sash : 101 ways to fix a cruciate by dr stephen m. fearnside

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“101 ways to fix a Cruciate” Stephen M Fearnside Veterinary Surgical Specialist Small Animal Specialist Hospital [email protected]

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Page 1: SASH : 101 ways to fix a cruciate by Dr Stephen M. Fearnside

“101 ways to fix a Cruciate”

Stephen M FearnsideVeterinary Surgical Specialist

Small Animal Specialist [email protected]

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Design: Multicentre prospective comparative study

“in the absence of a cohort of willing oxen as a control group” ……..

Chose to compare intelligence test scores and dominant hand grip strength in ortho surgeons (x36) and anaesthetists (x40)

3 UK District General Hospitals

VS

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Introduction• Incidence of CrCL disease in the USA in

dogs exceeds that in humans (Helliker, Wall St Journal 2006)

• Estimated repair costs in USA (2003) are $1.23 billion annually

• Recent studies demonstrate that no single technique returns patients to normal function consistently

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Summary Anatomical considerations Biomechanical analysis Review of Pathogenesis Review of traditional techniques What about the poor old meniscus? Current trends and issues

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Anatomy Diarthrodial joint 2 distinct articulations

1. Femoral-tibial2. Femoropatella

Joint Capsule:3 distinct interconnecting cavities. Reinforced by fibrous retinaculum, local ligaments and tendons

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Menisci Semilunar fibrocartilages Cranial and caudal

meniscotibial ligaments Meniscofemoral ligament

(lateral meniscus) Intermeniscal ligament Blood supply –

peripheral 10-15% Function: stress transfer,

joint stability, lubrication, proprioception (horn innervation)

Lateral meniscus

Medial meniscus

Intermeniscal ligament

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Ligamentous support

Primary support via femorotibial ligaments:1. Cruciate ligaments2. Medial and lateral collateral

ligaments.

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Cruciate Ligaments Blood supply – from

synovial tissue sheath, fat pad, caudal joint soft tissue.

Intra-articular but extrasynovial

Primary stabilisers against cranial/caudal tibial translation, axial rotation (twisting on each other), hyperextension and excess valgus/varus in flexion.

Cruciate ligaments’ blood supply

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Cranial Cruciate Lig Origin = caudomedial

aspect of lateral femoral condyle

Insertion = cranial intercondyloid area of tibia

2 functional componants1. Craniomedial band2. Caudolateral band

Ligament spirals laterally approx 900

collagen bundles grouped into fascicles – tightening/relaxing through motion.

Craniomedial Band

Caudolateral Band

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Stifle Joint Motion Flexion and extension in sagittal plane Slight cranio-caudal movement – not uniplanar

motion Secondary restraints to cr-ca motion = joint

capsule, menisci, collat ligs, articular surface shape, muscle forces

“Screw-home” mechanism

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Stifle Joint MotionCranial Tibial Thrust

Result of ground reaction forces + extensor muscle forces = compressive forces through tibia shear force generated

Countered by CrCL (passive restraint) and hamstrings/biceps m (active restraints)

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Pathogenesis“rupture of the cranial cruciate ligament is seen for the most part in active jumpers, and especially in those individuals having the defect in conformation where stifle and tarsus are carried in over-extension. The absence of normal flexion angle of these joints in the standing position appears to be a predisposing cause”Erwin Schroeder, 1939

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PathogenesisTrauma

20% cases Cranial tibial thrust

mechanism – eg jumping. Magnitude of thrust > breaking strength of ligament

Excessive internal rotation

Hyperextension

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PathogenesisDegeneration

Age related changes in ligament (Vasseur et al, 1985). Stress/strain energy of ligament decreases with age Age related changes significantly greater for dogs>15kg Histological changes

Tissue changes identified during progressive rupture (Muir et al 2002, Vasseur et al 1985)

Loss of ligament fibroblasts Transformation of fibroblasts to ovoid or spheroid phenotype Disruption of normal type I collagen – loss of crimp, disruption of

fascicles Contribution of blood supply Bilateral disease – 37% within average 17months

(Doverspike et al, 1993) Young large breed dogs - <4ys, Rottweilers over

represented. Postulated cause = inadequate exercise when young?? (Bennett et al, 1988)

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Sagittal section through cranial cruciate ligament demonstrating chondroid metaplasia of fibroblasts and failure to maintain collagen fibrils

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PathogenesisConformation

Contributing factors = internal rotation, hyperextension, tibial plateau slope

Young large breed dogs -Read & Robins (1982) Small breed dogs – Macias et al 2002, Selmi &

Padhilla 2001 Medial patella luxation Congenital narrowing of the intercondylar notch

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PathogenesisImmune mediated joint disease

Plasmacytic lymphocytic synovitis (Galloway & Lester, 1995).

Anticollagen antibodies in serum and synovium (Nierbauet et al 1987, DeRooster et al, 2000)

The chicken or the egg??? Osteoarthritis

OA a primary lesion?? (Hulse & Aron, 1994). Role of genetics and conformation.

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Epidemiology

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Epidemiology Breed: large breed dogs predisposed

Rottie, Newfowndland, SBTerrier (Whitehair & Vasseur, 1993)

N.Mastiff, Retriever, Labrador, SBTerrier (Duval et al, 1999)

Breed variation in physical properties – Rottie ligament requires ½ load per unit body mass that the GH ligament requires to rupture (Wingfield et al, 2000)

Comparison of TPA between clinically normal GH and Labradors with and without cruciate lig disease (Wilke et al 2002).

Body Size: <22kg lower prevalence (Whitehair et al 1993)<15kg tend – degenerative changes occur later in life

(Vasseur et al, 1985) Obesity = increase load.

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Epidemiology Sex: Whitehair & Vasseur, (1993) reported higher

prevalence in neutered and female dogs Duval et al (1999) increased risk in desexed dogs

but no male/female difference.

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Clinical Signs and Diagnosis Gait assessment: reducing external limb load, limb carried in greater

flexion (Vilensky et al 1994, Korvick et al 1994) Joint effusion Cranial draw and tibial compression (mimics loading to elicit

cranial tibial thrust)What % of patients have drawer????? (Carobbi & Ness

2009) Radiography – Degenerative joint disease

effusion, Compression stress radiography (de Rooster & Van Bree

1999) Joint fluid analysis: WCC<5000/mm3, mononuclear cells

predominate.

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Radiography

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TreatmentConservative management

Cats – mean follow-up 20.5 months all cats (n=18) clinically normal. Mean time to normal function 4.8wks (Scavelli & Schrader 1987)

Small dogs <15kg :90% success rate if <20kg (Pond & Campbell 1972). 86% clinically normal or improved after mean f/up 36.6mths

(Vasseur, 1984). 73% (8/11) free of lameness after mean 5.5mths (Strande

1967) Dogs >15kg: 81% of dogs had persistent or worsening

lameness after mean f/up 10.2mths (Vasseur, 1984)

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Surgical Management Methods of conventional repair:

1. Primary repair – only for avulsion injuries.

2. Intra-articular or intra-capsular repair3. Extra-articular or extra-capsular

repair.

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Intra-articular reconstruction Graft selection:

Biological tissue (autograft, allograft, xenograft)

Synthetics eg goretex, dacron, braided polyester

Combination (composite grafts)

Graft Placement: isometric points of attachment to maintain graft length through ROM.

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Graft issues Arnoczky et al 1982:

• Patella tendon graft revascularisation by 20 weeks – vulnerable during the first 20weeks

• Initial necrosis revascularisation remodelling• Revascularisation from: fat pad, posterior synovial

tissues• 12mths = vascular and histological characteristics of

normal ligament Biomechnical studies:

• Material properties decline significantly after implantation

• Ultimate stiffness and load <35% of original ligament

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Extra-articular reconstruction Quicker, easier (except fibula head

transposition) Changes the ‘instant centre of

motion” of the stifle which results in compressive forces at the tibio-femoral contact points (Arnocsky et al 1977)

Designed to rotate tibia externally allowing the MCL to act synergistically with the laterally placed suture to inhibit draw. Stifle therefore becomes “hinge joint” altering stifle kinematics (Patterson et al 1991)

Ultimate joint stability due to periarticular fibrosis.

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Isometry“For a suture that spans a joint to provide support without limiting range of motion, its attachment points on either side of the joint must remain the same distance from each other from full extension to full flexion”

Roe et al, VCOT 2008

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Isometry: Roe et al VCOT 2008

Most isometric = Tibia site:1,2,5 if femoral anchor site 4 used

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Materials Braided non-absorbable suture

material – draining sinus tracts reported in 21% cases.

Monofilament nylon leader line

Orthofibres Sterilisation Knotting vs crimping –

Crimping shown to result in less elongation (knots tend to slip) but also reduces strength (Sicard et al 2002).

Crimping superior in all biomechanical assessment parameters (Anderson et al, 1998)

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Instrumentation

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Materials – transcondylar systems

Tightrope CCL Securos

systems:• XGen CCR• Bone anchors

and orthofibre

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Results Postoperative results: 85-90% improve. Complete

soundness = Less than 50% (Moore & Read, 1996). Studies evaluating factors that influence prognosis

found that surgery type had little influence (Fallon & Thomlinson 1986, Moore & Read 1995)

Studies report that DJD progresses despite satisfactory clinical results (Vasseur & Berry 1992)

Biomechanically intra-articular techniques more consistent with normal state using “instant centre of motion” model (Arnoczky et al 1977) – the future??.

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Meniscal Injury Incidence varies – low

frequency for partial ruptures (25% reported by Scavelli et all 1990) up to 80% in some reports with complete tearing of CrCL

Vascular supply – outer 10-25%

Mechanism of damage – crushing injury during cranial subluxation of tibia

Lesion classification – 7 types (Bennett & May, 1991)

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The Meniscus Human studies suggest that degree of

degenerative change directly proportional to amount of meniscus removed (Cox et al 1975).

Meniscal release – controversial. Simple transection has been shown to result in loss of load bearing capacity – loss of ability to resist circumferential strain.

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Management of meniscal injury

Healing potential – peripheral tears, radial tears

Experimental techniques – vascular access channels, exogenous fibrin clots, allograft, prosthesis.

Porcine small intestinal submucosa implants – Welch et al (2002), Cook et al (1999).

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Tibial Plateau Leveling Osteotomy The Slocum approach:

1. Slocum B, Devine T. Cranial tibial thrust: a primary force in the canine stifle. JAVMA, 183:456, 1983

2. Slocum B, Devine T. Tibial plateau leveling osteotomy for eliminating cranial tibial thrust in cranial cruciate ligament repair. JAVMA, 184:564, 1984.

Procedure does not attempt to restore function, but rather provide stability during weight bearing by reducing cranial tibial thrust

Note – does not eliminate passive drawer!!

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Determining the tibial plateau angle (TPA)

True lateral of stifle (femoral and tibial condyles superimposed).

Tibia parallel to table top Slope of medial tibial plateau

determined Tibial functional axis

determined TPA defined as angle between

slope of the medial tibial condyle and the perpendicular to tibial long (functional) axis.

Tibial long axis

Medial tibial plateau

Perpendicular to long tibial axis

TPA

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Procedures Slocum Technique –

patented Meniscal release –

recommended to allow caudal pole of medial meniscus to remain in caudal compartment of joint during cranial translation of tibia.

Medial arthrotomy – routine or limited caudomedial approaches.

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T.P.L.O

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T.W.O

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P.T.I.O.Proximal tibial intra-articular osteotomy

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Chevron Wedge

Osteotomy

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T.T.O.Triple Tibial

Osteotomy

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T.P.L.O + Cranial Tibial

Wedge Osteotomy

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T.T.A.Tibial Tuberosity

Advancement

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So where do we go from here?

Initially I think we need to slow down!

Rob McCarthy JSAP 2009

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Thoughts on TTA

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TTA – “the beginning”

Cranialisation of the tibial tuberosity

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Thoughts on TTA Case selection Newer systems To graft or not to

graft? Stifle mechanics Meniscal release? Complications Outcomes

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TTA Complications

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TTA Complications

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1 week postop

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TTA modifications – “Archie” WHWT Partial cruciate

tear Modified

Marquet technique

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Archie

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Medial Patella LuxationKyon Washer/Spacer

XGEN Securos

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TTO – “Vader”35 degrees

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Postoperative rehabilitation – the forgotten science?

Marsolais et al 2002: Prospective clinical trial with 51 dogs.

Limb function evaluated before and after surgery using force plate analysis

Dogs assigned into rehabilitation or exercise restriction groups.

Rehab programme – leash walking, massage, passive ROM, swimming.

Significant increase in limb usage in rehab gp compared with exercise restricted gp at 6mths.

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“My Opinion – for what it is worth ” Cruciate surgery in the dog = strong

opinion based on weak data. A good extracap = a good TPL

surgery……BUT TTA provides a more consistently good

outcome in large breed dogs Small breeds???? Going forward with extracap – focus on

isometry.

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Inspect the joint - Resect damaged ligament and meniscus – controversial!

Adhere to strict aseptic principles. Antibiotic use Don’t over-tighten extracap sutures –

achieve stability Rehabilitation is important!

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The unanswered questions There are many!!! Preventative strategies remain in their infancy If TPL restore mechanical stability then why does DJD

progress? Why do only 60% of dogs with confirmed CrCL disease

have drawer Why are we seeing so many cases of CrCL disease What role does genetics play – shown to play a role in

Newfies (Wilkie et al, 2006)

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The Future?? Lars Ligament

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Stifle Joint Replacement We have the

technology!!! Long recovery times Complicated and

challenging surgery Case selection!

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Tables

Table 1 Participants’ demographics, intelligence, and grip strength

Characteristic Orthopaedic surgeons (n=36) Anaesthetists (n=40)

Mean (SD) age (years) 42.2 (8.82) 42.5 (8.63)

Grade—consultant:specialist registrar 20:16 21:19

Handedness—right:left 36:0 38:2

Mean (SD) intelligence 105.19 (10.85) 98.38 (14.45)

Mean (SD) grip strength (kg) 47.25 (6.95) 43.83 (7.57)

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Study ConclusionsThe stereotypical image of male orthopaedic surgeons as strong but stupid is unjustified in comparison with their male anaesthetist counterparts.The comedic repertoire of the average anaesthetist needs to be revised in the light of these data.

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The author’s recommendations:

“we would recommend caution in making fun of orthopaedic surgeons, as unwary

anaesthetists may find themselves on the receiving end of a sharp and quick witted

retort from their intellectually sharper friends or may be greeted with a crushing

handshake at their next encounter”.

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Clinical Update – Wound Therapy using PICO (Smith & Nephew)

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PICO – Negative pressure for wound therapy

Single use negative pressure wound therapy system

Provides -80mm Hg negative pressure to wound bed

7 day use, 2 dressing per pack Dressing consists of:

Silicone adhesive contact layer

Airlock layer that distributes –ve pressure evenly

Absorbent layer High MVTR that allows

excess fluid to transpire

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Advantages of NPWT: Promotion of closed moist

wound environment Reduction of tissue oedema Enhances wound contraction Mechanical stimulation of

wound bed Stimulation of angiogenesis

and alteration of blood flow at wound edge

Aids in GT formation Physical splinting of wound

and aids graft adherence.

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“Ashleigh”

Grade II MCT right antebrachium

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