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Swan neck deformityw

Swan neck deformityw






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    Swan neck deformityw Swan neck deformityw Presentation Transcript

    • Swan Neck Deformity
    • Swan neck deformity. The volar plate is torn, causing the joint toopen abnormally under the pull of the extensor ligaments .
    • Swan-Neck Deformity• Typically defined as: – proximal interphalangeal (PIP) joint hyperextension – with concurrent distal interphalangeal (DIP) joint flexion• Not necessarily unique to RA but rather an end result of muscle and tendon imbalance caused by RA.
    • Swan-Neck Deformity• Not necessarily unique to RA but rather an end result of muscle and tendon imbalance caused by RA
    • Nalebuff Classification 1989• Type I - PIP joints flexible in all positions – No intrinsic tightness or functional loss• Type II - PIP joint flexion limited in certain positions – Intrinsic tightness – Limited PIP motion with extended MCP with ulnar deviation• Type III - PIP joint flexion limited in all positions – Near normal radiograph• Type IV - PIP joints stiff with poor radiographic appearance
    • Pathophysiology• The intercalated joint collapse concept of Landsmeer means that collapse of a joint in one direction will result in deformity of the next distal joint in the opposite direction. – Z deformity
    • Pathophysiology• In a normal finger, intrinsic muscles serve as: – flexors of the MCP joint – extensors of the PIP and DIP joints• By being located volar to the MCP joint axis and dorsal to the PIP and DIP joint axes
    • Pathophysiology• Intrinsic tightness increases the flexor pull on the MCP joint and hyperextension of PIPJ• Weak flexor power aggravates this by being unable to pull the middle phalanx. – DIPJ and MCPJ hyperextension follows• Constant efforts to extend the finger against this pull then leads to stretching of the collateral ligaments and weakening of the volar plate at the PIPJ.
    • Pathophysiology• the lateral bands are constrained in their dorsal position with the extensor apparatus migrating proximally – therefore upsetting the flexor-extensor balance,• The lateral bands in this position act to increase the pull of the central slip that attaches to the dorsal base of the middle phalanx. – Leading to hyperextension of PIPJ
    • Pathophysiology• The increase of FPL tension resulting from hyperextension of the PIP joint leads to a reciprocal flexion of the DIP joint.• DIP mallet deformity also from: – Joint erosion – Extensor tendon attentuation or rupture• Progressive disease leads to joint destruction and fixed contracture.
    • Hashemi-Nejad and Goddard (1994)-multidisciplinary approach is best-an affected joint will affect other joints-early synovectomy is worthwhile after a 6-month trial ofnon-operative treatment-tenosynovectomy decreases the risk of tendon rupture,-the wrist is the key in the RA hand-the thumb is a very important source of disability-silastic MCPJ arthroplasty is successful in reducing painand improving function
    • Feldon (1993) lists the aims of surgery in the RA hand:1. pain relief2. functional improvement3. preventing disease progression4. cosmetic improvement Note that the presence of a painless deformity with minimal function deficit is not an indication for surgery.
    • Management• Millender and Nalebuff staging system (1975) is a good guideline for identifying treatment options in RA
    • Principles• Prevention• Correct PIPJ hyperextension• Restore DIPJ extension
    • Type1– Silver ring splint to flex PIPJ– Volar dermatodesis– Correction of any MCPJ abnormality first– Flexor tenosynovectomy (if synovitis is present)– Flexor tenodesis - FDS slip through A2 pulley then looped back to itself– Retinacular ligament reconstruction– Release ulnar lateral band proximally and pass volar to PIPJ axis → sheath
    • Silver Ring Splint• Permit active PIP • flexion and limit hyperextension of the PIP joint
    • DIP Fusion• Difficult and unreliable to restore the extensor apparatus at DIP level cause underlying RA disease will destroy the repair• Also secondary arthritis within DIP may make attempts to mobilise joint unwise•
    • Dermadesis• Used to prevent PIP hyperextension bu creating a skin shortage volarly• Elliptical skin wedge (4-5mm at widest) is removed from volar aspect of PIP• Care not too disturb venous drainage or violate the flexor sheath• Skin closed with PIP in flexion• Only useful if done in conjunction with other procedures ie DIP fusion
    • Flexor Tendon Tenodesis “sublimis sling”• Used as checkrein against hyperextension ie restoration of strong volar support• One slip of FDS is divided ~1.5cm proximal to PIP• This is then separated from its corresponding slip bit left attached distally• With joint at 20-30 degrees the detached slip is fixed proximally – Anchored to thickened margin of sheath, distal edge of A2 or Mitek• Nalebuff did simpler procedure whereby he passed split tendon around A1 pulley
    • Reticular Ligament Reconstruction• Credited to Littler• Ulnar lateral band is freed from extensor mechanism proximally but left attached distally• Passed volar to Cleland’s fibres to bring it volar to axis of PIP• Band is sutured to the fibrous tendon sheath under enough tension to restore DIP extension and prevent hyperextension at PIP• However, in RA may have destruction of terminal tendon so no amount of tension applied to the relocated tendon will achieve DIP extension
    • Type 2• Looks like Type 1 but PIP movement is limited in certain positions related to position of MCPJ – MCPJ extended/radial deviation then limited passive PIP ROM – MCPJ flexed/ulnar deviated then PIP ROM increased• As MCPJ subluxates and the intrinsics get tight a secondary swan neck develops as a result of muscular imbalance• Not sufficient to restrict PIPJ hyperextension, intrinsics must be released plus MCPJ subluxation must be corrected +/- arthroplasty
    • Intrinsic Release• Photo on camera• A rhomboid portion of the ulnar extensor aponeurosis is then resected• This procedure resects the lateral band through which the abnormally tight intrinsics have caused MP flexion and PIP hyperextension
    • Type 3• unlike type 1 & 2 have significant functional disability due to inability to grasp objects• Not joint destruction but restriction due to: – Extensor mechanism – Collateral ligaments – Skin• First goal is to restore passive ROM – PIPJ manipulation – Skin release – Lateral band mobilisation – Then correction of deformity after motion restored
    • PIPJ Manipulation• MUA possible up to 80-90 degrees• Usually in conjunction with intrinsic release, arthroplasty or tenosynovectomy
    • Skin Release• Dorsal skin may limit the amount of passive flexion that is achieved during manipulation• Tension minimised with an oblique incision just distal to the PIPJ – Allowing skin edges to spread – Closes 2-3 weeks by secondary intention – PHOTO 2112
    • Lateral Band Mobilisation• Lateral bands are displaced dorsally• Free lateral bands from central slip using 2 parallel incisions allows flexion without releasing lateral bands or lengthening central slip• PHOTO 2113
    • Type 4• Patients with stiff PIPJ and radiographic evidence of advanced intra-articular changes require salvage procedure – Fusion or arthroplasty• PHOTO 2114