Musculoskeletal Nursing Guide

Medical and Surgical Nursing
Musculoskeletal Disorder
Prepared: Mark Fredderick Abejo RN, MAN

MEDICAL AND SURGICAL NURSING

Musculoskeletal System

Lecturer: Mark Fredderick R. Abejo RN,MAN
______________________________________________________________________________________________

DISEASES OF THE MUSCULOSKELETAL SYSTEM COMMON HEALTH PROBLEMS OF THE NEONATES
AND INFANTS

I. COMMON HEALTH PROBLEMS OF THE NEONATES
AND INFANTS I. CONGENITAL HIP DYSPLASIA
 DEVELOPMENTAL HIP DYSPLASIA
(CONGENITAL HIP DYSPLASIA)  Improper formation and function of the hip socket 
 CLUB FOOT (TALIPES DEFORMITIES) subluxation or dislocation of the head of femur
 TORTICOLLIS (WRY NECK)  acetabulum is either flattened or shallow
 SUBLUXATION  femoral head is “riding high” in
II. COMMON HEALTH PROBLEMS OF THE CHILD shallow acetabulum
 DISORDERS OF BONE DEVELOPMENT  DISLOCATION  femoral head out of acetabulum
A. FLAT FEET (PES PLANUS)
B. BOWLEGS (GENU VARUM)
C. BLOUNT’S DISEASE (TIBIA VARA)
D. KNOCK KNEES (GENU VALGUM)
E. TOEING-IN (PIGEON TOE)
F. LIMPS
G. OSTEOGENESIS IMPERFECTA
H. LEGG-CALVÉ-PERTHES DISEASE (COXA
PLANA)
I. OSGOOD-SCHLATTER DISEASE
J. SLIPPED CAPITAL FEMORAL EPIPHYSIS
(COXA VERA)

 JUVENILE RHEUMATOID ARTHRITIS
 RICKETS

III. COMMON HEALTH PROBLEMS OF THE
A. ETIOLOGY
ADOLESCENT
1. Unknown
 SCOLIOSIS
2. Polygenic inheritance pattern
3. Uterine position (?)
IV. COMMON HEALTH PROBLEMS OF THE YOUNG
4. Children of Mediterranean ancestry
ADULT
5. 6x > in girls
 OSTEOGENIC SARCOMA
6. Relaxin (?)
7. Unilateral
V. COMMON HEALTH PROBLEMS OF ADULT
8. Socio-cultural
 RHEUMATIC DISEASES
9. Manner of carrying infants
 GOUT
 CARPAL TUNNEL SYNDROME
B. SIGN AND SYMPTOMS
 DEGENERATIVE JOINT DISEASE
Early detection is important
1. Affected leg shorter
VI. COMMON HEALTH PROBLEMS ACROSS LIFESPAN
 1 knee lower: child supine, thigh flexed 90°
 FRACTURE
 Ortolani’s sign
 AMPUTATION
 Barlow’s sign
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2. Unequal number of skin folds on posterior thigh h. Pavlik’s Harness
3. Prominence of trochanter  adjustable chest halter that abducts legs
4. Assessment of hip abduction during health  method of choice for long term treatment
maintenance visits (4-6 wks) reduces time interval for treatment to 3-4
wks
Ortolani’s sign - Pull with click sound
Barlow’s sign - Push back with click sound

C. MANAGEMENT

1. Position hip into a flexed, abducted (externally
rotated) position
a. Traction
b. Splints
c. Halters
d. Casts
e. Pins to stabilize hips
f. Multiple diapers (cloth)
 bulk separates legs  frog-leg, externally
rotated  worn continually except when bathing
g. Hip abduction splint (Frejka)  assess skin under straps
 made of plastic and buckles
 keep splint in place at all times except i. Spica cast (6-9 months)
when bathing/changing diapers  if hip is fully dislocated or if with severe
 firm pressure but caution vs. forcible subluxation
abduction  compromise of blood supply  Bryant’s traction for 1 week
 assess hourly for circulatory constriction
 temperature and circulation in toes

 good diaper care
 wash area w/ clear water
 A & D ointment
 Vaselin
 Desitin
 Padding edges of brace
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II. CLUB FOOT (TALIPES DEFORMITIES) B. MANAGEMENT
 1/1000 children 1. Cast application in overcorrected position; extends
 boys > girls above knee
 polygenic inheritance pattern 2. Frequent diaper changes  prevent case soaked
 usually unilateral vs. pseudotalipes  2° to intrauterine with urine/ meconium
position 3. Check the coldness & capillary refill
 TRUE TALIPES 4. Circulatory compression  change cast q1-2 weeks
 (4 types): due to rapid growth
1. Plantar flexion: (Talipes equinus) 5. 6 weeks casting  passive foot exercises
2. Dorsiflexion 6. Denis Browne splints
3. Varus
4. Valgus:

Plantar flexion (Talipes Equinus)
 Foot lower than heel

Dorsiflexion ( Talipes Calcaneus)
 heel lower than feet or anterior
 foot flexed toward anterior leg

Talipes valgus
 foot turns out

Talipes varus
 foot turns in

7. Surgery – final option

III. TORTICOLLIS (WRY NECK)
 tortus – twisted; collus – neck
 congenital anomaly when sternocleidomastoid muscle is
injured & bleeds during birth trauma – delivery of
shoulders
 head tilted to side of involved muscle; chin rotates to
opposite side
 may not be immediately evident
 fibrous contraction age 1-2 mos. w/ thick mass over
muscle

A. ASSESSMENT
1. Early detection
2. Straighten all newborn feet to midline as part of
initial assessment

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C. BLOUNT’S DISEASE (TIBIA VARA)
A. MANAGEMENT   retardation of growth of the epiphyseal line on
1. Parent to initiate passive stretching exercises & the medial side of the proximal tibia (inside of the
encourage infants to look in the direction of affected knee)  bowed legs
muscle, e.g. feeding position   serious disturbance in bone growth
2. If simple exercises not effective ≈1 year of age 
surgical correction followed by neck immobilizer
3. Adults  Botox injections (not recommended for
children)

COMMON HEALTH PROBLEMS OF THE CHILD

DISORDERS OF BONE DEVELOPMENT
 Assessment of Blount’s disease
A. FLAT FEET (PES PLANUS)
  X-ray shows medial aspect of the proximal tibia
 relaxation of the longitudinal arch of the foot;
will show a sharp beaklike appearance
 Normal  newborn foot is flatter &
  Treatment of Blount’s Disease:
proportionately wider than adult’s
 Osteotomy
  longitudinal arch rarely visible until child has
 Bracing
been walking for months

  Assess: ask child to stand on tiptoe  visible
longitudinal arch
  Exercises to strengthen
 Tiptoe walking ≈5-10 min
 Picking marbles w/ toes
  Sports shoes
D. KNOCK KNEES (GENU VALGUM)
B. BOWLEGS (GENU VARUM)   opposite of Genu Varum
  Lateral bowing of the tibia   medial surfaces of knees touch
  Malleoli are touching   medial surfaces of ankle malleoli
  Medial surface of knees is >2in (5cm) apart separated >3cm (7.5cm)
  Gradually corrects itself ≈2y/o   children 3-4y/o;
  If unilateral or worsening  orthopedist  no treatment necessary

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E. TOEING-IN (PIGEON TOE) 3. INWARD FEMORAL TORSION
  2° foot, tibial, femoral or hip displacement  Normal
  “awkward”  Internal rotation ≈ 30°
  “always falling over her feet”  Outward rotation ≈ 90°
 With Inward femoral torsion
 Internal rotation ≈ 90°
 No treatment required but w/
compensating tibial torsion

4 Cases of Toeing In:
1. METATARSUS ADDUCTUS
 turning in of forefoot – heel has good
alignment 4. DEVELOPMENTAL HIP DYSPLASIA
 R/T Infants who sleep prone w/ feet
adducted F. LIMPS
 older children who watch TV kneeling,   may reflect serious bone or muscle involvement,
feet turned in e.g. CP, Osteomyelitis
 >1year  passive stretching exercises   History: -- Pain
 May require casts or splints   measurement of leg length
 Early detection & treatment before   Range Of Motion
walking N   growing pains (?)
 biphosphonates

G. OSTEOGENESIS IMPERFECTA
  connective tissue disorder: fragile bone
formation  recurring pathologic fractures

2. INWARD TIBIAL TORSION
 line drawn from anterior superior iliac
crest through center of patella intersects
4th or 5th toe (normal = 2nd toe)
 No treatment required

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TYPE 1: Severe A.D.
  countless fractures related to birth trauma
  X-ray ribbon like or mosaic bone pattern
  blue sclera related to poor connective tissue
formation

TYPE 2: A.R.
  assoc deafness & dental deformities
 No treatment is curative
  preventive & safety measures
 Growth Hormone
 Calcitonin
 Biphosponates

H. LEGG-CALVÉ-PERTHES DISEASE (COXA PLANA)
  avascular necrosis of proximal femoral
epiphysis related to unknown cause
  boys > girls
  peak incidence 4-8y/o J. SLIPPED CAPITAL FEMORAL EPIPHYSIS (COXA
  unilateral but may be bilateral VERA)
  slipping of femur head in relation to neck of
femur at the epiphyseal line
  Proximal femur head displaces posteriorly &
inferiorly
  < preadolescence
  2x African Americans
  2x boys than girls
  more on obese & rapidly growing

  Pain in hip joint w/ spasm & LOM
 Differential Diagnosis: Synovitis
1. Stage I: Synovitis stage
2. II: Necrotic stage – 6-12 months
3. III: Fragmentation stage – 1-2 yr
4. IV: Reconstruction stage

 Treatment for Legg Calve Perthes
1. NSAIDS
2. containment devices
 abduction braces, casts
 leather harness slings
3. reconstructive surgery  osteotomy to center
femoral head
4. in acetabulum  cast

I. OSGOOD-SCHLATTER DISEASE JUVENILE RHEUMATOID ARTHRITIS
  thickening and enlargement of tibial tuberosity   collagen – vascular disease; 1° involves joints also
resulting from microtrauma blood vessels and connective tissue
  pain/swelling over tibial tubercle   symptoms before 16 y/o
  more during early adolescence   symptoms last longer than 3 months
 Treatment:   peak incidence: 1-3 y/o, 8-12 y/o
1. Limiting strenuous physical exercises   slightly more common in girls
2. Immobilization ≈ 6 wks   acute changes rarely continue past 19
3. children   cause unknown
 probably autoimmune
 (+) ANA
 Some w/ genetic predisposition

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A. ASSESSMENT
1. persistent fever & rash  joint involvement  Nursing Diagnosis for Juvenile Rheumatoid Arthritis
2. medical diagnosis  Deficient knowledge related to care necessary to
3. Nursing Assessment: control disease symptoms
a. Effect on Individual & Family
b. Self-care  Health Teaching for Juvenile Rheumatoid Arthritis
c. Ex: elevated toilet, Velcro strips  Active role in treatment
d. Complications  Need for follow-up care
e. Ex: slit lamp examinations q6 months  Plan & schedule – balance rest & exercise

B. MANAGEMENT
1. - Long term illness RICKETS
a. Exercise   disorder in which mineralization of organic matrix is
b. Heat application defective
c. Splinting   assoc with Vit D deficiency or resistance
d. Nutrition   growing skeleton; defective mineralization both in
e. Medications bones and cartilage
2. Exercise: Rationale – to preserve muscle and joint   vs. Osteomalacia – mineralization disorder in adults
function in whom epiphyseal growth plates are closed
a. Daily ROM exercises  Bowing deformities, knocked knees
b. Incorporate into dance routine or game  Stunting of growth of long bones
c. Family participation  Severe muscle weakness
d. Avoid excessive strain on joints
 Running A. PATHOPHYSIOLOGY
 Jumping 1. Disorders causing alteration of Vit D nutrition or
 Prolonged walking metabolism or phosphate wasting
 Kicking 2. Hypovitaminosis D
 Shortened school day – fatigue easily; 3. Inadequate prod. Vit D3 in skin
start midmorning 4. insufficient dietary supplementation
3. Heat application: 5. inability of small intestine to absorb Vit from diet
4. Rationale – reduces pain & inflammation, increases 6. resistance to effects of Vit D
comfort & motion  drugs which interfere w/ Vit D action
a. Warm water soaks 20-30 min 7. anticonvulsants, glucocorticoids
b. Paraffin soaks for finger & wrists  alteration in Vit D metabolism
5. Splinting: rarely prescribed because of more 8. Chronic renal failure
effective NSAIDS 9. Intoxication  cadmium, lead, expired tetracycline
6. Nutrition: Altered nutrition related to chronic pain
a. GIT irritation – NSAIDS B. SIGN AND SYMPTOMS
b. Plan mealtimes 1. Skeletal deformities – children unable to walk
7. Medications 2. Susceptibility to fractures
c. Tolmetin 3. Weakness & hypotonia
d. Naproxen 4. Growth disturbances
e. Ibuprofen 5. CRANIOTABES: soft calvariae, widening of
f. Celecoxib less GIT irritation sutures
g. Rofecoxib 6. RACHITIC ROSARY: prominence of
h. NSAIDS: reduce/control pain & inflammation costochondral junctions
 6-8 wks
 Health teachings:
 GIT irritation (w/
meals)
 Give even if w/o pain
to exert anti-
inflammatory action
i. SAARDs (Slow Acting Anti-Rheumatic drugs)
j. DMARDs (Disease Modifying Anti-Rheumatic
drugs)
 Ex. Gold salts, Penicillamine,
Hydroxychloroquinine
k. Cytotoxic Drugs: side effects
 Cyclophosphamide
 Chlorambucil
 Methotrexate
l. Steroids
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7. HARRISON’S GROOVE: indentation of lower  family history = 30% but no specific inheritance
ribs at site of attachment of diaphragm pattern
 5x more girls > boys
 Peak incidence 8-15 y/o
 Most marked during pre-puberty (rapid growth)

8. Bowing of tibia, femur, radius, ulna
9. Flattening of pelvis
10. Enamel defects
11. Radiologic Features:
 Increased thickness of growth plate (physis)
due to ↓ calcification & inadequate
mineralization

C. TREATMENT
1. Vit D2 (Ergocalciferol) 800-4000 IU
2. Vit D3 (Cholecalciferol) (0.02-0.1 mg) daily for 6-
12 wks followed by 200-600 IU daily
3. Calcium supplements  Uneven Shoulders
 Curve in Spine
 Uneven hips
COMMON HEALTH PROBLEMS OF THE ADOLESCENT A. ASSESSMENT
1. Bra straps adjusted to unequal length
2. Difficulty buying jeans
I. SCOLIOSIS 3. Skirts & dresses hang unevenly
 lateral curvature of spine 4. Bend forward
  may involve all or only a portion of SC 5. Scoliometer: reading >7° ≈ 20°
  may be functional (2°) or structural (1° deformity) 6. PPT
 I. FUNCTIONAL SCOLIOSIS 7. Chest Xray
 II. STRUCTURAL SCOLIOSIS
B. MANAGEMENT
I. FUNCTIONAL SCOLIOSIS 1. Scoliosis (Long term)
  compensatory mechanism related to unequal leg 2. <20° = no treatment; close observation until 18y/0
length, EOR  constantly tilt head sideways 3. >20° = conservative non-surgical treatment, body
  pelvic tilt related to unequal leg length & head brace, traction
tilt  spinal deviation 4. >40° = surgery, spinal fusion
  C shaped curve - little change in shape of 5. Bracing > 20° - 40° skeletally immature
vertebrae 6. Milwaukee brace (Thoracolumbar support)
 THERAPEUTIC MANAGEMENT of Functional 7. worn under clothing
Scoliosis 8. worn 23H/day
1. correct the difficulty causing spinal curvature 9. at night  Charleston Bending brace
2. unequal leg length (as is to medial malleolus) 10. Milwaukee Brace
3. shoe lift
4. correct EOR
5. maintain good posture
6. sit-ups, pushups, swimming

II. STRUCTURAL SCOLIOSIS
 idiopathic
 permanent curvature of spine accompanied By
damage to vertebrae
 primary lateral curvature
 ® Thoracic convexity+ Compensatory second curve
↓
 S-shaped curve appearance (rotation angulation)

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A. ASSESSMENT
11. Braces 14 ½ y/o ♀ 1. usually taller children (rapid bone growth)
16 ½ y/o ♂ 2. pain & swelling at tumor site
3. History of recent trauma  not the cause
12. Halo Traction 4. Pathologic fracture
5. Diagnostic biopsy
6. ↑ alkaline phosphatase fm rapidly growing bone cells
7. Metastatic workup
 CBC, UA
 CXR
 Chest CT Scan
 Bone scan

B. Therapeutic Management of Osteogenic Sarcoma
1. small tumor in leg – child has reached adult size
↓
Surgical removal of bone
+
Bone or metal prosthesis
If extensive  total hip amputation

2. lung managements  thoracotomy - lobectomy,
C. NURSING MANAGEMENT pneumonectomy
1. Health teaching how to apply braces 3. pre-op chemotherapy
2. Right fit  methotrexate
3. Adjustment q3mos  cisplatin
 doxorubicin
 ifosfamide
4. present prognosis
COMMON HEALTH PROBLEMS OF THE YOUNG ADULT  early detection  60-65% cure rate

C. NURSING MANAGEMENT
I. OSTEOGENIC SARCOMA 1. Post-op: swelling disrupting neurologic & circulatory
  malignant tumor of long bone involving rapidly function
growing bone tissue 2. proper position
 more commonly in boys > girls 3. monitor
 common sites  Capillary refill < 5s
 Distal femur (40-50%)  (-) numbness & tingling
 Proximal tibia (20%)  Warm, pink
 Proximal humerus (10-15%) 4. Post-op: Phantom Pain Syndrome
 History of radiation 5. Nerve trunks continue to report pain
 Early metastasis 2° to ↑vascularity of bones 6. Need analgesics!
 Lungs – 25% brain, other bones
 Chronic cough
 Dyspnea
 Chest pains COMMON HEALTH PROBLEMS OF ADULT
 Leg pains

I. RHEUMATIC DISEASES – “Arthritis”
 1° affects skeletal MS, bones, cartilages, ligaments,
tendons, joints of males & females of all ages.
 RHEUMATIC ARTHRITIS – Inflammatory
Arthritis
 2-3x women > men
 Autoimmune reaction primarily occurs in synovial tissue

A. PATHOPHYSIOLOGY
1. Phagocytosis produces enzymes within joint
2. Enzymes break down collagen
1. Edema
2. Proliferation of synovial membrane
3. Pannus formation
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 Destroys cartilage, erodes bones C. Assessment & diagnostic of Rheumatoid Arthritis
 Loss of articular surfaces & joint motion 1. Hx & PE
3. Muscle  degenerative Δs  Bilateral & symmetric stiffness
4. Tendon & ligament elasticity & contractile  Tenderness & swelling
power lost  Temperature Δs in joints
 Extraarticular Δs
2. Rheumatoid Factor (+) 80%
3. ESR ↑
4. RBC C4 & C4 complement ↓
5. C Reactive proteins maybe (+)
6. ANA
7. Arthrocentesis: cloudy, milky, or dark yellow
8. X-ray: bone erosions, narrowed joint spaces

II. GOUT

B. SIGNS AND SYMPTOMS
1. joint pain, swelling, warmth, erythema, lack of
function
2. joint fluid
3. small joints in hands, wrists, hips, elbows, ankles,
cervical spines, temporo-mandibular joint
4. acute
5. bilateral and symmetric
  heterogenous group of conditions related to genetic
6. joint stiffness in AM > 30min
defect of purine metabolism  hyperuricemia
 oversecretion of uric acid
 renal defect  ↓excretion of UA
 combination
  males > females
  ↑ incidence w/ ↑ age & Body Mass Index
 PRIMARY HYPERURICEMIA >7 mg/dl (0.4 fmol/L)
 usually faulty uric acid metabolism
 severe dieting or starvation
 food high in purines
 heredity
 SECONDARY HYPERURICEMIA
 ↑ cell turnover
 Leukemia
 Multiple myeloma
 Anemia
 Psoriasis
 Uric acid under excretion
Extra - Articular Manifestations of Rheumatoid
 SE of drugs (thiazide & furosemides)
Arthritis
 Low dose salicylates
1. fever, wt loss, fatigue, anemia, LN enlargement,
Raynaud’s phenomenon, Arterities, Scleritis,
A. PATHOPHYSIOLOGY
Sjogren’s pericarditis, splenomegaly
1. Hyperuricemia  monosodium urate crystal
2. Rheumatoid nodules – with Rheumatoid Factors
deposition
3. ≈50% of Patients
2. Sudden ↑ or ↓ of serum acid levels
4. Usually non-tender & movable in subcutaneous
3. Inflammatory response
tissues
4. Tophi formation
5. Over bony prominences
5. great toe, hands, ear
6. May disappear spontaneously
6. Renal urate lithiasis
7. Chronic renal disease
8. IgG coating urate crystals – immunologic
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 Interrupts breakdown of purines before uric
B. SIGNS AND SYMPTOMS acid is formed
1. Acute Gouty Arthritis  Inhibits xanthine oxidase
 recurrent attacks of sever articular & peri-  S.E. BM depression, vomiting, abdominal pain
articular inflammation 10. Corticosteroids: Anti-inflammatory
2. Tophi
 Crystalline deposits
3. Gouty Nephropathy III. CARPAL TUNNEL SYNDROME
4. Uric Acid Calculi  entrapment neuropathy; median nerve at the wrist is
5. Tophi in hand and ears compressed by
 thickened flexor tendon sheath
 skeletal encroachment
 edema
 soft tissue mass

Stages of Gout
a. Asymptomatic Hyperuricemia
b. Acute Gouty Arthritis
c. Intercritical Gout
d. Chronic Tophaceous Gout

6. Metatarsophalangeal joint of big toe
7. 75% of patients
8. attack may be triggered by
 Trauma
 Alcohol
 Dieting  repetitive hand activities
 Medications  also assoc w/ pregnancy, arthritis, hypothyroid
 Surgical stress  characterized by pain & numbness, paresthesias,
 Illness weakness along median nerve (thumb & 1st 2 fingers)
9. Abrupt onset awakening patient at night  (+) Tinel’s sign
10. Subdues within 3-10 days even w/o treatment  (+) Night pain
11. Symptom free period (intercritical stage)  Treatment for Carpal Tunnel Syndrome
12. Tophi also found in aortic walls, heart valves, etc  rest splints
13. Definite Diagnosis  avoidance of repetitive flexion
 Polarized microscopy of synovial fluid  NSAIDs
 Uric acid crystals  Cortisone injections
 (+)  Laser release
 PMN Leukocytes

C. MANAGEMENT IV. DEGENERATIVE JOINT DISEASE (Osteoarthritis)
1. Colchicine, NSAIDs  treatment of acute attack  functional impact on quality of life
2. Then management of Hyperuricemia after  primary (idiopathic) no prior event/disease
inflammatory process has subsided  secondary: r/t previous joint disease or inflammatory
3. Colchicine disease
4. lowers deposition of uric acid & interferes w/  increasing age
leukocytes & kinnin formation, thus reducing  often begins 34d decade
inflammation  peaks between 5th and 6th decade
5. Does not alter serum or urine levels of uric acid,  by age 75- 85 % either xray or clinical evidence
used in acute and chronic mgt.  But is 15-25% with significant symptoms
6. administer until pain relief or diarrhea  ability of articular cartilage to resist microtrauma
7. prolonged use  ↓Vit B12 absorption, GI upset
8. Probenecid:Uricosuric agent A. RISK FACTORS
 Inhibits renal reabsorption of urates 1. increased age – wear and tear
 ↑ urinary excretion of UA 2. obesity
 Prevents tophi formation 3. previous joint damage
 S.E. nausea, rash, constipation 4. repetitive use (occupational or recreational)
9. Allopurinol: Xanthine oxidase inhibitor 5. anatomic deformity

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6. genetic susceptibility D. ASSESSMENT
7. congenital sublaxation-dislocation of hip 1. Physical Exam
8. acetabular dysplasia 2. tender and enlarged joints
9. Legg-Calves Perthes 3. X-Ray
10. slipped capital femoral epiphysis 4. 30-50%
progressive loss of joint cartilage “narrowing of
B. SIGNS AND SYMPTOMS joints spaces”
1. pain 5. spur=ostephyte formation -> cartilage attempts to
2. stiffness regenerate
3. functional impairment
4. PAIN inflammation of synovium E. MEDICAL MANAGEMENT of Osteoarthritis
5. inflammation of nerve endings in periosteum over 1. Preventive measures to slow progress
osteophytes b. weight reduction
6. stretching of joint capsules or ligaments c. prevention of injuries
7. trabecular microfracture d. joint rest
8. intraosseous hpn e. perinatal screening (congenital hip dysplasia)
9. bursitis f. ergonomic modification
10. tendinitis 2. Conservative Measures to Slow Progress of
11. muscle spasm Osteoarthritis
12. STIFFNESS “morning” or after awakening<30 a. use of heat
min/ decreases with movement b. weight reduction
c. joint rest
d. avoidance of joint overuse
e. orthostatic devices (splints, braces)
f. isometric and postural exercises
g. aerobic exercises
h. OcTherap and PhysTher

F. SURGICAL MANAGEMENT
1. use of heat
2. weight reduction
3. joint rest
4. avoidance of joint overuse
5. orthostatic devices (splints, braces)
6. isometric and postural exercises
7. aerobic exercises
8. OcTherap and PhysTher
9. Osteotomy- to alter the force distribution of the
joint
10. Arthroplasty- to replace diseased joint
C. PATHOPHYSIOLOGY compnonents
11. Viscosupplemetation-reconstitution of joint fluid
viscosity using hyaluronic acid
Genetic and Mechanical Previous joint
hormonal injury damage 12. (Hyalgan, Synvise Rx)
factors 13. Tidal Lavage of Knee – stimulate production of
Others synoviocytes
14. Approximately 6 months pain relief
Chondrocyte response G. NURSING MANAGEMENT
1. Pain management
Release of cytokines 2. Optimizing functional ability
3. Pt referral
4. Lifestyle changes
Stimulation, production and release of proteolytic 5. Planning daily activities
enzymes, metalloproteases, collagensase

Resulting damage predisposes to more,,,

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14. Open, Compound, Complex skin or muscle
extends thru fractured bone
COMMON HEALTH PROBLEMS ACROSS LIFESPAN

I. FRACTURE
 FRACTURE- break in the continuity of bone and
adjacent structures
 soft tissue edema
 hemorrhage into muscles and joints
 joint dislocation
 ruptured tendons
 severed nerves
 damaged blood vessels
 body organ damage secondary to force or fracture
fragments A. CLINICAL MANIFESTATIONS
1. pain
Types of fractures 2. loss of function, abnormal movement
1. Complete break across entire cross section of bone 3. deformity: displacement, angulation, rotation,
(displacement) swelling – VISIBLE or PALPABLE
2. Open, Compound, Complex skin or muscle 4. shortening- 2.5-5cm r/t contraction of muscles
extends thru fractured bone 5. crepitus – grating sensation
a. Grade I clean wound <1cm 6. swelling and discoloration
b. Grade II larger wound without extensive soft
tissue damage B. MANAGEMENT
c. Grade III highly contaminated OPEN FRACTURE
d. Compressed – bone has been compressed 1. cover wound with a clean / sterile dressing
(ie. Vertebral fractures) 2. do not attempt to reduce fracture
3. Depressed- fragments driven inwards 3. ASSESS NEUROVASCULAR STATUS DISTAL
e. (ie. Skull and facial bones) TO INJURY
4. Epiphyseal- fracture thru epiphysis
5. Impacted- bone fragment is driven thru another C. MEDICAL MANAGEMENT
bone fragment 1. Reduction “setting the bone”
6. Pathologic- occurs thru an area of diseased bone 2. restore the fracture fragments to anatomical
7. Stress- results from repeated loading without bone alignment and rotation
and muscle recovery  OPEN
8. Incomplete (greenstick) break thru only part of  CLOSED
cross section of bone 3. early Fracture reduction, gentle manipulation
9. Transverse-fracture straight across the bone 4. Nursing consideration written consent / analgesia
10. Closed (simple)- no break in skin
CLOSED REDUCTION
-bring bone fragments into apposition (ends in
contact) via
a. manipulation
b. traction and counter traction (thru patients
weight and bed position)
c. splint or cast
d. x-rays
e. traction (skin or skeletal) for fracture
reduction/ for fracture immobilization

PRINCIPLES OF TRACTION
1. traction must be continuous to be effective
2. skeletal muscle traction is never interrupted
3. do not remove weights unless intermittent is
prescribed
11. Oblique occur at an angle across the bone (less 4. eliminate any factor that reduces effective pull or
stable than transverse) alter resultant line of pull
12. Comminuted one that produces several bone  good body alignment in center of bed
fragments  ropes unobstructed
13. Spiral fracture that twists around shaft of bone  weights should hang free

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 knot in rope or footplate must not touch pulley
or foot of bed EARLY COMPLICATIONS
5. VECTOR OF FORCE  SHOCK
6. RESULTANT LINE OF PULL  FAT METABOLISM
 SYSTEMIC EMBOLIZATION
7. Types of Traction
1. Straight or running traction
2. balanced suspension traction SHOCK
3. skeletal  hypovolemia, traumatic shock leads to blood
4. skin: traction tape/foam boot loss and ECF – extracellular fluid
5. manual  -restore blood volume and circulation
6. SKELETAL TRACTION  -pain relief
7. BUCK’S EXTENSION TRACTION  -splint
 -protect from other injuries
OPEN REDUCTION (ORIF) Open
reduction internal FAT METABOLISM
fixation  -usually young adults (20-30%) and elderly
adults with fracture proximal femur
D. NURSING MANAGEMENT  fat globules  blood
1. encourage patient to return to usual activity as  As marrow pressure > capillary pressure
rapidly as possible secondary to increase catecholamines
2. teach patient to control selling and pan mobilization of fatty acids
3. teach exercises, use assistive devices  Occlude small blood vessel lungs, brain,
4. environmental modification kidney, etc.
5. self-care, medications, potential complications  usuall approx. 24-48 degrees ~ week after
6. open fracture injury
a. prevent infection (monitor)  Hypoxia, tachypnea, pyrexia
b. delayed closure (5-7 days)  Dyspnea, crackles, wheezes
c. bone grafting (4-8 weeks to bridge defects)  Chest pain, thick white sputum, tachycardia
r/t increase pulmonary pressure
FRACTURE HEALING AND COMPLICATIONS  ABG PaO2 < 60 mmHg
 Respiratory alkalosis ~ respiratory acidosis
 Factors that Enhance Fracture Healing  Chest XRay: Snowstorm infiltrates ~>
1. immobilization of fracture fragments pulmonary edema. AARDS, CHF
2. maximum bone fragment contact  CNS: r/t fat emboli in brain and hypoxis
3. sufficient blood supply
4. nutrition SYSTEMIC EMBOLIZATION
5. exercise: weight bearing for long bones  pale
6. Hormones: GH, Thyroid, Calcitonin, Vit. D.  thrombocytopenia- petechiae
anabolic Steroids  hyperpyrexia (39.5C)
7. electric potential across fracture  fat emboli kidney failure

1. Factors that Inhibit Fracture Healing PREVENTION
1. extensive local trauma 1. immediate immobilization
2. bone loss 2. minimal fracture manipulation
3. inadequate mobilization 3. adequate support
4. space between fragments 4. fluid and electrolyte
5. infection 5. prompt invitation of respiratory support- high oxygen
6. local malignancy
7. Metabolic bone disease (ie. Paget’s disease) MANAGEMENT
8. irradiated bone (radiation necrosis) 1. respiratory support controlled volume ventilation
9. avascular necrosis PEEP (positive expiratory e pressure)
10. intra-articular fracture (synovial fluid contains 2. prevents respiratory and metabolic acidosis
fibrolysis, which lyse initial clot and retard clot 3. steroids- inflammatory lung reaction and cerebral
formation) edema
11. age 4. vasoactive meds
12. steroids 5. accurate fluid Input and Output
13. flat bones heal rapidly (pelvis, scapula) 6. morphine
14. fx at ends of ling bones heal rapidly than 7. nursing reassurance
midshaft fracture – more vascular and
cancellous
15. weight bearing stimulates healing of stabilized
fractures
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EARLY COMPLICATIONS: BONE GRAFT
 osteogenesis-bone formation occurs after
Compartment Syndrome transplantation of bone containing osteoblasts
 Tissue Perfusion < tissue viability  osteoconduction-provision by graft of structural
 Signs and Symptoms matrix for ingrowth of blood vessels and osteoblasts
 unrelenting pain resistant to opioids r/t  osteoinduction-stimulation of host stem cells to
 reduction in size of muscle compartment differentiate into osteoblasts b several growth factor
because enclosing muscle fascia is too tight or including bone morphogenic proteins
constricting cast or dressing  autograft- tissue harvested from the donor to the
 increase in muscle compartment because of edema donor
or hemorrhage  Allograft: tissue harvested from donor other than the
 Esp. forearm, leg muscle person who will receive the tissue
  decrease microcirculation nerve, muscle  Healing= 6-12 months
anoxia  necrosis  Problems:
 Loss of function > 6 hours 1. Wound or graft infection
2. Graft fracture
3. Non-union
4. Partial acceptance
5. Graft rejection
6. Transmission of disease (rare)

 Electrical Bone Stimulation
 Modifies tissue environment making it
electronegative  enhances mineral
deposition and bone formation
 Non-invasive inductive coupling
 Pulsing electromagnetic field delivered to
fracture approximately 10 hours each day
with electromagnetic coiled over non-union
site 3-6 months
Assessment and Diagnostic findings NURSING MANAGEMENT
1. paresthesis – early sign 1. Provide emotional support and encouragement
2. motor weakness: late sign of nerve ischemia 2. encourage compliance
3. paralysis – nerve damage 3. pain management
Assessment of peripheral circulation 4. monitor for signs and symptoms of infection
1. color- cyanotic- venous congestion, 5. health teaching-reinforcement
2. pale, cold 6. Immobilization
3. prolonged capillary refill
4. decrease arterial perfusion
5. pulselessness if with arterial occlusion, not
compartment syndrome REACTION TO INTERNAL FIXATION DEVICES
6. Doppler ultrasound 1. usually not removed unless with symptoms
7. Pain 2. pain and decreased function
8. Hypoesthesia 3. mechanical failure: inadequate insertion and stabilize
9. Anesthesia 4. material failure
10. Nerve tissue pressure = 8 mmg Hg or less 5. corrosion
 Compromised = 30 mmHg 6. allergic reaction
MEDICAL MANAGEMENT of Compartment Syndrome 7. osteoporotic remodeling adjacent to fixation device
1. elevate above level of heart r/t disuse osteoporosis
2. release restrictive dressings
3. if unsuccessful  fasciotomy 1 hour COMPLEX REGIONAL PAIN SYNDROME (CRPS)
4. splint and elevate  reflex sympathetic dystrophy (RSD)
5. Passive range of motion Q 4-6Hours  upper extremity
6. Deep vein thrombosis  > women
7. Thromboembolism  painful sympathetic nervous system problem
8. Pulmonary Embolism  CLINICAL MANIFESTATIONS of Complex
9. DIC Regional Pain Syndrome
1. severe burning pain
2. local edema
3. hyperesthesia
4. stiffness
5. discoloration
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MS Abejo


 vasomotor changes NURSING DIAGNOSIS of AMPUTATION
 trophic changes  acute pain r/t amputation
 Risk for disturbed sensory perception: phantom limb
Management of Complex Regional Pain Syndrome pain r/t amputation
1. -elevation  impaired skin integrity r/t surgical amputation
2. -immobility device with greatest ROM  disturbed body image r/t amputation of body part
3. -pain control  self-care deficit r/t loss of extremity
4. -NSAIDS  impaired physical mobility r/t loss of extremity
5. -Steroids
6. -anti-depressants NURSING INTERVENTION after Amputation
7. -avoid BP and venipuncture 1. PAIN RELIEF
 opioid analgesics
 non pharmaceutical
AMPUTATION  evac of hematoma / fluid
 removal of body parts (extremity)  counteract muscle spasm
peripheral vascular disease *  may be expression of grief
 folminating gas gangrene 2. Minimizing altered sensory perceptions
 trauma-crushing, frostbite, electrical  phantom limb approx. 2-3 months post-op
 malignant tumor  acknowledge feelings
 chronic osteomyelitis  keep patient active
 early intensive rehab and stump
 desensitization with kneading massage
 distraction activities
3. TENS (transcutaneous electrical stimulation)
4. Ultrasound
5. local anesthetics
6. identify patient’s strength and resource to facilitate
rehab
7. help patient resolve grieving
8. promote independent self-care
9. help patient achieve physical mobility

LEVEL OF AMPUTATION
1. circulation
2. functional usefulness (prosthesis)

COMPLICATIONS OF AMPUTATION
1. hemorrhage
2. infection
3. skin break down
4. phantom limb: r/t severing of peripheral nerves
5. joint contracture: r/t positioning and protective
flexion withdrawal pattern associated with pain and
muscle imbalance

MEDICAL MANAGEMENT of Amputation
1. Objective
 healing of amputation wound
 Non-tender stump
 health skin for prosthesis
2. 1. gentle handling of stamp
3. 2. control of edema by rigid or soft compression
dressings
4. 3. use of aseptic technique in wound care
5. CLOSED RIGID CAST DRESSINGS: uniform
compression for support soft tissues, control pain
and prevent joint contractures
6. SOFT DRESSINGS- if there is significant wound
drainage require frequent inspection

16
MS Abejo

Musculoskeletal Nursing Guide

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