CHAPTER 12: HAND - ARTHRITIS, DUPUYTREN'S, TUMOURS Flashcards
What is osteoarthritis?
What is the incidence and pathogenesis?
OA = degenerative arthritis
- 10% of adults over 50 have some OA
- X-ray evidence in almost everyone over 60
PATHOGENESIS
- Destruction of articular cartilage
- Sclerotic periarticular bone, +/- areas of porosity (cysts)
Mild synovitis and inflammatory joint effusions
- Idiopathic / after joint injury → joint instability, joint surgery, inflammatory joint disease
What is arthritis?
How is it classified?
Arthritis = joint disease associated with inflammation
Degenerative Arthritis
- Erosive arthritis → Osteoarthritis
Inflammatory Arthritis
- Rheumatoid arthritis
- Psoriatic arthritis
- Gout
- Pseudogout
- Systemic lupus erythematosus (SLE)
Infective Arthritis
- Septic arthritis
How is osteoarthritis classified?
Swanson Classification (JHS 1985) JSECS! I Joint narrowing II + Subchondral sclerosis, hypertrophic nodes III + Erosions IV + Cyst formation, deviation V + Dislocation or subluxation
What are the clinical features of OA?
- Most upper limb = DIPJ and basal joints of thumbs
- Pain, stiffness, ↓ movement
- Bony swelling (osteophytes), effusions, tenderness
- DIPJ bony swellings = Heberden’s nodes
- PIPJ = Bouchard’s nodes
What are the typical features on X ray?
- Narrow joint space
- Sclerosis
- Cyst formation within the bone underlying the joint
- Periarticular osteophytes
What is the treatment for OA?
Non Op → activity modification, splint, NSAIDs, Intra-articular steroids, Physio
Surgery - for
pain/stiffness/deformity/cosmesis
DIPJ → fusion
CMCJ → Arthrodesis/ Trapeziectomy, Osteotomy of base of 1st MC, Ligament reconstruction. (Trap can be replaced by nothing, implant, rolled FCR, or PL)
Arthrodesis e.g. index finger:
- MCP 25deg
- PIPJ 40deg
- DIPJ 15deg max
Techniques:
- 90/90 box wires
- Lister loop
- Tension band wiring (around x2 k-wires)
- Parallel K-Wires
Arthroplasty (next slide)
What are the risks of finger joint replacements?
Infection – 1%
Pain – This usually settles over the first week and is usually moderate.
Stiffness – Often the joint that is being replaced is very stiff. If this is the case the resultant movement after the operation will be limited. This is the most common complication in small joint replacements.
Swelling – The finger will remain swollen for 3 to 6 months
Nerve injury – Localised numbness around the wound may occur. It usually resolves with time.
Dislocation – This is a risk in the short term, before the tissues tighten. The risk is low, but if it does occur, a short anaesthetic is required to relocate the joint.
Loosening – This is the long term complication of the joint replacement and is almost inevitable. Once the joint is loose, it may become painful and swollen again. At that stage the majority of patients would have their replacement converted to a fusion. Hopefully though there have been many years of benefit!
What types of arthroplasty do you know?
Soft tissue and Perichondrial arthroplasty:
- Cartilage graft with/without silicone spacer
- Tupper arthroplasty MCPJ - volar plate into joint
- Volar plate arthroplasty for PIPJ - a different op to Tupper
Replacement Arthroplasty
- Pyrolytic Carbon - good for high demand hands i.e. OA as opposed to RA £800 each
- Swanson silastic spacer - low demand hands as wear out - £80 each. Good for MCP and PIP
- Neuflex - silicone implants with special hinges, less strain on implant, fingers are in more anatomical position
1 = unconstrained - complications: subluxation, dislocation, loosening, implant fracture and joint stiffness
2 + 3 = constrained hinge: loosening, fracture. Neuflex’s centre of rotation is more volar
How does psoriatic arthropathy present? What xray findings are there?
10% of pts with psoriasis
Clinically → DIPJs or whole finger (sausage finger)
X-ray → Joint surface erosions, Concave cup deformity of the distal phalanx surface and convex pencil deformity of the middle phalanx (pencil in cup deformity)
What is gout and pseudo gout?
♂>♀ 8:1
Gout → intra- and periarticular deposits of needle shaped crystals of monosodium urate monohydrate → inflammatory arthritis.
Pseudogout → Calcium pyrophosphate deposits.
Hyperuricaemia – Primary or Secondary
Primary → ↑ intake (red wine and meat), enzyme abnormality, ↓ excretion
Secondary → Diuretics (esp. thiazides), Myeloproliferative disorders.
How does gout present and what is the treatment?
Clinical Presentation
Acute gout → painful synovitis, red, inflamed, 90% self limiting, 60% affect 1st MTPJ, also wrists and fingers. Main DD = infection.
Chronic gout → tophi - sc nodules w crystals, may ulcerate through skin, erosive arthritis.
Diagnosis
- MUM crystals on polarised light microscopy (negative birefringence)
- High uric acid levels are NOT diagnostic
- X-ray → large punched out erosions away from the joint margin, soft tissue swelling.
Treatment
Acute → high dose NSAIDs, Colchicine
Chronic → Low purine diets, xanthine oxidase inhibitor → allopurinol, uricosuric drugs such as probenecid.
what is RA? Incidence and aetiology?
RhA is inflammation / expansile / invasive - 3 phases -
1. Proliferative
2. Destructive
3. Reparative (burnt out)
Originates in synovium (joints and tendons)
2% of population worldwide
♀>♂ 3:1
90% some hand involvement, 10% significant
? due to autoimmune reaction to agent within synovial tissue → interacts with IgG and IgM antibodies → synovial inflammation.
70% rheumatoid factor +ve (IgG / IgM)
How is RA hand disease classified?
Monoarthropathy → single joint Pauciarthropathy → 2-4 joints Polyarthropathy → over 4 joints or Monocyclic disease → one attack Polycyclic disease → recurrent attacks Progressive disease → chronic worsening disease
What is the 1987 American College of Rheumatology classification
criteria for rheumatoid arthritis?
1-4 >6wks
- Morning stiffness of >1 hour most mornings
- Arthritis and soft-tissue swelling of >3 of 14 joints/joint groups
- Arthritis of hand joints
- Symmetric arthritis
- Subcutaneous nodules in specific places
- Rheumatoid factor at a level above the 95th percentile
- Radiological changes suggestive of joint erosion
At least four criteria have to be met for classification as RA.
What are the 3 clinical stages of RA?
What changes are seen in the bones and cartilage?
- Proliferation → synovial swelling and pain
- Destruction → erosion of tendon, bone and joint
- Reparation → ↓ synovial activity and fibrosis – burn-out.
Bone Disease in RA
- Sclerotic
- Lytic
- Mutilans
Cartilage Destruction in RA
- Articular Lysosomes
- Free radicals from neutrophils - damage
- Inhibition of cartilage production
What is the 2010 American College of Rheumatology/European League Against Rheumatism classification
criteria for rheumatoid arthritis?
Target population : Patients who
1) have at least 1 joint with definite clinical synovitis (swelling)
2) with the synovitis not better explained by another disease
Classification criteria for RA
Cutoff score for RA is 6/10
A. Joint involvement
1 large joint = 0
2 - 10 large joints = 1
1 - 3 small joints (with or without involvement of large joints) = 2
4 - 10 small joints (with or without involvement of large joints) = 3
>10 joints (at least 1 small joint) = 5
B. Serology (at least 1 test result is needed for classification)
Negative RF and negative ACPA = 0
Low-positive RF or low-positive ACPA = 2
High-positive RF or high-positive ACPA = 3
C. Acute-phase reactants (at least 1 test result is needed for classification)
Normal CRP and normal ESR = 0
Abnormal CRP or abnormal ESR = 1
D. Duration of symptoms
=6 weeks = 1
ACPA = anticitrullinated protein antibody
What extra-articular manifestations of RA?
Eyes →
Iritis, Scleritis, uveitis,
Sjögren’s syndrome = dry eyes –keratoconjunctivitis sicca, xerostomia and RhA.
Nervous system →
Peripheral neuropathy , carpal tunnel + other nerve entrapment syndromes, cervical myelopathy, mono neuritis multiplex.
Haemopoietic syn →
Anaemia, Felty’s syn (RA, splenomegaly, neutropenia).
Heart → Pericarditis, myocarditis, pericardial effusions, valvular heart disease, conduction defects.
Lungs → Pleural effusions, nodules, fibrosing alveolitis, Caplan’s syndrome: RA + pneumoconiosis.
Kidneys→ Amyloidosis
Skin → vasculitic ulcers and rashes, pyoderma gangrenous,, pretibial lacerations Rh Nodules (20% of pts) esp. olecranon, thin skin due to steroids.
How do RA patients present?
- Joint or systemic symptoms
- Upper limb joints → elbow, wrist, MCPJ and PIPJ.
- Numbness, paraesthesiae, weakness.
- Record time period over which symptoms have occurred.
- Degree of functional impairment
What investigations are there for RA?
Blood → Rh factors, ACPA, CRP. X-ray → - Joint space widening (effusion) - then narrowing and ankylosis due to joint destruction. - Juxta-articular erosions, - Fusiform soft tissue swelling, - Periarticular bone cysts, - Generalised osteopenia.
What is the conservative treatment of RA?
Aim: induce remission with no active joint inflammation and no erosive or functional deterioration.
MDT
GP, rheumatologist, hand surgeon, nurse specialist, physiotherapist, occupational therapist, dietitian, podiatrist, pharmacist, and social worker
Steroid injections, physio, splints, activity modification
What is the medical treatment of RA?
Analgesics + Anti-inflammatories
- paracetamol, opiates
- NSAIDs
- COX-inhibitors (celecoxib, etoricoxib)
Corticosteroids
Non- biological DMARDS
- azathioprine, ciclosporin, d-penicillamine, hydroxychloroquine, leflunomide, methotrexate, mycophenolate mofetil (MMF), sulfasalazine
Biological DMARDS = cytokine modulators (used if patient resistant to methotrexate)
- Tumour necrosis factor (TNF) inhibitors: adalimumab (Humira), certolizumab pegol, Etanercept (Enbrel), golimumab, infliximab.
- Anti-interleukin-1 therapy: Anakinra (Kineret).
- T-cell co-stimulator modulator: abatacept.
- Anti-CD20 therapy: rituximab.
- Anti-interleukin-6 receptor therapy: tocilizumab.
What are the indications for surgery?
- Pain
- Loss of function
- Disease progression (Prophylactic surgery to prevent future deformity)
- Cosmesis
Deformity without loss of function is not an indication for surgery
NICE guidelines on referral for surgery
If failed non-surgical therapy:
- Persistent pain (from e.g. joint damage or other soft tissue cause).
- Worsening joint function.
- Progressive deformity.
- Persistent localised synovitis.
Refer people with complications for a specialist surgical opinion before damage or deformity becomes irreversible:
- Imminent or actual tendon rupture.
- Nerve entrapment (e.g. carpal tunnel syndrome).
- Any stress fracture.
Refer urgently for:
- Suspected or proven septic arthritis (especially in a prosthetic joint).
- Any symptoms or signs that suggest cervical myelopathy.
What are the principles of surgery?
- Best shot first
- Minimum intervention for maximal result
- Treat the patient, not the x-ray
- Midline, longitudinal incisions to allow repeat surgery
How should procedures be prioritised?
Flexors before MPs before Extensors
Start proximal then go distal - wrist is the key
Soutar’s Winners 1979 - Groups
I
Thumb MPJ fusion
Extensor synovectomy + excision ulna head
II
Flexor tendon synovectomy
MP joint arthroplasty
III
PIP joint fusion
Wrist stabilisation
IV
Correction of swan-neck deformity
MP & PIPJ synovectomy
Thumb IPJ fusion
V
PIPJ arthroplasty
Boutonniere correction
What wrist deformities are noted in rheumatoid arthritis?
Carpal supination (ulnar side of wrist dropped)
Volar translocation
Ulnar translation
Radial rotation
Caput ulnae = prominent ulnar head
What is ulnar shift vs ulnar drift?
Ulnar drift = ulnar deviation + ulnar shift
Ulnar deviation = ulnar rotation of the PP in relation to MC head
- can be normal (index is always ulnar deviated unless 1st dorsal interosseus is actively abducting finger)
- becomes abnormal when it cannot be corrected
Ulnar shift = ulnar translation of PP in relation to MC head
- is always pathological
In RA the MCPJ also develops volar dislocation / subluxation
What is ulnar shift vs ulnar drift?
Ulnar drift = ulnar deviation + ulnar shift
Ulnar deviation = ulnar rotation of the PP in relation to MC head
- can be normal (index is always ulnar deviated unless 1st dorsal interosseus is actively abducting finger)
- becomes pathological when uncorrectable.
Ulnar shift = ulnar translation of PP in relation to MC head, causing joint incongruity and eventual subluxation.
- is always pathological.
In RA the MCPJ also develops volar dislocation / subluxation
How do you correct extensor tendon rupture?
- Tends to occur in ulnar to radial direction
EDM EDC EI (ECU is protected) - Direct repair not normally possible
- Suture to adjacent tendon is best
- Both little and ring together → both to middle finger, or EIP to little and ring to middle.
- If all ruptured → FDS ring transferred from palm (Boyes transfer)
Describe the classic wrist deformity
Caput ulnae syndrome
- Volar subluxation of carpus
→ Volar subluxation of ECU + tendon swings around & acts more as flexor
- Supination of carpus
- Prominent ulnar (piano key sign)
- Dorsal swelling = synovial proliferation within ext compartments
Surgery
- Synovectomy
- extensor tendons
- DRUJ - ECRL to ECU transfer to correct radial deviation and carpal supination.
- Excision of distal ulna
- limited (Bowers)
- complete (Darrachs) + sling of extensor retinaculum can be used to support subluxed ECU tendon.
- segmental resection of distal ulna shaft and fusion of DRUJ (Sauve-Kapandji) - Wrist-Fusion
- radio-lunate (Chamay)
- radio-scaphoid
- total
- Intermetacarpal placement of Stanley pin (instead of through 3rd MC) to extend wrist for better grip, or
- Dorsal locking wrist plate (suitable for osteopenic bone).
What is Z deformity and why does it occur?
- When a joint adopts angulation in one direction, the next joint down/up adopts compensatory opposite angle
- Swan neck can be thought of as same in palmar/volar plane
How does flexor tenosynovitis present?
Pain on finger flexion ↓ range of finger movement Trigger finger Carpal tunnel syndrome Crepitus on finger flexion Synovial erosion → flexor tendon rupture.
Treatment → flexor synovectomy
- small nodules (rice bodies) may be found in flexor sheaths
- DO NOT RELEASE A1 PULLEY
How does flexor tenosynovitis present?
- Swelling proximal to wrist crease
- Pain on finger flexion
- ↓ active and passive ROM
- Trigger finger
- Carpal tunnel syndrome
- Crepitus on finger flexion
- Synovial invasion → flexor tendon rupture.
Treatment → flexor synovectomy
- small nodules (rice bodies) may be found in flexor sheaths
- DO NOT RELEASE A1 PULLEY
What is the commonest flexor tendon rupture and how do you treat it?
Mannerfelt lesion = FPL most common, attrition on scaphoid osteophytes.
- Reconstruction by direct repair / tendon graft / middle or ring FDS transfer or IPJ arthrodesis if joint is unstable or destroyed.
Fingers: rupture of
- FDP in palm → transfer distal stump to adjacent FDP.
- FDP in finger → arthrodese DIPJ + tenosynovectomy to preserve FDS.
- FDS → not usually noticed clinically → synovectomy to protect FDP.
- FDP + FDS → reconstruct FDP using FDS tendon graft.
What changes are observed at the MCPJs?
MCPJ synovitis → erodes through dorsal joint capsule → sagittal bands stretches & radial is thinnest therefore ulnar deviation + volar subluxation occurs.
Ulnar drift = ulnar deviation + ulnar shift
Factors for volar subluxation:
- Weak or stretched dorsal extensor expansion
- Dislocation of the extensors into valleys between MCs
- Detached or stretched collaterals
Factors for ulnar drift are:
1. Thumb pressure on index from key pinch
2. Intrinsic tightness
3. Pull of abductor digiti minimi
4. Ulnar inclination of MC heads
5. Radial deviation of the wrist causing compensatory ulnar deviation of MCPJs by Z
mechanism.
6. Ulnar deviating forces of flexor tendons
What are the surgical options of MCPJ treatment?
- Synovectomy
- Synovectomy
+ intrinsic release,
+/- crossed intrinsic transfer,
+ extensor tendon stabilisation. - Replacement Arthroplasty
What are the steps in MCPJ arthroplasty?
Swanson
- ‘a flexible hinge or a dynamic spacer’.
- Implant + capsule form new joint.
- Skin incision – longitudinal
- Through ulnar sagittal band, intrinsic release ulnarly
- Sagittal arthrotomy
- Excise MC head at metaphyseal flare (cutting block)
- Synovectomy
- Volar plate release from base of P1
- Reaming, broach
- Trials
- Drill dorsoradial MC for collateral reattachment radially
- Implant
- Reef radial sagittal band, Centralise and Radialise Extensor
- Close
What changes are observed in the PIPJ and what deformities result?
Synovial inflammation + proliferation → stretching of extensor mechanism → imbalance in extensor mechanism → swan neck or boutonnière deformity
What is a swan-neck deformity and what is the classification?
Hyperextension at PIPJ and flexion at DIPJ
Causes
- PIPJ volar plate rupture
- Attenuation of FDS (synovitis)
- Intrinsic tightness
- MCPJ subluxation
- Mallet deformity
Classification (Nalebuff 1989)
I PIPJ flexible in all positions
II PIPJ flexion limited in some positions
III PIPJ flexion limited in all positions
IV Stiff PIPJ with poor radiographic appearance
Surgery - depends on PIPJ mobility
- PIPJ flexible in all positions (I) → silver ring splint limiting extension or flexor tendoesis (FDS sling detached proximally and anchored to hold PIPJ in some flexion)
- PIPJ flexion limited (II+III) → intrinsic release, extensor tenolysis, capsulodesis or tenodesis.
- Stiff PIPJ, joint destruction (IV) → arthroplasty or arthrodesis.
