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Not affiliated with the Royal Australasian College of Surgeons.

Rheumatoid Arthritis of the Hand

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Rheumatoid Arthritis of the Hand

Comprehensive guide to rheumatoid arthritis affecting the hand - pathophysiology, classification, medical and surgical management including synovectomy, arthroplasty, and arthrodesis

complete
Updated: 2025-12-24
High Yield Overview

RHEUMATOID ARTHRITIS - HAND

Inflammatory | Synovitis | Deformity | Multijoint

90%have hand involvement
3:1female to male ratio
70%RF or anti-CCP positive
2 yearswindow for DMARD efficacy

NALEBUFF THUMB DEFORMITIES

Type I
PatternBoutonniere (MCP flexion, IP extension)
TreatmentMCP arthroplasty
Type II
PatternSwan-neck (MCP extension, IP flexion)
TreatmentCMC/MCP fusion
Type III
PatternSwan-neck from CMC subluxation
TreatmentCMC stabilization

Critical Must-Knows

  • Ulnar drift from MCP radial collateral destruction + extensor subluxation
  • Boutonniere = PIP flexion + DIP extension (central slip rupture)
  • Swan-neck = PIP hyperextension + DIP flexion (volar plate laxity)
  • Medical optimization before surgery - stop methotrexate 2 weeks pre-op
  • Proximal-to-distal surgery - wrist before digits, correct deforming forces first

Examiner's Pearls

  • "
    RF positive 70%, anti-CCP more specific (95%) for RA diagnosis
  • "
    Caput ulnae syndrome = dorsal ulnar head prominence from DRUJ destruction
  • "
    Vaughan-Jackson lesion = EDM/EDC rupture from attrition on ulnar head
  • "
    Synovectomy only effective if done under 6 months of synovitis onset

Clinical Imaging

Imaging Gallery

There is extensive soft tissue calcinosis in the visualized portion of the distal forearm as well as within the dorsum of the right hand. There is also acro-osteolysis of the fingers with calcinosis i
Click to expand
There is extensive soft tissue calcinosis in the visualized portion of the distal forearm as well as within the dorsum of the right hand. There is alsCredit: Hsu V et al. via Clin. Rheumatol. via Open-i (NIH) (Open Access (CC BY))
AP view of right hand reveals flexion deformities, acro-osteolysis, and calcinosis of all five fingers. A representative sagittal CT image with bone windows and 3-D volume rendered CT of the third fin
Click to expand
AP view of right hand reveals flexion deformities, acro-osteolysis, and calcinosis of all five fingers. A representative sagittal CT image with bone wCredit: Hsu V et al. via Clin. Rheumatol. via Open-i (NIH) (Open Access (CC BY))
Oblique volume rendered 3-D CT, a single image from the coronal CT with bone windows, and an oblique radiograph of the left hand are shown: CT imaging shows better views of the extensive calcinosis su
Click to expand
Oblique volume rendered 3-D CT, a single image from the coronal CT with bone windows, and an oblique radiograph of the left hand are shown: CT imagingCredit: Hsu V et al. via Clin. Rheumatol. via Open-i (NIH) (Open Access (CC BY))

Critical RA Hand Exam Points

Ulnar Drift Mechanism

Radial collateral ligament destruction. Extensor tendon subluxates ulnarly. Intrinsics pull fingers into ulnar deviation. Progressive worsening with grip.

Deformity Recognition

Boutonniere vs Swan-neck. Boutonniere = PIP flexion from central slip rupture. Swan-neck = PIP hyperextension from volar plate laxity or FDS rupture.

Tendon Rupture Sequence

Vaughan-Jackson lesion. EDM ruptures first, then EDC ring, then EDC middle. Attrition on dorsal ulnar head (caput ulnae). Early Darrach or hemiresection.

Surgical Timing

Disease control first. Optimize medical management before reconstructive surgery. DMARDs within 2 years critical. Address proximal deformities before distal.

Quick Decision Guide - RA Hand Surgery

DeformityStageTreatmentKey Pearl
Early synovitis under 6 monthsNo deformity yetSynovectomy + medical optimizationWindow of opportunity - DMARDs critical
MCP ulnar drift, flexiblePassively correctableMCP arthroplasty + soft tissue rebalancingSilicone implants standard, 80% satisfaction
Boutonniere deformity, fixedPIP flexion contracture over 40°PIP arthrodesis in functionArthroplasty fails in fixed contracture
Caput ulnae + tendon ruptureEDM/EDC ruptureDarrach + tendon transfer/graftPrevent further ruptures with DRUJ excision
Mnemonic

BUTTONBoutonniere Deformity Pathomechanics

B
Band (central slip) disruption
Central slip ruptures or attenuates
U
Ulnar/radial bands migrate volar
Lateral bands slide volar to PIP axis
T
Terminal extension preserved
DIP extends (lateral bands intact)
T
Tight lateral bands
Shortened lateral bands resist correction
O
Oblique retinacular ligament contracts
ORL shortens, worsens deformity
N
No passive correction if chronic
Fixed after 6-12 months, needs arthrodesis

Memory Hook:BUTTON yourself up wrong - PIP stuck flexed, can't extend like a buttonhole!

Mnemonic

SWANSwan-Neck Deformity Causes

S
Slip (central) hypertrophy
Intrinsic tightness pulls PIP into extension
W
Weak volar plate
Volar plate attenuation allows hyperextension
A
Attenuated FDS
FDS rupture removes PIP flexion force
N
Nodules in flexor tendon
Trigger finger causes MCP flexion, compensatory PIP extension

Memory Hook:SWAN with elegant neck extended - PIP hyperextends while DIP flexes!

Mnemonic

BMI-CSSNalebuff Thumb Classification

B
Boutonniere (Type I)
MCP flexion, IP extension - MCP synovitis
M
MCP unstable (Type II)
MCP hyperextension, IP flexion - MCP ligament laxity
I
IP flexion (Type III)
Swan-neck from CMC subluxation
C
CMC arthritis (Type IV)
CMC joint destruction, adduction contracture
S
Swan-neck combination (Type V)
MCP hyperextension + IP flexion, multiple joints
S
Stiff arthritis mutilans (Type VI)
Global destruction, bone resorption

Memory Hook:BMI-CSS classification - B (boutonniere) vs swan-neck types, CMC to catastrophic!

Overview and Epidemiology

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease affecting approximately 1% of the population worldwide. The hand is involved in 90% of patients, making it the most common site of RA manifestation. Early diagnosis and treatment with disease-modifying antirheumatic drugs (DMARDs) within the first 2 years significantly impacts disease progression and outcomes.

Why RA Hand Management Matters

Hand involvement in RA causes progressive functional disability through synovitis, tendon rupture, and joint destruction. Modern biologic DMARDs have revolutionized medical management, but surgical intervention remains critical for correcting established deformities. The key is medical optimization before surgery and addressing deformities in a proximal-to-distal sequence to correct deforming forces.

Demographics

  • Age: Peak onset 40-60 years
  • Gender: 3:1 female predominance
  • Genetics: HLA-DR4 association (70%)
  • Smoking: Doubles RA risk, worsens severity

Hand Involvement Patterns

  • MCP joints: Most commonly affected (95%)
  • PIP joints: 80% involvement
  • Wrist: 60-70% early in disease
  • DIP joints: Rarely affected (under 10%)
  • Thumb: Nalebuff deformities in 50%

Pathophysiology

Synovial Inflammation Cascade

RA begins with immune-mediated synovial inflammation driven by T cells, B cells, and inflammatory cytokines (TNF-alpha, IL-6). Synovial hypertrophy (pannus formation) invades cartilage and bone, causing progressive joint destruction. Unchecked inflammation leads to ligament destruction, tendon attrition, and bone erosion.

Pathophysiologic Sequence in RA Hand

Disease Progression

Early (0-2 years)Synovial Inflammation
  • Pannus formation: Synovial hypertrophy with inflammatory cells
  • Cartilage invasion: Proteases degrade articular cartilage
  • Bone erosion: Marginal erosions at joint edges
  • Ligament weakening: Collateral and volar plate stretch
Intermediate (2-5 years)Tendon and Ligament Failure
  • Extensor subluxation: Radial collateral destruction allows ulnar drift
  • Central slip attenuation: Boutonniere deformity develops
  • Volar plate laxity: Swan-neck deformity from PIP hyperextension
  • Tendon rupture: Attrition on roughened bone (Vaughan-Jackson, Mannerfelt)
Late (over 5 years)Fixed Deformities
  • Joint destruction: Bone-on-bone arthritis
  • Contractures: Soft tissue shortening prevents passive correction
  • Ankylosis: Spontaneous fusion in some joints
  • Arthritis mutilans: Severe bone resorption (opera-glass hand)

Specific Deformity Mechanisms

Deformity Pathomechanics

DeformityPrimary PathologySecondary ChangesResult
Ulnar drift (MCP)Radial collateral ligament destructionExtensor subluxates ulnarly, intrinsics pull fingers ulnarProgressive ulnar deviation, worst with grip
Boutonniere (PIP)Central slip rupture/attenuationLateral bands migrate volar to PIP axis, ORL contractsPIP flexion, DIP extension, fixed after 6-12 months
Swan-neck (PIP)Volar plate laxity or FDS ruptureIntrinsic tightness extends PIP, lateral bands tightenPIP hyperextension, DIP flexion, can't hook
Z-deformity (thumb)CMC subluxation (Type III) or MCP hyperextension (Type II)Compensatory IP flexion for pinchLoss of opposition and pinch strength

Classification Systems

Nalebuff Classification of RA Thumb Deformities

TypeDeformity PatternPrimary PathologyTreatment
Type I (Boutonniere)MCP flexion, IP extensionMCP synovitis → volar plate stretchingMCP arthroplasty or arthrodesis
Type II (Swan-neck)MCP hyperextension, IP flexionMCP ligament laxity → hyperextensionMCP fusion or volar capsulodesis
Type III (CMC swan-neck)CMC subluxation, MCP hyperext, IP flexCMC synovitis → adduction collapseCMC stabilization + MCP fusion
Type IV (CMC arthritis)CMC arthritis, adduction contractureCMC joint destructionCMC arthroplasty or arthrodesis
Type V (Combined)Multiple joint involvementProgressive pannus at all jointsStaged reconstruction, proximal to distal
Type VI (Arthritis mutilans)Bone resorption, instabilitySevere osteolysisFusion if salvageable, otherwise adaptive

Type I vs Type II Distinction

Type I (Boutonniere): MCP is the problem joint (flexed from synovitis), IP compensates with extension. Type II (Swan-neck): MCP ligaments fail allowing hyperextension, IP compensates with flexion for pinch. Type III is swan-neck but driven by CMC subluxation proximally. Knowing the primary pathology determines surgical target.

Boutonniere vs Swan-Neck Deformities

Finger Deformity Comparison

FeatureBoutonniereSwan-Neck
PIP positionFlexionHyperextension
DIP positionExtensionFlexion
Primary pathologyCentral slip ruptureVolar plate laxity or FDS rupture
Lateral bandsMigrate volar to PIP axisTighten dorsally
Functional lossCannot extend PIP (no hook)Cannot flex PIP (no grip)
Surgical approachCentral slip repair (early) or PIP fusion (late)Volar plate reconstruction or FDS tenodesis

Staging of Boutonniere Deformity

Stage I (under 30° lag): Splinting + central slip repair may work

Stage II (30-50° lag): Consider central slip reconstruction or terminal tendon tenotomy

Stage III (over 50° lag, fixed): PIP arthrodesis in 30-40° flexion (functional position)

MCP Ulnar Drift Classification

GradeDeviation AnglePassive CorrectionTreatment
MildUnder 20 degreesFully correctableMedical optimization, splinting, observe
Moderate20-40 degreesPartially correctableMCP arthroplasty + soft tissue rebalancing
SevereOver 40 degreesFixed deformityMCP arthroplasty + intrinsic release, may need bone work

Clinical Presentation

History

  • Morning stiffness: Over 1 hour (vs OA under 30 min)
  • Symmetric involvement: Both hands, multiple joints
  • Systemic symptoms: Fatigue, fever, weight loss
  • Pain pattern: Worse with rest, improves with activity
  • Functional loss: Difficulty with grip, pinch, fine motor
  • Extra-articular: Nodules, lung involvement, vasculitis

Examination

  • Look: Swelling (boggy, soft), deformities, nodules, skin thinning
  • Feel: Warm, boggy MCP/PIP synovitis, ulnar head prominence
  • Move: Reduced ROM, pain at end-range, crepitus
  • Function: Pinch/grip strength, ulnar drift with grip
  • Tendons: Trigger fingers, palpable ruptures

Key Physical Findings

Caput ulnae syndrome: Dorsal prominence of distal ulna from DRUJ destruction. Ulnar head becomes:

  • Prominent dorsally
  • Painful with forearm rotation
  • Site of extensor tendon attrition (Vaughan-Jackson lesion)

Vaughan-Jackson lesion: Sequential rupture of ulnar-sided extensors:

  1. EDM (extensor digiti minimi) - first to rupture
  2. EDC ring finger - second
  3. EDC middle finger - third
  4. Pattern: ulnar to radial progression

Mannerfelt lesion: FPL rupture from attrition on volar scaphoid osteophyte. Less common than Vaughan-Jackson but causes complete loss of thumb IP flexion.

Distinguish RA from OA

RA features:

  • Morning stiffness over 1 hour
  • Soft, boggy swelling (synovitis)
  • Symmetric involvement
  • Spares DIP joints (unlike OA)
  • Systemic features
  • RF/anti-CCP positive

OA features:

  • Morning stiffness under 30 minutes
  • Hard, bony swelling (osteophytes = Heberden's/Bouchard's nodes)
  • Asymmetric, wear pattern
  • Affects DIP joints (Heberden's nodes)
  • No systemic features

Investigations

Diagnostic Workup

First LineSerologic Testing

Rheumatoid factor (RF):

  • Positive in 70% of RA patients
  • Sensitivity 70%, specificity 85%

Anti-CCP antibodies:

  • Positive in 70% of RA patients
  • More specific (95%) than RF
  • Predicts erosive disease

Inflammatory markers:

  • ESR, CRP elevated during flares
  • Track disease activity
ImagingPlain Radiographs

Standard hand series: PA, lateral, oblique views

Early findings:

  • Periarticular osteopenia
  • Soft tissue swelling
  • Joint space narrowing (symmetric)

Late findings:

  • Marginal erosions (at joint edges)
  • Subluxations and deformities
  • Bone resorption (arthritis mutilans)
  • Ankylosis
Advanced ImagingMRI or Ultrasound

Indications:

  • Early disease detection (synovitis before x-ray changes)
  • Assess tendon integrity pre-operatively
  • Monitor DMARD response

MRI findings:

  • Synovial enhancement with contrast
  • Bone marrow edema
  • Tendon tenosynovitis
  • Early erosions

Anti-CCP Specificity for RA

Anti-CCP antibodies are 95% specific for RA compared to RF at 85%. Presence of anti-CCP predicts more aggressive, erosive disease and guides earlier DMARD initiation. Patients with high anti-CCP titers benefit from biologic agents earlier in the disease course.

Management Algorithm

📊 Management Algorithm
rheumatoid arthritis hand management algorithm
Click to expand
Management algorithm for rheumatoid arthritis handCredit: OrthoVellum

Medical Management (Primary)

RA Medical Management Protocol

DiagnosisFirst Line

Methotrexate:

  • Gold standard DMARD
  • 10-25mg weekly, oral or subcutaneous
  • Add folic acid 5mg daily
  • Monitor LFTs, FBC every 3 months

Alternative: Sulfasalazine, hydroxychloroquine

If inadequate response at 3 monthsSecond Line

Add biologic DMARD:

  • TNF-alpha inhibitors (adalimumab, etanercept)
  • IL-6 inhibitors (tocilizumab)
  • B-cell depletion (rituximab)
  • JAK inhibitors (tofacitinib)

Target: Low disease activity or remission

Symptom controlAdjuncts

NSAIDs: Short-term for pain/inflammation

Corticosteroids:

  • Prednisolone 5-10mg daily during flares
  • Intra-articular injection for single joint synovitis
  • Bridge therapy while DMARDs take effect (6-12 weeks)

Window of Opportunity - First 2 Years

DMARD initiation within 2 years of symptom onset is critical. Early aggressive treatment prevents erosive disease, preserves joint function, and reduces need for surgery. Delay beyond 2 years results in irreversible joint damage.

Pre-operative Medical Management

Medication Management

Methotrexate: Stop 2 weeks before, restart 2 weeks after (reduces infection risk)

Biologics (TNF-alpha inhibitors): Hold 1 dosing cycle before surgery

Corticosteroids: Continue (adrenal suppression risk if stopped)

NSAIDs: Stop 7 days before surgery

Disease Activity Assessment

Optimize disease control before elective surgery:

  • Low disease activity score (DAS28 under 3.2)
  • CRP/ESR trending down
  • No active synovitis at surgical site
  • Defer surgery during acute flares

Timing pearl: Schedule surgery during remission or low disease activity. Active synovitis increases infection risk and impairs healing.

Surgical Indications

Surgery indicated when:

  • Persistent pain despite optimal medical management
  • Functional impairment affecting ADLs or work
  • Tendon rupture or impending rupture (tenosynovitis)
  • Progressive deformity with joint destruction
  • Nerve compression (carpal tunnel syndrome common in RA)

Surgical Technique

MCP Joint Arthroplasty with Soft Tissue Rebalancing

Consent Points

  • Implant fracture/failure: 10-20% at 10 years
  • Recurrent deformity: 10-15% ulnar drift recurrence
  • Infection: 2-3% risk (higher in RA)
  • Stiffness: ROM reduced from pre-op in 30%
  • Sensory loss: Digital nerve injury rare (under 2%)

Equipment Checklist

  • Silicone implants: Swanson or Sutter design, sizes 0-3
  • Bone reamers: MCP head and base reamers
  • Saw: Sagittal saw for bone resection
  • Sutures: 3-0 and 4-0 for soft tissue repair
  • K-wires: 0.045" for temporary fixation

Surgical Steps

MCP Arthroplasty Procedure

Step 1Approach

Dorsal longitudinal incision over MCP joints:

  • Can do single incision for index through small (4 joints)
  • Or individual incisions per digit
  • Elevate skin flaps to expose extensor mechanism
Step 2Extensor Tendon Management

Split extensor hood longitudinally:

  • Incise between sagittal band and extensor tendon
  • Reflect radial-sided hood ulnarly
  • Expose MCP joint capsule
Step 3Synovectomy
  • Excise hypertrophic synovium completely
  • Remove pannus from joint and tendon sheath
  • Send specimen for culture (rule out infection)
Step 4Joint Resection

Resect MCP joint:

  • Remove metacarpal head with sagittal saw
  • Ream intramedullary canal of metacarpal
  • Ream proximal phalanx base
  • Preserve collateral ligament origins if possible
Step 5Implant Insertion
  • Trial silicone implant sizing
  • Insert implant into metacarpal canal first
  • Reduce MCP joint
  • Insert distal stem into phalanx
  • Confirm alignment and smooth ROM
Step 6Soft Tissue Rebalancing (CRITICAL)

Correct ulnar drift:

  • Release ulnar sagittal band and intrinsics
  • Tighten radial sagittal band (reef)
  • Centralize extensor tendon over MCP
  • Consider radial collateral ligament reconstruction

Extensor hood repair:

  • Close hood with 3-0 braided suture
  • Ensure tendon centralizes with finger flexion
Step 7Closure and Splinting
  • Close skin with 4-0 nylon
  • Apply bulky dressing
  • Dynamic extension splint with MCP extension, radial deviation
  • Outrigger splint worn for 6 weeks

Soft Tissue Rebalancing is Key

Implant alone will fail without soft tissue rebalancing. The deforming forces (intrinsics pulling ulnar, sagittal band incompetent radially) persist after arthroplasty. Ulnar intrinsic release + radial sagittal band tightening prevents recurrent ulnar drift. 30% of recurrent deformity is from inadequate soft tissue balancing.

Wrist Synovectomy and Darrach Procedure

Indications:

  • Persistent wrist synovitis despite medical management
  • Caput ulnae with extensor tendon attrition
  • Vaughan-Jackson lesion (EDM/EDC rupture)

Surgical Steps

Step 1Dorsal Approach
  • Longitudinal incision over distal ulna and DRUJ
  • Identify and protect dorsal sensory branch of ulnar nerve
  • Elevate EDC and ECU to expose DRUJ and ulnar head
Step 2Synovectomy
  • Extensive dorsal wrist synovectomy
  • Remove pannus from radiocarpal and DRUJ
  • Inspect extensor tendons for attrition
Step 3Darrach (Distal Ulna Excision)
  • Divide DRUJ capsule
  • Osteotomize distal 1.5-2cm of ulna
  • Smooth ulnar stump with rongeur
  • Critical: Preserve TFCC attachment to ulnar stump
Step 4Tendon Transfers (if ruptured)

If EDM ruptured:

  • Transfer EIP (extensor indicis proprius) to EDM

If multiple ruptures (EDM + EDC ring/middle):

  • Use FDS slips as free grafts
  • Or perform side-to-side tendon transfers to intact EDC
Step 5Closure
  • Close extensor retinaculum over tendons
  • Skin closure
  • Splint wrist in neutral, forearm in neutral rotation

Prevent Ulnar Stump Instability

After Darrach, the ulnar stump can become painful and unstable (convergence). Preserve TFCC attachment to stump. Consider hemiresection arthroplasty (Sauvé-Kapandji) in young, active patients to maintain DRUJ stability while decompressing caput ulnae.

PIP Arthrodesis for Fixed Boutonniere

Indication: Fixed boutonniere deformity with PIP flexion contracture over 40 degrees that is not passively correctable.

Fusion position: 30-40 degrees flexion (functional position for grip)

Surgical Technique

Step 1Approach
  • Dorsal curved incision over PIP joint
  • Elevate skin flaps
  • Split central slip longitudinally or reflect laterally
Step 2Joint Preparation
  • Remove all cartilage to bleeding bone
  • Shape bone ends to congruent surfaces
  • Remove osteophytes
  • Aim for 30-40° flexion angle
Step 3Fixation

Options:

  • Two crossed K-wires (most common)
  • Tension band wiring
  • Headless compression screw (Herbert/Acutrak)
  • Plate fixation (if bone quality poor)
6 weeksPost-operative
  • Protective splint/buddy tape for 6 weeks
  • K-wire removal at 6 weeks if used
  • Confirm fusion on x-ray (bridging bone 3/4 cortices)

Thumb Reconstruction (Nalebuff Types)

Surgical Approach by Nalebuff Type

TypeDeformitySurgical TreatmentOutcome
Type IMCP flexion, IP extensionMCP arthroplasty or arthrodesis + IP capsulodesisGood pinch restoration
Type IIMCP hyperextension, IP flexionMCP arthrodesis in 15-20° flexionStable pinch platform
Type IIICMC sublux, MCP hyperext, IP flexCMC stabilization (ligament reconstruction) + MCP fusionComplex, staged procedures
Type IVCMC arthritisCMC arthroplasty or arthrodesisPain relief, maintain grip

Key surgical principle: Address the primary deformity (e.g., CMC in Type III) before correcting secondary compensatory deformities distally.

Complications

ComplicationIncidenceRisk FactorsManagement
Infection2-5%Immunosuppression (MTX, biologics), corticosteroids, diabetesAggressive antibiotics, consider implant removal if deep
Implant fracture (MCP arthroplasty)10-20% at 10 yearsHigh-demand activities, poor bone qualityObservation if painless, revision arthroplasty or fusion if symptomatic
Recurrent ulnar drift10-15%Inadequate soft tissue rebalancing, poor compliance with splintingRevision soft tissue balancing, intrinsic release
Stiffness (worse ROM)20-30%Prolonged immobilization, poor therapy complianceHand therapy, dynamic splinting, may need manipulation
Nonunion (arthrodesis)5-10%Smoking, corticosteroids, poor bone qualityRevision fusion with bone graft if symptomatic
Tendon rupture (extensor)3-5%Unaddressed caput ulnae, continued attritionTendon transfer or reconstruction, Darrach if not done

Infection Risk in RA Patients

RA patients are immunosuppressed from disease and medications (methotrexate, biologics, corticosteroids). Infection risk is 2-5 times higher than non-RA patients. Strategies to reduce infection:

  • Stop methotrexate 2 weeks pre-op, restart 2 weeks post-op
  • Hold biologics 1 dosing cycle before surgery
  • Prophylactic antibiotics (first-generation cephalosporin)
  • Meticulous sterile technique
  • Monitor closely post-op for signs of infection

Postoperative Care and Rehabilitation

Post-MCP Arthroplasty Rehabilitation

Immediate ProtectionWeeks 0-2
  • Splinting: Dynamic extension splint with outrigger
  • MCP held in extension and radial deviation
  • Passive ROM exercises initiated day 3-5
  • Critical: Maintain radial pull to prevent recurrent ulnar drift
Active MobilizationWeeks 2-6
  • Continue dynamic splint full-time
  • Active ROM exercises 5x daily (remove splint)
  • Blocking exercises to isolate MCP motion
  • Scar massage and edema control
StrengtheningWeeks 6-12
  • Wean from splint (nighttime only)
  • Progressive grip strengthening
  • Functional activities (ADLs)
  • Assess for recurrent drift, adjust therapy
Long-termWeeks 12+
  • Resume normal activities
  • Continue nighttime splint for 3-6 months
  • Monitor for implant fracture, recurrent deformity
  • Annual follow-up indefinitely

Splinting Compliance is Critical

Recurrent ulnar drift occurs in 10-15%, mostly from poor splinting compliance. The dynamic extension splint provides radial-directed force to counteract ulnar pull during healing. Patients must understand that splint wear for 6 weeks full-time, then nighttime for 6 months, is essential to prevent recurrence.

Post-Wrist Synovectomy Rehabilitation

ProtectionWeeks 0-2
  • Volar wrist splint in neutral
  • Finger ROM exercises (gentle)
  • Elevate, ice, edema control
MobilizationWeeks 2-6
  • Remove splint for exercises
  • Active wrist ROM (flexion, extension, radial/ulnar deviation)
  • Forearm rotation exercises
  • No strengthening yet
StrengtheningWeeks 6-12
  • Progressive wrist strengthening
  • Grip exercises
  • Functional activities
  • Return to work (light duty) by week 8

Outcomes and Prognosis

Functional Outcomes by Procedure

ProcedurePain ReliefFunctionSatisfactionRevision Rate
MCP arthroplasty80-90% significant improvementROM improved in 60%, reduced in 30%80% satisfied10-20% at 10 years (implant fracture)
PIP arthrodesis90% complete reliefStable grip platform, no motion85% satisfied5-10% (nonunion, malunion)
Wrist synovectomy70% relief if done early (under 6 months synovitis)Preserves ROM, prevents tendon rupture75% satisfied30% require repeat synovectomy at 5-10 years
Darrach (distal ulna excision)90% relief of ulnar-sided wrist painForearm rotation improves80% satisfied10% instability/convergence requiring revision

Predictors of Poor Outcome

Factors associated with worse surgical outcomes in RA hand:

  • Active disease at time of surgery (defer until remission)
  • Poor medical compliance (methotrexate, biologics)
  • Smoking (impairs wound healing, increases nonunion)
  • Advanced age with poor bone quality (implant failure, nonunion)
  • Inadequate soft tissue rebalancing (recurrent deformity)
  • Poor rehabilitation compliance (stiffness, recurrent drift)

Evidence Base and Key Trials

Silicone MCP Arthroplasty: Long-Term Outcomes

3
Chung et al • Journal of Hand Surgery (Am) (2009)
Key Findings:
  • Systematic review of 1,015 Swanson silicone MCP arthroplasties
  • Mean follow-up 7.2 years
  • Implant fracture: 18% at 10 years, 63% asymptomatic
  • Patient satisfaction: 81% satisfied or very satisfied
  • Recurrent ulnar drift: 12% overall, higher without soft tissue balancing
  • Revision rate: 7% for symptomatic implant fracture or recurrent deformity
Clinical Implication: Silicone MCP arthroplasty provides durable pain relief and acceptable function in RA with high satisfaction despite frequent asymptomatic implant fracture. Soft tissue rebalancing is critical to prevent recurrent deformity.
Limitation: Heterogeneous surgical techniques and rehabilitation protocols across studies. Lack of patient-reported outcome measures in older studies.

Early DMARD Therapy in RA: Impact on Hand Function

1
TICORA Trial Investigators • Lancet (2004)
Key Findings:
  • RCT of intensive DMARD therapy vs routine care in 111 early RA patients
  • Primary outcome: DAS28 (disease activity score)
  • Intensive therapy arm: MTX + 2 other DMARDs, tight control protocol
  • Results: DAS28 improved by 3.5 vs 1.9 (control), p < 0.001
  • Radiographic progression: Less erosion progression in intensive arm
  • Hand function: Improved HAQ scores by 0.6 vs 0.3 (control)
Clinical Implication: Intensive DMARD therapy within first 2 years preserves hand function and prevents erosive disease. Early aggressive medical management reduces long-term need for reconstructive surgery.
Limitation: Single-center trial with relatively short follow-up (18 months). Cost-effectiveness of intensive regimen not assessed.

Anti-CCP Antibodies: Predictive Value for Erosive Disease

2
van der Helm-van Mil et al • Arthritis and Rheumatism (2007)
Key Findings:
  • Prospective cohort of 454 early arthritis patients followed for 3 years
  • Anti-CCP positive patients: 74% developed RA, 68% had radiographic erosions
  • Anti-CCP negative patients: 30% developed RA, 25% had erosions
  • High anti-CCP titers (over 3x ULN): 85% developed severe erosive disease
  • Combination RF + anti-CCP positive: 90% predictive of erosive RA
Clinical Implication: Anti-CCP antibodies are highly predictive of erosive RA and guide early aggressive DMARD therapy. High titers warrant biologic DMARD consideration within first year.
Limitation: Predominantly Caucasian population, may not generalize to all ethnic groups. Antibody assay standardization varies between laboratories.

Exam Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

Scenario 1: MCP Ulnar Drift Assessment

EXAMINER

"A 55-year-old woman with 8-year history of seropositive RA presents with progressive ulnar deviation of MCP joints in both hands. She is on methotrexate and adalimumab with good systemic disease control. Her ulnar deviation is approximately 30 degrees and partially correctable passively. What is your assessment and management?"

EXCEPTIONAL ANSWER
This patient has rheumatoid arthritis with moderate MCP ulnar drift, which is Nalebuff Grade 2 (20-40 degrees deviation, partially correctable). My systematic approach: First, assess her disease activity - she appears to be in remission on DMARDs which is ideal for surgery. Second, examine both hands for the pattern of involvement: ulnar drift suggests radial collateral ligament destruction with ulnar extensor subluxation and intrinsic contracture. Third, assess for other deformities proximally (wrist, DRUJ) and distally (PIP boutonniere or swan-neck) as these affect surgical planning. Fourth, plain radiographs to assess bone quality and joint destruction. My management would be MCP silicone arthroplasty with soft tissue rebalancing for all four fingers (index through small). The critical components are: implant insertion to replace destroyed MCP joint, ulnar intrinsic release to remove ulnar-deviating force, and radial sagittal band tightening to centralize the extensor tendon. Post-operatively, she requires a dynamic extension splint with radial outrigger for 6 weeks to prevent recurrent drift. I would counsel about 80% satisfaction, 10-20% implant fracture risk at 10 years (mostly asymptomatic), and 10-15% risk of recurrent ulnar drift if splinting compliance is poor.
KEY POINTS TO SCORE
Assess disease activity - surgery only in remission
MCP arthroplasty indicated for Grade 2 deformity (partial correction)
Soft tissue rebalancing is critical: ulnar intrinsic release + radial sagittal band reef
Dynamic splinting compliance prevents recurrent drift
COMMON TRAPS
✗Operating during active disease flare (high infection risk)
✗Implant alone without soft tissue balancing (30% recurrent drift)
✗Not addressing wrist deformity if present (proximal deformity causes distal recurrence)
✗Inadequate post-op splinting protocol
LIKELY FOLLOW-UPS
"What would you do if the wrist also has significant deformity?"
"How do you manage recurrent methotrexate in the peri-operative period?"
"What if the deformity was fixed and not passively correctable?"
VIVA SCENARIOChallenging

Scenario 2: Extensor Tendon Rupture (Vaughan-Jackson Lesion)

EXAMINER

"A 60-year-old man with longstanding RA presents unable to extend his small and ring fingers at the MCP joint. Examination reveals prominent dorsal ulnar head and loss of EDM and EDC ring finger function. What is your assessment and surgical management?"

EXCEPTIONAL ANSWER
This patient has a Vaughan-Jackson lesion - sequential extensor tendon rupture from attrition on a prominent distal ulna (caput ulnae syndrome). The typical pattern is EDM ruptures first, followed by EDC ring, then EDC middle, progressing from ulnar to radial. My assessment: First, confirm tendon rupture by asking patient to extend fingers while palpating tendons - absent EDM and EDC ring with intact EDC middle/index. Second, examine DRUJ for caput ulnae - dorsal prominence, painful rotation, and instability. Third, plain radiographs showing DRUJ destruction with ulnar head erosion. My surgical management addresses both the ruptured tendons and the underlying bony pathology to prevent further ruptures. Approach is dorsal wrist exposure. First, I perform wrist synovectomy to remove inflammatory pannus. Second, Darrach procedure - excise distal 1.5-2cm of ulna to decompress the caput ulnae and remove the source of attrition, preserving TFCC attachment. Third, tendon reconstruction: since EDM and EDC ring are ruptured and cannot be primarily repaired, I transfer EIP (extensor indicis proprius) to EDM, and perform side-to-side transfer of EDC ring to the intact EDC middle. If multiple tendons are ruptured and EIP transfer insufficient, I would use FDS slips as free tendon grafts. Post-operatively, splint wrist neutral for 4 weeks, then begin ROM and therapy. I would counsel about good functional recovery but permanent loss of independent small finger extension, and 5-10% risk of further rupture if disease not controlled medically.
KEY POINTS TO SCORE
Vaughan-Jackson lesion = sequential EDM, EDC ring, EDC middle rupture from caput ulnae attrition
Must address bony pathology (Darrach) to prevent further ruptures
Tendon reconstruction: EIP to EDM transfer + side-to-side or FDS graft for other ruptured tendons
Medical optimization critical to prevent progression
COMMON TRAPS
✗Attempting tendon repair without addressing caput ulnae (further ruptures inevitable)
✗Missing diagnosis of tendon rupture vs MCP synovitis (test extension with wrist flexed)
✗Inadequate synovectomy allowing continued inflammation and attrition
✗Not counseling about further rupture risk if RA not controlled
LIKELY FOLLOW-UPS
"What is the alternative to Darrach procedure in a young patient?"
"How would you reconstruct if all four extensors (EDM, EDC ring, EDC middle, EDC index) are ruptured?"
"What is a Mannerfelt lesion and how does it differ?"
VIVA SCENARIOChallenging

Scenario 3: Thumb Z-Deformity (Nalebuff Type III)

EXAMINER

"A 50-year-old woman with RA has progressive thumb deformity with CMC joint subluxation, MCP hyperextension to 40 degrees, and compensatory IP flexion. She has weak pinch and difficulty with activities requiring precision grip. Describe your classification and surgical approach."

EXCEPTIONAL ANSWER
This patient has a Nalebuff Type III thumb deformity - swan-neck pattern driven by CMC joint subluxation. The pathomechanics: CMC synovitis causes ligamentous laxity and adduction collapse of the thumb metacarpal. To compensate and achieve thumb-index opposition for pinch, the MCP hyperextends and the IP flexes (Z-deformity). This is distinct from Type II (primary MCP laxity) - here the CMC is the primary problem. My surgical approach addresses the deformity proximally to distally: First, stabilize the CMC joint. Options include ligament reconstruction using FCR slip or LRTI (ligament reconstruction tendon interposition) if there is significant CMC arthritis. If CMC joint destruction is severe, CMC arthrodesis is an option but sacrifices motion. Second, correct MCP hyperextension. Since MCP hyperextension is secondary and the ligaments are attenuated, I would perform MCP arthrodesis in 15-20 degrees of flexion to provide a stable post for pinch. Volar capsulodesis alone would likely fail given the severity. Third, the IP flexion is compensatory and typically improves once proximal deformities are corrected, but if fixed, IP capsulotomy may be needed. Surgical sequence is staged: CMC stabilization first (allow 3 months healing), then MCP fusion. I would counsel about 70-80% improvement in pinch strength and function, with trade-off of MCP motion lost but stable pinch platform gained. Recovery is 3-6 months for full rehabilitation.
KEY POINTS TO SCORE
Nalebuff Type III = swan-neck driven by CMC subluxation (primary pathology)
Surgical sequence: proximal to distal (CMC first, then MCP)
CMC ligament reconstruction or fusion + MCP arthrodesis for stability
IP deformity usually secondary and improves with proximal correction
COMMON TRAPS
✗Treating MCP alone without addressing CMC (deformity will recur)
✗Attempting MCP soft tissue reconstruction in severe laxity (will fail - needs fusion)
✗Operating distal to proximal (wrong sequence - proximal deformity drives distal)
✗Not counseling about loss of MCP motion and prolonged recovery
LIKELY FOLLOW-UPS
"How do you differentiate Nalebuff Type II from Type III clinically?"
"What would you do if there is significant CMC arthritis with bone loss?"
"How would your approach differ for Nalebuff Type I (boutonniere thumb)?"

MCQ Practice Points

Ulnar Drift Mechanism Question

Q: What is the primary pathologic mechanism of MCP ulnar drift in rheumatoid arthritis? A: Radial collateral ligament destruction with ulnar subluxation of the extensor tendon. The radial collateral ligament fails from synovitis, allowing the extensor tendon to subluxate ulnarly. Intrinsic muscles then pull the fingers into progressive ulnar deviation, worsened with grip.

Vaughan-Jackson Lesion Question

Q: What is the typical sequence of extensor tendon rupture in Vaughan-Jackson lesion? A: EDM (extensor digiti minimi) ruptures first, followed by EDC ring, then EDC middle. The sequence progresses from ulnar to radial as tendons attrit on the prominent dorsal ulnar head (caput ulnae). EDM ruptures first because it is most ulnar and has the thinnest cross-section.

Boutonniere vs Swan-Neck Question

Q: What is the primary pathology distinguishing boutonniere from swan-neck deformity? A: Boutonniere: Central slip rupture/attenuation causes PIP flexion and DIP extension. Lateral bands migrate volar to PIP axis. Swan-neck: Volar plate laxity or FDS rupture causes PIP hyperextension and DIP flexion. Intrinsics pull PIP into hyperextension.

Anti-CCP Antibody Question

Q: What is the specificity of anti-CCP antibodies for rheumatoid arthritis diagnosis? A: 95% specificity for RA (compared to RF at 85%). Anti-CCP antibodies are highly predictive of erosive disease and indicate need for early aggressive DMARD therapy. Combination of RF + anti-CCP positive is 90% predictive of erosive RA.

Soft Tissue Rebalancing Question

Q: What is the most important soft tissue procedure to prevent recurrent ulnar drift after MCP arthroplasty? A: Ulnar intrinsic release combined with radial sagittal band tightening. Releasing the ulnar intrinsics removes the ulnar-deviating force, while tightening the radial sagittal band centralizes the extensor tendon over the MCP joint. Implant alone without soft tissue rebalancing has 30% recurrence rate.

Nalebuff Type III Question

Q: In Nalebuff Type III thumb deformity, what is the primary pathology and surgical target? A: CMC joint subluxation is the primary pathology (not MCP). The thumb metacarpal adducts and subluxates at CMC from ligamentous laxity. MCP hyperextension and IP flexion are compensatory to achieve pinch. Surgical treatment must address CMC stabilization first before correcting MCP deformity, otherwise recurrence is inevitable.

Australian Context and Medicolegal Considerations

Australian RA Management

  • PBS coverage: DMARDs (methotrexate, sulfasalazine) fully covered
  • Biologic access: TNF-alpha inhibitors, IL-6 inhibitors on PBS with rheumatologist authority
  • Public hospital wait times: Elective hand surgery 6-18 months
  • Hand therapy: Medicare rebate for post-surgical therapy (CDM plan)

ACSQHC Guidelines

  • Surgical site infection: Target rate under 2% for clean hand surgery
  • Pre-operative optimization: Documented medical clearance and disease control assessment
  • DMARD management: Stop MTX 2 weeks pre-op, restart 2 weeks post-op
  • VTE prophylaxis: Risk assessment, mechanical prophylaxis for high-risk

Medicolegal Considerations for RA Hand Surgery

Key documentation requirements:

  • Medical optimization: Document rheumatology consultation, disease activity score (DAS28), medication management plan pre-op
  • Consent specifics: Infection risk (2-5% in RA), implant fracture (10-20% at 10 years), recurrent deformity (10-15%), need for revision surgery
  • Medication management: Document methotrexate hold and restart plan, biologic hold duration
  • Splinting protocol: Document splinting requirements and consequences of non-compliance (recurrent drift)

Common litigation issues:

  • Infection in immunosuppressed patient (document pre-op optimization and antibiotic prophylaxis)
  • Recurrent deformity (document soft tissue rebalancing performed and splinting compliance counseling)
  • Implant fracture requiring revision (ensure consent documented realistic implant longevity)
  • Worse ROM post-operatively (pre-op counseling that ROM may decrease but pain improves)

RHEUMATOID ARTHRITIS - HAND

High-Yield Exam Summary

Key Pathophysiology

  • •Synovial inflammation (pannus) invades cartilage and bone causing progressive destruction
  • •Ulnar drift = radial collateral ligament destruction + ulnar extensor subluxation + intrinsic contracture
  • •Boutonniere = central slip rupture, PIP flexion, DIP extension (lateral bands volar to PIP axis)
  • •Swan-neck = volar plate laxity or FDS rupture, PIP hyperextension, DIP flexion
  • •Vaughan-Jackson = EDM, EDC ring, EDC middle sequential rupture from caput ulnae attrition

Classification

  • •Nalebuff Thumb Type I = boutonniere (MCP flexion, IP extension) = MCP synovitis
  • •Type II = swan-neck (MCP hyperext, IP flex) = MCP ligament laxity
  • •Type III = swan-neck from CMC subluxation (treat CMC first!)
  • •Boutonniere deformity staging: Stage I (under 30° lag, correctable), Stage II (30-50°), Stage III (over 50°, fixed)

Medical Management

  • •DMARDs within 2 years critical - window of opportunity to prevent erosions
  • •Anti-CCP 95% specific for RA, predicts erosive disease
  • •Methotrexate gold standard, add biologic if inadequate response at 3 months
  • •Pre-op: stop MTX 2 weeks before, biologics 1 dosing cycle, continue corticosteroids

Surgical Pearls

  • •Proximal-to-distal surgery sequence - correct wrist before MCP, MCP before PIP
  • •MCP arthroplasty requires soft tissue rebalancing: ulnar intrinsic release + radial sagittal band reef
  • •Darrach (distal ulna excision) for caput ulnae prevents further extensor ruptures
  • •Dynamic extension splint for 6 weeks post-MCP arthroplasty prevents recurrent drift
  • •Synovectomy only effective if done under 6 months of synovitis onset

Complications

  • •Infection 2-5% (immunosuppression from RA medications)
  • •MCP implant fracture 10-20% at 10 years (mostly asymptomatic)
  • •Recurrent ulnar drift 10-15% (inadequate soft tissue balancing or poor splinting compliance)
  • •Stiffness 20-30% (ROM may worsen but pain improves)
  • •Arthrodesis nonunion 5-10% (smoking, corticosteroids, poor bone quality)
Quick Stats
Reading Time116 min
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