Chest tube insertion

1. Osteomyelitis, osteoarthritis,
Rheumatoid arthritis
Getu Mosisa(BSc, MSc).
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2. Objectives
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By Getu M( Bsc, Msc)
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At the end of the session the students will able to:
 Describe osteomyelitis, osteo-arthritis, rheumatoid arthritis
 Describe patho-physiology of osteomyelitis, osteo-arthritis,
rheumatoid arthritis
 List clinical features of osteomyelitis, osteo-arthritis, rheumatoid
arthritis
 Identify managements of osteomyelitis, osteo-arthritis,
rheumatoid arthritis
 Develop nursing process for the patients with osteomyelitis,
osteo-arthritis, rheumatoid arthritis

3. Osteomyelitis
 Osteomyelitis is an infection of the bone.
PATHOPHYSIOLOGY
 Bone is normally resistant to infection.
 When microorganisms are introduced into bone
hematogenously from surrounding structures or from direct
inoculation related to surgery or trauma, osteomyelitis can
occur.
 Bone infection may result from the treatment of trauma, which
allows pathogens to enter bone and proliferate in the traumatized
tissue.
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4. Cont.…..
 When bone infection persists for months, the resulting infection is
referred to as chronic osteomyelitis and may be polymicrobial.
 Although all bones are subject to infection, the lower extremity is most
commonly involved.
Important factors in the pathogenesis of osteomyelitis include
the following:
 Virulence of the infecting organism
 Underlying disease
 Immune status of the host
 Type, location, and vascularity of the bone
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5. Cont.……
 Bacteria may possess various factors that may contribute to
the development of osteomyelitis.
 For example, factors promoted by S aureus may promote
bacterial adherence, resistance to host defense mechanisms,
and proteolytic activity
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6. Cont.……
Hematogenous osteomyelitis
 In adults, the vertebrae are the most common site of
hematogenous osteomyelitis, but infection may also occur in
the long bones, pelvis, and clavicle.
 Primary hematogenous osteomyelitis is more common in
infants and children, usually occurring in the long-bone
metaphysis; it may spread to the medullary canal or into the
joint.
 Secondary hematogenous osteomyelitis is more common
and can develop from any primary focus of infection or from
reactivation of a previous infection in the presence of
immuno-compromised status.
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7. Contiguous-focus and posttraumatic osteomyelitis
 The initiating factor in contiguous-focus
osteomyelitis often consists of:
 Direct inoculation of bacteria via trauma,
 Surgical reduction and internal fixation of fractures,
prosthetic devices,
 Spread from soft-tissue infection,
 Spread from adjacent septic arthritis, or nosocomial
contamination.
 Infection usually results approximately 1 month after
inoculation.
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8. Cont.……
 Posttraumatic osteomyelitis more commonly affects adults and
typically occurs in the tibia.
 The most commonly isolated organism is S aureus.
 At the same time, local soft-tissue vascularity may be compromised,
leading to interference with healing.
 Compared with hematogenous infection, posttraumatic infection begins
outside the bony cortex and works its way in toward the medullary
canal.
 Low-grade fever, drainage, and pain may be present.
 Loss of bone stability, necrosis, and soft-tissue damage may lead to a
greater risk of recurrence
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9. Cont.……
 Septic arthritis may lead to osteomyelitis.
 Abnormalities at the joint margins or centrally, which may arise
from overgrowth and hypertrophy of the synovial pannus and
granulation tissue,
 may eventually extend into the underlying bone, leading to
erosions and osteomyelitis.
 One study demonstrated that septic arthritis in elderly persons
most commonly involves the knee and that, despite most of the
patients having a history of surgery, 38% developed osteomyelitis.
 Many patients with vascular compromise, as in diabetes mellitus,
are predisposed to osteomyelitis owing to an inadequate local
tissue response
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10. Cont.……
 Infection in neuropathic or vascular-compromised feet is most
often caused by minor trauma to the feet with multiple organisms
isolated from bone,
 including Streptococcus species, Enterococcus species, coagulase-positive
and -negative staphylococci, gram-negative bacilli, and anaerobic
organisms.
 Fungal infections are also known in neuropathic feet with
osteomyelitis.
 Foot ulcers allow bacteria to reach the bone.
 Patients may not experience any resulting pain, because of
peripheral neuropathy, and may present with a perforating foot
ulcer, cellulitis, or an ingrown toenail.
 Treatment of osteomyelitis in diabetic feet is multidisciplinary and
prolonged, involving complex debridements, soft-tissue cover, and
antimicrobial and antifungal treatments.
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11. Vertebral osteomyelitis
 The incidence of vertebral osteomyelitis generally increases
progressively with age, with most affected patients being older
than 50 years
 The infection usually originates hematogenously and generally
involves two adjacent vertebrae with the corresponding
intervertebral disk.
 The lumbar spine is most commonly affected, followed by the
thoracic and cervical regions.
 Potential sources of infection include skin, soft tissue, respiratory
tract, genitourinary tract, infected intravenous (IV) sites, and dental
infections.
 S aureus is the most commonly isolated organism.
 However, Pseudomonas aeruginosa is more common in IV drug
users.
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12. Cont.……
 Most patients with vertebral osteomyelitis present with localized
pain and tenderness of the involved vertebrae with a slow
progression over 3 weeks to 3 months.
 Fever may be present in approximately 50% of patients.
 Some 15% of patients may have motor and sensory deficits.
 Laboratory studies may reveal peripheral leukocytosis and an
elevated erythrocyte sedimentation rate (ESR).
 Extension of the infection may lead to abscess formation.
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13. Etiology
 The major causes of osteomyelitis include the following:
 Primary - Hematogenous
 Secondary - Secondary to trauma, surgery, or sepsis of
any etiology
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14. Risk factors
 Poorly nourished
 Elderly
 Obese
 Impaired immune system (long-term corticosteroid therapy or
immunosuppressive agents)
 Chronic illness (diabetes, rheumatoid arthritis)
 History of previous injury or infection
 Postoperative
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15. Epidemiology
 Approximately 20% of adult cases of osteomyelitis are
hematogenous, which is more common in males for unknown
reasons.
 The overall incidence of vertebral osteomyelitis is believed to
have increased as a consequence of IV drug use, increasing age of
the population, and higher rates of nosocomial infection due to
intravascular devices and other instrumentation.
 The overall incidence of osteomyelitis is higher in developing
countries.
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16. Presentation
History
 Acute osteomyelitis requires that the clinician maintain a high
degree of suspicion so as to minimize delayed diagnosis and the
consequences.
 Osteomyelitis is often diagnosed clinically on the basis of
nonspecific symptoms such as fever, chills, fatigue, lethargy, or
irritability.
 The classic signs of inflammation, including local pain, swelling, or
redness, may also occur and usually disappear within 5-7 days
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17. Cont.……
 Chronic posttraumatic osteomyelitis requires a detailed
history for diagnosis, including information regarding the
initial injury and previous antibiotic and surgical
treatment.
 Weightbearing and function of the involved extremity are
typically disturbed.
 Local pain, swelling, erythema, and edema may also be
reported
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18. Physical examination
 On physical examination, scars or local disturbance of wound
healing may be noted along with the cardinal signs of
inflammation.
 Range of motion ROM), deformity, and local signs of impaired
vascularity are also sought in the involved extremity
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19. DIAGNOSTIC METHODS
 A complete blood count (CBC) is useful for evaluating
leukocytosis and anemia.
 Leukocytosis is common in acute osteomyelitis before therapy.
The leukocyte count rarely exceeds 15,000/µL acutely and is
usually normal in chronic osteomyelitis.
 The erythrocyte sedimentation rate (ESR) and the C-reactive
protein (CRP) level are usually increased.
 Alkaline phosphatase (ALP), calcium, and phosphate are elevated,
but they are within normal limits in osteomyelitis.
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20. Cont.……
 Blood cultures are positive in only 50% of cases of
osteomyelitis.
 They should be obtained before or at least 48 hours after
antibiotic treatment.
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21. Imaging studies
Radiography
 Conventional radiography is the initial imaging study at
presentation of acute osteomyelitis.
 Radiographic findings include periosteal thickening or elevation, as
well as cortical thickening, sclerosis, and irregularity.
 Other changes include loss of trabecular architecture, osteolysis,
and new bone formation.
 These changes may not be evident until 5-7 days in children and
10-14 days in adults.
 Plain films show lytic changes after at least 50-75% of the bone
matrix is destroyed.
 Therefore, negative radiographic studies do not exclude the
diagnosis of acute osteomyelitis.
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22. Cont.……
 Computed tomography (CT) is useful for guiding needle
biopsies in closed infections and for preoperative planning
to detect osseous abnormalities, foreign bodies, or necrotic
bone and soft tissue.
 It may assist in the assessment of bony integrity, cortical
disruption, and soft-tissue involvement. It may also reveal
edema
 Magnetic resonance imaging (MRI) is a very useful modality
in detecting osteomyelitis and gauging the success of
therapy because of its high sensitivity and excellent spatial
resolution.
 The extent and location of osteomyelitis is demonstrated
along with pathologic changes of bone marrow and soft
tissue
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23. Cont.……
 Bone biopsy leads to a definitive diagnosis by isolation of
pathogens directly from the bone lesion.
 Bone biopsy should be performed through uninfected tissue
and either before the initiation of antibiotics or more than
48 hours after discontinuance.
 Open or percutaneous needle bone biopsy with
histopathologic examination and culture is the routine for
the diagnosis of osteomyelitis.
 This procedure may not be necessary if blood cultures are
positive with consistent radiologic findings
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24. Treatment
 The principles of management of osteomyelitis necessitate a
multipronged, multidisciplinary approach that may involve a team
consisting of the following:
 Orthopedic surgeon
 Infectious disease consultant
 Plastic surgeon
 Microbiologist
 Nurses
 Others as needed
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25. Cont.……
 This approach should first determine whether the disease is
acute, chronic, or an acute exacerbation of a chronic disease
or (in some cases) a partially treated subacute osteomyelitis.
 Acute osteomyelitis must be treated surgically to drain pus
and prevent bone necrosis.
 Antibiotics suited to the patient's age and the organism are
given to control hematogenous spread and to treat the local
infection.
 In other words, antibiotics save life, and surgery helps save
bone.
 Debridement of necrotic tissues, removal of foreign materials,
and sometimes skin closure of chronic unhealed wounds are
necessary in some cases.
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26. Differential Diagnoses
 Ewing Sarcoma
 Gout and Pseudogout
 Septic Arthritis
 Sickle Cell Disease (SCD)
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27. Medical Therapy
 Antibiotic treatment should be based on the identification
of pathogens from bone cultures at the time of bone biopsy
or debridement
 Bone cultures are obtained first, and suspected pathogens
are then covered by initiation of a parenteral antimicrobial
treatment.
 However, treatment may be modified once the organism is
identified.
 Parenteral and oral antibiotics may be used alone or in
combination, depending on microorganism sensitivity
results, patient compliance, and infectious disease
consultation.
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28. Cont.……
 Traditionally, antibiotic treatment of osteomyelitis has
consisted of a 4- to 6-week course.
 Animal studies and observations show that bone
revascularization following debridement takes about 4 weeks.
 However, if all infected bone is removed, as in forefoot
osteomyelitis, antibiotic therapy can be shortened to 10 days
 Oral antibiotics that have been proved to be effective include
clindamycin, rifampin, trimethoprim-sulfamethoxazole, and
fluoroquinolones.
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29. Cont.……
 Clindamycin is given orally after initial intravenous (IV)
treatment for 1-2 weeks and has excellent bioavailability.
 It is active against most gram-positive bacteria, including
staphylococci.
 Linezolid is active against methicillin-resistant
staphylococci and vancomycin-resistant Enterococcus.
 It inhibits bacterial protein synthesis, has excellent bone
penetration, and is administered IV or orally.
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30. Cont.……
 Oral quinolones are often used in adults for gram-negative
organisms.
 Quinolones have excellent oral absorption and may be used as
soon as patient is able to take them.
 Rifampin has an optimal intercellular concentration and a good
sensitivity profile for methicillin-resistant staphylococci.
 It is used in combination with cell wall–active antibiotics to
achieve synergistic killing and to avoid rapid emergence of
resistant strains.
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31. Cont.……
 The use of rifampin in combination with other antibiotics has
been found to be more effective than monotherapy for treating
infection associated with surgical hardware.
 Extensive studies of suppressive therapy with administration of
rifampin, ofloxacin, fusidic acid, and trimethoprim-
sulfamethoxazole for 6-9 months have been performed in patients
with infected orthopedic implants.
 Studies have shown that, after discontinuance of antibiotics, no
recurrence of infection occurred in 67% of patients treated with
trimethoprim-sulfamethoxazole, 55% of patients treated with
rifampin and fusidic acid, and 50% of patients treated with
rifampin and ofloxacin.
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32. Surgical Management
 Surgical debridement of bone to remove purulent and necrotic
material followed by irrigation is performed; IV antibiotics are
continued.
 Antibiotic-impregnated beads may be placed directly in the
wound.
 Chronic osteomyelitis: Sequestrectomy (removal of necrotic
bone) is performed, with sufficient bone removed to convert a
deep cavity into a shallow saucer (saucerization).
 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.
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33. Cont.…..
 Wounds are closed tightly to obliterate the dead space or
packed and closed later by granulation or grafting with
muscle flap.
 Internal fixation or external supportive devices may be
needed to stabilize or support the bone to prevent
pathologic fracture.
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34. Nursing process with patient with osteomyelitis
Assessment
 Assess for risk factors (eg, older age, diabetes, long-term
steroid therapy) and for previous injury, infection, or
orthopedic surgery.
 Assess for acute onset of signs and symptoms (e.g.
localized pain, edema, erythema, fever) or recurrent drainage
of an infected sinus with associated pain, edema, and low-
grade fever.
 Observe for guarding or patient avoiding pressure on area.
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35. Cont.…..
 Assess for generalized weakness due to systemic
reaction to infection.
 Observe for inflammation, edema, tenderness, and purulent
drainage.
 Monitor for elevated temperature.
 Patients with chronic osteomyelitis may have minimal
temperature elevations, occurring in the afternoon or
evening
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36. Nursing Diagnoses
 Acute pain related to inflammation and edema
 Impaired physical mobility related to pain, immobilization
devices, and weight-bearing limitations
 Risk for extension of infection: Bone abscess formation
 Deficient knowledge about treatment regimen
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37. Planning
 Goals include:-
 Relief of pain,
 Improved physical mobility within therapeutic
limitations, control and
 Eradication of infection, and knowledge of the
treatment regimen.
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38. Nursing Interventions
Relieving Pain
 Splint affected area to decrease pain and muscle spasm.
 Monitor neurovascular status of affected extremity
 Handle affected part with great care to avoid pain.
• Elevate affected part to reduce swelling and discomfort.
• Administer prescribed analgesics in conjunction with other
techniques to reduce pain
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39. Cont.…..
Improving Physical Mobility
 Teach patient to adhere to activity restrictions and
reduce stress on the bone, as bone is weakened due to
infectious process.
 Encourage activities of daily living within physical
limitations.
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40. Cont.…..
 Controlling Infectious Process
• Monitor response to antibiotic therapy. Observe IV sites
for evidence of phlebitis, infection, or infiltration.
• Monitor for signs of super-infection, such as oral or vaginal
candidiasis, and loose or foul-smelling stools, secondary to
long-term antibiotic therapy.
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41. Cont.…..
 If surgery is necessary, maintain wound suction, elevation
of area, avoidance of pressure on grafted area; maintain
immobility and compliance with weight-bearing
restrictions.
 Change dressings using aseptic technique to promote
healing and prevent cross-contamination.
 Monitor general health and nutrition; provide a diet high
in protein and vitamin C to promote positive nitrogen
balance and healing; encourage adequate hydration
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42. Cont.…..
Teaching Patients Self-Care
 Teach patient and family to adhere strictly to the antibiotics
regimen and to prevent falls or other injuries that could result in
fracture.
 Teach patient and family how to maintain and manage the IV
access site and IV administration equipment.
 Provide education about medication name, dosage, frequency,
administration rate, safe storage and handling, adverse reactions,
and necessary laboratory monitoring.
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43. Cont.…..
 Teach about aseptic dressing and warm compress
techniques.
 Monitor for and instruct patient to report elevated
temperature, drainage, odor, signs of increased
inflammation, adverse reactions, and signs of super-
infection.
 Assess need for home care or home infusion.
 Stress importance of follow-up health care appointments
and recommend age-appropriate health screening
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44. Evaluation
Expected Patient Outcomes
• Experiences pain relief
• Increases physical mobility
• Has absence of infection; negative wound cultures,
normalWBCs
• Adheres to therapeutic plan
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45. Osteoarthritis
 Osteoarthritis (OA) is the most common type of arthritis.
 Its high prevalence, especially in the elderly, and its negative
impact on physical function make it a leading cause of
disability in the elderly
 OA has been classified as primary (idiopathic), with no
prior event or disease related to the OA, and secondary,
resulting from previous joint injury or inflammatory disease.
 The distinction between primary and secondary OA is not
always clear.
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46. Cont.…….
Commonly affected joints include
 The hip, knee, and first metatarsal phalangeal joint (MTP) and
cervical and lumbosacral spine.
 In the hands, the distal and proximal inter-phalangeal joints
and the base of the thumb are often affected.
 Usually spared are the wrist, elbow, and ankle.
 OA often begins in the third decade of life and peaks
between the fifth and sixth decades.
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47. Joints commonly affected by osteoarthritis
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48. Epidemiology
 Studies continue to illustrate the high prevalence of OA
worldwide, with a greater burden among:-
 older individuals, women, some racial and ethnic groups, and individuals
with lower socioeconomic status
 Statistical figures are influenced by how the condition is defined—
that is, by self-report, by radiographic or symptomatic criteria, or
by a combination of these.
 On the basis of the radiographic criteria for osteoarthritis, more
50% of adults older than 65 years are affected by the disease.
 Internationally, osteoarthritis is the most common articular
disease.
 Estimates of its frequency vary across different populations.
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49. Cont.…..
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50. Age-related demographics
 Primary osteoarthritis is a common disorder of the elderly,
and patients may present asymptomatic.
 Approximately 80-90% of individuals older than 65 years
have evidence of radiographic primary osteoarthritis
 The prevalence of the disease increases dramatically among
persons older than 50 years.Why?
 Because of age-related alterations in collagen and
proteoglycans that decrease the tensile strength of the
joint cartilage and because of a diminished nutrient supply
to the cartilage
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51. Sex related characteristics
 In individuals older than 55 years, the prevalence of osteoarthritis
is higher among women than among men.
 Women are especially susceptible to osteoarthritis in the DIP
joints of the fingers.
 Women also have osteoarthritis of the knee joints more
frequently than men do, with a female-to-male incidence ratio of
1.7:1.
 Women are also more prone to erosive osteoarthritis, with
a female-to-male ratio of about 12:1.
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52. Race-related demographics
 In persons older than 65 years, osteoarthritis is more
common in whites than in blacks.
 Knee osteoarthritis appears to be more common in black
women than in other groups.
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53. RISK FACTORS
 Joint vulnerability and joint loading are the two major factors
contributing to the development of OA.
 On the one hand, a vulnerable joint whose protectors are
dysfunctional can develop OA with minimal levels of loading,
perhaps even levels encountered during everyday activities.
 On the other hand, in a young joint with competent protectors, a
major acute injury or long-term overloading is necessary to
precipitate disease.
 Risk factors for OA can be understood in terms of their effect
either on joint vulnerability or on loading
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54. Risk factors for osteoarthritis (OA) either contribute to the susceptibility of the joint
(systemic factors or factors in the local joint environment) or increase risk by the load they
put on the joint. Usually, a combination of loading and susceptibility factors is required to
cause disease or its progression.
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55. PATHOPHYSIOLOGY
 OA falls into two major etiologic classes.
 Primary (idiopathic) OA, the more common type, has no identifiable
cause.
 Secondary OA is associated with a known cause such as
rheumatoid or another inflammatory arthritis, trauma, metabolic
or endocrine disorders, and congenital factors
 The old view of OA as a “wear-and-tear” or degenerative disease,
largely focused on joint cartilage, has long been superseded by an
appreciation of the dynamic nature of OA and that it represents a
failure of the joint and surrounding tissues.
 Some changes in the OA joint may reflect compensatory
processes to maintain function in the face of ongoing joint
destruction.
 Not only biomechanical forces but also inflammatory, biochemical,
and immunologic factors are involved.
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56. Function, Structure, and Composition of
Cartilage
 Articular cartilage possesses viscoelastic properties that
provide lubrication with motion, shock absorbency during
rapid movements, and load support.
 In synovial joints, articular cartilage is found between the
synovial cavity on one side and a narrow layer of calcified
tissue overlying subchondral bone on the other side
 The layer of cartilage is narrow, with human medial femoral
articular cartilage being approximately 2 to 3 mm thick.
 Despite this, healthy articular cartilage in weight-bearing
joints withstands millions of cycles of loading and unloading
each year.
 Cartilage is easily compressed, losing up to 40% of its
original height when a load is applied.
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57. Cont.…..
 Compression increases the area of contact and disperses
force more evenly to underlying bone, tendons ligaments,
and muscles.
 In addition, cartilage is almost frictionless, and together with
its compressibility, this enables smooth movement in the
joint, distributes load across joint tissues to
prevent damage, and stabilizes the joint
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58. Cont.…..
 Normal cartilage turnover helps repair and restore cartilage in
response to demands of joint loading and during physical activity.
 In adults, cartilage chondrocyte metabolism is slow and is
regulated by growth factors, including bone morphogenetic
protein 2, insulin-like growth factor-1, and transforming growth
factor, and by catabolism and proteolysis stimulated by matrix
metalloproteinases (MMPs), tumor necrosis factor-α (TNF-α),
interleukin-1, and other cytokines.
 Tissue inhibitors of metalloproteinase (TIMP) also contribute to
the balance by restraining the catabolic actions of MMPs.
 If cartilage is injured, chondrocytes react by removing the
damaged areas and increasing synthesis of matrix constituents to
repair and restore cartilage
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59. Cont.…..
 Another component supporting healthy joints are the joint
protective mechanisms,
 such as muscles bridging the joint, sensory receptors in feedback
loops to regulate muscle and tendon function, supporting
ligaments, and subchondral bone that has shock-absorbent
properties.
 Finally, it is important to note that adult articular cartilage is
avascular, with chondrocytes nourished by synovial fluid.
 With movement and cyclic loading and unloading of joints,
nutrients flow into the cartilage, whereas immobilization
reduces nutrient supply.
 This is one of the reasons that normal physical activity is
beneficial for joint health.
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60. Characteristics of osteoarthritis in the diarthrodial joint
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61. Osteoarthritic Cartilage
 Important contributors to the development of OA are
local mechanical influences, genetic factors,
inflammation, and aberrant chondrocyte function leading to
loss of articular cartilage.
 At a molecular level, OA pathophysiology involves the
interplay of dozens, if not hundreds, of extracellular
and intracellular molecules with roles including:
 chondrocyte regulation, phenotypic changes, proteolytic
degradation of cartilage components, and interactions between
articular cartilage, underlying subchondral bone, and the joint
synovium.
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62. Cont.…..
 OA most commonly begins with damage to articular cartilage,
through trauma or other injury, excess joint loading from obesity
or other reasons, or instability or injury of the joint that causes
abnormal loading.
 In response to cartilage damage, chondrocyte activity increases in
an attempt to remove and repair the damage.
 Depending on the degree of damage, the balance between
breakdown and re-synthesis of cartilage can be lost, and a vicious
cycle of increasing breakdown can lead to further
cartilage loss and apoptosis of chondrocytes
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63. Cont.…..
 There is an increased appreciation of the role of tissues beyond
cartilage, within the joint and surrounding it, subchondral bone.
 Subchondral bone undergoes pathologic changes that may
precede, coincide with, or follow damage to the articular
cartilage.
 In OA, subchondral bone releases vasoactive peptides and
MMPs, and damage to subchondral bone may trigger further
damage to articular cartilage.
 Neovascularization and subsequent increased permeability of
the adjacent cartilage occur and contributes further to cartilage
loss.
 Joint space narrowing resulting from loss of cartilage can lead to
a painful and deformed joint.
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64. Cont.…..
 Remaining cartilage softens and develops fibrillations (vertical
clefts into the cartilage), followed by splitting off more cartilage
and exposure of underlying bone.
 During this time, adjacent subchondral bone undergoes further
pathologic changes, cartilage is eroded completely, leaving
denuded subchondral bone, which becomes dense, smooth, and
glistening (eburnation).
 A more brittle, stiffer bone results, with decreased weight-bearing
ability and development of sclerosis and microfractures.
 New bone formations, or osteophytes, also appear at joint
margins, distant from cartilage destruction and are thought to
arise from local and humoral factors.
 There is direct evidence that osteophytes can help stabilize
osteoarthritic joints
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65

65. Cont.…..
 In the joint capsule and synovium, inflammatory changes and
pathologic changes can occur.
 Contributors to inflammation may include crystals or cartilage
shards in synovial fluid.
 Other possible players are interleukin-1, prostaglandin E2, TNF-α,
and nitric oxide which are found in synovial fluid.
 With inflammatory changes in the synovium, effusions and
synovial thickening occur.
 The pain of OA is not related to the destruction of cartilage but
arises from the activation of nociceptive nerve endings within the
joint by mechanical and chemical irritants.
 OA pain may result from distension of the synovial capsule by
increased joint fluid, microfracture, periosteal irritation, or
damage to ligaments, synovium, or the meniscus.
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66. SOURCES OF PAIN
 Because healthy cartilage is aneural, cartilage loss alone in a joint
is not accompanied by pain.
 Thus, pain in OA likely arises from structures outside the
cartilage.
 Innervated structures in the joint include the synovium, ligaments,
joint capsule, muscles, and subchondral bone.
 Most of these are not visualized by x-ray, and the severity of x-ray
changes in OA correlates poorly with pain severity.
 However, in later stages of OA, loss of cartilage integrity
accompanied by neurovascular invasion may contribute to pain
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67. Diagnosis
 The diagnosis of OA is made through history, physical
examination, characteristic radiographic findings, and
laboratory testing.
 The major diagnostic goals are:
1. To discriminate between primary and secondary OA and
2. To clarify the joints involved, severity of joint
involvement, and response to prior therapies, providing a
basis for a treatment plan
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68. Cont.…..
 The American College of Rheumatology has published
traditional diagnostic criteria and “decision trees” for OA
diagnosis.
 As with all guidelines, the authors stress these are for
assisting the clinician rather than replacing clinical judgment.
 For example, traditional criteria are as follows:
 (1) For hip OA, a patient must have pain in the hip and at
least two of the following three: an erythrocyte
sedimentation rate less than 20 mm/h (<5.6 µm/s), femoral
or acetabular osteophytes on radiography, or joint space
narrowing on radiography.
 This provides a sensitivity of 89% and a specificity of 91%.
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69

69. Cont.…..
2. For a clinical diagnosis of knee OA, a patient
must have
 Pain at the knee and osteophytes on radiography
 Plus one of the following: age older than 50 years, morning
stiffness not more than 30 minutes, crepitus on motion, bony
enlargement, bony tenderness, or palpable warmth.
 This provides a sensitivity of 95% and a specificity of 69%.
 The addition of laboratory or radiographic data further
improves accuracy of diagnosis
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70

70. Clinical features
Symptoms
 Pain
 Deep, aching character
 Pain on motion
 Stiffness in affected joints
 Resolves with motion, recurs with
rest (“gelling phenomenon”)
 Usually duration <30 minutes
 Often related to weather
 Limited joint motion
 May result in limitations of
activities of daily living
 Instability of weight-bearing joints
Signs, history, and physical
examination
 Monoarticular or oligoarticular,
asymmetrical involvement
 Hands
 Distal interphalangeal joints
Herberden nodes (osteophytes or
bony enlargements)
 Proximal interphalangeal joints
Bouchard’s nodes (osteophytes)
First metacarpal joint
 Osteophytes give characteristic
square appearance to hands
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71. Cont.…..
 Knee
Pain related to climbing
stairs
Transient joint effusion
Genu varum (“bow-legged”)
 Hips
Groin pain during weight
bearing exercises
Stiffness, especially after
activity
Limited joint movement
 Spine
Lumbar involvement is most
common at L3 and L4
Paresthesias
Loss of reflexes
 Feet
Typically involves the first
metatarsalphalangeal joint
Shoulder, elbow,
acromioclavicular,
sternoclavicular,
tempomandibular joints may
also be affected
 Observation on joint
examination
Bony proliferation or occasional
synovitis
Local tenderness
Crepitus
Limited motion with
passive/active movement
Deformity
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72. Cont.…..
 Radiologic Evaluation
 Early Mild OA
 Radiographic changes often absent
 Progressive OA
 Joint space narrowing
 Subchondral bone sclerosis
 Marginal osteophytes
 Late OA
Abnormal alignment of joints
Effusions
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73. Desired Outcome
 Management of the patient with OA begins with a diagnosis
based on a careful history, physical examination, radiographic
findings, and an assessment of the extent of joint
involvement.
 Treatment should be tailored to each individual.
Goals are
A. To educate the patient, family members, and
caregivers;
B. To relieve pain and stiffness;
C. To maintain or improve joint mobility;
D. To limit functional impairment; and
E. To maintain or improve quality of life
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74. Treatment
 Non pharmacologic
– Encourage weight reduction if obese or overweight
– Increase physical activity, specific exercise, physiotherapy
– Weight supports (crutches, walking sticks or frames)
– Arthroscopic interventions (irrigations, debridement and
synovectomy) in refractory cases
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75. Cont.…..
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76. 11/15/2022
77

77. Pharmacologic treatment
Pain management
Inflammatory osteoarthritis
First line-NSAIDS,
 Ibuprofen, 200-400mg P.O.,TID
 Diclofenac, 50-75mg P.O., BID or rectal suppository 100mg/daily
 Indomethacin, 25-50mg, P.O., 2-3 times/day; maximum dose is
200mg/day or rectal suppository 100mg/daily.
 Avoid indomethacin in hip OA.
 Piroxicam, 10-20mg, P.O., once per day. Maximum dose is
20mg/day
 Dosage forms: Capsule, 10mg, 20mg ;Tablet, 10mg, 20mg
 Meloxicam, 7.5-15mg/day. Maximum dose is 15 mg/day
 Dosage forms:Tablet, 7.5mg, 15mg
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78. Cont.….
Plus
 GI protection for high risk individuals: a history of peptic ulcer
disease, on antiplatelet therapy, concomitant anticoagulant
therapy, or have more than one of other risk factors (Age ≥60
years, Corticosteroid use, Dyspepsia or GERD symptoms)
 First line PPIs
Omeprazole, 20mg, P.O., once daily or BID.
Esomeprazole, 20-40mg, P.O., once daily
Pantoprazole, 40mg, P.O., once daily
 Alternative-H2 blockers
Cimetidine, 400mg P.O., BID
Ranitidine, 150mg, P.O, BID
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79. Non inflammatory osteoarthritis
 First line
 Paracetamol, 1g 4–6 hourly P.O., when required to a
maximum of 4 doses per 24 hours
If ineffective: start NSAIDS as above.
 First line
 Tramadol, 50mg to 100mg, P.O., once to twice per day.
Dosage forms: tablet/capsule, 50mg, 75mg, 100mg, 200mg
 Alternative
 Codeine phosphate 30mg P.O., QID. USE CODEINE FOR
SHORT DURATION ONLY.
Dosage forms: Tablet 30mg
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80

80. Cont.…..
Intra-articular steroids
– Consider in inflammatory osteoarthritis of the knee and
shoulder when it is refractory to NSAIDS
– To be prescribed and administered by a specialist only
– Not more than 2–3 injections per year per joint are
recommended.
First line
Methylprednisolone acetate, 20–80mg depending on joint
size
 Dosage forms: Injection, 40mg/ml in 1ml ampoule
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81. Cont.…..
OR
 Triamcinolone acetonide: Initial: Smaller joints: 2.5-
5mg, larger joints: 5-15mg, up to 40mg for large joints
Dosage forms: Injection, 10mg/ml, 40mg/ml in vial
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82. Rheumatoid arthritis
 Rheumatoid arthritis (RA) is the most common systemic
inflammatory disease characterized by symmetrical joint
involvement.
 Extra-articular involvement, including rheumatoid nodules,
vasculitis, eye inflammation, neurologic dysfunction,
cardiopulmonary disease, lymphadenopathy, and
splenomegaly, can be manifestations of the disease.
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83. Epidemiology
 RA affects ∼0.5–1% of the adult population worldwide
 It can occur at any age, with increasing prevalence up to
the seventh decade of life.
 The disease is three times more common in women.
 In people aged 15 to 45 years, women predominate by a
ratio of 6:1; the sex ratio is approximately equal among
patients in the first decade of life and in those older than
60 years.
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84

84. Cont.…….
 Epidemiologic data suggest that a genetic predisposition and
exposure to unknown environmental factors may be necessary
for expression of the disease.
 The major histocompatibility complex molecules, located on T
lymphocytes, appear to have an important role in most patients
with RA.
 These molecules can be characterized using human lymphocyte
antigen (HLA) typing.
 A majority of patients with RA have HLA-DR4, HLA-DR1, or
both antigens in the major histocompatibility complex region.
 Patients with HLA-DR4 antigen are 3.5 times more likely to
develop RA than those patients who have other HLA-DR
antigens
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85. Patho-physiology
 In RA, the autoimmune reaction primarily occurs in the
synovial tissue.
 Phagocytosis produces enzymes within the joint.
 The enzymes break down collagen, causing edema,
proliferation of the synovial membrane, and ultimately
pannus formation.
 Pannus destroys cartilage and erodes the bone.
 The consequence is loss of articular surfaces and joint
motion.
 Muscle fibers undergo degenerative changes.
 Tendon and ligament elasticity and contractile power are
lost
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86

86. Pathophysiology and associated physical signs of
rheumatoid arthritis. ROM, range of motion.
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87

87. RISK FACTORS
 Autoimmune
 RA affects 1% of the population worldwide, affecting
women two to four times more often than men
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88

88. Clinical features
 The incidence of RA increases between 25 and 55 years of age,
after which it plateaus until the age of 75 and then decreases.
 The presenting symptoms of RA typically result from inflammation
of the joints, tendons, and bursae.
 Patients often complain of early morning joint stiffness lasting >1
hour that eases with physical activity.
 The earliest involved joints are typically the small joints of the
hands and feet.
 The initial pattern of joint involvement may be monoarticular,
oligoarticular (≤4 joints), or polyarticular (>5 joints), usually in a
symmetric distribution.
 Some patients with inflammatory arthritis will present with too
few affected joints to be classified as having RA so-called
undifferentiated inflammatory arthritis.
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89. Extra articular manifestations
 Extra articular manifestations may develop during the clinical
course of RA in up to 40% of patients, even prior to the onset of
arthritis.
 Patients most likely to develop extraarticular disease have a history
of cigarette smoking, have early onset of significant physical
disability, and test positive for serum RF or Anti-Citrullinated
Protein Antibody (ACPA).
 Subcutaneous nodules, secondary Sjögren’s syndrome,
interstitial lung disease (ILD), pulmonary nodules, and anemia are
among the most frequently observed extraarticular manifestations.
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90. Extra articular manifestations
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91

91. Cont.……
 Subcutaneous nodules have been reported to occur in
30–40% of patients and more commonly in those with the
highest levels of disease activity, the disease-related shared
epitope (SE), a positive test for serum RF, and radiographic
evidence of joint erosions.
 Secondary Sjögren’s syndrome is defined by the
presence of either keratoconjunctivitis sicca (dry eyes) or
xerostomia (dry mouth) in association with another
connective tissue disease, such as RA.
 Approximately 10% of patients with RA have secondary
Sjögren’s syndrome
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92

92. Cont.…..
 Pleuritis, the most common pulmonary manifestation of RA,
may produce pleuritic chest pain and dyspnea, as well as a
pleural friction rub and effusion.
 The most frequent site of cardiac involvement in RA is the
pericardium.
 Up to 20% of patients with RA may have asymptomatic
pericardial effusions on echocardiography.
 Cardiomyopathy, another clinically important manifestation
of RA, may result from necrotizing or granulomatous
myocarditis, coronary artery disease, or diastolic
dysfunction
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93

93. Cont.…..
 Rheumatoid vasculitis typically occurs in patients with
long-standing disease, a positive test for serum RF or anti–
cyclic citrullinated peptide (CCP) antibodies, and
hypocomplementemia
 A normochromic, normocytic anemia often develops in
patients with RA and is the most common hematologic
abnormality.
 The degree of anemia parallels the degree of inflammation,
correlating with the levels of serum C-reactive protein (CRP)
and erythrocyte sedimentation rate (ESR).
 Platelet counts may also be elevated in RA as an acute-phase
reactant.
 Immune-mediated thrombocytopenia is rare in this disease.
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94

94. Cont.…..
 Felty’s syndrome is defined by the clinical triad of
neutropenia, splenomegaly, and nodular RA and is seen in
<1% of patients
 It typically occurs in the late stages of severe RA and is
more common in whites than other racial groups.
 Large cohort studies have shown a two- to fourfold
increased risk of lymphoma in RA patients compared with
the general population.
 The most common histopathologic type of lymphoma is a
diffuse large Bcell lymphoma.
 The risk of developing lymphoma increases if the
patient has high levels of disease activity or Felty’s
syndrome.
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95

95. Cont.…..
 Osteoporosis is more common in patients with RA than
an age- and sex-matched population, with an incidence
rate of nearly double that of the healthy population and a
prevalence of approximately one-third in postmenopausal
women with RA
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96

96. Investigations
- ESR/CRP
- Rheumatoid factor
- ANA (antinuclear antibody)
- X-ray of involved joints
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97. Treatment
 Objectives
- Reduce pain, swelling and stiffness
- Prevent deformities
- Delay disease progression and onset of long term
complications
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98

98. Treatment
 Non pharmacologic
- Rest of affected joints during acute flares
- Physiotherapy
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99

99. Pharmacologic
 Disease-modifying anti-rheumatic medicines (DMARD):
Initiate early in the course
First line
Methotrexate, 7.5mg P.O., once per week. Increase dose
gradually to a maximum of 25mg per week.
N.B. Monitor: Liver function and CBC before and 12 weekly
during treatment.
PLUS
Folic acid, 5mg P.O., per week with methotrexate at least 24
hours after the methotrexate dose
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100

100. Cont.…..
AND/OR
 Chloroquine phosphate, 150mg P.O., (as base) daily for 5
days of each week for 2–3 months.
 Then reduce dose if possible and administer 5 days a week
with an annual medicine holiday for 1 month.
 Do ophthalmic examination annually to monitor for ocular
damage.
AND/OR
Sulfasalazine, 500mg P.O., 12 hourly.
Gradually increase over one month from 500mg to 1 g 12
hourly.
 Liver function and CBCs monthly for first 3 months then
every 3–6 months
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101

101. Cont.…..
 Oral corticosteroids
Indications:
- As bridging therapy while waiting for DMARDs to take
effect.
- The elderly if threatened by functional dependence and
intolerant to NSAIDs.
- Extra-articular manifestations, e.g. pleural effusion, scleritis.
- Acute flare
Prednisolone, 40mg P.O., daily for 2 weeks during acute
flares.
 Thereafter gradually reduce the dose to < 7.5 mg daily.
 Maintenance low dose prednisolone may be needed in many
patients
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102. Joint pain management-NSAIDs
Use for active inflammation with pain.
NSAIDs are used for symptomatic control only, as they have no
long-term disease modifying effects.
NSAID dose should be reduced and then stopped once the
DMARDs have taken effect.
Ibuprofen, 800mg, P.O.,TID with meals. If not tolerated: 400mg 8
hourly.
An extra night-time dose of a NSAID may be added in some
patients with severe nocturnal pain/morning stiffness
OR
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103

103. Cont.…..
 Diclofenac, Immediate or delayed release tablet: 150-
200mg/day P.O., in 2-4 divided doses.
 Rectal suppository, insert 50mg or 100 mg rectally as single
dose to substitute for final daily dose (maximum combined
dose [rectal and oral]: 150 mg/day)
OR
Indomethacin, 25-50mg P.O., BIDTO TID; maximum dose:
200mg/day.
Rectal suppository, insert 100mg, BID or once, at bed time
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