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rheumatoid arthritis, osteoarthritis, inflammatory arthritis, Lupus and scleroderma, others > Arthritis (all types) > Flashcards

Arthritis (all types) Flashcards

1
Q

Define osteoarthritis

A

· Degenerative osteoarthritis of the hand/wrist can involves all of the tissues around the synovial joint, including the articular cartilage, joint capsule, ligaments, subchondral bone, metaphyseal bone, and the muscles acting across the joint

· Principle pathological change –> loss of articular cartilage.

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2
Q

Describe the pathophysiology of osteoarthritis

A
  • Changes to articular cartilage
    • Biochemical: cytokine release –> cellular response, cartilage damage
    • Biomechanical: loss of proteoglycans, increase vascular ingrowth, increased water - cartilage becomes soft (chrondromalacia)
    • Structural changes: chondrocytes respond to mechanical forces and cartilage develops fibrillations on surface, clefts, fractures, decrease thickness
  • Changes to subchrondral bone
    • sclerosis (increased bone density where exposed), cysts, osteophyte formation
  • Changes to peri-articular structures
    • inflamed synovium, swelling, stiffness
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3
Q

how do you classify osteoarthritis?

A
  • Primary vs. secondary:
  • Primary – idiopathic (combo of genetics, joint shape/anatomy, endocrine changes)
  • Secondary – Antecendent event or underlying etiology that accelerates loss of cartilage
    • Mechanical – change to joint architecture – trauma, infection
    • Metabolic – gout, cppd, Wilson’s disease, hemochromatosis (MCPJ, 2nd & 3rd)
    • Inflammatory – rheumatoid / inflammatory arthopathy
    • Endocrinopathy: DM (neuropathic joint), acromegaly, hyperparathyroidism
    • Miscellaneous (AVN, genetic skeletal disorders)
  • Non-Erosive (classic OA) vs. Erosive – features of inflammatory OA, often post-menopausal & hereditary; PIPJ
  • By joint & disease stage (see below)
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4
Q

list findings on physical exam for OA hand

A

THUMB OA

  • dorsal subluxation
  • MCPJ hyperextension
  • adduction contracture*
  • tenderness*
  • pain and/or crepitus with axial loading (and/or traction)*
  • decreased a/pROM*

rest of hand see * above and:

  • heberden’s nodes (DIPJ)
  • Bouchard’s nodes (PIPJ)
  • mucous cyst formation
  • instability
  • decreased grip strength
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5
Q

xray findings of OA

A

o joint space narrowing, subchondral sclerosis, subchondral cysts, osteophytes

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6
Q

what are goals for treatment of OA

A

(in order) – control pain, improve function, correct deformity, improve appearance

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7
Q

outline a general treatment approach to OA

A
  • Conservative: all patients start here; often intra-articular steroid after other modalities first (unless severe)
  • NSAIDS, Tylenol, splinting, activity modification, steroid injection (triamcinalone), mechanical assists (PT/OT)
  • Surgical management – Indications à intractable functional pain, deformity impacting function after non-operative trial
  • Options: arthrodesis, arthroplasty (including tenoplasty, ligamentoplasty)
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8
Q

why is the volar beak ligament important? how does its pathology contribute to thumb CMC OA?

A
  • volar oblique ligament is most important stabilizing structure (pinch produces a dorsal force)
  • volar beak of bone on MC base ® trapezial tuberosity (controls pronation & prevents radial translation)

pathology

  • volar beak ligament attrition –> ligamentous laxity –> abnormal joint position and loading –> abnormal transmission of force across joint surface –> biomechanical change and loss of articular cartilage
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9
Q

why does the thumb assume a hyperextension posture at MCP w/ CMC OA?

A
  • Lateral/dorsal subluxation d/t capsular / intermetacarpal ligamentous laxity, hypertrophic medial spurs, pull of APL ® compensatory MPJ hyperextension & thumb adduction
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10
Q

what is the differential diagnosis for thumb cmc oa?

A

· Tendonitis/tenosynovitis: FCR; de Quervain’s (1st dorsal compartment); intersection syndrome (2nd compartment)

· Inflammatory arthritis: RA

· Crystal arthropathy: gout, cppd

· Ligamentous: Chronic UCL injury (Gamekeeper’s thumb)

· Neuropathy: Radial sensory neuritis (Wartenberg); CTS

· Arthritis at other joint: SLAC wrist; isolated STT arthritis; radiocarpal, MCP

· Scaphoid trauma

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11
Q

in addition to usual views on XR, what additional imaging would you want for thumb cmc oa?

A
  • X-rays: Stress view – PA at 30° (shows MC base lateral subluxation); Roberts view – AP of hyperpronated hand (all 4 trapezial articulations)
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12
Q

describe eaton classification for thumb cmc oa

A

Stage I

  • Normal X-ray, joint space may be wide

Stage II

  • Joint space narrow, minimal subchondral sclerosis, debris<2mm, STTJ normal

Stage III

  • ++narrow, cystic changes/sclerosis/debris>2mm, variable subluxation. STTJ normal

Stage IV

  • Pantrapezial arthritis, large osteophytes, ++ subchondral sclerosis, STTJ arthritis
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13
Q

list surgical options for thumb cmc oa?

A

Stage 1

  1. Palmar/volar oblique ligament reconstruction
  2. MC osteotomy

Stages 2-4

  1. Trapeziectomy ± hematoma/distraction arthroplasty
  2. Trapeziectomy w/ interposition graft
  3. Trapeziectomy, LR(±TI)
  4. Arthrodesis
  5. Arthroplasty
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14
Q

describe MC osteotomy for thumb CMC OA

A
  • Designed to restore abduction and extension
  • 4 cm longitudinal incision over radial border of 1st metacarpal
  • Resect radially based 20-30o wedge within 2 cm of joint
  • Distal MC extended and compressed through wedge excision; fixation K wires, intraosseus loops, plate
  • Advantages: pain relief, improved function (increased grip & pinch @ 2 yrs)
  • Nonunion up to 50%
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15
Q

describe trapeziectomy and LRTI

A
  • Trapeziectomy & LRTI
  • Incise: rad bord 1st MC, dissect between APL/EPB or EPL / EPB
  • Trapezial resection (in quadrants) - FCR tendon is at base
  • drill hole through base of MC in line with nail plate, and out through base of MC
  • FCR harvest (1/2 or all) through 2 transverse volar forearm incisions, pull into joint
  • Pass FCR through base of MC, sutured onto itself (as tight as possible), interpose into joint, (± Kwire)
  • Alternative = APL à one slip harvested, passed through base 1st MC (or around FCR), through 2nd MC (radial/volar à dorsal ulnar), free end woven through ECRB and secured to itself (± Kwire)
  • Capsular & wound closures
  • Postop: cast for 4 weeks, splint for 4 weeks, normal function at 12 weeks
  • Advantage: most common, durable/reliable outcome, pain relief, increased grip/pinch
  • Disadvantage: loss of trapezial space height; no advantage over trapeziectomy alone (PRS 2011 Thoma, Sys. Rev)
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16
Q

describe considerations for management of MCPJ hyperextension during thumb cmc oa operations

A
  • Degree of hyperextension
    • <20 - no Rx
    • 20-30 deg - EPB tenotomy à transfer to base of MC to augment APL; K-wire x 4/52
    • >30° – fusion vs. volar capsulodesis MPJ + EPB tenotomy vs. sesamoid arthrodesis vs. palmaris longus volar plate reconstruction (No evidence of approach superior to another, no long term comparative prospective studies)
  • Non-operative management – figure of 8 splint
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17
Q

describe use of arthroplasty for pipj oa

A
  • Arthroplasty – less active patients with stiff, painful joints, flex/ext arc 60-80⁰ –> ½ pre-op ROM expected
  • Volar plate arthroplasty (limited use)
  • Silastic arthroplasty: joint spacer (RA pt), pain relief, less stable, limited ROM
    • dorsal, volar or lateral approach; must preserve central slip insertion
    • oblique osteotomies, remove minimal bone
  • Surface replacement arthroplasty
    • constrained prosthesis, chromium-cobalt alloy, pyrocarbons
    • PP head and articular base of MP (looks like a mini total knee)
    • Greater stability, likely higher complications, higher cost, ? long-term durability
  • Immobilize x 2/52, then limited ROM x 2/52 more (can be more aggressive with constrained implants
  • Advantages: preserve ROM (avg ROM post-op: 40’-60’ TAM)
  • Disadvantages: not full ROM/ ROM may deteriorate; compliance w/ therapy, implant failure, instability, deformity
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18
Q

describe use of arthrodesis for pipj oa

A
  • Arthrodesis – young, high demand patient, significant loss of bone, symptom relief, stability (preference for D2/3
  • Dorsal approach, splint extensor tendon and joint capsule; cup & cone vs osteotomies/rongeur
  • Plating is best. Alternatives – K-wire, screw, Fig of 8 tension band
  • Best for index +/- small (pinch, stability)
  • Advantage stable and reliable
  • Distadvantage: PIPJ contributes 85% to finger ROM and ~ 25% to hand flexion, loss of grip, NU/DU/MU
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19
Q

what is your differential for mono- arthritis of joints in hand?

A

MONOARTHRITIS

  • Crystal induced
  • Infection (acute, chronic)
  • Trauma, hemarthrosis
  • Osteoarthritis
  • Foreign body
  • Pigmented villonodular synovitis
  • Joint neoplasms
  • Aseptic necrosis
  • Osteochondritis dissecans
  • Mechanical internal derangement
  • Sarcoidosis
  • Neuropathic (Charcot) joint
  • Onset of polyarthritis
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20
Q

describe XR finding in psoriatic arthritis

A
  • Imaging – osteolysis, pencil in cup (typically DIP), arthritis mutilans (osteolysis hand with collapse), ankyloses
  • Distal to joint = bone proliferation; proximal side joint = bone wasting
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21
Q

what is presentation for psoriatic arthritis?

A
  • Presentation – psoriasis, joint pain/stiffness >30 mins in AM, relieved with activity
  • Classic PE – psoriatic plaque, distal & asymmetric, nail lesions (pitting, onycholysis); PIPJ 95% (flexion deformity, no boutonniere), polyarthritis 25%, DIP 5%
  • Associated features: enthesitis, dactylitis (fusiform), pitting edema, uveitis
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22
Q

what is your treatment approach to psoriatic arthritis?

A
  • Medical – NSAIDS, steroids (systemic), DMARDs (MTX, penicillamine)
  • Surgical (rare) – synovectomy/tenosynovectomy, tendon release/repair/transfer (DIP usually autofuses; PIP fusion, MCP arthroplasty, fusion/bone graft arthritis mutilans to maintain length
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23
Q

what is the classic presentation and diagnostic criteria for lupus arthritis

A
  • Presentation – F>>M, onset 15-25yo, black>white, morning stiffness, pain, +/- Raynaud’s
  • Classic PE – Erythematous maculopapular eruption fingers & palm, symmetric joint swelling & pain, tenosynovitis
  • Joint deformities – see below (ligamentous and volar plate laxity, tendon subluxation
  • 11 criteria: Serositis, oral ulcers, arthritis, photosensitivity, blood (pancytopenia), renal disorder (proteinuria), ANA+, immunologic (anti-dsDNA, anti-Smith, APLA), neurologic (seizures, psychosis), malar rash, discoid rash
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24
Q

discuss treatment approach to lupus arthritis

A

Treatment

o Medical – Rheum/Medicine, NSAIDS, steroids, hand therapy & splints (to delay surgery)

o Surgical – soft tissue procedures (extensor tendon relocation & tenodesis) – do not provide long-term results; selective arthrodesis is often the best choice

Wrist

MCP

PIP

DIP

Thumb

Deformity

Caput unlna

  • SL dissoc.
  • Radial dev
  • Ulnar trans carpus
  • Dorsal sublux ulna
  • Ulnar deviation PP
  • Volar subluxation PP
  • Ulnar subluxation EDC
  • Hyperextension
  • Flexion
  • Lateral deformity
  • Hyperextension
  • Flexion
  • Lateral deformity
  • MP hyperextension
  • Lateral subluxation at distal joint
  • Subluxation of extensor tendons

Mgmt.

  • Limited & total wrist fusion
  • (Darrach w/ ECU stabilization)
  • Swanson arthroplasty
  • Extensor tendon relocation
  • Early – soft tissue re-alignment
  • Late – arthrodesis
  • Early – soft tissue re-alignment
  • Late – arthrodesis
  • EPL rerouting
  • Arthrodesis in 15-20° flexion
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25
Q

describe classic presentation of gout

A
  • Presentation – M>>F, ↑ with age
  • Classic PE – MTP great toe most common (acute monoarticular inflammatory condition), exquisitely tender, tophi
  • DDx – sept arth, suppur tenosynovitis, RA, cancer
  • Labs – CBC, serum urate, Xray, urine (crytals), Joint aspirate –> gout = negatively birefringent crystals (polarized light)
  • Imaging – early – no change; late = punched out erosions or lytic areas with overhanging edges
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26
Q

describe classic presentation of scleroderma

A
  • Presentation – F>M, CREST –> Calcinosis, Raynaud’s, Esophageal dysfunction, Sclerodactyly, Telangiectasia
  • Classic PE – progressive PIPJ contracture, hyperextension MCPJ, 1st web contracture, extensor tendon rupture, soft tissue breakdown/ulcers/gangrene with exposed tendon/bone/joint
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27
Q

describe approach to treatment of scleroderma arthritis and hand problems

A

Treatment

o Medical – Rheum, D-penicillamine, MTX, interferon

o Surgical – Avoid GA and tourniquet

§ Wound management to minimize infection

§ Optimize: vascularity, function, cosmesis, improve pain

DIP

PIP

MCP

1st Web

Deformity

Gangrene, tuft resorption

Fixed flexion deformity

Hyperextension

Contracture

Mgmt.

  • Fusion
  • Amputation if gangrenous, infected, osteomyelitis
  • Fusion: angle depends on MCPJ ROM
  • Resection of joint to overcome contractures
  • ± Arthroplasty
  • Release of thumb adductor, FTSG
  • Standard web release techniques
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28
Q

what is hypothenar hammar syndrome and classic presentation?

A
  • Thrombembolic occlusion or aneurysm UA à digital ischemia
  • Repetitive blunt palmar or hypothenar trauma
  • PE – Pain, cold sensitivity, sensory disturbances, hypothenar mass, dig ischemia, ulceration, abnormal Allen’s test
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29
Q

what is your approach to treatment of hypothenar hammar syndrome?

A
  • Conservative/Medical – vasodilation for acute ischemia (warm room, compresses, lidocaine plain injections, CCB, nitroglycerin paste; ↓ sympathetic tone (pain control, rest)
  • activity modification, cold protection, CCBs, quit smoking
  • Operative/interventional: thrombolysis, excision & ligation, excision & vein grafting
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30
Q
A
31
Q

Define and describe rheumatoid arthritis

A
  • RA is a chronic progressive inflammatory disorder driven by a T-cell mediated autoimmune process
  • that preferentially affects synovial tissue
  • leading to pain, deformity and destruction of soft tissue (tendon, subcut) and joints (ligaments, capsule, synovium, bone); also extra-articular invovlement in some
32
Q

what is the etiology of RA?

A
  • is idiopathic, with a
  • complex interaction between genetic and environmental factors
  • genetic factors include HLA-DR4 and PTPN22
  • environmental include smoking, infectious exposure
33
Q

what is the pathophysiology of RA?

A
  1. an autoimmune disease, where an antigen (trigger) is presented to the synovium/synoviocytes
  2. incites a cell mediated MHC type II response - leading to cellular and chemical influx - T cells, B cells (and antibodies), macrophages/monocytes, synoviocytes, cytokine and other systemic inflammatory modulators
  3. local effects - synovium targeted first, then tissue, cartilage and bone
    1. inflamed and proliferating synovium (pannus)
    2. synovial pannus produces proteolytic enzymes (such as metalloproteinases, serine proteases, cathepsins, and aggrecanases) and activates osteoclasts
    3. mechanical distention of supporting soft tissue structures and erosion of cartilage and bone
34
Q

what is rheumatoid factor?

A

§ IgM antibody that attacks native IgG Ab, immune complex deposited in end tissue (eg kidney)

35
Q

what cell and what cytokines are primary mediators of tissue destruction

A
  • monocyte
  • TNF and IL-1
36
Q

WHAT ARE THE GOALS OF SURGERY IN PATIENTS W RA?

A

· Pain relief

· Improve function

· Limit disease progression

· Address aesthetic deformity

37
Q

DISCUSS PRINCIPLES IN THE SEQUENCE/PLANNING OF SURGERY for RA

A

· Painful before painless

· Proximal to distal

· Lower before upper (so hands don’t get ruined on crutches or wheelchair)

· Stabilizing before mobilizing

· Flexor tendon reconstruction before MPJ arthroplasty before extensor tendon reconstruction (controversial)

· Predictable procedures first

o Tenosynovectomy (flexor before extensor), Wrist fusion, Distal ulna resection

o Then proceed with more complicated and less predictable procedures

· Tendon rupture and nerve compression are high priority

38
Q

LIST DIAGNOSTIC CRITERIA FOR ADULT RA

A
  • 4 of 7 is diagnostic; Numbers 1 through 4 present > 6 wks.
  1. Morning stiffness > 1 hr
  2. 3+ joints
  3. Hand involvement (wrist/MCP/PIP)
  4. Symmetrical
  5. RF+
  6. Subcutaneous nodules
  7. XR evidence of peri-articular bone erosion and osteopenia of wrist/hand
39
Q

WHAT ARE EXTRA ARTICULAR MANIFESTATIONS OF RA?

A
  • Rheumatoid nodules
  • Rheumatoid vasculitis
  • Cardiac: pericarditis,
  • Pulmonary: pleural effusion or interstitial disease
  • Peripheral neuropathy: CTS, cubital tunnel etc
  • Ocular: keratoconjunctivitis sicca
  • Felty’s syndrome (RA with splenomegaly and leukopenia)
  • Still’s disease (acute onset RA with fever, rash and splenomegaly)
  • Sjogren’s syndrome (autoimmune condition affecting exocrine glands)↓secretions from salivary & tear duct glands, Lymphoid tissue proliferation
40
Q

DESCRIBE HOW ATTACKING SYNOVIAL TISSUE INFLUENCES OUR UNDERSTANDING OF THE ARTICULAR / PERIARTICULAR MANIFESTATIONS OF RA

A
  • Hand joints 1st (high synovium to joint surface ratio), larger/proximal joints later (lower ratio); DIPJ often spared (low synovial content)
    • inflammed synovium leads to inflamation, distension of periarticular soft tissue
  • Synovial lining of tendons (therefore see also: CTS, trigger, rupture, tendonitis)
41
Q

describe peri-operative considerations in RA patients

A
  • TMJ invovlement and limited mouth opening
  • glottic narrowing
  • atlanto-axial instability (pre-op cspine flexion-extension XR)
  • Felty’s syndrome: splenomegaly, neutropenia, and secondary thrombocytopenia
  • pulmonary: disease and drug effects – nodules, interstitial fibrosis
  • medications: steroids (stress dose), MTX (plt #), ASA/NSAIDS (plt fxn) etc
42
Q

what is the peri-operative work up and management of medications in patients w RA

A
  • anaesthesia consult, ECG, metabolic panel, CBC + diff, chest X-ray, and cervical spine radiographs
  • If >5mg/day prednisone require steroid coverage if undergoing GA, prolonged or invasive surgery (generally not for outpatient hand procedures)
    • Solucortef 100mg IV pre-op, then 100mg IV q8hrs x 24hrs (day of surgery), then 50mg IV q8hrsx24hrs (POD1), restart daily dose PO/IV POD #2
  • MTX: continue normal pre-op dose
  • other conventional DMARDs: discuss w/ rheumatologist, but in general continue
  • biologic DMARDs: discuss w/ rheumatologist, but in general hold for 2-4 wks before and after surgery
43
Q

Describe your history and physical exam for RA patient

A

History

oPresence, duration, rate of change of symptoms, current & previous joint involvement

oCurrent and past medications and surgery

oUse of aids (ambulatory or for ADLs), splints, OT/PT

oSocial history, occupation, habits

Physical

oFull UE exam, joint ROM/stiffness/subluxation, tendon function (active/passive/adhesions/triggering), sensory/motor

oObjective measures: ROM (Goniometer), grip strength (dynanometer), pinch strength (pinchmeter)

44
Q

describe XR findings in RA patient

A
  • Early – Osteopenia (diffuse)
  • Joint space widening (from the joint effusion)
  • Rheumatoid nodules
  • Late – Blurring of cortical outline (destruction of joint margins)
  • Deep erosions irregular cup-shaped appearance (rat-bite)
  • Narrowing of joint space (loss of cartilage)
  • Subluxation (ligamentous laxity)
  • Marginal sclerosis and ostoephyte formation denotes secondary osteoarthritis
45
Q

describe medical management of RA

A
  • Medical: 3 classes
  • NSAIDS – reduce acute inflammation à pain relief, improve function, DO NOT ALTER DISEASE COURSE
  • Corticosteroid (systemic) – prednisone, methylpred: reduce inflammation, regulate immune system function (for pts whom NSAIDS no longer effective) à effective for symptom control, improve function, DO NOT ALTER DISEASE COURSE OR PROGRESSION OF JOINT DESTRUCTION, +++ side effects
  • DMARDS: decrease pain, improve function, induce remission, halt radiographic progress’n of joint destruction, safe, long-lasting effects
    • Conventional: methotrexate (also azathiprine, gold, anti-malarial)
    • Biologic: anti-TNF (etanercept [Enbrel], infliximab [Remicade], adalimumab [Humira]) & anti-IL-1 (anakinra [Kineret])
    • Combined thereapy (usually MTX + biologic) – most effective. Disadv of DMARD / cominbed tx = COST
46
Q

describe a different in treatment approach to CTS in RA patient

A

distal and proximal extensions of incision, CT decompression and tenosynovectomy, excision of bone spur on scaphoid

47
Q

what is the mechanism for tendinopathies among patients w/ RA

A

· Direct invasion/erosion of tendon by synovitis

· Mechanical disruption within sheath

· Attrition across bony (eroded) prominences

48
Q

describe flexor tenosynovitis in RA patient

A
  • Trigger digit: usually coming after failed non-surg including failed intralesional; if not then release 1st line
    • Brunner incision, tenosynovectomy and excise nodules, leave A1 intact (prevent further volar sublux’n and ulnar drift), consider excision of 1 slip of FDS
  • Flexor synovitis at volar wrist in carpal tunnel and distal forearm: with CTS; get XR (for scaphoid bone spur)
49
Q

describe surgery for extensor tenosynovitis in RA patient

A

§ tenosynovectomy if failed medical mngmt x mos; can improve pain/swelling - do wrist capsulotomy and assess for need for wrist synovectomy

+/- Darrach procedure if dorsal dislocation of distal ulna

+/- rongeur of lister’s tubercle

+/- side-to-side tenodesis if impending tendon rupture

+/- dorsal reposition of ECU (can use the ulnar base flap)

• dorsal longitudinal incision, divide retinaculum in “step ladder” or “zig-zag” (radial flap hinged off 1,2 septum; ulnar flap hinged off 4,5 septum), close - 1/2 under tendons and 1/2 over tendons

§ Complications: nerve injury, adhesions, tendon rupture

50
Q

what is classic presentation of flexor tendon rupture in RA patient

A
  • radial to ulnar
  • FPL most common
51
Q

why does the FPL rupture? What is that called? How do you manage?

A
  • FPL rupture on scaphoid erosion = Mannerfelt lesion
    • tenosynovectomy and excision of boney spicules
    • primary repair with tendon graft
    • or FDS (d3/d4) tendon transfer and pull-through at insertion
    • or IP arthrodesis (allow for stable pinch)
52
Q

describe management of extrinsic finger flexor rupture in RA patient

A
  • FDS rupture
    • zone IV: to adjacent tendon
    • Zone III: to adjacent FDP or FDS
    • Zone II: leave alone, 2-stage recon, PIP/DIP arthrodesis
  • FDP rupture
    • no tendon repair +/- DIPJ arthrodesis
    • end-to-side with adjacent FDP or intact FDS +/- tendon graft
53
Q

what is differential diagnosis of inability to extend finger(s)[thumb] in RA patient?

A

§ extensor tendon rupture

§ extensor tendon subluxation at MCPJ

§ MCPJ volar subluxation/dislocation

§ Trigger digit (stuck in flexion)

§ PIN compression

§ Also (not related to RA): dupuytren’s

54
Q

why would a patient be unable to extend their long finger, but maintain extension when passively placed there? how would you manage this problem?

A
  • Extensor tendon subluxation at MCPJ due to laxity of radial sagital band (passively correct and pt can maintain ext’n)
    • Centralization & soft tissue rebalancing: transverse incision across MCP, mobilize tendon, imbricate radial SB, ulnar intrinsic release with/without cross-finger intrinsic transfer
55
Q

what is it called when there is a progression of extensor tendon ruptures in RA?

how would you manage the following scenarios?

  • extensors to D5
  • D4 & D5
  • D3,4,5
  • EDC 2,3,4,5
  • EIP & EDC 2,3,4,5
  • EPL - how manage, why does it happen?
A
  • Vaughn–Jackson syndrome: ulnar to radial progression of extensor tendon rupture
    • EDM+EDC5: end-to-side or EIP transfer
    • EDC4+EDC5: EDC4 end-to-side to 3; EIP tendon transfer to EDC5 (or EIP to EDC4,5)
    • EDC3,4,5: EDC3 end-to-side EDC2; EIP to EDC4/EDQ
    • or EIP to EDC3 and FDS4 to EDC4,5
    • EDC2,3,4,5: EDC3 end-to-side to EIP; FDS4 to EDC4/EDQ
    • or FDS3 to EDC2,3 and FDS4 to EDC4,5
    • all: FDS4 to EDC4/EDQ; FDS3 to EDC2 + EIP/EDC3
    • consider treating all tendons like a radial nerve palsy
    • FCR for EDC, PL for thumb EPL, PT for wrist/ECRB
    • never to more than 2 tendon to 1 transfer
    • possibly combine with tenosynovectomy, Darrach procedure
  • EPL on Lister’s tubercle (vs. synovial invasion): EIP transfer vs. EPB vs. PL
56
Q

describe the net effect of wrist and hand deformity in RA

A

Net effect: caput ulna syndrome + SUV of carpus + Zig-Zag deformity

  • Caput-ulna syndrome – dorsal dislocation of the ulnar head (or volar displ radio carpal jt), carpal supination and volar subluxation of the ECU 2’ destruction ligamentous complex from synovitis of ulnar wrist/DRUJ
  • SUV carpus: supination, ulnar translation, volar subluxation
  • “Zig-Zag” deformity: ulnar translation of carpus, radiation deviation of MC, ulnar deviation of phalanges
57
Q

describe the pathomechanics of RA wrist & hand deformities

A

Radial side – Attenuation of radioscapholunate ligament and radiocapitate ligament

  • Rotatory displacement of scaphoid: scaphoid volar-flexed, ↓ carpal height –> Scapholunate dissociation –> Radiocarpal collapse
  • Carpus supinates, slides ulnar & volar, then radial deviation of MC and ulnar deviation at MCP (pathology of zig-zag)

Ulnar side – Attenuation of ulnocarpal ligaments

  • Radioulnar dissociation with dorsal prominence of distal ulna
  • Volar displacement of ECU tendon
  • Caput Ulnae –> DRUJ incongruity –> impaction of distal ulna on carpus
58
Q

list and briefly describe the surgical options to TREAT THE WRIST in RA

A
  • Prophylactic options
  • Synovectomy / tenosynovectomy: ongoing edema/inflammation and pain despite > 6 mos medical tx
    • Dorsal longitudinal incision; split extensor retinaculum between 3rd and 4th compartments; excise synovitis; consider PINectomy on floor of 4th compartment; open joint capsule for synovectomy; secure ECU dorsally
  • ECU relocation
  • Tendon transfer to rebalance wrist (ECRL to ECU)
  • Radiocarpal fusion: RL (Chamay) or RSL – disease isolated to RC (disease free mid-carpal): address pain, add stability, preserve some motion; disadv: risks w/ bone & hardware
  • Corrective: remember, painless stable wrist is foundation for reconstruction of hand
  • Total wrist arthroplasty – for painful but low demand wrist w stable soft tissue & good bone stock; adv is preserve ROM; disadv are “relatively” great – bone& hardware + implant complications; arthrodesis for failure more difficult
  • Total wrist arthrodesis (often combined w/ Darrach) – for recalcitrant, disabiling pain, unstable wrist: predictable & reliable results (painless, stable wrist) & correction of deformity; disadv: w/ bone & hardware; goal is straight MC (fixate 3rd MC base, capitate, distal radius); use ICBG – if good bone then limited contact dynamic compression plate (LCDCP); if poor bone stock then Steinmann pins
59
Q

list and briefly describe surgical options to treat the DRUJ in RA

A
  • Can be combined w/ tenosynovectomy, ECU translocation, tendon transfer; arthordesis (doing w/ RL/RSL arthrodesis (preserved mid-carpus) or total wrist arthrodesis)
  • Darrach: procedure of choice (most common) – distal ulna resection; risk is further ulnar carpal translocation (combine w/ one of arthrodesis above): preserve TFCC, undertake sub-periosteal resection, interpose PQ btwn distal radius & ulna
  • Sauve-Kapanji: fusion of DRUJ combined with proximal ulna ostectomy & pseudarthrosis; helps to support ulnar carpus / prevent translation
  • Bower’s Hemi-Resection: interposition arthroplasty
60
Q

describe the deformity at MCPJ in RA

what is the pathophysiology of that deformity?

A
  • Predictable deformity: pain, with volar subluxation and ulnar drift
  • Intrinsic factors
    • Synovitis with distension of joint capsule
    • Synovial invasion of collateral ligaments with secondary laxity
    • Attenuation of radial sagittal band allows ulnar subluxation of extensor tendon
  • Extrinsic factors
    • Volar and ulnar forces on joint cause subluxation in those directions
    • Forces of gravity and pinch
  • Anatomic factors
    • Normal mechanical advantage of ulnar intrinsics
    • Asymmetry and slope of MC head of index & middle fingers
    • Asymmetry of collateral ligaments
    • Flexor tendon mechanics – enter sheath at angle to allow ulnar palmar pull
    • Carpal collapse causes wrist radial deviation – compensatory MP ulnar drift
61
Q

how do you first consider treating an MCPJ that is passively correctable

A
  • MCPJ synovectomy and tendon rebalancing
  • Centralize extensor tendon by:
    • Imbricating radial sagittal band
    • Ulnar intrinsic release
    • Cross-intrinsic transfer: divide ulnar lateral band distally in D2/3/4 & transfer to radial side extensor tendons of D3/4/5)
    • Release ADM for D5
62
Q

describe the surgical options to consider when an MCPJ is not passively correctable (fixed deformity) and/or there is radiologic evidence of joint destruction (and pain)

A
  • Unable to passively correct MCP (or sig erosion on x-ray): arthroplasty vs. arthrodesis
  • MCPJ arthroplasty with soft tissue recon as needed (reconstruction radial sagittal band, ulnar intrinsic release, centralization extensor tendon)
    • Swanson arthroplasty = procedure of choice good pain relief, modest ↑ROM
  • Transverse incision across dorsal MC heads, expose subcapsule/periosteal, osteotomies at MC flare, awl to create hole for stem, size generally D2&3=5, D4=4, D5=3, close capsule over top, ± tendon repositioning
  • Post-op 6/52 MCP extension, PIPJ free, ROM daily
    • Alternatives: unconstrained pyrocarbon (more unstable in context of already unstable soft tissues) or volar plate arthroplasty (proximal VP on dorsal MC, when MCP medulla too small for implant)
  • Arthrodesis is risky, because so much motion comes from that joint
63
Q

discuss arthroplasty vs arthrodesis in PIPJ in RA patient

A

· Generally, the soft-tissue instability of PIPJ precludes use of arthroplasty for RA (consider more in OA)

· Never for index +/- small; Use silicone (more stabl than pyrocarbon) if at all

64
Q

what is more problematic for a patient? Swan-Neck or Boutonniere? (why)

what is more problematic for a surgeon? Swan-Neck or Boutonniere? (why)

A
  • For a patient SWAN NECK IS MORE PROBLEMATIC
    • because SND patients cannot flex their finger/pipj - no grasp, sig decr fxn
  • For a surgeon BOUTONNIERE IS MORE PROBLEMATIC
    • because there is more to lose; it is a difficult problem to correct, and you are taking a more functional deformity and risking PIPJ hyperextension (and dysfxn like SND)
65
Q

DESCRIBE THE ETIOLOGIES OF SWAN NECK DEFORMITY IN RA; COMPARE TO ETIOLOGY OF BOUTONNIERE

A

SWAN NECK:

  • DIPJ: Mallet deformity
  • PIPJ: Volar plate/ligamentous laxity, FDS rupture
  • MCPJ: volar subluxation & intrinsic muscle tightness

BOUTONNIERE

  • Problem always originates from PIPJ: central slip avulsion/rupture —> volar subluxation lateral band à tightening of retinacular ligaments —> hyperextension at DIPJ
66
Q

DESCRIBE YOUR TREATMENT APPROACH TO PATIENT W SWAN NECK DEFORMITY

A
  • TREAT THE JOINT OF ORIGIN
  • If early/ passively correctable in all positions (no intrinsic tightness) consider non-op mngmt w/ figure of 8 splint
  • If etiology is at the DIPJ (Mallet) then arthrodesis of DIPJ with trial post-op of splint for PIPJ hyperextension
  • If etiology is at MCPJ: any subluxation and intrinsic tightness should be managed first with arthroplasty +/- soft tissue procedures (above)
  • Passively correctable / no joint destruction, etiology @ PIPJ (or not corrected by above procedures): need to address PIPJ hyperextension (via extension block) and intrinsic tightness (via release): choose one/several of as appropriate:
    • Volar plate proximal advancement to restrain PIPJ
    • FDS lasso (tenodesis): divide proximal slip, suture to A1 pulley
    • Oblique retinacular ligament reconstruction (ORL, Littler): ulnar lateral band is detached proximally, passed volar (in to axis of PIPJ/volar to Cleland’s ligament (in a spiral), sutured to PP w/ PIPJ in flexed posture
    • Distal/ulnar intrinsic release
    • Relocaiton of lateral bands (if lateral bands are tight, dorsal incision, incise btwn central slip & lateral bands to allow volar migration; combine with other procedure)
    • Consider: lateral band release, capsulotomy, central slip step-lengthening
  • Fixed deformity w/ joint destruction
    • Athrodesis >>>> arthroplasty (soft tissue laxity increases failure rate of ‘plasty)
67
Q

describe your treatment approach to Boutonniere deformity

A
  • intervention for moderate to severe deformity that is very debilitating only, because risk destabilizing the PIPJ +/- causing a PIPJ hyperextension/SND (ie can still make a fist w/ a Boutonniere, but you cannot w SND, therefore that is worse)
  • Non-operative management is first line:
  • PT/OT, serial splints/casts of PIPJ (keep DIPJ free to help reposition the lateral bands volar)
  • To optimize a passively correctible joint that is not a full pROM
  • Passively correctable:
  • PIPJ synovectomy
  • Reposition of lateral bands to dorsal position
  • Tenotomy of terminal tendon @ DIPJ
  • Central slip reconstruction (shortening)
  • Fixed deformity:
  • Arthrodesis >>>> arthroplasty (for RA, as above)
68
Q

what is gout?

A
  • metabolic disorder
  • characterized by hyperuricemia
  • deposition of monosodium urate crystals in joints
69
Q

list important considerations for small joint arthroplasty

A
  1. Indications: stiff, painful or deformed joint
  2. Contraindications: insufficient bone stock, poor soft tissue cover, infection, paralysis of extrinsic tendons
  3. Preferred in sedentary vs. heavy laborers
  4. Anticipate therapy and motion to begin within a few days after surgery
  5. Set realistic expect ions for post op ROM
  6. Advise pts of potential complications of
    1. early: wound, infection, prosthetic dislocation, nerve injury
    2. late: stiff / loss of motion, recurrent deformity, prosthetic loosening, prosthetic fracture
70
Q

List the indications for bone graft in arthrodesis

A
  1. revision
  2. insufficient bone stock / traumatic bone loss
  3. infection
  4. arthritis mutilans
71
Q

what is silicone synovitis?

A
  • a reactive synovitis in response to silicone particulate debris released w wear & tear of silicone prostheses, driven partially by migration of macrophages (foreign body giant cells) which promote inflammation and further arthorplasty wear, exposing underlying bone
72
Q
A
73
Q

what is your differential for polyarthritis of joints of hand

A

- inflammatory arthropathies (ex: RA, SLE, ankylosing spondylitis, psoriatic arthritis)

  • Primary generalized (erosive) osteoarthritis
  • Secondary osteoarthritis
  • Calcium pyrophosphate dehydrate
  • deposition disease
  • Neuropathic joint disease
  • Acromegaly
  • Arthrogryposis
  • Hemachromotosis
  • Wilson’s disease
  • Osteodystrophy
  • Heritable disorders of connective tissue

rheumatoid arthritis, osteoarthritis, inflammatory arthritis, Lupus and scleroderma, others (38 decks)

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