6. Causes of Soft Tissue Rheumatism
Overuse or Injury
Incorrect Posture
Structural abnormalities
Associated with Arthritides e.g. RA, Gout, OA
Occasionally from an Infection
Very often unknown
15. Management of Soft Tissue
Rheumatism
Rest during the acute phase
Splints, bands, soft pads etc.
Heat and/or cold applications
Physical Therapy
Medications e.g NSAIDS, analgesics (systemic & topical)
Prevention e.g exercises, avoid repetitive motion, weight reduction
16. LOW BACK PAIN:
GENERALITIES
◦ Low back pain is a very common disorder
◦ Mostly related to dysfunction of muscles, ligaments,
tendons & fascia
◦ Symptoms & x-rays seldom correlate in most cases of the
back pain
◦ May be associated with several musculoskeletal & other
medical disorders
17. SIMPLE BACK ACHE
◦ Patients aged 20-50 years
◦ Pain in the lumbosacral region, buttocks & thighs
◦ Pain is mechanical in nature
◦ Pain varies with physical activity
◦ Patient is otherwise well
18. SPECIAL CONSIDERATIONS IN
CHRONIC LOW BACK PAIN
◦ Examine the person more than the pain & its
mechanisms
◦ Stay alert for secondary gains & malingering
◦ Treatment modalities attempt to modify the pain
to tolerable levels e.g, excercises, TENS,
biofeedback, acupuncture etc.
◦ Analgesics, anti-inflammatory drugs, anti-
depressants
◦ Treatment can be difficult (and frustating)
19. OSTEOARTHRITIS: GENERALITIES
• Cartilage degradation: loss of matrix integrity
• Role of cytokines, enzymes, nitric oxide
• Age is the strongest risk factor
• Other risk factors: obesity, injury, muscle weakness
• Knees & hips are most commonly affected
• Herbenden's & Bouchard's nodes
• Mechanical pain, no systemic features
22. MANAGEMENT OF
OSTEOARTHRITIS
-NON-PHARMACOLOGIC
◦ Heat and cold treatments
◦ Joint protection e.g. weight reduction,
orthotics, assitive devices
◦ Exercises e.g. isometrics, stationary
cycling
-PHARMACOLOGIC
◦ Analgesics- systemic and topical
◦ Nonsteroidal anti-inflammatory drugs
(especially specific COX-2 inhibitors)
◦ Intra-articular steroid
◦ Intra-articular hyaluronate
◦ Disease-modifying drugs
-SURGERY
23. MANAGEMENT OF KNEE OA
If inadequate, surgery
If inadequate, joint lavage or arthroscopic debridement
If inadequate, use full-dose NSAID with gastric protectants
Acetaminophen; If necessary, add capsaicin cream
Consider aspiration of effused joint & intaarticular steroids
Nonpharmacologic modalities
24. Exercise Considerations in Hip or Knee
Osteoarthritis-I
• Maintain proper weight
• Maintain range of motion and flexibility
• Exercise in water, on a bicycle or a rowing machine
• Alternate weight-bearing and non-weight-bearing
activities
• Use cane on contralateral side
25. Exercise Considerations in Hip or Knee
Osteoarthritis-II
• Do not carry loads more than 10% body weight
• Minimize use of stairs, one-legged stance, low seating
• Walking speed should not exacerbate joint symptoms
• Select shoes and insoles for shock attenuation
• Warm-up prior to walking exercise
26. THE
SPECTRUM
OF GOUT
◦ Hyperuricemia
◦ Acute gouty arthritis
◦ Tophaceous deposition of urate
crystals
◦ Urolithiasis
◦ Interstitial deposition of urate
crystals in renal parenchyma
◦ Uric acid nephropathy
27. GOUTY ARTHRITIS :
GENERALITIES
◦ Extremely painful episodes of arthritis
◦ Intermittent course, usually monoarticular involving the big
toe, ankle, knee
◦ May later be oligo- or polyarticular
◦ Tendency to abuse NSAIDS (and steroids)
◦ May be precipitated by stress e.g surgery, blood transfusion
28. Acute Gouty
Arthritis
◦ Precipitated by local trauma
unaccustomed excercise & alcohol
consumption
◦ Acute arthritis is the most common
manifestation
◦ Excruciating pain over hours
frequently nocturnal
◦ Swelling, redness & tenderness
◦ Monoarticular & lower extremities
-May affect knees, wrist, elbow &
rarely SI & hips
32. GOUT &
DIET
Purine content in the diet DOES NOT
USUALLY CONTRIBUTE more than 1.0
mg/dl to SUA concentration
MODERATION in dietary purine
consumption (rather than a constant low
purine diet) is indicated in those who
habitually eat large amounts of purine-
containing food
Consumption of LARGE AMOUNTS of
food containing a small concentration of
purines provides a GREATER PURINE
LOAD than consumption of a small amount
of food containing a large purine load
33. When to treat Hyperuricemia?
The cause cannot be corrected e.g. obesity,
hypertension, hypercholesterolemia
Two or three definite gout attacks
Tophaceous gout
Urinary calculi and/or urinary UA >800 mg/day
Tumor lysis (risk of acute uric acid nephropathy)
35. Do not overlook the Septic Joint
• Fever before and during monoarthritis suggests septic
arthritis
• Persistent monoarthritis (and fever) despite NSAIDs
or colchicine, suggests septic arthritis
• In case of doubt, treat as septic arthritis
• Gout and septic arthritis can co-exist
47. Systemic Lupus
Erythmatosus
◦ More commonly
reported among (Filipinos)
orientals. This is a disease
with a myriad of
potential manifestations
ranging from mild to
severe/life threatening.
48. Polymyositis – dermatomyositis
• Usually presents with
proximal muscle weakness
• Characteristic rashes,
include heliotrope rash on
the eyelid
51. OTHER LABORATORY TESTS
• Azotemia – poor prognosis in SLE, vasculitides
• ALT, AST elevation – hepatitis or myositis
• Hypocomplementemia – SLE
52. Approach to Arthritis
Treatment
Regardless of the type of arthritis, the
treatment goals are the same:
◦ Optimize treatment of pain &
inflammation
◦ Minimize joint damage
◦ Maximize functional independence
◦ Provide access to care at reasonable cost
◦ Enhance quality of life
53. Anti-inflammatory Drug Therapy
NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
(NSAIDs)- I
• Widely used for various conditions with pain &
inflammation
• May be the only dug required by the patient
• Different patients & diseases respond differently to
different NSAIDs
54. Anti-inflammatory Drug Therapy
NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
(NSAIDs)- II
• Use only one NSAID at a time
• Note for possible drug interactions e.g.
antihypertensives, warfarin
55. Anti-inflammatory Drug Therapy
NON-STEROIDAL ANTI-INFLAMMATORY DRUGS
(NSAIDs)- III
• Most common side effects include gastropathy;
occasionally renal & liver SE
• New anti-inflammatory drugs e.g. specific COX-2
inhibitors or coxibs have less potential for GI side-
effects
56. Anti-inflammatory Drug Therapy
CORTICOSTEROIDS-I
• Anti-inflammtory activity directly correlates with
dosage
• Adrenal suppression directly correlates with dosage,
duration, frequency and schedule of administration
• Chronic side effects include Cushing's, osteoporosis,
AVN, cataract, hyperglycemia, infections etc.
57. Anti-inflammatory Drug Therapy
CORTICOSTEROIDS-II
• Determine minimum effective dose to control signs
& symptoms
• Steroids may be abruptly discontinued within 5 to 7
days of administration
• If steroid history is unclear, do not abruptly
discontinue steroids
66. ACR 1987
CLASSIFICATION
CRITERIA FOR
RHEUMATOID
ARTHRITIS
Requires four out of the seven
criteria:
◦ Morning stiffness*
◦ Arthritis of three or more joints*
◦ Arthritis of hand joints*
◦ Symmetric arthritis*
◦ Rheumatoid nodules
◦ Serum rheumatoid factor
◦ Radiologic changes
◦ *Must have been present for at
least six weeks
69. ACR GUIDELINES IN RA TREATMENT
– I
ESTABLISH
RA DIAGNOSIS
EVALUATE
• Disease activity/extent of synovitis
• Structural damage
• Functional/psychosocial status
INITIATE TREATMENT
• Patient education
• Physical & occupational therapy etc.
• NSAIDs
• Possible local or oral steroids (≤ 10mg. Prednisone)
ASSESS DISEASE ACTIVITY
70. ACR GUIDELINES IN RA TREATMENT
– II
ASSESS DISEASE ACTIVITY
START DMARD
Consult Rheumatologist
MONITOR DISEASE ACTIVITY
MONITOR DISEASE ACTIVITY
MONITOR DISEASE ACTIVITY
PERIODICALLY
REVISE TREATMENT PLAN
• Consult Rheumatologist
• Change NSAIDs
• Change/add DMARDs
• Local or oral steroids
• Rehabilitation
Persistent Active Disease
Spontaneous Remission
Reactivation of Disease
Remission or Satisfactory Control
Reactivation of Disease
Remission or Satisfactory Control
Persistent Active Disease
71. ACR GUIDELINES IN RA TREATMENT
– III
REVISE TREATMENT PLAN
• Consult Rheumatologist
• Change NSAIDs
• Change/add DMARDs
• Local or oral steroids
• Rehabilitation
MONITOR DISEASE ACTIVITY
PERIODICALLY
SURGICAL INTERVENTION
REFRACTORY RHEUMATOID
ARTHRITIS
• Consult Rheumatologist
• Most effective NSAID
• Most effective DMARD
• Possible local or oral steroids
• Rehabilitation
Mechanical Joint Symtoms
Mechanical Joint Symtoms
Persistent
Active
Disease
Reactivation of Disease
Remission or Satisfactory Control
77. CHARACTERISTICS OF PATIENTS
WITH MILD SLE
• Diagnosed or highly suspected SLE
• Clinically stable disease
• Not life-threatening
• Normal & stable body systems: kidneys, skin, joints,
hematologic, lungs, heart, GI, CNS
• No significant toxicities from SLE therapies
78. TREATMENT OF MILD SLE
• Patient education
• Analgesics as needed
• NSAIDs as needed (caution on side effects)
• Topical steroid & sunscreens
• Adequate rest, especially during disease flare
• Low-dose glucocorticoid, i.e. <10mg Prednisone
daily
80. REASONS FOR REFERRAL TO A
RHEUMATOLOGIST
• To confirm the diagnosis or consider other
possibilities
• To assess disease activity & severity
• To provide general disease management
• To mange uncontrolled or life-threatening disease
• To manage/prevent treatment toxicities
• Other special circumstances e.g. antiphospholipid
syndrome, pregnancy, surgery
88. Some pitfalls in
Rheumatic
Disease
Diagnosis
◦ Present polyarthritis may have
started as intermittent
monoarthritis of gout
◦ Knee pain in a perfectly
healthy looking knee may be
coming from the hip
◦ A rash is not a rash if you do
not look for it
◦ Gout may occur without
hyperurcemia & vice versa
◦ ANA positivity does not
always indicate SLE
89. SUMMARY
◦ Most rheumatic diseases are
diagnosed by history & physical
examination, occasionally with the
use of basic laboratory tests
◦ Analgesics & anti-inflammatory
drugs are a mainstay of therapy in
most rheumatic diseases
◦ Therapy is highly individualized
even in patients with the same
rheumatic disease
◦ Recognition of a serious rheumatic
disorder may be more important
than making an actual diagnosis
