musculoskeletal Disorders

1. Management of a patient with
musculoskeletal system disorders
By
Mr.A.Sanjaikumar M.Sc Nursing, PhD Fellow
Medical Surgical Nursing
Critical Care Department
Associate Professor
School of Health Sciences
Madda Walabu University
Bale Goba.
1

2. Anatomy and physiology review of
MSS
Assessment of pt with MSS problem
Intervention for clients with
musculoskeletal disorders
Intervention for clients with
musculoskeletal trauma:
Soft tissue injuries
Sprain 2

3. Dislocations
Fracture
Amputation
Joint and connective tissue diseases
Rheumatoid arthritis
Gouty Arthritis
Osteomyelitis
Osteoporosis
Osteoarthritis septic arthritis
3

4. Anatomy and
physiology of the
musculoskeletal
system
4

5. Anatomy and physiology of the MSS
Musculoskeletal system includes:
Bones Joints Muscles
Tendons Ligaments bursae
Musculoskeletal system
5

6. Anatomy and physiology of the MSS
(cont’d…)
Their functions are highly integrated
Therefore, disease in or injury to one adversely affects
the others.
For instance, an infection in a joint (septic arthritis)
causes degeneration of the articular surfaces
6

7. Bones
•At birth ≈ 270 bones
•Adult ≈ 206 bones through ossification and divided in
five shape categories:
•Long bones (e.g., Femur),
•Short bones (e.g., Metacarpals),
•Flat bones (e.g., Sternum)
•Irregular bones (e.g., Vertebrae).
•Sesamoid bones(e.g. patella & the pisiform bone of
carpals )
7

8. 8

9. Bones (cont’d…)
 Arranged in two
divisions:
Axial skeleton
( 80 bones)
Appendicular
skeleton (126
bones)
9

10. Bones (cont’d…)
Bone is composed of cells, protein matrix, and
mineral deposits.
Three bone cells:-
•Osteoblasts
•Osteocytes
•Osteoclasts
10

11. Bones (cont’d…)
•Osteoblasts
• Bone formation by secreting bone matrix.
•Matrix consists of collagen & ground substances
(glycoprotein & proteoglycans)
•Osteocytes –
•Mature bone cells
• Involved in bone maintenance;
•Osteoclasts
•Multinuclear cells
•Involved in dissolving & desorbing bone.
11

12. Parts of Bones
12

13. 13

14. 14

15. Bone Healing
Gross injuries(fractures ) heal by stages with new
bone with no scar
15
Inflammation/
hematoma
formation
Precallus
formation
Callus
formation
Replacement
of callus
Remodeling
of bone

16. 16

17. Muscle Tissue
17

18. Types of Muscle Tissue
Skeletal muscle
 >650 muscles & located throughout the body
Striated in appearance ,multi- nucleated
Under voluntary nervous control.
Smooth or visceral muscle
•Located in the walls of organs
•No striations, & under involuntary control.
Cardiac muscle
oLocated only in the heart, striated ,1-3 central nuclei &
involuntary control.
18

19. Structure of a joint and surrounding
tissues.
19

20. 20
Type of
Joint
Extent of
Movement
Example
Synovial Freely movable.
Bones do not
Touch each other
Knee, shoulder
Cartilaginou
s
Slightly movable Vertebral bodies
of the spine
Fibrous Immovable Skull sutures

21. Some movements at synovial joints
Rotation
Movement :
•Internal or
medial
rotation
•External or
lateral rotation
Angular
Movements:
• Flexion
• Extension
• Abduction
• Adduction
Special movements:
• Pronation
• Supination
• Dorsiflexion
• Plantar flexion
• Inversion
• Eversion
• Protraction
• Retraction
21

22. Test ROM of elbow

23. Supination and pronation

24. Test ROM of wrist

25. TEST ROM
Ask the client to:
• Spread the fingers apart.

26. ROM of fingers

27. TEST ROM

28. Abduction and adduction

29. Internal rotation

30. External rotation

31. Flexion and extension

32. TEST ROM

33. Connective tissues
Ligaments( skeletal
component )
• Join bones to bones or
cartilage to cartilage
– Joint capsule
– Stabilizer of joints (degree
of stiffness or laxity of
joints )
– Limited ROM & not elastic
Tendons(cord like)
• Connect muscle to
Bone
• Inelastic and transmit
muscle power/forces to
bones
• Respond well to tensile
stress.
Read more
: http://www.ehow.com/fac
ts_5558153_functions-
ligaments-tendons.html
33

34. Connective tissues (cont’d…)
• The point where a tendon or ligament joins a bone
is called an enthesis and may be the site of
inflammation
34

35. Cartilages
Pad and cushion of the end of bone - protects
the end of the bones.
35

36. Function– Support
• Provides the framework to support the body’s
fat, muscle, and skin.
– Protection
• Protects the body’s vital organs.
– Leverage
• Serves as a point of attachment for skeletal
muscles responsible for movement.
– Storage
• Stores most of the body’s calcium supply.
– Blood cell production
• Forms red and white blood cell and platelets.
– Form
• Gives shape to the body. 36

37. Assessment of
patient
with
Musculoskeletal
system problems
37

38. MSS assessment methods
History
Physical examination
• Inspection and
• palpation
Diagnostic Evaluation
•Imaging Procedures
•Laboratory Studies
38

39. Diagnostic evaluation
Imaging procedures
X-rays
Computed tomography (CT) scan
Magnetic resonance imaging
Arthrography - Acute or chronic tears of the:
Joint capsule / Supporting ligaments
 Bone densitometry
•Estimate bone mineral density (BMD).
Bone scan
39

40. Diagnostic evaluation (cont’d..)
Arthroscopy
•Direct visualization of a joint
Electromyography (EMG)
•Electrical potential of the muscles and the
nerves
 Biopsy
•Determine the structure and composition
of bone marrow, bone, muscle, or synovium
40

41. Laboratory studies
Coagulation studies - detect bleeding tendencies
Serum calcium levels - altered in osteomalacia,
parathyroid dysfunction,, metastatic bone tumors.
Serum phosphorus levels - diminished in
osteomalacia
Acid phosphatase- elevated in paget’s disease and
metastatic cancer.
Alkaline phosphatase - elevated during early
fracture healing
41

42. Laboratory (studies cont’d)
Serum enzyme level- creatine kinase and aspartate
aminotransferase become elevated with muscle damage
Urine calcium levels - increase with bone destruction
Complete blood count (CBC)
Hgb- normochromic, normocytic anaemia occurs in chronic
inflammatory and autoimmune diseases
WBC- neutrophilia is seen in bacterial infection (e.g. Septic
arthritis
Platelets- thrombocythaemia in chronic inflammation
42

43. Laboratory (studies cont’d)
 ESR and C-reactive protein (CRP).
increase reflects inflammation
 Uric acid for gout
Serum auto antibody studies
IgM rheumatoid factors
 Synovial fluid examination
43

44. Synovial fluid examination
Colour Diagnosis WBC per mm3
Clear, yellow and
viscous
OA < 3000
Translucent and
thin
RA 3000-40 000
Very cloudy Seronegative
arthritis
Crystal arthritis
Purulent Sepsis 750 000
44

45. MSS assessment methods (cont’d…)
 Musculoskeletal assessment includes:
• Assessment of joint
• Assessment muscle and
• Assessment bones
 (Give attention to pain, tenderness,
tightness, and abnormal sensations)
45

46. Assessment of Joint
 Joints are assessed for :
A. Range of motion
B. Any sign of inflammation
C. Crepitation
D. Deformities
E. Condition of surrounding tissue
F. Symmetry of involvement
46

47. TEMPOROMANDIBULAR JOINT(TMJ)
• Inspect, palpate, and test ROM

48. Assessment of Muscle
• Assess muscles
A. Bulk (Hypertrophy with proportionate
strength)
B. Tone( resistance to passive stretch, Normal
Decreased, Increased (Spasticity ,Rigidity)
C. Strength
– Check each component in the arms, legs, and
trunk.
48

49. Rating scale
Movement Classification Score
Active motion against full
resistance
Normal 5
Active motion against some
resistance
Slight weakness 4
Active motion against gravity Average weakness 3
Passive range of motion Poor ROM 2
Slighter flicker of contraction Severe weakness 1
No muscular contraction Paralysis 0

50. Assessment of Bone
• Inspect
– Any deformity,
– Malalignment
– Abnormality in the cervical, thoracic or lumbar
curvature .
– lateral curvature.
51

51. 52

52. 53
Spinal
deformities

53. Testing knee effusion
54
Patellar tap
Ripple test:
(A) Empty the suprapatellar
pouch, as for the patella
tap test.
(B) Stroke the medial side
of the joint to displace
excess fluid to the lateral
side of the joint.
(C) Stroke the lateral side
while watching the
medial side closely for a
bulge or ripple as fluid
re-accumulates.

54. Cruciate ligament stability
• Flex knee to 90°
Anterior drawer sign
• Hands behind the upper tibia and
both thumbs over the tibial
tuberosity, pull the tibia anteriorly
• If there is significant movement the
anterior cruciate ligament is lax.
• Movement of >1.5 cm suggests ACL
rupture.
Posterior drawer sign
• Push tibia
backwards
• Posterior movement
of the tibia suggests
PCL laxity
55

55. Patellar apprehension test /patellar stability
• Patient's knee fully extended
• Push the patella laterally and flex the knee slowly
• If the patient actively resists flexion, this suggests
previous patellar dislocation or instability
56

56. WRISTS
INSPECT AND PALPATE
• Inspect for size, shape, symmetry, color,
and swelling.
• Palpate for tenderness and nodules.

57. test for carpal tunnel syndrome(phalen’s test)

58. Tinel’s sign

59. Thomas’s test.

60. trendelenberg test.

61. KNEES
• INSPECT AND PALPATE

62. TEST FOR SWELLING
bulge test.

63. ballottment test.

64. ANKLES AND FEET
Inspect and palpate
• With the client sitting, standing, and walking,
inspect position, alignment, shape, and skin.
• Palpate for tenderness, heat, swelling, or
nodules.

65. Abnormal spinal curvature

66. Abnormal Wrists, Hands, And Fingers
• Boutonniere and swan-neck deformities

67. • Ganglion.

68. • Osteoarthritis.

69. • Tenosynovitis.

70. • Acute rheumatoid arthritis.

71. • Chronic rheumatoid arthritis

72. • Thenar atrophy

73. Abnormal Ankles, Feet, And Toes
• Acute gouty arthritis.

74. • Callus.

75. • Corn.

76. • Flat feet.

77. • Hallux valgus

78. • Hammer toe.

79. Tests for meniscal tears
Meniscal provocation tests
• Medial meniscus
– Passively flex the knee to its full extent.
– Externally rotate the foot and abduct the upper
leg at the hip, keeping the foot towards the
midline (i.e. creating a varus stress at the knee).
– Extend the knee smoothly.
– In medial meniscus tears a click or clunk may be
felt or heard, accompanied by discomfort
80

80. Meniscal tears…
• Lateral meniscus /valgus stress
– Passively flex the knee to its full
extent
– Internally rotate the foot and
adduct the leg at the hip (i.e.
creating a valgus stress at the
knee).
– Extend the knee smoothly.
– In tears of the lateral meniscus a
click or clunk may be felt or heard,
accompanied by discomfort.
Squat test
• Squat, keeping the feet &
heels flat on ground.
• If cannot - incomplete
knee flexion on the
affected side.
• May be- tear of the
posterior horn of the
menisci.
81

81. Intervention for clients with Musculo
skeletal system trauma
82

82. Sprain….
 Injury to the ligaments that surround a joint
A torn ligament causes joint unstablility
Cause - twisting motion/ hyperextension of a
joint.
Blood vessels rupture & edema forms
Joint is tender, & movement of the joint
becomes painful.
83

83. Sprains (cont’d…)
Sprains are graded as:
First-degree
sprain
• Stretching the
ligamentous
fibers
• Minimum
damage
• Mild edema,
local
tenderness,
and pain
Second-degree
sprain
•Partial tearing of
the ligament.
•Increased
edema,
tenderness, pain
with motion,
• Joint
instability
•Partial loss of
normal joint
function
Third-degree sprain
• Completely
ligament torn or
ruptured.
• May cause bone
avulsion.
• severe pain,
tenderness,
increased edema,
and abnormal
joint motion.
84

84. Sprains (cont’d…)
85

85. Strain (pulled muscle or tendon)
An injury caused by overuse, overstretching, or
excessive stress of tendon.
86

86. Strain (cont’d…)
Three types of strain are recognized:
First-degree
strain
• Mild stretching
of muscle/
tendon.
• Signs &
symptoms:
minor edema,
tenderness,
and mild
muscle spasm,
without
noticeable loss
of function.
Second-degree
strain
 Partial tearing
of muscle/
tendon.
Signs and
symptoms: loss
of load-bearing
strength with
edema,
tenderness,
muscle spasm,
and ecchymosis.
Third-degree strain
• Severe muscle or
tendon stretching
with rupturing and
tearing of the
involved tissue.
• Signs and
symptoms:
significant pain,
muscle spasm,
ecchymosis, edema,
and loss of
function.
87

87. Strain (cont’d…)
X-ray
Should be obtained to rule out bone injury b/c of
avulsion fracture in a third-degree strain.
MRI
 Will reveal a third-degree strain, but x-rays do
not reveal injuries to soft tissue or muscles,
tendons, or ligaments.
88

88. Nursing management
Treatment of strains, and sprains
consists of the acronym “RICE”
R-Resting - Prevents additional injury& promotes
healing
I-Ice- produces vasoconstriction w/c decreases
bleeding, edema & discomfort.
C-Compression with bandage controls bleeding,
reduces edema, and
E-Elevation- controls swelling
89

89. Nursing management (cont’d..)
For third degree sprain or strain:
• Surgical repair
•Immobilization to keep joint stability by:
•Splint, Brace, or Cast
90

90. Joint dislocations
91

91. Joint dislocations
 Dislocation of a joint :
•Articular surfaces of the distal and proximal
bones that form the joint are no longer in
anatomic alignment.
Complete dislocation- bones are literally “out of
joint.”
92

92. Types of dislocation
Traumatic dislocations
- orthopedic emergencies caused by trauma.
 Pathological /spontaneous dislocation
- Pathological condition in the joint causes abnormality the
joint. e.g. Septic hip dislocation
 Recurrent dislocation
- Repeatedly occurs due to weakening of the supportive joint
structures
Congenital dislocation
- e.g. Congenital hip dislocation 93

93. Joint dislocations (cont’d…)
Signs and symptoms of a traumatic dislocation:
Acute pain,
Change in positioning of the joint,
Shortening of extremity,
Deformity, and
Decreased mobility.
X-rays confirm the diagnosis and associated fracture.
94

94. Diagnosis of dislocation
Limb assumes an abnormally fixed position with
loss of normal ROM
Associated soft tissue injuries
e.g. Poplital artery in knee dislocation, sciatic
nerve in posterior hip dislocation
X-ray in various planes and views confirms
diagnosis
95

95. Management joint dislocations
Medical Management
Immobilized affected joint
Displaced parts are placed back in proper
anatomic position
Closed reduction( analgesia, muscle relaxants, and
possibly anesthesia)
After reduction, if the joint is stable, progressive,
active and passive movement to preserve ROM and
restore strength.
96

96. Management joint dislocations (cont’d…)
Nursing management
Frequent neurovascular assessment
Education:
Proper exercises and activities
 Danger signs and symptoms
•Increasing pain (even with analgesics),
•Numbness or
• Tingling, and
• Increased edema in the extremity.
97

97. Fracture
98

98. Fractures
• A complete or incomplete disruption in the
continuity of bone structure (structural breech
in normal continuity of bone)
99

99. Fractured by compression
Injuries from high impact sports
Forceful movements and traumatic blows
Overuse that causes bone stress
Falls from heights
Accidents
Tumors growing near the bone - bone compression
• osteoporosis and other bone debilitating conditions
100

100.  Complete fracture- entire cross-section of the
bone and is frequently displaced.
 Incomplete fracture - only part of the cross-
section
 Comminuted fracture -several bone fragments.
 Closed fracture(simple fracture) - not cause a
break in the skin.
 Open fracture(compound, or complex) - skin or
mucous membrane wound extends to the fractured
bone. 101

101. Types of Fractures (Cont’d...)
102

102. Types of Fractures (Cont’d...)
103

103. Types of Fractures (Cont’d...)
104

104. Types of Fractures (Cont’d...)
• Open fractures are graded as:
– Grade I is a clean wound less than 1 cm
long.
– Grade II is a larger wound without
extensive soft tissue damage.
– Grade III is highly contaminated, has
extensive soft tissue damage, and is the
most severe.
105

105. Pathophysiology of fracture
Fracture initiate inflammatory response & hemostasis
Bleeding
Edema stretches periosteum and swelling of soft
tissues—pain
Release of bradykinin and other chemical mediators---
contributes to pain
Clot forms at fracture sites
Systemic sign of inflammation may occur
106

106. Clinical manifestations of fractures
107

107. Clinical manifestations of fractures
Pain
• Continuous and increases in severity until the
bone fragments are immobilized.
Loss of Function
– B/c normal function of the muscles depends on
the integrity of the bones to which they are
attached.
– Pain contributes to the loss of function.
108

108. C/M of fractures (cont’d...)
Deformity
– Displacement, angulations, or rotation of the
fragments
Shortening
– B/C of the compression of the fractured bone.
– Muscle spasms can cause the distal & proximal
site of the fracture to overlap, causing the
extremity to shorten. 109

109. C/M of fractures (cont’d...)
Crepitus
– Crumbling sensation felt caused by the rubbing of
the bone fragments against each other.
Localized edema and ecchymosis
– Localized edema & ecchymosis occur after a
fracture as a result of trauma & bleeding into the
tissues. 110

110. Clinical: - history of trauma
- Pain, swelling, inability to use the injured part
- Tenderness, swelling and bruising
Deformity, abnormal movement (sure signs of
fracture)
X-ray: A suspected fractured bone should be x-rayed.
- X-ray should be taken in at least two planes (AP and
lateral) 111

111. Management of fractures
112

112. 1. Emergency Management fracture
 Immobilization
– Adequate splinting
– In open fracture,
• wound is covered with a sterile dressing
• No attempt is made to reduce the fracture
– The fractured extremity is moved as little as
possible to avoid more damage.
113

113. Immobilization (cont’d...)
Methods of immobilization:
 Plaster of Paris (POP) cast
• Safest and cheapest
 Traction
I. Using gravity:
II. Skin traction: using
bandage,( children)
max.wt = 2kg.
III. Skeletal traction: via a
pin
 Fixation
 External fixation
 Fixing by metal pins
 Mostly in compound
fractures
 Internal fixation
 Operative fixation of
fractures by plates, nails,
screws, pins and wires
 Indicated in poly
traumatized patients
114

114. Plaster of Paris (POP) cast
115

115. 116
Traction

116. 2. Medical Management of fracture
a. Reduction
– Restoration of the fracture fragments to anatomic
alignment and positioning.
– Can be closed or open reduction
– The patient is prepared for the procedure
– An analgesic is administered .
117

117. Reduction (cont’d...)
Closed reduction
• Fragments aligned into anatomic alignment through
manipulation and manual traction with a cast, splint,
or other device.
• X-rays are obtained to verify correct alignment.
• Traction (skin or skeletal) may be used until the patient
is physiologically stable to undergo surgical fixation.
118

118. Reduction (cont’d...)
Open Reduction
– surgical aligning fracture fragments
– Internal fixation devices (metallic pins, wires,
screws, plates, nails, or rods) may be used to hold
the bone fragments in position until solid bone
healing occurs.
– Devices may be attached to the sides of bone, or
may be inserted through the bony fragments or
directly into the medullary cavity of the bone.
119

119. Open reduction (cont’d...)
• Internal fixation devices ensure firm approximation and
fixation of the bony fragments.
• External fixation -makes a small percutaneous incision so that
pins may be implanted into the bone.
• Pins are held in place by an external metal frame to prevent bone
movement.
120

120. Open reduction (cont’d...)
External fixation indication
– Fracture with extensive soft tissue
injury
– Unstable closed fractures
– Closed fractures with compartment
syndrome, head injury, burns, or
impaired sensation.
– Fracture with loss of bone
121

121. Open reduction (cont’d...)
Internal fixation indication
• A displaced intra- articular
fracture
• Metaphyseal junction
fractures of the knee or ankle
• Mal-unions
• Non-unions .
122

122. Medical Management of fracture
(cont’d...)
b. Immobilization
 After fracture reduction, the bone
fragments must be immobilized and
maintained in proper position and
alignment until union occurs.
123

123. Medical Management of fracture
(cont’d...)
C. Maintaining & restoring function
– Reduction and immobilization
– Controlled edema
– Routine neurovascular status monitoring
– Control restlessness, anxiety, and
discomfort
– Encouraged (ADLS) is to promote
independent functioning & self-esteem.
124

124. 3. Nursing Management
I. Patients with closed fractures
• Instruct the pt regarding controlling edema & pain .
• Teach:
– Exercises
– Assistive devices crutches, walkers, and special
utensils)
– Self-care, medication information, potential
complications,
– Fracture healing and restoration(max.of 6 to 8 wks)
125

125. Nursing management (cont’d...)
II. Patients With Open Fractures
• Risk for osteomyelitis, tetanus, and gas
gangrene.
• Immediately Iv antibiotics- give upon arrival
• Wound irrigation and debridement are initiated
• Wound is cultured and bone grafting
• Carefully reduced and stabilized by external
fixation & wound is usually left open for 5 to 7
days for intermittent irrigation and cleansing.
126

126. Nursing management (cont’d...)
 Primary wound closure is usually delayed.
 Heavily contaminated wounds are left
unsutured and dressed with sterile gauze
 Assess neurovascular status frequently.
 Monitored temperature & signs of infection at
regular intervals
 In 4 to 8 weeks, bone grafting
127

127. Fracture Healing
• Takes longer than soft tissue healing ( wks-months
)
– Long bone - 6-12 weeks to heal in an adult and
3-6 weeks in children
– Flat bones (pelvis, sternum, and scapula) heal
rapidly.
– Comminuted fracture may heal slower.
– More vascular and cancellous, heal more quickly
than fractures in dense and less vascular
128

128. Fracture Healing
• Factors that
enhance fracture
healing
• Factors that inhibit
fracture healing
129

129. Factors that affect fracture healing
Factors that enhance fracture healing
Immobilization of fracture fragments
Maximum bone fragment contact
Sufficient blood supply
Proper nutrition
Exercise: weight bearing for long bones
Hormones: growth hormone, thyroid, calcitonin,
vitamin D, anabolic steroids
130

130. Factors that affect fracture healing
(cont’d...)
Factors that inhibit fracture healing
Extensive local trauma , bone loss
Weight bearing prior to approval
Malalignment of the fracture fragments
Inadequate immobilization
Space or tissue b/n bone fragments
Infection , local malignancy
131

131. Factors that inhibit fracture
healing(cont’d..)
Metabolic bone disease
Irradiated bone (radiation necrosis)
Avascular necrosis
Intra-articular fracture
Age (elderly persons heal more slowly)
Corticosteroids (inhibit the repair rate)
132

132. Complications of fractures
Early (first 48 hours)
Delayed/ Late (weeks,
months, years)
Systemic
Hypovolaemia and shock
Fat embolism
Acute respiratory distress
syndrome
Venous thrombo-
embolism(DVT)
Chest infection
Urinary tract infection
Bone Osteomyelitis
Bone healing abnormalities
Delayed or non-union /Malunion
Osteomyelitis
Necrosis
Heterotopic ossification
Joint
Stiffness
Osteoarthritis
Instability
Soft tissues
Compartment syndrome
Muscular/tendon injury
Neural injury
Vascular injury
Adjacent structural damage
Complex regional pain syndrome
(CRPS) (Reflex sympathetic
dystrophy(RSD)
Peripheral and cord injury
Ischaemic contracture
Pneumothorax 133

133. Amputation
134

134. Amputation….
Amputation is the removal or excision of part
or whole of a body part, often an extremity/limb.
Frequency: upper extremity < a lower
extremity( often necessary b/c of progressive
peripheral vascular disease
135

135. Causes of amputations
Diabetes mellitus
 Fulminating gas gangrene
 Trauma (crushing injuries, burns, frostbite,etc
Congenital deformities,
Chronic osteomyelitis,
 Malignant tumor.
Peripheral vascular disease accounts for most
amputations of lower extremities 136

136. Levels of amputation
Performed at the most distal level that provide a
functional stump & heal successfully
Choice is determined by:
Age
Nature and extent of the pathology
Circulation in the part
Presence of infection
Status of the joints
Functional usefulness (Access to prosthesis)
137

137. Levels of amputation(cont’d…)
A. Levels of amputation of upper extremity.
B.Levels of amputation of lower extremity. 138

138. Lower limb…
139

139. Levels of amputation(cont’d…)
Upper limb:
Attempt should be made to conserve every possible
inch.
 Lower limb:
Most important factor is to try & conserve the knee
joint whenever possible.
Amputation of toes & foot can cause changes in
gait & balance
A Syme amputation ( ankle disarticulation) -
extensive foot trauma 140

140. Levels of amputation(cont’d…)
Below-knee amputation (BKA) is preferred to
above-knee amputation (AKA) b/c of :
Importance of the knee joint
Energy requirements for walking.
Knee disarticulations - successful with:
 Young
Active patients who can develop precise control of
the prosthesis.
141

141. 142

142. Complications of amputation
Hemorrhage (secondary & reactionary)
Edema & hematoma
Ischemic necrosis
 Infection
 Skin breakdown
 Phantom limb
 Flexion contracture
143

143. Medical Management
Objective - to achieve healing
•Immediately after surgery, a sterilized residual
limb sock is applied to the residual limb.
•Padding is placed over pressure-sensitive areas.
•Healing is enhanced by gentle handling of the
residual limb, control edema, use of aseptic
technique
144

144. Medical Management(cont’d…)
A closed rigid cast dressing/elastic residual limb
shrinker that covers the residual limb may be used:
To provide uniform compression,
To support soft tissues,
To control pain, and
To prevent joint contractures.
145

145. Medical Management(cont’d…)
•The cast is changed in about 10 to 14 days.
•Rigid dressing is removed several days after
surgery
•An immobilizing splint may be incorporated in
the dressing.
•Wound drainage devices to minimize infection
146

146. Nursing process for amputating
patient
Assessment
 Evaluate the neurovascular and functional
status of the extremity
 Evaluates the nutritional status
147

147. Assessment…
148

148. Assessment cont’d..
Concurrent health problems
 Use of corticosteroids, anticoagulants,
vasoconstrictors, or vasodilators (influence mg't
and delay wound healing.
Evaluation emotional reaction to amputation and
grief responses
149

149. 150

150. 151

151. 152

152.  Evaluate the neurovascular and
functional status of the extremity(
residual limb & unaffected
extremity).
 Infection or gangrene status
153

153. Nursing diagnoses
154

154. Nursing diagnoses…
• Acute pain related to amputation
• Disturbed sensory perception: phantom limb pain
related to amputation
• Impaired skin integrity related to surgical
amputation
• Disturbed body image related to amputation of body
part
• Grieving and/or risk for complicated grieving related
to loss of body part and resulting disability 155

155. Nursing diagnoses cont’d…
• Self-care deficit: feeding, bathing/hygiene,
dressing/grooming, or toileting, related to loss of
extremity
• Impaired physical mobility related to loss of
extremity
Collaborative problems/potential complications
• Postoperative hemorrhage
• Infection
• Skin breakdown
156

156. Planning and goals(major)
Relief of pain
Absence of altered sensory perceptions,
Wound healing,
Acceptance of altered body image,
Resolution of the grieving process,
Independence in self-care,
Restoration of physical mobility, and
Absence of complications.
157

157. Nursing interventions
Relieving pain
Minimizing altered sensory perceptions-
(phantom limb pain )
Promoting wound healing
Enhancing body image- communicate to accept
& to care the residual
158

158. Nursing interventions cont’d…
Helping the patient to resolve grieving
Promoting independent self-care
Helping the patient to achieve physical mobility
Monitoring & managing potential complications
Promoting home & community-based care
159

159. Joint and connective tissue
diseases
160

160. Arthritis
 Inflammation of joints & breakdown of cartilage,
which normally protects the joint
 Women affected twice than men
 Acute forms - caused by bacteria & treated with
antibiotics (septic arthritis).
Chronic forms (osteoarthritis, rheumatoid
arthritis, and gouty arthritis)
161

161. 1. Osteoarthritis
 Degenerative synovial joint disease(DJD)
characterized by cartilage loss with an
accompanying periarticular bone response
 No simple definition b/c of consideration of three
overlapping areas –
 Pathologically- alteration in cartilage structure,
 Radiologically - osteophytes and joint space
narrowing
 Clinically - complain of pain and disability.
162

162. Osteoarthritis (cont’d…)
 Most common & frequent disabling joint
disease and prevalence increases with age -
Probably related to normal aging process
 “Wear and tear” arthritis; affects the
articular cartilages, causing them to soften,
fray, crack, and erode
 It is non inflammatory- only cartilage is
affected, not synovial membrane
163

163. Osteoarthritis (cont’d…)
• Deterioration of cartilage produces bone
spurs- Restricts movement
• Pain upon awakening—disappears with
movement
164

164. Osteoarthritis (cont’d…)
Causes and types
• Osteoarthritis can be primary or secondary
1. Primary /Idiopathic/ OA:-
– The cause is Unknown
– Genetic factors and allergy is the most
common predisposing factors
– It is not inflammatory joint disease
165

165. Causes and types (cont’d...)
2. Secondary OA
• Caused by other conditions:
– Previous joint infection e.g. RA ,Gout, SA
– Inflammation
– Trauma , surgery
– Certain occupation or activities
– Endocrine is order (acromegally or hyperparathyroidism
– Skeletal deformity
– Hemophilia
166

166. Causes and types (cont’d...)
Other Predisposing factors to OA:
•Age
•Weight- Obesity
•genetic indisposition
•Sex - women; a higher after the menopause
suggests a role for sex hormones.
•Hypermobility - Increased range of joint motion
and reduced stability
167

167. Pathophysiology of osteoarthritis
Damage of articular cartilage
Surface of cartilage becomes rough and wear
Enzymes released - accelerate disintegration of cartilage
Subchondral bone may be exposed
Cysts/ oseophytes –new bone spurs developed
Osteophytes and cartilages break of
Joint space narrowed
Secondary inflammation of surrounding tissues
Loss of normal joint ROM
Pain with weight bearing and use
168

168. Clinical manifestations OA
Symptoms
• Joint pain - improve with
rest
• Joint gelling (stiffening and
pain after immobility)
• Joint instability
• Loss of function
Signs
• Joint tenderness
• Crepitus on movement
• Limitation of range of movement
• Joint instability
• Joint effusion and variable
levels of inflammation
• Bony swelling
• Wasting of muscles due to
disuse.
169

169. 170

170. Diagnosis of osteoarthritis
History
Physical examination
 Investigations:
• Blood tests.
• No specific test
• ESR and CRP are normal.
•Rheumatoid factor and antinuclear antibodies
are negative.
•X-rays - abnormal only when the damage is
advanced.
•MRI - early cartilage and subchondral bone
changes.
•Arthroscopy - reveals early fissuring and surface
erosion of the cartilage.
171

171. Management (Medical and Nursing
care) of osteoarthritis
 Objective : treat the symptoms and
disability, not the radiological appearances
– Relief pain
– Restoration of joint functions
– Prevention of disability and complication
172

172. Management of osteoarthritis (cont’d..)
Pharmacological Rx:
•Acetaminophen
•NSAID
•Analgesics
•Intra articular steroid injection
173

173. Management of osteoarthritis (cont’d..)
 Non-pharmacological mgt
 Weight reduction
 Heat application to relief pain and relaxing muscles
before exercise
 Application of cold after exercise to decrease pain
and swelling
 Exercise and prevent injuries
 Surgical management like
Arthrodesis or joint fusion
Joint replacement
174

174. 2. Rheumatoid arthritis(RA)
• Systemic,symetrical disease
characterised by chronic
recurrent inflammation of
joint and surrounding soft
tissue .
• Has periods of remission &
exacerbation.
– Remission-period when
disease symptoms are
reduced or absent.
– Exacerbation –a period when
disease symptoms occur or
increased.
175
Ulnar deviation of the
fingers, small muscle
wasting and synovial
swelling at carpus,
metacarpophalangeal
and proximal
interphalangeal joints.

175. Rheumatoid arthritis (cont’d…)
 Symptoms begin with bilateral inflammation of
certain joints
 Often leads to deformities
 Cartilage attacked
 Inflammation, swelling & pain
 Final step is fusion in joint
176

176. Rheumatoid arthritis (cont’d…)
– Occurs in around 3% of women and 1% of
men
– Caused by a cell-mediated (T-cell)
autoimmune response
– Rheumatoid factor positive in 80%
– Often starts with symmetrical disease
affecting small joints of the hands and feet
177

177. Etiology of rheumatoid arthritis
• Cause unknown
• Suggested – response to an infectious agent in a genetically
susceptible host.
• Predisposing includes
– Autoimmune reaction
– Genetic predisposition
– Infection – viral & bacterial (rubella, mycoplasma, CMV and
EBV virus)
– Other factors such as metabolic ,nutritional &
environmental factors.
178

178. Pathophysiology rheumatoid arthritis
Stage -1: Unknown etiologic factor initiates joint
inflammation with swelling of the synovial lining
membrane & production of excess synovial fluid.
Stage-2: Pannus formation (Proliferation of synovial
membrane)
Stage-3: Pannus destroys the cartilage & erodes the bones
results in loss of articular surfaces & loss of joint motion
,malignant & deformity
Stage-4 :As fibrous tissue calcifies bony ankylosis may result.
(Ankylosis –immobility of a joint)
179

179. C/F of RA
 Early symptoms include:
• Fatigue
• Weight loss
• Fever
• Malaise
• Morning stiffness of joints
• Pain at rest and with movement
• Edematous, Erythemataus “baggy” joint
180

180. C/F of RA (cont’d…)
 Late symptoms include
• Color changes of digitalis (bluish, rubor, pallor)
• Muscle weakness, atrophy
• Joint deformity
• Decreased joint mobility , Contractures
• Subluxation or complete dislocation
• Increasing pain
• Formation of rheumatoid nodules are aggregate of
inflammatory cues
181

181. C/F of RA (cont’d…)
 Extra- articular manifestations of RA:
– Skin – subcutaneous nodules
– Eyes – scleritis, iritis
– Lungs – interstitial lung disease, pleural effusion
– Heart – myocarditis
– Kidneys – nephritis
– Amyloid – lungs, kidneys, heart, bowel
– Compression and vascular neuritis
182

182. C/F of RA (cont’d…)
• Problems in the hand and wrist caused by RA:
– Radial deviation of the wrist
– Extensor tendon ruptures
– Ulnar deviation metacarpophalangeal joints
– Z-deformity of the thumb
– Boutonnière deformity of the fingers
– Swan neck deformities
– Carpal tunnel syndrome
183

183. 184

184. C/F of RA (cont’d…)
• Virtually all joints can be involved, but most
commonly involved joints are:
• Hand joints, wrists , Ankles, Elbow
and knees
• Most often it evolves bilaterally or
symmetrical pattern
185

185. Diagnosis of rheumatoid arthritis
Clinical features
Positive rheumatoid factor
Titer increases at active diseases (antinuclear antibody)
Lab finding
Indicator of active inflammation
ESR - increased,
RBCS- decreased
C-reactive protein (CRP)
Abnormal synovial fluids
X-ray study
Biopsy
186

186. Diagnosis of rheumatoid arthritis
(cont’d…)
Diagnostic Criteria:
• Morning stiffness > 1 hours & at least 6 weeks
duration
• Soft tissue swelling of 3 or more joints for at least 6
weeks (wks)
• Swelling of wrist, metacarpophalangeal or proximal
interphalangeal joints at least 6wks
187

187. Diagnosis of RA (cont’d…)
• Criteria for the diagnosis of rheumatoid
arthritis (American College of Rheumatology,
1987 revision)
188
Morning stiffness > 1 hour
For ≥6
weeks
Arthritis of three or more joints
Arthritis of hand joints and wrists ,metacarpophalangeal
or proximal interphalangeal
Symmetrical arthritis
Subcutaneous nodules
A positive serum rheumatoid factor
Typical radiological changes (erosions and/or
periarticular osteopenia)
N.B: four of the seven criterias are necessary to diagnosis RA

188. Diagnosis of RA (cont’d…)
189
Rheumatoid nodules and
olecranon bursitis

189. Management of rheumatoid arthritis
Goals :
 Short term :
 Controlling pain and reducing inflammation
without causing undesired side effects
 Long term:
 Preservation of joint function and the ability to
maintain life-style
190

190. Management of RA (cont’d..)
Pharmacological Rx:
1) First line : NSAIDs
 Control symptoms & signs of local inflammatory
process.
 Rapid alleviation pain and symptoms ,
 Minimal long term effect
• Aspirin 900 mg PO TID, Ibuprofen 400 mg PO BID or
TID Diclofenac 50 mg PO BID , indometacin 50 mg PO
BID.
191

191. Pharmacological Rx RA (cont’d…)
2) Second line :
Low dose potent anti-inflammatory oral
corticosteroids
• Systemic administration in sever
progressive articular diseases and extra
articular involvement
Start with 5-10 mg/day in the morning
and taper the dose with improvement
192

192. Pharmacological Rx RA (cont’d…)
3) Third line: Disease modifying antirheumatic
drugs- (DMARD)
 Methotrexate , gold compounds , d-penicillamine ,
antimalarials and sulfasalazine
Have the capacity to alter the course of RA.
Used in NSAIDS non -respondent
Methotrexate is the most frequently used &
relatively rapidly acting ( given in an intermittent
low dose: 7.5-30 mg once weekly)
193

193. Pharmacological Rx RA (cont’d…)
4) Fourth line: Anti cytokine agents:
Biological agents that bind & neutralize TNF.
effective in controlling signs & symptoms failed to
respond with DMARDs.
5) Fifth line : immunosuppressive therapy :
Include azathioprine, cyclsosporine, and
cyclophosphamide.
Same therapeutic effect as DMARDs 194

194. Non pharmacologic therapy RA
Nursing management
 Health teaching about balance of rest and
exercise, drug side effects
 Give the prescribed drugs
 Encourage physiotherapy & occupational therapy
 Physiotherapy
 Surgical mgt (Arthroplasty, synovectomy, tendon
transplants) 195

195. Complications of rheumatoid arthritis
– Ruptured tendons
– Ruptured joints
– Joint infection
– Spinal cord compression (atlantoaxial or
upper cervical spine)
– Amyloidosis (rare)
– Side-effects of therapy
196

196. 3. Gouty arthritis/Gout
• Gout is a clinical syndrome resulting from the
deposition of urate crystals in the synovial fluid, joints
or articular cartilage
• Gout syndromes - serum uric acid concentration
above 7 mg/dl.
• Results from prolong hyperuricemia (elevated serum
uric acid) caused by
– Higher synthesis of purines or
– Poor renal excretion of uric acid
197

197. Gouty arthritis/Gout (cont’d…)
 It Primary affects adult men & postmenopausal women
 Uric crystals build up in joints—pain
- Waste products of DNA & RNA metabolism
- Builds up in blood
- Deposited in cartilage causing inflammation and
swelling
- Bones fuse
- Middle-aged men with abnormal gene
- Can usually be controlled with diet
198

198. Causes of gouty arthritis/gout
• It can be primary or secondary gout
• In general:
– It is caused by excess levels of uric acid
• Primary gouty arthritis is caused by
– Sever dieting or starvation,
– Excessive intake of food that is high in
purines (shellfish, organ meat)
199

199. Causes of gouty arthritis/gout (cont’d..)
 Secondary gout is caused by:
 Over production of uric acid caused by:
 Polycythemia vera, cancer ,cytotoxic drugs
 Hemolytic anemia , leukemia ,multiple myeloma
 Decreased excretion uric acid by:
• Chronic renal insufficiency
• Lactic acids & Keto acidosis
• Drugs enhance under excretion of uric acid like
diuretics like thiazides, frusomide.
200

200. Causes of gout (cont’d..)
Predisposing factors/Risk factors:
• Family history(18%)
• Men gender
• Obesity ,diabetes insipidus, psoriasis,
preeclampsia
• Excessive alcohol in take
• Hypelipidemia
• Hypertension , diuretic uses
• down syndrome, hypothyroidism
201

201. C/F of gout
It has four stages :
1. Asymptomatic hyperuricemia
 Increased serum uric acid level in the absence of
clinical evidences
1. Acute gouty arthritis –
• Abrupt onset often at night, symptoms awakening:
– Sever pain, swelling, erythematic of the involved
joint, tenderness and warmth.
202

202. C/F of gout (cont’d..)
3. Intercritical gout stage
 Symptom free period after the attack until
the next attack, may stay for months or
years
4. Chronic tophaceous gout stage
Tophi (crystalline deposits in the
articular tissue, soft tissue & cartilage)
Gouty nephropathy (renal impairment)
203

203. Diagnostic work up of gout
A) Acute gouty arthritis ;
• Serum uric acid value - nonspecific (normal in
10 %) & often is not helpful.
• used to assess the effectiveness of
hypouricemic therapy.
• special urate crystals WBC of 10,000- 60,000
/μl (predominant neutrophils) in Synovial
fluid analysis:
204

204. Diagnostic work up of gout
B) chronic tophaceous gout:
• Physical appearance of tophi
Firm movable and superficial located.
Chalky material if ulcerate and extrudes.
• Radiologic findings:
 Tophaceous deposits appear
•Punched out erosions of the subchondral bone.
• In first metatarso phalangal joint (MTP) 205

205. Management of gout
Asymptomatic hyperuricemia:
No need for treatment
Correction of the underlying causes.
 Acute gouty arthritis :
Drug treatment is most effective if started early
a) Colchicine
 Given early, it is effective in 85 % of patients.
 0.6 mg is given every hr until the relief of
symptoms or GIT toxicity occurs.
206

206. Management of acute gouty (cont’d...)
b) NSAID:
Used in high but quickly tapered dose.
Drugs that affect uric acid clearance should be
avoided like aspirin
•Indomethacine: 25-50 mg PO TID, ibuprofen:
800 mg po TID, Diclofenac: 25-50 mg PO TID
c) Corticosteroids:
Prednisolone, 30-50 mg/day as the initial dose &
tapered over 5-7 days.
207

207. Management of gout(cont’d...)
Intercritical gout:
Prophylactic treatment
•small dose of colchicines (0.6 mg once or
2X per day)
small doses of a NSAID
208

208. Management of gout(cont’d...)
Chronic tophaceous gout :
a) Uricosuric agents (E.G. Probenicide,
sulfinpyrazone).
 Facilitate the renal excretion of uric acid.
 Probenicide 200 mg po bid increased up to 2 gm
B) xanthine oxide inhibitors: include allopurinol;
Drug competitively inhibits xanthine oxidase.
300 mg single morning dose initially and may be
increased up to 800 mg
209

209. Management of gout (cont’d…)
Nursing management
• Monitor drug side effects
• Avoid the predisposing factors
• Advise the patient to avoid alcohol intake
• Rest and immobilization until the acute attack
subside
• Avoid heat application since of increase the
inflammation
• Encourage life style modification
210

210. 4. Septic(infectious) arthritis
• Septic arthritis is inflammation of the joint that
resulted of invasion of the synovial membrane by
microorganisms.
211

211. Causes of septic arthritis
Neisseria gonorrheal
Meningococcal
Streptococci
Staphylococcus aureus
Salmonella
Haemophilus influenza
212

212. Causes of septic arthritis (cont’d…)
• S . aureus causes at least 50% of all joint infections,
and 80% of cases of septic arthritis in pts with RA
and diabetes.
• knee is the joint - most commonly infected (50% of
cases ), followed by the hip & the shoulder
,respectively.
213

213. Causes of septic arthritis (cont’d…)
Method of entry for the bacteria in to the
joints include:
Hematogenous spread/blood the most
common
Direct inoculation
Extension from an adjacent infection
214

214. Risk factors for septic arthritis
• Advanced age
• Immunodeficiency
• Chronic diseases e.g., diabetes
• Rheumatoid arthritis
• Preexisting joint disease or joint replacement
• Intravenous drug abuse (corticosteroid or
immunosuppressive drugs
• Local joint surgery or trauma
• Intraarticular injection
215

215. Pathophysiology septic arthritis
• Bacterial invasion of synovial space
• inflammation of the synovial tissue
• Accumulation pus in the synovial membrane
and synovial fluid
• Abscess accumulation in the synovium and
subchondral bone
• Destroying of the cartilage and ankylosis of
joints.
216

216. C/Ms of septic arthritis
• Pain, swelling and tenderness of the joint
• Pus in the synovial membrane
• Abscess in the synovium and subchondral bone
• Ankylosis of joints,
• Loss of the normal joint motion, erythema
217

217. Diagnosis of septic arthritis
Joint aspiration/synovial fluid analysis
WBC count
X-ray
Culture
CT scan & MRI may reveal damage to the
joint lining
Radioisotope scanning may be useful in
localizing the infectious process.
218

218. Management septic arthritis
– Antibiotics e.g. cloxacillin
– Pain control
– Immobilization
– Aspiration & drainage when indicated
(atrthrocentesis)
– When infection subside and motion is
tolerated initiate active ROM
219

219. Bone disorders
220

220. Bone disorders....
 Bone is a specialized connective tissue,
serving three major functions:
• Mechanical - providing structure and muscular
attachment for movement
• Metabolic - as a reserve of calcium and
phosphate
• Protective - enclosing bone marrow and vital
organs
221

221. Bone disorders....
 Bone disorders includes :
Metabolic bone disorders
Osteoporosis
Osteomalacia
Infectious bone disorders
Osteomyelitis
222

222. Metabolic bone disorders
Osteoporosis
 Most prevalent bone disease in the world.
 It is a disease characterized by:
 Reduced bone quantity and quality
 Low bone mass & density
 Micro architectural deterioration of bone tissue
• Leading to:
 Enhanced bone fragility
 Increase in fracture risk
3

223. Osteoporosis (cont’d…)
 WHO defines osteoporosis as a condition in
which a BMD is less than -2.5 standard
deviations (SD) below peak bone mass
 The consequence of osteoporosis is bone
fracture.
224

224. Osteoporosis (cont’d…)
 Peak adult bone mass at ages of 18 & 25 years
 Bone mass during these years is affected by:
– Nutrition,
– Physical activity,
– Medications, endocrine status,
– & general health
 Failure to develop optimal peak bone mass
contributes to the development of osteoporosis.
225

225. Osteoporosis (cont’d…)
• Primary osteoporosis
– Occurs
• women after menopause ( 45 -55
years)
• Men later in life, but it is not merely a
consequence of aging.
226

226. Osteoporosis (cont’d…)
 Secondary osteoporosis
– Is the result of medications or other
conditions & diseases that affect bone
metabolism.
• Metabolic problem
227

227. Osteoporosis (cont’d…)
Women develop osteoporosis more
frequently and more extensively than men
b/c of
Lower peak bone mass and
The effect of estrogen loss during
menopause.
More than half of all women older than 50
years show evidence of osteopenia.
228

228. Risk factors for osteoporosis.
• Predisposes to low
bone mass
Genetics
• Caucasian or Asian
• Female
• Family history
• Small frame
• Hormones (estrogen,
calcitonin, &
testosterone) leads to
bone loss
Age
• Post menopause
• Advanced age
• Low testosterone in men
• Decreased calcitonin
• Reduces nutrients
needed for bone
remodeling
Nutrition
• Low calcium intake
• Low vitamin D intake
• High phosphate intake (carbonated
beverages)
• Inadequate calories
229

229. Risk factors for osteoporosis.
• Bones need stress for
bone maintenance
Physical exercise
• Sedentary
• Lack of weight-bearing
exercise
• Low weight and body mass
index
• Reduces osteogenesis
in bone remodeling
Lifestyle choices
• Caffeine
• Alcohol
• Smoking
• Lack of exposure to sunlight
• Affects calcium
absorption and
metabolism
Medications
e.g., corticosteroids, antiseizure
medications, heparin, thyroid
hormone
Co-morbidity
e.g., anorexia nervosa,
hyperthyroidism, malabsorption
syndrome, renal failure 230

230. 231

231. Pathophysiology of osteoporosis
 Osteoporosis is characterized by
• Reduced bone mass,
• Deterioration of bone matrix, and
• Diminished bone architectural strength.
 Normal homeostatic bone turnover is altered;
– Rate of bone resorption > rate of bone
formation
– Resulting in a reduced total bone mass.
232

232. Pathophysiology of osteoporosis
(cont’d...)
 The bones become progressively porous, brittle, &
fragile;
 Fracture easily under stresses that would
not break normal bone.
 This fractures may be the first c/ of
osteoporosis.
233

233. 234

234. Pathophysiology of osteoporosis
(cont’d...)
• Increase susceptibility to fracture
– Compression fractures of thoracic and lumbar
spine, hip fractures, & colles’ fractures of wrist.
• Gradual collapse of a vertebra - progressive
kyphosis.
• Associated loss of height.
• Postural changes result in relaxation of the
abdominal muscles & a protruding abdomen.
• Produce pulmonary insufficiency.
235

235. 236

236. Diagnosis of osteoporosis
• Osteoporosis may be undetectable on routine
x-rays until there has been 25% to 40%
demineralization
• Dual-energy x-ray absorptiometry (DXA),
provides information about BMD at the
spine and hip.
237

237. Diagnosis of osteoporosis(cont’d...)
P/E
 Height loss
 Body weight
 Kyphosis
 Tooth loss
 Skin fold thickness
 Arm span-height difference
 Wall- occiput distance
 Rib-pelvis distance 238

238. Medical Management of osteoporosis
 Diet (rich in calcium & vitamin D)
• Throughout life,
• During adolescence, young adulthood, &
the middle years, protects against
skeletal demineralization.
 Regular weight-bearing exercise promotes
bone formation.
239

239. Medical Management of
osteoporosis(cont’d..)
Pharmacologic
 Calcium and vitamin D
 Hormone replacement therapy
 Selective estrogen receptor modulators
 Bisphosphonates
 Calcitonin
 Parathyroid hormone
240

240. Infectious bone disorder
Bone infections are more difficult to eradicate
than soft tissue infections because :
Infected bone is mostly avascular & not
accessible to the body’s natural immune
response.
 There is decreased penetration by antibiotic
241

241. Infectious bone disorder (cont’d...)
Osteomyelitis
• Is an infection of the bone that results in
inflammation, necrosis, and formation of
new bone.
242

242. Osteomyelitis (Cont’d...)
• Severe infection of the
–Bone
–Bone marrow
–Surrounding soft tissue
• Caused by a variety of microorganisms
• Most common infecting microorganism is
Staphylococcus aureus
243

243. Osteomyelitis (Cont’d...)
Osteomyelitis is classified as:
– Hematogenous - due to blood borne spread of
infection
– Contiguous-focus - from contamination of bone(
surgery, open fracture, or traumatic injury)
– Osteomyelitis with vascular insufficiency,
• Seen most commonly among patients with
diabetes & peripheral vascular disease, most
commonly affecting the feet .
244

244. Osteomyelitis (Cont’d...)
• Patients at high risk for osteomyelitis:
– Poorly nourished, elderly, or obese.
– Impaired immune systems,
– Chronic illnesses (e.g., Diabetes,
rheumatoid arthritis),
– Receiving long-term corticosteroid therapy
or other immunosuppressive agents.
245

245. Pathophysiology of osteomyelitis
• Pathogens entered to bone and infection
• Initial response to infection is inflammation,
increased vascularity, & edema.
• After 2 or 3 days, thrombosis of the local blood
vessels → ischemia with bone necrosis.
• Infection extends into the medullary cavity &
may spread into adjacent soft tissues and joints.
• A bone abscess forms.
246

246. Pathophysiology of osteomyelitis
(cont’d...)
• Abscess cavity contains dead bone tissue
(sequestrum), w/c does not easily liquefy and drain.
• New bone growth forms and surrounds the
sequestrum.
• Although healing appears to take place, a chronically
infected sequestrum remains & produces recurring
abscesses throughout the patient’s life.
• This is referred to as chronic osteomyelitis.
247

247. Pathophysiology of osteomyelitis
(cont’d...)
248

248. Clinical manifestations of
osteomyelitis
• When the infection is blood borne, the onset
is usually sudden,
– Chills, high fever, rapid pulse, general
malaise.
– The infected area becomes painful,
swollen, & extremely tender.
– constant, pulsating pain that intensifies
with movement (i.e., due to pus).
249

249. Clinical manifestations of
osteomyelitis(cont’d...)
When osteomyelitis occurs from spread of
adjacent infection or from direct
contamination,
There are no symptoms of sepsis.
 The area is swollen, warm, painful, and
tender to touch
250

250. C/M of acute osteomyelitis
• Initial infection
– Infection of <1 month in duration
– Both systemic and local
• Systemic
– Fever , Night sweats , Chills
– Restlessness , Nausea
• Local
– Constant bone pain that worsens with activity
– Swelling, tenderness, warmth at infection site
– Restricted movement of affected part
– Later signs: drainage from sinus tracts
251

251. C/M of chronic osteomyelitis
• A non healing ulcer with sinus that will
intermittently and spontaneously drain pus .
• Lasting longer than a month
• Infection failed to respond to initial antibiotic
• Systemic signs may be diminished
• Local signs of infection more common
– Constant bone pain
– Swelling, tenderness, warmth at infection
site
252

252. Diagnostic findings of osteomyelitis
• X-ray
– Demonstrate soft tissue edema - early
acute osteomyelitis
– Large, irregular cavities; raised periosteum;
sequestra; or dense bone formations in
chronic osteomyelitis,
• Blood studies- leukocytosis & elevated ESR.
• Wound and blood culture performed,
although they are only positive in 50% of cases.
253

253. Medical Management of
osteomyelitis
• Initial goal of therapy is to:
– Control & halt the infective process.
• Antibiotic therapy depends on the results of blood
and wound cultures.
• Supportive measures (e.g., Hydration, diet high in
vitamins and protein, correction of anaemia)
should be instituted.
• Immobilized affected area
254

254. Medical Management osteomyelitis
(cont’d..)
Pharmacologic Therapy
• Culture specimens are obtained, IV antibiotic
• After results of the culture and sensitivity studies are
known, an antibiotic to which the causative organism
is sensitive is prescribed.
• Iv antibiotic therapy continues for 3 to 6 weeks.
• After the infection appears to be controlled, the
antibiotic may be administered orally for up to 3
months.
255

255. Surgical Management osteomyelitis
• Chronic & does not respond to antibiotic, surgical
debridement
– Infected bone is surgically exposed, and irrigated with
sterile saline solution.
• Iv antibiotic therapy is continued.
• A sequestrectomy is performed.
• A closed suction irrigation system may be used to
remove debris.
• Wound irrigation using sterile physiologic saline
solution may be performed for 7 to 8 days. 256

256. Surgical Management of OM (cont’d...)
• The débrided cavity may be packed with
cancellous bone graft to stimulate healing.
• With a large defect, the cavity may be filled
with a vascularized bone transfer or muscle
flap
• These microsurgery techniques enhance the
blood supply.
257

257. Nursing management osteomyelitis
 Relieving pain
 Improving physical mobility
 Controlling the infectious process
 Promoting home and community-based care
258

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