Musculoskeletal System

Musculoskeletal

Heberden’s nodes osteoarthritis
Painless bony enlargement of distal interphalangeal joint

Swan neck deformity rheumatoid arthritis
Hyperextended proximal interphalangeal joint
Slightly flexed distal interphalangeal joint
Also:
Volar subluxation of metacarpophalangeal joint
Ulnar deviation of fingers

Tophi gout
Painless, nodular swelling (uric acid deposits)
Ear, hands and feet

Abduction Movement of part away from the midline of the body

Adduction Movement of part toward the midline of the body

Circumduction Combination of flexion, extension, abduction, and adduction resulting in circular motion of the body part

Eversion Turing of sole outward away from midline of body

Extension Straightening of joint that increases angle between two bones

External rotation Movement along longitudinal axis away from midline of body

Flexion Bending of joint as a result of muscle contraction that results in decreased angle between two bones

Hyperextension Extension in which angle exceeds 180 degrees

Internal rotation Movement along longitudinal axis toward midline of body

Inversion Turning of sole inward toward midline of body

Pronation Turning of palm downward

Supination Turning of palm upward



Muscle Strength Scale
0 No detection of muscular contraction
1 A barely detectable flicker or trace of contraction with observation or palpation
2 Active movement of body part with elimination of gravity
3 Active movement against gravity only and not against resistance
4 Active movement against gravity and some resistance
5 Active movement against full resistance without evident fatigue (normal muscle strength)

Physical Assessment of Musculoskeletal System
Full range of motion of all joints without pain or laxity
No joint swelling, deformity or crepitation
Normal spinal curvatures
No tenderness on palpation of spine
No muscle atrophy or asymmetry
Muscle strength of 5

Common Abnormalities
Finding Description Poss. Etiology and significance
Ankylosis Scarring w/i joint leading to stiffness or fixation Chronic joint inflammation
Atrophy Wasting of muscle, characterized by decreased circumference and flabby appearance leading to decreased function and tone Muscle denervation, contracture, prolonged disuse as a result of immobilization
Contracture Resistance of movement of muscle or joint as a result of fibrosis of supporting soft tissues Shortening of muscle or ligaments, tightness of soft tissue, incorrect positioning of immobilized extremity

Crepitation (crepitus) Crackling sound or grating sensation as a result of friction or broken bone or cartilage bits in joint Fracture, dislocation, chronic inflammation, osteoarthritis
Effusion Fluid in joint possibly with swelling and pain Trauma, especially to knees; inflammation
Ganglion Small fluid-filled synovial cyst usually on dorsal surface of wrist or foot Degeneration of connective tissue close to tendons and joints leading to formation of small cysts
Hypertrophy Increase in size of muscle as a result of enlargement of existing cells Exercise or other increased stimulation, increased androgens

Kyphosis (dowager’s hump) Anteroposterior or forward bending of thoracic spine with convexity of curve in posterior direction Poor posture, tuberculosis, arthritis, osteoporosis, growth disturbance of vertebral epiphyses
Lordosis Lumbar spinal deformity resulting in Anteroposterior curvature with concavity in posterior direction Secondary to other spinal deformities, muscular dystrophy, obesity, flexion contracture of hip, congenital dislocation of hip
Pes planus Flatfoot Congenital condition, muscle paralysis, mild cerebral palsy, early muscular dystrophy
Scoliosis Deformity resulting in lateral curvature of thoracic spine Idiopathic of congenital condition, fracture or dislocation osteomalacia
Subluxation Partial dislocation of joint Instability of joint capsule and supporting ligaments. (e.g. from trauma, arthritis)
Valgus (bow legs) Angulation of bone away from midline Alteration in gait, pain, arthritis
Varus (knock-knees) Angulation of bone toward midline Alteration in gait, pain, arthritis

Sports-related injuries
Injury Definition Treatment
Impingement syndrome Entrapment of soft tissue structures under coacromial arch of the shoulder NSAIDs; rest until symptoms decrease and then gradual ROM and strengthening exercises
Rotator cuff tear Tear w/i muscle or ligaments of shoulder If minor tear, rest, NSAIDs, and gradual mobilization with ROM and strengthening exercises
If major tear, surgical repair
Shin splints Inflammation along tibial shaft from tearing away of tendons caused by improper shoes, overuse, or running on hard pavement Rest, ice, NSAIDs, proper shoes; gradual increase in activity; if pain persist x-ray should be done to rule out stress fracture of tibia
Tendonitis Inflammation of tendon in upper or lower extremity or as a result of overuse or incorrect use Rest, ice, NSAIDs; gradual return t sport activity; protective brace (orthosis) may be necessary if symptoms recur
Ligament injury Tearing or stretching of ligament; usually occurs as a result of direct blow; characterized by sudden pain, swelling, and instability Rest, ice, NSAIDs; protection of affected extremity by use of brace; if symptoms persist, surgical repair may be necessary
Meniscal injury Injury to fibrocartilage of the knee characterized by popping, clicking, or tearing sensation, swelling Rest, ice, NSAIDs; gradual return to regular activities; if symptoms persist, surgical arthroscopy to diagnose and repair meniscal injury ma be necessary


ARTHRITIS
Rheumatoid arthritis Osteoarthritis
Autoimmune disease

Onset: young to middle age
Female/male ratio is 2:1 or 3:1; less marked gender difference after age 60

Lose or maintain weight

Systemic disease with exacerbations and remissions

Small joints first, wrists, elbows, shoulders, knees; usually bilateral, symmetric

Stiffness: 1 hr to all day

Effusions: common

Synovial fluid: WBC count>2000/μl with mostly neutrophils

Morning stiffness
Swelling of 3 or more joints
Involves: wrist, MCP and PIP

Subcutaneous nodules: Present, especially on extensor surfaces

Rheumatoid factor in serum (80% of patients)
Elevated ESR, CRP indicative of active inflammation

Characteristic hand deformity:
Ulnar deviation of digits
“swan neck” deformity

X-Ray:
Joint space narrowing, erosions, subluxations with advanced disease; osteoporosis related to corticosteroid use
Periarticular bone erosions Degenerative disease

Onset: usually >40 yr of age
Before age 50, more men than women; after age 50, more women than men

Often overweight

Localized disease with variable, progressive course

Weight-bearing joints (knees, hips), MCPs, DIPs, PIPs, cervical and lumbar spine; often asymmetric

Stiffness: on arising but usually subsides after 30 minutes
Progressive pain
Relieved by rest

Synovial fluid: WBC count <2000/μl (mild leukocytosis
RF negative
Transient elevation in ESR related to synovitis

Effusions: uncommon

Nodules: Heberden’s (DIPs,) and Bouchard’s (PIPs) nodes

X-ray:
Loss of cartilage
Narrowed joint space
Subchondral cysts and sclerosis
New bone formation (marginal osteophytes)


Analysis
Impaired mobility----risk of injury Impaired mobility---risk of injury
Implementation
Range of motion exercises
Encourage self-care: provide privacy and pain relief
Apply local heat or cold
MEDICATIONS:
Analgesics
Anti-inflammatory drugs Range of motion exercises
Exercises to maintain muscle strength (but minimize weight-bearing activities)
Encourage weight loss to reduce stress on joints
Warm tub baths to relieve stiffness
CLIENT EDUCATION
Serious risk of gastric ulceration from anti-inflammatory drugs.

Osteoarthritis
The most common form of joint disease in North America. A slowly progressive noninflammatory disorder of the diarthrodial (synovial) joints, sometimes called degenerative joint disease. No longer considered to be a normal part of the aging process. May be primary (idiopathic or secondary disorder
Causes of Secondary Osteoarthritis
Cause Effects on joint cartilage
Trauma Dislocations or fractures may lead to avascular necrosis or uneven stress on cartilage
Mechanical stress Repetitive physical activities (e.g., sports activities) cause cartilage deterioration
Inflammation Release on enzymes in response to local inflammation can affect cartilage integrity
Joint instability Damage to supporting structures causes instability, placing uneven stress on articular cartilage
Neruologic disorders Pain and loss of reflexes from neruologic disorder, such as diabetic neuropathy, and Charcot joint cause abnormal movements that contribute to cartilage deterioration
Skeletal deformities Legg-Calve-Perthes disease or dislocated hip contribute to cartilage deterioration
Hematologic/endocrine disorders Chronic hemarthrosis (e.g., hemophilia) can contribute to cartilage deterioration
Use of selected drugs Drugs such as indomethacin (Indocin), colchicines, and corticosteroids can stimulate collagen-digesting enzymes in joint synovium


Common in the elderly: more than 70% of people older than 65.

Clinical manifestations:
Pain and stiffness in one or more of the joints, commonly the hands, wrists, feet, knees, upper and lower spine, hips and shoulders
Swelling of the affected joints, with a decreased ROM. Joins may appear deformed
Heberden’s nodes may develop at the distal interphalangeal joints.

Diagnosis:
Arthroscopy, MRI, and CT scan

Treatment:
A balance between resting and exercising the joints, geared toward minimizing inflammation by preserving range of motion is helpful
Analgesics and anti-inflammatory drugs to reduce swelling and inflammation
Surgery ay be required to correct a deformity or replace a joint


Rheumatoid Arthritis

Chronic, inflammatory disease that causes degeneration of connective tissue, usually starting with the synovial membrane. The inflammation than spread to the surrounding structures of the joint including the articular cartilage and the fibrous joint capsule. After that the ligaments and tendon become inflamed. The inflammation is characterized by whit blood cell accumulation; complement activation, extensive phagocytosis and scarring. /The synovial membrane hypertrophies and thickens, occludes blood flow and stimulates further cell necrosis and more inflammation. Pannus, an inflammatory granular tissue covers the synovium; it may spread throughout the joint causing further inflammation and scarring. This process destroys the bone and causes massive amounts of pain.

Causes:
This is an autoimmune disease that develops in individuals after an immune response against an unknown trigger. That trigger may be a bacterium, mycoplasma, or virus that infects the joints or resembles the joint antigenically. Usually the original antibody response is IgG mediated. It may successfully destroy the microorganism, but then the person begins to produce antibodies, usually IgM or IgG against the original IgG antibody. Theses are called rheumatoid factors (RFs). These persist in the joint capsule, cause chronic inflammation and destruction of the tissue. There may be a genetic predisposition to the autoimmune disease. Women are more often affected than men. Various cytokines, especially tumor necrosis factor alpha, may contribute to the problem.

Clinical manifestations:
Onset characterized by general symptoms of inflammation including fever, fatigue, body aches, and joint swelling.
Joint tenderness and stiffness develop because of acute inflammation and from scar formation. Finger and wrist joints are usually the first to be involved. Stiffness is worse in the morning and affects joints bilaterally. Inflammation and remission are interspersed.
Decreased ROM. Joint deformity and muscular contraction
Extrasynovial rheumatoid nodules develop in approximately 20% of individuals with RA. These consist of WBCs and cell debris and are located at areas of trauma or increased pressure. They usually develop in subcutaneous tissue over the elbows and fingers.

Diagnostic tools:
Elevated serum rheumatoid factor in 80% of cases.
X-ray changes such as bony decalcification of the joints
Synovial fluid aspirating may show WBCs.

Complications:
Extrasynovial rheumatoid nodules may develop on cardiac valves, in the lungs, eyes, or spleen. They may cause respiratory and cardiac problems. Glaucoma my result is the nodules block outflow of ocular fluid in the eye.

Treatment:
Rest of the joins during exacerbations.
Rest periods each day.
Alternating hot and cold packs.
ASA, NSAIDs or steroids. Gold treatment may be tried.
Anti-TNF medications are used t block cytokine-mediated inflammation.
Surgery to remove the synovial membrane or to correct deformity.

Anatomic Stages of Rheumatoid Arthritis
Stage I-Early No destructive changes on x-ray, possible x-ray evidence of osteoporosis
State II-Moderate x-ray evidence of osteoporosis, with or without slight bone or cartilage destruction, no joint deformities (although possible limited joint mobility), adjacent muscle atrophy, possible presence of extraarticular soft tissue lesion (e.g., nodules, tenosynovitis)
Stage III-Severe x-ray evidence of cartilage and bone destruction in addition to osteoporosis; joint deformity, such as subluxation, ulnar deviation, hyperextension, without fibrous or bony Ankylosis; extensive muscle atrophy; possible presence of extraarticular soft tissue lesion (e.g., nodules, tenosynovitis)
Stage IV-Terminal Fibrous or bony Ankylosis, criteria of Stage III



GOUT
Deposits of urate crystals in synovial tissue----acute inflammation
90% of cases are due to under-excretion of uric acid
10% of cases are due to over-production of uric acid
ASSESSMENT
May be asymptomatic for a long time
Acute attack: pain in joint of great toe (“podagra”)
Elevated serum uric acid
Tophi: urate deposits in subcutaneous tissue
Primary gout: hereditary error of purine metabolism leads to the overproduction or retention of uric acid (90% of cases)
Predominantly in middle-aged men
Secondary gout: may be related to another acquired disorder or may be the result of drugs known to inhibit uric acid excretion. May also be caused by drugs that increase the rate of cell death (chemo).
IMPLEMENTATION
Bed rest during acute attack
Use cradle to keep bedcovers elevated
Encourage fluid intake (3L/day)
Hot packs (reduce swelling and pain)
Cold packs (reduce swelling and pain)
MEDICATIONS:
Asymptomatic hyperuricemia: no medication necessary
Mild attacks: analgesics (acetaminophen)
Sever attacks: colchicines, NSAIDs
Allpurinol: reduces uric acid production
Probenecid: increases renal uric acid excretion
CLIENT EDUCATION
Encourage weight loss but avoid crash diets!
Avoid alcohol
Limit food high in purines (anchovies, shellfish, organ meats)
Factors that inhibit uric acid secretion: (increase risk of gout)
Alcohol
Aspirin
Diuretics

SPONDYLOARTHROPATHIES
Autoimmune diseases involving spine and sacroiliac joint
Ankylosing spondylitis
(more common in men)
Symmetric sacroiliitis and progressive inflammatory arthritis of the axial skeleton
Inflammatory spine pain usually precedes dx.
Iritis most common nonskeletal symptom.
May have chest pain that mimics angina or pleurisy
Severe postural abnormities and deformity can lead t significant disability, impaired spinal ROM and fixed Kyphosis can lead to altered visual function (safe ambulation concerns), aortic insufficiency and pulmonary fibrosis are frequent complication
Cauda equina syndrome can occur and contribute to lower-extremity weakness and bladder dysfunction
Risk for spinal fracture due to osteoporosis
Care: maintaining maximal skeletal mobility with decreasing pain and inflammation
Heat, NSAIDs and salicylates
DMARDs (sulfasalazine, methotrexate)
Etanercept for active AS
Remicade shows promise.
Exercise is essential
Postural control to minimize spinal deformity. Regimen should include back, neck, and chest stretches.
Hydrotherapy to decrease pain and facilitate spinal extension.
Surgery: for severe deformity and mobility impairment
Reiter’s syndrome
(reactive arthritis) (more common in men)

Sudden onset
Urethritis or cervicitis, conjunctivitis and mucocutaneous lesions (small, painless, superficial ulcerations on the tongue, oral mucosa and glans penis)
May have Achilles tendonitis or plantar fasciitis
ESR may be elevated
Arthritis (knees and ankles)-may be symmetric, frequently involving the large joints of the lower extremities and the toes.
Lower back pain may occur with severe disease
Follows dysentery (Shigella, Salmonella, Campylobacter, or Yersinia)
Follows STD (Chlamydia)
Most recover in 2-16 weeks
Up to 50% may develop chronic or recurring disease.
Psoriatic arthritis (more common in women)
Approx. 10% of the 3 million people (20%) with psoriasis develop psoriatic arthritis

Variable onset
Progressive inflammatory disease.
Cause is unknown, but combination of immune, genetic and environmental factors suspected.
Five forms:
1. Arthritis involving primarily the small joints of the hands and feet
2. Asymmetric arthritis involving joints of the extremities
3. Symmetric polyarthritis resembling RA
4. Arthritis of the sacroiliac joints and spine (psoriatic spondylitis)
5. Arthritis mutilans, a rare but very deforming and destructive disease
Nail pitting
“sausage toes”

X-ray:
Cartilage loss and erosion similar to that or RA
Widened joint spaces and “pencil in cup” deformity in the DIP joints
Elevated ESR, mild anemia and elevated blood uric acid level in some patients (gout must be excluded)
Treatment: splinting
Joint protection
Physical therapy
Gold therapy has been tried with some success
Methotrexate in most effective agent for cutaneous and articular manifestations
Sulfasalazine has been successful too
Physical therapy, postural and breathing exercises are extremely important to maintain mobility and posture!
Septic arthritis (infectious or bacterial arthritis) Invitation of the joint cavity with microorganisms
Hematogenous seeding of joints (transport through blood of infection)
Organisms can be introduced through trauma or surgical incision
Any bacteria can cause the infection
Causative organisms: Staphylococcus aureus, Streptococcus hemolyticus, Neisseria gonorrhoeae
Occurs twice as often as osteomyelitis
Factors that increase the risk: decreased host resistance (leukemia, diabetes mellitus, corticosteroids or immunosuppressive drugs, debilitation chronic illness
Inflammation of the joint cavity causes severe pain, erythema and swelling.
Fever or chill
Diagnosis: aspiration of the joint and culture of the synovial fluid
Blood cultures
Medical emergency
Antibiotics are used; infection may respond within 2 weeks or may take from 4-8 weeks
Open surgical drainage may be required
Nursing intervention: assessment and monitoring of joint inflammation, pain and fever. Immobilization to control pain, gentle ROM exercises on regular schedule
Lyme disease A spirochetal infection caused by Borrelia burgdorferi
Transmitted by the bite of an infected deer tick
Most U.S. cases occur in three endemic areas: Northeastern coast from Maryland to Massachusetts
Midwestern states of Wisconsin and Minnesota
Northwestern coast of Northern California and Oregon

Reported incidence of Lyme disease has doubled in the last 10 years (16,700 cases annually)

“Great imitator” it symptoms can mimic diseases such as MS, mononucleosis and meningitis

Most characteristic clinical symptom: erythema migrant: skin lesion that occurs at the site of the bite within 2 to 30 days
Often accompanied by acute viral-like symptoms (fever, chills, headache stiff neck, fatigue, swollen lymph nodes, migratory joint and muscle pain)

Can progress to include nervous system (weeks or months) such as severe headaches, temporary facial paralysis (Bell’s palsy), poor motor coordination

Late disease (months to years): Arthritis pain and swelling may occur in a few large joints
Often temporary but may become chronic if untreated

Dx: based on clinical manifestations (EM lesion, hx. of exposure in endemic area
Labs: Serology tests for antibodies not usually positive fore weeks
CSF should be examined when neruologic involvement

Treatment: Active lesions: oral doxycycline or amoxicillin
IV ceftriazone for cardiac or neruologic abnormalities
Vaccine: recently withdrawn from market
Teaching for prevention


SYSTEMIC LUPUS ERYTHEMATOSUS
Chronic inflammatory disease of connective tissues (autoimmune)
Systemic lupus Weakness, fatigue
Anorexia, weight loss
Photosensitivity
Butterfly rash (spares nasolabial fold)
Discoid rash
Anemia
Arthritis
Nephritic syndrome
LAB:
Leucopenia, lymphopenia
Thrombocytopenia
Antinuclear antibodies
False positive tests for syphilis
Drug induced lupus Often fairly mild
History of hydralazine, procainamide, other drugs
Reversible after drug cessation
ANALYSIS:
Complications related to organs affected
IMPLEMENTATION
Emotional support
Protective clothing and sun screen if client is photosensitive
Heat packs for joint pain
Monitor for signs of renal damage: edema, hypertension
MEDICATIONS:
Steroids (topical for skin, systemic if organ involvement)

Systemic lupus erythematosus: chronic multisystem inflammatory disease associated with abnormalities of the immune system.
Affects: skin, joints, serous membranes, renal, hematologic and neruologic systems

Incidence: 2-8 per 100,000. Women in their childbearing years are most common. African Americans, Asian American and Native Americans are 3 times more likely to develop SLE than whites.
Characterized by variability within and among persons
It has a chronic unpredictable course marked by alternating periods of exacerbations and remissions

Etiology: unknown A disorder of immunoregulation. Autoimmune reactions are directed against constituents of the cell nucleus, particular DNA. The overaggressive antibody response is related to B and T cell hyperactivity. Autoantibodies bind to their antigens , complement activation occurs and immune complexes are deposited in the basement membranes of capillaries in the kidneys, heart, skin, brain, and joints.
Poss. genetic influence
Hormones know to play a role.
Onset or exacerbation sometimes occurs after the onset of menarche, with the use or oral contraceptives and during and after pregnancy. Tends to worsen in the immediate postpartum period

Environmental factors: sun exposure and burns are triggers; Infectious agents could serve as stimulus. May also be precipitated or aggravated by certain drugs (procainamide, hydralazine, and some antiseizure drugs

Ranges from mild to rapidly progressing affecting many organ systems. No characteristic pattern occurs in the organ involvement.

Dermatologic Manifestations: cutaneous vascular lesions can appear in any location but most likely in sun exposed areas. May be photosensitive. Butterfly rash over the cheeks and bridge of the nose in 50% of patients
Sub acute cutaneous lupus: mild systemic disease characterized by persistent lesions, photosensitivity and systemic disease

Musculoskeletal Problems: Polyarthralgia with morning stiffness. Arthritis in 90% of patients. Diffuse swelling accompanied by joint and muscle pain.

Cardiopulmonary Problems: Tachypnea and cough suggestive of restrictive lung disease
Pleurisy with or without pleural effusion is possible.
Cardia: arrhythmias resulting from fibrosis of the SA and AV nodes
Hypertension and hypercholesterolemia require treatment and monitoring
Accelerates CAD and the chance of developing CAD

Renal Problems: Lupus nephritis occurs in about 50% of patients with 1 year of dx. Manifestations vary from mild proteinuria to rapid, progressive glomerulonephritis.
Nearly all patients show renal histologic abnormalities in renal biopsy studies or autopsy results.

Nervous Ststem Problems: Neurologic effects are the most prevalent in SLE. Generalized or focal seizures are the most common manifestation involving the CNS and occur in as man as 15% of patients.

Hematologic Problems: formation of antibodies agains blood cess
Anemia, mild leucopenia and leucopenia and thrombocytopenia are often present

Infection: increased suscepitibility to infections. Pneumonia most common infection

Diagnostic Studies:
Dx based on the presence of distinct criteria based on history, physical examination and lab finding.

Lab: Anti nuclear antibodies, anti-DNA, antineuronal, anticoagulant, anti-WBC, anti-red blood cell (RBC), anti-platelet and anti-basement membrane.
Most specific: anti-double-stranded DNA and anti-Smith.

Treatment: NSAIDs, Antimalarial agents (hydroxychloroquine, antileprosy drug (dapsone), corticosteroids (limited) Methotrexate, folic acid, Ma use axathioprine and cyclophosphamide to reduce need for long-term steroid use.

OSTEOPOROSIS
Loss of bone mass----risk of fractures
All elderly persons are at risk!!
Bone loss is accelerated in postmenopausal women (lack of estrogen)
ASSESSMENT
Backache
Kyphosis
Loss of height
Serum calcium and phosphate levels are normal
x-ray: decreased density of vertebrae
ANALYSIS
Risk of injury: femur (hip) fractures, vertebra compression fractures
IMPLEMENTATION
DIET:
High-protein diet
Calcium and vit. D
MEDICATIONS:
Estrogen replacement
CLIENT EDUCATION
Encourage physical activity to prevent atrophy
Prevent falls: Slippery bathroom floors, loose rugs, etc.
Estrogens slight increase the risk of endometrial cancer. Regular check-ups for clients on estrogen replacement are recommended.


Risk factors for osteoporosis
Female gender
Thin, small framed
Family history of osteoporosis
Diet low in calcium
White or Asian ethnicity
Excessive use of alcohol


Collaborative Care
Osteoporosis
Diagnostic
History and physical examination
Serum calcium, phosphors, and alkaline phosphatase levels
Bone mineral densitometry
Dual energy x-ray absorptiometry (DEXA)
Quantitative ultrasound

Collaborative Therapy
Calcium supplements
Diet high in calcium
Vitamin D supplements
Exercise program
Estrogen replacement therapy
Bisphosphonates
Etidronate (Didronel)
Alendronate (Fosamax)
Raloxifene (Evista)
Calcitonin (Calcimar)

HERNIATED DISK
ASSESSMENT
Sever lower back pain
Pain radiating down buttocks and legs
Usually unilateral
Neurological exam: motor or sensory deficits are a serious sign!
Diagnosis: CT or MRI
ANALYSIS
Risk of injury to spinal cord and nerve roots
Level of mobility?
IMPLEMENTATION
Apply local heat or cold
CERVICAL:
Cervical herniation: collar or traction required
LUMBAR:
Bed rest until inflammation is reduced
Provide firm mattress
Recommend high-fiber diet with plenty of fluid (to prevent constipation and straining)
CLIENT EDUCATION
Avoid prolonged sitting
Use legs when lifiting objects (keep spine straight)
Exercise to strengthen abdominal and back muscles


CARPAL TUNNEL SYNDROME
Compression of median nerve at wrist joint
ASSESSMENT
Pain in wrist or palm of hand
Paresthesias in radial palmar aspect of hand
Weakness of thumb
IMPLEMENTATION
Relieve pressure on median nerve: hand elevation, splinting of hand and forearm)
Cortisone injections into carpal tunnel
CLIENT EDUCATION
Avoid prolonged flexion of wrist
Teach proper hand position when typing or using computer

OSTEOMYELITIS
Infection of bone, usually by Staphylococcus aureus
ASSESSMENT
Malaise
Pain and tenderness of bone
Swelling and redness over bone
Fever
Diagnosis: bone scan or culture from needle biopsy
IMPLEMENTATION
Immobilization of affected limb
No weight-bearing on affected limb
Explain client need for long-term antibiotics (oral for 6 weeks after fever normalizes)

LEG AMPUTATION
ASSESSMENT
Peripheral vascular disease----claudication (pain when walking, rapid relief when resting)
Cyanosis
Ulcer formation
Gangrene: foul smell, blackened wound
ANALYSIS
Risk of injury
Effective coping with altered body image?
IMPLEMENTATION
Watch for signs of infection and sepsis
POSTOPERATIVE:
Bandages should be applied in a diagonal figure 8 pattern
Elevate stump for first 12 hours
Monitor wound drainage (keep tourniquet at bedside for emergencies)
Exercise to improve arm strength
CLIENT EDUCATION
Explain “phantom pain”
Encourage frequent repositioning in bed
Massage stump to improve vascularity
“Phantom pain” is REAL pain!


CRUTCHES & CANES
CRUTCHES:
Fitting Measure from anterior fold of axial to heel, add six inches
There should be 2 inch space between axillary fold and underarm piece to prevent damage to brachial plexus (“crutch paralysis”)
Basic stance Crutches should rest in front and lateral of feet
2-point gait 1. advance right crutch and left foot together
2 advance left crutch and right foot together
3-point gait Used if only one leg is injured

1. advance both crutches and involved leg forward
2. advance healthy foot while keeping body weight on crutches
4-point gait Similar to 2- point gait, but slower and more stable

1. advance right crutch
2. advance left foot
3. advance left crutch
4. advance right foot
CANES
Fitting Highest point should be at level of greater trochanter
Handpiece should allow 30 flexion at elbow
Use Use cane in hand opposite to injured leg
Advance cane and injured leg at same time
Don’t lean body over cane
Walking upstairs: “good” leg first-walking downstairs: “bad” leg first

Clinical manifestations of fracture
Manifestations Significance
Edema and swelling Disruption of soft tissues or bleeding into surrounding tissues Unchecked edema in closed space can occlude circulation and damage nerves (risk of compartment syndrome)
Pain and tenderness Muscle spasm as a result of involuntary reflex action of muscle, direct tissue trauma, increased pressure on sensory nerve, movement of fracture parts Pain and tenderness encourage splinting of fracture with reduction in motion of injured area
Muscle spasm Protective response to injury and fracture Muscle spasms may displace nondisplaced fracture or prevent it from reducing spontaneously
Deformity Abnormal position of bone as result of original forces of injury and action of muscles pulling fragment into abnormal position; seen as a loss of normal bony contours Deformity is cardinal sign of fracture; if uncorrected, it may result in problems with bony union and restoration of function of injured part
Ecchymoses Discoloration of skin as a result of extravasation of blood in subcutaneous tissues Ecchymoses may appear immediately after injury and may appear distal to injury. The nurse should reassure patient that process is normal.
Loss of function Disruption of bone, preventing functional use Fracture must be managed properly to ensure restoration of function.
Crepitation Grating or crunching together of bony fragments, producing palpable or audible crunching sensation Crepitation may increase chance for nonunion if bone ends are allowed to move excessively.

Complications of fracture healing
Problem Description
Delayed union Fracture healing progresses more slowly than expected; healing eventually occurs.
Nonunion Fracture fails to heal properly despite treatment, resulting in fibrous union of pseudarthrosis.
Malunion Fracture heals in expected time but in unsatisfactory position, possibly resulting in deformity or dysfunction.
Angulation Fracture heals in abnormal position in relation to midline of structure (type of malunion)
Pseudarthrosis Type of nonunion occurring at fracture site in which false joint is formed on shaft of long bones. It is a fracture site that failed to fusel. Each bone end is covered with fibrous scar tissue.
Refracture New fracture occurs at original fracture site.
Myositis ossificans Condition occurring in response to muscle hemorrhage caused by trauma. Hematoma ossifies.

Characteristics of impending compartment syndrome
Paresthesia Numbness and tingling
Pain Not relieved by narcotic and on passive stretch of muscle (+ Homan’s sign in LE)
Pressure In compartments
Pallor Coolness and loss of normal color of the extremity
Paralysis Loss of function
Pulselessness Diminished/absent peripheral pulses


Types of Muscular Dystrophy
Type Genetic basis Clinical manifestations
Duchenne ((pseudohypertrophic) x-linked
mutation of dystrophin gene Onset before age 5; progressive weakness of pelvic and shoulder muscles; unable to walk after age 12; cardiomyopathy; respiratory failure in second or third decade; mental impairment
Becker (benign pseudohypertrophic) x-linked
mutation of dystrophin gene Onset between 5 and 15 years; slower course of pelvic and shoulder muscle wasting than Duchenne; cardiomyopathy; respiratory failure; may survive into fourth or fifth decade
Landouzy-Dejerine (facioscapulohumeral) Autosomal dominant deletion of chromosome 4q35 Onset before age 20 slowly progressive weakness of face, shoulder muscles,, and foot dorsiflexion; deafness
Erb (limb-girdle) Autosomal recessive or autosomal dominant Onset ranges from early childhood to early adulthood; slow progressive weakness of shoulder and hip muscles