Dr.

Henry Pebruanto, SpOT

CURICULUM VITAE

EDUCATION UNDER-POST GRADUATE TRAININGS

 Medical Faculty of Udayana University, Denpasar – Bali; 2005
 Orthopaedic Training (Airlangga Univ., Sby/ Udayana Univ., Dps); Jan 12
 Overseas Observership Programme (Hip and Knee Arthroplasty): Perth – WA; Nov 10
 ASEAN Cadaveric Knee Course: Chiang Mai Univ. – Thailand; Apr 12.
 Australian Educational Program (Knee &Shoulder): Sydney – NSW; Jun 12
 ASEAN Cadaveric Knee Course: Bangkok – Thailand; May 14.
 ASEAN EASE (Express Arthroplasty and Arthroscopy Skills Education) Knee Course : Bangalore –
India; May 15.

COURSES
 Advanced Trauma Life Support (Denpasar – Bali); Jan 06
 Basic Orthopedic Skill Course (Surabaya – East Java); Aug 07
 Basic Surgical Skills Course (Surabaya – East Java); Jan 08
 Ultrasonography for Abdominal and Chest Trauma Course (Jakarta); Apr 08
 Total Nutritional Treatment Course (Tanah Lot – Bali); Dec 08
 Basic AO Trauma Course (Nusa Dua – Bali); May 09
 Bali Hand Course (Denpasar – Bali); Jul 09
 Post Graduate Course : Musculoskeletal Trauma (Jakarta); Nov 09
 8th Annual Meeting of Indonesian Spine Society & 1st International Society for Minimal
Intervention in Spinal Surgery (Denpasar – Bali); Jun 10
COURSES
 Workshop Hemiarthroplasty and Bone Substitute (Malang – East Java); Jun 10
 Ponsetti Course (Denpasar – Bali); Dec 10
 4th Arthroplasty Workshop : Jump Start on Total Knee Replacement (Jakarta); Apr 11
 3rd Arthroplasty Workshop : Jump Start on Total Hip Replacement (Jakarta); Apr 11
 AO Spine Principles Course (Jakarta); Jun 11
 Current Diagnosis and Comprehensive Treatment of Brachial Plexus Injury (Surabaya –
East Java); Oct 11
 3rd Pelvic and Acetabular Course and Workshop (Surabaya – East Java); Oct 11
 Lower Extremity Trauma Course (Denpasar – Bali); Jan 12
 RA ~ most common cause of chronic inflammatory
joint disease.
 Typical features :
 a symmetrical polyarthritis and tenosynovitis,
 morning stiffness,
 elevation of the erythrocyte sedimentation rate (ESR)
 appearance of autoantibodies (rheumatoid factor (RF)
and anti-citrullinated peptide antibodies (ACPAs)) in the
serum.

 Individuals with RA tend to die younger than their

peers as a result of the effects of chronic
inflammation on a number of organ systems.
 ~ Early ischaemic heart disease.
 Prevalence of RA ~ 1–2%,
 Peak incidence ~ 4th or 5th decades.
 Women (3x) > men.
 More common ~ in Caucasians
~ still incompletely worked out.
 Important factors :
 genetic susceptibility;
 an immunological reaction ~ focused on synovial
tissue;
 inflammatory reaction joints & tendon sheaths;
 the appearance of rheumatoid factors (RF) and anti-
citrullinated antibodies (anti-CCP or ACPA) in the blood
and synovium;
 perpetuation of the inflammatory process;
 articular cartilage destruction.
Genetic susceptibility
 RA is more common in first-degree relatives
 Human leucocyte antigen (HLA) DR4 ~ 70% of
people with RA
 HLA-DR4 is encoded in the major
histocompatibility complex (MHC) region on
chromosome 6.
 Strong associations between HLA-DR4 and RA.
The inflammatory reaction
 Marked proliferation of cells in the synovium, with new
blood vessel formation.
 Immune cells coordinate their action by the use of ‘short-
range hormones’ (cytokines)
 Activate inflammatory cells such as macrophages and B cells.
 Some cytokines (~chemokines) attract other inflammatory cells
to the area.
 Certain cytokines are important in RA.
 Tumour necrosis factor (TNF), interleukin-1 (IL-1) and
interleukin-6 (IL-6).
 The resulting synovitis, both in joints and in tendon sheath
linings, is the hallmark of early RA.
Rheumatoid factor
 B-cell activation  production of anti-IgG
autoantibodies, which are detected in the
blood as ‘rheumatoid factor’ (RF).
 Low levels of RF ~ ‘normal’ individuals
 Other autoimmune conditions such as SLE &
Sjögren’s syndrome ~ presence of RF.
 Anti-cyclic citrullinated peptide antibodies
(anti-CCP).
 Very specific for RA.
Chronic synovitis and joint destruction
 ~ associated with the production of proteolytic
enzymes, prostaglandins and the cytokines TNF
and IL-1.
 Immune complexes are deposited in synovial
joints  to augment the inflammatory process.
 ~ leads to depletion of the cartilage matrix and
damage to cartilage and underlying bone.
 Vascular proliferation and osteoclastic activity,
most marked at the edges of the articular
surface  cartilage destruction and periarticular
bone erosion.
 RA ~ systemic disease
 But the most characteristic lesions are seen in
the synovium or within rheumatoid nodules.
 The synovium is engorged with new blood vessels
and packed full of inflammatory cells.
JOINTS AND TENDONS
 The pathological changes proceed in four
stages (Figure 3.1)
 Stage 1: Pre-clinical
 Stage 2: Synovitis
 Stage 3: Destruction
 Stage 4: Deformity
JOINTS AND TENDONS
 The pathological changes proceed in four
stages (Figure 3.1)
 Stage 1: Pre-clinical
 Immune pathology is already beginning.
 Raised ESR, CRP and RF may be detectable years
before the first diagnosis.
JOINTS AND TENDONS
 The pathological changes proceed in four
stages (Figure 3.1)
 Stage 2: Synovitis
 Early changes are vascular congestion with new blood
vessel formation, proliferation of synoviocytes and
infiltration of the subsynovial layers by polymorphs,
lymphocytes and plasma cells (Figure 3.2).
 Thickening of the capsular structures, villous
formation of the synovium and a cell-rich effusion into
the joints and tendon sheaths.
 Painful, swollen and tender
 Structures are still intact and mobile,
 The disorder is potentially reversible.
JOINTS AND TENDONS
 The pathological changes proceed in four
stages (Figure 3.1)
 Stage 3: Destruction
 Articular cartilage is eroded
 by proteolytic enzymes, by vascular tissue of the
synovium, and direct invasion by a pannus of
granulation tissue
 At the margins of the joint, bone is eroded by tissue
invasion and osteoclastic resorption.
 Tenosynovitis
 Partial or complete rupture of tendons.
 Swelling of the joints, tendons and bursae.
JOINTS AND TENDONS
 The pathological changes proceed in four
stages (Figure 3.1)
 Stage 4: Deformity
 The combination of articular destruction, capsular
stretching and tendon rupture leads to progressive
instability and deformity of the joints.
 Mechanical and functional effects of joint and tendon
disruption now become vital.
EXTRA-ARTICULAR TISSUES
 Rheumatoid nodules
 ~ small granulomatous lesion consisting of a
central necrotic zone surrounded by a radially
disposed palisade of local histiocytes, and by
inflammatory granulation tissue.
 Nodules occur under the skin (especially over
bony prominences), in the synovium, on tendons,
in the sclera and in many of the viscera.
EXTRA-ARTICULAR TISSUES
 Lymphadenopathy
 mediastinal nodes can be affected.
 mild splenomegaly,
 due to hyperactivity of the reticuloendothelial
system.
EXTRA-ARTICULAR TISSUES
 Vasculitis
 Can be a serious and life-threatening
complication of RA.
 Nailfold infarcts
 Muscle weakness
 Common ~ due to a generalized myopathy or
neuropathy,
 Sensory changes ~ part of a neuropathy
 localized sensory and motor symptoms ~ nerve
compression by thickened synovium
 e.g. carpal tunnel syndrome
EXTRA-ARTICULAR TISSUES
 Visceral disease
 The lungs, heart, kidneys, gastrointestinal tract
and brain are sometimes affected.
 Ischaemic heart disease and osteoporosis are
common complications.
 In the early stages
 Polysynovitis, with soft-tissue swelling and
stiffness (Figure 3.3).
 Typically, a woman of 30–40 years ~ pain,
swelling & loss of mobility in the proximal joints
of the fingers.
 ~ ‘muscle pain’, tiredness, loss of weight and a
general lack of well-being.
 Classic feature ~ generalized stiffness after
periods of inactivity (especially after rising from
bed in the early morning).
 > 30 minutes.
 Physical signs ~ minimal
 Symmetrically distributed swelling and
tenderness of the MCPJ, the PIPJ and the wrists.
 Tenosynovitis is common in the extensor
compartments of the wrist and the flexor
sheaths of the fingers
 Thickening, tenderness and crepitation ~ wrist or
the palm while passively moving the fingers.
 Local warmth, synovial hypertrophy and intra-
articular effusion
 Movements are often limited.
 In the later stages
 Joint deformity
 The combination of joint instability and tendon
rupture produces the typical ‘rheumatoid’
deformities:
 ulnar deviation of the fingers,
 radial and volar displacement of the wrists,
 valgus knees,
 valgus feet and clawed toes.
 Joint movements are restricted
 Very painful.
 pain and stiffness in the cervical spine.
Extra-articular features
 Nodules
 found as small subcutaneous lumps,
 rubbery
 also develop in tendons ~ cause ‘triggering’ or rupture
(in the viscera and the eye).
 ~ pathognomonic of RA
 Less specific features :
 muscle wasting, lymphadenopathy, scleritis, nerve
entrapment syndromes, skin atrophy or ulceration,
vasculitis and peripheral sensory neuropathy.
X-rays
 Early ~ features of synovitis (soft-tissue
swelling and periarticular osteoporosis).
 Later ~ marginal bony erosions and narrowing
of the articular space, especially hands and
feet (Figure 3.4)
 Advanced ~ articular destruction and joint
deformity
 Flexion and extension views of the cervical spine
~ subluxation at the atlantoaxial or mid-cervical
levels
Ultrasound Scanning and MRI
 to look at soft-tissue changes and early
erosions within joints
 Ultrasound ~ presence of synovitis and early
erosions
 Vascularity ~ Doppler techniques
Blood investigations
 Normocytic, hypochromic
 ~ abnormal erythropoiesis
 aggravated by chronic gastrointestinal blood loss
caused by NSAIDs drugs
 ESR and CRP ~ raised.
 RF (+) ~ in about 80% of patients
 Antinuclear factors (+) ~ in 30%
 Anti-CCP antibodies ~ greater specificity but
at the expense of sensitivity.
Synovial biopsy
 via the arthroscope, or by open operation.

 non-specific.
 Criteria for diagnosing RA
 bilateral, symmetrical polyarthritis
 involving the proximal joints of the hands or feet
 persisting for at least 6 weeks.
 Subcutaneous nodules or X-ray signs of
periarticular erosions  the diagnosis is
certain.
 RF (+) in the absence of the above features is
not sufficient
 Chief value of the RF tests is in the assessment of
prognosis
 High titres ~ more serious
 Inthe differential diagnosis of polyarthritis
several disorders must be considered.
 Seronegative inflammatory polyarthritis
 Ankylosing spondylitis
 Reiter’s disease/reactive arthritis
 Polyarticular gout
 Calcium pyrophosphate deposition disease
 Sarcoidosis
 Lyme disease
 Viral arthritis
 No cure for RA.

 Medical treatment is guided by the principle

that inflammation should be reduced rapidly
and aggressively.

 Poor prognosis is associated with

 female sex, multiple joint involvement, high ESR
and CRP, positive RF and anti-CCP, younger age,
high BMI, smoking and the presence of erosions
at diagnosis.
PRINCIPLES OF MEDICAL MANAGEMENT
 Treatment ~ controlling inflammation as rapidly as
possible.
 Corticosteroids for their rapid onset
 initially oral doses of 30 mg of prednisolone or 120 mg i.m.
methylprednisolone
 Steroids should be rapidly tapered to prevent significant side
effects.
 Disease-modifying antirheumatic drugs (DMARDs) should
be started at this time.
 The first choice : methotrexate at doses of 10–25 mg/week.
 Alone or in combination with sulphasalazine and
hydroxychloroquine.
 Leflunomide
 if methotrexate is not tolerated.
 Gold and penicillamine ~ significant side effects and are
now used very rarely.
PRINCIPLES OF MEDICAL MANAGEMENT
 Control of pain and stiffness  NSAIDs
 Maintaining muscle tone and joint mobility 
exercise

 If there is no satisfactory response to DMARDs 

biological therapies such as
 TNF inhibitors
 infliximab, etanercept, golimumab, certolizumab and
adalimumab.
 Inhibitors of T-cell costimulation (abatacept),
 IL-6 (tocilizumab)
 B-cell depleting therapies (rituximab).
PRINCIPLES OF MEDICAL MANAGEMENT
 Injection of corticosteroid preparations into
inflamed joints and tendon sheaths.
 Injections ~ cause damage to articular cartilage
or tendons.
 Little evidence that they are harmful
 used sparingly and with full precautions against
infection.
 Prolonged rest and immobility ~ weaken
muscles and lead to a worse prognosis.
 Splinting can be helpful at any stage of the
disease.
PHYSIOTHERAPY AND OCCUPATIONAL THERAPY
 Preventative splinting and orthotic devices
 It is important to encourage activity.
 If these fail to restore and maintain function,
operative treatment is indicated.
SURGICAL MANAGEMENT
 Soft-tissue procedures (synovectomy, tendon
repair or replacement and joint
stabilization);
 Osteotomy may be more appropriate.
 Indications for reconstructive surgery :
 severe joint destruction, fixed deformity and loss
of function
 Types of reconstuction :
 arthrodesis,
 osteotomy and
 arthroplasty
Fixed deformities
 ~ due to joint contractures.

Muscle weakness
 ~ myopathy or neuropathy, when combined
with prolonged inactivity
 Prevented by control of inflammation,
physiotherapy and pain control
Joint rupture
 Treatment ~ underlying synovitis, i.e. splintage and
injection of the joint, with synovectomy.

Infection
 ~ susceptible to infection.
 possibility of septic arthritis  joint aspiration.

Spinal cord compression

 ~ complication of cervical spine (atlantoaxial)
instability.

 ~ immobilization of the neck is essential and spinal

fusion should be carried out as soon as possible.
Systemic vasculitis
 ~ rare but potentially serious complication.
 Corticosteroids and immunosuppressives such
as intravenous cyclophosphamide may be
required.

Amyloidosis
 ~ rare but potentially lethal complication
 Proteinuria and progressive renal failure.
 Finding amyloid in a rectal or renal biopsy
 Aggressive control of inflammation
 High titres of RF and anti-CCP, periarticular
erosions, rheumatoid nodules, severe muscle
wasting, joint contractures and evidence of
vasculitis are bad prognostic signs.
 Women ~ worse than men.

 10% of patients improve steadily

 60% have intermittent phases of disease activity
and remission
 20% have severe joint erosion (Figure 3.6)
 10% end up completely disabled.
 Reduction in life expectancy by 5–10 years
 due to premature ischaemic heart disease