Arthritis (all types) Flashcards

Question 1

Q

Define osteoarthritis

Answer

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.

Question 2

Q

Describe the pathophysiology of osteoarthritis

Answer

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

Question 3

Q

how do you classify osteoarthritis?

Answer

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, 2^nd & 3^rd)
- 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)

Question 4

Q

list findings on physical exam for OA hand

Answer

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

Question 5

Q

xray findings of OA

Answer

A

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

Question 6

Q

what are goals for treatment of OA

Answer

A

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

Question 7

Q

outline a general treatment approach to OA

Answer

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)

Question 8

Q

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

Answer

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

Question 9

Q

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

Answer

A

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

Question 10

Q

what is the differential diagnosis for thumb cmc oa?

Answer

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

Question 11

Q

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

Answer

A

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

Question 12

Q

describe eaton classification for thumb cmc oa

Answer

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

Question 13

Q

list surgical options for thumb cmc oa?

Answer

A

Stage 1

Palmar/volar oblique ligament reconstruction
MC osteotomy

Stages 2-4

Trapeziectomy ± hematoma/distraction arthroplasty
Trapeziectomy w/ interposition graft
Trapeziectomy, LR(±TI)
Arthrodesis
Arthroplasty

Question 14

Q

describe MC osteotomy for thumb CMC OA

Answer

A

Designed to restore abduction and extension
4 cm longitudinal incision over radial border of 1^st metacarpal
Resect radially based 20-30^o 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%

Question 15

Q

describe trapeziectomy and LRTI

Answer

A

Trapeziectomy & LRTI
Incise: rad bord 1^st 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 1^st MC (or around FCR), through 2^nd 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)

Question 16

Q

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

Answer

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

Question 17

Q

describe use of arthroplasty for pipj oa

Answer

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

Question 18

Q

describe use of arthrodesis for pipj oa

Answer

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

Question 19

Q

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

Answer

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

Question 20

Q

describe XR finding in psoriatic arthritis

Answer

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

Question 21

Q

what is presentation for psoriatic arthritis?

Answer

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

Question 22

Q

what is your treatment approach to psoriatic arthritis?

Answer

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

Question 23

Q

what is the classic presentation and diagnostic criteria for lupus arthritis

Answer

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

Question 24

Q

discuss treatment approach to lupus arthritis

Answer

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

Question 25

Q

describe classic presentation of gout

Answer

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

Question 26

Q

describe classic presentation of scleroderma

Answer

A

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

Question 27

Q

describe approach to treatment of scleroderma arthritis and hand problems

Answer

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

1^st 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

Question 28

Q

what is hypothenar hammar syndrome and classic presentation?

Answer

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

Question 29

Q

what is your approach to treatment of hypothenar hammar syndrome?

Answer

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

Question 30

Q

Question 31

Q

Define and describe rheumatoid arthritis

Answer

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

Question 32

Q

what is the etiology of RA?

Answer

A

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

Question 33

Q

what is the pathophysiology of RA?

Answer

A

an autoimmune disease, where an antigen (trigger) is presented to the synovium/synoviocytes
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
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

Question 34

Q

what is rheumatoid factor?

Answer

A

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

Question 35

Q

what cell and what cytokines are primary mediators of tissue destruction

Answer

A

monocyte
TNF and IL-1

Question 36

Q

WHAT ARE THE GOALS OF SURGERY IN PATIENTS W RA?

Answer

A

· Pain relief

· Improve function

· Limit disease progression

· Address aesthetic deformity

Question 37

Q

DISCUSS PRINCIPLES IN THE SEQUENCE/PLANNING OF SURGERY for RA

Answer

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

Question 38

Q

LIST DIAGNOSTIC CRITERIA FOR ADULT RA

Answer

A

4 of 7 is diagnostic; Numbers 1 through 4 present > 6 wks.

Morning stiffness > 1 hr
3+ joints
Hand involvement (wrist/MCP/PIP)
Symmetrical
RF+
Subcutaneous nodules
XR evidence of peri-articular bone erosion and osteopenia of wrist/hand

Question 39

Q

WHAT ARE EXTRA ARTICULAR MANIFESTATIONS OF RA?

Answer

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

Question 40

Q

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

Answer

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)

Question 41

Q

describe peri-operative considerations in RA patients

Answer

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

Question 42

Q

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

Answer

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

Question 43

Q

Describe your history and physical exam for RA patient

Answer

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)

Question 44

Q

describe XR findings in RA patient

Answer

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

Question 45

Q

describe medical management of RA

Answer

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

Question 46

Q

describe a different in treatment approach to CTS in RA patient

Answer

A

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

Question 47

Q

what is the mechanism for tendinopathies among patients w/ RA

Answer

A

· Direct invasion/erosion of tendon by synovitis

· Mechanical disruption within sheath

· Attrition across bony (eroded) prominences

Question 48

Q

describe flexor tenosynovitis in RA patient

Answer

A

Trigger digit: usually coming after failed non-surg including failed intralesional; if not then release 1^st 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)

Question 49

Q

describe surgery for extensor tenosynovitis in RA patient

Answer

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

Question 50

Q

what is classic presentation of flexor tendon rupture in RA patient

Answer

A

radial to ulnar
FPL most common

Question 51

Q

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

Answer

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)

Question 52

Q

describe management of extrinsic finger flexor rupture in RA patient

Answer

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

Question 53

Q

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

Answer

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

Question 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?

Answer

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

Question 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?

Answer

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

Question 56

Q

describe the net effect of wrist and hand deformity in RA

Answer

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

Question 57

Q

describe the pathomechanics of RA wrist & hand deformities

Answer

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

Question 58

Q

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

Answer

A

Prophylactic options
Synovectomy / tenosynovectomy: ongoing edema/inflammation and pain despite > 6 mos medical tx
- Dorsal longitudinal incision; split extensor retinaculum between 3^rd and 4^th compartments; excise synovitis; consider PINectomy on floor of 4^th 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 3^rd MC base, capitate, distal radius); use ICBG – if good bone then limited contact dynamic compression plate (LCDCP); if poor bone stock then Steinmann pins

Question 59

Q

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

Answer

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

Question 60

Q

describe the deformity at MCPJ in RA

what is the pathophysiology of that deformity?

Answer

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

Question 61

Q

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

Answer

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

Question 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)

Answer

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

Question 63

Q

discuss arthroplasty vs arthrodesis in PIPJ in RA patient

Answer

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

Question 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)

Answer

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)

Answer 64

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

Answer 65

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)

Answer 66

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)

Answer 67

A

metabolic disorder
characterized by hyperuricemia
deposition of monosodium urate crystals in joints

Answer 68

A

Indications: stiff, painful or deformed joint
Contraindications: insufficient bone stock, poor soft tissue cover, infection, paralysis of extrinsic tendons
Preferred in sedentary vs. heavy laborers
Anticipate therapy and motion to begin within a few days after surgery
Set realistic expect ions for post op ROM
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

Answer 69

A

revision
insufficient bone stock / traumatic bone loss
infection
arthritis mutilans

Answer 70

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

Answer 71

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

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Arthritis (all types) Flashcards

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