weeks of local bone pain, swelling, low grade fever,
malaise and weight loss.
 Investigations - Clinical, CBC, ESR, C-reactive protein,
X-ray of the affected bone - Culture of pus/sequester
(if debridement is done)

 Treatment Objectives - Control infection - Prevent
disability Non pharmacologic - Rest/immobilization -
Surgical debridement

 Pharmacologic Empiric antibiotic – duration of
antibiotics is for at least six weeks First line
 Vancomycin, 30mg/kg/day, IV, in two divided doses
PLUS
 Ciprofloxacin, 750mg, P.O., BID
 Alternative
 Cloxacillin, 2gm, I.V. QID
 PLUS
 Ciprofloxacin, 750mg, P.O., BID

 Further treatment is guided by culture sensitivity tests
 For pain and fever – Analgesic/antipyretic e.g.
Paracetamol, 500-1,000mg P.O. as needed (4-6 times
daily) can be given.

Osteoporosis
 Osteoporosis means ―porous bone.‖
 Viewed under a microscope, healthy bone looks like a
honeycomb.
 When osteoporosis occurs, the holes and spaces in the
honeycomb are much larger than in healthy bone.
 Osteoporotic bones have lost density or mass and
contain abnormal tissue structure.
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Osteoporosis…..
 One in two women and one in four
 Osteoporosis is known as the “silent thief”
 because it slowly and insidiously over many
years robs the skeleton of its banked resources.
 Bones can eventually become so fragile that they
cannot withstand normal mechanical stress.
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Why Osteoporosis is more common in
women reasons:
 lower calcium intake than men throughout their lives
 have less bone mass because of their generally smaller
frames;
 bone resorption begins at an earlier age and
accelerated at menopause;
 pregnancy and breastfeeding deplete a woman’s
skeletal reserve
 longevity increases the likelihood of osteoporosis
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Osteoporosis………
 initial bone scan in women before the age of 65. If the
results are normal and
 the person is at low risk for osteoporosis, another scan is
not needed for 15 years.
 Testing should start earlier and be done more
frequently if a person is at high risk for fractures (e.g., low
body weight, smoker, prior fractures). Men should be
screened before the age of 70 years old and by age 50 if
at high risk for fractures
 (e.g., low body weight, hypogonadism).
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Etiology and Pathophysiology
 risk is associated with regular weight-bearing exercise
and fuoride, calcium, and vitamin D ingestion.
 Low testosterone levels are a major risk factor in men.
 Peak bone mass (maximum bone tissue) is primarily
achieved before age 20.
 It is determined by a combination of four major
factors: heredity, nutrition, exercise, and hormone
function.
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Etiology and Pathophysiology
 Heredity may be responsible for up to 70% of a
person’s peak bone mass.
 Bone loss from midlife (ages 35 to 40 years) onward is
inevitable, but the rate of loss varies.
 At menopause, women experience rapid bone loss when
the decline in estrogen production is the sharpest.
 Tis rate of loss then slows, and eventually matches the
rate of bone lost by men 65 to 70 years old.
 Long-term use of corticosteroids, thyroid replacements,
heparin, long-acting sedatives, or antiseizure
medications
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Etiology and Pathophysiology……
 Bone is continuously being deposited by osteoblasts
and resorbed by osteoclasts, a process called remodeling.
 Normally the rates of bone deposition and resorption
are equal to one another so that the total bone mass
remains constant.
 In osteoporosis, bone resorption exceeds bone deposition.
 Many drugs can interfere with bone metabolism, including
corticosteroids, antiseizure drugs (e.g., divalproex
sodium [Depakote], phenytoin), aluminum-containing
antacids, heparin, certain cancer treatments, and
excessive thyroid hormones.
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Osteoporosis Can Sneak up on You
 Osteoporosis is often called a silent disease
because one can’t feel bones weakening.
 Breaking a bone is often the first sign of
osteoporosis or a patient may notice that he or she is
getting shorter or their upper back is curving forward.
 experiencing height loss or your spine is curving, pre
alarming sign
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Clinical Manifestations of OP
 Osteoporosis occurs most commonly in the bones of the
spine, hips, and wrists.
 Usual first manifestations are back pain or spontaneous
fractures.
 weakened bone and spontaneous fractures or
fractures from minimal trauma.
 Over time, wedging and fractures of the vertebrae
 produce gradual loss of height and a humped back
known as kyphosis,or ―dowager’s hump‖
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Clinical Manifestations of OP…..
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Diagnostic
 conventional x-ray can not detect until more than 25%
to 40% of calcium in the bone is lost.
 Serum calcium, phosphorus, and alkaline phosphatase
levels usually are normal, although alkaline phosphatase
may be elevated afer a fracture.
 Bone mineral density (BMD) :- quantitative ultrasound
(QUS) and dual-energy x-ray absorptiometry (DXA).
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Collaborative Therapy
• Diet high in calcium Calcium supplements
 Vitamin D supplements Exercise program
 Drug therapy
 Bisphosphonates, alendronate (Fosamax, Binosto)
 clodronate (Bonefos), etidronate (Didronel)
 Selective estrogen receptor modulator (e.g., raloxifene
[Evista])
 Recombinant form of parathyroid hormone (e.g.,
teriparatide [Forteo]), denosumab (Prolia)
 Minimally invasive procedures, Vertebroplasty,
Kyphoplasty
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Rheumatoid arthritis (RA)
 Systematic autoimmune inflammatory disease
 Persistent inflammation of synovial tissue especially of
the wrists, hands and feet.
 long-term disease that can affect surrounding structures
like the tendon sheath, the bursa and tendons.
 Without treatment, RA can possibly lead to joint
deformities and permanent function loss.

Rheumatoid Arthritis (RA)
 RA is commonly used as the prototype for inflammatory
arthritis.
 The incidence rate is approximately 3%, with a two to
three times greater incidence in women.
 In RA, the autoimmune reaction primarily occurs in the
synovial tissue.
 Phagocytosis produces enzymes within the joint.

 The enzymes break down collagen, causing edema,
proliferation of the synovial membrane, and ultimately
pannus formation.
 Pannus destroys cartilage and erodes the bone.
 The consequence is loss of articular surfaces and joint
motion.
 Muscle fibers undergo degenerative changes.
 Tendon and ligament elasticity and contractile power are
lost.

Risk factors
 Etiology is Unknown
 Age: risky age groups; 40 - 60 .
 Sex: more common among women than men.
 Genetics
 Weight
 Smoking
 Diet: Lower intake of vitamin D and antioxidants and
higher intake of sugar, sodium, red meats, protein, or
any food with much vitamin C
89

Factors decreased risk
 Fish and omega-3 fatty acid consumption
 Moderate alcohol intake
 Healthy diet
 Statin use
 Oral contraceptive use/hormone replacement
90

Clinically Relevant Anatomy
 inflammation and destructive erosion of bone and loss
of joint integrity - disability.
 Under normal circumstances, the synovium consists of 2
- 3 layers of cells.
 In patients with rheumatoid arthritis, the synovium is
strongly thickened and inflamed.
 Due to the inflammation production of enzymes occurs,
which breaks down the cartilage.
 This can cause local damage to the bone-tissue and
cartilage.
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Clinical Manifestations RA
 The disease course typically follows three possible
paths
Monocyclic: Having one episode that does not
reoccur. This usually ends within 2-5 years of
initial diagnosis.
Polycyclic: The disease severity varies over the
course of the progression of the condition.
Progressive: Condition continues to become
more severe and non-remitting
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Clinical Manifestations RA……
 Clinical manifestations of RA vary, usually reflecting the
stage and severity of the disease.
 The three most important complaints are the pain, morning
stiffness(>30 minute) and fatigue.
 joint swelling, warmth and redness
 a chronic, symmetrical inflammation of
metatarsophalangeal joints (MTP), the wrists, the
metacarpophalangeal joints (MCP) and the proximal
interphalangeal joints (PIP).
 Softening of the ligaments can lead to deformation of the
fingers

(RA)…….
 Other symptoms can include:
 a poor appetite (not feeling hungry)
 weight loss
 a high temperature, or a fever
 sweating
 dry eyes – as a result of inflammation
 chest pain – as a result of inflammation.

(RA)
 Characteristically, the pattern of joint involvement begins
with the small joints in the hands, wrists, and feet.
 As the disease progresses, the knees, shoulders, hips,
elbows, ankles, cervical spine, and temporomandibular
joints are involved.
 The onset of symptoms is usually acute.
 Symptoms are usually bilateral and symmetric.
 Deformities of the hands and feet are common in RA.
 RA is a systemic disease with multiple extra-articular
features.

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Stage Description
Stage I Mild
No destructive changes on radiographic examination Radiographic
evidence of osteoporosis may be present
Stage II
Moderate
Radiographic evidence of osteoporosis, with or without slight
subchondral bone destruction; slight cartilage destruction may be
present No joint deformities, although limitation of joint mobility may
be present
Adjacent muscle atrophy
Extra-articular soft tissue lesions, such as nodules and tenosynovitis may
be present
Stage III
Severe
Radiographic evidence of cartilage and bone destruction in addition to
osteoporosis Joint deformity, such as subluxation, ulnar deviation, or
hyperextension, without fibrous or bony ankylosis Extensive muscle
atrophy Extra-articular soft tissue lesions, such as nodules and
tenosynovitis may be present
Stage IV
Terminal
Fibrous or bony ankylosis Stage III criteria

Clinical Manifestations RA……
98

RA……99

RA……100

RA……101

Differential Diagnosis
 There is no unique test or feature that is pathognomonic
for RA. Common disorders to consider as differential
diagnoses with RA are:
 Osteoarthritis: the absence of systemic inflammatory
signs and symptoms, onset in later life, and the pattern of
joint involvement.
 Infectious arthropathies: the important consideration in
the setting of fever and polyarthritis. joint aspiration and
synovial fluid cultures and blood cultures are often
helpful in establishing the diagnosis.
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Differential Diagnosis
 Lyme disease: negative synovial fluid cultures.
Apparent in endemic region where tick exposure was
likely.
 Seronegative spondyloarthropathies (reactive
arthritis, ankylosing spondylitis, inflammatory bowel
disease–associated arthropathy): muscle weakness
and antibodies associated with these disorders most
often readily distinguish these disorders from RA.
 Fibromyalgia (FMS): absence of synovitis, the lack of
pain on motion, and normal laboratory and imaging
studies.
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Other pathologies to consider as
ddx
 Osteoarthritis Paraneoplastic syndrome
 Myelodysplastic syndrome
 Polychondritis
 Polymyalgia
 Rheumatica Psoriatic Arthritis
 Sarcoidosis Sjogren Syndrome
 Systemic Lupus
 Erythematous
 Reiter Syndrome
 Gout
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Note: RA diagnosed if at least four of these criteria are
satisfied (the first four must have been present for at least
six weeks).
The major drawback of the criteria is insensitivity in
identifying early disease which subsequently develop into
typical RA .

Investigations - ESR/CRP
- Rheumatoid factor
- ANA (antinuclear antibody) –
- X-ray of involved joints
- Treatment
- Objectives - Reduce pain, swelling and stiffness ,
Prevent deformities , Delay disease progression and
onset of long term complications

Medical Management
EARLY-STAGE RA
 Begins with education, a balance of rest and exercise,
and referral to community agencies for support.
 Medical management begins with therapeutic doses of
salicylates or NSAIDs.

Medical Management
EARLY-STAGE RA
 When used in full therapeutic dosages, these
medications provide both anti-inflammatory and
analgesic effects.
 Several COX-2 inhibitors, another class of NSAIDs, have
been approved for treatment of RA.
 COX (cyclo-oxygenase) is an enzyme involved in the
inflammatory process.

Medical Management
Moderate, Erosive RA
 For moderate, erosive RA, a formal program with
occupational and physical therapy is prescribed
 Educate the patient about principles of joint protection,
pacing activities, work simplification, range of motion,
and muscle-strengthening exercises.

Medical Management
Persistent, Erosive RA
 Reconstructive surgery and corticosteroids are often
used.
 Reconstructive surgery is indicated when pain cannot be
relieved by conservative measures.

Medical Management
Persistent, Erosive RA
 Surgical procedures include
 Synovectomy (excision of the synovial
membrane),
 Tenorrhaphy (suturing a tendon),
 Arthrodesis (surgical fusion of the joint), and
 Arthroplasty (surgical repair and replacement of
the joint).

Medical Management
Advanced, Unremitting RA
 immunosuppressive agents are prescribed.
 These include high-dose:
 Methotrexate
 Cyclophosphamide and
 Azathioprine
 These medications, however, are highly toxic and can
produce bone marrow suppression, anemia,
gastrointestinal disturbances, and rashes.

 Medical Management
 Through all stages of RA, depression and sleep
deprivation may require the short-term use of low-dose
antidepressant medications.
 They may include:
 amitriptyline,
 paroxetine , or
 sertraline ,

MGT of RA…..
Initiate early in the course First line Methotrexate, 7.5mg
P.O., once per week. Increase dose gradually to a
maximum of 25mg per week.
N.B. Monitor: Liver function and CBC before and 12
weekly during treatment.
PLUS Folic acid, 5mg P.O., per week with methotrexate at
least 24 hours after the methotrexate dose.
AND/OR Chloroquine phosphate, 150mg P.O., (as base)
daily for 5 days of each week for 2–3 months.

MGT of RA…..
 Then reduce dose if possible and administer 5 days a
week with an annual medicine holiday for 1 month.
 Do ophthalmic examination annually to monitor for
ocular damage. AND/OR Sulfasalazine, 500mg P.O.,
12 hourly.
 Gradually increase over one month from 500mg to 1
g 12 hourly.
 Liver function and CBCs monthly for first 3 months then
every 3–6 months.
118

MGT of RA…..
 Oral corticosteroids
 Indications: - As bridging therapy while waiting for
DMARDs to take effect. - The elderly if threatened by
functional dependence and intolerant to NSAIDs. -
Extra-articular manifestations, e.g. pleural effusion,
scleritis. - Acute flare Prednisolone, 40mg P.O., daily
for 2 weeks during acute flares. Thereafter gradually
reduce the dose to < 7.5 mg daily. Maintenance low
dose prednisolone may be needed in many patients



MGT of RA…..
 Joint pain management-NSAIDs
 Use for active inflammation with pain.
 NSAIDs are used for symptomatic control only, as they
have no long-term disease modifying effects.
 NSAID dose should be reduced and then stopped once
the DMARDs have taken effect
 Ibuprofen, 800mg, P.O.,TID with meals. If not tolerated:
400mg 8 hourly.

MGT of RA…..
 An extra night-time dose of a NSAID may be added
in some patients with severe nocturnal pain/morning
stiffness OR
 Diclofenac, Immediate or delayed release tablet:
150-200mg/day P.O., in 2-4 divided doses.
 Rectal suppository, insert 50mg or 100 mg rectally as
single dose to substitute for final daily dose OR
 Indomethacin, 25-50mg P.O., BID TO TID; maximum
dose: 200mg/day. Rectal suppository, insert 100mg,
BID or once, at bed time.
121

 Nutrition Therapy
 Patients with RA frequently experience anorexia,
weight loss, and anemia.
 Foods high in vitamins, protein, and iron for tissue
building and repair are usually prescribed.
 For the extremely anorexic patient, small, frequent
feedings with increased protein supplements may be
prescribed.

3. GOUT
 The deposition of microcrystals of uric acid in the
joints and peri-articular tissues
 May be present even when the level of uric acid in the
blood is normal
 Acute symptoms may precipitated by the consumption of
alcohol and foods rich in purines e.g. red meat, sea foods,
as well as trauma, surgery, starvation and infection.
 The incidence increases with age and body mass index.
 It occurs more commonly in males than females
 not caused by the level of uric acid but by acute changes in
the uric acid level

GOUT
 Primary gout is related to underexcretion or
overproduction of uric acid, which associated with
dietary excesses or overuse of alcohol and
metabolic syndrome.
 Secondary gout is related to medications or
conditions that cause hyperuricemia, such as
myeloproliferative diseases and their treatment,
hyperproliferative skin disorders, enzymatic
defects, and renal failure
 The prevalence of gout is reported to be 1.6 to 13.6
per thousand.

GOUT
 Attacks of gout appear to be related to sudden
increases or decreases of serum uric acid levels.
 When the urate crystals precipitate within a joint, an
inflammatory response occurs and an attack of gout
begins.
 With repeated attacks, accumulations of sodium
urate crystals, called tophi, are deposited in
peripheral areas of the body, such as the great toe,
the hands, and the ear.
 Renal urate lithiasis (kidney stones) with chronic renal
disease secondary to urate deposition may develop.

Gout…..
 Gout can be a manifestation or complication of
other diseases such as;
 metabolic syndrome,
 hematological malignancies,
 chronic kidney disease and
 medicines like thiazide and loop diuretics, cytotoxic
medicines and pyrazinamide
127

Gout…..
 Acute gouty arthritis (recurrent attacks of severe
articular and periarticular inflammation),
 Tophi (crystalline deposits accumulating in articular
tissue, osseous tissue, soft tissue, and cartilage),
 Gouty nephropathy (renal impairment), and
 Uric acid urinary calculi.

GOUT…….
Four stages of gout can be identified:
1. asymptomatic hyperuricemia,
2. acute gouty arthritis,
3. intercritical gout, and
4. chronic tophaceous gout.

GOUT………..
 The subsequent development of gout is directly related
to the duration and magnitude of the hyperuricemia.
 Therefore, the commitment to lifelong pharmacologic
treatment of hyperuricemia is deferred (delayed) until
there is an initial attack.

Gout…..
 Typical acute attack
 Excruciating pain, redness, swelling, and disability.
 Maximal severity of the attack is usually reached within
12 to 24 hours.
 80% of initial attacks involve a single joint, most often at
the base of the great toe (known as podagra), or the
knee
 - Affected joint is inflamed, swollen and tender
131

GOUT
Diagnosis & Medical Management
 A definitive diagnosis of gouty arthritis is established by
polarized light microscopy of the synovial fluid of the
involved joint.
 Uric acid crystals are seen within the polymorphonuclear
leukocytes within the fluid.
 Investigations
 - CBC, ESR,BUN, creatinine, Serum uric acid, Blood
glucose, Serum lipids
 - X-ray of affected joint

Positive finding of gout
 Uric acid level in the blood >7.2 normal( 3.5 -7.2
mg/dl.
 Uric acid urine test
 A uric acid level > 750mg ( normal 250 - 750 mg)
Joint x-ray: If there is chronic gout, to see if any
joint damage.
 Ultrasound: to look for urate crystals or tophi in
your joints.
133

Positive x-ray finding in gout
134

Positive x-ray finding in gout…..
135

Treatment of gout
 Objectives :-Relieve pain immediately ,Reduce joint
inflammation ,Prevent recurrent attacks and joint
damage, Prevent uric acid crystal deposition in soft
tissues
 Non Pharmacologic
 Rest affected joint
 Identify and manage underlying or predisposing factors
 Weight reduction in obese or overweight individuals
 Dietary modification (low purine diet)
136

Pharmacologic
1. Acute Gout
 Ibuprofen, 800mg P.O.TID with meals. If not tolerated: 400
mg 8 hourly
 An extra night-time dose of a NSAID may be added in
some patients with severe
 nocturnal pain/morning stiffness
OR
 Diclofenac, Immediate or delayed release tablet: 150-
200mg/day P.O., in 2-4
137

Pharmacologic mgmt….
OR
 Indomethacin, 25-50mg P.O. BID or TID; maximum
dose: 200mg/dayor Rectal
 suppository, 100mg, BID or once at bed time
 Alternative(when NSAIDS are not tolerated or
contraindicated)
 Prednisolone, 20-40mg P.O. for one to two wks and
tapered over another one to
138

Pharmacologic mgmt.….
2. Chronic gout
 If possible, avoid known precipitants
 Treat secondary causes when possible
 Assess renal function and blood uric acid level
 Uric acid lowering therapy
 Indicated for
 >2 acute attacks per year
 chronic tophaceous gout
 Uric acid renal stones
 urate nephropathy
139

Pharmacologic mgmt.….
 Allopurinol, 100 mg P.O. daily.
 - Increase monthly by 100mg according to uric acid
blood levels and eGFR.
 - Most patients will be controlled with a dose of
300 mg daily
 N.B. Do not stop uric acid lowering medicines during
an acute attack
140

GOUT
Nursing Management
 While severe dietary restriction is not necessary,
patients should be encouraged to restrict consumption
of foods high in purines, especially organ meats, and to
limit alcohol intake.
 Maintenance of normal body weight should be
encouraged.

GOUT
Nursing Management
 In an acute episode of gouty arthritis, pain
management is essential.
 During the intercritical period, the patient feels well
and may abandon preventive behaviors, which may
result in an acute attack.
 Acute attacks are most effectively treated if therapy is
begun early in the course.

4. Septic (Infectious)
Arthritis

Septic (Infectious) Arthritis
 Joints can become infected through:
Spread of infection from other parts of the
body (hematogenous spread) (80-90%)
Directly through trauma or surgical
instrumentation (10-15%).
 Previous trauma to joints, joint replacement, coexisting
arthritis, and diminished host resistance contribute to the
development of an infected joint.

 Some inflammation of joints, tendons, and bursae is
directly related to infection caused by bacterial, viral,
fungal, or parasitic agents.
 Bacterial arthritis is the most rapidly destructive form of
infectious arthritis.

 There are two major classes of bacterial arthritis:
 arthritis caused by Neisseria gonorrhoeae and
 Arthritis caused by non gonococcal bacterium.
 The most prevalent of the non gonococcal organisms
include Staphylococcus aurous and the various
streptococcal variants.

Septic Arthritis
 Chills Fatigue and generalized weakness
 The characteristic symptom is single swollen and painful
joint.
 The patient often immobilizes the joint and elevates the
affected extremity because of pain and swelling.
 Fever may be high or it may be absent.
 Signs of systemic infection may be lacking in elderly
patients, those with diabetes, and those with suppressed
immune systems.

How Is Septic Arthritis
Diagnosed?
 CBC: usually very high
 ESR>22 mm/hour for men and 29 mm/hour for
women
 CRP>3 mg/L
 - synovial fluid analysis including Gram stain and
culture will help to reach the right diagnosis.
 X-ray of the affected joint should also be done.
 MRI scanning is sensitive in evaluating joint
destruction (not sensitive at early phase)
149

Positive x ray finding of SA
150

Treatment SA
Objectives - Treat infection promptly and prevent joint
destruction
Non pharmacologic –
 Aspiration/drainage when indicated
 Splintage, but early immobilization if joints are
mobile.
 The joint must be splinted with a POP slab or skin
traction to relieve pain and prevent contractures

Management SA
 medical emergency : early diagnosis and treatment
eliminate distribution of infection;
 Otherwise, the joint may be destroyed relatively
quickly.
 Empiric antibiotics with duration of If synovial fluid
gram stain is unavailable or negative:
 At least the first two weeks of antibiotics should be
through intravenous route.

Treatment of SA……
 First line Vancomycin, 30mg/kg/day IV in two divided
doses, not to exceed 2g per day PLUS
 Ceftriaxone, 2gm, I.V, daily
 Alternatives Cloxacillin, IV, 2g every 6 hr QID for 4-6
weeks OR
 Ceftriaxone 2gm,IV, daily
 If gram postive organism- vancomycin as first line and
Cloxacillin as alternative.
 If gram negative organism-use ceftriaxone with the
above dose as first line.

Nursing Management
 Nursing management focuses on providing pain relief,
administering antibiotics, and assisting the patient with
self-care activities.
 If the patient is sent home on intravenous antibiotics,
the nurse arranges home care and instructs the patient
and care providers in safe administration and changes
to report to a health care provider.

PYOMYOSITIS
 Pyomyositis is a purulent infection of skeletal muscle that
arises from hematogenous spread, usually with abscess
formation.
 By definition, it is not secondary to a contiguous infection
of the soft tissue or bone, nor due to penetrating trauma.
 Pyomyositis has a predilection for large-muscle groups
and often results in localized abscess formation.
 Pyomyositis often is called tropical myositis because of its
prevalence in tropical areas, where pyomyositis accounts
for 3% to 5% of hospital admissions
158

Predisposing factors for pyomyositis
 Immunodeficiency; HIV infection, diabetes mellitus,
malignancy, cirrhosis, renal insufficiency, organ
transplantation, and administration of immunosuppressive
agents.
 trauma, injection drug use,
 concurrent infection( Toxocariasis)
 malnutrition.
159

MICROBIOLOGY
 S. aureus is the most common cause of
pyomyositis;
 Methicillin-resistant S. aureus (MRSA), including
community acquired strains, is also an
increasingly important pathogen.
 Group A streptococci ;second most common
pathogen.
 Less common causes ;non-group A streptococci,
pneumococci and gram-negative enteric bacilli.
 E. coli among patients with hematologic
malignancy.
160

Clinical manifestation
 Pyomyositis presents with fever and pain with
cramping localized to a single muscle group.
 usually affect lower extremity (sites include
the thigh, calf and gluteal muscles),
 but other muscles may be involved, including
the iliopsoas, pelvic, trunk, paraspinal and
upper extremity muscles.
161

Stage of Pyomyositis
 Stage 1Characterized by
 crampy local muscle pain, swelling, and low-grade fever
 Mild leukocytosis and induration of the affected muscle
may be present.
 A deep abscess may not be discretely palpable, but the
muscle may have a "woody" texture on palpation.
 Fluctuation is not present, and aspiration of the muscle
will not yield purulent material.
 Only 2 percent of patients present at this stage.
162

Stage 2 of pyomyocities
 Occurs 10 to 21 days after the initial onset of symptoms
and is
 characterized by fever, exquisite muscle tenderness, and
edema.
 A frank abscess may be clinically apparent, and
aspiration of the affected muscle typically yields pus.
 Marked leukocytosis is usually present.
 More than 90 percent of the patients present at this
suppurative stage
164

Stage 3 of pyomyocities
 systemic toxicity.
 The affected muscle is fluctuant.
 bacteremia such as septic shock, endocarditis (S.
aureus )
 septic emboli, pneumonia, pericarditis, septic
arthritis, brain abscess, and
 acute renal failure can occur.
 Rhabdomyolysis has also been described.
 bacteremia, may cause endocarditis.
165

DIFFERENTIAL DIAGNOSIS
 muscle strain, contusion, hematoma, cellulitis,
deep vein thrombosis, osteomyelitis, septic
arthritis, or neoplasm.
 clostridial myonecrosis, necrotizing fasciitis,
spontaneous gangrenous myositis, diabetic
muscle infarction, septic arthritis, and other forms
of myositis.
166

Case report of pyomyocities
 A 58 year-old woman with type 2 diabetes was
admitted with a one month history of increasing pain
of the left thigh and the left arm. She complained for
two months of polyuropolydipsic syndrome, weight
loss and weakness. On presentation, the patient was
febrile (38.5°C). Physical exam showed a firm and
painful swelling of the left thigh with erythema . In the
left arm we noticed an indurated painfull mass
without erythema. There was no abdominal pain or
vomiting.
167

Case report of pyomyocities ….
 Laboratory findings shows a high white blood cell count
of 17910/mm3, hemoglobin 12.4 g/dL, platelets count
458000/mm3, erythrocyte sedimentation rate 107 mm, C
reactive protein: 213 mg/L, serum creatinine: 77µmol/L,
serum glucose: 27.5 mmol/L, CPK: 208 U/L, LDH: 265
U/L. The urine dipsticks demonstrate ketosis and
glucosuria. Blood gases parameters showed metabolic
acidosis: PH: 6.98, PaO2: 64 mmHg, PCO2: 27 mmHg,
HCO3-: 17 mmol/L. The culture of urine analysis was
negative. Three serial blood cultures were negative.
Ultrasonography of the painful areas was in favor
myositis.
168

Case report of pyomyocities ….
169

DIAGNOSIS
 Radiographic can defining the site(s) of infection and for
ruling out other entities.
 Computed tomography (CT) is helpful for detecting
muscle swelling and well-delineated areas of fluid
attenuation that display rim enhancement with contrast,
as well as for radiographic-guided drainage of purulent
material
 CT is preferable if available, ultrasonography is also a
potentially useful
 Magnetic resonance imaging (MRI) can be helpful for
identification of the extent of infection
170

DIAGNOSIS………
 Cultures:- Bacteriologic diagnosis can be made by
cultures of drainage prior to antibiotic therapy.
 Laboratory data:- leukocytosis with left shift,
elevated ESR and C-reactive protein.
 Eosinophilia for a concomitant parasitic infection.
 Counterintuitively , creatine kinase levels are often
normal.
171

TREATMENT
 Although stage 1 pyomyositis can be treated with
antibiotics alone, most patients present with stage
2 or 3 disease and therefore require both antibiotics
and drainage for definitive management
 In the setting of deep infection or extensive muscle
involvement with significant necrosis, surgical
intervention may be required.
172

TREATMENT…….
 For immunocompetent individuals, initial empiric
parenteral antibiotic therapy should be directed
against staphylococci and streptococci.
 Empiric therapy for MRSA should be initiated for
patients with a previous episode of proven MRSA
infection, patients with risk factors for MRSA, and
patients with systemic toxicity.
 In addition, it should be considered in communities
where the prevalence of MRSA is greater than 30
percent.
173

TREATMENT…….
 For immunocompromised cover both gram-positive,
gram-negative and anaerobic organisms with
vancomycin
 The course of therapy for patients with other
sequelae of bacteremia (such as endocarditis or
osteomyelitis) should be adjusted based on the
nature of infection at these other sites.
174

Necrotizing fasciitis
 A progressive life-threatening softtissue
infection (with liquifactive necrosis of
subcutaneous fat and fascia) ± skin .
175

Necrotizing fasciitis has also been
referred to as
 Hemolytic streptococcal gangrene
 Meleney ulcer
 Acute dermal gangrene
 Hospital gangrene
 Suppurative fasciitis
 Synergistic necrotizing cellulitis
176

CAUSITIVE ORGANISMS
 Group A Hemolytic streptococci (Streptococcus
pyogenes) and Staphylococcus aureus, alone or in
synergism, are frequently the initiating
 other aerobic and anaerobic pathogens
 Bacteroides fragilis
 Clostridium perfringens
 Peptostreptococcus
 Enterobacteriaceae
 Pseudomonas
 Klebsiella
177

Pathophysiology
178
This deep infection causes vascular occlusion,
ischemia, and tissue necrosis. Superficial nerves
are damaged, producing the characteristic
localized anesthesia

Types of necrotizing fasciitis
 Type I:- Polymicrobial (aerobic and
anaerobic;enterobacter +Non Group A streptococi)
 Common with DM and PVD, after surgical
procedures
 Type II:- Monomicrobial (primarily by GAS,
 occasionally caused by community associated
MRSA).
 TYPE 3:- Gas Gangrene by clostridial myo necrosis
 TYPE 4 (recently placed under of classification)
 Fungal cause
179

Sign and symptoms
 Small, red, painful lump or bump on the skin-
Changes to a very painful bruise-like area and
grows rapidly, sometimes in less than an hour
 The center may become black and die
 The skin may break open and ooze fluid
 Severe pain
 Bullae formation (thin walled fluid filled blisters)
 Other symptoms may include:
 Fever, Chills, Sweating, Nausea, Weakness,
Lightheadedness or dizziness
180

DIAGNOSIS
 Laboratory Testing:
 elevated WBC, azotemia, abnormal coagulation profiles,
and decreased platelet and fibrinogen levels.
 elevated lactate and blood glucose levels,
hypocalcaemia, hypoalbuminemia, and anemia are also
commonly found.
 Imaging studies:
 Plain radiography, ultrasonography, CT, and MRI have
all been used to help diagnose NSTI.
183

X ray findings of necrotizing fasciitis
184

Positive findings of necrotizing fasciitis
185

Treatment
 Intravenous antibiotic :Chloramphenicol, Erythromycin.
 Process of debridement is done for removal of heavily
contaminated tissue and all devitalized tissues by surgery.
 Amputations of affected limbs, in some cases.
 Hyperbaric oxygen therapy (HBO): Increased oxygen
partial pressure has been associated with the reversal of
basic pathophysiologic mechanisms of necrosis
187

OSTEOMYELITIS
 Osteomyelitis is an infection of the bone.
 The bone becomes infected by one of three modes:
Extension of soft tissue infection (e.g., infected
pressure or vascular ulcer, incisional infection)
Direct bone contamination from bone surgery, open
fracture, or traumatic injury (e.g., gunshot wound)
Hematogenous (bloodborne) spread from other sites of
infection (e.g., infected tonsils, boils, infected teeth,
upper respiratory infections).

OSTEOMYELITIS
 Patients who are at high risk for osteomyelitis
include:
Poorly nourished,
Elderly
Obese
Impaired immune systems,
Chronic illness (e.g., diabetes,
rheumatoid arthritis),
Long-term corticosteroid therapy

OSTEOMYELITIS
 Bone infections are more difficult to
eradicate than soft tissue infections because
the infected bone becomes walled off.
 Natural body immune responses are
blocked, and there is less penetration by
antibiotics.
 Osteomyelitis may become chronic and may
affect the patient’s quality of life

OSTEOMYELITIS
 If bloodborne sudden onset of the ff
manifestations of septicemia like:
 chills, high fever, rapid pulse, general malaise
 pain, swellining, and extreme tenderness.
 Constant, pulsating pain that intensifies with
movement as a result of the pressure of the
collecting pus.

OSTEOMYELITIS
 If from spread of adjacent infection or from direct
contamination:
 No symptoms of septicemia
 Swollen, warm, painful, and tender to touch.
 Chronic osteomyelitis
Presents with a continuously draining sinus or
Recurrent periods of pain, inflammation, swelling,
and drainage.

OSTEOMYELITIS
Medical Management
 IV antibiotic therapy
 An antibiotic to which the causative organism is sensitive
is prescribed after results of the culture and sensitivity
studies are known.
 IV antibiotic therapy continues for 3 to 6 weeks.
 After the infection appears to be controlled, the
antibiotic may be administered orally for up to 3 months.

OSTEOMYELITIS
SURGICAL MANAGEMENT
 If the patient does not respond to antibiotic therapy, the
infected bone is surgically exposed, the purulent and
necrotic material is removed, and the area is irrigated
with sterile saline solution.
Nursing Interventions
 Reliefing pain
 Improving physical mobility
 Controlling the infectious process

OSTEOMYELITIS
Prevention
 Elective orthopedic surgery should be postponed if the
patient has a current infection (e.g., urinary tract
infection, sore throat) or a recent history of infection.
 Use of aseptic surgical environment and other
techniques to decrease direct bone contamination.
 Prophylactic antibiotics 24 hours before and after surgery
 Aseptic postoperative wound
 Prompt management of soft tissue infections

ANKYLOSING SPONDYLITIS
 It is a form of arthritis that primarily affects the spine,
although other joints can become involved.
 It causes inflammation of the spinal joints (vertebrae) that
can lead to severe, chronic pain and discomfort.
 In more advanced cases this inflammation can lead to
ankylosis new bone formation in the spine
 causing sections of the spine to fuse in a fixed, immobile
position.
 AS can also cause inflammation, pain, and stiffness in
other areas of the body such as the shoulders, hips, ribs,
heels, and small joints of the hands and feet.

ANKYLOSING SPONDYLITIS….
 Sometimes the eyes can
become involved rarely the
lungs and heart can be
affected.
 The hallmark sign is the
involvement of the sacroiliac
(SI) joints during the
progression of the disease.
 The SI joints are located at
the base of the spine, where
the spine joins the pelvis

Ankylosing Spondylitis
 Ankylosing spondylitis affects the
cartilaginous joints of the spine and
surrounding tissues.
 Occasionally, the large synovial joints, such
as hips, knees, or shoulders, may be
involved.
 Ankylosing spondylitis is usually diagnosed
in the second or third decade of life.

 Mainly affects men than women.
 Back pain is the characteristic feature.
 As the disease progresses, ankylosis
(stiffness) of the entire spine may occur,
leading to respiratory compromise and
complications.

Newer SpA Classification System
 Axial Spondyloarthritis (AxSpA)
 Axial SpA causes inflammation in the spine and/or
pelvis that typically brings on inflammatory back pain.
 Peripheral Spondyloarthritis (pSpA)
 causes inflammation in joints and/or tendons outside the
spine or sacroiliac joints. Commonly involved sites
include joints in the hands, wrists, elbows, shoulders,
knees, ankles, and feet.
 Many people with SpA have or will develop both axial
SpA and peripheral SpA. Others will have only axial
SpA or only peripheral SpA.
202

Medical Management of Spondylitis
 Focuses on treating pain and maintaining mobility by
suppressing inflammation.
 Good body positioning and posture are essential, so
that if ankylosis (fixation) does occur, the patient is in
the most functional position.
 Maintaining range of motion with a regular exercise
and muscle-strengthening program is especially
important.

Pharmacologic therapy
 Salicylates, NSAIDs, and corticosteroids often produce
marked improvement in back, skin, and joint symptoms.
Surgical management
 Surgical management may include total hip
replacement.
Nursing Management of Spondylitis
 Manage symptom and maintain optimal functioning.

ACUTE LOW BACK PAIN
Most low back pain is caused:
Acute lumbosacral strain due to lifting
heavy objects
Unstable lumbosacral ligaments and
weak muscles,
Osteoarthritis of the spine,
Spinal stenosis, Herniated disk
Intervertebral disk problems, and
Unequal leg length

ACUTE LOW BACK PAIN
 In older patients it is associated with osteoporotic
vertebral fractures or bone metastasis.
 Other causes include:
◦ Kidney disorders,
◦ Pelvic problems,
◦ Retroperitoneal tumors,
◦ Abdominal aneurysms,
◦ Obesity,
◦ Stress,

Causes of low back pain
 chemical substances are released in response to tissue
irritation.
 ―stimulate‖ the surrounding pain sensitive nerve fibers,
resulting in the sensation of pain.
 Some of these chemicals trigger the process of
inflammation, or swelling, which also contributes to pain.
 The chemicals associated with this inflammatory process
feed back more signals which perpetuate the process of
swelling.
 The inflammation attributable to this cycle of events may
persist for days to weeks.
208

Causes of low back pain…..
 Muscular tension (spasm) in the surrounding tissues may
occur resulting in a ― trunk shift‖ (the body tilts to one
side more than the other) due to muscular imbalance.
 Additionally, a relative inhibition or lack of the usual
blood supply to the affected area may occur
 nutrients and oxygen are not optimally delivered and
removal of irritating byproducts of inflammation is
impaired.
209

ACUTE LOW BACK PAIN
 Acute back pain or
 Chronic back pain (lasting more than 3
months without improvement) and
 Fatigue.
 Pain radiating down the leg, which
suggests nerve root involvement.

ACUTE LOW BACK PAIN
 The patient’s gait, spinal mobility, reflexes,
leg length, leg motor strength, and sensory
perception may be altered.
 Paravertebral muscle spasm (greatly
increased muscle tone of the back postural
muscles) with a loss of the normal lumbar
curve and possible spinal deformity.

Diagnosed Of back pain
 In most cases of acute low back pain, diagnostic
testing is not required.
 X-ray : in cases of pain associated with severe
trauma, history of cancer, fever, diabetes, other
medical problems, illicit IV drug use, age over 50,
bowel or bladder dysfunction, nocturnal pain or
osteoporosis.
 CT scan and magnetic resonance imaging (MRI).
212

ACUTE LOW BACK PAIN
Medical Management
 Most back pain is self-limited and resolves within 4
weeks with analgesics, rest, stress reduction, and
relaxation.
 Management focuses on relief of pain and discomfort,
activity modification, and patient education.
 Heat or cold therapy frequently provides temporary
relief of symptoms.

Treatment of back pain
 Remain active ―as tolerated‖- cardiovascular activities,
such as walking,
 stretching muscles and tissues in the legs and back
during an acute episode, but stretching should not
cause more severe pain.
 Local application of heat or ice can temporarily reduce
pain and heat may facilitate stretching,
214

OSTEOMALACIA
 Osteomalacia is a metabolic bone disease characterized
by:
 Inadequate mineralization of bone.
 softening and weakening of the skeleton,
 causing pain, tenderness to touch, bowing of the bones, and
pathologic fractures.
 Skeletal deformities (spinal kyphosis and bowed legs) give
patients an unusual appearance and a waddling or limping
gait.
 As a result of calcium deficiency, muscle weakness, and
unsteadiness, there is an increased risk for falls and
fractures.

OSTEOMALACIA
Causes
 Deficiency of activated vitamin D (calcitriol),
 Failed calcium absorption (e.g., malabsorption syndrome)
or from excessive loss of calcium from the body.
 Liver and kidney diseases can produce a lack of vitamin
D because these are the organs that convert vitamin D to
its active form.
 Hyperparathyroidism
 Deficiency in vitamin D often associated with poor intake
of calcium (malnutrition)

OSTEOMALACIA
Medical Management
 Correcting underlying cause of
 If osteomalacia is caused by malabsorption, increased
doses of vitamin D, along with supplemental calcium.
 Exposure to sunlight for ultraviolet radiation to transform
a cholesterol substance (7-dehydrocholesterol) present in
the skin into vitamin D may be recommended.

OSTEOMALACIA
Medical Management
 If osteomalacia is dietary in origin, a diet
with adequate protein and increased calcium
and vitamin D is provided
 Dietary sources of calcium and vitamin D (eg,
fortified milk and cereals, eggs, chicken
livers) are recommended

Bone Tumors
 Neoplasms of the musculoskeletal system are of various
types, including osteogenic, chondrogenic, fibrogenic,
muscle (rhabdomyogenic), and marrow (reticulum) cell
tumors as well as nerve, vascular and fatty cell tumors.
 They may be primary tumors or metastatic tumors from
primary cancers elsewhere in the body (e.g., breast, lung,
prostate, kidney).
 Metastatic bone tumors are more common than primary
bone tumors.

Bone Tumors
Benign Bone Tumors
 Benign tumors of the bone and soft tissue are
more common than malignant primary bone
tumors.
 Benign bone tumors generally are slow
growing and well circumscribed, present few
symptoms, and are not a cause of death.

Bone Tumors
Benign Bone Tumors
 Benign primary neoplasms of the musculoskeletal system
include:
Osteochondroma (tumor of bone),
Enchondroma (tumor of hyaline cartilage),
Osteoid osteoma (painful tumor in children and
young adults),
Rhabdomyoma, and
Fibroma
 Some benign tumors, such as giant cell tumors, have the
potential to become malignant.

Bone Tumors
Malignant Bone Tumors
 Primary malignant musculoskeletal tumors are
relatively rare.
 Malignant primary musculoskeletal tumors
include:
Osteosarcoma,
Chondrosarcoma,
Ewing’s sarcoma, and
Fibrosarcoma.

Bone Tumors
Malignant Bone Tumors
 Soft tissue sarcomas include:
Liposarcoma,
Fibrosarcoma of soft tissue, and
Rhabdomyosarcoma.
 Bone tumor metastasis to the lungs is
common.

Bone Tumors
Metastatic bone disease
 Metastatic bone disease (secondary bone
tumor) is more common than any primary bone
tumor.
 Tumors arising from tissues elsewhere in the
body may invade the bone and produce
localized bone destruction (lytic lesions) or
bone overgrowth (blastic lesions).

Bone Tumors
 The most common primary sites of tumors
that metastasize to bone are:
The kidneys,
Prostate,
Lung,
Breast,
Ovary, and
Thyroid.

Bone Tumors
 Metastatic tumors most frequently
attack the:
Skull,
Spine,
Pelvis,
Femur, and
Humerus and involve more than one
bone (polyostotic).

Bone Tumors
 Some may be symptom free or
 have pain (mild and occasional to constant and severe),
 varying degrees of disability and,
 at times, obvious bone growth.
 Weight loss, malaise, and fever may be present.
 The tumor may be diagnosed only after pathologic
fracture has occurred.

Bone Tumors
 With spinal metastasis, spinal cord
compression may occur.
 It can progress rapidly or slowly.
 Neurologic deficits (eg, progressive pain,
weakness, gait abnormality, paresthesia,
paraplegia, urinary retention, loss of bowel
or bladder control)

Bone Tumors
Medical Management
PRIMARY BONE TUMORS
 The goal of primary bone tumor treatment is to destroy or
remove the tumor.
 Surgical excision (ranging from local excision to
amputation and disarticulation),
 Radiation therapy if the tumor is radiosensitive,
 Chemotherapy (preoperative, intraoperative,
postoperative, and adjunctive for possible
micrometastases).

Bone Tumors
Medical Management
METASTATIC BONE DISEASE
 The treatment of metastatic bone cancer is
palliative.
 The therapeutic goal is to relieve the
patient’s pain and discomfort while
promoting quality of life.

Bone Tumors
 Similar in many respects to that of other
patients who have had skeletal surgery.
 Vital signs are monitored;
 Blood loss is assessed; and
 Observations are made to assess for the
development of complications.

Trauma and Soft Tissue
Injuries

1, Contusions, Strains,
and Sprains

Contusions, Strains, and Sprains
 Contusion: is a soft tissue injury produced by blunt force,
such as a blow, kick, or fall.
 Many small blood vessels rupture and bleed into soft tissues
(ecchymosis, or bruising).
 A hematoma develops when the bleeding is sufficient to
cause an appreciable collection of blood.
 Local symptoms (pain, swelling, and discoloration) are
controlled with intermittent application of cold.
 Most contusions resolve in 1 to 2 weeks.

 Strain: is a ―muscle pull‖ caused by overuse,
overstretching, or excessive stress.
 Strains are microscopic, incomplete muscle tears with
some bleeding into the tissue.
 The patient experiences soreness or sudden pain, with
local tenderness on muscle use and isometric
contraction.

 Sprain: is an injury to the ligaments surrounding a joint
that is caused by a wrenching or twisting motion.
 The function of a ligament is to maintain stability while
permitting mobility.
 A torn ligament loses its stabilizing ability.
 Blood vessels rupture and edema occurs; the joint is
tender, and movement of the joint becomes painful.

 Sprain:
 The degree of disability and pain increases during the
first 2 to 3 hours after the injury because of the
associated swelling and bleeding.
 An x-ray should be obtained to rule out bone injury.
 Avulsion fracture (in which a bone fragmented is
pulled away by a ligament or tendon) may be
associated with a sprain.

Management
 Treatment of contusions, strains, and sprains consists of
resting and elevating the affected part, applying cold,
and using a compression bandage.
 (The acronym RICE Rest, Ice, Compression, Elevation—is
helpful for remembering treatment interventions.)

Management
 Rest prevents additional injury and promotes healing.
 Moist or dry cold applied intermittently for 20 to 30
minutes during the first 24 to 48 hours after injury
produces vasoconstriction, which decreases bleeding,
edema, and discomfort.
 Care must be taken to avoid skin and tissue damage
from excessive cold.

Management
 An elastic compression bandage controls bleeding,
reduces edema, and provides support for the injured
tissues.
 Elevation controls the swelling.
 If the sprain is severe (torn muscle fibers and disrupted
ligaments), surgical repair or cast immobilization may be
necessary so that the joint will not lose its stability.
 The neurovascular status (circulation, motion, sensation)
of the injured extremity is monitored frequently.

Joint Dislocations
 A dislocation of a joint is a condition in which the
articular surfaces of the bones forming the joint are no
longer in anatomic contact.
 The bones are literally ―out of joint.‖
 A subluxation is a partial dislocation of the articulating
surfaces.

Joint Dislocations
 Traumatic dislocations are orthopedic emergencies
because the associated joint structures, blood supply,
and nerves are distorted and severely stressed.
 If the dislocation is not treated promptly, avascular
necrosis (tissue death due to anoxia and diminished
blood supply) and nerve palsy may occur.

Joint Dislocations
 Dislocations may be congenital, or present at birth
(most often the hip); spontaneous or pathologic, caused
by disease of the articular or periarticular structures;
or traumatic, resulting from injury in which the joint is
disrupted by force.

Joint Dislocations
 Signs and symptoms of a traumatic dislocation are:
pain,
change in contour of the joint,
change in the length of the extremity,
loss of normal mobility, and
change in the axis of the dislocated bones.
 X-rays confirm the diagnosis and demonstrate any
associated fracture.

Joint Dislocations
Medical Management
 The affected joint needs to be immobilized while the
patient is transported to the hospital.
 The dislocation is promptly reduced (ie, displaced parts
are brought into normal position) to preserve joint
function.
 Analgesia, muscle relaxants, and possibly anesthesia
are used to facilitate closed reduction.
 The joint is immobilized by bandages, splints, casts, or
traction and is maintained in a stable position.

Joint Dislocations
Medical Management
 Neurovascular status is monitored.
 After reduction, if the joint is stable, gentle,
progressive, active and passive movement is begun to
preserve range of motion (ROM) and restore strength.
 The joint is supported between exercise sessions.

Joint Dislocations
Nursing Management
 Nursing care is directed at:
 Providing comfort,
 evaluating the patient’s neurovascular status, and
 protecting the joint during healing
 Teaching the patient how to manage the immobilizing
devices and how to protect the joint from reinjury.

Fractures
 A fracture is a break in the continuity of bone and is
defined according to its type and extent.
 Fractures occur when the bone is subjected to stress
greater than it can absorb.
 Fractures are caused by direct blows, crushing forces,
sudden twisting motions, and even extreme muscle
contractions.

Fractures
 When the bone is broken, adjacent structures are also
affected,
 Resulting in soft tissue edema, hemorrhage into the
muscles and joints, joint dislocations, ruptured tendons,
severed nerves, and damaged blood vessels.
 Body organs may be injured by the force that caused
the fracture or by the fracture fragments.

Types of Fractures
 Based on cross-section of the bone involved:
1. Complete fracture: involves a break across the entire
cross-section of the bone and is frequently displaced
(removed from normal position).
2. Incomplete fracture (eg, greenstick fracture): the break
occurs through only part of the cross-section of the
bone.
3. Comminuted fracture: is one that produces several
bone fragments.

Types of Fractures
 Based on involvement of the skin:
1. Closed fracture (simple fracture): is one that does
not cause a break in the skin.
2. Open fracture (compound, or complex, fracture): is
one in which the skin or mucous membrane wound
extends to the fractured bone.

Types of Fractures
 Open fractures are graded according to the following
criteria:
◦ Grade I: is a clean wound less than 1 cm long.
◦ Grade II: is a larger wound without extensive soft
tissue damage.
◦ Grade III: is highly contaminated, has extensive soft
tissue damage, and is the most severe.
 Fractures may also be described according to
the anatomic placement of fragments,
particularly if they are displaced or nondisplaced.

Fracture
 The clinical manifestations of a fracture are:
◦ pain,
◦ loss of function,
◦ deformity,
◦ shortening of the extremity,
◦ crepitus (a grating sensation palpation), and
◦ local swelling and discoloration.
 Not all of these clinical manifestations are present
in every fracture.

Emergency Management of Fractures
 Immediately after injury, whenever a fracture is
suspected, it is important to immobilize the body part
before the patient is moved.
 If an injured patient must be removed from a vehicle
before splints can be applied,
 The extremity is supported above and below the
fracture site to prevent rotation as well as angular
motion.

Emergency Management of Fractures
 With an open fracture, the wound is covered with a
clean (sterile) dressing to prevent contamination of
deeper tissues.
 No attempt is made to reduce the fracture, even if
one of the bone fragments is protruding through the
wound.
 Splints are applied for immobilization.

Medical Management of Fractures
1. REDUCTION
 Reduction of a fracture (―setting‖ the bone) refers to
restoration of the fracture fragments to anatomic alignment
and rotation.
1. Closed Reduction: closed reduction is accomplished by
bringing the bone fragments into apposition (ie, placing the
ends in contact) through manipulation and manual traction.
2. Open Reduction. Through a surgical approach, the fracture
fragments are reduced. Internal fixation devices (metallic
pins, wires, screws, plates, nails, or rods) may be used to
hold the bone fragments in position

2. IMMOBILIZATION
 After the fracture has been reduced,
 The bone fragments must be immobilized, or held in
correct position and alignment, until union occurs.
 Immobilization may be accomplished by external or
internal fixation.

3. MAINTAINING AND RESTORING FUNCTION
 Reduction and immobilization are maintained as prescribed
to promote bone and soft tissue healing.
 Swelling is controlled by elevating the injured extremity and
applying ice as prescribed.
 Neurovascular status (circulation, movement, sensation) is
monitored, and the orthopedic surgeon is notified
immediately if signs of neurovascular compromise are
identified.
 Isometric and muscle-setting exercises are encouraged to
minimize disuse atrophy and to promote circulation.

Complications of Fracture
 Complications of fractures fall into two categories—early
and delayed.
 Early complications include:
 Shock,
 Fat embolism,
 Compartment syndrome,
 Deep vein thrombosis,
 Thromboembolism (pulmonary embolism),
 Disseminated intravascular coagulopathy (DIC), and
 Infection.

Complications of Fracture
 Delayed complications include:
Delayed union and nonunion,
Avascular necrosis of bone,
Reaction to internal fixation devices,
Complex regional pain syndrome (formerly
called reflex sympathetic dystrophy), and
Heterotrophic ossification.

Care of the Patient
in a Cast
267

Care of the Patient in a Cast
268
 A cast is a rigid external immobilizing device that is
molded to the contours of the body.
 It permit mobilization of the patient while restricting
movement of a body part.
 The purposes of a cast are:
 To immobilize a body part in a specific position,
 To apply uniform pressure on encased soft tissue,
 To immobilize a reduced fracture,
 to correct a deformity,
 To apply uniform pressure to underlying soft tissue,
or
 To support and stabilize weakened joints.

Types of Cast
269
 Short arm cast: Extends from below the elbow to the
palmar crease, secured around the base of the
thumb. If the thumb is included, it is known as a
thumb spica or gauntlet cast.
 Long arm cast: Extends from the upper level of the
axillary fold to the proximal palmar crease. The
elbow usually is immobilized at a right angle.
 Short leg cast: Extends from below the knee to the
base of the toes. The foot is flexed at a right angle
in a neutral position.

Types of Cast
270
 Long leg cast: Extends from the junction of the upper
and middle third of the thigh to the base of the toes.
The knee may be slightly flexed.
 Walking cast: A short or long leg cast reinforced for
strength.
 Body cast: Encircles the trunk.
 Shoulder spica cast: A body jacket that encloses the
trunk and the shoulder and elbow.
 Hip spica cast: Encloses the trunk and a lower extremity.
A double hip spica cast includes both legs.

CASTING MATERIALS
271
 Nonplaster (fiberglass casts): they are water-
activated polyurethane materials and have the
versatility of plaster but are lighter in weight,
stronger, water resistant, and durable.
 Plaster (POP): Rolls of plaster bandage are wet in
cool water and applied smoothly to the body.
 The plaster cast requires 24 to 72 hours to dry
completely, depending on its thickness and the
environmental drying conditions.

Management of undried cast
272
 While damp (wet), the cast can be dented.
Therefore,
it must be handled with the palms of the hand
and
not allowed to rest on hard surfaces or sharp
edges
should be exposed to circulating air to dry
and should not be covered with clothing or bed
linens

Management of undried cast
273
 Cast dents may press on the skin causing irritation
and skin breakdown.
 A wet plaster cast appears dull and gray, sounds
dull on percussion, feels damp, and smells musty.
 A dry plaster cast is white and shiny, resonant,
odorless, and firm.

POTENTIAL COMPLICATIONS OF CAST
AND THEIR MANAGEMENT
274
Compartment Syndrome
 Compartment syndrome occurs when there is
increased tissue pressure within a limited space
(eg, cast, muscle compartment) that compromises
the circulation and the function of the tissue within
the confined area.

POTENTIAL COMPLICATIONS OF
CAST AND THEIR MANAGEMENT275
Compartment Syndrome
 Management: To relieve the pressure, the cast must be
bivalved (cut in half longitudinally) while maintaining
alignment, and the extremity must be elevated no
higher than heart level.
 If pressure is not relieved and circulation is not restored,
a fasciotomy may be necessary to relieve the pressure
within the muscle compartment.
 The nurse records neurovascular responses and
promptly reports changes to the physician.

Pressure Ulcers
 Pressure of the cast on soft tissues may cause
tissue anoxia and pressure ulcers.
 Lower extremity sites most susceptible to pressure
are the heel, malleoli, dorsum of the foot, head of
the fibula, and anterior surface of the patella.

Pressure Ulcers
 Management: To inspect the pressure area, the
physician may bivalve the cast or cut an opening
(window) in the cast.
 If the physician elects to create a window to inspect the
pressure site, a portion of the cast is cut out.
 The portion of the cast is replaced and held in place by
an elastic compression dressing or tape.
 This prevents the underlying tissue from swelling through
the window and creating pressure areas around its
margins.

Disuse Syndrome
 While in a cast, the patient needs to learn to tense
or contract muscles (eg, isometric muscle
contraction) without moving the part.
 This helps to reduce muscle atrophy and maintain
muscle strength.

Disuse Syndrome
 Management: The nurse teaches the patient with a leg
cast to ―push down‖ the knee and teaches the patient in
an arm cast to ―make a fist.‖
 Muscle-setting exercises (e.g., quadriceps-setting and
gluteal setting exercises) are important in maintaining
muscles essential for walking.
 Isometric exercises should be performed hourly while
the patient is awake.

Managing the
Patient in Traction
280

Managing the Patient in Traction
281
 Traction is the application of a pulling force to
a part of the body.
 Traction is used:
to minimize muscle spasms;
to reduce, align, and immobilize fractures;
 to reduce deformity; and
 to increase space between opposing
surfaces.

Managing the Patient in Traction
282
 Traction must be applied in the correct direction and
magnitude to obtain its therapeutic effects.
 As muscle and soft tissues relax, the amount of weight
used may be changed to obtain the desired effect.
 The effects of traction are evaluated with x-ray studies,
and adjustments are made if necessary.
 Traction is used primarily as a short-term intervention
until other modalities, such as external or internal
fixation, are possible.
 At times, traction needs to be applied in more than one
direction to achieve the desired line of pull.

PRINCIPLES OF EFFECTIVE TRACTION
283
1. Whenever traction is applied, counter-traction (forces
in opposite direction) must be used to achieve effective
traction.
2. Traction must be continuous to be effective in reducing
and immobilizing fractures.
3. Skeletal traction is never interrupted.
4. Weights are not removed unless intermittent traction is
prescribed.
5. Any factor that might reduce the effective pull or alter
its resultant line of pull must be eliminated.

TYPES OF TRACTION
284
 Straight or running traction: applies the pulling
force in a straight line with the body part resting
on the bed. E.g. Buck’s extension traction
 Balanced suspension traction (Fig. 67-5): supports
the affected extremity off the bed and allows for
some patient movement without disruption of the
line of pull.
 Skin traction: Traction applied to the skin.

TYPES OF TRACTION
285
 Skeletal traction: traction directly applied to the
bony skeleton.
 The mode of application is determined by the
purpose of the traction.
 Manual traction: Traction applied with the hands.
 This is temporary traction that may be used when
applying a cast, giving skin care under a Buck’s
extension foam boot, or adjusting the traction
apparatus.

Potential Complications of Skin
Traction287
 Skin breakdown,
 nerve pressure, and
 circulatory impairment

288
 Monitor and prevent skin breakdown
 Regularly assess sensation and motion.
 Immediately investigate any complaint of burning
sensation under the traction bandage or boot.
 Promptly report altered sensation or motor function.
 Circulatory assessment consists of the following:
 Peripheral pulses, color, capillary refill, and
temperature of the fingers or toes
 Indicators of DVT, including calf tenderness, and
swelling.

Nursing Interventions for Skin
Traction289
 Maintaining effective traction
 Maintaining positioning
 Preventing skin break down
 Monitoring neurovascular status
 Promoting pin site care
 Promoting exercise (iso-metric excersice for
immobilized parts)

Amputation
291
 Amputation is the removal of a body part, usually an
extremity.
 Amputation of a lower extremity is often made
necessary by progressive peripheral vascular disease
(often a sequela of diabetes mellitus), fulminating gas
gangrene, trauma (crushing injuries, burns, frostbite, and
electrical burns), congenital deformities, chronic
osteomyelitis, or malignant tumor.
 Of all these causes, peripheral vascular disease accounts
for most amputations of lower extremities.

Purposes of Amputation
292
 Amputation is used to:
relieve symptoms,
improve function, and
save or improve the patient’s quality of life.

Levels of Amputation
293
 Amputation is performed at the most distal point that
will heal successfully.
 The site of amputation is determined by two factors:
1. circulation in the part, and
2. functional usefulness (ie, meets the requirements
for the use of the prosthesis).
 The objective of surgery is to conserve as much
extremity length as possible.
 Preservation of knee and elbow joints is desired. Almost
any level of amputation can be fitted with a prosthesis.

Levels of Amputation
295
 Upper extremity amputations are performed to
preserve themaximum functional length.
 The prosthesis is fitted early for maximum function.
 A staged amputation may be used when gangrene and
infection exist. Initially, a guillotine amputation is
performed to remove the necrotic and infected tissue.
 The wound is débrided and allowed to drain. Sepsis is
treated with systemic antibiotics.
 After the infection has been controlled and the
patient’s condition has stabilized, a definitive
amputation with skin closure is performed.

Complications of Amputation
296
 Complications that may occur with amputation
include:
hemorrhage,
infection,
skin breakdown,
phantom limb pain, and
joint contracture

Medical Management
297
 The objective of treatment is to achieve healing of
the amputation wound, the result being a non
tender residual limb (stump) with healthy skin for
prosthesis use.
 Healing is enhanced by gentle handling of the
residual limb, control of residual limb edema
through rigid or soft compression dressings, and
use of aseptic technique in wound care to avoid
infection.

Medical Management
298
 A closed rigid cast dressing is frequently used to
provide uniform, to support soft tissues, to control pain,
and to prevent joint contractures.
 Immediately after surgery, a sterilized residual limb
sock is applied to the residual limb.
 Felt pads are placed over pressure-sensitive areas.
 The residual limb is wrapped with elastic plaster-of-
paris (POP) bandages while firm, even pressure is
maintained.
 Care is taken not to constrict circulation.

Medical Management
299
 A removable rigid dressing may be placed over a soft
dressing to control edema, to prevent joint flexion
contracture, and to protect the residual limb from
unintentional trauma during transfer activities.
 This rigid dressing is removed several days after
surgery for wound inspection and is then replaced to
control edema.
 The dressing facilitates residual limb shaping.

Medical Management
300
 A soft dressing with or without compression may be
used if there is significant wound drainage and
frequent inspection of the residual limb (stump) is
desired.
 An immobilizing splint may be incorporated in the
dressing.
 Stump (wound) hematomas are controlled with wound
drainage devices to minimize infection.

Medical Management
301
 Rehabilitation: Because the amputation is the
result of an injury, the patient needs
psychological support in accepting the sudden
change in body image and in dealing with the
stresses of hospitalization, long-term
rehabilitation, and modification of lifestyle.
 Patients who undergo amputation need support
as they grieve the loss, and they need time to
work through their feelings about their permanent
loss and change in body image.

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