🔹🔹Mainly involves the joints.
Joints of the wrist, hand, knee, ankle and foot are
Psoriatic arthritis:
Psoriatic arthropathy can involve the small joints of the hands and feet but 🔹Elbow, shoulder, hip and spine are not commonly
commonly affected.
🔹
can also cause a large effusion in a single joint.
🔹
affected.
🔹
🔹 Affects men and women equally and tends to run in families. Monoarticular involvement is rare.
The arthritis is not as clearly symmetrical as in RA and –it occurs mainly Involvement of soft tissue structures surrounding the
🔹
in the interphalangeal joints of the fingers and toes.
🔹 Definition
joint too occurs, eg the synovium, capsule, tendons,
Bone destruction may be so severe that the digits are completely flail or
🔹Lungs, pericardium, eyes, vessels and nerves are the
muscles,..
🔹
badly deformed (‘arthritis mutilans’). It is an autoimmune systemic disorder wherein the body defence
About one-quarter of the patients develop sacroiliac and vertebral mechanism identifies the normal tissue as antigen and evokes a
🔹Exact 🔹
other structures that can get involved.
🔹Age
🔹
changes. chain of inflammatory reaction resulting in destruction. 20-40 yr.
🔹 HLA-B27 occurs in about 60% of those with overt sacroiliitis. Etiology M:F ratio is 3:1
Beware of the patient with psoriasis who has a swollen joint without cause is not known. Following factors are considered as
🔹
obvious explanation: operation is unlikely to be helpful. triggering factors.
Treatment is similar to rheumatoid arthritis, but the condition is seldom a. Chronic infection —bacterial, fungal or viral. Pathology
as severe. b. Environmental factors —polluted atmosphere, smoking, etc. Although tissues throughout the body are affected, the brunt of the attack falls on
c. Genetic factors —HLA with DR4 specificity is observed.
🔹
synovium.
🔹
d. Endocrinal factors. The pathological changes, proceed in four stages:
e. Poor quality food with constant assault on the gut. ■■ Stage 1: preclinical: well before RA becomes clinically apparent the immune
🔹
pathology is already beginning.
■■ Stage 2: synovitis: synovial membrane becomes inflamed and thickened, giving
🔹
rise to a cell rich effusion.
■■ Stage 3: destruction:persistent inflammation causes joint and tendon destruction.
🔹
Articular cartilage is eroded.
■■ Stage 4: deformity:the combination of articular destruction, capsular stretching
and tendon rupture leads to progressive instability and deformity.
Reiter’s disease and reactivearthritis
🔹 Reiter’s disease is acquired through sexual contact or as a sequel to
dysentery and includes the following features:
Clinical Features
Systemic features start insidiously with low grade fever, malaise, fatigue and
🔹
Extra-articular features
The most characteristic extra-articular lesion is the rheumatoid nodule, a small
1. Conjunctivitis.
🔹
joint pains.
The joints are swollen edematous, warm, tender with effusion and the
granuloma occurring under the skin (especially over bony prominences), on tendons,
2. Urethritis.
🔹
3. Synovitis.
🔹
movements are painful and limited.
Early morning stiffness is characteristic. Synovial thickening is
🔹
in the sclera and in viscera.
Other systemic features are lymphadenopathy, vasculitis, muscle weakness and
🔹
The condition can affect any joint but the small joints of the hands and feet
are most often involved. A number of conditions usually associated with seronegative polyarthritis 🔹
appreciable.
Subcutaneous nodules may be palpable.
🔹 brain and gastrointestinal tract.
visceral disease affecting the lungs, heart, kidneys,
🔹
🔹🔹
Large joints such as the knee are affected less often. (i.e. without serum RFs)
The diagnosis should be considered in any patient, especially men, with these may show changes in the spine and sacroiliac joints
🔹
symptoms.
TreatmentThe condition usually resolves spontaneously but anti-
inflammatorydrugs are helpful.
The best defined of these conditions are:
-psoriatic arthritis.
-Reiter’s disease.
-Arthritis that sometimes accompanies ulcerative colitis or Crohn’s disease;
🔹
Ankylosing spondylitis.
The exact relationship between these disorders is unknown, but
they share certain important features:
Seronegative spondarthritis
(1) the characteristic spondylitis and sacroiliitis occur in all of them.
(2) they are all associated with HLA-B27.
(3) they show familial aggregation.
(4) there is considerable overlap within families, some members having one
disorder and close relatives another
🔹 X-rays
The cardinal sign – and often the earliest – is erosion and
🔹
fuzziness of the sacroiliac joints.
The earliest vertebral change is flattening of the
🔹
X-rays
normal anterior concavity of the vertebral body
🔹
(‘squaring’).
🔹 In the early stages diffuse rarefaction is the only finding.
🔹
Later, ossification of the ligaments around the Later other changes develop such as
Investigations
intervertebral discs produces delicate bridges
🔹
🔹 🔹 • Narrowing of the joint space.
🔹
Hb%—may be low.
🔹
(syndesmophytes) between adjacent vertebrae. • Destruction of the articular surfaces.
Bridging at several levels gives the appearance of a
‘bamboo spine’. 🔹
🔹
TC—leukocytosis.
DC—neutrophil> in the early acute phase & lymphocytes > in chronic phase.
🔹 • Subchondral sclerosis.
• Subchondral cysts.
🔹
🔹
ESR—elevated.
CRP—elevated. It is nonspecific and only suggests that there is active inflammation.
ANA—when positive suggests sensitization has occurred and autoimmunity has
🔹
developed. (Normal titer is 1:40. Higher titer indicates presence of autoimmunity).
RA factor—positive in 80% of the patients. > 20 IU/ml is considered positive. Neither of
Ankylosing spondylitis 🔹
these tests is specific and neither is required for a diagnosis of RA.
🔹
CCP (Citruline antibody)—elevated. It is more sensitive than RA factor. Can be positive
Ankylosing spondylitis is essentially a even when RA factor is negative.
disease of the spine but it also involves the
large joints, such as hip, knee and shoulder. The
disease is commoner in men than women by 6 : 1
and usually presents between the ages of 15
and 30 years.
Diagnosis
Treatment consists of
anti-inflammatory drugs
Rheumatoid Arthritis
🔸
🔸 The diagnosis of rheumatoid arthritis is essentially clinical.
The minimal criteria for diagnosing RA are:
🔹
and physiotherapy.
Cervical and lumbar
osteotomy may be needed
(1) bilateral, symmetrical polyarthritis, involving
(2) the proximal joints of the hands or feet,
🔶 Rheumatoid arthritis – differential diagnosis All three
(3)present for at least 6 weeks. If, in addition, there are subcutaneous nodules or periarticular
🔹
for late deformities.
Joint replacement is 🔸
erosions on x-ray, the diagnosis is certain.
A useful screening tool is the inclusion of one or more of the following:
🔸
patients presented with painful swollen fingers. In:
🔸 (a) mainly the proximal joints were affected (rheumatoid arthritis);
often unsuccessful
because the new joints also
1. Morning stiffness > 1 h.
2. Swelling (synovitis).
🔸 (b) in the distal joints were the worst (Heberden’s osteoarthritis)
(c) in there were asymmetrical nodular swellings around the joints
become ankylosed. 3. Characteristic distribution of joints.
4. ESR 20 mm/h.
🔸Swollen finger joints:
(gouty tophi).
Proximal joints = inflammatory arthritis.
5. Nodules.
Distal joints = osteoarthritis.
6. Positive laboratory tests.
🔹 Juvenile idiopathic arthritis (JIA) is the preferred term for non-infective inflammatory
7. Radiographic findings – erosions of hands and feet.
8. Non-steroidal anti-inflammatory drugs are beneficial.9. First degree relative with inflammatory joint
🔹
joint disease of more than 3 months’ duration in children under 16 years.
It embraces a group of disorders in all of which pain, swelling and stiffness of the joints are
disease.
🔹
common features.
The prevalence: is about 1 per 1000 children, and boys and girls are affected with equal
🔹
frequency
The cause: is probably similar to that of rheumatoid disease: an abnormal immune response
Complications Of R.A
🔸 Infection:
🔹
to some antigen in children with a particular genetic predisposition, However, RF is usually absent.
The term juvenile chronic arthritis includes Still's disease and a number of less well - defined
conditions, some of which may be monoarticular or may have minimal joint involvement — so –
Patients with RA – and even more so those on corticosteroid therapy – are susceptible to
infection. Sudden clinical deterioration, or increased pain in a single joint, should alert one to
🔸
the possibility of septic arthritis and the need for joint aspiration.
🔹
called pauciarticular .
🔹 The onset is often insidious, but may be acute.
Fever, lymph gland involvement and anaemia are usually present in addition to the joint pains
Tendon rupture:
Nodular infiltration may lead to tendon rupture. This is seen most often at the wrist, where it
🔸Joint rupture
contributes significantly to the development of the characteristic rheumatoid deformities.
🔹
and stiffness.
🔹 Uveitis occasionally occurs.
Occasionally the joint lining ruptures and synovial contents spill into the soft tissues. Treatment
🔹 The main joints affected are the knees, ankles, wrists and occasionally the spine.
The degree of pain varies, children occasionally presenting with chronically swollen joints
Juvenile idiopathic arthritis
is directed at the underlying synovitis – i.e. splintage and injection of the joint, with
🔸
which are painless and functioning normally synovectomy as a second resort.
Secondary osteoarthritis
Articular cartilage erosion may leave the joint so damaged that, even if the rheumatoid disease
Deformities occur, as in the adult form, and there is a more subsides or is kept under control, the end stage will be very similar to advanced osteoarthritis.
marked tendency to ankylosis, especially in the cervical spine.
🔹
Treatment
The same local and general measures are
Epiphyseal growth may be disturbed.
🔶Conservative measures in rheumatoid arthritis:
🔹
needed as in the adult. 1. Drugs.
🔸
Physiotherapy is important in maintaining -Non-steroidal anti-inflammatory drugs:
joint movements, particularly when the disease Non-steroidal anti-inflammatory drugs. These are the first line of treatment and include aspirin, ibuprofen,
🔹 Surgery is rarely needed,
is beginning to settle.
🔸
naproxen, etc.
🔸 Patients may require steroids taken orally, or injected into affected joints in severe cases.
These drugs help modify joint pain and inflammation.
🔸🔸These
-Second line drugs or disease-modifying antirheumatic drugs (DMARDS):
May help prevent joint destruction and subsequent deformity.
🔸
🔸 Crystals can be deposited in joints or soft tissue because of a metabolic abnormality.
The accumulation of crystals probably begins in infancy but is not usually apparent 🔸
slow-acting drugs may take months to become effective and are often used for long periods of time,
sometimes years.
These DMARDS may promote remission, and they are often used in combination and together with first line
🔺added from chat Gbt
🔸
until the third or fourth decade
Deposits of crystals in and around joints often remain asymptomatic but they can also
cause two types of arthritis:
🔸
drugs.
Second-line drugs include quinine, sulfasalazine, gold, penicillamine or immunosuppressive therapies such
1. Acute self-limiting attacks of inflammation. 🔸
as methotrexate, azathioprine and cyclophosphamide.
Newer drugs aim to block the production of the inflammatory mediators such as tumor necrosis factor
🔸
2. Chronic destructive joint disease.
Gout and its imitators form a group of conditions characterized by the presence of
(antiTNF) and interleukin-1.
2. Rest during an attack and mobilization during remission:
🔸
crystals in and around the joints, bursae and tendons.
Three clinical disorders in particular are associated with this phenomenon:
🔸
-Rest and immobilization
■ Gout: urate crystal deposition disorder. Affection Of The Splintage and rest will also reduce the swelling of joints and it can induce remission of the disease in an
🔸The aim of treatment is to:
Treatment
🔸
acute attack.
■ Pseudogout: calcium pyrophosphate dihydrate (CPPD) deposition disease.
■ Basic calcium phosphate (BCP) deposition disease. Joints Control synovitis and pain. 🔸 Rest may require admission to hospital.
Restoration of joint movement by physiotherapy when the attack has passed is essential.
Arthritis Maintaining joint function.
🔹
clinic picture
The disease is chronic, but characterized by acute attacks in which the 🔸
Prevention of long-term deformities.
A multidisciplinary approach between rheumatologists, orthopaedic surgeons and 🔸
3. Aids and appliances:
🔸 Patients with rheumatoid arthritis need a host of appliances.
Sticks, frames and crutches take the weight of lower limbs; splints and braces protect painful joints from
affected joints, usually single, become severely painful, swollen, often red and physical therapists is often necessary.
🔹
impossible to move. unnecessary movement; and soft protective footwear relieves the pressure on vulnerable skin.
🔹
🔹
This usually settles spontaneously in less than 3 weeks.
The joint may be gradually damaged by repeated attacks.
Other features include the formation of gouty tophi —collections of urate 🔶 Operative treatment:
crystals in the soft tissues, especially in the ear lobes, hands and feet. Operative treatment may be required for three reasons, but only if medical
treatment has failed.1. To remove inflamed synovium by synovectomy.2. To
🔸 The most useful investigation is the serum
repair damaged soft tissue.3. To salvage destroyed joints.
uricacid, which is usually well above normal,
although occasionally isolated readings may be
Gout
🔸 🔸
Surgery in rheumatoid arthritis.
🔸Synovectomy.
🔸
This is a metabolic disease characterized by the deposition of Tendon repair.
🔸
within normal limits.
🔸Arthrodesis.
urates in the tissues, hyper - uricaemia and, in about 10% of cases,
The X - ray appearance may be typical, with
well -demarcated, rounded erosions close to the 🔸
increased excretion of uric acid in the urine.
It is a common disease, affecting men in 95% of cases and post -
Arthroplasty
🔸
joint margins, usually in the hands.
🔸 Joint destruction maybe seen later. 🔸
menopausal women.
The arthritis usually affects the distal joints of the hands and Crystal arthropathies
🔸
The most useful investigation is the serum feet, and the knees.
uricacid, which is usually well above normal, Osteoarthritis (OA) is a chronic joint disorder in which there is progressive softening and disintegration of
It particularly (and characteristically)affects the articular cartilage accompanied by new growth of cartilage and bone at the joint margins (osteophytes), and
although occasionally isolated readings may be metatarsophalangeal joints of the great toes.
within normal limits.
🔹
capsular fibrosis.
🔹 It is defined as primary when no cause is obvious,and secondary when it follows a demonstrableabnormality 🔺 The basic difference in joint destruction
Treatment 🔹
🔹
The condition is the result of degenerative changes taking place in the joint. occurring inRheumatoid arthritis and
🔸
The articular cartilage and the subchondral bone progressively degenerates. Osteoarthritis is that, in rheumatoid arthritis:
Two drugs are useful for treating the acute attack:
1 Colchicine, which is very specifi c and may be used as a therapeutic test. It 🔹 This results in inflammation and mechanical derangement which promotes further degeneration.
Ultimately results in badly deranged joint,associated with deformityand ligamentous laxity.
inflammation occurs first. The joint destruction
that follows is the result of inflammation. Whereas
in Osteoarthritis: the joint destruction occurs
by fatema okoff is, however, toxic and unpleasant to take. Types
🔸
2 NSAIDs, such as indometacin or diclofenac, are usually effective.
Many patients are also treated with a drug such as allopurinol which lowers
a. Primary osteoarthritis Is the type where there is no preexisting abnormality or damage (incongruity) as a
cause for progressive degeneration. secondary to joint destruction. 🔺
first and the inflammation that follows is
🔸
the serum uric acid in the anticipation of preventing further attacks. b. Secondary osteoarthrit
Nevertheless, acute attacks may be precipitated by allopurinol or is Is the type where there is a preexisting pathology or damage (incongruity) which is responsible for the
probenecid if given without NSAID cover progressive degeneration.
Primary
With advancing age the proteoglycan content of the articular
cartilage decreases thereby reducing the water content of the
Pseudogout
🔸 This is a condition, similar to gout, but is usually less acute, and
the crystals deposited in the affected joint are of calcium
cartilage.
Such a cartilage becomes less resilient and cracks during activities
of daily living.
🔸
pyrophosphate rather than uric acid.
Both pyrophosphate and hydroxyapatite deposition may follow
either local or systemic disorders and be associated with acute
This is responsible for the onset and progression of degenerative
process.
It starts innocuously in the beginning, progresses slowly over a
🔸
inflammatory synovitis or chronic joint destruction.
A common feature is calcification of the menisci of the knees,
although this is rather non -specific.
period of time and then becomes severe.
Secondary
🔹
There is usually evidence of osteoarthritis.
🔹
No specific treatment is known, but NSAIDs are usually There is a joint incongruity which has developed due to some disease in the past.
helpful in relieving symptoms. Thus degeneration occurs secondary to a pre-existing mechanical abnormality.This is secondary
osteoarthrosis.
Secondary causes of osteoarthritis include:
1 Fractures (especially intra - articular injuries).
2 Joint infection.
🔹 This is known by various names as acute pyogenic arthritis, acute septic arthritis,
3 Inflammatory joint disease.
4 Congenital joint abnormalities.
🔹
acute pyoarthrosis and acute infective arthritis.
🔹 It refers to presence of pus in the joint secondary to infection of the joint.
Osteoarthritis
5 Joint instability.
6 Cartilage damage.
🔹 Age of onset—common in infants and children can occur at any age.
🔹 Sex—M:F 🔹
7 Obesity
🔺
ratio 5:1 Weight - bearing joints, especially the hip and theknee, are most frequently affected.
Site—Any joint. Common in hip and knee. Osteoarthritis, once established, is usually a progressive disorder.
🔹 Septic arthritis can arise in three ways:
1. Spread from an infected bone.
Rarely, a patient presents with widespread osteoarthritic changes in many joints. This is sometimes
an inherited condition.
2. Direct infection from a penetrating wound.
🔹
3. Bacteraemia. Diagnosis
Organism Clinical Features It is not difficult.
Staphylococcus aureus 90%, Streptococcus, H. influenzae,E. coli, Proteus, etc. are A. Pain is the primary feature of osteoarthritis. It is gradual in onset and slowly Clinical features and X-rays confirm the
🔹
responsible in remaining 10% of the patients. progressing in severity. There can be pain free intervals too. diagnosis.
Focus of infection—spreads from the synovium or fromthe bone B. Swelling and joint effusion.Swelling in osteoarthritis is due to effusion.
C. Limitation of movement.Painful limitation of movement is a late feature of Radiological Findings
O.A. In the early phase the joint movements are associated with pain but not • Narrowing of the joint space (due to loss
Pathology limited. of articular cartilage.)
Once the infection gets into the joint there is seropurulent exudate formation. The D. Heberden’s nodes and Bouchard’s nodes. These are nodular formation • Sclerosis of the subchondral bone.
articular cartilage gets destroyed very rapidly due to the enzymatic degradation occurring in the DIP and PIP joints respectively in osteoarthrtis. • Subchondral cysts.
resulting from the enzymes released from the bacteria as well as from the inflamed E. Deformitytends to develop as a result of more severe destruction of the • Osteophytes (the bony excrescenceor
synovium and inflammatory cells. underlying bone surface, especially at the knee and the ankle. outgrowth, usually branched in shape)•
The subchondral bone gets exposed and later gets eroded too. Deformities.
If the pus is not drained surgically, a sinus develops.
Sequel depends on the speed at which the infection is controlled.
If the infection is controlled before the destruction of the cartilage, the joint becomes
normal. No residual deformity is seen.
🔹
Management
Non - operative
The condition is a slowly progressive and painful one, and most patients can be managed
After some destruction of cartilage, the joint goes in for fibrous ankylosis.After conservatively for many years.
considerable destruction of cartilage, the joint goes in for bony ankylosis. 1-Analgesics are usually the mainstay of treatment.Anti - inflammatory analgesics are of less
If the infection takes natural course then bony ankylosis with deformity is the result. help in osteoarthritis than in rheumatoid arthritis.
2-Protection of the joint, e.g. the patient may benefit by losing weight, and a stick, splint or
other support may be helpful.
Diagnosis 3-Change of life style, such as a more sedentary job.
Diagnosis is mainly on clinical grounds. 4-Physiotherapy, i.e. intermittent heat treatment or short - wave diathermy, with supervised
Signs of acute infection, i.e. calor, rubor, dolor, tumor with painful exercises to maintain movements.
immobile joint. Signs of systemic toxicity such as high grade fever
with delirium may also be present.
Investigations such as TC, DC, ESR, CRP, ultrasound, X-ray, MRI are
Acute Suppurative Arthritis
🔹 Surgical (Operative) Management
It is done late in the course of the disease when the joint isdegenerated and clinically
useful and should be done as per indication. associated with pain and deformity.
-Total joint arthroplasty is the treatment of choice .In selective cases osteotomies can be
done.
🔺
Treatment
Emergency surgical drainage of the joint of pus and debris under cover of systemic
antibiotics is the treatment of choice.
-Osteotomy alters the line of weight bearing and distribution of stress and is known to give
relief, e.g. high tibial osteotomy.
-Arthroscopic lavage and excision of loose bodies is donein high risk patients who are not
Continuous irrigation and suction can be employed for achieving good control of infection. fit for joint replacementsurgery. This procedure gives temporary relief.
Immobilization is essential till control of infection is achieved. This is followed by gradual
mobilization as early as possible to avoid stiffness of the joint.
Systemic antibiotics are used for considerable period to get rid of any residual focus of infection
depending on the organism isolated in culture and its antibiotic sensitivity
Arthrodesis is the treatment of choice for unsound ankylosis.
In selected cases of hip and knee ankylosis with no reactivation of the disease, total joint
arthroplasty can be considered.
This procedure considerably reduces the morbidity
Neonatal septicaemia causes widespread septic
arthritis.
Once common, and known as Tom Smith’s arthritis, the
condition is now rare in developed countries but is
sometimes seen after exchange transfusion and invasive
procedures on the newborn.
Prompt and early attention with an accurate diagnosis
followed by drainage of pus under antibiotic cover may Neonatal
reduce the morbidity septicaemia
Joints of the wrist, hand, knee, ankle and foot are
Psoriatic arthritis:
Psoriatic arthropathy can involve the small joints of the hands and feet but 🔹Elbow, shoulder, hip and spine are not commonly
commonly affected.
🔹
can also cause a large effusion in a single joint.
🔹
affected.
🔹
🔹 Affects men and women equally and tends to run in families. Monoarticular involvement is rare.
The arthritis is not as clearly symmetrical as in RA and –it occurs mainly Involvement of soft tissue structures surrounding the
🔹
in the interphalangeal joints of the fingers and toes.
🔹 Definition
joint too occurs, eg the synovium, capsule, tendons,
Bone destruction may be so severe that the digits are completely flail or
🔹Lungs, pericardium, eyes, vessels and nerves are the
muscles,..
🔹
badly deformed (‘arthritis mutilans’). It is an autoimmune systemic disorder wherein the body defence
About one-quarter of the patients develop sacroiliac and vertebral mechanism identifies the normal tissue as antigen and evokes a
🔹Exact 🔹
other structures that can get involved.
🔹Age
🔹
changes. chain of inflammatory reaction resulting in destruction. 20-40 yr.
🔹 HLA-B27 occurs in about 60% of those with overt sacroiliitis. Etiology M:F ratio is 3:1
Beware of the patient with psoriasis who has a swollen joint without cause is not known. Following factors are considered as
🔹
obvious explanation: operation is unlikely to be helpful. triggering factors.
Treatment is similar to rheumatoid arthritis, but the condition is seldom a. Chronic infection —bacterial, fungal or viral. Pathology
as severe. b. Environmental factors —polluted atmosphere, smoking, etc. Although tissues throughout the body are affected, the brunt of the attack falls on
c. Genetic factors —HLA with DR4 specificity is observed.
🔹
synovium.
🔹
d. Endocrinal factors. The pathological changes, proceed in four stages:
e. Poor quality food with constant assault on the gut. ■■ Stage 1: preclinical: well before RA becomes clinically apparent the immune
🔹
pathology is already beginning.
■■ Stage 2: synovitis: synovial membrane becomes inflamed and thickened, giving
🔹
rise to a cell rich effusion.
■■ Stage 3: destruction:persistent inflammation causes joint and tendon destruction.
🔹
Articular cartilage is eroded.
■■ Stage 4: deformity:the combination of articular destruction, capsular stretching
and tendon rupture leads to progressive instability and deformity.
Reiter’s disease and reactivearthritis
🔹 Reiter’s disease is acquired through sexual contact or as a sequel to
dysentery and includes the following features:
Clinical Features
Systemic features start insidiously with low grade fever, malaise, fatigue and
🔹
Extra-articular features
The most characteristic extra-articular lesion is the rheumatoid nodule, a small
1. Conjunctivitis.
🔹
joint pains.
The joints are swollen edematous, warm, tender with effusion and the
granuloma occurring under the skin (especially over bony prominences), on tendons,
2. Urethritis.
🔹
3. Synovitis.
🔹
movements are painful and limited.
Early morning stiffness is characteristic. Synovial thickening is
🔹
in the sclera and in viscera.
Other systemic features are lymphadenopathy, vasculitis, muscle weakness and
🔹
The condition can affect any joint but the small joints of the hands and feet
are most often involved. A number of conditions usually associated with seronegative polyarthritis 🔹
appreciable.
Subcutaneous nodules may be palpable.
🔹 brain and gastrointestinal tract.
visceral disease affecting the lungs, heart, kidneys,
🔹
🔹🔹
Large joints such as the knee are affected less often. (i.e. without serum RFs)
The diagnosis should be considered in any patient, especially men, with these may show changes in the spine and sacroiliac joints
🔹
symptoms.
TreatmentThe condition usually resolves spontaneously but anti-
inflammatorydrugs are helpful.
The best defined of these conditions are:
-psoriatic arthritis.
-Reiter’s disease.
-Arthritis that sometimes accompanies ulcerative colitis or Crohn’s disease;
🔹
Ankylosing spondylitis.
The exact relationship between these disorders is unknown, but
they share certain important features:
Seronegative spondarthritis
(1) the characteristic spondylitis and sacroiliitis occur in all of them.
(2) they are all associated with HLA-B27.
(3) they show familial aggregation.
(4) there is considerable overlap within families, some members having one
disorder and close relatives another
🔹 X-rays
The cardinal sign – and often the earliest – is erosion and
🔹
fuzziness of the sacroiliac joints.
The earliest vertebral change is flattening of the
🔹
X-rays
normal anterior concavity of the vertebral body
🔹
(‘squaring’).
🔹 In the early stages diffuse rarefaction is the only finding.
🔹
Later, ossification of the ligaments around the Later other changes develop such as
Investigations
intervertebral discs produces delicate bridges
🔹
🔹 🔹 • Narrowing of the joint space.
🔹
Hb%—may be low.
🔹
(syndesmophytes) between adjacent vertebrae. • Destruction of the articular surfaces.
Bridging at several levels gives the appearance of a
‘bamboo spine’. 🔹
🔹
TC—leukocytosis.
DC—neutrophil> in the early acute phase & lymphocytes > in chronic phase.
🔹 • Subchondral sclerosis.
• Subchondral cysts.
🔹
🔹
ESR—elevated.
CRP—elevated. It is nonspecific and only suggests that there is active inflammation.
ANA—when positive suggests sensitization has occurred and autoimmunity has
🔹
developed. (Normal titer is 1:40. Higher titer indicates presence of autoimmunity).
RA factor—positive in 80% of the patients. > 20 IU/ml is considered positive. Neither of
Ankylosing spondylitis 🔹
these tests is specific and neither is required for a diagnosis of RA.
🔹
CCP (Citruline antibody)—elevated. It is more sensitive than RA factor. Can be positive
Ankylosing spondylitis is essentially a even when RA factor is negative.
disease of the spine but it also involves the
large joints, such as hip, knee and shoulder. The
disease is commoner in men than women by 6 : 1
and usually presents between the ages of 15
and 30 years.
Diagnosis
Treatment consists of
anti-inflammatory drugs
Rheumatoid Arthritis
🔸
🔸 The diagnosis of rheumatoid arthritis is essentially clinical.
The minimal criteria for diagnosing RA are:
🔹
and physiotherapy.
Cervical and lumbar
osteotomy may be needed
(1) bilateral, symmetrical polyarthritis, involving
(2) the proximal joints of the hands or feet,
🔶 Rheumatoid arthritis – differential diagnosis All three
(3)present for at least 6 weeks. If, in addition, there are subcutaneous nodules or periarticular
🔹
for late deformities.
Joint replacement is 🔸
erosions on x-ray, the diagnosis is certain.
A useful screening tool is the inclusion of one or more of the following:
🔸
patients presented with painful swollen fingers. In:
🔸 (a) mainly the proximal joints were affected (rheumatoid arthritis);
often unsuccessful
because the new joints also
1. Morning stiffness > 1 h.
2. Swelling (synovitis).
🔸 (b) in the distal joints were the worst (Heberden’s osteoarthritis)
(c) in there were asymmetrical nodular swellings around the joints
become ankylosed. 3. Characteristic distribution of joints.
4. ESR 20 mm/h.
🔸Swollen finger joints:
(gouty tophi).
Proximal joints = inflammatory arthritis.
5. Nodules.
Distal joints = osteoarthritis.
6. Positive laboratory tests.
🔹 Juvenile idiopathic arthritis (JIA) is the preferred term for non-infective inflammatory
7. Radiographic findings – erosions of hands and feet.
8. Non-steroidal anti-inflammatory drugs are beneficial.9. First degree relative with inflammatory joint
🔹
joint disease of more than 3 months’ duration in children under 16 years.
It embraces a group of disorders in all of which pain, swelling and stiffness of the joints are
disease.
🔹
common features.
The prevalence: is about 1 per 1000 children, and boys and girls are affected with equal
🔹
frequency
The cause: is probably similar to that of rheumatoid disease: an abnormal immune response
Complications Of R.A
🔸 Infection:
🔹
to some antigen in children with a particular genetic predisposition, However, RF is usually absent.
The term juvenile chronic arthritis includes Still's disease and a number of less well - defined
conditions, some of which may be monoarticular or may have minimal joint involvement — so –
Patients with RA – and even more so those on corticosteroid therapy – are susceptible to
infection. Sudden clinical deterioration, or increased pain in a single joint, should alert one to
🔸
the possibility of septic arthritis and the need for joint aspiration.
🔹
called pauciarticular .
🔹 The onset is often insidious, but may be acute.
Fever, lymph gland involvement and anaemia are usually present in addition to the joint pains
Tendon rupture:
Nodular infiltration may lead to tendon rupture. This is seen most often at the wrist, where it
🔸Joint rupture
contributes significantly to the development of the characteristic rheumatoid deformities.
🔹
and stiffness.
🔹 Uveitis occasionally occurs.
Occasionally the joint lining ruptures and synovial contents spill into the soft tissues. Treatment
🔹 The main joints affected are the knees, ankles, wrists and occasionally the spine.
The degree of pain varies, children occasionally presenting with chronically swollen joints
Juvenile idiopathic arthritis
is directed at the underlying synovitis – i.e. splintage and injection of the joint, with
🔸
which are painless and functioning normally synovectomy as a second resort.
Secondary osteoarthritis
Articular cartilage erosion may leave the joint so damaged that, even if the rheumatoid disease
Deformities occur, as in the adult form, and there is a more subsides or is kept under control, the end stage will be very similar to advanced osteoarthritis.
marked tendency to ankylosis, especially in the cervical spine.
🔹
Treatment
The same local and general measures are
Epiphyseal growth may be disturbed.
🔶Conservative measures in rheumatoid arthritis:
🔹
needed as in the adult. 1. Drugs.
🔸
Physiotherapy is important in maintaining -Non-steroidal anti-inflammatory drugs:
joint movements, particularly when the disease Non-steroidal anti-inflammatory drugs. These are the first line of treatment and include aspirin, ibuprofen,
🔹 Surgery is rarely needed,
is beginning to settle.
🔸
naproxen, etc.
🔸 Patients may require steroids taken orally, or injected into affected joints in severe cases.
These drugs help modify joint pain and inflammation.
🔸🔸These
-Second line drugs or disease-modifying antirheumatic drugs (DMARDS):
May help prevent joint destruction and subsequent deformity.
🔸
🔸 Crystals can be deposited in joints or soft tissue because of a metabolic abnormality.
The accumulation of crystals probably begins in infancy but is not usually apparent 🔸
slow-acting drugs may take months to become effective and are often used for long periods of time,
sometimes years.
These DMARDS may promote remission, and they are often used in combination and together with first line
🔺added from chat Gbt
🔸
until the third or fourth decade
Deposits of crystals in and around joints often remain asymptomatic but they can also
cause two types of arthritis:
🔸
drugs.
Second-line drugs include quinine, sulfasalazine, gold, penicillamine or immunosuppressive therapies such
1. Acute self-limiting attacks of inflammation. 🔸
as methotrexate, azathioprine and cyclophosphamide.
Newer drugs aim to block the production of the inflammatory mediators such as tumor necrosis factor
🔸
2. Chronic destructive joint disease.
Gout and its imitators form a group of conditions characterized by the presence of
(antiTNF) and interleukin-1.
2. Rest during an attack and mobilization during remission:
🔸
crystals in and around the joints, bursae and tendons.
Three clinical disorders in particular are associated with this phenomenon:
🔸
-Rest and immobilization
■ Gout: urate crystal deposition disorder. Affection Of The Splintage and rest will also reduce the swelling of joints and it can induce remission of the disease in an
🔸The aim of treatment is to:
Treatment
🔸
acute attack.
■ Pseudogout: calcium pyrophosphate dihydrate (CPPD) deposition disease.
■ Basic calcium phosphate (BCP) deposition disease. Joints Control synovitis and pain. 🔸 Rest may require admission to hospital.
Restoration of joint movement by physiotherapy when the attack has passed is essential.
Arthritis Maintaining joint function.
🔹
clinic picture
The disease is chronic, but characterized by acute attacks in which the 🔸
Prevention of long-term deformities.
A multidisciplinary approach between rheumatologists, orthopaedic surgeons and 🔸
3. Aids and appliances:
🔸 Patients with rheumatoid arthritis need a host of appliances.
Sticks, frames and crutches take the weight of lower limbs; splints and braces protect painful joints from
affected joints, usually single, become severely painful, swollen, often red and physical therapists is often necessary.
🔹
impossible to move. unnecessary movement; and soft protective footwear relieves the pressure on vulnerable skin.
🔹
🔹
This usually settles spontaneously in less than 3 weeks.
The joint may be gradually damaged by repeated attacks.
Other features include the formation of gouty tophi —collections of urate 🔶 Operative treatment:
crystals in the soft tissues, especially in the ear lobes, hands and feet. Operative treatment may be required for three reasons, but only if medical
treatment has failed.1. To remove inflamed synovium by synovectomy.2. To
🔸 The most useful investigation is the serum
repair damaged soft tissue.3. To salvage destroyed joints.
uricacid, which is usually well above normal,
although occasionally isolated readings may be
Gout
🔸 🔸
Surgery in rheumatoid arthritis.
🔸Synovectomy.
🔸
This is a metabolic disease characterized by the deposition of Tendon repair.
🔸
within normal limits.
🔸Arthrodesis.
urates in the tissues, hyper - uricaemia and, in about 10% of cases,
The X - ray appearance may be typical, with
well -demarcated, rounded erosions close to the 🔸
increased excretion of uric acid in the urine.
It is a common disease, affecting men in 95% of cases and post -
Arthroplasty
🔸
joint margins, usually in the hands.
🔸 Joint destruction maybe seen later. 🔸
menopausal women.
The arthritis usually affects the distal joints of the hands and Crystal arthropathies
🔸
The most useful investigation is the serum feet, and the knees.
uricacid, which is usually well above normal, Osteoarthritis (OA) is a chronic joint disorder in which there is progressive softening and disintegration of
It particularly (and characteristically)affects the articular cartilage accompanied by new growth of cartilage and bone at the joint margins (osteophytes), and
although occasionally isolated readings may be metatarsophalangeal joints of the great toes.
within normal limits.
🔹
capsular fibrosis.
🔹 It is defined as primary when no cause is obvious,and secondary when it follows a demonstrableabnormality 🔺 The basic difference in joint destruction
Treatment 🔹
🔹
The condition is the result of degenerative changes taking place in the joint. occurring inRheumatoid arthritis and
🔸
The articular cartilage and the subchondral bone progressively degenerates. Osteoarthritis is that, in rheumatoid arthritis:
Two drugs are useful for treating the acute attack:
1 Colchicine, which is very specifi c and may be used as a therapeutic test. It 🔹 This results in inflammation and mechanical derangement which promotes further degeneration.
Ultimately results in badly deranged joint,associated with deformityand ligamentous laxity.
inflammation occurs first. The joint destruction
that follows is the result of inflammation. Whereas
in Osteoarthritis: the joint destruction occurs
by fatema okoff is, however, toxic and unpleasant to take. Types
🔸
2 NSAIDs, such as indometacin or diclofenac, are usually effective.
Many patients are also treated with a drug such as allopurinol which lowers
a. Primary osteoarthritis Is the type where there is no preexisting abnormality or damage (incongruity) as a
cause for progressive degeneration. secondary to joint destruction. 🔺
first and the inflammation that follows is
🔸
the serum uric acid in the anticipation of preventing further attacks. b. Secondary osteoarthrit
Nevertheless, acute attacks may be precipitated by allopurinol or is Is the type where there is a preexisting pathology or damage (incongruity) which is responsible for the
probenecid if given without NSAID cover progressive degeneration.
Primary
With advancing age the proteoglycan content of the articular
cartilage decreases thereby reducing the water content of the
Pseudogout
🔸 This is a condition, similar to gout, but is usually less acute, and
the crystals deposited in the affected joint are of calcium
cartilage.
Such a cartilage becomes less resilient and cracks during activities
of daily living.
🔸
pyrophosphate rather than uric acid.
Both pyrophosphate and hydroxyapatite deposition may follow
either local or systemic disorders and be associated with acute
This is responsible for the onset and progression of degenerative
process.
It starts innocuously in the beginning, progresses slowly over a
🔸
inflammatory synovitis or chronic joint destruction.
A common feature is calcification of the menisci of the knees,
although this is rather non -specific.
period of time and then becomes severe.
Secondary
🔹
There is usually evidence of osteoarthritis.
🔹
No specific treatment is known, but NSAIDs are usually There is a joint incongruity which has developed due to some disease in the past.
helpful in relieving symptoms. Thus degeneration occurs secondary to a pre-existing mechanical abnormality.This is secondary
osteoarthrosis.
Secondary causes of osteoarthritis include:
1 Fractures (especially intra - articular injuries).
2 Joint infection.
🔹 This is known by various names as acute pyogenic arthritis, acute septic arthritis,
3 Inflammatory joint disease.
4 Congenital joint abnormalities.
🔹
acute pyoarthrosis and acute infective arthritis.
🔹 It refers to presence of pus in the joint secondary to infection of the joint.
Osteoarthritis
5 Joint instability.
6 Cartilage damage.
🔹 Age of onset—common in infants and children can occur at any age.
🔹 Sex—M:F 🔹
7 Obesity
🔺
ratio 5:1 Weight - bearing joints, especially the hip and theknee, are most frequently affected.
Site—Any joint. Common in hip and knee. Osteoarthritis, once established, is usually a progressive disorder.
🔹 Septic arthritis can arise in three ways:
1. Spread from an infected bone.
Rarely, a patient presents with widespread osteoarthritic changes in many joints. This is sometimes
an inherited condition.
2. Direct infection from a penetrating wound.
🔹
3. Bacteraemia. Diagnosis
Organism Clinical Features It is not difficult.
Staphylococcus aureus 90%, Streptococcus, H. influenzae,E. coli, Proteus, etc. are A. Pain is the primary feature of osteoarthritis. It is gradual in onset and slowly Clinical features and X-rays confirm the
🔹
responsible in remaining 10% of the patients. progressing in severity. There can be pain free intervals too. diagnosis.
Focus of infection—spreads from the synovium or fromthe bone B. Swelling and joint effusion.Swelling in osteoarthritis is due to effusion.
C. Limitation of movement.Painful limitation of movement is a late feature of Radiological Findings
O.A. In the early phase the joint movements are associated with pain but not • Narrowing of the joint space (due to loss
Pathology limited. of articular cartilage.)
Once the infection gets into the joint there is seropurulent exudate formation. The D. Heberden’s nodes and Bouchard’s nodes. These are nodular formation • Sclerosis of the subchondral bone.
articular cartilage gets destroyed very rapidly due to the enzymatic degradation occurring in the DIP and PIP joints respectively in osteoarthrtis. • Subchondral cysts.
resulting from the enzymes released from the bacteria as well as from the inflamed E. Deformitytends to develop as a result of more severe destruction of the • Osteophytes (the bony excrescenceor
synovium and inflammatory cells. underlying bone surface, especially at the knee and the ankle. outgrowth, usually branched in shape)•
The subchondral bone gets exposed and later gets eroded too. Deformities.
If the pus is not drained surgically, a sinus develops.
Sequel depends on the speed at which the infection is controlled.
If the infection is controlled before the destruction of the cartilage, the joint becomes
normal. No residual deformity is seen.
🔹
Management
Non - operative
The condition is a slowly progressive and painful one, and most patients can be managed
After some destruction of cartilage, the joint goes in for fibrous ankylosis.After conservatively for many years.
considerable destruction of cartilage, the joint goes in for bony ankylosis. 1-Analgesics are usually the mainstay of treatment.Anti - inflammatory analgesics are of less
If the infection takes natural course then bony ankylosis with deformity is the result. help in osteoarthritis than in rheumatoid arthritis.
2-Protection of the joint, e.g. the patient may benefit by losing weight, and a stick, splint or
other support may be helpful.
Diagnosis 3-Change of life style, such as a more sedentary job.
Diagnosis is mainly on clinical grounds. 4-Physiotherapy, i.e. intermittent heat treatment or short - wave diathermy, with supervised
Signs of acute infection, i.e. calor, rubor, dolor, tumor with painful exercises to maintain movements.
immobile joint. Signs of systemic toxicity such as high grade fever
with delirium may also be present.
Investigations such as TC, DC, ESR, CRP, ultrasound, X-ray, MRI are
Acute Suppurative Arthritis
🔹 Surgical (Operative) Management
It is done late in the course of the disease when the joint isdegenerated and clinically
useful and should be done as per indication. associated with pain and deformity.
-Total joint arthroplasty is the treatment of choice .In selective cases osteotomies can be
done.
🔺
Treatment
Emergency surgical drainage of the joint of pus and debris under cover of systemic
antibiotics is the treatment of choice.
-Osteotomy alters the line of weight bearing and distribution of stress and is known to give
relief, e.g. high tibial osteotomy.
-Arthroscopic lavage and excision of loose bodies is donein high risk patients who are not
Continuous irrigation and suction can be employed for achieving good control of infection. fit for joint replacementsurgery. This procedure gives temporary relief.
Immobilization is essential till control of infection is achieved. This is followed by gradual
mobilization as early as possible to avoid stiffness of the joint.
Systemic antibiotics are used for considerable period to get rid of any residual focus of infection
depending on the organism isolated in culture and its antibiotic sensitivity
Arthrodesis is the treatment of choice for unsound ankylosis.
In selected cases of hip and knee ankylosis with no reactivation of the disease, total joint
arthroplasty can be considered.
This procedure considerably reduces the morbidity
Neonatal septicaemia causes widespread septic
arthritis.
Once common, and known as Tom Smith’s arthritis, the
condition is now rare in developed countries but is
sometimes seen after exchange transfusion and invasive
procedures on the newborn.
Prompt and early attention with an accurate diagnosis
followed by drainage of pus under antibiotic cover may Neonatal
reduce the morbidity septicaemia
