MUSCULOSKELETAL Part1

8/6/2019 MUSCULOSKELETAL Part1

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MUSCULOSKELETALDISORDERS

Learning Contents Time Framed Learning

activities

Learning assessment



Assessment of musculoskeletalfunction

History

Subjective assessment:

I. Pain

Characteristic of pain(onset, location,intensity, duration)

Patterns and types

Differentiate pain of musculoskeletalorigin from systemic origin

Aggravating factors

Relieving factors

Associated signs and symptoms



11. Altered Sensation

Sensory disturbances may beassociated with musculoskeletalproblems

Parasthesias(burning, tingling

sensation or numbness)PHYSICAL ASSESSMENT

I. POSTURE

Assessment is performed from theposterior and lateral views takingnote of any asymmetry orabnormalities of the spine and itssurrounding structures



Common Deformities:

1. Kyphosis an increased forward

curvature of the spine2. Lordosis excessive posterior curvature

of the lumbar spine

3. Scoliosis lateral deviation of the spine

11. GAIT: Assessed by having the patient walk

away from the examiner for a shortdistance, or as soon as the patient walks

into the examining room Note for smoothness and rhythm of gait.

Inequality in step and stride lengths,limping or abnormal pelvic dipping may

indicate muscular imbalances oratholo in the ad oinin structures



111. Bone Integrity

Compare the left and right sides ofthe body, take note any deformitiesand anatomical misalignment

1V. JOINTS

Evaluate ROM, deformities, stability andnodular formation

Active ROM the joint can be moved bythe patient through active contraction of

the surrounding muscle

Passive ROM only the examiner canmove the joint without participation fromthe patient



MUSCLES Note of the ability to change position,

strenght and coordination, presence ofatrophy or hyperthrophy

Check carefully the origin of muscleweakness because patients fear,unwillingness, or malingering might give

false-positive results(muscle strength)

Note for muscle tone (sensation ofresistance felt as one manipulates a jointthrough its ROM)

Measure the muscle girth at the bulkiestportion of the extremity(location andposition must be the same on bothextremities)



Diagnostic Evaluation A. Radiography

1. Computed Tomography(CT scan)- Shows in detail a specific plane of

involved bone and can reveal tumors ofthe soft tissue or injuries to the

ligaments or tendons- Identifies the location and extent of

fracture in areas difficult to evaluate

11. X-Rays

- Imaging technique use to determine bonedensity, texture, erosion and changes inbone relationship



B. Magnetic Resonance Imaging- noninvasive, special imaging technique, which

uses magnetic fields, radio waves, and computers

to determine abnormalities of soft tissue, such asmuscle. tendons, cartilage, nerve and fat

C. RADIONUCLIDE IMAGING

1. Arthrography-

- identifies acute or chronic tears of the jointcapsule or supporting ligaments of the knee,shoulder, ankle, hip or wrist

- A radiopaque substance or air is injected into a joint cavity to outline soft tissue structure and

the contour of the joint- Joint is put through its ROM to distribute the

contrast agent while series of X-rays areobtained

- If a tear is present, the contrast agent leaks out

of the joint and is evident on the radiographs



D. Bone Scan

- Performed to determine certain fractures, osteomyelitis,

metastatic and primary bone tumors and asepticnecrosis

E. Special Tests/Invasive Tests of Structure

1. Arthroscopy- To visualize joints to confirms and rule out joint

disorders

2. Arthrocentesis

- To obtain synovial fluid for diagnostic purposes and torelieve pain due to effusion

3. Electromyography- To determine abnormalities and differentiates nerve and

muscle functions

4. Bone Biopsy

-To help diagnose diseases by determining thestructure and composition of the bones



Laboratory Studies

1. CBC

2. Coagulation studies

3. Blood chemistry

4. Thyroid Studies



Degenerative Bone Disorder:

Osteoarthritis(OA)

Wear and Tearr/t aging

- Progressive loss of the joint cartilage

- most common and frequently disabling

-K nown as degenerative joints disease orosteoarthrosis

Classification:

1. Primary (Idiopathic) with no prior disease

2.Secondary result from previousinjury/inflammatory disease



Etiology/Risk Factors

Increased Age: by 40 = 90 % develop the

disease- Prevalence of OA 70% in age=55 to 74

Obesity

Previous joint damage

Genetic susceptibility and hormonalfactors

Mechanical injury

Anatomic deformity

Congenital and developmental disorder Cartilage degradation

Bone stiffening

Reactive inflammation of synovial



Pathophysiology of OA

MechanicalinjuryGenetic &

hormonalfactors

Previous jointsdamage

Chondrocytes response

Release of cytokines

Stimulation, production and release of proteolytic enzyme,metalloproteases,collagenase

Damage predisposes tomore injury

others



OAS&S:

Pain & Stiffness in AM due to inflamedsynovium; irritation of nerve ending,muscle spasm, stretching of jointcapsule/ligament

Redness & SwellingPainless bony nodules

Knee effusions

Tender and enlarged joints

CrepitusDX:

History and Physical

X-rays narrowing of the joint space



TX: Medications

Analgesics: acetaminophen

NSAIDS

Steroids-RARE

Treatments ROM exercises

Rest the joint

Assistive devices = walker, cane, crutches



Surgical TX:Joint A rthroplasty

(Reconstruction or

Replacement



Hip Replacement





Total Joint Replacement

Candidate selection Several devices available

Significant relief of pain

Good return to ADL

OOB in 1 -2 days with PT help

Best results with PT program for re-strengthening muscles

Post op CPM

Continuous Passive Motion see next slide



Continuous Passive Motion



Post Op Care Joint Hip Replacement

Monitor incision for bleeding

Cough, turn, deep breath OOB as ordered

Neurovascular checks hourly 12-24 hours (color,temp, pulses, capillary refill, movement, sensation)

Pain management

Prevent new hip displacement

Nursing Care Plan

Pain assessment

Position changing with Trapeze

Sequential compression

Incentive spirometer

Abduction pillow for hip replacement

Monitor temperature and other VS

Surgical site assessment

Quadriceps and foot exercises



Discharge Health Teaching

Hazards assessment Chronic disease

ROM

Prevent Overuse/Overstess Pain Management



Metabolic Bone Disorder

Osteoporosis (Bone Atrophy)

- Rate of bone resorption is greaterthan bone formation resulting ina decreased total bone mass

- Reduction of bone density and achange of bone structure

- Loss of bone mass

- Bones becomes porous, brittle and

fragile- Increase risk of fractures



Cause of Osteoporosis

¡

Low Calcium





Who is at Risk for OsteoporosisMenopause

Small frame, non-obese with sedentarylifestyle

Inadequate dietary calcium and Vitamin Dintake

Bidridden status(r/t effects of immobility)

Use of antacids and laxatives

Calcium deficiencies

Skeletal Loss

High intake of Sodas

Vitamin D Deficiency

Smokers and intake of ceffeineExcess ETOH

Decrease Estrogen

Sedentary Lifestyle



Risk factors and its Effects:

Genetics:Caucasian/asian;Female; family hx;small frame

Nutrition: low calcium intake; Low Vit.Dintake; High Phosphateintake(carbonated beverages);Inadequate calories

Physical exercise: sedentary;lack of weight bearingexercise; low weight andbody mass index

Lifestyle choices: caffeine;alcohol ;smoking

Age: post menopause;advancedage;low testosterone inman;decreased calcitonin

Medicaton:corticosteroids; antiseizuremedicatio; heparin; thyroid hormoe

Co-morbidity: anorexia;hyperthyroidism,malabsorption syndrome, renal failure

Predispose to bonemass

Hormones (estrogen,calcitonin and testosterone)Inhibit bone mass

Reduces nutrientsneeded for boneremodeling

Bone needs stress for bonemaintenance

Reduces osteogenesisin bone remodelling

affectscalciumabsorptionandmetabolism



Cardinal Signs and Symptoms

Loss of height

Curvature of Spine

Dowagers Hump

Lordosis

Low Back Pain

Other S&S:

Difficulty of bendingover Pulmonary insufficiency and

easy fatigability

Protrusion of the abdomen



Medical /Surgical MGT:

Medication of Osteoporosis

Biphosphonates

Fosamax Actonel

Didronel

Calcitonin

Sodium Flouride

Raloxifene (Evista)



Medical /Surgical MGT:

Brace for vertebral fracture Calcium Supplements; dietary

modification and HRT

Regular weight-bearingexercise

Repair of fractures



Nursing Interventions:

Promote regular weight bearing execise

Promote modification of lifestyle Emphasize the needs to have sufficient

intake of calcium. Vit D and exposure tosunshine

Instruct client to increase fluid intake toreduce the risk of renal calculi

If HRT is prescribed, educate about theimportance of compliance and periodic

screening for breast and endometrialcancer

Apply intermittent local heat and backrubs

Instruct to move trunks as a unit and toavoid twisting and strenuous lifting



B. Osteomalacia(Adult Rickets)

Is a metabolic bone disease Characterized by an excess of

unmineralized bone matrix

The bone becomes abnormally softdue to a disturbed calcium andphosphorusbalance secondary to Vitamin D deficiency

May result from failure of theintestines to absorbcalcium(malabsorption syndrome),or excessive loss of calcium from

the body



Risks factors:

Hypoparathyroidism

Renal tubulardisorder(hypophosphatemicrickets)

Hepatobiliary disease Diseases of small intestine

Prolonged anti-convulsant therapy

Excessive intake of chelating

agents



Signs and Symptoms:

Bone pain and tenderness

Referred pain to the pelvis, back or hipsand muscle cramps

Severe progressive muscular weakness

Bowing and bending deformities of the

long bones X-rays reveals generalized

demineralization of bone

Hypocalcemia and hypophosphatemia,

low urine calcium and creatinineexcretion

Bone biopsy reveals increase amount ofosteoid



Medical/Surgical MGT:

Vit D replacement and

supplemental calcium High-calcium and high-phosphorus

diet

Repair of fracture and corrective

osteotomiesNURSING INTER VENTION:

Monitor calcium and phosphoruslevels

Encourage high calcium and high-phosphorus diet



C. Pagets Disease Osteitisdeformans

- Is a disorder of localized rapid boneturnover, affecting the skull, femur,tibia, pelvic bones and vertebrae

Incidence:

- Greater in men than woman- Increasing in aging

Etiology: UNKNOWN

Predisposing factors: Family hx

Aging



Pathophysiology

Primary proliferation of osteoclast-produces bone resorption

Compensatory increase in osteoblastic activity thatreplace the bone

A classic mossaic(disorganized) patternof bone develop

Highly vacularized and structurally weak Fx occur

Inc. old age; rapid bone turnover



Signs and Symptoms: Skeletal deformity; bowing of femur and tibia =

wading gait

Enlargement of the skull

Spine is bent forward and rigid

The chin rest on the chest

The thorax is compressed and immobile onrespiration

The trunk is flexed on the legs to maintainbalance

Deformity of the pelvic bone

Cortical development of the long bones

Cranium enlarge Face small, triangular appearance

Impaired hearing due to cranial nervecompression and dysfunction

Pain, tenderness and warmth over the bones

X-ray result= sclerotic changes



Dx. and Assessment findings

Elevated serum alkalinephosphatase

Urinary Hydroxyproline excretionreflect inc. osteoblastic activity

X-rays bone overgrowth

Bone Biopsy



Medical Mgt

Pharmacologic therapy:

- NSAIDs

- Calcitonin: retard bone resorption bydecreasing the number and availability ofosteoclast. Facilitate remodeling; relieve

bone pain- Biphosphonates (Didronel) and Fosamax

= produce rapid reduction in boneturnover and relief pain

- Caicium1

500mg- Vitamin D(400 to 600 IU)

- Plicamycin(Mithracin)cytotoxicantibiotic



D. Arthritis:

Inflammation of a joint usuallyaccompanied by pain swelling andchanges in structure

Etiology

Degenerative Joint Disease

Osteoarthritis, Rheumatoid

Metabolic disturbances Gout

Infection Gonococcus, TB, Pneumonia



Gout and Gouty Arthritis

Metabolic disorder Inflammation 2°

deposits of uricacid crystals in

joint Body produces too

much uric acid

Or

Body excretes toolittle uric acid



What is Uric Acid

Uric acid is a waste product formedfrom the breakdown of purines

High levels of purines are found inorgan meats (liver, brains, kidney),anchovies, herring, mackerel.

Alcohol and some drugs may affectpurine excretion.



Stage 1: AsymptomaticHyperuricemia

Uric acid levels elevated to 9-10range (normals ~ 3 6)

No symptoms

Client may not progress tosymptomatic disease



Stage 2 Acute Gouty Arthritis

Sudden onset, acute pain, redness,swelling

Usually hits the big toe, may affect

another joint Fever, chills

Elevated WBC, sed rate

Attack lasts hours to weeks 60% have recurrent attack in 1 yr



Stage 3Chronic Tophaceous Gout

Hyperuricemia untreated

Tophi (urate crystals deposits)

develop in cartilage, synovialmembranes, tendons, softtissues

Pain, ulceration, nerve damage Uric acid crystals>kidney

stones



Gout and Gouty Arthritis

Assessment:- Articular and

periarticularinflammation

- Presence of tophi- Hyperurecemia

- Acute attack usuallyhappens during thenight

- Severe pain, swelling,redness and warmth

- Joint enlargement



Nursing Diagnoses

Acute Pain

Impaired Physical Mobility



Nursing Intervention



Medical MGT:

Pain

Indocin NSAIDS, Narcotics

Steroids (po/intra-articular)

Interrupt urate crystal formation Colchicine: Does NOT alter uric acid

levels

Inhibit tubular reabsorption of uric

acid Probenecid (Benemid)

Reduce the production of uric acid

Allopurinol (Zyloprim)

Treatment of Gout Attack



Treatment of Gout AttackContinued

Dietary Management Drink 3-4 quarts of fluids daily

Avoid alcohol

Sometimes no diet is prescribed

Low purine diet Meats, seafood, yeast, beans,

peas, lentils, oatmeal, spinach,asparagus, cauliflower,

mushrooms



Nursing Intervention

Instruct to avoid purine-rich foods Limit alcohol intake

Encourage client to maintainnormal body weight

Avoid stress and trauma



Musculoskeletal infectionOSTEOMYELITIS infection of the

bone¡ Acute or Chronic

¡ Usually Caused By¡

Staphylococcus Aureus¡Fungus¡Parasite¡ Virus



Ways that Bones become



Ways that Bones becomeInfected

Extension of soft tissueinfection(e.g. infectedpressure/vascular ulcer, incisionalinfection)

Direct bone contamination frombone surgery, open fx., traumaticinjury(gunshot wound)

Hematogenous(bloodborne) spread

from other sites ofinfection(infected tonsils, boils)trauma



RISK FACTORS

¡ Trauma¡ Diabetes

¡ Hemodialysis

¡ Splenectomy¡ Advanced age

q Immune function

¡ Poor circulation



CAUSES

¡ Direct Contamination

¡ Surgical Infection

¡ Adjacent Soft Tissue Infection

¡ Hematogenous¡ Originating in the blood



STA GES OF OSTEOMYELITIS

Pathophysiology Osteomyelitis



Pathophysiology-Osteomyelitis

Bone infection 70- 80% caused by staphylococcus Aureus, other: Pseudomonas. Escherichia coli, Proteus

Inflammationinc. vascularity, edema-thrombosis

Ischemia with bone necrosis to

=Periosteum soft tissue - joints

A bscess formation abscess cavity contains dead bone tissue(thesequestrum) Does not liquiffy and drain

The cavity can not collapse and heal = involucrum(new bone

growth formed and surround the sequestrum

Sequestrum remain infected chonically thus produced recurring

abscessess thru out life = osteomyelitis occur

S O S



MANIFESTATIONS

¡ Pain¡ Swelling, redness, warmth

¡ Purulent exudate

¡

Systemic¡ Fever

¡ Chills

¡ Nausea

¡ Malaise

DIAGNOSTIC STUDIES



DIAGNOSTIC STUDIES

¡ MRI¡ CT

¡ Bone Scan

¡

Ultrasound¡ Labs:

¡ Sed Rate

¡WBCs

¡ Cultures

TREATMENT



TREATMENT

¡ Medications¡ Antibiotics

¡Pain Management

¡ Surgical debridement

¡ Amputation



Common Nursing Diagnoses for

Clients with Osteomyelitis?

Risk for Infection

HyperthermiaImpaired physical mobility

A cute pain

A nxietyBody Image

Self Esteem



Prevent Osteomyelitis?

Risk Factors?

Trauma

DM

PVD

SHOES, SOCKS

Arthirtis



Arthirtis

Septic Arthritis

-results from the activity of pus-formingbacteria in a synovial joint

- Most common sites of infection: hip andKnee

-Most common infectingagent:Staphyloccocus aureus

ASSESSMENT:

Fever and chills

Painful, warm and wollen joint MRI and CT scan show damage to joint

lining

Culture of synovial fluid show presence

of pathogens

i i i



Nursing intervention

Immobilized affected joints

Progressive ROM exercise after theinfection subsides

Monitor nutritional intake and fluidstatus of the patient

MEDICAL Mgt:

Broad spectrum antibiotic

Analgesic(codeine)

NSAIDs

Rh t id A th iti



Rheumatoid Arthritis

Chronic, Systemic AutoimmuneDisease

Inflammation of the connective tissue,

Inflammation of the joint

Sit ff t d



Sites affected

M if t ti f RA



Manifestations of RA

Joint symptoms Pain, swelling, stiffness (in morning)

Deformity and muscle atrophy

Limited ROM

Other Symptoms

Fatigue

Anorexia

Low-grade fever

Inflammatory changes of heart andlungs

Di g i f RA



Diagnosis of RA

History and physical exam Labs

Rheumatoid factors (RF)

ESR (Erythrocyte Sedimentation Rate)

Synovial fluid exam

X-rays

Narrowing joint space

T eatment of RA



Treatment of RA

NO CURE

Goals of Treatment

Relieve pain

Reduce inflammation

Stop or slow joint damage anddeformity

Improve well-being and ability to

function

T t t f RA



Treatment of RA

Medications

NSAIDS Steroids (po or intra-articular)

Disease-modifying drugs Modify immune system

Gold, antimalarial,

Modify the autoimmune andinflammatory response

Enbrel- Tumor necrosis factor blocker

Kineret- Interleukin 1 receptor antagonist

Surgery

Joint replacement

Tendon reconstruction

MUSCULAR DYSTROPHY



MUSCULAR DYSTROPHY

- A genetic disorder characterized by

gradual degeneration of musclefibers and is usually accompaniedby deformity and disability

Treatment:

supportive and symptomatic

The aim of tx is to increase comfortand functional ability

Respiratory exercise is encouraged

Care of Patient with



Musculoskeletal Trauma

1. Contusion, strain, spraina. contusion: bruising of soft tissue caused

by a blunt force; results in rupture ofblood vessels and bleeding into the softtissue

b. Strain: incomplete muscle tears withsome bleeding into the tissuessecondary to over-stretching, overuse orunaccustomed repeated trauma of

minor degree; less severe than a sprainS&S:

Muscle soreness or sudden pain andtenderness upon isometric and active

muscle contractions

Sprain



Sprain- Severe stress, stretch, ot tear of

ligaments surrounding a joint

NURSING INTER VENTION:

- PRICE method:

a. Protect

b. Rest

c. Ice

d. Compression

e. Elevation

- avoid skin and tissue damage due toexcessive cold

- Apply elastic bandage

- Heat application is done after 24 hr to48 hr after injury

Joint Dislocation



Joint Dislocation

Dislocation

- Articular surfaces within a joint are beingdisplaced, leading to soft tissue damage,

inflammation, pain and muscle spasm

Subluxation

- An incomplete or partial dislocation involvingsec. trauma to surrounding soft tissue

Assessment:

- Pain

- Change in length of extremity

- Loss of normal mobility

- Change in the axis of the dislocated bones

Nursing Intervention:



Nursing Intervention:

Joint immobilization

Reduction method to preserve jointfunction

Progressive ROM andstrengthening exercise

Provide comfort

Evaluate neurovascular status

Protect the joint during the healing

process

Fracture



Fracture

- Any break in the continuity of a bone

Types of Fracture:

1. Open or compound

- Communication between the bone andthe outside is present

2. Closed or simple

- Does not produce a break in the skin

3. Complete

- Involves a break across the entire cross-section of the bone

4. Incomplete

- Break occurs only on a part of the bonescross-section(greenstick fx)

5. Comminuted



- Bone is broken into fragments

6. Pathologic

- Occurs in bones weakened by pre-existingdisease

7. Stress fx

- Repetitive unaccustomed loading and

inadequate muscular support results in bonefatigue

8. Oblique

- Line of breakage runs in a slanted direction

across the shaft of the bones9. Transverse fx

- Caused by simple angulatory forces

10. Spiral

- Results from torsional injury

Assessment



Assessment

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MUSCULOSKELETAL Part1