TENDONS - flexor, extensor and tendon transfer Flashcards Preview

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Flashcards in TENDONS - flexor, extensor and tendon transfer Deck (77)
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1

List principles of tendon transfer

  1. Supple joints, full pROM
  2. stable soft tissue bed
  3. Expendable donor
  4. Adequate excursion
  5. Adequate force/motor function
  6. Synnergistic
  7. Straight line of pull
  8. 1 function per tendon transfer

2

List the contents of dorsal extensor compartments and pathologies specific to each compartment

  1. EPB, APL: de Quervain's
  2. ECRB, ECRL: intersection syndrome (w/ 1st)
  3. EPL: traumatic/attrition rupture s/p non-operative mngmt distal radius #
  4. EIP, EDC: extensor tenosynovitis
  5. EDM: Vaughn-Jackson syndrome (ulnar to radial attrition rupture in RA)
  6. ECU: snapping/subluxation

3

describe common anatomic variations of 1st dorsal extensor compartment

  • vertical septum creating 2 subcompartments
  • multiple slips of APL

4

why can a person independently extend the index finger after EIP tendon transfer?

  1. lack of junctura teninae between D2 and D3
  2. individually innervated independent muscle bellies

5

are EIP and EDM ULNAR OR RADIAL to respective EDC tendon?

  • ulnar

6

what is a seymour fracture and what is your treatment plan?

  • a seymour fracture is a trans-epiphyseal fracture of the distal phalanx in a skeletally immature patient
  • closed fractures have intact nail plate (and underlying nail bed)
  • open fractures often present w subluxation of nail plate from under the perionychium w associated nail bed (germinal, sterile) injury
  • treatment closed:
    • splint x 6 wks, then night/activity x 6 wks
  • treatment open - need to recognize bc "like" an intra-articular fracture
    • remove nail plate
    • copiously irrigate fracture
    • repair nail bed
    • replace nail plate
    • splint x 6 wks, then night/activity x 6 wks vs. k-wire & splint if unstable
    • consider PO antibiotics (no evidence)

7

how would you treat a zone III BLUNT/CLOSED extensor injury?

  • blunt, no fracture
    • splint PIPJ in extension, DIP free x 3 wks, protected range of motion x 2 wks
    • if lag, unstable consider splinting whole finger vs k-wire stabilization
  • Blunt, fracture (central slip is w fracture fragment)
    • if piece large, consider screw fixation then splint vs. k-wire as above
    • if piece is small, consider excise and advance (mitek screw anchor vs. transverse wire across base of MP) then splint vs k-wire as above

8

a blunt injury to MCPJ and extensor lag

how would you differentiate between sagittal band vs central tendon injury?

  • sagittal band: can MAINTAIN extension when place passively
  • central slip, cannot maintain or initiate extension

9

for complete laceration to zone 5, what is treatment approach?

  • repair EDC - running horizontal mattress vs. core suture +/- dorsal epitendinous
  • repair sagittal band - figure of 8
  • wrist 20' ext, MCP neutral or slight hyperext, IPJ free x 3 wks; protected motion x 2 wks
  • vs. yoke splint x 3 wks, protected motion x 2 wks

10

what is the mechanism of rupture for EPL after distal radius managed closed.

  1. ischemic rupture: decrease diffusion / blood flow
  2. attrition rupture: hematoma, inflammation/synovitis, callous narrows the 3rd compartment, leads to mechanical irritation and attrition rupture

11

how would you treat a non-inflammatory rupture of EPL or EDC

  • options include address etiology and intercalary graft or tendon transfer (eip to epl; edc to edc end to side)

12

what is the suspected etiology of extrinsic extensor tightness?

  • common post-traumatic or post-operative
  • too tight repair / transfer
  • muscle or soft tissue contractures
  •  

13

what is your treatment plan for a patient with post-operative or post-traumatic extrinisc extensor tendon tightness

  • after immobilization, initiate protected motion protocol after 6 (zone 1,2), 3 (zones 3,4,5), 4 (zones 6+) weeks
  • if presenting late, then initiate static and dynamic splinting
  • progress to exercise program of assisted flexion/extension for several months (3-6) prrio to OR
  • operative interventions
    • tenolysis
    • extrinsic extensor release (excise portion of central tendon between sagittal band and prior to emergence of lateral bands/PIPJ

14

what is the etiology of intrinsic contracture?

  • trauma/burns: adhesions, ischemic contracture, nerve injury
  • inflammatory joint disease / RA / SLE: volar MCP subluxation, inflammatory adhesions
  • CP/stroke, parkinsons, encephalitis (CNS): spasticity

15

describe a treatment plan for intrinsic contracture

  • essential hand therapy, static/dynamic splinting pre-operatively
  • operative
    • excise lateral bands
    • excise ulnar lateral band and step-lengthen (vs zplasty) radial lateral band

16

what are operative interventions to address late presentation of sagittal band injury

  • first need to centralize the EDC (may need to partially release ulnar sagittal band)
  • numerous options described
    • ulnar junctura, proximally based partial slip of EDC, proximally based partial slip of ulnar sagittal band, free tendon graft - used to maintain central position of EDC - sutured to / around adjacent radial lumbrical, radial collateral ligament
  • post-op immobilize MCP & finger in extension until first post-op, then IPs free, then gentle aROM to MCP at 2-3 wks, then graduated increase activity (initial extension splint, then yoke splint)

17

discuss the patho-etiology of Boutonniere deformity

  • problem is always initiated at PIPJ
  • with injury/attenuation of the central slip leads to unopposed flexion at PIPJ
  • with time, there is volar migration of lateral bands
  • lateral bands become flexors of PIP and extenders of DIP
  • over time, oblique retinacular ligament becomes contracted and triangular ligament becomes lax, and there is loss of passive extension of PIP/passive flexion of DIP and joint contracture
  • eventually this abnormal posture imparts abnormal forces of joint surfaces, leading to degenerative arthritis

18

describe classification of boutonniere deformity

burton classification

  1. extensor lag, full passive extension (supple joint)
  2. fixed contracture, lateral band contracture
  3. fixed contracture, joint fibrosis, volar plate fibrosis/contracture
  4. with degenerative joint changes

Essential features to differentiate clinically and classify the injury to guide treatment:

acute vs. chronic (will respond to early initiation of spinting protocol / prophylaxis against worsening deformity)

supple & passively corrected joint vs. fixed contracture (will/should respond to non-operative program to rebalance extension mechanism (lateral bands); contracted joints may need preliminary surgical stage of capsulotomy);

with / without associated degenerative joint changes (consider rebalancing + joint arthroplasty vs. arthrodesis in better functional position)

19

Discuss treatment plan for early and/or supple boutonniere deformity

  • non-operative management is usually sufficient to rebalance extensor mechanism / lateral bands, and restore normal motion / more functional motion
  • 3 step program
  • stage 1: achieve full passive extension (serial splinting, dynamic casting, physio; for aptients not completely responsive, may need to consider capsulotomy as prelim operative stage)
  • stage 2: rebalance extensor apparatus: add exercises to DIPJ - active and passive flexion to lengthen lateral band, move volar
  • stage 3: maintain PIP extension: PIP extension splint alone, DIPJ free x 8 wks
    • if extensor lag recurs, then resume splinting
  • if failed, or extensor lag > 30', consider surgical intervention

20

LIST surgical options to treat chronic boutonniere

  • all patients have central slip, triagular ligament, oblique retinacular ligament tenolysis
  • Fowler terminal tenotomy (tenotomy distal to triangular ligament)
  • Central slip reconstruction
    • resection of attenuated / scarred portion and primary repair
    • central slip shortening
    • Tendon graft procedures to restore central slip
  • Lateral band rebalancing / mobilization centrally

21

what would you do for a patient with a chronic boutonniere, failed appropriate course of non-operative management, and with extensor lag of 47' but partial passive extension

 

  • ensuring that full passive ROM (extension) has been achieved - if unable to do via non-operative management, undertake preliminary stage of capsulotomy; then post-operatively re-institute 3-stage program of non-operative therapy (many patients will improve at this point to lag < 30')
  • if still extensor lag 47': long discussion with patient regarding ongoing benefit from non-operative management, risks of surgery (stiff finger with limited flexion) vs. benefits of surgery (depends on limitations w extensor lag)
  • if proceeding with surgery, my plan is:
    • extensive tenolysis
    • folwer distal tenotomy (of terminal tendon distal to triangular ligament)
      • lateral band insertion to terminal tendon preserved but tension at terminal tendon released and hyperextension released
      • proximal migration of rest of extensor apparatus increases tone at central slip
    • mobilization and dorsal centralization of lateral bands
      • effectively to act as PIP extensor like central lip
      • extension of DIPJ facilitated through intact oblique retinacular ligament to lateral bands

22

For a Swan Neck Deformity, describe the acute and chronic changes that occur to the extensor mechanism and periarticular structures

  • acute
    • volar plate laxity
    • dorsal subluxation of lateral bands
    • attenusation of transverse retinacular ligament
  • chronic
    • extensor tendon adhesions
    • contracture of lateral band
    • PIP and DIP fixed contractures
    • degenerative joint changes

23

list the potential etiologies for swan neck deformity:

  • swan neck deformity originates in pathology at or proximal to PIP or at the DIP
  • PIPJ
    • extrinsic tightness
    • intrinsic extensor tightness: CNS pathology, trauma, nerve injury, inflammatory joint disease
    • MCPJ volar subluxation: inflammatory joint disease
    • laxity of volar plate / ligamentous structures of PIPJ: injury (dislocation), inflammatory joint disease, other chronic joint effusion/synovitis
    • FDS injury / laxity or repair or transfer
  • DIPJ
    • chronic mallet
    • short MP (sequellae of MP#)

24

describe the pathophysiology of development of swan neck deformity when originating from PIP vs DIP

  • pip hyperextension
    • primary hyperextension at PIPJ from extrinsic or intrinsic tightness, MCP volar subluxation, FDS laxity/injury, laxity of volar plate/ligamentous structures @ joint
    • laxity and dorsal subluxation of lateral bands - inability to extend DIP
    • attenutation of FDP when passing over hyperextended PIP - increased flexor tone at DIP
  • dip flexion
    • disruption of the terminal tendon
    • extesnor force focussed at central slip
    • gradual weakening of volar joint structures
    • PIP hyperextends

25

describe a classification of swan neck deformity, outline the important components for decision making

  • a classification for swan neck proposed by feldon (described originally for RA)
  1. fully passively flexible PIP and DIP
  2. joints passively flexible in certain positions, given presence of intrinsic tightness
  3. fixed PIP deformity, normal articular surfaced
  4. fixed PIP deformity, abnormal / destructive articular surfaces

Important components for decision making are:

- passive flexion in all positions?

- presence of intrinsic tightness?

- fixed PIP +/- DIP contracture

- destructive joint changes

26

what are surgical options to treat swan neck deformity when problem originates at PIP or proximal?

  • MCPJ
    • intervention at this joint indicated by presence of intrinsic tightness
    • if present, then intrinsic release (often ulnar intrinsics, because there is ulnar deviation)
    • if chronic MCPJ subluxation & joint destruction, then MCPJ arthroplasty recommended
  • PIPJ - several options for flexible PIPJ in all / some positions:
    • Volar plate capsulodesis
    • FDS sling / tenodesis (distally based ulnar slip of FDS is advanced proximally to PP istelf or around A2
    • Intrinsic re-routing described by Littler - ulnar lateral band is sectioned at musc-tend jxn, re-routed volar cleland/grayson and attached to volar PP or flexor sheath
    • spiral ORL reconstruction (free tendon graft dorsal to volar through DP, spiral proximal and volar through base of MP)
  • PIPJ - when there is fixed contracture in all positions
    • PIPJ capsulotomy, joint mobilization, +/- lateral band mobilization (separation from dorsal position and ass'n w/ central slip), +/- skin release if relative insufficiency, +/- short k-wire immobilization
    • vs PIPJ capsulotomy, joint mobilization, and approaches listed above
  • DIPJ
    • do nothing (when all joints supple, rebalancing at PIP may be sufficient)
    • vs arthrodesis

27

what are the surgical options to treat swan neck deformity when problem originates w chronic mallet?

  • address the chronic mallet
  • if < 2-6 mos or if still tender at DIPJ then period of splinting may be beneficial
    • extension splint for DIP plus figure of 8 for PIP
  • fowler central slip tenotomy
  • spiral ORL reconstruction
  • advance terminal tendon

28

WHAT IS THE FUNCTION OF THE FLEXOR SHEATH?

  • nutrition via diffusion
  • tendon gliding
  • improve exurusion of flexion by prevention of bowstringing

29

List special considerations for each zone for a flexor tendon injury

  • zone 1: FDP only
    • consideration is whether there is sufficient stump for direct primary repair or if a pull-through suture over a wire is required
    • consideration is whether there is proximal retraction of FDP to palm (depending on vinculae/bone avulsion as per leddy classification)
    • should preserve or reconstruction A4 pulley
    • immobilization protocol for pull-through suture technique, otherwise passive motion
  • Zone 2:
    • consideration is that both FDP and FDS have likely been injured
    • should aim to repair both, or at least 1 slip of FDS
    • should preverse or reconstruct A2 pulley
    • early motion protocol essential to improved outcomes, early active when possible (> 4 strand repair)
  • zone 3
    • typically good tendon outcomes, but sharp injuries in this zone associated with neurovascular injury to common (or proper) digital vessels and nerves
    • early motion protocol (passive or active)
  • zone 4
    • need to explore for associated median nerve injury
    • may be adhesions through small space;
    • need to repair and step-lengthen (or z-plasty) transverse carpal ligament
    • early motion protocol (passive or active)
  • zone 5
    • often associated w other major neurovascular injury, need to explore widely
    • if at MT junction or muscle belly then repair w vicryl, figure of 8 sutures
    • immobilization protocol

30

discuss timing of repair

  • optimal timing is early repair (wihtin 2 wks)
  • no benefit of immediate over early repair
  • delayed primary repair wihtin 3-4 wks
  • secondary repair/delayed repair/reconstruction when:
    • associated extensive soft tissue injury wiht inability to cover repair immediately
    • associated devitalized or infected tissue
    • late presentation
    • rupture of previous repair