-is a break or disruption in the

continuity of a bone
CLASSIFICATION OF FRACTURES:
by the extent of the break
1. COMPLETE FRACTURE
-involves a break across the entire
cross-section of the bone
2. INCOMPLETE FRACTURE
-the break occurs through only part
of the cross-section of the bone
by the extent of associated soft-tissue
damage
1. Closed / Simple
-does not cause a break in the skin
2. Open / Compound / Complex
-one in w/c the skin or mucous
membrane wound extends to the
fractured bone
Specific types of fracture:
Fractures are characterized by their CAUSE:
1. Pathologic /Spontaneous fracture
-occurs after minimal trauma to a bone that has been weakened by
disease -ex. client with bone cancer or osteoporosis
2. Fatigue/ Stress fracture
-results from excessive strain or stress on the bone
3. Compression fracture
-produced by loading force applied to the long axis of cancellous bone
-often occur in the vertebrae of clients with osteoporosis

CLINICAL MANIFESTATIONS:
PAIN –continuous & ↑ses in severity until bone fragments are immobilized
LOSS OF FX –fx of muscles depends on the integrity of the bones to w/c
they are attached
DEFORMITY –displacement, angulation or rotation of fragments either
visible or palpable
SHORTENNG –due to the contraction of muscles attached above & below
the site
CREPITUS –caused by rubbing of bone fragments against each other
SWELLING as a result of trauma & bleeding into the tissues;
DISCOLORATION may not develop for several hrs after the injury
4 R’s Management of Fracture

1. RECOGNITION
2. REDUCTION
-Closed Reduction
-Open Reduction
3. RETENTION
-Fixation (internal/ external)
-Cast
-Traction
-Braces & Splints
-Bandage
4. REHABILITATION
Fracture Reduction
is the procedure by which a fractured bone is realigned in
normal position
it can be either closed or open

 Closed reduction
-refers to realigning bones without breaking the skin
It is performed with manual manipulation and/or traction and is
commonly done with some kind of anesthetic (LA or GA).
-cast or splint may be applied after
 Open reduction
-primarily refers to surgery that is performed to realign bones or
fragments
-may be treated with internal fixation devices
-cast or traction may be applied after the procedure
Fractures with little or no displacement may not require any form of
reduction.
Open Reduction with
Internal Fixation
An internal fixation device may be used to keep fractured
bones stabilized and in alignment.
The device is inserted surgically to ensure the bones
remain in an optimal position during and after the healing
process.
An external fixation device

-commonly used in children

-when the skin over the
fracture has been damaged
-provides more freedom of
movement than with
traction
ILIZAROV EXTERNAL FIXATION DEVICE
Stages of Bone Healing
within 48-72 hrs after the injury , hematoma (a localized swelling filled with
blood) forms at the site of the fracture because bone is extremely vascular
blood supply to and within the bone usually diminishes bec. of the injury
causes an area of bone necrosis

dead cells prompt the migration of fibroblasts and osteoblasts to the
fracture site / inflammatory process

formation of fibrocartilage=providing foundation for bone healing within
3 days -2 weeks

due to vascular & cellular proliferation
fracture site is surrounded by callus= a new vascular tissue within 2-6
weeks
Callus formation is the beginning of a nonbony union

as healing continues, callus is transformed from loose, fibrous tissue
into bone within 3weeks- 6 months

excess callus is resorbed

healing, consolidation & remodeling continues up to a year
 FRACTURE HEALING COMPLICATIONS
2 CATEGORIES:
1. EARLY
SHOCK
-Hypovolemic shock resulting from hemorrhage
-may occur in fractures of extremities, thorax, pelvis or spine
-Tx: restoring of blood volume &circ
relieving patient’s pain
provide adeq splinting
protect patient from further injury & other complications

FAT EMBOLISM
-most freq in young adults (20-30 y.o.) & elderly w/ proximal femur fractures
-fat globules may move into the blood bec.
 marrow pressure >capillary pressure
cathecolamines ↑by the patient’s stress rxn mobilize fatty acids ►promote
devt.
of fat globules in the bloodstream
- fat globules (emboli) occlude small blood vessels that supply the lungs, brain,
kidneys, etc
-onset of sxs is rapid ,occurring w/in 24-72 hrs
-but may occur up to a week after injury
Clinical Features
a. Pulmonary features:
•respiratory insufficiency occurs in 75% of patients with FES
presenting with dyspnea, tachypnea, and fine inspiratory crackles
2-3 days after injury.
The chest x-ray is often normal initially but bilateral fluffy shadows
develop as respiratory insufficiency worsens  ARDS
b.Cerebral features:
•neurological features often precede pulmonary features by 6-12
hours. Patients often present in an acute confusional state.
Seizures and decorticate posturing have also been seen in FES.
Fortunately, almost all neurological deficits are reversible.
c. Cutaneous features:
•due to embolisation within the dermal capillaries
This produces a petechial rash in the conjunctiva, oral mucous
membrane and skin folds of the upper body, especially the neck
and axilla.
The rash appears within the first 36 hours and is self-limiting,
disappearing completely within 7 days.
-Tx:
Notify MD immediately
Support respiratory system
increased pressure within one or more compartments

massive compromise of circulations to an area

leads to decreased perfusion and tissue anoxia

within 1hr, w/o tx

irreversible neuromuscular damage
-Tx:
Notify MD immediately
>bec delay may result in permanent
nerve & muscle damage or even
necrosis
==Elevation of extremity to the heart
level
==Release of restrictive devices like
dressings or cast
>>if it doesn’t relieve pain w/in 1 hr
►Fasciotomy may be needed
DVT

THROMBOEMBOLISM

PULMONARY EMBOLUS

DIC

INFECTION
2. LATE
-DELAYED UNION=occurs when healing does not occur @ a normal
rate for the location &
type of fracture
=assoc w/ distraction (pulling apart) of bone fragments, systemic or
local infection, poor nutrition or comorbidity; eventually, the fracture
heals

-NONUNION=failure of the ends of the fractured bone to unite

=problems include infection, interposn of tissue bet. The bone ends,
inadq immobilization or manipulation that disrupts callus formation,
excessive bone gap, limited bone contact, impaired blood supply ►
avascular necrosis
Tx: internal fixation, bone grafting, electrical bone stimulation or
combination of these

-MALUNION=heal incorrectly
-occurs after a fracture w/
disruption of blood
supply esp in femoral neck
fractures
-also seen in dislocations, bone
transplantation, prolong high
dosage corticosteroid therapy,
chronic renal dse, sickle cell
anemia, etc
-sxs: pain, limited movt,
 sensation
x-ray: Ca loss & structural
collapse
-Tx: bone grafts,
prosthetic replacement or
arthrodesis ( joint fusion)
SLE
-prevalence is 100 per 100,00 persons
-occurs 10x more freq in women
-2-3x times more prevalent among people of
color, including African-Americans,
Hispanics, Asians, and Native Americans
PATHOPHYSIOLOGY:
combination of:
•genetic
•hormonal (evidenced by the usual onset during the childbearing yrs bet
15-40 y.o)
•environmental factors (sunlight, thermal burns)
•chemical or drug-induced:
hydralazine(Apresoline), procainamide (Pronestyl), isoniazid (INH),
chlorpromazine (Thoraxine) & some antiseizure medications

immunoregulatory disturbance

exaggerated production of autoantibodies

w/c resulted from abN suppressor T-cell fx

immune complex deposition & tissue damage

inflamm stimulates more antigens w/c stimulate addtnal antibodies

these complexes invade organs directly or cause vasculitis (vessel
inflamm), which deprives the organs of arterial blood and O2
Onset may be insidious or acute.
SLE may remain undiagnosed for yrs.
CLINICAL FEATURES:
-involves multiple body systems
Systemic Manifestations
Musculoskeletal Sys
-arthralgias (joint pain) & arthritis (synovitis) is a
common presenting sx
-joint swelling, tenderness & pain on movt are also common, freq accompanied by
morning stiffness
Skin
a. subacute cutaneous lupus erythematosus
=papulosquamous or annular polycyclic lesions
b. discoid lupus erythematosus
=chronic rash that has erythematous papules/ plaques
& scaling & can cause scarring & pigmentation changes
c. acute cutaneous lesion
=butterfly-shaped rash across the bridge of the nose &
cheeks & most familiar occurring in <half of patients
-lesion worsen during flare ups (exacerbations) & provoked
by sunlight or artificial UV light

-oral ulcers may also occur

Cardiac
-pericarditis is the most
common
Renal
-screening: serum creatinine
levels & urinalysis
-may lead to HPN
Kidney involvement
-leading cause of death
-renal biopsies show progressive changes
within the glomeruli:
► glomeruli slightly irregular
=minimal lupus nephritis
►further glomerular changes; shows clinical signs of renal impairment
=focal/mild lupus nephritis
►50% of glomeruli are affected; client is in renal failure
=diffuse/ severe proliferative nephritis
CNS
-widespread, encompassing the entire range of
neurologic dses
-neuropsychiatric presentations as demonstrated by
> subtle changes of in behavior patterns or cognitive ability
> depression
> psychosis
DXTICS:
Hx, physical examination & blood tests
BUT NO SINGLE LAB TEST CONFIRMS SLE

MEDICAL MGMNT:
There is no cure for SLE.
TX is aimed to manage the disease aggressively until remission.
=NSAIDs for minor clinical manifestations.
=Corticosteroid=single most impt. medication available
-topically to promote fading of the skin lesions
-low oral doses for minor dse activity
-high doses or IV doses for major dse activity
=Anti-malarial agent called hydroxychloroquine (Plaquenil) for
cutaneous, musculoskeletal & mild systemic features of SLE
=Immunosuppressive agents (alkylating agents & purine analogs)
bec of its effect on immune function & for patients w/ serious forms
of SLE who have not responded to conservative therapies

NSG MGMNT:
Instruct patient abt the importance of continuing prescribed
meds.
Addresses the changes & side effects likely w/ the use of these
meds.
Remind patient of the importance of monitoring bec of the risk for
systemic involvement including renal & cardiovascular effects.
-CAN OCCUR @ ANY AGE, USUALLY 25 &
55 Y.O.
-2-3x greater incidence in women

PATHOPHYSIOLOGY

T- & B- cell proliferation.

Angiogenesis in synovial lining.

Neutrophil accumulation in synovial fluid.
Cell proliferation. No cartilage invasion

Synovitis. Early pannus (proliferation of
synovial tissue) invasion. Degradation of
cartilage.

Subchondral bone (bony plate that
support the articular cartilage) erosion.
Pannus invasion of cartilage. Laxity of
ligaments.
CLINICAL MANIFESTATIONS:
-may vary, depends on the stage & severity of the dse.
CLASSIC: joint pain, swelling, warmth, erythema & lack of fx
upon palpation: joints reveal spongy or boggy tissue
begins w/ small joints in the hands, wrists & feet progresses to the knees,
shoulder, hips, elbows, ankles, cervical spine & temporomandibular joints

BILATERAL & SYMMETRIC

JOINT STIFFNESS ESP IN THE MORNING LASTING FOR >30 MINS
IMMOBILIZATION FOR EXTENDED PERIODS = RESULTS TO CONTRACTURES,
CREATING SOFT TISSUE DEFORMITY
SYSTEMIC: fever, wt loss, fatigue, anemia, lymph node enlargement, Raynaud’s
phenomenon ( cold- & stress-induced vasospasm causing episodes of digital
blanching or cyanosis)
ADVANCED: NODULES ARE PRESENT = nontender & movable in the subq
tissues
= appear over bony prominences like
elbows; vary in size & disappear
spontaneously
Other extra-articular features: neuropathy, scleritis, pericarditis, spenomegaly &
Sjögren’s syndrome ( dry eyes & dry mucous membranes.
Wrist subluxation
MEDICAL MGMT:

EARLY-STAGE RA
-education, balance of rest & exercise & referral to community agencies for
support
-sx control within the first 2 yrs of dse onset
-more aggressive pharmacologic approach earlier in the dse.
-COX-2 inhibitors = a class of NSAIDs;
cyclo-oxygenase blocks enzyme involved in inflammatory process while
leaving intact the enzyme involved in protecting the stomach lining► less
likely to cause gastric irritation & ulceration
=antirheumatic agents: antimalarials, gold, penicillamine or sulfasalazine
initiated early
-if sx appears to be aggressive ( x-ray: early bony erosions)
=methotrexate to pain, tender & swollen joints ►improve the quality of life

MODERATE, EROSIVE RA
-formal program w/ occupational & physical therapy
-medication program is reevaluated periodically w/ appropriate changes made
=cyclosporine an immunomodulator may be added
PERSISTENT, EROSIVE RA
-reconstructive surgery when pain cannot be relieved by conservative
measures;
cannot be performed during dse flares
Synovectomy-excision of the synovial membrane
Tenorrhaphy-suturing a tendon
Arthrodesis-surgical fusion of the joint
Arthroplasty-surgical repair & replacement of the joint
-systemic corticosteroids for unremitting inflamm or pain or needs
“bridging” medication while waiting for the slower dse-modifying
antirheumatic agent (methotrexate) to begin working
-local injection of corticosteroid for severely inflamed joint

ADVANCED, UNREMITTING RA
-immunosuppressive agents are prescribed: high dose methotrexate
(Rheumatrex), cyclophosphamide (Cytoxan) & azathioprine (Imuran)
-however, these are highly toxic meds S/E: bone marrow suppression,
anemia, GI disturbances & rashes
-Prosorba= a protein A Immunoiadsorption column used in 12 weekly 2-hr
apheresis tx to bind IgG (circulating immune complex)

NSG MGMNT:
Assess & intervene in patient concerns & issues with this kind of chronic
illness.
-most common & frequently disabling of the joint disorders

CLASSIFICATION:
1. Primary / Idiopathic
-no prior event or dse related to OA
2. Secondary
-resulting from previous joint injury or
inflammatory dse
=distinction is not always clear
-OFTEN BEGINS DURING 30s AND PEAKS
BET. 50s & 60s
- @ 75 YEARS, 85% OF POPULATION HAS
X-RAY OR CLINICAL EVIDENCE OF OA
but only 15%-25% experience significant sxs
PATHOPHYSIOLOGY:
Risk factors: age, obesity, previous joint damage,
repetitive use (occupational/ recreational), anatomic deformity, genetic
susceptibility

affects the articular cartilage, subchondral bone & snynovium

combination of cartilage degradation, bone stiffening & reactive inflamm of
synovium occurs
CLINICAL MANIFESTATIONS:
>primary:
-pain due to an inflamed synovium, stretching of the joint capsule or
ligaments, irritation of the nerve endings, bursitis, tendonitis & muscle
spasm
-JOINT STIFFNESS MOST COMMONLY EXPERIENCED IN THE
MORNING OR AFTER AWAKENING & LASTS <30 MINS & DECREASES
W/ MOVT
-functional impairment is due to pain on movt & limited motion caused
by structural changes in the joint
>OCCURS MOST OFTEN IN WEIGHT-BEARING JOINTS (hips, knees,
cervical & lumbar spine), PROXIMAL & DISTAL FINGER JOINTS ARE ALSO
OFTEN INVOLVED
>BONY NODES MAY BE PRESENT ONINSPECTIONN & PALPATION
= PAINLESS UNLESS INFLAMM IS PRESENT

DXTICS:
physical examination reveals tender & enlarge joints
INFLAMM IS NOT THE DESTRUCTIVE TYPE AS IN RA
X-ray: narrowing of joint space bec there progressive loss of joint
cartilage
-blood tests are not useful
Bouchard’s nodes
MEDICAL MGMT:

=Preventive measures
wt reduction
prevention of injuries
perinatal screening for congenital hip dse
ergonomic modifications

=Conservative txs
use of heat
wt reduction
joint rest /avoidance of joint overuse
orthotic devices (splint or braces)
isometric, postural & aerobic exercises
=Meds

initial analgesic therapy: acetaminophen

COX-2 inhibitors
Opioids
Intra-articular corticosteroids
Topical analgesics: capsaicin & methysalicylate
SURGICAL MGMNT:
Osteotomy –surgical cutting of bone to alter the force distribution in the
joint

Arthroplasty –diseased joint components are replaced with artificial

products

Viscosupplementation –reconstitution of synovial fluid viscosity,

hyaluronic acid is used w/c stimulates the production of synoviocytes, 3-
5 weekly intra-articular injections►pain relief for 6 months

Tidal irrigation -(lavage of the knee) involves the introduction & removal
of large volume of saline into the joint thru cannulas ►pain relief for 6
months

NSG MGMNT: Goal » pain mgmt & optimizing functional ability

Referral for physical therapy or to an exercise program.
Reinforce exercise programs
Teach in the proper use of assistive devices.
Osteoarthritis, the most common form of arthritis, involves the wearing
away of the cartilage that caps the bones in your joints.

Rheumatoid arthritis, the synovial membrane that protects and

lubricates joints becomes inflamed, causing pain and swelling.
Joint erosion may follow.
OA vs RA
Rheumatoid Arthritis
[RA] or
Osteoarthritis [OA]:
Which is it?
1.
Though either form of
arthritis can occur at
any age, this form of
arthritis usually
affects older people.
2.
Ulnar deviation and
wrist subluxation are
common deformities
seen with ___
3.
Morning stiffness which lasts
no more than 30 minutes,
and joint pain which typically
is worse later in the day after
repetitive use of the joint are
characteristic of ___
4.
Degenerative arthritis
or degenerative joint
disease are other
names for ___
5.
This type of arthritis is
considered an
inflammatory,
autoimmune disease.
6.
Joint damage which
occurs with bilateral
symmetry (same joint
on both sides of body)
is characteristic of ___
7.
This type of arthritis is
also known as wear-
and-tear arthritis.
8.
It is a systemic
disease, involving
other body organs.
9.
An elevated sedrate and
anemia are diagnostic
lab tests consistent with
___
10.
The most common
type of arthritis is ___
-is considered a hereditary
disease resulting from defective
uric acid metabolism.

Purine rich foods > end product:

uric acid > metabolized by the
body and excreted === GOUT,
uric acid is not excreted > urates
form > goes to the joints

There are recurrent attacks of

the pain and swelling of the
joints. 

This is a famous image drawn by

James Gillray which is a
representation of gout.
2 Major Types of Gout:

1. Primary gout
-most common type
-results from inborn errors of purine metabolism –end product is uric
acid
-production of uric acid exceeds the excretion capability of the kidneys
-sodium urate is deposited in synovium & other tissues resulting in
inflammation
-inherited as an X-linked trait - males are affected through female
carriers
-25% of clients have a family hx
-85%-90% affects middle-aged & older men
-peak time of onset: during a person’s 30s & 40s

2. Secondary gout
-involves hyperuricemia (excessive uric acid in the blood) caused by
another disease
-affects people of all ages
-renal insufficiency, diuretic therapy & certain chemotherapeutic agents=
 in the normal excretion of uric acid & other waste products
PATHOPHYSIOLOGY:
4 Phases of the Primary Disease
1. Asymptomatic hyperuricemic phase
-serum uric acid level is elevated but no
overt sign of the disease are present
2. Acute phase
-first “attack” begins
-excruciating pain & inflamm in one or
more small joints
-75% of clients experience inflamm of
metatarsophalangeal joint of the big toe
=podagra as initial manifestation
(severe pain in the big toe caused by gout)
-also in tarsal area, ankle or knee
-less common: wrists, fingers &elbows
-ESR & WBC count are ed due to the
inflammatory process
3. Intercritical (Intercurrent)
-months or years can pass before addtnal
attacks occur
-client is asymptomatic & no abnormalities
are found in the joints
4. Chronic tophaceous phase
-deposits of urate crystals (TOPHI)
develop under the skin and within the major organs, particularly in the renal
system
-urate kidney stone formation
DEFINITIVE DX:
=established by polarized light
microscopy of the synovial fluid of
the involved joint
Arthrocentesis…

This special light will reveal the

presence of monosodium urate
(MSU) crystals, which will nearly
always confirm a diagnosis of gout.
OTHER DXTICS:
 Elevated serum uric acid level
 Joint x-rays which show damage
consistent with gouty arthritis
MEDICAL MNGMT:
Drug therapy is the primary component of management for clients with gout.
Acute gouty attacks, inflamm subsides spontaneously within 3-5 days.
1. Acute gout
-combination of colchicine (Colsalide, Novocolchicine) & NSAIDs such as
indomethacin (Indocin, Novomethacin of ibuprofen (Motrin, Amersol)
-IV colchicine works within 12 hrs.
-client takes oral meds until inflamm subsides, usually 4-7 days
2. Chronic gout
-Uricosuric agents: Probenecid (Benemid, Benuryl)  urinary excretion of
uric acid; prevents tophi formation
Allopurinol (Zyloprim) is the drug of choice when patient
has or at@ risk for renal insufficiency or renal calculi ; xanthine oxidase
inhibitor= interrupts the breakdown of purines before uric acid is formed ;
use is limited bec of the risk for toxicity
===Aspirin is avoided because it inactivates the effects of the drug-

-Corticosteroids may be used in resistant cases

NSG MGMNT:
=Patients are encouraged to restrict consumption of
foods high in purines, esp organ meats & limit alc
intake; maintain N body wt
=In acute episodes: pain management is essential
 Diet and gout
Purines (specific chemical compounds found in some foods)
are likely to be broken down into uric acid.

Foods to limit (very high in purines):

·     Beef
·     Pork
·     Lamb
·     Seafood
·     Yeast (used in beer and bread)
·     Alcoholic beverages, particularly beer
·     Bacon
• Liver
Foods to eat occasionally
(moderately high in purines, but
may not raise your risk of gout):

·     Asparagus, cauliflower,

mushrooms, peas, spinach
·     Whole-grain breads and
cereals
·     Chicken, duck, ham, and
turkey
·     Kidney and lima beans
Dairy products that may lower
your risk of gout:
·     Low-fat or skim milk
·     Low-fat yogurt
Foods that are safe to eat (low in
purines):
·     Green vegetables and tomatoes
·     Fruits and fruit juices
·     Breads and cereals that are not
whole-grain
·     Butter, buttermilk, cheese, and
eggs
·     Chocolate and cocoa
·     Coffee, tea, and carbonated
beverages
·     Peanut butter and nuts
REVIEW QUESTIONS: MUSCULO DISORDERS SLE-GOUT
1. Which of the ff nursing diagnosis is a priority for a patient with gout?
A. fatigue C. risk of peripheral neurovascular dysfunction
B. risk of infection D. pain
2. In gout, the foods to limit are A. apples B. liver C. milk D. carrots
3. Serum level of patient’s uric acid was elevated. In order to hasten excretion of
serum uric acid, a uricosuric agent is prescribed which is
A. Allopurinol C. Alendronate
B. Colchicine D. Ibuprofen
4. A client asks for information about Osteoarthritis. Which of the following
statements about Osteoarthritis is correct?
A. Osteoarthritis is a rare form of arthritis.
B. Osteoarthritis is affects joints symmetrically.
C. Osteoarthritis is a rarely debilitating disease.
D. Osteoarthritis affects people over age of 60.
5. All but one are deformities associated with rheumatoid arthritis.
A. Heberden’s nodes C. Wrist subluxation
B. Ulnar deviation D. Boutonniere deformity
6. Nursing intervention for Gouty arthritis is / are the following, EXCEPT
A. Increase fluid intake
B. Avoid legumes, organ meat, and nuts
C. Avoid intake of seashells and seafoods
D. Decrease fluid intake
 7. True of SLE:
A. Chronic sunlight exposure exacerbates the disease.
B. It affects male population.
C. It is a degenerative process.
D. Leading cause of death is due to seizure.

8. In which of the following disorders may the patient require surgery to relieve
pressure on the nerve as it passes through the wrist into the hand.
A. Fractures B. Gout C. Carpal Tunnel Syndrome D. Osteoarthritis

9. Which muscular disorder has the following signs and symptoms: stiff joints
for a short time in the morning, usually 15 minutes or less; joint pain with
movement or weight bearing; and enlargement of joint due to bony overgrowth
and remodeling?
A. Fractures B. Gout C. Carpal Tunnel Syndrome D. Osteoarthritis

10. Aspirin should be given to help reduce inflammatory response in patients

with Gout.
A. TRUE
B. FALSE