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Сеченовский Университет

Кафедра поликлинической терапии


ИКМ  им. Н.В.Склифосовского 

Joint syndrome in outpatient


practice (Part I).
Osteoarthritis.

Доцент кафедры, к.м.н.


Солоденкова К.С.
Joint syndrome

• Сomplex of symptoms,
including subjective changes in
the joint and periarticular
tissues, confirmed by clinical,
laboratory and instrumental
examination methods
Subjective symptoms
• Arthralgia (nature and intensity of pain,
localization, duration of pain symptom, time of
manifestation during the day, symmetry or
asymmetry of the lesion, speed of development,
connection with physical activity);
• Restriction of movement in the joints (the
severity of this symptom is usually directly
proportional to the severity of organic and
functional changes in the joints);
Objective signs
Objective signs
• Joint defect is a change in the shape of the joint
due to inflammatory edema of the synovial
membrane and periarticular tissues, effusion
into the joint cavity, hypertrophy of the synovial
membrane and fibrosclerotic changes in the
periarticular tissues.
• Joint deformation is a persistent change in the
shape of the joints due to bone changes, the
development of ankylosis, subluxations.
Objective signs
• Swelling in the joint can occur in both of
these conditions.
• Redness of the skin over the affected joints is
due to a local increase in skin temperature
and indicates an active inflammatory process
in the joint.
• When examining and palpating the affected
joints, a restriction of the range of
movements characteristic of this joint is
approximately established (restriction of
active and passive movements in the joints).
CLASSIFICATION OF ARTHRITIS

1.Purulent Arthritis
2.Arthritis as a manifestation of systemic rheumatic diseases
• RA
• Systemic lupus erythematosus
• Acute rheumatic fever
• systemic vasculitis
• spondyloatropathy
3.Reactive arthritis
• intestinal infections (yersiniosis, salmonellosis,
shigellosis, campylobacteriosis)
• urogenital infections (chlamydiosis, mycoplasmosis,
ureaplasmosis)
• respiratory tract infections (post-streptococcal arthritis)
4.Arthritis on the background of primary osteoarthritis
(osteoarthritis)
5.Gouty arthritis
6.Arthritis in case of calcium pyrophosphate crystals deposition
disease (pseudogout)
Demographic factors:

1.Age of onset of the disease


2.Patient gender
•Young women - more often Systemic lupus
erythematosus
•Women in general - RA
•Young men - ankylosing spondylitis
COMPLAINTS AND ANAMNESIS:

1.Localization of pain (in addition to the main


localization)
2.Features of pain:
• rhythm of pain during the day
• the presence of night pain indicates severe
arthritis and/or damage of bone structures
3.The presence of other musculoskeletal system
sensations, except pain
4.Paresthesia (damage of the peripheral nervous
system)
5.Muscle weakness (tests that objectively evaluate
the strength of individual muscles).
Anamnesis:

Is important for diagnosis of:


•gout (typical acute monoarthritis),
•acute infections prior to arthritis
•intestinal or urogenital infections
•spondylitis (family history)

Valuable information can be obtained by


analyzing concomitant diseases and their
treatment.
LABORATORY :

The minimum necessary laboratory tests for diagnosis and


differential diagnosis of inflammatory joint diseases:

♦ general blood test


♦ cytological analysis of synovial fluid
♦ biochemical analysis of blood (uric acid, cholesterol,
transaminases, creatinine, alkaline phosphatase, calcium,
phosphorus, creatine phosphokinase, iron, etc.)
♦ determination of CRP, RF and ANF in serum.

Other studies (microbiological, immunological, studies of


synovial fluid for the presence of crystals, etc.) are carried
out according to indications in specialized laboratories.
INSTRUMENTAL METHODS:

X-ray examination of joints

♦ Examination of symmetrical joints is always necessary.


♦ In RA, the earliest changes are noted in the joints of the fingers
of the hands, wrist joints and metatarsophalangeal joints (a direct
projection is sufficient).
♦ If there is a suspicion of spondylitis (regardless of clinical
manifestations), an examination of the sacroiliac joints is indicated
(overview picture of the pelvis).
♦ A complete X-ray examination of the knee joint includes images
in the direct, lateral and axial projections.
♦ X-ray images of the knee and hip joints in a direct projection
should be performed in a standing position of the patient
(especially if osteoarthritis is suspected).
♦ Radiological changes in the joints should always be analyzed
taking into account clinical data.
Ultrasound examination of the joints:

•effusion in the joint cavity


•pathology of tendons attached in the joint
area (tears, tenosynovitis),
•pathology of deeply located bags (bursitis)
•assessment of the condition of ligaments
and menisci of the knee joint (more reliable
in this regard are MRI and arthroscopy).
X-ray computer
tomography (CT):

•condition mainly of bone structures of the


joints.
•diagnosis of those diseases of the joints, the
primary changes in which are localized in the
bone tissue (tuberculosis, septic arthritis due
to osteomyelitis),
•differential diagnosis of arthritis with bone
tumors (for example, with osteoid osteoma).
Magnetic Resonance Imaging (MRI)

•Visualization of the state of soft tissues (cartilage,


menisci, intraarticular ligaments, synovial membrane,
tendons, synovial bags)
•Identifies bone marrow edema
•Apply for:
 early diagnosis of osteoarthritis
 ischemic bone necrosis
 hidden bone fractures (stress fractures)
 sacroileitis
 for detecting traumatic pathology of menisci and
cruciate ligaments of the knee joint
 pathology of periarticular soft tissues.
Purulent Arthritis

•It is characterized by an acute developing


lesion of one joint (usually large or
medium).

Typical:
•very severe pain (including at rest),
•significant effusion,
•severe dysfunctions,
•fever.
Caution regarding the development of purulent
arthritis should occur in the following situations:
•in young, previously healthy men and women (gonorrhea;
sepsis)
•in people using iv drug administration;
•in people of any age with chronic diseases (diabetes
mellitus, tumors, HIV infection, etc.);
•in individuals receiving drug therapy with glucocorticoids,
cytotoxic drugs, inhibitors of tumor necrosis factor-α, etc.
•in patients with RA in the case of an unusually bright
inflammation of any one joint;
•upon detection of neutrophilic leukocytosis in the synovial
fluid (> 50,000 in 1 mm3);
•in persons with joint endoprostheses.
MICROBIOLOGICAL DIAGNOSTICS OF SEPTIC
ARTHRITIS:

•Cultural study of the synovial membrane!

                If this is not possible:

•Bacteriological examination of synovial fluid (Gram stain


bacterioscopy and culture).

•PCR (often false positive for non-infectious joint diseases


due to very high sensitivity)

Currently, these methods are used only for screening


analysis.
Do not allow to determine the sensitivity of
microorganisms to antibiotics.
Osteoarthritis
Osteoarthritis - is a heterogeneous group of
diseases of various etiologies with similar
biological, morphological, clinical
manifestations and outcome, which are based
on the defeat of all components of the joint,
especially cartilage, as well as subchondral
bone, synovial membrane, ligaments, capsules,
periarticular muscles.
EPIDEMIOLOGY
INCIDENCE - 8.2 PER 100 000 POPULATION
PREVALENCE: 20% OF THE WORLD'S POPULATION
MORTALITY: THE DISEASE IS NOT FATAL
PREVAILING AGE: 40-60 YEARS
PREVAILING GENDER:
     - FOR OA OF THE KNEE JOINTS - FEMALE,
     - FOR OA OF THE HIP JOINTS - MALE
PREVENTION
•AT THE HEART OF OA PREVENTION IS A REDUCTION
IN JOINT STRESS.
•MAINTAINING NORMAL BODY WEIGHT (BMI NO
MORE THAN 25 KG / M2).
•A DECREASE IN WEIGHT OF 2 UNITS (BASED ON BODY
MASS INDEX) LEADS TO A 50% REDUCTION IN THE
RISK OF DEVELOPING OA OF THE KNEE JOINTS.
•AVOID LIFTING WEIGHTS AND MOVEMENTS
ASSOCIATED WITH FREQUENT BENDING OF THE KNEE
JOINTS TO REDUCE THE RISK OF DEVELOPING OA OF
THE KNEE JOINTS AND CLIMBING STAIRS - FOR OA OF
THE HIP JOINTS.
CLINICAL CLASSIFICATION

1.Primary (idiopathic) OA:


• Localized: joints of the hands, joints
of the feet, knees, hips, spine, other
joints.
• Generalized: defeat of three or more
different articular groups
2. Secondary OA
It develops due to a number of reasons:
•Post-traumatic.
•Congenital, acquired or endemic diseases: Perthes
disease (osteochondropathy of the femoral head),
hypermobility syndrome, etc.
•Metabolic diseases: ochronosis (homogentizine
acid), hemochromatosis (iron), Wilson-Konovalov
disease (hepatolenticular degeneration, copper),
Gaucher disease (glucosylceramide lipidosis,
glucocerebroside)
In the development of OA take part:
Key factors:
•Mechanical factor (macro- and
microtraumatization)
•Violation of microcirculation (particulary
in venous stasis)
•Changing in the synovial fluid structure
and the deterioration of its "lubricating"
function.
Predisposing factors:
•Hypodynamia
•Age
•Infectious and allergic factors
•Overweight
•Hypothermia
Diagnosis:
1. Pain
• After a long load
• "Start" pain
2. The symptom of crepitus (crunch) when moving
3. Secondary (reactive) synovitis
4. Joint deformation
5. Radiological changes
Diagnostic criteria:
1. Night pain in the joints.
2. Pain during joint movements.
3. Pain after rest.
4. Involvement of the hip, knee, distal and proximal
interphalangeal joints.
5. Restrictions of movement and crunching in joints.
6. On radiographs: bone growths in the joint cavity,
narrowing of the joint space, marginal osteophytes and
nodules, subchondral sclerosis, cystic enlightenments
7. The absence of inflammatory changes in the blood.
6 or more criteria - defined OA
3-6 criteria - probable OA
less than 3 criteria - OA can be excluded
CLASSIFICATION:
Stage I:
•Moderate restriction of movement in the
joint.
•Pain in the joint is absent at rest and in a
small load,
•Pain occurs during prolonged exercise.
•X-ray: slight narrowing of the joint space
Stage II:
•Progression of restriction of movement in the
joint, accompanied by a crunch.
•Pain syndrome is pronounced and decreases
after prolonged unloading of the joint.
•X-ray:
narrowing of the joint space by 2-3 times compared
with the norm
rough bone growths along the edges of the articular
cavity
zones of subchonal sclerosis appear.
Stage III:
•Complete loss of mobility in the joint:
only swinging movements are
preserved.
•X-ray: the joint gap is practically
absent.
Leken index:
1–4 points – light OA
5–7 - moderate
8–10 - severe
11–13 - very severe
14 - extremely severe OA
TREATMENT

1. exercise therapy
2. pharmacotherapy
–   NSAIDs
– chondroprotectors
3. joint replacement
Chondroitin sulfate and glucosamine
sulfate medications.

1.Symptomatic action:
– reduce joint pain in OA
2.Disease-modifying effect:
– slow down the narrowing of the joint space, the
formation of osteophytes
• Chondroitin sulfate
750 mg 2 times a day - first 3 weeks.
then 500 mg x 2 times a day
course duration - 6 months.
• Glucosamine sulfate
orally 1500 mg/day (once) or IM 2-3 times a
week.
general course 4-12 weeks.
courses are repeated 2-3 times a year.
Derivatives of hyaluronate
•are used for intraarticular administration.
•reduce pain in the knee joints
•the effect lasts from 60 days to 12 months.
Currently, two hyaluronate medications are used:
•low molecular weight (mol. mass 500-730 kilodaltons)
•high molecular weight (mol. mass of 6000 kilodaltons).
NSAIDs:
• Indomethacin 100 mg 2 times/day.
• Diclofenac 25 mg 3 times/day.
• Ibuprofen 200 mg 3-4 times/day.
• Meloxecam 15 mg 1 time/day.
• Celecoxib 100 mg 2 times/day or 200 mg once
• etoricoxib 120mg up to 8 days in an acute attack
• Local treatment with ointment (Dicloran, Voltaren on affected joint
3-4 times/day )
Glucocorticosteroids
• Methylprednisolone 40 mg - 1 injection in the affected area not
more than 1 time per month.
Analgesics
• Paracetamol - 500-1000 mg 1-3 times/day;
MAX daily dose - 3000 mg.
• Tramadol (opioid analgesic) - 500 mg, up to 3
mg / day. In the first days: 50 mg/day with a
gradual increase in dose to 200-300 mg/day)
for the relief of severe pain, if paracetamol or
NSAIDs are ineffective.
Thank you!

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