Knee

History and Examination Summary

History

1. pain: where,rad,type,when,nocte,agg,rel.,how long, stairs, start up
2. other: lock,swell,giveway,stiffness.deformity
3. function: walking,limp,support,squat,kneel,stairs,toes,socks
4. past history: treatment,injury,surgery,sim episodes

Exam (Standing)

1. look: shoes,sticks,spine,back,side,front,scars,swelling, deformity,wasting,redness
2. feel: LLD (Trendel)
3. move; gait,single leg, hop,squat

Exam

1. look: swelling,wasting,deformity,ffd
2. feel: pulses tape,effusion & synovium(X-fluct,tap, bulge), temp, posterior whole knee systematically
3. move: creps:passive ext,active ext.,act.flex.,passive flex.
4. ligs:
   1. var/valg
   2. Lachman.ant draw,slocum,frd,p/s,jerk,cros
   3. Lacmann,post draw,push back,90/90+dynamic rev. p/s(Jakob),ext rot. recurvatum(Hughston)
5. menisci: McMurray(flex,abd,e.r.>ext.,add,i.r.),Steinman

Exam PFJ

1. look: size,shape,posn,vmo
2. feel: artic,quadrant glide,tilt(n=0-15),grind,Q(N=15M20F)
3. move: creps,passive apprehension,
4. rotational alignment

Exam (Prone)

Special Tests

Patellar Glide test

( Kolowich etal " Lateral release of the patella: indications and contraindications" Am J Sports Med 18: 359, 1990)
-knee flexed 20-30^o, quads relaxed. Patella divided into quadrants and displaced in med and lat directions to assess tightness of parapatellar structures
- a medial glide of 1 quadrant = tight lat structures

Patellar Tilt test

( Kolowich etal Am J Sports Med 18: 359, 1990)
- knee extended, quads relaxed. Examiner lifts lat edge of patella from the lat femoral condyle- tight lat structures indicated in neutral or negative angle to the horizontal

A-P drawer

(Marshall etal "The Anterior Drawer Sign - What is it? J Sports Med 3: 152, 1975)
First inspect to determine if any posterior sag ( may get false +ve anterior drawer in a knee that is really PCL defic -not ACL)
knee at 90^o, do ant drawer in neutral as well as 30^o IR and 15^oER
in ER, med complex should become tight - abnormal laxity = injury to posteromedial corner
in IR, lat complex should tighten and in the normal knee reduce anterior drawer; abnormal laxity= injury to posterolat corner
( the IR/ER part is called the Slocum test- Slocum etal CORR 118: 63, 1976)

Pivot Shift

(Galway, Beupre, Mackintosh JBJS 54B: 763-764, 1972)
3 requisites: a non functioning ACL, an intact medial complex and an intact iliotibial tract
foot held in int rotation with one hand and the leg slightly abducted, the other hand is placed on the lat side of the leg at the level of the fibular head- applying a valgus thrust to the leg and gently flexing it
if +ve, subluxation will occur at 20-30^o with the lat fem condyle sliding forward on the tibial plateau to a reduced position

Flexion Rotation Drawer Test

Anterior force is applied to the tibia in 15^o of flexion, resulting in anterior subluxation as in the Lachman test. With further knee flexion the tibia reduces beneath the femur with a clunk and internal rotation of the femur.

Jerk Test

Start with the knee flexed and apply a valgus and IR force to sublux the lat tibial condyle anteriorly. As the knee is extended the tibia reduces with a clunk

Quadriceps Active Test

(Daniel etal JBJS 70A:386, 1988 "Use of the Quadriceps Active test to diagnose PCL disruption and measure posterior laxity of the knee")
Pt supine, knee flexed to 90^o, foot flat on the table. In the PCL defic knee the tibia assumes a resting position posterior to normal. Quads contraction against resistance produces anterior tibial translation

Dynamic Posterior Shift Test

(Shelbourne etal Am J Sports Med 17:275, 1989 )
Leg positioned with the hip at 90^o flexion and the knee is slowly extended from 90^o of flexion. As the knee extends, the tibia is in a posteriorly subluxed position - in PCL insufficiency, as the knee nears extension, the knee suddenly reduces with a clunk

Posteromedial Pivot Shift

(Owens JBJS 76A:532-539, 1994)
Elicited by flexing the knee more than 45 deg while applying a varus stress, compression and IR. As the knee is brought into extension, the tibia suddenly reduces, ~ 20-40 deg short of full extension
Requires divided PCL, MCL and posterior oblique lig to be present

External Rotation Recurvatum Test

(Hughston and Norwood- CORR 147:82, 1980)
Pt supine - lift the legs by the great toe. +ve test when knee falls into varus hyperextension and tibial ER.
Hughston stated this test to be specific for injury to the arcuate complex ( LCL, arcuate lig, popliteus, lat gastroc). Insall believes that the test will be mildly positive with isolated injury to the posterolat corner but that for excessive hyperextension and varus to be present the ACL must be torn and possibly the PCL also

Posterolateral Drawer Test

( Hughston and Norwood- CORR 147:82, 1980)
Perform posterior drawer test knee at 90^o flexion and foot 15^o ER
- if +ve lat tibial plateau moves posteriorly on the femoral condyle- in contrast the medial condyle does not move
- when assymetrical = pathological ER of tibia
When the posterolat structures are sectioned, ER of tibia increases ~5^o at 90^o of flexion. When the PCL is then sectioned, ER at 90^o flexion increases another 15^o if this test grossly +ve PCL probably damaged

Reverse Pivot Shift Test

( Jakob, Acta Orthop Scand (supp) 52: 1, 1981)
elicited by bringing the knee from a position of 90^o flexion, where it is subluxed to the fully extended position under a valgus load and the foot externally rotated where it is reduced
- Jakob: test grossly +ve in 3% and weakly +ve in 8% of normal knees - this has been found to correlate with ligamentous laxity
- indicates posterolat instability where is assymetrical with other side, reproduces symptoms, are other signs to correlate also

External Tibial Rotation

Prone, knees at 30^o and at 90^o, foot is forcefully rotated externally- the degree of rotation of the medial border of the foot is measured relative to the femur + compared with the contralateral side. NB palpate the tibial plateau to determine its relative position to the femoral condyles - this is to confirm that the increased ER is due to posterolat instability rather than anteromed instability
- NB considerable interindividual variation in degree of maximal ER
at 30^o flexion: av 30^o, range 15-45^o
at 90^o flexion: av 37^o, range 15-70^o

Meniscal Tests

Numerous rotation tests for meniscal pathology have been described- all have the common purpose of trapping abnormally mobile or torn fragments of menisci between the joint surfaces, causing pain or clicking.

McMurray Test

( McMurray, TP: "The Semilunar Cartilages"
Br J Surg 29: 407, 1941 )
- intended to diagnose lesions of the posterior horn of the meniscus
Pt supine, hip flexed 90^o and knee flexed more than 90^o. For examining the R knee, the examiner stands to the pts R side with L hand on the knee and R hand holding the foot. The foot is taken from a position of abduction and ER to one of adduction and IR- this is repeated for various angles bw full flexion and 90^o- trapping of damaged meniscus is felt as a clunk by the fingers on the jt line

Steinmann Test

( Ricklin etal, " Meniscal lesions: Problems of clinical diagnosis , arthrography and therapy", Grune and Stratton, Orlando, FL, 1971)
Pt seated and with knee hanging loose over the edge of the table- knee flexed at least 90^o, foot grasped and tibia is sharply rotated into IR then ER- a meniscal lesion is demonstrated by pain at the appropriate jt line

Apley Test

( Apley AG: " The diagnosis of meniscus injuries: some new clinical methods" JBJS 29B:78, 1947)
Pt prone , knee flexed > 90^o, downward pressure is applied to the foot and the jt surfaces thereby rotated and compressed slightly. The maneuvre is repeated this time with sistraction rather than compression. Meniscal lesions will be demonstrated by clicking or pain in the compression part of the test, while ligamentous injuries cause pain when the jt is distracted.

Patella

Anatomy

Radiology of the PF jt

Blumensaats line:

Line drawn on a lateral radiograph with the knee flexed 30^o through the dome of the inter condylar notch which should intersect the lower pole of the patella
If the patella is above this line = patella alta

Labelle and Lavine:

Line drawn along the anterior cortex of the femur with the knee flexed to 90^o should not intersect the patella (in 97% of normals the proximal pole of the patella was below this line)
At 90^o of flexion the patella should sit between the lines drawn along the anterior and posterior cortex of the femur

Insall / Salvati Ratio:

T/P ratio : normal = 1.0 in the normal knee the length of the patella and tendon should not vary by more than 20%
recurrent dislocation = 1.2
ref: Insall and Salvati "Patellar position in the normal knee jt" Radiology 101: 101, 1971

Merchant view:

pt supine with knees flexed 45^oover the end of the table. A cassette is placed below the knees and XR taken 30^o to line of the femur- 2 angles are measured:

1. sulcus angle: N = 138^o
   abN greater than 150^o
2. congruence angle: angular difference bw a line bisecting the sulcus angle and a line joining the sulcus apex to the lowest point on the patella
   N = av -6^o
   abN = greater than 16^o
   NB: Congruence angle negative if bisecting line lateral to the other
   ref: Merchant etal "Roentgenographic analysis of patello-femoral congruence" JBJS 56A:1391, 1974

Laurin view:

Tangential view with knee flexed 20^o, measure the lateral patellofemoral angle- draw a line tangent to the top of the med and lat femoral condyles and a second line tangential to the lat facet of the patella.
N = the angle is open laterally
abN = angle is closed laterally or parallel
ref: Laurin etal JBJS 60A: 55, 1978

Bipartite patella

Classification (Saupe)

Type I: Distal pole
Type II: Lateral
Type III: Supero-lateral

Extensor Mechanism

Rupture:

Site varies with age
Elderly usually rupture above the patella
Young adults usually rupture patella ligament
Middle aged usually fracture patella
Young and adolescent ® avulsion of tibial apophysis
Disruption of quads mechanism with inability to SLR requires repair at the appropriate level
Rupture of rectus femoris ® characteristic lump in the thigh on muscle contraction and no treatment is required
Beware 'sleeve' fracture of the patella ® disruption of quads mechanism as the cartilage covering of the distal pole is pulled away from the patella distally ® ORIF with modified tension band wire

Osgood Schlatters Disease

Clinically

Treatment

Sindig / Johanson / Larsen Syndrome

Dislocation of the Patella

Classification

1. Congenital dislocation (rare) associated with Downs syndrome and arthrogryposis
2. Habitual dislocation ® dislocation each time the knee is flexed and reduction on extension of the knee
3. Traumatic dislocation ® injury with acute symptoms and signs
4. Recurrent dislocation (repeated dislocation / subluxation in 55% of cases)

Congenital

is an irreducible lat patellar dislocation
Pathology: small patella, laterally positioned over a hypoplastic condyle fixation of patella to lat condyle and iliotibial band
Treatment: operative correction- mobilisation of quads, med plication, medial hemitransfer of the patellar tendon- done in infancy

Habitual

characterised by recurrent dislocation of patella each time the knee flexes- due to abnormal contracture of vastus lateralis and the iliotibial band
Treatment: operative - release to centralise patella

Traumatic

Usually due to sudden twisting , more rarely to direct blow.
pt usually falls to ground, may tell of lat displaced patella at the time
DDx: ACL rupture, other disruption of extensor mechanism, meniscal tear
Treatment: conservative - for first time dislocation- immob in extension splint for 4 wks, quads rehab immed , can WB prn in splint
approx 1/3 will redislocate after conservative treatment
Operative- for osteochondral #

1. Generalised joint laxity
   
2. Genu valgum
   
3. Rotational malalignment- esp femoral antetorsion and tibial lateral torsion
   
4. High 'Q' angle (greater than 15^o in a male and greater than 20^o in a female) should be measured with the knee slightly flexed ® test during quads contraction which results in a lateralising force
5. Small high riding patella-
   Insall-Salvati ratio: T/P: normal = 1.0 ( in the normal knee length of the patella and of the tendon should not differ by more than 20%)
   recurrent dislocation = av 1.2
   
6. Lateral condylar hypoplasia ie a flat trochlea
   - assessed by: the Merchant view sulcus angle: normal = av 140^o
   Abnormal greater than 150^o
   CT scan
   
7. Incongruence of the PF jt
   - assessed by the Merchant view congruence angle: normal = av -6^o
   abnormal = greater than + 16^o
8. Weak medial restraints: Hypoplasia or atrophy of VMO
   attenuated medial retinaculum
   
9. Iliotibial tract attachments to the patella

Clinically

History:

Pain is usually antero-medial and aggravated by bent knee activities
Patients often report clicking, catching and giving way

Pt standing:

varus / valgus
patellar squinting
signs of hypermobility

Pt supine:

look: VMO wasting
size + position of patella
feel: measure Q angle
local tenderness- palpate artic surfaces, retinaculae, insertions
patellar tracking and PF crepitus
Patella apprehension test of Fairbank or Apley (displacement of the patella laterally in slight flexion ® pain and expectation of pending dislocation)
Patellar shift test
Patellar tilt test

Pt prone:

Staheli test

Pathology

Treatment

1. lateral release- commencing on the lateral side of patella tendon from 4cm below the patella to the commencement of fibres of vastus lateralus (coagulate the superior lateral geniculate vessels) and should be able to tilt the patella 90^o on itself after the release
2. VMO advancement / medial plication
3. Hemitransfer of the patellar tendon ( Goldthwaite)
4. semitendinosus tenodesis (Galeazzi procedure)

1. distal realignment procedures: Elmslie Trillat type procedure and aim for 'Q' angle of 10^o, never move tubercle posteriorly
   
2. Maquet procedure (elevation of tibial tubercle) recommended elevation of 2 - 2.5cm but may ® skin necrosis therefore elevation of 1cm usually performed (use of a tissue expander may enable considerable elevation without risk of skin necrosis). May ® help symptoms of patello femoral OA or improve the mechanical effect of patellectomised quads
3. Patellectomy is the final option but ® weakness of quads mechanism and usually an extensor lag and decreased flexion range (Kaufer, 1979)
   May relieve pain of patello femoral OA but if subluxation / dislocation a problem this may continue post patellectomy unless anatomical problems
   addressed

Prognosis

After conservative treatment of acute dislocations:

Cofield and Bryan "Acute dislocation of the patella -results of conservative treatment" J Trauma 17: 526, 1977
52% unsatisfactory results, 27% required further surgery
Cash and Hughston " Treatment of acute patellar dislocation" Am J Sports Med 16: 244, 1988
43% recurrence rate if signs of patello- femoral dysplasia
20% recurrence rate if no signs of dysplasia

After surgical Treatment of acute dislocations:

Cash and Hughston ( see above)
medial reefing in 16 knees, satisfactory results in 87%

After surgical treatment of recurrent dislocations

Chrisman etal " A long term prospective study of the Hauser and Roux- Goldthwaite procedures for recurrent patellar dislocation " CORR 144:27, 1979
Hauser: 17% redislocation, 8.5% PF OA ( due to overcorrection)
Roux- Goldthwaite: 5% redislocation, 5% PF OA
Cerullo etal " Evaluation of the results of Extensor mechanism reconstruction"
Am J Sports Med 16:93, 1988
Results of prox and dist realignment - 100% satisfactory in dislocating patellae, 80% satisfactory in subluxing patellae

Chondromalacia Patellae and Patellofemoral OA

Aetiology

- Trauma ( or repeated microtrauma) may initiate cartilage degeneration by initiating the release of PGE2, causing increased synthesis of proteases which break up matrix proteins. This creates a vicious cycle where more destruction and inflammation ensue.
50% idiopathic
15% post traumatic
20% secondary to maltracking- lateral patellar compression syndrome
15% due to unstable (recurrent dislocaters) patellae

Wiberg: described 3 types of patella morphology- found no association bw patellar shape and chondromalacia
ref: Wiberg G. Roentgenographic and anatomic studies of the patellofemoral jt. With special reference to chondromalacia patella. Acta Orthop Scand 12:319, 1941

1. Equal medial and lateral facets which are both slightly concave (normal anatomy)
2. Smaller medial than lateral facet, medial facet is flat or slightly convex
3. Very small medial facet which is convex
4. Without a medial ridge or medial facet ( described by Baumgartl, 1944)

Classification: (Outerbridge)

Stage I:

Localised softening of the cartilage with minimal or no break in the surface

Stage II:

Fissuring within the softened area (often longitudinal 'shark' gill type)

Stage III:

Breakdown of the surface and fibrillation extending down to subchondral bone

Stage IV:

Really early osteoarthritis ® erosive changes and exposure of subchondral bone, usually also involves the opposite articular surface (more often the lateral than the medial femoral surface)

Pathology

Treatment

1. rest
2. Activity modification
3. Quads training- esp VMO- SLR type are best ( are isometric), after some strength has ben achieved can start short arc isotonic exercises in last 30^o of extension. NB- knee exercise from 90^o to full ext with weight on the ankle is contraindicated as applies high load on PF jt
   
4. NSAID- may have protective role in artic cartilage by decreasing PG synthesis
5. McConnell program ref: McConnell J "The management of chondromalacia patellae- along term solution" Aust J Physiother 32: 215, 1986
   - stretching of tight lateral restraints
   - taping of patella to maintain stretch
   - VMO training
   This program will help in ~ 60% of cases
   

1. Patellar shaving- unstable flaps of cartilage are removed
2. Subchondral bone drilling , cortical abrasion, and spongialisation
   - all aim to encourage fibrocartilage ingrowth from the underlying cancellous bone
   
3. Lateral release- useful in the pt with lateral patellar tilt, without subluxation
   (if subluxation as well- need to realign either prox or dist)
   - useful in ~60%
   
4. Elevation of the tibial tubercle- aims to reduce contact pressures- Maquet calculated that a 2 cm advancement of the tibial tuberosity would reduce contact forces by 50%. Most of the force reduction occurs in the initial 1-1.5 cm of elevation - this is now the recommended distance for advancement
   - Results:
   :Maquet procedure ( Rozbruk etal Orthop Trans 3:291, 1979)
   -60% satis results in 30 knees at 1-5 yrs
   -complications- skin necrosis, infection
   :Fulkerson procedure ( Fulkerson etal " Anteromedial tibial tubercle transfer without bone graft" Am J Sports Med 18: 490, 1990)
   -89% satis results in 30 knees ,greater than 2 yr FU
   - no skin sloughs or infections
   
5. Patellar resurfacing- not indicated- poor long term results
   
6. Patellectomy- last resort
   the patella increases the moment arm of the quads mechanism
   patellectomised knees have a decreased torque cf normal side of ~ 50%- this leads to difficulties in stair climbing and rising from chairs
   Ref: Kelly and Insall " patellectomy" OCNA 17:289, 1986
   Lewis etal " Patellectomy- an analysis of 100 cases" JBJS 58A: 736, 1976
   Lennox etal "Knee function after patellectomy" JBJS 76B:485-487, 1994
   - excellent or good in ~ 75% of pts ( ~ 50% in PF OA)
   - poorer results with cont weakness / instability- thus must rehab pts aggressively

Bowed Legs & Knocked Knees

Normal development

In early infancy, lateral tibial bowing is common
later infancy- physiologic bowing is common, involving both the femur and tibia
By 3-4 yrs physiologic knock knee is most pronounced, usually more extreme in girls
Most physiologic variations improve with time

Evaluation

History:

note family history and racial background
note progression or resolution over time
nutritional problems

Examination:

Knee Joint laxity
Motion of all lower extremity joints
Assessment of the level of the angulation
Assess the alignment of the limb

Investigation:

Use long leg standing radiographs

Differential diagnosis

Physiologic:

early infancy- lateral tibial bowing
late infancy- common bowing
early childhood- common knock knees

Pathologic:

Varus

Tibia vara (Blounts)
Unresolved physiologic varus

Valgus

post tibial metaphyseal fracture
lateral condylar hypoplasia
unresolved physiologic valgus

Either Valgus or Varus

Trauma malunion
partial physeal arrest
Metabolic rickets
renal disease
Osteopenia Osteogenesis Imperfecta
Rheumatoid Arthritis

Genu Valgum

Aetiology

Clinically

Treatment

Genu Varum

Aetiology

Clinically

Treatment

Blounts Disease

Aetiology:

Classification:

Infantile Form

onset at 5 yo or less
occurs predominantly in Negro's
Male : Female 2:1
50 - 75% are bilateral
Patients are usually over weight
Pain is frequently the presenting symptom
Deformity is slight and slowly progressive
Leg length discrepancy averages 2cm
Deformity varies from 10^o to 45^o (average 20^o)

1. Age 2 - 3 with irregularity of entire metaphysis with medial metaphyseal beaking
   
2. Age 2.5 - 4 years with a propensity for healing at this stage and sharp antero-medial depression evident
   
3. Age 4 - 6 years with deepening of the depression ® step
   
4. Age 5 - 10 years a step develops which is filled in by the epiphysis
   
5. Age 9 - 11 years a triangular fragment separates
   
6. Age 10 - 13 years growth plate ossification, growth continues in the normal lateral part
   

ref: Feldman and Shoenecker " Use of the metaphyseal- Diaphyseal angle in the evaluation of bowed legs" JBJS 75A: 1602- 1609, 1993
- Children with physiological bow leg - av m-d angle was 9 +/- 4 deg
Blounts - av m-d angle was 19 +/- 5.7 deg
this difference was significant to p less than . 0000001

Juvenile Form

Onset between 6 and 9 years

Adolescent Form

Usually present between 8 - 14 years

Pathology:

Treatment:

Stage 1+ 2

long leg bracing - try night bracing first as it does not disable the child - if still does not improve - go to day bracing as well
- deformity is often reversible at this stage

Stage 3 + 4

if the deformity persists or increases to this stage, osteotomy indicated
- osteotomise prior to age 4 if possible

Stage 5 + 6

Deformity severe - osteotomy
- if tomograms show a bony physeal bridge - can excise as well as osteotomy - esp if signif growth remaining
- Severe depression of the joint may require osteotomy and elevation of the plateau
- Premature medial growth plate closure recommended to ® epiphyseodesis of the lateral plate in addition to tibial osteotomy. Use of an opening wedge may avoid the need for operative correction of LLD
- in osteotomy aim to correct to ~ 10 deg valgus

Prognosis:

Infantile Form

The first 4 years ® main period for progression and deformity may be from 10 - 60o, after which the deformity remains the same or progresses slowly
From 9 years to skeletal maturity there is usually a gradual increase in deformity

Adolescent Form

Varus deformity ® increased incidence of degenerative joint disease at an early stage

Genu Recurvatum

Congenital:

1. secondary to intra uterine posture - these are flexible and respond to conservative management - gentle manipulation should start at birth- the tibia is brought posterior to the femur as the knee is flexed- aftermanipulation the desired correction may be held with a cast
2. severe cases may be associated with congenital dislocation of the knee
Is most common with arthrogryposis and myelodysplasia- and is often associated with club feet, CDH, and other congenital anomalies
treatment- begin nonop as above- if < 30° flexion at 3 mths - operative release

Laxity of ligaments:

eg in prolonged splintage in hyperextension and neurological problems

Bone injury

® faulty growth or malunion of a fracture

Treatment

Cysts about the knee

Pre-patella Bursitis (Housemaids' knee)

Infra patella Bursitis (Clergyman's knee)

Semimembranosus Bursa

Popliteal cyst (Bakers when in association with OA)

Meniscal cyst

Loose bodies

Clinically:

Treatment:

Osteochondritis dissecans

Definition

Incidence

Aetiology

1. the occurrence of OCD esp in athletic young people
   
2. assoc with trauma to the jt eg direct blow, patellar dislocation
   
3. assoc with other knee internal derangement
   signif valgus or varus deformity - 14%
   ACL deficiency - 7%
   patellar subluxation/ dislocation - 16%
   
4. production of OCD lesions in cadavic knees by applying axial compression and rotatory forces
   
5. cadaveric studies showing that direct blow to the flexed knee can produce the classic OCD lesion at the lat MFC
   
   

Clinically

Treatment

1. if cartilage intact- simple drillingof fragment with 1mm K- wire
   
2. loose or sequestered lesions should be replaced and fixed- if lesion small eg < 5mm can excise
   

Prognosis

Knee Ligament Problems

Definitions:

Instability:

Abnormal increased range of motion due to ligamentous, capsular, meniscal, cartilage or bone injury / abnormality

Strain:

Stretching injury to a musculo tendinous attachment to bone

Sprain:

Injury limited to ligaments (connective tissue attaching bone to bone)
Injury ® stretch or tear ligament fibres but does not completely disrupt the ligament (as apposed to ligament rupture)

1st Degree sprain:

Tearing of minimal fibres resulting in local tenderness and no instability

2nd Degree sprain:

Partial tear of the ligament with increased loss of function and joint reaction again with no instability

3rd Degree sprain:

Complete tear or disruption resulting in instability
The instability is graded according to its severity
+ (0 - 5mm) laxity
++ (5 - 10mm) laxity
+++ (> 10mm) laxity

Clinically:

Haemarthrosis:

ACL rupture (accounts for 70% of haemarthrosies)
Acute patella dislocation
Osteochondral fracture
Peripheral meniscal tear

Pathology:

Ligament Healing;

Phase 1: Acute inflammation occurs in the first 24 hours and is associated with haematoma formation and acute inflammation

Phase 2: Repair and regeneration (48 - 72 hours post injury continuing for ~ 6/52) ® subsidence of inflammation and commencement of healing

Phase 3: Remodelling and maturation (requires 6 - 9 months)
Contraction of ligament ® change collagen predominance with increased cross linking and increased tensile strength
The original strength is not reached (probably 50 - 70%)

Treatment:

Knee Instability

Straight instability

Medial Opens

with valgus stress test in full extension- indicates tear MCL, med capsular lig, ACL, posterior oblique lig and the medial portion of the post capsule- the PCL may be also torn but not necessarily so
Opens with valgus stress test in 30° flexion- indicates tear to med lig only

Lateral

Opens with varus stress test in full extension- indicates tear of lat capsular lig, LCL, and commonly PCL
Opens with varus stress test in 30° flexion- may be present in minor lat complex tears or may be normal

Posterior Demonstrated by posterior drop back of the tibia with no rotation
- indicates tear of PCL, arcuate lig complex, posterior oblique lig complex

Anterior

Demonstrated by the anterior drawer test in neutral rotation with both tibial condyles subluxing anteriorly with no rotation. In this type of instability the test becomes negative as the tibia is internally rotated as in this posotion the PCL becomes taut
- indicates tears of ACL, lat capsular lig, med capsular lig

Rotatory instability

Anteromedial

tear of med capsular lig, MCL, post oblique lig, ACL
the med tibial plateau subluxes forward on the femur
The medial meniscus is an important adjunct to anteromed stability- thus should be conserved if at all possible
Repair of the posterior oblique lig is essential for stability

Anterolateral

tear of lat capsular lig, arcuate complex, ACL
results in excess internal rotation of the tibia on the femur at 90° flexion
With an internal rotation /varus stress injury, an avulsion fracture of the attachment of the lateral capsule from the tibia may occur (= Segond fracture)- high assoc with torn ACL

Posterolateral

the lat tibial plateau rotates posteriorly wrt the femur with lateral opening of the jt
implies tear of popliteus tendon, arcuate complex, lat capsular lig, occasionally the PCL, and the biceps from its insertion
-results in an ER subluxation where the tibia rotates about an axis of the intact PCL

Posteromedial

the medial tibial plateau rotates posteriorly wrt the femur with med opening of the jt
implies tear of MCL, posterior oblique lig, ,ACL, med portion of posterior capsule. May be stretching / injury to semimembranosus tendon

Combined

Anterolat- anteromed combined: results from tears of ACL and both med and lat capsular ligs in their middle third. PCL is intact
-the ant drawer test is markedly positive in neutral, exaggerated in ER, but negative in IR ( PCL tightens in IR)

Anterolat- posterolat combined: results from tear of all of the lat comp capsular ligs and ACL, with or without tear of the iliotibial band , PCL remains intact
- varus instability marked, Ant + post drawer tests in neutral show lat tibial plateau rotation ant + post

Anteromed- posteromed combined: medial and posteromed structures are torn with ACL and often PCL
- valgus instability marked, ant + post drawer tests in neutral show med tibial plateau rotation ant and post

Medial Collateral Ligament

Superficial layer:

A continuation of the deep fascia of the thigh

Middle layer:

Superficial medial ligament from medial condyle just below the adductor tubercle to medial subcutaneous surface of the tibia 6 - 7cm below the joint line behind the axis of rotation

Deep layer:

Condensation in the medial joint capsule from the medial epicondyle of the femur to the medial meniscus and via the coronary ligament to the tibia

Natural History of disruption:

Healing of mid substance tear not improved by surgery
Bony avulsions respond well to reattachment

Treatment:

Isolated MCL injury- early motion +/- bracing depending on the severity of the injury
Ref: Indelicato etal CORR 256: 174-177, 1990
- concluded complete isolated tears of the MCL can be successfully managed nonsurgically provided there is no associated meniscal or ACL damage

If MCL injury assoc with another major ligamentous injury eg ACL/PCL then surgery is
indicated -but repair /reconstruction of the ACL or PCL may be all that is necessary

Hughston JBJS 76A: 1328, 1994 - in MCL tears with ACL tears- advocates treatment of the ACL only in the case of a 1+ or 2+ medial instability. However , in those with 3+ med instability he states that these must have a posteromedial disruption and this should be repaired with emphasis on repair of the post oblique lig and semimembranosus insertion

Lateral Collateral Ligament

Superficial layer:

The ilio-tibial band continuous with deep fascia inserts into the antero-lateral surface of the proximal tibia (Gerdy's Tubercle)

Middle layer:

Superficial lateral ligament from the lateral epicondyle to the styloid process of the fibula and is tight in extension but lax in flexion (femoral attachment lies behind the axis of rotation)

Deep layer:

Capsular thickening which is poorly developed and runs from the lateral condyle to the head of the fibula and does not attach to the meniscus ® lateral meniscus is more mobile

Natural History of disruption:

Usually associated with cruciate injuries or posterolat corner injuries and significant instability
Isolated LCL injuries are rare and can be treated nonsurgically
If assoc secondary restraints are torn- therefore if complete lateral complex injury (ie opens in extension) should be repaired
Direct repair +/- biceps tenodesis to lateral epicondyle of femur
Chronic instability- advancement , augmentation or reconstruction
eg ITB augmentation, biceps tenodesis of the posterolat corner

Anterior Cruciate Ligament

Anatomy:

Tibial attachment is on the non articular surface of the tibial plateau extending from just behind the medial and lateral spines forward for about 3cm
Femoral attachment is the lateral and posterior portion of the medial femoral condyle in the inter condylar notch and some fibres of the ligament are taut in all positions of the knee
Anterior fibres are the most isometric with the postero-lateral fibres relaxing somewhat in flexion
No fibres are truly isometric but the antero-medial fibres have the least variation in length (~ 1.5mm)
Most of the fibres of the ACL are taught in extension
Primary function is to prevent anterior displacement of the tibia on the femur

Pathology:

Unhappy triad of O'Donaghue ® MCL, ACL and medial meniscus
As MCL attaches to the meniscus disruption forces ® pull on the MCL may disrupt the medial meniscus and if strain sufficient will go on to rupture the ACL

Natural History of disruption:

70% of these injuries are sustained during sporting activities-mainly in non contact sports involving jumping or cutting
50% of all acute ACL tears are assoc with meniscal tears
Conservative treatment is not satisfactory in high risk patients (conservative treatment resulting in unsatisfactory results in 60 - 85% of patients) where as satisfactory results are achieved in 85 - 95% of reconstructed patients
For low risk patients non operative treatment is satisfactory in 85 - 90% of cases
ref: Ciciotti etal JBJS 76A:1315-1321, 1994
52 pts with ACL rupture bw 40-60 yo, 30 followed av 7 yrs
25 of these 30 pts had good result with nonop treatment

Treatment:

ACL injury in the skeletally immature
Conservative treatment and muscle exercises
Avoid any procedure involving bony tunnelling until skeletal maturity
If indicated ® extra-articular reconstruction (eg McIntosh repair)

McIntosh procedure: Iliotibial band mobilised proximally and re-routed beneath the LCL around the intermuscular septum and back beneath the LCL to be reattached to Gerdies tubercle

Therefore reconstruct if:

less than 35 years of age and closed growth plates
Moderate to severe instability
Participates in high risk sports or work

Rehabilitation: Post operation ® CPM 0 - 90^o
Mobilise in a splint when leg control and allow 0 - 90^o ROM in the splint for 3 weeks
Physio ® ROM exercises and muscle toning ® mobilise unrestrained after 3 weeks
Recommence activity on the basis of muscle tone, power and control and when within 90% of normal power ® resume sporting activities

Posterior Cruciate Ligament

Anatomy:

From the medial surface of the inter condylar notch to a groove in the posterior surface of the tibia below the level of the articular surface
There are no truly isometric fibres but the most posterior portion has the least variation in length
Most of the fibres of the PCL are lax in extension becoming taught in flexion limiting anterior displacement of the femur on the tibia in flexion
The average length of the PCL is 38mm and the diameter is 13mm with a width of 8mm
Posterior menisco-femoral ligament of Wrisberg extends from the posterior horn of the lateral meniscus to the femur behind the PCL and the anterior menisco-femoral ligament of Humphrey if present passes in front of the PCL

Mechanism of injury

post directed force on a flexed knee
forced hyperextension
posterior rotatory force

Natural History of disruption:

Isolated PCl injuries rarely assoc with meniscal pathology and result in little functional disability
85 - 90% satisfactory results despite persistent laxity in the PCL and surgical repair is recommended for bony avulsions only
Many are only slightly impaired and return to sport without reconstruction
Increased shear forces transmitted to articular surfaces may lead to early degenerative arthritis
At this time there is not sufficient evidence to prove the benefit of surgical reconstruction over non operative treatment
Surgical intervention reserved for those who fail conservative therapy, those with combined ligamentous injury, those with multidirectional instability
Surgical options include: primary repair with augmentation with semitendinosus/ gracilis
reconst with patellar tendon or achilles tendon auto- or allo-graft
Maintenance of quads strength emphasised, hamstring strengthening delayed

Dislocated Knees

Classification (anatomical)

anterior (hyperextension injury)
Posterior (direct force to the tibia)
Medial
Lateral
Rotational

Pathology:

At least three of the four major ligaments as well as capsule must be ruptured in order for the knee to dislocate

Complications:

Arterial injury in 30 - 40% of cases with anterior or posterior dislocations usually at the level of the adductor hiatus or the trifurcation of tibial vessels
Amputation rate for knee dislocation are ~10%
Peroneal nerve palsies in 20-40%- half are permanent

Treatment:

Dependant on general state of patient and demand on the leg
Arthroscopy not indicated as ® soft tissue extravasation
Usually ® primary repair of external ligaments and capsule and subsequent reconstruction of the anterior cruciate if found to be necessary.
Bony avulsions should be repaired acutely & CPM used post operatively

Meniscal Injuries

Function

1. Load bearing: at least 50% of the commpressive load of the knee jt is transmitted through the meniscus in extension , and approx 85% of the load is transmitted in 90° flexion.
   In the meniscectomised knee the contact area is reduced approx 50%
   Partial meniscectomy also increases the contact pressures

2. Shock absorption: menisci may attenuate the intermittent shock waves generated by impulse loading during gait- the shock absorbing capacity of normal knees is ~ 20% higher than in meniscectomised knees.
   The ability of a system to absorb shock has been implicated in development of OA
   ( Radin and Rose " The role of subchondral bone in the initiation and progression of Osteoarthritis" CORR 213:34-40, 1986)

3. Knee jt stability: meniscectomy alone may not seriously affect stability. However, in assoc with ACL tears, meniscectomy increases ant laxity of the knee

4. Lubrication:

5. Proprioception: this has been inferred from the finding of type 1 and type 2 nerve endings in the ant and post horns of the menisci

Clinically:

Investigation

Classification

Pathology:

Differential Diagnosis

Treatment:

Options

Conservative ® restrict activity
Manipulative to reduce ® conservative treatment
Operative ® arthroscopic partial menisectomy or meniscopexy
Discoid meniscus ® excise the central portion of the disc for Types I & II and resect the meniscus if Type III (Wrisberg Type)
Meniscal cysts in adults need to address pathology in the joint and not just the cyst as excision of the cyst alone is likely to ® recurrence
Meniscal transplantation- experimental

Meniscal repair

ref: DeHaven and Arnoczky " Meniscal repair- Part 1: Basic science, Indications for repair and open repair" JBJS 76A: 140-152, 1994
Dehaven etal " Open meniscal repair. Technique and 2-9 yr results"
Am J Sports Med 17:188-795, 1989
Cannon and Morgan " Meniscal repair- Part 2: Arthroscopic repair techniques" JBJS 76A: 294-311, 1994
Blood supply to the meniscus is age dependent- in the adult the periph 3mm as well as the ant and post horns are well vascularised
Blood supply originates from the lat + med geniculate arteries ( sup and inf)- branches from these give rise to a perimeniscal capillary plexus in the synovial and capsular tissue- this plexus supplies the meniscus on its peripheral attachment to the jt capsule. the degree of vascular penetration is 10-30% of med and 10-25% of lat meniscus.
repair should be reserved for traumatic tears in the vascular region of the meniscus
within 3mm of periphery = vascular ( = red- red tears)
3-5 mm from periphery = grey zone ( = red- white tears)
> 5mm from periphery = avascular ( = white- white tears)

Healing :

similar to other connective tissues- exudation, organisation, vascularisation cellular proliferation , remodelling
: following injury there is formation of a fibrin clot rich is inflammatory cells.
Vessels from the perimeniscal capillary plexus proliferate into this fibrin scaffold , followed by mesenchymal cell proliferation forming a cellular fibrovascular scar. Modulation of this scar tissue into normal appearing fibrocartilage requires several months
Approx 80% of repairable menisci are found in knees with an acute or chronic tear of the ACL- thus repair of the meniscus is linked to the management of the ACL tear
NB risk of injury to peroneal n in lat meniscus repair, saphenous n in medial repair

Aftercare:

6 wk period of maximal protection to allow initial healing and a subsequent 6 mth period of protection from vigorous stresses to allow for maturation of the healing collagen tissue
Min touch down WB 6 wks in hinged splint, initially locked
Isometric Q+H setting exercises begun immediately post op
limited ROM 30-70° at 2 wks
remove splint 4 wks , increase stretching exercises bw 4-6 wks
from 6 wks WB increased to FWB by 8 wks
Low impact activity from 3 mths
Full activity at 6 mths

Results of meniscal suture

62% heal, 17% heal incompletely and 21% do not heal
92% are clinically stable
80% return to active sport
NB: 30-40% failure rate in 5 yrs in meniscal repair in knees that are ACL deficient- therefore need to reconstruct ACL to protect meniscal repair
- the success rate in stable knees is ~ 90% at 9 yrs

Osteoarthritis of the knee

As the cartilage becomes less capable of taking load, the subjacent bone becomes more dense in response to loading. The reduced compliance of the subchondral bone further contributes to the loss of articular cartilage. Osteophytes form in an attempt to increase the weight bearing area.

Adult mature chondrocytes do not appear to be able to undergo mitosis- Chondrocyte clustering is probably due to loss of matrix between previously separated cells rather than from cell division

Thus true healing of an articular cartilage defect cannot occur- However, healing by scar formation can occur ie healing by fibrocartilage derived from underlying cancellous bone. For this to occur need to have connection bw jt and underlying cancellous bone eg by drilling. For this fibrocartilage to persist and effectively line the jt surface - need to remove the primary mechanical cause for the initial cartilage destruction eg by osteotomy

Rheumatoid arthritis

Management
Synovectomy if fail to respond to medical management and no evidence of joint destruction
Tibial osteotomy, many feel this is contraindicated due to bi-compartmental disease process
Arthrodesis, only if hip normal, usually reserve for failed TKR or when TKR can not be performed

TKR; Loosening ~ 1.3%
Infection ~ 0.4%
Pain relief 95%
Cement fixation and replacement of all cartilaginous surfaces advocated by many surgeons

Synovectomy of the Knee

Indications RA

PVNS
Synovial chondromatosis
Haemophilic synovitis

Rheumatoid:

Synovectomy reduces at least temporarily the pain and synovitis of RA
pts should have failed at least 6 mths of maximal nonoperative treatment
surgical: may be open or arthroscopic
ref: Olgilvie-Harris and Basinski " Arthroscopic synovectomy for RA"

Arthroscopy 7: 91-97, 1991
- 4 yr FU : 21% had pain at 4 yrs vs 56% preop
24% ha d synovitis vs 100% preop
Arthroscopic synovectomy
- advantages- low morbidity, ¯ infection, better ROM post op
- results similar to open synovectomy
Chemical: eg with alkylating agents - rarely done as damage to cartilage
Radiation: eg Yttrium 90
Dysprosium 165(attached to ferric hydroxide macroaggregates)
ref: Sledge etal " Intraarticular radiation synovectomy" CORR 182:37, 1984
- satisfactory results in 50% at 3 yrs

Haemophilia:

ref: Rivard etal JBJS 76A: 482-488, 1994
92 synoviortheses on 48 pts with haemophilia
reduced episodes of haemarthrosis
better ROM maintenance than after synovectomy
no need for extra factor replacement
procedure almost painless
does not alter the rate of jt degeneration ( same for synovectomy) - suggesting that once initated, haemophilic arthropathy progresses regardless of treatment

Osteotomy

Treatment

Prognosis

Unicompartmental Knee Replacement

Indications

Contraindications

• Weight > 82kg
• Inflammatory arthropathy
• Dynamic instability
• Cruciate deficiency of the knee
• FFD greater than 15 ^o
• Flexion of less than 90^o

Technique

Results

Complications

Unique to UKR: progression of degen changes to the opposite compartment
impingement of the patella on the edge of the femoral component

Total Knee Replacement

Indications for TKR

1. To relieve pain
   
2. To provide motion with stability
   
3. To correct deformity

1. RA- regardless of age , including JCA
   
2. OA- consider age, wght, occupation,sex, activity level
   avoid in <60 yo, manual labourers, high demand pts, obese
   
3. post traumatic OA- a rare indication in the younger pt
   
4. Failure of HTO
   
5. Patellofemoral OA- rare in isolation- if so , the best treatment in the older pt is TKR
   
6. Neuropathic jt- controversial - Insall believes it is feasible as long as correct alignment and stability are achieved
   

Contraindications for TKR:

1. Neuropathic joint (see above)
   
2. Recent or current sepsis
   
3. Age (relative)
   
4. stable arthrodesis- prospects of a successful arthroplasty are not good, a constrained prosthesis is usually required, in the event of failure rearthrodesis may not succeed
   
5. Genu Recurvatum- assoc with muscular weakness or paralysis - is likely to recur following TKR and places stresses on the prosthesis which increase likelihood of loosening
   
6. Quads weakness- arthrodesis better choice

Investigations:

Technique

Difficult exposures: when exposing a stiff or ankylosed knee the standard exposure will risk damage to the tibial tubercle- options include:

1. Quads turndown- a narrow inverted V incision distally based, extended until the patella can be everted
   
2. Rectus Snip- standard approach but at the apex of the quads tendon incision continued laterally across the tendon
   
3. Tibial tubercle osteotomy- a long portion ~ 3-6 cm in length is elevated - must be fixed back with screws

Ligament balance
ensure flexion and extension gaps are equal
if ligament rebalancing is needed - best done by appropriate releases rather than advancements
If fixed deformities greater than 15^o, the best results for correction are obtained by excision of the PCL and use of a cruciate substituting prosthesis

Varus release remove med osteophytes from the prox tibia
raise a sleeve of soft tissue from the prox tibia that is allowed to slide proximally- includes periosteum, deep and superfic med lig, insertion of the pes tendons

Valgus release NB risk of peroneal nerve palsy
Order of release:

1. ITB from Gerdys tubercle
2. Lat capsular attachments to the tibia
3. Posterolat capsule +/- PCL
4. Popliteus tendon
5. LCL
6. Lat head of gastroc
7. lat intermusc septum with V lateralis

May be coupled with medial soft tissue advancement in which case lateral release usually restricted to ilio-tibial band and postero-lateral joint capsule
If ® advancement of medial structures splint leg post op for 3 - 4 weeks

Flexion release:

more prox femoral bone resection
r/o post osteophytes
Elevation of post capsule +/- release of the PCL
Post capsule can be divided transversely near to the origin from the femur with great care
In order to minimise bone resection ® division or stripping of posterior capsular attachment to the femur which may include both heads of gastroc.Additional resection from the distal femur then undertaken if unable to obtain full extension

Sagittal:

most systems aim for 3-7^o posterior slope
too much femoral comp extension may ® notching ant femur ® ­ risk #
too much femoral comp flexion® FFD

Axial:

IR of the tibial comp ® lat displacement of the tibial tubercle® ­ Q angle
®patellar maltracking
-align tibial comp to point to med 1/3 of tibial tubercle
IR of femoral comp also affects patellar tracking- aim for 3-4° ER of femoral component to improve patellar tracking- this amount of rotation also helps equalise collateral structure balancing as the lat collat structures are slightly more lax in flexion

Jt line:

level of jt line should be maintained as close to normal as possible- esp if using PCL retaining design where tension of the retained PCL must be as normal as possible to ensure FROM and even pressure transfer throughout the range to the tibial component

Patellar Tracking

lateral release if required

Component Design

1. PCL sacrificing
   
2. PCL sacrificing with substitution
   
3. PCL retaining
   

1. restore more normal knee motion- including axial rotation of the tibia and roll back of femur on tibia
   
2. maintain proprioception of the PCL
   
3. maintain load transfers by PCL
   
4. in gait analysis pts with retained PCL have a more normal stair climbing gait- no difference in level gait
   

1. more difficult collateral balancing
   
2. need to reproduce the preop jt line- or get ­ jt reaction forces® ­ wear
   
3. partial release of the PCL may be necessary for correct ligament balance
   
4. exposure may be more difficult in PCL retention
   

Fixation
Cement remains the gold standard

ref Scuderi etal "Survivorship of cemented knee replacements"
JBJS 71B: 798-803 , 1989
- posterior stabilised prosthesis- 15 yr success rate of 90%
- all poly tibia - 10 yr success rate of 97%
- metal backed tibia- 7 yr success rate of 98.75%

Cementless tibial components are more prone to failure than cemented - probably due to failure to obtain sufficient initial stability for adequate bone ingrowth
Thus hybrid TKR is now being performed- early results are equal to all cemented
ref: Wright etal CORR 260: 80-86, 1990
- hybrid - good or excellent in 93%
no sign of component loosening

Polyethylene
wear influenced by: limb alignment, component design, presence of metal backing, poly thickness, modularity
less conforming surfaces have more point loading ® ­ wear
Metal backing - may lead to use of poly which is too thin- need min 8mm thick poly
may get wear bw poly and metal backing

Prognosis:

94% 11 year survival for total condylar prosthesis
Specific Groups
TKR after Patellectomy

ref: Joshi etal JBJS 76B: 926-929, 1994
- 19 pts, av FU 63 mths , high complication rate - 36% overall
3 supracondylar #'s, 3 coronal instabilities ( no AP instabilities)

TKR in severe deformity ref: Karachalios etal JBJS 76B: 938-942, 1994
- 51 knees with varus or valgus >20 deg
14 knees had persisting deformity esp in the case of valgus , 4 knees with valgus > 30 deg had lat dislocation / subluxation of the patella post TKR

Complications of TKR

1. neurovascular damage
   arterial damage rare - < .05%
   Peroneal n damage- usually in correction of flexion and valgus deformity
   - prognosis - all have partial recovery, 1/2 full
   
2. blood loss ~ 1500 ml
   
3. Fat embolism assoc with stemmed intramedullary components and guides
   ~ 3%
   

1. Wound healing - ­ problems in RA, diabetes, haematoma, low albumin, leucopenia
   
2. Sepsis: Infection affects 1 - 2.5% of TKRs

treatment

1. Long term antibiotic suppression if prosthesis removal not feasible, for low virulence or highly sensitive organisms and the prosthesis not loose

2. Debridement, irrigation and suction if in the immediate post operative period (2 - 4 weeks) but chance of sucess not good

   Once the infection has been treated the options are

3. Removal of implants if excessive bone loss and low demand patient with limited rehab potential- requires prolonged cast/bracing, results are unpredictable
   Resection arthroplasty aim for 7o valgus and 15o flexion and if unhappy ® arthrodesis

4. Arthrodesis ® painless stable extremity with usually 2 - 8cm shortening but often difficult due to bone loss
   - resurfacing implants have less bone loss
   - ~ 75% fusion rate with ex fixation
   - ~ 80% fusion rate with internal fixation eg IM nail, plating
   - internal fixation requires a clean wound
   - fusion usually in 4-6 mths

5. Re implantation in two stages (Insall, 1983) ® removal of implants followed by 6 weeks appropriate antibiotics and reimplantation if operative site appeared sterile ® No recurrent infections and good or excellent results in 75%
   Insert an antibiotic impregated spacer and reimplant prosthesis between 6 weeks and 3 months after debridement
   Reimplantation difficult after about 3/12 due to soft tissue contracture and extensor lag and poor power being the most common problem post-operatively
   ref: Windsor, Insall and Urs "2 stage reimplantation for the salvage of total knee arthroplasty complicated by infection: further follow up and refinement of indications" JBJS 72A: 272-278, 1990

6. Immediate re implantation ® only 35% success

7. Amputation if life threatening infection
   multiple failed attempts at control
   elderly nonambulant pt

Postoperative

1. DVT evident on venography in 50 - 70% of patients and asymptomatic PE in 17% of patients (prophylaxis with warfarin ® complications in 17%)
   - see section on DVT/PE in HIP notes
   
2. Loss of Quads power
   
3. Limited ROM (less than 90^o flexion)
   
4. Fractures:
   1. Around the prosthesis which may be secondary to stress risers produced by femoral notching (0.6% of knees and 42% are rheumatoid patients)
      ORIF should be reserved for patients who do not have osteopenia and where stable fixation can be achieved, and adequate closed r eduction can not be maintained
      
   2. Fractures of the patella in 1 - 11% of those replaced ? secondary to AVN or increased tension in quads or excessive resection
      -min displaced # - treat in extension splint for 6 wks
      - displaced # not involving patellar comp- TBW
      - displaced # involving loosened comp- ® r/o implant as bone stock usually too poor for reimplantation
      
5. Problems of the patella :
   
   1. Patellar tendon avulsion ­ risk in revision, prior HTO
      treat with primary repair

   2. Patellar resurfacing: complications occur in as many as 10% of patients and account for almost 50% of all long term complications of TKR
      - include: failure of metal backed components
      patellofemoral instability
      component loosening
      patellar # and AVN
      - recommend replace patella in RA and advanced degen changes of patella, preop PF pain
      ref: Keblish etal JBJS 76B: 930-937, 1994 "Patellar resurfacing or retention in TKA"
      52 pts with bilat TKA - no difference bw the 2 sides

   3. Patellofemoral instability: causes include-
      IR of tibial comp
      IR and med translation of fem comp
      residual valgus deformity
      inadequate resection of bone in resurfacing® too thick patella
      failure to check tracking
      - treat by release or distal realignment

6. Loosening:
   Most common complication and increases with time and in association with more constrained prostheses
   Major cause malalignment, poor cement techniques
   Wear debris is uncommon in TKR but may be a problem with patella prostheses

Revision TKR

Preop planning

physical examination- test for lig integrity
quality of skin
previous incisions
XR full length wght bearing films , routine AP/lat/ sunrise views
-determine patellar position, jt line location, loosening, bone stock loss
CT assess bone stock
Aspiration to rule out infection

Results

Elia and Lotke "Results of revision total knee arthroplasty associated with significant bone loss" CORR 271: 114-121, 1991
-good or excellent in 75%
Friedman etal " results of revision total knee arthroplasty"
CORR 255: 235-241, 1990
- 5.8% failure rate at 5 yrs
Goldberg etal "the results of revision total knee arthroplasty"
CORR 226: 86-92 ,1988
- 46% good or excellent results

Complications

infection up to 5%
¯ ROM
­ risk patellar maltracking
DVT
Component malalignment

Arthrodesis

1. Charcot joint
   
2. Limb paralytic or no muscular control of lower leg
   
3. Persistent infection
   
4. Unilat post traumatic OA in a young pt
   
5. Painful ankylosis
   
6. Failed TKR

1. compression arthrodesis by external fixation
   advantages is extra articular
   disadvantages pin tract problems
   poor pt compliance
   often need to remove early and go to cast immobilisation

2. intramedullary rod ~ 85% fusion rate
   advantages- immed wght bearing
   no problems with pin sites
   disadvantages difficulty in obtaining correct alignment
   may need to remove rod

3. plates and screws
   Desired alignment: 0-5^o
   valgus, flexion 10-15^o
   Complications: fusion may not occur
   breakage or backing out of the IM rod
   pin site infection
   patient dissatisfaction- stiff knee not well accepted
   \ pt should have trial of long leg POP