Inflammatory & infective arthritis
Rheumatoid arthritis (RA)
This is the most common form of inflammatory arthritis, affecting 3% of women and 1% of men. RA is a symmetrical, deforming polyarthritis. The disease process is a cell-mediated (mononuclear cells) immune response within the synovium of joints, leading to inflammation and destruction initially of the peri-articular soft tissues and later cartilage and bone. Inflammatory mediators, including cytokines (particularly IL-1 and TNF-alpha) and lymphokines, initiate a destructive cascade within the joint, degrading the cartilage and damaging surrounding tissues. Inflamed synovium has a proliferation of blood vessels forming the ‘pannus’ which invades the joint and further damages the cartilage.
Clinically, this manifests as insidious onset of joint swelling and nodules with associated stiffness, followed by joint pain with radiographic changes of erosive joint narrowing and destruction with periarticular osteopenia +/- subluxation or dislocation. X-ray changes are commonly seen at MCPJs, PIPJs and carpal bones of hands, wrists, cervical spine, knees and hips (the latter commonly with protrusio = medial deepening of acetabulum).
Laboratory tests include:
Systemic manifestations include:
Diagnostic criteria from the American College of Rheumatology include morning stiffness, joint swelling, arthritis of joints of the fingers lasting >6 weeks, nodules, positive laboratory results and specific X-ray findings (see above).
Common hand signs include:
Synovitis leading to attenuation of finger stabilising structures, causing:
Boutonnière deformity - proximal interphalangeal joint (PIPJ) flexion with distal interphalangeal (DIPJ) hyperextension
Swan-neck deformity - PIPJ hyperextension with DIPJ flexion
Metacarpo-phalangeal joints (MCPJ) ulnar and volar deviation and subluxation
Tenosynovitis of hands and wrist tendon sheaths (leading to swelling, pain and stiffness and eventually tendon rupture)
Rheumatoid wrist with tenosynovitis eventually leading to tendon subluxation, combined with joint destruction causing:
Carpus subluxation in a volar and ulnar direction
Dorsal subluxation of the ulnar head (caput ulnae)
Management
The goals are:
Treatment is in a multidisciplinary setting and includes therapeutic drugs, physiotherapy (to maintain joint range of motion and strength), occupational therapy (for splints and functional aids) and occasionally surgery.
Drug therapy used to start with NSAIDs and then progress to antimalarials, remittent agents (sulfasalazine, gold and penicillamine), steroids and cytotoxic drugs. Recently, rheumatologists have shown the benefit from treating much earlier in the disease process
with new disease-modifying anti-rheumatic drugs (DMARDs). These include methotrexate, azothioprine and TNF-alpha inhibitors (including infliximab and etanercept).
Surgery, in the form of synovectomy and joint replacement, has become increasingly rare due to this more aggressive therapeutic regime. Patients requiring surgery under general anaesthetic require evaluation of cervical spine stability with pre-operative radiographs. Most DMARDs are halted a few weeks prior to surgery. Surgery now is predominantly for hand tendon repair or re-routing, finger and wrist joint replacement or fusion and total knee or hip replacement.
This is the most common form of inflammatory arthritis, affecting 3% of women and 1% of men. RA is a symmetrical, deforming polyarthritis. The disease process is a cell-mediated (mononuclear cells) immune response within the synovium of joints, leading to inflammation and destruction initially of the peri-articular soft tissues and later cartilage and bone. Inflammatory mediators, including cytokines (particularly IL-1 and TNF-alpha) and lymphokines, initiate a destructive cascade within the joint, degrading the cartilage and damaging surrounding tissues. Inflamed synovium has a proliferation of blood vessels forming the ‘pannus’ which invades the joint and further damages the cartilage.
Clinically, this manifests as insidious onset of joint swelling and nodules with associated stiffness, followed by joint pain with radiographic changes of erosive joint narrowing and destruction with periarticular osteopenia +/- subluxation or dislocation. X-ray changes are commonly seen at MCPJs, PIPJs and carpal bones of hands, wrists, cervical spine, knees and hips (the latter commonly with protrusio = medial deepening of acetabulum).
Laboratory tests include:
- Raised CRP and ESR
- Rheumatoid factor (Immunoglobulin M) - +ve in 80% of patients
- HLA-DR4 - +ve in 70% of patients
Systemic manifestations include:
- Vasculitis
- Pericarditis
- Pulmonary fibrosis
- Felty's syndrome (RA with splenomegaly and leukopenia)
- Still's disease (acute onset juvenile RA with fever, rash and splenomegaly)
- Sjögren's syndrome (autoimmune exocrinopathy often associated with RA leading to lymphoid proliferation and decreased salivary and lacrimal secretion - keratoconjunctivitis sicca complex)
Diagnostic criteria from the American College of Rheumatology include morning stiffness, joint swelling, arthritis of joints of the fingers lasting >6 weeks, nodules, positive laboratory results and specific X-ray findings (see above).
Common hand signs include:
Synovitis leading to attenuation of finger stabilising structures, causing:
Boutonnière deformity - proximal interphalangeal joint (PIPJ) flexion with distal interphalangeal (DIPJ) hyperextension
Swan-neck deformity - PIPJ hyperextension with DIPJ flexion
Metacarpo-phalangeal joints (MCPJ) ulnar and volar deviation and subluxation
Tenosynovitis of hands and wrist tendon sheaths (leading to swelling, pain and stiffness and eventually tendon rupture)
Rheumatoid wrist with tenosynovitis eventually leading to tendon subluxation, combined with joint destruction causing:
Carpus subluxation in a volar and ulnar direction
Dorsal subluxation of the ulnar head (caput ulnae)
Management
The goals are:
- Control pain and synovitis
- Maintain joint function
- Prevent deformity
Treatment is in a multidisciplinary setting and includes therapeutic drugs, physiotherapy (to maintain joint range of motion and strength), occupational therapy (for splints and functional aids) and occasionally surgery.
Drug therapy used to start with NSAIDs and then progress to antimalarials, remittent agents (sulfasalazine, gold and penicillamine), steroids and cytotoxic drugs. Recently, rheumatologists have shown the benefit from treating much earlier in the disease process
with new disease-modifying anti-rheumatic drugs (DMARDs). These include methotrexate, azothioprine and TNF-alpha inhibitors (including infliximab and etanercept).
Surgery, in the form of synovectomy and joint replacement, has become increasingly rare due to this more aggressive therapeutic regime. Patients requiring surgery under general anaesthetic require evaluation of cervical spine stability with pre-operative radiographs. Most DMARDs are halted a few weeks prior to surgery. Surgery now is predominantly for hand tendon repair or re-routing, finger and wrist joint replacement or fusion and total knee or hip replacement.
Juvenile Rheumatoid Arthritis - see paediatric chapter
Systemic Lupus Erythatosus (SLE)
This is a chronic inflammatory disease of unknown origin probably related to immune complexes. It is common in Afro-Caribbean women. 75% patients have joint involvement with similar findings to rheumatoid arthritis, with acutely swollen, tender PIPJs, MCPJs, wrists and other joints.
Systemic findings:
Laboratory tests:
Management
Same as for rheumatoid arthritis, using the same multidisciplinary approach and drugs.
This is a chronic inflammatory disease of unknown origin probably related to immune complexes. It is common in Afro-Caribbean women. 75% patients have joint involvement with similar findings to rheumatoid arthritis, with acutely swollen, tender PIPJs, MCPJs, wrists and other joints.
Systemic findings:
- Fever
- Butterfly malar rash
- Pancytopenia
- Pericarditis
- Nephritis
- Polyarthritis
Laboratory tests:
- Raised CRP and ESR
- Antinuclear antibody (ANA) - usually +ve
- HLA-DR2 & 3 - +ve in ~50% of patients
- Rheumatoid factor - may be +ve
Management
Same as for rheumatoid arthritis, using the same multidisciplinary approach and drugs.
Polymyalgia rheumatica
Aching and joint stiffness, particularly around the shoulders and hips. Cause unknown. Associated with headache, malaise and anaemia. May have raised ESR, anaemia and raised alkaline phosphatase.
Treated symptomatically with NSAIDs and analgesia with steroids for severe cases.
Associated with temporal arteritis (requires urgent temporal artery biopsy and steroids to
reduce risk of blindness).
Aching and joint stiffness, particularly around the shoulders and hips. Cause unknown. Associated with headache, malaise and anaemia. May have raised ESR, anaemia and raised alkaline phosphatase.
Treated symptomatically with NSAIDs and analgesia with steroids for severe cases.
Associated with temporal arteritis (requires urgent temporal artery biopsy and steroids to
reduce risk of blindness).
Seronegative arthropathies
Characterised by -ve rheumatoid factor and +ve HLA-B27. Typically occur at ligament insertions into bone (enthesopathy) or spine (spondyloarthropathy).
Characterised by -ve rheumatoid factor and +ve HLA-B27. Typically occur at ligament insertions into bone (enthesopathy) or spine (spondyloarthropathy).
Ankylosing spondylitis (AS)
AS typically presents with insidious onset of back pain and morning stiffness with hip pain in males between 30-50 years of age. Bilateral sacroiliitis +/- anterior uveitis with a positive HLA-B27 is diagnostic. The condition progresses over several years with increasing spinal
rigidity and kyphotic deformity, eventually leading to the ‘chin on the chest’ position. Spine X-rays demonstrate obliteration of sacroiliac joints with squaring and fusion of vertebrae. The spine becomes one rigid, brittle column and is prone to fracture after trivial falls with a
high risk of epidural haemorrhage and neurological impairment.
Systemic findings:
Management
Hip pain and stiffness with spinal deformity often improve with bilateral total hip replacement. Clinicians must maintain a high degree of suspicion for spine fracture after injury - if in doubt, CT scan the whole spine. Spine fractures usually require fixation by a spinal surgeon in a specialist centre.
AS typically presents with insidious onset of back pain and morning stiffness with hip pain in males between 30-50 years of age. Bilateral sacroiliitis +/- anterior uveitis with a positive HLA-B27 is diagnostic. The condition progresses over several years with increasing spinal
rigidity and kyphotic deformity, eventually leading to the ‘chin on the chest’ position. Spine X-rays demonstrate obliteration of sacroiliac joints with squaring and fusion of vertebrae. The spine becomes one rigid, brittle column and is prone to fracture after trivial falls with a
high risk of epidural haemorrhage and neurological impairment.
Systemic findings:
- Iritis
- Aortitis
- Colitis
- Amyloidosis
- Sarcoidosis
- Pulmonary fibrosis and restricted chest excursion
- Heart disease
Management
Hip pain and stiffness with spinal deformity often improve with bilateral total hip replacement. Clinicians must maintain a high degree of suspicion for spine fracture after injury - if in doubt, CT scan the whole spine. Spine fractures usually require fixation by a spinal surgeon in a specialist centre.
Reiter's syndrome
This presents in young men with conjunctivitis, urethritis and oligoarthritis ("can't see, pee or bend the knee"!). It usually causes acute single joint swelling and pain (commonly knee), which may recur. Most are HLA-B27 positive and many chronic patients have
sacroiliitis. Rheumatoid factor is negative.
Treatment involves physiotherapy and NSAIDs/analgesia.
This presents in young men with conjunctivitis, urethritis and oligoarthritis ("can't see, pee or bend the knee"!). It usually causes acute single joint swelling and pain (commonly knee), which may recur. Most are HLA-B27 positive and many chronic patients have
sacroiliitis. Rheumatoid factor is negative.
Treatment involves physiotherapy and NSAIDs/analgesia.
Psoriatic arthritis
This commonly causes swelling and pain in the small joints of hands and feet, usually in young men. It affects between 5-10% patients with psoriasis and about half are HLA-B27 positive. Pitting is seen in fingernails with swollen "sausage" digits and DIPJ deformity and
erosion.
Treatment is similar to rheumatoid arthritis.
This commonly causes swelling and pain in the small joints of hands and feet, usually in young men. It affects between 5-10% patients with psoriasis and about half are HLA-B27 positive. Pitting is seen in fingernails with swollen "sausage" digits and DIPJ deformity and
erosion.
Treatment is similar to rheumatoid arthritis.
Crystal deposition disease
This presents with recurrent attacks of exquisitely painful single joint arthritis. It commonly affects the lower extremity, especially the great toe. Razor-sharp crystals form within the synovium, leading to inflammation and pain with eventual joint destruction due to mechanical wear.
Gout
A disorder of nucleic acid metabolism leading to hyperuricaemia and monosodium urate crystal deposition. Serum urate may be elevated but this is not diagnostic. Joint fluid microscopy shows intracellular crystals that are strongly negatively birefringent.
Treatment during acute attack is with indomethacin or other NSAIDs. Allopurinol (a xanthine oxidase inhibitor) is used to lower serum urate levels in chronic gout but stopped during acute flares.
Pseudogout
Calcium pyrophosphate crystal deposition due to a disorder of pyrophosphate metabolism can be mistaken for gout. Crystals are weakly positively birefringent under microscopy. Pseudogout may lead to chondrocalcinosis (deposition of calcium in cartilage) within joints, especially the knee.
Treatment is with NSAIDs symptomatically.
This presents with recurrent attacks of exquisitely painful single joint arthritis. It commonly affects the lower extremity, especially the great toe. Razor-sharp crystals form within the synovium, leading to inflammation and pain with eventual joint destruction due to mechanical wear.
Gout
A disorder of nucleic acid metabolism leading to hyperuricaemia and monosodium urate crystal deposition. Serum urate may be elevated but this is not diagnostic. Joint fluid microscopy shows intracellular crystals that are strongly negatively birefringent.
Treatment during acute attack is with indomethacin or other NSAIDs. Allopurinol (a xanthine oxidase inhibitor) is used to lower serum urate levels in chronic gout but stopped during acute flares.
Pseudogout
Calcium pyrophosphate crystal deposition due to a disorder of pyrophosphate metabolism can be mistaken for gout. Crystals are weakly positively birefringent under microscopy. Pseudogout may lead to chondrocalcinosis (deposition of calcium in cartilage) within joints, especially the knee.
Treatment is with NSAIDs symptomatically.
Septic arthritis
This must be suspected in any acutely swollen, painful and stiff joint and must be ruled out as an emergency. Infection within a joint rapidly kills cartilage, which if left to continue, can completely destroy a joint within hours.
Septic arthritis occurs following haematogenous spread or by extension of osteomyelitis and is common in children. Risk factors in adults include immunocompromise, diabetes mellitus, rheumatoid arthritis, intravenous drug users and previous invasive procedures into an infected joint.
Clinically the joint is hot, swollen, red with an effusion and the patient is in extreme pain with any active or passive movements. Suspicion is raised with fever, increased CRP, white cell count (specifically neutrophils in bacterial infection) and ESR. X-rays may be normal. Confirmation of diagnosis is by joint aspiration (under sterile conditions) with urgent Gram stain and microscopy (for organisms and crystals).
The most common organisms are Staphylococcus aureus, streptococci and Gram negative bacilli.
Management
This is with rapid diagnosis followed by urgent surgical joint debridement and washout. At the time of surgery, multiple tissue samples are sent for microscopy and culture prior to starting empirical antibiotic therapy dependent on local hospital antibiotic policy (usually a third generation cephalosporin +/- penicillinase resistant penicillin).
Once culture and sensitivities have been finalised, antibiotics may be altered as needed. Further joint washout and debridement may be required at 48-72 hours if joint pain and swelling is not improving. Antibiotics may continue for up to 6-8 weeks, dependent on the joint remaining quiescent and the return of all inflammatory markers and clinical signs to normal levels.
This must be suspected in any acutely swollen, painful and stiff joint and must be ruled out as an emergency. Infection within a joint rapidly kills cartilage, which if left to continue, can completely destroy a joint within hours.
Septic arthritis occurs following haematogenous spread or by extension of osteomyelitis and is common in children. Risk factors in adults include immunocompromise, diabetes mellitus, rheumatoid arthritis, intravenous drug users and previous invasive procedures into an infected joint.
Clinically the joint is hot, swollen, red with an effusion and the patient is in extreme pain with any active or passive movements. Suspicion is raised with fever, increased CRP, white cell count (specifically neutrophils in bacterial infection) and ESR. X-rays may be normal. Confirmation of diagnosis is by joint aspiration (under sterile conditions) with urgent Gram stain and microscopy (for organisms and crystals).
The most common organisms are Staphylococcus aureus, streptococci and Gram negative bacilli.
Management
This is with rapid diagnosis followed by urgent surgical joint debridement and washout. At the time of surgery, multiple tissue samples are sent for microscopy and culture prior to starting empirical antibiotic therapy dependent on local hospital antibiotic policy (usually a third generation cephalosporin +/- penicillinase resistant penicillin).
Once culture and sensitivities have been finalised, antibiotics may be altered as needed. Further joint washout and debridement may be required at 48-72 hours if joint pain and swelling is not improving. Antibiotics may continue for up to 6-8 weeks, dependent on the joint remaining quiescent and the return of all inflammatory markers and clinical signs to normal levels.
