Knee Replacement Surgery

Knee Replacement Surgery

Knee replacement surgery involves replacing some or all the components of the knee joint with a synthetic implant, to repair the damaged weight-bearing surfaces that are causing pain.

A total knee replacement surgeryreplaces all three compartments of the diseased knee joint.

A partial knee replacement involves an implant in just one or two compartments of the knee, retaining any undamaged parts. While there are  non-surgicaland  surgical interventions short of knee  replacement which will often provide temporary relief, the long-term resolution to most knee degeneration will be joint replacement. There are several different implant designs (  total implants- partial  implants) but each will offer renewed stability and movement. there are two main benefits to be gained from knee replacement surgery:

(1)   elimination of pain and

(2)   improved range of motion.

Of all possible surgical interventions, total knee replacement offers the greatest quality of life improvement. The procedure has a high rate of success.

Indications

●                   most commonly performed in people with advanced  osteoarthritis. It should be considered when conservative treatments have been exhausted. espetially in patients over 65 years .

●                 Total knee replacement is also an option to

correct significant knee joint or bone trauma.

● Similarly, total knee replacement can be performed to correct mild  valgus or  varus deformity. Serious  valgus or  varus deformity should be corrected

by  osteotomy. Physical therapy has been shown to improve function and may delay or prevent the need for knee replacement

●                      extreme pain when performing physical activities requiring a wide range of motion in the knee joint.

●                   Rheumatoid arthritis causing severe destruction.

  Contraindications

➢ Absolute contraindications

•         knee sepsis including previous osteomyelitis .

•             a remote source of ongoing infection .

•         extensor mechanism dysfunction .

•         severe vascular disease .

•            recurvatum deformity secondary to muscular weakness, and the presence of a well functioning knee arthrodesis.

➢ Relative contraindications include

•         medical conditions that preclude safe anesthesia,the demands of surgery and rehabilitation.

•

•         skin conditions within the field of surgery e.g psoriasis, a neuropathic joint and obesity.

  Surgical approach

•          anterior longitudinal incision allows full exposure of the proximal tibia;

•          this incision allows exposure of both medial & lateral aspects of joint w/o the necessity for large skin flaps

•         this incsion has advantage that it leaves strong cuff of fibrous tissue attached to vastus medialis obliquus muscle

•         this strong cuff facilitates suture placement and secure closure at the end of the case

•         - straight incisions are less disruptive to the  blood supply to  knee than curved incisions;

- a gentle medially curved incision is an alternative which may

Knee Disorders

[Knee Disorders] Page | 1
Knee Anatomy
MUSCLES
Biceps Femoris
• multiple insertions
• 3 layers:
o superficial layer - superficial to LCL
o middle layer - surrounds LCL
o deep layer - attaches to head of fibula & Gerdy's tubercle on tibia
• Function - flex knee & externally rotate tibia
Popliteus
• forms floor of popliteal fossa
• muscle attached to posterior tibia - tendon passes intraarticularly deep to femoral
attachment of LCL to attach to femur
• Functions
o flex & internally rotate tibia when leg is free OR externally rotate femur on tibia
when tibia is fixed.
o dynamic reinforcement of PCL, preventing post. displacement of tibia on femur
Semimembranosis 5 distal attachments:
1]. Oblique Popliteal ligament
2]. Posterior Oblique Ligament
3]. Deep Head - deep to MCL (Pars reflexa)
4]. Direct Head - to post medial tibial condyle
5]. Anterior Expansion - over anterior leg fascia
6]. Popliteal expansion: over the popliteus fascia
Pes Anserinus
1. Sartorius, gracilis & semitendinosis (Say Grace before Tea)
2. sartorius - very broad insertion, forming a sheath over gracilis & semiT
3. Gracilis - smaller & anterior to semiT
4. Semitendinosis - enveloping muscle belly extending more distally
5. Functions - flexor of knee & internal rotator of tibia
Iliotibial Tract
1. inserts into GERDY'S tubercle on the tibia & extends to form the lateral patellar
retinaculum
2. also attaches to the lateral femoral condyle forming a static lateral restraint
3. Function: since it crosses the centre of rotation of the knee moving from flexion to
extension it acts as a flexor in flexion & an extensor in extension
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KNEE STABILISERS (ANATOMICAL)
I- EXTRA-ARTICULAR: see later
II- INTRA-ARTICULAR STRUCTURES
1]. Anterior Cruciate Ligament
• Intraarticular extrasynovial
• Anteromedial fibers - tight in flexion - limits anterior
translation of tibia on femur
• Posterolateral fibers - tight in extension - limits anterior
translation plus external rotation
• Bl.supply - middle genicular a. (post) & synovial vv (ant)
• Mechanoceptors with a proprioceptive role
• Acl strength = 50% pcl strength
• Load to failure = 1700n
• STRAIN RATE plays a role in the failure location
1. Midsubstance tears occur at higher rates
2. Avulsions occur at lower rates
2]. Posterior cruciate ligament
• 2 bundles: posteromedial and anterolateral
• Function:
1]. Limits hyperextension
2]. Prevents post translation of tibia on
femur especially during flexion
3]. Meniscofemoral ligaments:
1. Ligament of HUMPHREY - anterior
2. Ligament of WRISBERG - posterior
4]. Meniscii
• Fibrocartilagenous crescent; triangular in cross-section
• Lateral meniscus is more circular; medial meniscus more c-shaped
• Lateral meniscus has twice the excursion of the medial meniscus during knee motion.
• Anterior horn of LM & post horns of both menisci attach to the intercondylar eminence
• Anterior horns attached to each other by the intermeniscal ligament
• Popliteus muscle is attached to lateral meniscus (not the tendon)
• Semimembranosis is attached to medial meniscus
• Blood supply:
o From branches of the lateral, middle & medial genicular arteries
o Vascular synovial tissue from the capsule supplies the peripheral 25% of
meniscus
• Constituents:
1. Type 1 collagen fibers arranged radially & longitudinally (circumferential)
􀂃 Longitudinal fibers - dissipate hoop stresses in the meniscus
􀂃 Radial fibers & longit fibers - allows meniscii to expand under
compression
2. Proteoglycans trapped within collagen fibers to absorb energy
• Functions:
o Provision of stability
o Shock absorption
o Provision of increased congruity
o Aids lubrication
o Prevents synovial impingement
o Limits extremes of flexion & extension
o Transmits loads across the joint – 50- 100% of load is transmitted through
menisci
o Reduces contact stresses
[Knee Disorders] Page | 3
• Mechanics:
o The circumferential fibers act in much the same way as metal hoops placed around a
pressurized wooden barrel. The tension in the hoops keeps the wooden staves in
place.
o The compression of the menisci by the tibia and the femur generates outward forces
that push the meniscus out from between the bones.
o The circumferential tension in the menisci counteracts this radial force.
o These hoop forces are transmitted to the tibia through the strong anterior and
posterior attachments of the menisci.
o This hoop tension is lost when a single radial cut or tear extends to the capsular
margin and that in terms of load-bearing, a single radial cut through the meniscus is
equivalent to meniscectomy.
• Following total menisectomy there is a decrease in tibiofemoral contact area and an
increase in the contact stresses
• With only one third of the meniscus removed, as with partial meniscectomy, there has been
shown to be an estimated 65% increase in articular contact stress
• total meniscectomy may increase peak loads up to 235%
• In the ACL-deficient knee the menisci, specifically the posterior margins aid in stabilising the
knee from anterior translation.
NERVE SUPPLY
Motor
• Femoral n. - All 4 Quad muscles and the sartorius [Picture]
• Tibial Component of the Sciatic n. - Semitendinosis, Semirnembranosis, and the LHB
• Common Peroneal Component of the Sciatic N. - Short head of Biceps
• Obturator n. - Gracilis
Sensory
• Saphenous nerve is the largest cutaneous branch of the femoral nerve, and supplies
sensation to the skin over the anteromedial aspect of the leg [Picture]
• The main terminal branch, the sartorial nerve, runs distally with the greater saphenous vein
• The infrapatellar branch of the saphenous n. arises proximal to the knee joint, around or
through the sartorius, and then crosses underneath the patella to innervate the skin over
the proximal anterior tibia
• Free nerve endings are prominent in the peripheral portions of the menisci 􀃆 transmit pain
• Mechanoreceptors have been identified in the anterior and posterior horns
• ACL & PCL receive nerve fibers branches of the tibial n. 􀃆 proprioceptive and sensory
PATELLA
• Largest sesamoid bone in the body (usually 3 - 5cm in length)
• Patella tendon to patella length usually ratio of 1:1 (+/- 20%)
• 10% of patients have complete supra-patella membranes and 75% will have at least one of
the 3 plica's even if only as a remnant (supra-patella, medial patella or infra-patella)
• Ossification centre appears between 2 and 3 years of age but can be as late as 6 years
• Blood supply is via the anastomosis of the genicular vessels via the anterior-middle 1/3 and
is directed mainly upwards, from the inferior pole vessels also enter from the deep surface
• Function:
1]. 􀁹 quadriceps lever arm 􀃆 􀁹 mechanical advantage of the quadriceps
2]. Aid articular cartilage nourishment of the femoral condyles
3]. Provide some protection of the femoral condyles
• Normal function depends on the alignment, stability, articular cartilage and muscle control
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Knee Mechanics
KINEMATICS
Instant Center of Rotation
• "If one rigid body rotates about another rigid body, its motion at any instant can be
described by a point or axis of rotation called the instant center of rotation (ICOR).
Surface Joint Motion
• Motion between the tibia and the
femur is both rotational and
translational. The femoral
condyles both ROLL BACK and
glide as they articulate with tibial
plateaus. As the knee moves from
full extension into flexion the ICOR
moves posteriorly relative to both
the femur and the tibia. This
increase the flexion range
Screw home mechanism
• It is the lateral rotation of the medial tibial plateau on femur during stance phase (extension), and
internal rotation during swing phase (flexion).
• 3 factors leads to this mechanism:
1]. The more distal alignment of the MFC
2]. The bigger radius of curvature of the MFC
3]. The cruciates crossing in-between; around which this rotation occur
• Its significance it that it tightens both cruciates and locks the knee in the position of maximal
stability
Patellofemoral Joint
1. 1ry function of the extensor mechanism of the knee is deceleration during the swing phase
2. FUNCTIONS:
1. increases the moment arm of the quadriceps
2. allows wider distribution of compressive stress between the patellar tendon & the
femur
3. from full extension to full flexion the patella glides caudally 7cm on the femoral condyles.
4. by 20 º of knee flexion the patella first begins to articulate with the trochlear groove. Beyond
90º the patella rotates externally & only the medial facet articulates. At extreme flexion the
patella lies in the intercondylar groove.
5. Initially the patella contact occurs distally and with increased flexion the contact areas shift
proximally on the patella
6. patellofemoral contact pressure is 0.5 times body weight with walking, and increases to 2.5
to 3.3 times body weight with stair climbing and descending
[Knee Disorders] Page | 5
Knee Instability
Definition
• It is the loss of normal relationship among the different parts of the joint throughout the
whole arc of motion
Anatomy: (knee stabilizers)
I. Extra-articular
Site Layer Content Importance
Medial
(WARREN &
MARSHALL):
Layer 1 Crural fascia investing sartorius & gastroc
Sartorius
Layer 2 Superficial MCL
POL
Semimembranosus
1ry restraint in 30º
2ry restraint in 0º
Layer 3 Deep MCL
Coronary lig
True capsule
2ry restraint in 0º
Lateral Layer 1 ITB
Biceps
Layer 2 Patello-femoral lig
Patellar retinacula
2ry restraint in 0º
Layer 3 LCL
Arcuate
Capsule
1ry restraint in 30º
2ry restraint in 0º
PMC = postero-medial quadruple
(NICHOLAS and MINKOFF
quadruple complexes)
1]. MCL
2]. Semi-membranosus & its 5 attacments…
3]. SGS
4]. OPL / POL / PMC
PLC= postero-lateral corner 1]. LCL
2]. ITB
3]. Arcuate
4]. Popliteus Tendon
5]. Biceps Tendon
6]. Popliteo-Fibular Ligament (PFL)
AMC AM capsule
Medial retinacula
Patellofemoral & patellotibial lig
ALC AL capsule
Lateral retinacula
ITB
1ry restraint
Anterior ACL
Mid med & lat capsule / ITB / Mensci / collatrals
1ry restraint
2ry restraints
Posterior PCL 1ry restraint
Internal Rotation ACL
POL / PMC
1ry restraint
2ry restraints in 45º
External Rotation PFL & MCL
POL / PMC / LCL / PLC
1ry restraint
2ry restraints in 45º
Arcuate Complex 1]. LCL
2]. Arcuate lig (Y shaped condensation)
3]. Popliteus tendon
4]. Biceps tendon
5]. Lateral head gastroc
II. Internal structures:
ACL, PCL, Menisci and their ligaments
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Knee biomechanics:
• The MECHANICAL AXIS of the femur ≠ anatomical axis = 7º
• This produces greater WB stresses on the LFC > MFC
• The mechanical axis generally passes slightly medial to the center of the normal knee
• Because of the disparity between the lengths of the articular surfaces of the femoral
condyles and the tibial condyles, TWO MOTIONS are produced; ginglymus (hinge) +
trochoid (pivot):
1]. Flexion & extension ............................ sagittal plane
2]. Some degree of IR &ER ...................... Horizontal plane (5º-25º é the IR > ER)
• The complex flexion-extension = ROCKING + GLIDING:
1]. Rolling motion is demonstrable in the first 20º of flexion
2]. Gliding motion predominates after 20º flexion
• The MENISCI MOVE é femoral condyles in flexion and extension & move é tibia in rotation
• LFC IS BROADER in frontal and sagittal planes > medial
• MFC is taller i.e. projects distally to compensate for the 7º valgus
• MFC is prolonged forward > LFC 􀃆 Screwing and unscrewing occurs around an AXIS NEAR
THE MFC & IS INFLUENCED BY PCL
• No rotation is possible when the knee is in full extension.
• In full extension; femur IR until the medial articular surfaces are in contact & LFC rotates
forward 􀃆 "SCREWING HOME" movement, locking the knee in the fully extended position.
• FLEXION AND EXTENSION are from 0-140º
• Normally there is SAGITTAL LAXITY of the tibia over the femur, but not > 3-5 mm
• Also there is a coronal laxity (abduction-adduction) but never > 0-15º (not with full
extension)
• When the MCL is ruptured ...................... the vertical axis of rotation shifts lat & vice versa.
• Changes in the "ICOR" are responsible for OA associated é knee instability
KNEE RESTRAINTS - Sectioning Studies
DIRECTION PRIMARY RESTRAINTS SECONDARY RESTRAINTS
Anterior
ACL • ITB ...................................... 25%
• mid medial capsule .... 20%
• mid lateral capsule: ... 20%
• MCL ................................... 15%
• LCL: ................................... 15%
• Menisci
Posterior PCL (large anterior bundle more) LCL
Internal rotation ACL POL/PMC has secondary effect éin 0 - 45 º
External rotation PFL (Popliteofibular ligament)
LCL and PLC .......... mainly at 30 º flexion
MCL .......................... at all degrees
POL/PMC
Valgus Superficial MCL .... at all deg (least at full ext)
PMC ........................... at full extension
Deep MCL .............. little resistance to valgus
POL - especially near or at full extension
ACL
Varus
LCL ............................ all degrees (more at 30º ,
least at full extension )
PLC (PFL)
ACL
[Knee Disorders] Page | 7
Palmer Mechanisms Of Injury
1]. flexion, Abd, IR of the femur on the tibia,
2]. flexion, Add, ER of the femur on the tibia,
3]. hyperextension,
4]. AP displacement.
• F ABD IR is the commonest 􀃆 medial side injury, respectively;
1]. MCL then Medial capsule
2]. ACL
3]. MM = “O'DONOGHUE UNHAPPY TRIAD”
• F ADD ER 􀃆 injury of lat ligaments of the knee;
1]. LCL then lateral capsule
2]. ACL
3]. Arcuate complex
4]. Popliteus tendon
5]. ITB
6]. Biceps femoris
7]. Common peroneal nerve,
• HYPEREXTENSION mechanism;
1]. ACL
2]. PCL & posterior capsule
• ANTERO-POSTERIOR DISPLACEMENT; e.g. dashboard accident:
1]. ACL or
2]. PCL
• ISOLATED LIGAMENT DISRUPTION;
1]. Some say all ligaments work in concert especially the ACL, and probably no single
ligament can be disrupted
2]. Isolated PCL disruption can result from a direct blow to the front of the tibia with the
knee flexed.
• AVULSIONS occur either at the femoral, tibial, or mid-substance
Classification of injury
1- PLANES CLASSIFICATION
• I. One-plane instability (simple or straight)
1]. One plane medial
2]. One plane lateral
3]. One plan posterior
4]. One plane anterior
• II. Rotary instability
1]. Anteromedial
2]. Anterolateral
3]. Posterolateral
4]. Posteromedial
• III. Combined instability
1]. Anterolateral-anteromedial rotary
2]. Anterolateral-posterolateral rotary
3]. Anteromedial-posteromedial rotary
2- O'DONAGHUE:
Degree Pathology
1st Degree Sprain Lig injury with no instability
2nd Degree Sprain partial tear with some laxity
3rd Degree Sprain complete tear é instability
3- NOYES
Grade
Grade 1 <5mm
Grade 2 6-10mm
Grade 3 11-15mm
Grade 4 16-20mm
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SYMPTOM SIGNIFICANCE
Pain at sitting & stairs Patellofemoral pathology
Locking Meniscal tear
Loose body
Pseudo Locking PF disorder + painful ext
Hge + hamstring spasm
Acute swelling ACL
Peripheral meniscal tear
Osteochondral fracture
Giving way Ligamentous injury
Patellar dislocation
Pseudo Giving way Anterior knee pain
(Reflex inhibition of quad)
History
INJURY SIGNIFICANCE
Noncontact + Pop ACL
Patellar dislocation
Contact + pop Collateral injury
Menical injury
Fracture
Anterior dashboard PCL or Patellar #
Ant + Plantar-flexion PCL
Ant + dorsi-flexion Patellar #
Hyper-ext + varus + ER PLC corner injury
Examination:
LOOK
• Skin- SCARS, redness, swelling ................. Remember to look in popliteal fossa
• Muscle- WASTING of quads ....................... compare diameter of thigh if quads wasted
• Varus Valgus DEFORMITY( measure intermalleolar distance if valgus)
• Q ANGLE
• Bone/joint- EFFUSION
• Walking - look for varus THRUST = dynamic varus collapse in stance loading (ð laxity)
FEEL
• Skin - Temperature, back of hand
• Muscle- Ask patient to contract quads
• Bone/joint- Effusion fluid displacement test, patellar tap test
• Synovial thickening
• Joint line tenderness (with knee bent)
MOVE
• Active then passive- Flexion & extension (0-140º normal)
• Feel for crepitus
[Knee Disorders] Page | 9
SPECIAL TESTS
1]. MCL + LCL
• leg under arm, 2 hands, 10º flexion to relax pos capsule (careful not to rotate knee)
• Valgus stress in flexion ........................... MCL
• Valgus stress in extension ..................... MCL + POL
• Varus stress (taut in full ext) .................. LCL (normally lax in flexion)
2]. Anterior Cruciate Ligament
1- ANTERIOR DRAW at 90º
2- LACHMAN'S TEST - at 15-30º (put patient's knee over your knee) - most sensitive
3- MACINTOSH THE PIVOT SHIFT TEST- Knee extended, valgus strain, foot internally rotated, if
instability present, tibia is subluxed anteriorly. Now flex knee, clunk at 30º is +ve
4- LOSEE PIVOT SHIFT TEST- knee & hip flexed 45º and the other hand thumb behind the
fibula. ER and valgus the tibia + slow extension + push the fibula forward 􀃆 tibial
condyle shifts or subluxes forwards in full extension.
5- MODIFIED PIVOT SHIFT TEST- Grasp foot between arm and chest, valgus IR stress, , then
flex knee, femoral condyle will 'appear' to sublux ant (but tibia is reducing)
6- JERK TEST (HUGHSTON) - patient supine. flex knee 90º & hip 45º. Internally rotate tibia. Let
knee slowly extend while applying a valgus stress. High false -ve rate
7- ALRI TEST (SLOCUM) - Patient lies on unaffected side, with unstable knee up & flexed 10º.
Medial aspect of foot rests on table. Patient maintains ipsilateral pelvis rotated posteriorly
30-50º. Knee pushed into flexion. Easier to do in heavy or tense patients.
3]. Posterior Cruciate Ligament
1- POSTERIOR SAG (in extension)
2- DANIAL DROP-BACK in 90º flexion (active & passive)
3- GODFREY CHAIR TEST: the same but on a chair
4- POSTERIOR DRAW
5- REVERSE PIVOT SHIFT TEST (JAKOB): knee 30º flexed (Subluxed) 􀃆 valgus ER slow
extension 􀃆 reduces anteior
4]. Posteromedial Corner
1- Hold heel, look for foot position
2- HUGHSTON POSTERO-MED DRAWER ............. ACL, MCL sup & deep, (possible: POL, PMC)
• knee flexed & IR then post drawer is done; if lax 􀃆 Postero-med instability
5]. Posterolateral Instability
1- DIAL TEST - pt prone & bend knees or perform supine with the knees at 30º (PLC
only) and 90º (PLC + PCL) &assistant holding the knees 􀃆 ER maximally 􀃆 note
the difference between the two sides; > 15º difference = arcuate / PFL tear
2- HUGHSTON POSTEROLATERAL DRAWER
• knee flexed & ER then post drawer is done; if lax 􀃆 Postero-lateral instability
3- EXTERNAL ROTATION RECURVATUM TEST - by holding big toes, lifting feet off table &
watching to see if tibia falls into ER & Recurvatum
6]. Antero-medial rotary instability ...................... MCL, ACL (possible : POL, PMC)
1- SLOCUM TEST: knee flexed & ER then ant drawer is done; if lax 􀃆 Antero-med instability
7]. Anterolateral rotary instability ......................ACL (possible: PLC, AC)
1- SLOCUM TEST: knee flexed & IR then anterior drawer is done; if lax 􀃆 Antero-lat
instability
2- MAC-INTOCH: .......................................... see before
3- LOSEE: ..................................................... see before
4- JERK: ....................................................... see before
8]. Meniscal, muscle flexibility, others: see later
10 | Page [Knee Disorders]
Figure : A; Daniel test, B; Godfrey test, C; Slocum AMRI and ALRI test,
D; Slocum ALRI test for unrelaxed patients, E; Losee Test,
F; Lateral Pivot Shift of MacIntosh, G; Noyes test, H&I; Jacob test.
Different Instabilities of the knee
Plane Direction Test Used Deficient Structure
One plane
Valgus Valgus (Full Extension)…………….……….. MCL sup & deep, ACL (possible: POL, PMC, PCL)
Valgus (20-30° Flexion)…………….……….. MCL (possible: POL) 􀃆 O’Donoghue or Hughston
Varus Varus (Full Extension)……………..………… LCL, PCL, AC, PLC, ACL, ITB
Varus (20-30° Flexion) …………..………….. LCL (possible: PLC, AC)
Anterior Lachman (Only)……………………..…………. ACL (PLF)
Anterior Drawer (Only)……………..……… ACL (AMF)
Lachman & Ant. Drawer…………………… ACL complete (possible: POL)
Posterior Posterior Drawer; Daniel; Godfrey …… PCL
Two
planes
AM Slocum ……………………………………………… MCL, ACL (possible : POL, PMC)
AL Slocum; MacIntoch; Losee; Jerk. .................... ACL (possible: PLC, AC)
PM Hughston………………………………………….. ACL, MCL sup & deep, (possible: POL, PMC)
PL Hughston; Jakob; Dial; ERR ……………… PCL, AC (possible: PLC, LCL)
8].
[Knee Disorders] Page | 11
Fig.: A; Abduction adduction test, B; Dehaven test, C; spring test
Meniscal Test
1- HELFET TEST é patient sitting mark the midline of the patella and the tibial tuberosity;
normally in 90° flexion, the tibial tuberosity is aligned with the mid-patellar line & in
extension, it moves laterally. This indicates the normal screw-home movement. If
rotation is blocked, possibly by a meniscal fragment this movement is lost
GRIND TESTS
2- McMurray: acute knee flexion as possible. The leg is then rotated internally and
externally with varus and valgus rotational stresses 􀃆 Trapping of damaged MM is felt
as a clunk
(at 90º= PHMM / at 60º or less = body or AHMM)
3- ANDERSON GRIND TEST (if full flexion is difficult) varus and valgus rotational stresses are
applied to 45º flexed knee as the knee is extending. The maneuver is repeated with
progressive loading 􀃆 a clunk may be felt
4- APLEY COMPRESSION TEST
5- STEINMANN 1ST test is done with the patient sitting the same as Apley
6- STEINMANN 2ND test is done with the pt supine; ER during flexion & extension 􀃆 pain moves
from posterior to anterior with extension
7- JUMP TEST (especially for pt with ACL tears): knee flexed to 130º-140º. The proximal tibia is
grasped as in anterior drawer and pulled anteriorly with a firm, prolonged force 􀃆 jump or
jerk
COMPRESSION TESTS
8- BRAGARD’S EXTENSION TEST the knee is hyperextended & ER; so the menisci are forced to
move forward so the injured meniscus is stretched producing pain over the joint line.
9- BOHLER’S ABDUCTION ADDUCTIONTEST valgus and varus stresses cause pain over the lateral
or medial joint line respectively.
10- DEHAVEN ABDUCTION GRAVITY TEST may help to demonstrate tears of the anterior or middle
segments of the lateral meniscus. With the patient on his sound side, the affected knee is
flexed and extended from 90°-0°, so the force of gravity apply compression to the lateral joint
space
11- PAYR’S TEST: is the same idea by applying varus stress while the pt is sitting in Buddha position
12- SPRING TEST is done by grasping the heel with the knee flexed as much as possible, and then
extended passively. When a painful “spring block” occur = torn meniscus (fig.2-14; C).
13- THESSALY TEST: é the pt. mono-pedal standing on the affected side at 5º & 20º flexion &
supported by holding his out-stretched hands; he is asked to rotate his body on his knee internally
& externally. Pain, locking, or catching is pathognomonic to meniscal tear (95% accuracy)
14- MERKE’S TEST: is the same but the patient is standing bipedal unsupported
15- DUCK WALK TEST: pain is produced at the corresponding joint line
Fig: A; McMurray test, B; Apley compression, C; Jump test, D; Steinmann test.
12 | Page [Knee Disorders]
9]. Patellofemoral joint
1- ALIGNMENT
2- GRASS HOPPER SIGN of lateral subluxation of patella
3- Q ANGLE: between line joining ASIS to mid-patella & line from mid-patella to tibial
tubercle.
4- 'J' SIGN TRACKING - = maltracking due to lateral subluxation.
5- Grinding/crepitus
6- CLARKE'S (SNATCH) test - patella fixed with hand on it's superior border. Patient asked to
contract quads. Reproduction of symptoms = +ve (all patients get some discomfort)
7- PATELLAR APPREHENSION TEST (for instability) - Flex knee whilst trying to push patellar
laterally, if positive patient will react with apprehension or try to push examiner away.
8- PLICA GRIND TEST: flexion 30º then push patella medially 􀃆 pain if medial plica
10]. Othe usually forgotten tests:
1]. Back of the knee
2]. Hip
3]. Muscle flexibility tests: Ely, Tripod, Ober, Silfverskiold
4]. Nerve assessment especially of the common peroneal nerve in PLC injuries
Radiological
1].X-RAY ACUTE INJURY CHRONIC INJURY
AP Lateral capsular sign = SEGOND # ACL deficiency: Central osteophytes + Peaking
of the tibial spines (TETON sign)
Growth plate fracture MCL: PELLEGRINI-STIEDA disease
Avulsed fibular styloid OCD
Torn ligaments. (stress film) FAIRBANK’S joint line changes;
Squaring of MFC
Narrowing of medial joint space
Osteoscelerosis
Marginal and central osteophytes
DISCOID Lateral meniscus :
Squaring of LFC
Widening of Lat. joint space
Cupping of lat tibial plateau
Bipartite patella
Tunnel In addition to above findings:
Loose body
Avulsed ACL, or PCL
OCD
Lateral Avulsed ACL at tibial spine Patella alta
Avulsed patellar tendon SINDING-JOHANSSON-LARSEN syndrome
Avulsed quadriceps tendon OSGOOD-SHLUTTER disease
Osteophyte (inf. and sup. patellar border)
Calcified fat pad (HOFFA’S disease)
Calcified prepatellar bürsa
Patellofemoral Avulsed medial capsule Subluxed patella (Merchant 45°&Lauren 20º)
Fractured lateral osteophyte Calcification
2].MRI
• Allows assessement of PLC injury as well as
ACL & PCL
• Assess which structures of the
posterolateral corner are injured and
whether the injuries are mid-substance or
whether they have been avulsed from the
fibula or femur
[Knee Disorders] Page | 13
Non-operative Treatment:
• Good results if:
o thigh circumference is equal or better than opp. side
o stable
• Poor results if:
o thigh atrophy
o meniscectomy performed
o instability
Arthroscopic findings:
• "DRIVE THROUGH SIGN" = >1cm of lateral opening and exceptional posterior visualization of the
lateral meniscus
Rationale:
• ACL & PCL arthroscopic reconstructions are usually delayed for 6wk then reconstruct
• PLC & PMC are best treated in the acute stage
ACL Instability with degenerative changes
• Ligamentous stabilisation alone often fails
• Usually medial compartment OA
• Rx: combined tibial osteotomy plus extra-articular reconstruction
ACL
• Completely intraarticular extrasynovial ligament measures 33mm X 11mm
• ACL max TENSILE STRENGTH = 50% PCL strength = 1700n
• STRAIN RATE plays a role in the location of ligament failure
o Midsubstance tears occurring at higher rates
o Bone ligament complex tears occurring at lower rates
• BLOOD SUPPLY - middle genicular artery (post) & synovial vessels (ant)
Function
1]. Anteromedial fibers - tight in flexion - limits anterior translation of tibia on femur
2]. Posterolateral fibers - tight in extension - limits anterior translation + ER
3]. Mechanoceptors with a proprioceptive role
4]. Important as a secondary restraint to varus and valgus stresses
5]. Screw home motion occurs around its axis
Isometry:
1. Isometric placement of ACL refers to the concept that a full range of knee can be
achieved without causing long-term ligament deformation
2. isometry can not exist because, during ROM, there is no one point on femur that
maintains a fixed distance from a single point on tibia; elongation always will occur
3. placement of graft as closely as possible to centers of tibial & femoral attachments of
anterior medial band results in least amount of strain (least change in the length of
ACL during complete ROM of knee)
14 | Page [Knee Disorders]
Operative Treatment:
1]. ACL TREATMENT
I. Direct Repair
1- Screw fixation or pull out sutures for avulsion fractures
• Not recommended for mid-substance tears due to poor healing potential.
II. Extra-articular reconstruction
2- MACINTOSH PROCEDURE: (historical)
• Pass a mobilised strip of ITB to the posterolateral corner of the knee through a tunnel
deep to the LCL
3- LOSEE MODIFICATION: Loop through bony tunnel & lat. Gastroc.
4- ANDREWS ITB tenodesis
III. Intra-articular Reconstruction
5- CLANCY BTB reconstruction
6- MACINTOCH : distally attched BTB reconstruction
7- ZARICZNYJ hamstring reconstruction - semitendinosis + gracilis
8- LIPSCOMB distally attached ST graft
9- PUDDU proximally unstripped ST graft
10- ALLOGRAFT reconstruction
11- SYNTHETIC grafts
IV. Intra & extra articular Reconstruction
12- ZARIN ITB & ST in the opposite direction
13- LOSEE modification of Zarin ITB &ST in opposite direction
[Knee Disorders] Page | 15
2]. PCL TREATMENT
• Traditionally, most authors have recommended NONOPERATIVE TTT FOR ISOLATED PCL
• Salvage procedures:
1]. MÜLLER OLECRONIZATION of Patella to prevent posterior sag of tibia
• Reconstruction procedures:
2]. O’DONOGHUE transosseous suturing
3]. If avulsed REFIXATION of the avulsed fragment
• Arthroscopic assisted PCL reconstruction:
4]. SINGLE BUNDLE PCL reconstruction
5]. DOUBLE BUNDLE PCL reconstruction
6]. INLAY PCL reconstruction
3]. POSTERO-MEDIAL RECONSTRUCTION:
1- Repair:
1]. Anatomical repair from the deepest structures to the most superficial structures
2]. O’DONOGHUE transosseous suturing method
2- Reconstruction
3]. HUGHSTON reconstruction of POL through trans-osseous suture
4]. SLOCUM Pes Anserinus transplantation + sartorius advancement to reinforce MCL
16 | Page [Knee Disorders]
4]. POSTEROLATERAL RECONSTRUCTION
1- Acute Repair:
1]. Anatomical repair from the deepest to superficial + BUNNEL LCL suturing
2]. O’DONOGHUE transosseous suturing method
2- Chronic reconstruction:
1]. HUGHSTON postero-lateral advancement
2]. MÜLLER LCL reconstruction using biceps slip
3]. CLANCY Biceps tenodesis
4]. WARREN two tailed graft reconstruction (both LCL & popliteo-fibular lig)
5]. NOYES allograft reconstruction
6]. LARSEN semitendinosus for reconstruction
POST-OP CARE:
• CPM range of motion immediate post-op
• Closed chain exercises (foot is maintained on the ground or a platform)
• Running & any activity that involves excessive knee rotation (cutting) is
discouraged for the first several months.
[Knee Disorders] Page | 17
Complications:
1. Loss of knee extension / Arthrofibrosis
o more common with early reconstruction
o incorrect tunnel placement can cause decreased motion and fibrosis
(diagnose with x-rays & MRI)
2. Tibial tunnel syndrome
o 􀁹 size of tibial tunnel over 1yr following surgery
3. Graft failures:
o Improper placement of graft tunnels
o Impingement of the graft in the femoral notch:
􀂃 due to improper tunnel placement
􀂃 due to inadequate notchplasty
o Inadequate graft fixation
o Associated injuries (varus knee, significant osteochondral defects)
o CRPS (0.5%)
o Infection (<1%)
4. Patellofemoral pain
5. Patella fractures
6. CRPS (0.5%)
7. Infection (<1%)
18 | Page [Knee Disorders]
Knee Dislocations
Clinical Findings:
1. Popliteal artery & vein injury is common
1. note that knee dislocations that have spontaneously reduced may look benign but
may lead to thrombosis of the popliteal artery
2. popliteal a. is usually tethered proximal at adductor hiatus & distal by soleus arch
3. injury to popliteal a. may initially manifest as an intimal tear or intraluminal thrombus
2. Peroneal nerve injury:
1. in 20% to 40% (half of these palsies are permanent)
2. w/ peroneal nerve injury, be highly suspect for vascular injury; - even if pulse
returns following reduction, consider need for arteriogram, since incidence of
intimal injury is high w/ concomitant nerve injury
3. Both cruciates and least one collateral ligament are usually disrupted
Classification:
• Anterior (31%)
o hyperextension of knee (may need > 30 º of hyperextension to produce this injury)
o often PCL & ACL torn
o either the MCL or LCL or both will usually be injured
o alternatively, hyper-extension 􀃆 ACL & posterior capsule while the PCL is spared
o Popliteal artery injury
• Posterior (25%)
o disruption of both cruciate ligaments
o possible extensor mechanism disruption
o avulsion of or complete disruption of popliteal artery
• Lateral (13%) & Medial ( 3%)
• Rotatory ( 4% - usually posterolateral)
Investigations:
1. X-Rays:
o Tibial plateau fracture & Proximal fibula fracture & Avulsion of Fibular Head
o Avulsion fracture of Gerdy's Tubercle
o Intercondylar spine fracture
2. Arteriogram - indications unclear
3. MRI - see above
Management:
• Reduction
o may be complicated by interposed soft tissue
o External fixation - it is important that the external fixator pin sites will not interfere
with the ACL/PCL tunnel sites (during future ligament reconstruction)
• Vascular Inuries
o the worst error to make is to underestimate the need to promptly treat these injuries
• Nerve injury:
o the location of the nerve injury may be well above the knee joint
• Assessment of ligament injuries:
o EUA
• Surgical Treatment of Ligament Injuries:
o if vascular injury has been previously repair, get clearance from the vascular
surgeon to utilize a tourniquet
o Deep to superficial (as above)
[Knee Disorders] Page | 19
Patellofemoral Disorders
Anatomy
WIBERG’S CLASSIFICATION of patella shape
Type I 10% Concave facets, symmetrical and equal
Type II 65% Medial is smaller. Lateral is concave
Type III 25% Marked lateral predominance
Type IV <1% Tiny medial facet
Jagerhut Rare No articulating medial facet
Extensor mechanism:
1]. Quad & Quad tendon
2]. Medial and lateral retinaculae
3]. PF ligaments
4]. Patello-tibial lig
5]. Patellar tendon
6]. Tibial tubercle
Patellofemoral kinematics
• Patellofemoral joint reaction force
o 0.5 times body weight with walking
o 3.3 times body weight with stairs
• Patella 􀁹 the moment arm of the quadriceps 􀃆 􀁹 quad strength by 33-50%
• The femur articulates only with a portion of the patella in each position of flexion
CLINICAL
HISTORY: Determine if complaint is instability or pain
EXAMINATION (Also see Torsional Profile Assessment)
• Standing examination
o Varus/ valgus alignment & Q-angle
o Pelvic obliquity and LLD
o MISERABLE MALALIGNMENT $ = femurIR + Tibial ER ± pronated foot ± pes planus
• Sitting examination
o GRASSHOPPER EYES appearance: high and lateral patellas
o Lateral patellar tilt
o Patellar tracking: pain and crepitation, 'J' SIGN
o Position of tibial tubercle é respect to trochlear midline ≈ < 20mm lateral to the midline
• Supine examination
o Quadriceps (Q) angle (Normal M 10° F 15)
o Quadriceps mass (VMO atrophy); hand breadth above patella
o Hamstring tightness (popliteal angle)
o Tenderness on quadriceps or patellar tendon insertion, patellar facets, retinaculum
o Crepitation and patellar compression
o Apprehension test (20-30°flexion)
o Examination for medial plica
o CLARKE'S SNATCH TEST (pain on contraction of the quadriceps with the patella fixed)
o PATELLAR TILT (evaluates tension of the lateral restraint)
o PATELLAR GLIDE TEST (knee flexed 20 to 30°)
􀂃 􀁺: 1 quadrant or less medial glide is indicative of tight lateral
􀂃 􀁹: subluxable, or dislocatable patella
• Prone examination
o Hip motion - femoral neck anteversion (abnormal if IR exceeds ER > 30°)
o Quadriceps tightness - ELY TEST (especially rectus femoris)
o Leg-heel alignment (Normal 2-3° of varus)
o Hindfoot-forefoot alignment: (N: long axis of heel ⊥ to transverse axis of forefoot)
20 | Page [Knee Disorders]
INVESTIGATIONS
RADIOGRAPHY
• AP
• True lateral view
• Skyline views:
o Sulcus angle of Brattström: 120º-140º
o Patellar index:
MedialPFW LateralPFW
PatellarWedth
−
=17
o Congruence angle: between the sulcus line and the patellar vector = -16º to + 4º
o Lateral PF angle: bet. the tangent on femoral condyles & Lat.PFJ line 􀃆 N: +ve
o Lateral PF index: PFJ space (
LateralPFJ space
CentralPFJ space )=1.6
CT
• More accurate assessment of sulcus & congruence angle
• Perform é knee in different flexion degrees ± quad contraction
MAGNETIC RESONANCE IMAGING
• Midpatella transverse images with knee flexed 15°
• Assess other areas of knee: articular cartilage, muscle and supporting retinacular structures
• Dynamic MRI to assess patella tracking
Patellofemoral Trauma
PATELLA FRACTURE
PATELLAR STRESS FRACTURES
• Rare overuse injury reported in endurance runners, volleyball players, and high jumpers
• Two types: longitudinal and transverse (Iwaya 1985)
• In cases with delayed diagnosis operative treatment
• Quadriceps or Patellar tendon rupture
Non-arthritic patellofemoral pain
1. PATELLAR TENDONITIS (JUMPERS KNEE)
• Secondary to repetitive trauma: running, jumping and kicking sports
• Tenderness usually on the inferior pole
Blazina Classification Affect Participation Treatment
I Pain only after activity N Activity modification, warm-up,
II Pain at the start of activity & fatigue N stretching, ice, NSAID's
III Pain during and after participation Y As above 􀃆 Steroid inj 􀃆 debridement
IV Complete tendon disruption Y Primary repair of the tendon
2. PLICA SYNDROME
• Medial patellar (most common), lateral and suprapatellar
• Inflammation and impingement on medial femoral condyle
• Treatment
o NSAID's, quadriceps exercises ± Steroid injection ± Arthroscopic excision
3. OSTEOCHONDRITIS DISSECANS (OCD)
• Knee is most common site
• Typically in teenage athletes
• Location in the patella is rare
• Medial facet (70%), lateral facet (30%)
• Hughston Prone ..... 55º
• Merchant view ........ 45º
• Laurin view .............. 30º
• Ficat ........... 30º,60º,90º
• Blumensaats line
• Insall / Salvati Ratio ≈1
• Blackburne Peel ≈ 1
[Knee Disorders] Page | 21
4. CHONDROMALACIA
• "softening" of the articular cartilage
• Aetiology
o 50% idiopathic
o 15% post traumatic
o 20% secondary to maltracking- lateral patellar compression syndrome
o 15% due to unstable (recurrent dislocaters) patellae
• Treatment is dependent on cause
Outerbridge Classification
I Articular cartilage softening
II Chondral fissures and fibrillation < 1.25mm
III Chondral Fibrillation > 1.25 mm (crabmeat changes)
IV Exposed subchondral bone
5. PATELLOFEMORAL MALALIGNMENT
MEDIAL PATELLAR SUBLUXATION/DISLOCATION
• Usually iatrogenic, secondary to realignment procedures, but has also been described without
previous surgery (Richman 1998)
• When associated with internal tibial torsion
􀂃 If Tibio-Tubercle distance 􀁺: external derotational tibial osteotomy proximal to
tibial tubercle
􀂃 If Tibio-Tubercle distance is normal: external derotational tibial osteotomy distal
to tibial tubercle
LATERAL PATELLAR SUBLUXATION/DISLOCATION
• 5% are associated with an osteochondral fracture
• Treatment
o First time instability episode with no malalignment and normal radiographs
o immobilisation followed by early range of motion and PT
o If osteochondral loose bodies are present 􀃆 arthroscopic removal or fixation
Fulkerson Clinically Q Angle Lateral Retinaculum Realignment
I Subluxation alone 􀁹􀁹 Normal Distal
II Subluxation and tilt 􀁹􀁹 Tight Distal + Proximal
III Tilt alone Normal Tight Proximal
IV No malalignment Normal Normal Physiotherapy ± Proximal
o Subdivided:
A]. Absence of articular lesion
B]. Presence of minimal chondromalacia
C]. Presence of osteoarthritis
6. DORSAL DEFECT OF THE PATELLA
• Benign lesion - Non-specific fibrous tissue
• Located along the superolateral aspect of the articular surface of the patella
• Radiolucency with sclerotic margins and intact overlying articular cartilage
• Frequently heals spontaneously by sclerosis
7. BIPARTITE PATELLA
• 15% of people in childhood & 2% in adulthood
• Sometimes a 3rd ossific centre appears (TRIPARTITIE)
• 57% are unilateral with a male: female ratio of 9:1
Saupe Classification
TYPE I 5% Distal pole
TYPE II 20% Lateral
TYPE III 75% Supero-lateral
22 | Page [Knee Disorders]
8. OSGOOD SCHLATTER’S
• Traction injury to the apophysis where patella tendon inserts (some inserts on either side)
• 11-15 y male, usually no history of injury and may be bilateral
• Symptoms are aggravated by running, squatting, jumping, stairs etc
• PXR: May show fragmentation of the apophysis
• Spontaneous recovery is usual but takes time
• Where symptoms are persistent and troublesome excision of a separate ossicle
9. SINDIG-JOHANSSON-LARSEN'S DISEASE: (traction tendinitis at lower pole of patella, w/ calcification)
• Traction apophysitis of the distal pole of the patella 􀃆 traction tendonitis develops
• Similar pathology to Osgood-Schlatter’s disease and usually resolves spontaneously
10. TORN MENISCUS
11. DISCOID MENISCUS
12. PATELLA BURSITIS
13. PATELLA CYSTS OR TUMOURS
14. REFLEX SYMPATHETIC DYSTROPHY
Relationship of patellofemoral malalignment to femoral and tibial torsion
INTERNAL FEMORAL TORSION / FEMORAL NECK ANTEVERSION
1. Toeing-in if it exists alone and external rotation of hip < 30 °
2. Feet straight: if compensatory external tibial torsion, pes planus, or external hip rotation at
least 30°
EXTERNAL TIBIAL TORSION
• Primary or secondary to medial femoral torsion
• Primary deformity responsible for PF malalignment
• Gait with normal foot progression angle (straight ahead) but with kneeing-in medial thrust
with stance phase.
Treatment
CONSERVATIVE
1. Activity modification, rest, NSAID's and rehabilitation are successful in 90%
2. Supervised exercise program should be continued for at least 6 months
3. Patellar taping (Powers et al, 1997):
o Average pain reduction of 78%
o Taping changes the timing of VMO and VL activity in subjects with patellofemoral pain
during step-up and step-down tasks
o When the patellofemoral joint was taped, the VMO was activated earlier.
[Knee Disorders] Page | 23
SURGICAL
A. PROXIMAL REALIGNMENT PROCEDURES:
• LATERAL RELEASE (OPEN OR ARTHROSCOPIC)
o Indication: for patellar tilt < 8 º or lateral retinacular tightness
o Do only when it is tight
o Adequate release should allow inversion of patella to 70-90 º
o The superficial and deep layers of the retinaculum must be divided.
o Best results in patients with pain. Worse in patients with instability and severe DJD.
o 85% good results in pts é pain and PXR evidence of tilt and Outerbridge I
o 92% good & excellent results in patients with minimal articular degeneration and tilt
• LATERAL RELEASE AND MEDIAL PLICATION (PROXIMAL REALIGNMENT)
o Attempt to decrease the valgus quadriceps moment on the patella
o Indication: retinacular tightness and medial laxity
o for recurrent lateral subluxation /dislocation in skeletally immature patients
o 82% good/excellent results in patients with instability (Scuderi 1988)
o Poor results in patients with significant chondromalacia
• GALLEAZI procedure (semitendonosis tenodesis)
o Reconstruction with semitendonosis tendon
o Tensioned at 30° of flexion
B. COMBINED PROXIMAL AND DISTAL REALIGNMENT PROCEDURES
• ELSMLIE-TRILLAT: Lateral release with medialisation of tibial tubercle
o Best candidates have recurrent instability, evidence of increased Q angle and minimal,
if any articular degeneration
• FULKERSON: Lateral release with antero-medialisation of the tibial tubercle
o Biomechanical studies have shown that the patellofemoral joint reaction force
decreases about 50 % after a 2-cm anteriorisation of the tibial tubercle
o Due to the obliquity of the osteotomy, no bone graft is necessary.
o Best for pts é lateral patellar tilt and with Outerbridge grade III-IV chondrosis
o See Later for details of distal osteotomies
C. PATELLOFEMORAL ARTHROPLASTY
• Hemiarthroplasty (PATELLAR RESURFACING) or total patellofemoral arthroplasty
• Indicated for OA of the patella and trochlea
• Great care must be taken to ensure that any malalignment or maltracking is identified and
corrected otherwise the procedure will fail
D. FEMORAL OSTEOTOMY (ALBEE)
• For trochlear dysplasia
• Elevation of the lateral facet of the femoral trochlea with osteotomy and bone graft
E. PATELLECTOMY
• Last resort surgery which may not eliminate pain
• Complicated by loss of quadriceps strength 30 to 50%
24 | Page [Knee Disorders]
B]. DISTAL REALIGNMENT PROCEDURES:
1]. HAUSER (ABANDONED)
• Tibial tubercle osteotomy with the tubercle moved medial, distal and posterior
• Complicated by development of patellofemoral DJD in 70 % of patients because of
increased PFJ joint reaction forces (Hampson et al, 1975)
2]. MAQUET
• Elevation (anteriorisation) of tibial tubercle
• Salvage operation in patellofemoral DJD without malalignment
• Risk of anterior skin necrosis when anteriorisation > 2 cm
3]. GOLDTHWAITE-ROUX
a. The patella tendon is split & the lateral half is passed under the medial half & attached
to the periosteum on the tibia in a medial position.
4]. HEMI-PATELLAR TENDON TRANSFER ± lateral release/medial reefing
5]. ELMSLIE-TRILLAT
• Medialization of tibial tubercle + lateral release + medial capsular reefing
• Considered when there is minimal or absent articular injury in patients with lateral
instability caused by malalignment
• Good/excellent results in 81% (Brown, 1984)
• Best results when postoperative congruence angle < 15° (Shelbourne et al, 1994)
6]. FULKERSON
• Anteromedial tibial tubercle osteotomy
• Malalignment and lateral facet chondrosis
• Slope of cut dependent on amount of subluxation and DJD
• Not as successful with medial facet chondromalacia
• 90% good/excellent results (Fulkerson et al.1990)
[Knee Disorders] Page | 25
Patello-Femoral Instability
Patello-Femoral Joint Mechanics
1. Patella increases moment ( lever ) arm of extensor muscles
2. Slides 7 cm in trochlear groove
3. Patello-femoral contact minimal until 20 º flexion
4. Contact area moves from proximal -> distal in trochlea & distal to proximal on patella
5. >90º flexion quads tendon is in contact with the trochlea
6. 10º flexion -> lever arm increased 10 %
7. 45º -> 30 % then decreases
8. Patello-femoral joint reaction force determined by quads force and amount of knee flexion
9. Normal walking -> joint compressive forces = half bodyweight
10. Up stairs -> 2.5 - 3.3 times body wt
11. Deep knee bends -> 7-8 x body wt
Presentation
PFJ instability may present as:
• Anterior Knee Pain
• Patello-femoral subluxation
• Patello-femoral Dislocation
Anterior Knee Pain
Other causes of anterior knee pain include:
1. Patello-femoral overload (Chondromalacia)
2. Plica Syndrome
3. 'Jump' knee (enthesitis of patella tendon origin)
4. Sinding-Johansson-Larsen $
5. Torn Meniscus
6. Discoid Meniscus
7. Osteochondritis Dissecans
8. Patella Bursitis
9. Bipartite Patella
10. Patella cysts or tumours
Risk Factors / Causes
A. Bony (Static Stability)
1. Shallow femoral trochlea
2. Hypoplastic LFC
3. Patella Shape (Shutzer et al.)
4. Patella Alta
B. Malalignment
• External tibial torsion
• Incr. femoral anteversion
• Incr. genu valgum
• Incr. Q angle (unreliable)
C. Soft Tissue (Dynamic stability)
• Ligamentous laxity
• contribution of distal oblique portion of vastus medialis muscle is critical
• (tight hamstring & gastrocnemius w/ pronated feet)
Clinical
• Mechanism of injury, acuity, previous treatment, and status of the opposite knee.
Fulkerson Clinically Q retinacula Realignment
I Subluxation alone 􀁹􀁹 Normal Distal
II Subluxation + tilt 􀁹􀁹 Tight Distal + Proximal
III Tilt alone N Tight Proximal
IV No malalignment N Normal Physiotherapy ± Prox
Subdivided:
A]. Absence of articular lesion
B]. Chondromalacia
C]. Osteoarthritis
[Knee Disorders] Page | 19
Patellofemoral Disorders
Anatomy
WIBERG’S CLASSIFICATION of patella shape
Type I 10% Concave facets, symmetrical and equal
Type II 65% Medial is smaller. Lateral is concave
Type III 25% Marked lateral predominance
Type IV <1% Tiny medial facet
Jagerhut Rare No articulating medial facet
Extensor mechanism:
1]. Quad & Quad tendon
2]. Medial and lateral retinaculae
3]. PF ligaments
4]. Patello-tibial lig
5]. Patellar tendon
6]. Tibial tubercle
Patellofemoral kinematics
• Patellofemoral joint reaction force
o 0.5 times body weight with walking
o 3.3 times body weight with stairs
• Patella 􀁹 the moment arm of the quadriceps 􀃆 􀁹 quad strength by 33-50%
• The femur articulates only with a portion of the patella in each position of flexion
CLINICAL
HISTORY: Determine if complaint is instability or pain
EXAMINATION (Also see Torsional Profile Assessment)
• Standing examination
o Varus/ valgus alignment & Q-angle
o Pelvic obliquity and LLD
o MISERABLE MALALIGNMENT $ = femurIR + Tibial ER ± pronated foot ± pes planus
• Sitting examination
o GRASSHOPPER EYES appearance: high and lateral patellas
o Lateral patellar tilt
o Patellar tracking: pain and crepitation, 'J' SIGN
o Position of tibial tubercle é respect to trochlear midline ≈ < 20mm lateral to the midline
• Supine examination
o Quadriceps (Q) angle (Normal M 10° F 15)
o Quadriceps mass (VMO atrophy); hand breadth above patella
o Hamstring tightness (popliteal angle)
o Tenderness on quadriceps or patellar tendon insertion, patellar facets, retinaculum
o Crepitation and patellar compression
o Apprehension test (20-30°flexion)
o Examination for medial plica
o CLARKE'S SNATCH TEST (pain on contraction of the quadriceps with the patella fixed)
o PATELLAR TILT (evaluates tension of the lateral restraint)
o PATELLAR GLIDE TEST (knee flexed 20 to 30°)
􀂃 􀁺: 1 quadrant or less medial glide is indicative of tight lateral
􀂃 􀁹: subluxable, or dislocatable patella
• Prone examination
o Hip motion - femoral neck anteversion (abnormal if IR exceeds ER > 30°)
o Quadriceps tightness - ELY TEST (especially rectus femoris)
o Leg-heel alignment (Normal 2-3° of varus)
o Hindfoot-forefoot alignment: (N: long axis of heel ⊥ to transverse axis of forefoot)
26 | Page [Knee Disorders]
• Q angle
• The integrity of the ACL (because similar derotation, deceleration mechanisms that cause
patellar instability can cause ACL injury)
Radiology
LATERAL X-RAY: (knee at 30º = Patella is centered in trochlear groove at 30º flexion)
• BLUMENSAAT'S Line: The superior patella pole should not be higher than intercondylar roof
line
• INSALL-SALVATI index- length of patella to length of patella tendon, normal=1. Patella Alta 􀁺
• BLACKBURNE-PEEL index- length of patella articular surface to the distance of its inferior
margin from the tibial plateau w/ knee in 30º. flexion. normal=0.8-1.1. More accurate.
SKYLINE VIEW:
• Sulcus angle of BRATTSTRÖM: 120º-140º
• Congruence angle: between the sulcus line and the patellar vector = -16º to + 4º
• Patellar index:
MedialPFW LateralPFW
PatellarWedth
−
=17
• Lateral PF index: PF joint space (
LateralPFJspace
CentralPFJspace )=1.6
• Lateral PF angle: bet. the tangent on femoral condyles & Lat.PFJ line 􀃆 N: +ve
• Trochlear signs- Crossing sign, 'Bump' sign, Dysplastic condyles, Trochlear depth < 8mm.
AP & Tunnel views: for osteochondral fractures.
CT Scan helpful in assessing the relationship of the PF joint in terms of tilt or translation, or both.
Arthroscopy
• Use a suprapatella portal to watch patella centre in trochlear groove betw. 30-60º.
[Knee Disorders] Page | 27
Treatment
• Treatment is individualized and is based on the patient's lower extremity alignment, joint
motion, ligamentous laxity, muscle strength, and quadriceps competence.
• The goal of treatment is to prevent recurrence.
Proximal Realignment
• to alter the tension of tissues attached to the patella.(Lat release & med. reefing)
• Lateral retinacular release
• Direct medial retinacular repair in acute dislocations.
• Quadriceps transfers, particularly the vastus medialis obliquus are used to restore medial
vector balance (Medial plication).
• Medial hamstring transfer (GALEAZZI technique) may be required to provide a tenodesis
effect in troublesome cases.
DISTAL REALIGNMENT = transpose the tibial tubercle
1]. HAUSER PROCEDURE: (HISTORICAL)
• Involves medialization of the tibial tubercle in order to decrease Q angle. due to the anatomy
of the proximal tibia, translating the tibial tubercle medially, will also translate the tubercle
posteriorly. Posterior translation of the tibial tubercle will have the effect of increasing
patellofemoral contact pressures ώ leads to pain & OA. Also can produce a low patella (baja)
2]. ELMSLIE-TRILLAT PROCEDURE:
• medial tibial tubercle transfer which has no posterior displacement
• does not involve anterior / posterior displacement of the tuberosity
3]. MAQUET PROCEDURE: (HISTORICAL)
• Anterior translation of the tibial tubercle which has the effect of decreasing patellofemoral
contact forces. Patients with pain due to early patellofemoral arthrosis may expect pain relief
following the Maquet Procedure. Disadvantages with this procedure include high incidence
of skin necrosis, compartment syndrome and no effect on the Q angle;
• A combination of tibial tubercle transfer, proximal lateral release, medial capsulorrhaphy and
tendon transfer may be required to establish appropriate alignment.
4]. GOLDTHWAITE-ROUX PROCEDURE:
• The patella tendon is split & the lateral half is passed under the medial half & attached to the
periosteum on the tibia in a medial position.
5]. FULKERSON
• Anteromedial tibial tubercle osteotomy
• Malalignment and lateral facet chondrosis
• Slope of cut dependent on amount of subluxation and DJD
• Not as successful with medial facet chondromalacia
Contra-indications to Re-alignment:
1]. Absence of clear physical examination and radiographic findings
2]. Patellofemoral pain which results from "dashboard" car accident injuries; often have significant
patellofemoral pain chondromalacia, but do not improve with surgery
3]. Patellar instability associated with abnormal ligamentous laxity; eg, Down $ & Ehlers-danlos $
28 | Page [Knee Disorders]
Osteochondritis Dissecans
Definition
• NON INFLAMMATORY pathologic condition of the cartilage é IMPENDING OR ACTUAL
separation of a segment of cartilage é underlying subchondral bone
• Tends to heal spontaneous in skeletally immatures
Ætiology:
1- Repeated TRAUMATA
2- May be AVN
Pathogenesis:
1]. Intraosseous odema 􀃆 capillary compression 􀃆 ischemia
2]. Subchondral collapse 􀃆 arteriolar compression 􀃆 necrosis
3]. Fragmentation 􀃆 NBF
Pathology:
SITE:
• Bilateral .........................................................................20-30%
• Poster-lateral MFC (ant to PCL foot print) ...........70%
• LFC ..................................................................................20%
• patella ............................................................................10%
MACROSCOPICALLY:
• DEGENERATED cartilage
• Underlying a segment of OSTEONECROSIS
• lesion DISSECTS 􀃆 early OA ....................................25%
• More common 􀃆 Spontaneous healing ............75%
• Healing takes 3-4 mo 􀃆 􀁌 pain
CLASSIFICATIONS
GUHL ARTHROSCOPIC CLASSIFICATION
STAGE PATHOLOGY CARTILAGE
A Subchondral # soft and yellowish
B Incomplete separation cracked cartilage
C Complete undetached Cartilage lesion all over
D Complete detached Crater
PAPPAS CLASSIFICATION: Depends on age at presentation:
TYPE PHYSIS PROGNOSIS
Juvenile Open Excellent
Adolescent Partial closure Either way
Adult Closed Poor
Clinically:
• Young male 10-20y ≠ SONK
• No history of major trauma, Usually physically active with multiple minor traumata
• PAIN:
o Insidious onset ≠ SONK
o Dull aching; if sharp = dissection
o Deep Pain ≠ SONK
o 􀁹é activity
• If fragmentation: locking, swelling, and sharp pain may occur
[Knee Disorders] Page | 29
INVESTIGATIONS
• PXR TUNNEL VIEWS (60º flexion é the beam // to the plateau)
o May be the only key view in 25% of cases
o shadow of scelerotic fragment of separation and crater
o Anterior to BLUMESAAT’S line and adjacent to PCL femoral foot print
o DD: CAFFEY ISLANDS of ossification defects develop posteriorly on the condyles
(posterior to Blumensaat’s line, painless, and tend to coalase)
• MRI:
o MRI T1, serpiginous 􀁺 signal lines
o MRI T2, Double line =􀁺 signal margin & 􀁹 signal inner border
o MRI T1Rho sequence can delineate the GAG of the cartilage
TREATMENT (based on Pappas & Ghul)
Other New Treatments for irreparable lesions in WB zone:
1- Electromagnetic pulsed cartilage delivery technique: An idea depends on the injection of Anti
CD44 antibody-magnetic beads labeled mesenchymal cells into the knee after very localized
provocation of the cartilage lesion by a strong magnetic field; this will affect the concentration
of the mesenchymal cells into the cartilage lesion
2- Salu Cartilage implantation
3- Arthro-surface implantation
Patellar OCD
• Uncommon & present as ant. knee pain
• Distal ½ of the patella
• 30% bilateral.
• PROGNOSIS: less clear; but subchondral sclerosis = poor prognosis (as femoral OCD)
• TREATMENT principles are similar to those for femoral OCD.
OCD
<12 y
Usually heal
spontaneously
>12
Usually progress
Usually heal
spontaneous
• PWB
• ROM
<3cm
ARTHROSCOPIC
>3cm
ARTHOROTOMY
Stage A Stage B,C
Fixation
Stage D
Fragment removal and
reconstruction
(usually swollen and larger)
Drilling via
single puncture
Biodegradable
• Screws
• pegs
Metal
• Herbert Screw
• K-wire
Osteochondral
• OATS
• Allograft
Cartilage alone
• ACI
• MACI
Soft tissue
• Periosteal
• Fascia
Matrix scaffolds
• Collagen
• Carbon fiber
• PLA
Stage D
30 | Page [Knee Disorders]
Knee Bone Infarction
Definition:
• Ischemic death of bone & BM of a portion of the knee = AVN, that usually heals
spontaneously
Ætiology:
1. Steroids
2. Alcohol
3. SLE
4. Renal transplantation
5. Gaucher disease
6. Sickle disease
7. Caisson disease
Pathology:
SITE:
• More metaphyseal than epiphyseal extending to the subchondral plate
MACROSCOPICALLY:
• Pale BM
• 2ry OA & cystic degeneration of the necrotic area
MICROSCOPICALLY:
• Bone death
• Marrow necrosis
• Granulation tissue healing
• NBF
CLASSIFICATION
CLASS SYMPTOMS HISTOLOGICAL RADIOLOGICAL
Stage 0 Asymptomatic Abnormal -ve
Stage I Preclinical Abnormal +ve MRI only
Stage II Pain Precollapse PXR: osteopenia, MRI: double line
Stage III Pain Collapse Collapse
Stage IV Arthrosis OA
Diagnosis:
Clinically:
• Race, age, and gender are according to the cause
• Generalized pain
PXR:
• Lucent lesion surrounded by sclerotic shell
MRI
• T1: serpiginous lines of 􀁺 signal
• T2: Double line sign: outer 􀁺 signal line + inner border of 􀁹 signal
• Chinese letters serpiginous lines
Tc: cold spot
DD:
• OCD ..........................................................................lateral part of the MFC, young, active, and healthy
• SONK ........................................................................WB portions of the knee, elder female
Prognosis
• Usually heals spontaneously
Treatment:
• if not ...........................................................................as OCD
[Knee Disorders] Page | 31
Spontaneous Osteonecrosis Of Knee
SONK = Ahlbäck disease
First reported by Alback et al. in 1968. They described a radioluscent area in the femoral condyle
surrounded by a sclerotic halo and associated with a focally active bone scan.
Aetiology
1]. Unknown
2]. Vascular theory: Thrombotic veno-occlusive disease 􀃆 venous hypertension and ischemia
3]. TRAUMA THEORY: in osteoporotic patients stress fractures may be followed by bone necrosis
(most accepted theory)
Pathology:
SITE:
1]. Wt bearing portion of MFC ≠ OCD
2]. Wt bearing portion of LFC
3]. Tibial plateau
MACROSCOPICALLY:
• Crescentic linear subchondral # line
• Over lying hyaline cartilage: discoloration 􀃆 detach 􀃆 OA
• Marrow oedema
MICROSCOPICALLY:
• Tide mark fibrillation
• Bone necrosis + NBF
Clinical
1. Typically female > 60yrs ≠ OCD
2. SUDDEN onset of severe pain on the medial side of the knee ≠ OCD
3. pain worse at night
4. WELL LOCALISED tenderness over the affected condyle ≠ OCD
Radiology
X-Rays
STAGE PATHOLOGY
Stage-1 Normal (PXR visible lesion never develops, & symptoms resolve spontaneously)
Stage 2 Flattening of the MFC
Stage 3 Radiolucency + sclerotic halo
Stage 4 Sclerosis enlarges + collapse
Stage 5 Secondary OA changes
Bone scans (+ve after 72hr)
• 􀁹uptake is necessary to diagnosis
• The osteonecrotic lesion appears
as a focally intense area of
uptake over the affected LFC
MRI
• Extremely Valuable In
Osteonecrosis About The Knee
• T1 - Discrete 􀁺 Signal In The Femoral Condyle
• T2 - 􀁺 Signal in the centre + 􀁹 Signal at the margin
32 | Page [Knee Disorders]
Synovial Diseases:
1]. PVN synovitis
2]. Synovial condromatosis
3]. Rheumatoid
4]. Hemophilia
5]. Plicae
6]. HOFFA’S disease (anterior fat pad $): fat pad fibrosis and ca 2ry to trauma
ITB syndrome:
• ITB friction with LFC 􀃆 localized OA especially in hill runners and cyclists
• +ve Noble’s test: Max tenderness at 30º flexion, 3 cm proximal to the joint line
• +ve Ober’s test
• DD:
1]. Lateral meniscal cyst or tear
2]. LCL injury
3]. Chondromalacia of lat patella
4]. Segond #
• Ttt is usually rehabilitation; other wise ellipse ITB excision may be required
DD:
• OCD ............................................................................. Lateral aspect of MFC (non WB portion) in
teenage
• Subchondral # ......................................................... younger patient
Prognosis
• Prognosis is related to the size of the lesion at presentation:
1]. > 50% of the width of MFC ..................... OA, and collapse
2]. < 50% ................................................................ 90% spontaneous recovery
Treatment
• Usually arthroscopy or meniscectomy are initiated before Dx is established till collapsed
• Initially, most patients should be treated conservatively, as the stage of the lesion and the size
of the osteonecrotic segment are not clearly defined at the onset:
1]. > 50% of the width of MFC:
1. Core decompression
2. Osteochondral Allografting
3. Arthroscopic debridement
4. Mosaicplasty
5. HTO
6. Prosthetic replacement
2]. < 50% ................................................................ 90% spontaneous recovery
OCD SONK AVN
Cause Traumatic Unknown Vascular
Site NWB WB Metaphysio-epiphyseal
Pt Young active Elder female Variable with a PF
Pain Insidious Acute Usually asymptomatic
PXR Demarked Sclerotic fragment Radiolucency + sclerotic halo Mottling + collapse + OA
MRI T1 serpiginous 􀁺 signal lines 􀁺 signal 􀁺 signal + surrounding oedema
MRI T2 Double line =􀁺 signal margin &
􀁹 signal inner border
􀁹 signal at margin
􀁺 signal at centre
􀁹 signal
TC 􀁹 uptake 􀁹 uptake 􀁺 uptake
[Knee Disorders] Page | 33
Osteoarthritis
DEFINITION
Non-inflammatory degenerative joint disease ccc by progressive softening & disintegration of
articular cartilage é associated new bone formation & capsular fibrosis
1. It is not a simple wear as it is: asymmetrical, localized, & related to abnormal loading
2. It is not purely degenerative (misnomer) as it is accompanied by a healing process in the form
of reactive new bone formation
Epidemiology: it is the commonest joint diseases and considered a universal disorder
1]. > 60y ..........................................................................50%
2]. Fingers, hip, knee, and spine are more affected than other sites
3]. OA hands are more common in females
4]. ♀:♂ = 2:1 (more DDH in ♀) unlike china & Africa
AETIOLOGY
• Primary - no obvious cause more é aging (effect of aging on cartilage)
• Secondary - occurs following certain predisposing factors:
o Trauma: ....................................................direct injury, deformity, joint instability
o Congenital: ..............................................DDH, Perthes, Blount,…etc
o Infection
o Metabolic: ................................................ochronosis, hemochromatosis, gout, Paget
o Endocrine disorder: .............................Acromegaly and hyperparathyroidism
o Occupation: knee (in benders)- UL (vibrating tools) –hands (boxers) –shoulder
(pitchers)
o Obesity: .....................................................􀁹 loads across the WB joints
• OA is uncommon in pts é osteoporosis
• OA is due to FAILURE OF CHONDROCYTES TO REPAIR DAMAGED CARTILAGE.
• There is a DISPARITY BET.STRESS APPLIED AND CHONDROCYTE RESPONSE. = 'wear vs. repair'
Mechanical causes of the disparity of the stress and strength:
ABNORMAL LOADS ON NORMAL JOINT:
• articular cartilage can withstand loads of up to 25MPa without damage. Loads exceeding this
􀃆 chondrocyte death & cartilage fissures.
• single impact loads or less intense multiple impact loads can cause articular damage.
• impact loading 􀃆 loss of proteoglycans from matrix 􀃆 􀁺 cartilage stiffness, 􀁹 hydraulic
permeability & disrupt collagen meshwork.
• if repair cannot keep up with damage 􀃆 degeneration.
NORMAL LOAD ON ABNORMAL JOINTS:
• Instability 􀃆 altered congruence 􀃆 􀁹 shear & compression forces on regions of cart.
• Partial loss of joint sensory innervation accelerates joint degeneration
• Forced activity following joint injury or ACL transection 􀃆 joint degeneration, whereas
immobilisation after injury prevents degeneration.
34 | Page [Knee Disorders]
PATHOGENESIS
Theory 1
• The initiating event is FATIGUE OF THE COLLAGEN MESHWORK 􀃆 􀁹 HYDRATION of the
articular cartilage 􀃆 LOSS OF PROTEOGLYCANS from the matrix into the synovial fluid
• Cartilage SOFTEN 􀃆 CHONDROCYTES DIE 􀃆 release of proteolytic enz 􀃆 further damage
• Cartilage deformation 􀃆 􀁹 stresses on collagen network 􀃆 􀁹 damage
• Cartilage can’t withstand stresses ώ are concentrated on the subchondral bone 􀃆 􀁹
subchondral degeneration, cyst, vascularity, sclerosis
• Repair occurs at the joint margin in the form of growth & endochondral ossification 􀃆
hypertrophic osteophytes (unlike the atrophic diseases e.g. RA)
• Evidence of 􀁹 collagenolytic activity; but collagen loss may be ð mechanical causes.
Theory 2:
• The initial lesions are SUBCHONDRAL MICROFRACTURES following repetitive loading.
• Healing of these microfractures 􀃆 undue subchondral bone & violation of Tide mark
• A stress gradient develops 􀃆 articular cartilage is lost in areas of maximum stress
• Underlying bone becomes hardened and eburnated
• Proliferative changes also occur at the joint margins with formation of osteophytes.
Molecular Pathology:
1- 􀁹 WATER content (unlike 􀁺 water content in ageing) – ð weakening of type 2 collagen
2- PROTEOGLYCANS (􀁺 size, 􀁺 chondroitin 6-sulphate, 􀁺 keratan sulphate, 􀁺hyaluronic)
3- 􀁹CHONDROITIN / KERATIN RATIO (unlike ageing).
4- 􀁹 PROTEOGLYCAN-DEGRADING ENZYMES (collagenase & stromelysin & plasmin)
5- 􀁹 collagen, and proteoglycans synthesis and loss 􀃆 net result 􀁺 level
6- Increased levels of:
o Matrix METALLOPROTEINASES (MMPs) (collagenase, gelatinase, and stromelysin).
o CATHEPSIN B & D (proteases found in synovium, chondrocytes, and PNL)
o IL1 - enhances enzyme synthesis & has a catabolic effect.
o IL6
o TNFα
o TGFβ
o GAGs and polysulfuric acid
[Knee Disorders] Page | 35
PATHOLOGY
• CARTILAGE DAMAGE: (in pressure areas)
􀂃 softening 􀃆 fibrillation (chondromalacia) 􀃆 cracks 􀃆 ulceration
􀂃 eburnation (loss of cartilage é sclerotic 'polished' bone)
􀂃 tufts of fibrocartilage on the bone surface
• OSTEOPHYTES (in non-pressure areas) due to:
􀂃 vascularization of subchondral bone
􀂃 develop in the path of least resistance
􀂃 capsule traction & synovial metaplasia
􀂃 proliferation of cartilage adjacent to WB area é endochondral ossification
• Subchondral SCLEROSIS, congestion, and 􀁹 IOP
• Subchondral CYSTS:
􀂃 In the areas of max damage
􀂃 containing thick gelatinous material
􀂃 ð microfractures that degenerate & accumulate synovial fluid
• CAPSULAR THICKENING and fibrosis 􀃆 deformity F AD IR (antero inferior capsule)
• Mild SYNOVITIS usually (sometimes thick and villous)
• FRAGMENTATION of osteochondral surfaces
• LOOSE BODIES: usually ð synovial metaplsia and extrusion and not separation of an osteophyte
Microscopically:
• Early:
􀂃 Superficial SPLITS and irregularities
􀂃 Deep METACHROMASIA (depletion of matrix proteoglycans)
􀂃 􀁹 CHONDROCYTES clusters
􀂃 SUBCHONDRAL OSTEOBLASTIC activity, marked vascularity
􀂃 Margin OSTEOPHYTES: ð cartilage hyperplasia and ossification
• Late:
􀂃 Extensive CLEFTS
􀂃 CYSTS é amorphous material (squeezed synofluid, disintegrated trabeculae, osteonecrosis)
􀂃 Bone NECROSIS and denuding
Types
1. Hypertrophic 75%
2. Atrophic 20%
3. Progressive 5%
Variants:
1. Polyarticular (generalized): commonest, 50y♀, hands painful stiffness, also trapMC OA
2. Monoarticular & Pauciarticular: is the classic form, WB OA or 2ry to a cause (DDH)
3. Endemic OA: either environmental factor or genetic dysplasia
4. Unusual site OA: Milwaukee shoulder
5. kashin-Beck disease: generalized OA in hands, elbows, knees + short stature
6. Mseleni joint disease: Polyarticular esp hips 􀃆 crippling deformities ð MED & protrusio
7. Rapid destructive OA: elder ♂ under strong NSAIDs, usually hip ð Ca2+ crystal deposition
8. Charcot’s disease: the most severe form of OA
36 | Page [Knee Disorders]
CP
• Old age, +ve family history, + PF
• WB joints (hands in females)
• Insidious onset & Intermittent course é attacks may lasts for few months
1. PAIN:
1- The main symptom: ð ms fatigue, capsular stretch, congestion, 􀁹 IOP
2- Site: anterior (sometimes posterior or lateral)
3- 􀁹 é exertion, WB, Cold
4- 􀁺 é rest (relief 􀁺 by time)
5- Progress to be even at rest
2. Stiffness &loss of function: after periods of inactivity 􀃆 constant
3. 􀁺 ROM ± crepitus
4. Ms Wasting
5. Flexion & Varus Deformity ð ms spasm 􀃆 capsular contracture
6. Tenderness
7. Swelling: intermittent (effusion) or constant (cap/synovial thickening, or osteophytes)
8. Heberden’s Nodes: thickening of the DIP joints (≠ BOUCHARD’S nodes of RA)
Radiography
• PXR
1- Asymmetrical narrowing of joint space
2- Subchondral sclerosis
3- Subchondral cysts
4- Osteophytes at the margins
5- Late bone destruction and joint deformity and instability
• Tc-HDP Scan
􀂃 􀁹 uptake in bone phase (􀁹vascularity & new bone formation)
• MRI (T1rho):
􀂃 new MRI sequence that delineates glycosaminoglycans distribution, so it can assess
early degenerative changes in symptomatic osteoarthritic subjects
COMPLICATIONS
1- Loose bodies
2- Backer’s cyst: capsular herniation
3- Spinal deformity 2ry to pelvic deformity 􀃆 lordosis & side bend
4- Ankylosis
TREATMENT: Vary according to the site, stage, age, severity, and symptoms
• Early: keep moving, prevent overload, relieve pain,
1. EXERCISE of supporting muscles around joints to avoid wasting and keep ROM
2. PROTECTION of affected joints from overloading: 􀁺 wt, walking stick
3. Pain relief by analgesics or NSAIDS.
4. Modify activity: avoid climbing stairs, squatting,… etc
5. HYALURONIC acid injections
6. GLUCOSAMINE &chondroitin
• Late Surgical treatment - is indicated for patients é persistent symptoms:
• Arthroscopic debridement, wash, removal of LBs, and removal of osteophytes
• Realignment osteotomies may be done in younger patients to redistribute WB load,
decompress the congested metaphysis relief pain dramatically
• Arthrodesis if young and stiffness is accepted
• Total joint arthroplasties for older patients (over 60) in advanced cases
} Fairbank’s changes
[Knee Disorders] Page | 37
• New & Experimental Treatments:
1. Soft tissue grafts - periosteal / perichondral
2. ACI
3. Mosaicplasty
4. Artificial matrix - carbon fibre, collagen, polylactic acid
5. Fresh osteochondral allografts
6. Doxycycline 􀃆 cartilage collagenase activity
7. Transforming growth factor beta (TGF beta) can repair partial thickness lesions
8. Metalloproteinase inhibitors matrix destroying enzymes & block cytokines
9. Gene therapy - Genes that have either anti-arthritic or synthetic properties can be delivered
into the joint via non-replicating viral vectors; e.g. IL1
The potential long-term treatment or cure of OA really lies in the development of agents that
reverse the balance bet. degradative and synthetic processes of the chondrocyte.
Forestier’s Disease
DISH (DIFFUSE IDIOPATHIC SKELETAL HYPEROSTOSIS)
• = a type of OA with significant amount of osteophyte formation
• more common in elderly men
• associated with diabetes & gout
• prevalence of DISH may be as high as 28%
• spine shows calcification of the anterior longitudinal ligament & peripheral disc margins (disc
space height is preserved)
• Marginal osteophytes may be seen in all peripheral joints
• Clinically have spinal stiffnes & heel pain (with spurs)
• Differs from Ankylosing Spondylitis by abscence of inflammatory markers & HLA-B27
• increased risk of heterotopic ossification following THR
38 | Page [Knee Disorders]
Rheumatoid Arthritis
• Affects 3% of women & 1% of men
• Hand > Knee > hip > cervical spine
Diagnosis:
• ARA Criteria (American Rheumatism Association):
1- Morning stiffness
Lasting at least 1 hour before maximal improvement.
2- Arthritis of 3 or more joint areas
At least 3 joint areas simultaneously have had soft tissue swelling or fluid (not bony
overgrowth alone) observed by a physician; the 14 possible joint areas are right or left
proximal interphalangeal (PIP) joints, metacarpophalangeal (MCP) joints, wrist,
elbow, knee, ankle, and metatarsophalangeal (MTP) joints.
3- Arthritis of hand joints
At least 1 area swollen (as defined above) in a wrist, MCP or PIP joint.
4- Symmetric arthritis
5- Rheumatoid nodules
Over bony prominences, or extensor surfaces, or in juxta-articular regions
6- Rheumatoid factor +ve
7- Radiographic changes
• At least 4 of 7 criteria.
• Criteria 1 through 4 (at least 6 weeks).
• Clinical Staging:
o 7 ccc ........................................ Classic
o 5 ccc ........................................ Definite
o 3 ccc ........................................ Probable
o 2 ccc ........................................ Possible
Aetiology:
• Genetic susceptibility: RA is common in first degree
relatives of RA patients and twins
• Immunological process: HLA-DR4 & DW4 encoded on
chromosome 6; and is found on the surface of APC (antigen
presenting cells); & when interact é the antigen (some times
the antigen with the HLA form the activating complex) 􀃆
autoimmune response
• When APC and T-cells interact 􀃆 cell proliferation +
cyokines secretion 􀃆 ⊕ phagocytes & B-cells
• Rheumatoid factor: Anti-IgG auto antibodies which is detected
in the serum of the patient
[Knee Disorders] Page | 39
Pathology:
Stage 1: Synovitis
• vascular congestion & effusion
• synoviocyte proliferation 􀃆 VILLOUS formation
• infiltration of subsynovial layers by PMNs, lymphocytes & plasma cells
Stage 2: Destruction
• a PANNUS of granulation tissue creeps over the articular surface eroding cartilage & bone
• cartilage destruction occur partly ð proteolytic enzymes & vascular tissue
• bone destruction occur partly by proteolytic enz, & osteoclastic activity
• direct invasion occurs at the margins of the joint
• similar changes occur in tendon sheaths 􀃆 rupture
Stage 3: Deformity:
• From:
a. articular destruction
b. capsular stretching
c. tendon ruptures
• acute inflammation subsided
Extra-articular Manifestations:
• Nodules - in 20% of RA - skin, synovium, tendons, sclera, viscera
• Lymphadenopathy & Splenomegaly ...... FELTY'S Syndrome (pancytopenia)
• 􀁺 salivary & lacrimal gland secretion .... SJORGEN Syndrome
• Pulmonary (pleurisy & rh nodules) ........ CAPLAN $
• Vasculitis
• Myopathy & neuropathy, or direct compression from synovitis
• Visceral: pericarditis, nodules
Clinically:
• 40 female may be é positive family history
• Early:
􀂃 Painful swollen HAND joints é morning stiffness
􀂃 PAINFUL LIMPING
􀂃 􀁺 ROM ± crepitus
􀂃 loss of WEIGHT, weakness
􀂃 O/E: symmetrical swelling, tenderness, crepitation, synovial hypertrophy
• Late:
􀂃 Valgus Deformity
􀂃 Instability, tendon rupture
􀂃 Path #: from the disease and drugs
􀂃 BOUCHARD’S nodules, Swan neck , Boutonniere, Z-thumb, fingers ulnar
deviation, wrist radio-volar deviation, valgus knee, valgus feet, clawed toes,
atlanto-axial subluxation
• Types of presentations:
􀂃 Palendromic: starts intermittent episodes of multi joint affection 􀃆 evolve to
classic
􀂃 Systemic: severe form é visceral affection
􀂃 Monoarticular: usually knee. Also, may present as tenosynovitis or CT$
􀂃 Myalgic: as fibromyalgia rheumatica but with +ve RF
40 | Page [Knee Disorders]
Laboratory Findings:
• 􀁹. ESR, CRP
• RF +ve in 80%, ANA 30%
• ACCP (anti Cyclic Cetrolinated Peptide): 97% early +ve in RA even in seronegative RA
• anemia: ð abnormal erythropoiesis, and chronic blood loss from analgesic gastritis
• WBC: Normal or 􀁹 (if 􀁺 suspect Felty)
• 􀁺 Complement
Synovial biopsy & fluid:
• Biopsy: is non specific to RA
• Fluid: 􀁺ptn, C, glucose / poor clot / 􀁹 RA cells & PNL
PXR: LARSEN - DALE RADIOLOGIC INDEX
1- Stage I: juxta-articular osteopenia
2- Stage II: Narrow joint space (usually bilateral, symmetrical, concentric ± protrosio)
3- Stage III: Bone erosion of the head near the neck + bone cysts
4- Stage IV: Deformity (don’t forget the cervical PXR)
• Usually no sclerosis nor osteophytes (except if 2ry OA)
• Other complications: AVN, fracture neck
DDx:
1- Seronegative: SLE, Still’s
2- AS: spondarthropathy
3- Reiter’s: Conjunctivits, urethritis, Arthritis
4- Gout & CPPD: crystals
5- OA: DIP affection, osteophytes
6- Polymyalgia rheumatica: pelvic, and pectoral weakness, and aching, +ve steroid test
7- Sarcoidosis: Erythema nodosum, Hilar LN, +ve Kveim test
Management Principles:
• Stop the Synovitis
o Rest
o DMAR Drugs (Disease Modifying Anti-Rheumatic) - Pyramid Approach =
NSAIDs - antimalarials - sulphasalazine – gold – MTX – D-penicillamine -
Azathioprine – Leflunomide + low dose steroids
o Synovectomy - chemical, irradiation, surgical
• Prevent Deformity
o Splintage
o Physiotherapy
o Tendon repairs & joint stabilisation
• Reconstruct (start é knee if > 45º flexion deformity)
o Arthroplasty is the gold standard
o Osteotomy not done:
􀂃 Doesn’t remove the cartilage ώ is a
source of inflammation
􀂃 RA is concentric & no healthy cartilage
o Arthrodesis not to be done (bilateral)
• Rehabilitate & keep moving
o Occupational therapists - aids, support
o Physiotherapy
[Knee Disorders] Page | 41
At Onset: NSAID, exercise
Early: NSAID, Steroids, DMD, local injections, physiotherapy, Rest and splitage
Erosive: DMD, splintage, operative (synovectomy, tendon repair, joint stabilization)
Late Reconstructive arthroplasty
Problems é surgery:
1- Bilateral knee involvement
2- Ipsilateral hip involvement ........................... start é knee if flexion def >45º start é it
3- UL affection .................................................. needed for PWB
4- Infections ....................................................... scan for oral, UTI, skin before surgery
5- Bad general condition & systemic disease
6- Cortisone therapy ......................................... need to 􀁹 the dose preop
7- Atlantoaxial subluxation .............................. difficult intubation
8- Femoral #s .................................................... be gentle & ready
9- Loosening ..................................................... Cemented or Hybrid are favored
Drugs Details:
Drug Mechanism A/E
NSAIDs PG synthesis 􀃆 􀁺 pain and inflammation Gastric Upset
Antimalaria PG & phagocytic activity of PNL Lucoma
Sulphaslsazine Anti-inflammatory Megaloblastic anemia
Gold Alters the function of macrophages and complement Thrombocytopenia
Methotrexate Immune suppression Liver toxicity
D-Penicillamine Dissolve RF complexes in joints to be excreted Late resp.& nephrotic
Azathioprine Immuno suppression Liver toxicity
Leflunomide DiHydro-Orotate Dehydrogenase 􀃆 􀁺 T-cell prolif
Complications:
1]. Fixed Deformities
2]. Joint Rupture
3]. Infection
4]. Spinal cord compression
5]. PN compression
6]. Vasculitis
7]. Amyloidosis, proteinuria
8]. progressive RF
Poor prognostic signs:
1]. Very high RF
2]. Peri-articular erosions
3]. Nodules
4]. Muscle wasting
5]. Joint contractures
6]. Vasculitis
Prognosis:
1]. 10% improve after first attack of synovitis
2]. 60% have remissions & exacerbations
3]. 20% have severe joint erosions requiring multiple operations
4]. 10% become completely disabled
42 | Page [Knee Disorders]
Sero-negative Inflammatory Arthroses
Common Clinical Features (diff. to rheumatoid arthritis)
1. Enthesopathy (inflammation of ligament & tendon insertions)
2. Axial skeleton involvement
3. Asymmetrical joint involvement
4. Heel pain (Achilles tendinitis, calcaneal bursitis, plantar fasciitis)
5. Extraskeletal involvement = skin, mucous membranes, GUT, GIT
6. HLA-B27
7. Radiological:
1. ankylosis
2. calcification of adventitia
3. No osteopaenia (typical of rheumatoid)
SLE
• young females
• Arthritis in 75% of SLE patients
Clinical:
• fever, anorexia, weight loss, malaise
• skin rashes (butterfly malar rash)
• Raynaud's phenomenon
• splenomegaly
• nephritis, carditis
Laboratory:
• anaemia, leucopenia
• high ESR
• ANA positive
Treatment:
• Corticosteroids for severe disease
Complications:
• AVN hip (? from steroids)
[Knee Disorders] Page | 43
ANKYLOSING HYPEROSTOSIS (FORESTIER'S DISEASE)
• common disorder in older men
• widespread ossification of tendons & ligaments
• Diff to AS:
o No erosive arthropathy
o Normal ESR
Ankylosing Spondylitis
Aetiology:
• Affects spine & sacroiliac joints primarily
• Prevalence = 0.2%
• Males > females & Familial involvement
• HLA-B27 marker
Pathology:
• Inflammation & erosive destruction of:
1. Diathrodial joints = sacroiliac, vertebral facet, costovertebral
2. Fibro-osseous junctions - intervertebral discs, sacroiliac ligaments, symphysis pubis
• 3 Stages:
1. Inflammation - round cell infiltration, granulation tissue, joint erosion
2. Fibrosis - replacement of granulation tissue with fibrous tissue
3. Ossification - of fibrous tissue (e.g. syndesmophytes)
Clinical:
1. Spinal stiffness (classical posture)
2. WALL TEST.
3. Chest expansion < 7cm
4. Hip involvement with FFD
5. Achilles tendon insertion pain
6. Difficult cervical spine fractures with epidural haemorhage
Extraskeletal:
1. Prostatitis
2. Conjunctivitis & uveitis in 20%
3. Carditis, aortic valve disease
4. Pulmonary fibrosis
Radiology:
• Squaring of vertebral bodies
• Syndesmophytes
• Bamboo spine
• erosive arthritis with progressive ankylosis
Laboratory:
• High ESR
• HLA-B27 in 90%
• RF negative
Management:
• Postural management
• NSAIDs
• Operations to correct deformity & restore mobility
o Lumbar / cervical spine osteotomies
o THR
44 | Page [Knee Disorders]
Reiter’s Syndrome
Hans Reiter, 1916
Triad = Urethritis + Arthritis + Conjunctivitis
Aetiology:
• follows dysentery or venereal infection
• Causative organisms:
o Chlamydia trachomatis
o shigella, salmonella, campylobacter, Yersinia
o Lymphogranuloma venereum
Clinical:
1. Acute Phase:
o inflammatory arthritis of: knee or ankle or foot joints
o pustular dermatitis of the feet (keratoderma blennorrhagicum)
o balanitis
o painless buccal ulceration
2. Chronic Phase:
o spondyloarthropathy
o sacroiliitis in 60%
Radiology:
• erosive arthropathy similar to AS
Laboratory:
• HLA-B27 in 80%
• ESR high in acute phase
• organism may be isolated from urethral fluids or faeces
Treatment:
• Supportive
• Tetracycline for persistent urethral infection
Enteropathic Arthritis
Peripheral arthritis - in 15% of people with Crohn's disease & ulcerative colitis
Sacroiliitis & spondylitis - in 10% of people with Crohn's disease & ulcerative colitis
Must exclude the following first:
1. Septic arthritis of the hip from direct spread from bowel
2. Psoas abscess
3. AVN from steroids
4. Osteopenia from malabsorption & steroids
[Knee Disorders] Page | 45
Psoriatic Arthritis
Prevalence of Psoriasis is 1-2%; only 5% of those will develop psoriatic arthritis.
Aetiology:
• Familial
• HLA-B27 in 60%
Pathology:
• similar to rheumatoid arthritis, but destruction usually severe (arthritis mutilans)
• rheumatoid nodules are not present
Clinical:
• IPJs of fingers & toes affected (ARTHRITIS MUTILANS)
• asymmetrical
• 'sausage digits'
• sacroiliac & spine involvement in 30%
• psoriasis of skin & nails usually precedes arthritis - nail pitting
• ocular inflammation in 30%
Radiology:
• 'pencil in cup' deformity
• arthritis mutilans
Laboratory:
• RF negative
• HLA-B27 in 60%
Diagnosis (diff. to RA):
1. RF Negative
2. asymmetrical
3. distal finger joints
4. sacroiliitis & spondylitis
5. No rheumatoid nodules
6. No tendon involvement
Treatment:
• immunosuppresive agents in severe disease
• prevent deformities arthrodesis of IPJs to improve function
46 | Page [Knee Disorders]
TB Knee
• Tuberculosis is common throughout the world
• Usually due to Mycobacterium tuberculosis or Mycobacterium bovis infection
Pathology:
1- 1ry lesion:
Site:
􀂃 Lung usually (sub-pleural GHON’S FOCUS and mediastinal lymphadenopathy)
􀂃 Pharynx ▪ Gut
Changes:
􀂃 Local inflammatory focus 􀃆 Lymphangitis 􀃆 Lymphadenitis
Seculae:
􀂃 TB bacilli remain dormant in LN
􀂃 Body is sensitized to toxins (Type IV cell mediated delayed
hypersensitivity)
2- 2ry lesion:
Due to reactivation, repeat exposure, 􀁺 immunity (e.g. drugs or HIV infection)
Results in more significant symptoms as it spreads to:
􀂃 Lung ............................... military TB, TB bronchopeumonia
􀂃 Meninges: ....................... TB meningitis
3- 3ry lesions (10% affect the musculoskeletal system)
a. Tuberculoma formation:
􀂃 Central CASEATION necrosis (coagulation necrosis)
􀂃 Surrounded by EPITHELIOID cells, LANGERHANS giant cells, LYMPHOCYTES
􀂃 They tend to coalesce to form a wide area of caseation necrosis
􀂃 Spread to cartilage 􀃆 destruction and spread to joint space
b. TB Spondylitis: (mainly throracic)
􀂃 Starts ant. in the body at multiple level; destroy bone & respect ! disc except late
􀂃 POTT’S PARAPLEGIA ð (kyphosis, abscess, 􀁺 blood supply to the cord)
c. TB Arthritis (hip, knee, ankle, shoulder, then wrist)
􀂃 Synovium is THICKENED é Cell rich EFFUSION
􀂃 Granulomatous PANNUS may form & creaps on the cartilage & bone
􀂃 Cartilage & bone EROSION (peripherally at synovial reflection)
􀂃 Juxta articular OSTEOPENIA ð hyperaemia
d. Appendicular skeleton:
􀂃 Metaphyseal bone destruction (no sclerosis, no periosteal reaction)
e. TB Dactylitis = Spina Ventosa (middle and distal phalanx)
􀂃 Digit is swollen spindle shape é little pain
􀂃 Starts diaphyseal é bone rarefaction + PNBF + soft tissue swelling
􀂃 PXR: Spina (spindle shaped digit) Ventosa (full of are i.e. rarefied)
f. Cold Abscess:
􀂃 Infected LN may COALASE together to form big area of caseation
􀂃 Caseation spread via soft tissue planes
􀂃 May burst to skin to form a sinus
􀂃 May collect at a distant site far from original pathology e.g lumbar TB 􀃆 groin
4- Healing:
a. Resolution
b. Fibrous Ankylosis
c. Dormant bacilli
[Knee Disorders] Page | 47
Clinically:
• General:
Night sweat, night fever
Loss of weight, loss of appetite
• Local:
NIGHT CRIES: joint is splinted at day time by spastic ms ⎯⎯⎯→ AtNight spasm is relieved
􀃆 stretch or compression of the damaged tissue 􀃆 pain
Marked MS WASTING
Marked SYNOVIAL THICKENING
􀁺 ROM & STIFFNESS
Joint DEFORMITY
Spine: pain, abscess kyphosis, neurological manifestation
PXR:
JUXTA ARTICULAR OSTEOPENIA 􀃆 washed out bone ends
􀁺 JOINT SPACE (in children epiphysis 􀁹 2ry to hyperaemia)
Peripheral bone EROSION and CYSTIC subchondral lesions
NO PERIOSTEAL reaction
NO SCLEROSIS
Spine erosion, collapse, paraspinal abscess calcification & kyphosis é crowded
related ribs 􀃆 SUN RAY APPEARANCE
In hip erosions occur in 3 areas (BABCOCK’S Δ); erosion of the superior acetabulum
􀃆 WANDERING ACETABULUM
Investigation
• 􀁹ESR
• Leucopenia é relative lymphocytosis
• 􀁺 Lymphocyte/monocyte ratio may reach 1
• +ve Mantoux test (indicate TB infection recent or old)
• +VE PCR
• Synovial fluid:
􀂃 􀁹 ptn, 􀁺glucose
􀂃 􀁺 viscosity, poor mucin clot
􀂃 Red acid-alcohol fast INTRACELLULAR bacilli é ZEAL NELSEN ....20%
􀂃 Cultivation on LOWENSTEIN JENSEN media or Dorset egg .........80%
• Difficult to culture needs adequate relevant conc. (centrifuged) sample
• Decontaminate & remove other organism (Petroff method)
• Keep 35º for 6 wk
􀂃 Organisms also FLUORESCE WITH AURAMINE staining
􀂃 Negative microscopy does not exclude tuberculosis
􀂃 Guinea pig inoculation
• Synovial biopsy:
􀂃 Granulomatous reaction (caseation + Langerhans + epitheliod + lymphocytes)
􀂃 Characteristic evidence of a delayed hypersensitivity reaction
}
PHEMISTER Triad
48 | Page [Knee Disorders]
Skin tests
• Delayed hypersensitivity reaction used to diagnose tuberculosis
• The two commonest tests are the Mantoux and Heaf test
• Mantoux test:
􀂃 0.1 ml of purified protein derivative is injected intradermally
􀂃 +ve if .................................. > 5 mm papule at 72 hours
• Heaf test
􀂃 PPD is inoculated into the skin using a gun to produce multiple punctures
􀂃 +ve if .................................. > 4 papules at puncture sites at 72 hours
• Positive skin test are indicative of active infection or previous BCG vaccination
DDx
• Transient synovitis
• Monarticular RA
• Subacute arthritis
• Old septic arthritis
Treatment
• Rest:
􀂃 Splintage and traction to prevent ms spasm and deformity
􀂃 Maintained till pain and inflammation is over
􀂃 Then motion is encouraged; if pain & spasm return, resume splints
• Chemotherapy:
􀂃 RIPES - Rifampicin, Isoniazid, Pyrazinamide, Ethambutol, Spectinomycin
􀂃 Rifampicin + Isoniazid 6-8 mo
􀂃 Ethambutol (or pyrazinamide, spectinomycin) for the initial 8wk
􀂃 Streptomycin is toxic
• When to start surgical ttt:
􀂃 Clinically: ................................................ No fever, no wt loss, no spasm
􀂃 PXR: ....................................................... 􀁹 calcification
􀂃 Lab: ................................................................ 􀁺 ESR, 􀁹 lymph/monocyte ratio >5
• Operative:
􀂃 Drainge of a TB focus is seldom done nowadays
􀂃 Cold abscess .................................................. calls for urgent drainage
􀂃 Young age ...................................................... synovectomy
􀂃 Clearance operation ....................................... debride all infected & dead tissue
􀂃 Painful fibrous ankylosis in middle age ....... arthrodesis
􀂃 Painful destroyed joint ...................................spacer then arthroplasty
[Knee Disorders] Page | 49
Charcot’s Osteoarthropathy
NEUROPATHIC JOINT
It is a severe form of Degenerative OA caused by loss of propriosensation to involved joints
Ætiology:
1- DM is the commonest cause ............................. 0.5% will have charcot
2- TABES DORSALIS: ...................................................... 10% will have charcot
• Charcot’s is not a syphilitic infection of the joint, it is 2ry to tabes dorsalis
• Knee & hip are the mostly affected
• Knee jerk is lost
• Argyll Robertson Pupil
3- SYRINGOMYELIA: ........................................................ 50% will have Charcot
• Degenerative condition of the spinal cord (at the shoulder girdle segment)
• Shoulder and elbow are the mostly affected
• Lost of reflexes & thermal sensation
4- Other causes:
• Congenital indifference to pain
• Meningomyelocele & dysraphism
• CPPD
• Multi steroid injections
• Alcoholic & amyloidosis
Pathogenesis:
• Loss of propriosensation 􀃆 repetitive trauma to unprotected joints 􀃆 OA
• Usually extreme movement and harmful strains are prevented by the protective
contraction of the ms evoked by the Proprioceptive reflex arc
• é loss of joint sensibility this function is lost + no pain 􀃆 trauma & strain are not appreciated
• On the long run this leads to severe OA & disorganization of joint
• Alternatively sympathetic reflexes may lead to hyperaemia & bone resorption
Pathology: exaggerated OA
• Articular cartilage ...................................................... Degenerated, destroyed, disorganized
• Metaphysis ................................................................... rarefied & irregular destruction
• Osteophytes & Loose bodies (LB) ........................ is a characteristic feacture
• Intra-articular .............................................................. ACL vanish
• Synovium...................................................................... thick, polypoid, chondromatosis, pannus
• Capsule ......................................................................... stretched & lax
• Joint ............................................................................... Disorganized, Grotesque, dislocated
Clinically: Painless joint + lost reflexes
TYPE INCIDENCE COURSE TYPE OF JOINT LB &OSTEOPHYTES
1-Hypertrophic commonest Chronic WB Marked
2-Atrophic Rare Acute NWB Not evident
PXR:
• Joint is markedly DESTROYED, DISORGANIZED, and DISLOCATED
• Hypertopic NBF
Scans: hot as infection ..................................................... but cold indium scan
Treatment
• Conservative ttt: 􀁺wt, orthotics ............................ (no NSAIDs, or steroids)
• Operative ttt: arthrodesis & Ilizarov ..................... (No arthroplasty)
• Aim is to achieve fibrous Ankylosis
• Amputation are rarely indicated ......................... if broken neglected & severely infected
50 | Page [Knee Disorders]
Haemophilia
• Combined incidence is 1 in 10 000 male births
Haemophilia A (Classic haemophilia)
• Deficiency of factor VIII
• Most common of severe disorders
• XR inheritance
• Only affects males. Carried by females. 30% are new mutations
• Severity varies depending on level of clotting factor VIII:
􀂃 50% ............................................normal
􀂃 25-50% .....................................seldom have problems
􀂃 5-25 % ......................................severe bleeding with operations (mild)
􀂃 1-5 % .........................................severe bleeding after minor injury (moderate)
􀂃 <1% ...........................................spontaneous bleeding (severe)
• 50% of known haemophiliacs are moderate or severe
• 5% of patients develop antibodies to factor VIII
• Very difficult to treat. Infused factors are destroyed
Christmas disease
• Deficiency of factor IX
• Less common
• Also XR inheritance
• Similar spectrum of severity
Von Willebrand's disease
• Deficiency of von Willebrand factor
• AD inheritance
Clinical Presentation
• Male with positive family history
• May present after circumcision; Otherwise first bruising appears at 3-4 months; Severe
bruising at walking age; May be spontaneous haemarthroses; Milder forms may present
after dental extraction or operative procedure
• Bleeding In the form of:
o Bruises
o Muscle hematomas
o Haemarthroses
o May occur sometime after injury
• Defect is in clot formation (2nd phase) rather than haemostasis (1st phase)
• May be no known trauma
• HIV .......................................................................70% of whom received pooled factor VIIII
Investigations
• Platelet count and bleeding time normal
• APTT prolonged and PT normal ie Intrinsic
• Low factor VIII coagulant activity diagnostic
Treatment
1. Blood products
• Initially fresh frozen plasma used ...............but the volume was too great
• Then cryoprecipitate used ...........................higher level of F VIII; stored at very low temp
• Then factor VIII concentrates ......................Available in convenient dried concentrate form
o Administration: 1 U/KG elevates VIII by 2% (½ life is 6-12 hrs) till 15-30%
[Knee Disorders] Page | 51
Haemophilic Arthropathy
• Recurrent intra-articular bleeding can cause:
1- Chronic synovitis
2- Progressive articular destruction
Pathology:
o HAEMOSIDERIN ACCUMULATION in synovial cells
o SYNOVITIS makes synovium more susceptible to further injury
o Intra-articular clots 􀃆 Organize 􀃆 ADHESIONS 􀃆 may tear 􀃆 bleed
o Cartilage gradually eroded ð LIBERATION OF LYSOSOMAL ENZYMES
o Vascular pannus covers articular surface and further destroys it
o Subchondral bone exposed - Subchondral cysts - Osteoporosis ð disuse
o 􀁹 blood flow to joint 􀃆 EPIPHYSEAL OVERGROWTH &osteophytes
Muscle
• Recurrent bleeds lead to FIBROSIS AND CONTRACTURE
• May result in deformity
• May be complicated by:
1. Compressive nerve palsy
2. Compartment syndrome
3. Cysts and pseudotumour
4. Cyst from massive ms bleed (before it is absorbed draw in more fluid by osmosis)
5. Erode through skin or viscus and become an abscess
Pseudotumour (From subperiosteal or intraosseous bleed )
1- SUBPERIOSTEAL .........................................shows periosteal stripping + NBF
2- INTRAOSSEOUS ..........................................ill-defined lesion + extensive osteolysis ± NBF
• May be confused with sarcoma, GCT, ABC
• May destroy bone and lead to pathological fracture
Clinical
1. ACUTE HAEMARTHROSIS
o Most commonly affects - Knee, Elbow, Ankle, Hip and shoulder
o Joint is Hot red and swollen, Acutely painful, Held in flexion
2. SUBACUTE HAEMARTHROSIS
o After 2 or more acute bleeds
o Synovium is thickened and boggy
o Moderate 􀁺 ROM
o Pain not prominent
3. CHRONIC DISEASE
o After subacute form present for 6 m or more
o Bleeds less frequent and more difficult to detect
o 􀁺 ROM due to
􀂃 Fibrous contracture
􀂃 Deformity
􀂃 Muscle wasting
o Muscles most commonly affected = Iliopsoas, Thigh, Calf, Forearm
X-rays ........... Progressive destruction
Stage
Stage 1 After acute haemarthrosis • Soft tissue swelling
Stage 2 Subacute haemarthropathy • Epiphyseal osteoporosis; overgrowth
Stage 3 Chronic é no narrrowing • Squaring off of patella
• Widened intercondylar notch of knee
• Widened trochlear notch in elbow
Stage 4 Chronic severe • Marked narrowing of joint space
Stage 5 Destructive • Joint disintegration
52 | Page [Knee Disorders]
Treatment
Acute haemarthrosis
• Usually treated at home; Usually single dose sufficient to 􀁺 pain quickly
• Immediate IV dose of factor VIII to achieve level above 30%
• Adequate analgesia (not aspirin or NSAIDs) + Immobilise limb for first 24 hrs
• Place of aspiration or washout controversial
o Reduces pain and swelling
o Removes blood 􀃆 􀁺 degradation with possible toxic effects
o No evidence that it decreases risk of arthropathy
Subacute haemarthropathy
• Further treatment indicated if:
i. Failure to respond to above treatment
ii. Two or three bleeds in short period of time
• Initially:
o Prednisolone 5 days
o 2 or 3 doses of factor VIII for level 30%
• If still not settled: 6-8 wk course of Prophylactic factor replacement + Active
physiotherapy
Chronic haemarthropathy
1- Nonoperative
o 6 months of small dose of prednisone, prophylactic factor replacement, active
physiotherapy
2- Synovectomy
o When nonoperative treatment fails
o Not indicated beyond stage 3
o Open or arthroscopic
o Reduces number of bleeds
o Does not slow cartilage degeneration
3- Corrective surgery
o For stage 4 and 5
o Presence of antibodies is contraindication to elective surgery
o Avoid pins that penetrate skin
o Screen for HIV and hepatitis B preoperatively
o Check factor levels intraoperatively
o METICULOUS HAEMOSTASIS
o Increase factor levels for procedures such as MUA
o OSTEOTOMY
􀂃 Most common deformity is flexion contracture with valgus of knee. Can be
corrected with supracondylar osteotomy
o ARTHRODESIS
􀂃 Not often indicated because multiple joints involved
􀂃 Useful for ankle and subtalar joints
o TOTAL JOINT REPLACEMENT of hip and knee
􀂃 Higher perioperative complication rate (esp. Haematoma and infection)
􀂃 Only 50% SURVIVAL AT 10 YRS
􀂃 Maintain factor VIII LEVELS AT 100-130% for 2 days post-op; 50-60% for 2
wks; 30-50% for 6 wks
o TENDON LENGTHENING of tendo Achilles for equinus deformity
[Knee Disorders] Page | 53
Gaucher’s Disease
Discussion:
• In 1882, Gaucher described idiopathic hypertrophy of spleen w/o leukemia
• AUTOSOMAL RECESSIVE deficiency of lysosomal enzyme GLUCOCEREBROSIDASE. It is the most
common genetic lysosomal storage disorder & results in accumulation of of glucocerebroside
in retinuloendothelia cells
• Commonly seen in children of Jewish descent.
Pathology:
• Bone involvement is common in Gaucher's disease:
• expansion of metaphyses - failure of remodeling 􀃆 'ERLENMEYER FLASK' distal femur (also
found in Niemann-Pick disease and osteopetrosis).
• erosion of the cortices of bone ('moth eaten')
• AVN femoral head ('Bone within bone' appearance)
• Bone crisis similar to Sickle Cell Anaemia
• Pathologic frx.
Histology: lipid-laden Histiocytes.
Classification:
• TYPE I: (adult form) - chronic noneuronopathic type; - central nervous system is spared &
disease is characterized by slowly progressive visceral and osseous involvement; enlarged
spleen may cause mechanical problems, including abdominal distention and abdominal pain
as well as shortness of breadth, as well as causing pan cytopenia; splenectomy may be
performed for thrombocytopenia; bone pain is a common complaint, which often resolves
after 1-2 days; bone pain may also be due pathologic frx, osteomyelitis, or DJD;
• TYPE II: acute neuropathic form; most patients don't survive more than 9 months;
• TYPE III: - sub acute neuronopathic; convulsions are frequent;
Clinical Presentation:
• BONE CRISES (episodes of pain and swelling), sometimes accompanied by fever but w/o x-ray
changes, are common, recurrent manifestations of the disease. - often the pain cannot be
controlled w/ narcotics; pain may last days or several weeks;
• AVN OF THE FEMORAL HEAD - is the most symptomatic lesion; bilateral disease is comon;
MRI:
• 􀁺T2 signal is seen in the marrow of long bones, vertebrae, & hips and is related to the areas
of marrow infiltrated by Gaucher's lipids.
Treatment:
• PATHOLOGIC FRX: - are best treated conservatively; frxs are esp common in yound children. Frx
proximal end of femur may occur in children & adults - these may be treated non operatively
although there may be with some varus deformity
• BONE CRISIS: ...................................................... brief bed rest + NSAIDs 􀃆 crutches as tolerated
• AVN: ............................................................... brief bed rest + NSAIDs 􀃆 crutches as tolerated
THR carry 􀁹risk of infection, bleeding, loosening
• ENZYME REPLACEMENT therapy is now available.
54 | Page [Knee Disorders]
• Pellegrini Stieda:
o Deep MCL laceration é hematoma formation
o Ossification of the hematoma 􀃆 painful lump deep to the MCL
o ttt: removal if symptomatic
• Semimembranosus Bursa
o The bursa between the semimembranosus and the medial head gastroc
o CP:
􀂃 painless lump behind the knee slightly to the medial side
􀂃 􀁹 é knee flexion
􀂃 Fluctuant lump and the fluid could not be pushed into the joint ð ms that obstruct
the communication
􀂃 Some times painful
o ttt: excision via transverse incision
o Recurrence is common
• Baker’s cyst
o Synovial herniation of the posterior capsule
o Occur é OA, RA, TB
o CP:
􀂃 Older people
􀂃 Midline at the level of the joint
􀂃 Fluctuant lump
􀂃 Some times rupture and become painful é release of the synovial content into the
calf (DD: DVT)
o Arthrography:
􀂃 Reveal the communication é the joint
o ttt: aspiration + cortisone instillation
o Excision is not recommended as the cyst usually recur unless the cause is treated
[Knee Disorders] Page | 55
56 | Page [Knee Disorders]
Knee - Osteotomies
• 60% of the load of the body weight passes through the medial compartment of the knee
Loads up to 4 times body weight are produced on climbing stairs
• Osteotomy redistributes the force
• Valgus osteotomy most commonly performed (varus knee) and is indicated in patients that have uni
compartmental disease, are less than 60 - 70 years old, are of optimal weight, have an active
occupation or lifestyle ώ they want to maintain and have a good range of motion
NB: ROM is not likely to improve with an osteotomy
INDICATIONS
1. AGE: physiologic age < 60 yrs in an athlete, laborer, or anyone who needs to knee down
such as for gardening (TKR will generally not allow the patient to kneel)
2. WEIGHT: > 80 kg are at increased risk for component failure;
3. ANGULAR DEFORMITY:
1. >15º varus deformity (often patients will have varus laxity)
2. > 10º valgus deformity
4. SAGITTAL RANGE OF MOTION:
1. < 15 º flexion contracture
2. > 90 º flexion
5. UNICOMPARTMENTAL INVOLVEMENT
Contraindications:
1. TIBIAL SUBLUXATION > 1 cm
2. Bicompartmental or tricompartmental arthritis
3. OCD lesion of more than 5 mm deep
4. ACL tear
5. RA & inflammatory arthritis
6. Inadequate bone stalk
CLINICAL
• Observe patient WALK (look for varus thrust & foot progression angle)
• Test LIGAMENTOUS STABILITY tests
• Q ANGLE
• COMPENSATORY ARC OF MOTION - to correct a valgus knee deformity - for a 20º varus
osteotomy, 20º of hip abduction is required so pt does not end up é an add deformity
• Examine the FOOT FIXED VARUS DEFORMITIES which may worsen med compartment
loading
• LLD Coventry closing wedge osteotomy might be indicated, where as, if the arthritic side
is shorter (than the other leg), then consider opening wedge osteotomy
• STAHELI ROTATIONAL PROFILE is done to role out rotational malalignment
Preoperative Planning
Radiology
• STANDING LONG-LEG film with patellae facing forward (rather than the patient's feet)
o Mechanical axis = centre of femoral head - medial tibial spine - centre of ankle
joint
o Weight-bearing axis = centre of femoral head - centre of ankle joint
o Anatomical axis = line along axis of the femur to the intercondylar notch and the
line formed by the interspinous region to the centre of the ankle
• SUPINE films
• Perform the ALIGNMENT TEST.
[Knee Disorders] Page | 57
Technique
Medial Compartment Disease
• High Tibial Osteotomy (HTO) above the tibial tubercle:
o Lateral closing wedge & fibular shortening
o Open medial wedge
o Dome shaped osteotomy
o Rap osteotomy in severe degrees and Blount’s
• OVERCORRECTION of the mechanical axis by 3º is ideal (the mechanical axis pass through
the medial 1/3 of the lateral plateau)
• COMPLICATIONS:
1. Undercorrection - most common
2. Overcorrection
3. Penetration of the articular surface
4. AVN of tibial plateau
5. Anterior compartment syndrome
6. Peroneal nerve injury
7. Patella baja
8. TKR may be more difficult
Lateral Compartment Disease
• >12º ...............................femoral (as the LFC usually erodes 􀃆 accentuating the valgus)
o Distal femoral medial closing wedge
o Distal femoral lateral opening wedge
• < 12º ............................HTO (if preop. plan shows no joint line obliquity will result)
Other Osteotomies Around The Knee:
• Osteotomies of the patellofemoral malalignment
• Osteotomies of Blount’s
58 | Page [Knee Disorders]
Ideal position:
• 10-15 º FLEXION
• 0-7º VALGUS
Knee Arthrodesis
Indications:
1. FAILED KNEE REPLACEMENT (most common)
1. better fusion rate following failed condylar components (80%) than failed hinged
prostheses (55%)
2. uncontrollable SEPTIC ARTHRITIS with complete joint destruction
3. young patient with SEVERE ARTICULAR DAMAGE as in joint tumors
4. SEVERE LIGAMENTOUS INSTABILITY that can not be addressed by TKA
5. NEUROPATHIC JOINT disease
Contra-indications:
1. Contralateral knee disease
2. Contralateral leg amputation
3. Ipsilateral ankle or hip disease
4. Ipsilateral severe segmental bone loss
Techniques of Arthrodesis:
1- External Fixation
o Ilizarov technique
o minimal soft tissue dissection
o allows for late adjustment
o allows arthrodesis in the presence of active
infection
2- Intramedullary Nailing Arthrodesis
o most reliable for achieving fusion
o 2 stage technique in active infection
o can insert nail antegrade thro the piriform fossa
or thro the knee joint
o complication rates of 20-50%
3- Plate Fixation
o 2 twelve hole plates
Complications:
1- Non-union- 20%
2- Malunion
3- Delayed union
[Knee Disorders] Page | 59
Uni Compartmental Knee replacement
Rational
• Used to treat unicompartmental knee arthroses where it is better than the osteotomies as it
offers less early complications and fast initial success
Indications
1]. Unicompartmental knee arthroses
2]. <60 y
3]. degenerative arthritis
4]. Range of motion at least 15-90º flexion
Contraindications
1]. Bicompartmental arthroses
2]. Crystalline deposition arthroses
3]. ACL & Ligamentous instability
4]. Subluxation > 1 cm
5]. Large intercondylar erosion (sign of subluxation) convert of TKR
6]. Marked coronal malalignment > 10º varus, > 15º valgus
Technique
• Midline, subvastus, or lateral approach
• Protect the ACL and anterior horn meniscus
• Keep moist the contralateral cartilage surface
• Distal femoral cut should be minimal
• Anterior cut should allow the anterior flange to be recessed below the level of the normal cart
• Tibial cut parallel to the femoral cut (8-10 cm)
• Soft tissue balance and gap measurement are done as in TKA
Complications
• Anterior impingement of the patella
• Pes Anserinus bursitis
• Arthritis of the contra lateral compartment
• Loosening, vascular, thromboembolic…
Results
• Controversial, most surgeons stick to the indications only
• Up to 90% success
Arthrodesis Osteotmy Unicompartmental TKR
Age Any <60 >60 Any age
Patient Active Heavy active Light sedentary Light sedentary
Arhtritis Severe uni uni Bi or tri
Pathology Infective degenerative degenrative Any
Range Any range 15º - 90º 15º - 90º Any
60 | Page [Knee Disorders]
Primary Total Knee Arthroplasty
Rational
1]. Pain relief
2]. Restoration of normal limb alignment
3]. Restoration of a functional range of motion
Indications
1]. The most common indication for TKA is Primary And Secondary Osteoarthritis
2]. The 2nd is Rheumatoid Arthritis
3]. Hemophilic Arthritis and other types of arthropathy
4]. End-Stage Arthritis that is nonresponsive to the usual nonoperative treatment
5]. Severe Intractable Pain
6]. Ideally indicated for old ages; although also done in young patient ώ severe pathology
7]. Failed Alignment Osteotomies
Contradictions
Absolute
• Active Infection in the knee, ipsilateral extremity, or elsewhere in the body
Relative
1]. Inadequate bone stock due to osteoporosis or other metabolic bone disease
2]. After arthrodesis ð scaring & muscle fibrosis that needs highly constrained knee
3]. Marked Recurvatum in polio as the prosthesis is unable to address the recurvatum such a
deformity that may lead to early loosening and failure
4]. Neuropathic Joint ώ preclude motor control of the knee or lead to a Charcot knee
5]. Weak Extensor Mechanism
6]. Generally Poor Health or Systemic Disease
Classification
Three broad types of arthroplasty are used in uncomplicated primary TKR today: Cruciate-
Retaining, Cruciate-Substituting, And Mobile-Bearing Knees. For more complex
reconstructions in which instability due to ligament failure is present, nonlinked constrained
arthroplasties have been used. (Linked constrained devices such as “hinges” are rarely used or
even indicated.) All of these arthroplasties are descendants of the successful Total Condylar
knee, the gold standard for resurfacing types of total knee replacement. In the best designed of
each category, long-term results are excellent in terms of fixation, function, pain scores, and
motion.
[Knee Disorders] Page | 61
PCL-Retaining Knees
1]. The theoretical basis for retention of PCL in TKA suggests that with a posterior tether
between the femur and the tibia, STRESS BYPASS the TKA components
2]. Proprioception is maintained, and normal motion (femorotibial rollback) is preserved.
3]. Preservation of QUADRICEPS power and
4]. Preservation physiologic ROLLBACK may theoretically result in a more normal gait in
walking stairs. The demands of balancing the anatomic function of the PCL dictate that
the normal joint line be closely restored, possibly further improving patellofemoral
kinematics. In order to facilitate the femoral rollback, tibial polyethylene components
were historically kept relatively flat in the anteroposterior (AP) direction, with a
physiologic posterior slope. This avoided the “Kinematic Conflict” of a dished
polyethylene, preventing normal rollback. Although some laxity is necessary to preserve
range of motion, more 1anametric posterior cruciate–sparing prostheses depend entirely
on the soft tissues to resist posterior translation. Later iterations of cruciate-retaining
implants have added more congruence to the articular polyethylene to improve stability
and contact stresses.
5]. Restoration of the proper posterior translation of the femoral component 􀃆 􀁹 flexion;
this is reproduced by High-Flexion Designs in ώ there is 􀁹 in the thickness of the
posterior condyle 􀃆 delay of the tibial impingement during flexion
Precautions:
1]. LEVEL OF THE JOINT LINE must be near normal height 􀃆 or may cause tight PCL
2]. Avoid TIGHT PCL, ώ will produce:
i. Restricted flexion
ii. Excess femur on tibia rollback = Booking
iii. High posterior polyethylene-bearing load 􀃆 Articular failure.
3]. FLAT TIBIAL INSERT avoids that conflict.
4]. The technical challenge with a PCL-retaining knee design is to realign the limb and
restore full motion while keeping the PCL under proper tension.
• Normal physiologic tension is found in only 1 /10 knees undergoing a PCL-retaining
• Well-functioning PCL-retaining TKAs may have nonphysiologic AP movement.
• Some cases demonstrated “ROLL FORWARD” rather than “roll back”
Kinematic conflict occurs if
concepts are mismatched. In
this case, the posterior
cruciate ligament is
preserved using a dished
tibial component.
Impingement occurs
posteriorly with flexion.
62 | Page [Knee Disorders]
PCL-Substituting Knees
• Sacrifice and substitution for the PCL gives predictable femorotibial kinematics and may
facilitate balancing knees with greater angular deformity, especially when secondary
changes in the PCL contribute to the deformity.
• The function of the PCL is partially replaced by:
1]. More CONGRUENT articular surface
2]. Tibial SPINE
3]. Femoral CAM mechanism
• Historically, the most popular designs had a higher rate of patellofemoral complications.
• Patellar pathology may be partially due to:
1]. Relative elevation of joint line
2]. Relative patella baja
3]. Impingement of fibrous tissue proximal to patella 􀃆 “PATELLAR CLUNK”
4]. Boxy femoral profile é no recession of trochlear groove 􀃆 􀁹 patellar retinacular tension
• Recently, improved designs replicate patellofemoral anatomy and mechanics.
Mobile-Bearing Knees
• Potential design advantages:
1]. Highly congruent femoral and tibial articular surfaces 􀃆 very low contact stresses
2]. 􀁺 PE wear
3]. Tibial articular surface “float” by gliding 􀃆 􀁺 kinematic conflict by highly congruent surfaces
• Fluoroscopic information suggests that in vivo kinematics may imperfectly replicate design goals
• In USA:
1]. 45%................................... PCL substituting
2]. 45% ................................. PCL retaining
3]. 10% ................................. Mobile bearing
PCL retaining PCL substituting Mobile bearing
Advantage
1]. Preserve anatomy
2]. Preserve Roll Back
3]. 􀁺stress; dissipated to soft tissue
4]. Enhance upstairs activities
1]. 􀁹 congruence
2]. Fixed roll back
3]. Less sensitive to JL changes
4]. Correct moderate deformity
1]. Ultraconforming
2]. Floating tibial insert 􀁺 conflict
3]. 􀁺 contact stress
4]. Automatic correction of
rotational deformity
Disadvantage
1]. Less congruent
2]. Paradoxical roll-back
3]. Late PCL instability
4]. Diff to correct big deformity
1]. Patello-femoral clunk
2]. Implant dislocation
3]. Loss of PCL proprioception
4]. Femoral notch resection
1]. Diff precise flex-ext gap
2]. Bearing dislocation
[Knee Disorders] Page | 63
Accurate limb alignment 􀁺 stresses. The main goal of instrumentation is to provide accurate alignment
• The mechanical axis = line that passes from hip center to ankle center & falls on the med side of knee
center
• Consistent reproduction of a mechanical axis landmarks are difficult intraoperatively
• Anatomic axis landmarks, by contrast, are available, easy to instrument, and approximate mechanical
axis
• Precision is paramount because an asymmetry of only 5% 􀃆 LIFT OFF of the femoral component on
tibia, with compressive forces all on one side and tensile forces on the other.
• Subtle malalignment 􀁹 by time as soft tissues attenuate under excessive forces
• Fixation is reliably achieved with both cemented and cementless techniques, but PMMA remains the
standard and generally the most widely used technique.
Planning of skin incision:
1- Medial Parapatellar Approach
2- The Subvastus Approach
3- Lateral Parapatellar Approach
4- Modified Lateral Capsular Approach
5- Mid-Vastus approach
Kinetics is the study of forces
Kinematics is the study of motion
64 | Page [Knee Disorders]
Surgical Procedure
Preoperative Evaluation
7]. TAKE GOOD-QUALITY RADIOGRAPHS on large cassettes in both the AP and lateral planes. AP
weight-bearing films demonstrate better any potentially dynamic instability. They also
accentuate joint space narrowing. A Merchant view (or other similar radiograph) is useful to
evaluate patellofemoral mechanics. A TUNNEL VIEW may be useful to evaluate for
osteonecrosis.
8]. Fixed ANGULAR DEFORMITIES and CONTRACTURES need to be released at the time of surgery
either through soft tissue or bony maneuvers.
9]. LIGAMENTOUS INSTABILITY, particularly in the medial-lateral plane, may need to have specially
stabilized components or ligamentous augmentation for a successful procedure.
10]. VASCULAR DISEASE in LL, may be there is a contraindication for use of a tourniquet
11]. Assess SKIN condition; avoid flaps and undermining of the skin, particularly laterally over the
patella to avoid potentially devastating problems. In general, old incisions performed. Cross
transverse incisions for patellectomy or high tibial osteotomy at 90°. More recent parapatellar
incisions are problematic. In general, include recent parapatellar incisions in the line of the
main incision if practical.
12]. In the absence of long bone and hip deformities, STANDARD 36-INCH RADIOGRAPHIC films with
the patient standing are adequate for preoperative planning.
13]. TEMPLATE for the size of prosthetic components on the radiographs with acetate overlays that
are compensated for radiographic magnification. Preoperative templating is only an
approximation of the required prosthetic sizing—never use templating to determine the
precise size used at surgery.
SURGICAL PREPARATION
.
• POSITION the patient carefully in the supine position on the operating table.
• Protect the elbows with foam pads and gently flex them approximately 30°.
• Elevate the patient's buttock é soft roll (hard ones 􀃆 sciatic nerve palsy)
• Contralateral leg often lies in external rotation; so pad the lateral side of the knee.
• Position &secure TWO SEPARATE BUMPS to the table as leg positioners:
• When the leg lie on top of both full extension
• When the foot lie on the 1st bump 30° flexion
• When the foot lie on the 2nd bump 100º flexion
• Rotate the table toward the opposite limb 􀁺 tendency to ER
• Confirm that PREOP AB have been given before tourniquet
inflation; cephalosporin is an appropriate choice.
• TOURNIQUET should have been placed on the thigh as high as
possible and the skin protected with soft webril padding.
• Finally, take a “WALK AROUND” the patient just before scrubbing.
Check all peripheral nerve sites for appropriate padding.
• SHAVE the skin around the knee immediately before op to 􀁺
compromise of the skin surface. Extended time between shaving
and surgery promotes colonization of small nicks with bacteria.
• Reaffirm that the CORRECT LIMB is being prepared. Although it is
rare, wrong limb side surgery does occur and is disastrous for patient and surgeon. AAOS
recommended confirmation of the side to minimize this complication
• Avoid EXCESSIVELY BULKY DRAPES as precise alignment in total knee replacement depends on
the ability to palpate the bony landmarks
[Knee Disorders] Page | 65
Operative Technique
• Flex the knee to a 30° position and mark the surgical incision. Flexion produces tension on the
anterior tissues, which allows a more precise surgical exposure.
• A midline incision is preferred, extending ~ five fingerbreadths above & below the patella
• Carry the incision through the midpoint of the knee and distally just medial to the tibial
tubercle
• Then carry the incision through the deep fat and the prepatellar bursa.
Preserve the epitenon for later closure
• Perform a medial arthrotomy with a new knife blade. The location of the
quadriceps tendon can be very deceiving proximally, as it may be biased
laterally if only the visual landmarks are used, and this may lead to
transection of the bulk of the quadriceps. Often, feel the tendon
• Use a #10 blade perpendicular to the tendon, longitudinally in a gentle
curve, which curve around the patella.
• In the inferior region of the arthrotomy, split the fat pad with the medial
bulk of fat maintained. This facilitates the lateral exposure, and leave a fair tissues for closure.
• When the incision comes to the tibial tubercle, bring the incision parallel to the shaft of the
tibia and carry it distally for a few more millimeters.
• Place a right angle retractor medially and transect the anterior horn of the medial meniscus,
witht the medial soft tissue from proximal to distal, staying strictly at the subperiosteal level to
maintain the vascularity of the medial flap of tissue.
• If severe varus knee, the medial exposure can be extended into a medial release.
• Once the deep portion of MCL has been elevated, place the Z-type retractor between the
MCL and bone to gain medial exposure.
• Remove large medial osteophytes at this point as part of the medial release.
• Flex the knee to 90° or 100°. The potential for patella tendon avulsion exists in the tight knee.
As the knee is flexed
• Watch the insertion of the patella tendon to avoid any excessive flexion that may avulse the
patella tendon. If the patella cannot be easily everted without the risk of patella tendon
avulsion, obtain more extensile exposure either by:
I. Extending the arthrotomy proximally
II. Doing more distal soft-tissue release
III. Quadriceps release
IV. Tibial tubercle osteotomy: this is mostly prefered
• This situation most often occurs in:
i. Very obese patient
ii. Patient with prior knee surgery, e.g. HTO 􀃆 patella tendon is scarred and tight
• Once patella tendon avulsion occurs, it is very difficult to treat, so this complication is best
avoided.
• Flex the knee 100º, patella is everted; so femoral condyles, and tibial plateau should be at least
partially visualized.
• ACL is resected to enhance exposure.
• Using a 1-inch osteotome, remove medial and lateral osteophytes to expose the PCL
attachment
• If the PCL is being intentionally sacrificed, it is best done at this point. The PCL should not be
sacrificed in a cavalier fashion, but it should be done precisely by electrocautery
subperiosteally off
• Release the lateral periphery of the meniscus with a #15 blade in a precise curvilinear fashion
along to its insertion next to the PCL.
• Branches of the lateral geniculate artery are just outside the insertion of the lateral meniscus
and should be cauterized at this time.
• Once the lateral meniscus is removed, place a Z-type retractor in the corner overlying the
lateral tibial condyle to gain extensile exposure of the flexed knee.
66 | Page [Knee Disorders]
After resection of the
distal femur and
proximal tibia, the
extension gap (B)
must equal the flexion
gap exactly
Principles of Balancing:
• At least four directions for spatial relations must be carefully maintained:
1]. CORONAL ANGULATION
2]. ROTATION
3]. SAGITTAL ANGULATION
4]. JOINT LEVEL
• In tibia use IM or extramedullary alignment guides, but in femur only use IM guides
1]. Angulation:
• Femoral medullary hole ≈ 9 mm, just med to notch center & above PCL insertion 􀃆 best
alignment
• Avoid midline drill hole in femur 􀃆 valgus angulation, as it is not aligned é medullary canal.
• Put your opposite hand on the femoral shaft to provide appropriate
directional control
• Once the hole is drilled, aspirate BM to 􀁺 embolization.
• Distal cut is made in a preset angle from mechanical axis = 5°-6° valgus
• Tibial cut is made to its long axis
2]. Rotation Of The Femoral Component
• Patello-femoral mechanics are altered dramatically by femoral rotation.
• Excessively IR of femoral component 􀃆 􀁹 patellar subluxation
• Some ER of femur is desirable to achieve equal flexion gap, as tibial
cut is done to tibial long axis, not in ! normal 3° MEDIAL INCLINATION
• ER of femoral cut is necessary to make flexion gap equal, achieved by;
1]. WHITESIDE'S LINE and draw the transverse axis ⊥ on it
2]. TRANSEPICONDYLAR AXIS gives 3-5° ER to post condylar axis
3]. POSTERIOR CONDYLAR AXIS in 􀔅 cut is made 3° ER to that line
4]. Parallel to the tibial cut (GAP TECHNIQUE)
• No one landmark is always reliable. Use all three in combination;
o Epicondylar Axis .................. is the most reliable, but difficult to palpate
o Post condylar axis ............. not for valgus knees or RA
o Transepicondylar ................ not for lat condylar hypoplasia
Femoral cut depth and rotation techniques:
1]. GAP TECHNIQUE
• Begins é tibial cut to tibial axis 5-10 mm below the articular surface of
the more normal side, then check ligament balance.
• Measure the WHITESIDE'S LINE (AP axis) is the line between the deepest
part of the patellar groove anteriorly & the center of the intercondylar
notch posteriorly; this gives you an idea about the femoral size
• Posterior femoral cut is made // to tibial cut
• Disadvantages:
o Midrange laxity (only 0° - 90° are checked)
o Possible elevation of JL (in flexion contracture + 􀁹 flexion gap cut
􀃆 undersized femoral)
2]. MEASURED RESECTION TECHNIQUE
• Replace resected bone from femur & tibia = thickness of implant
• = Joint Line Technique, as the joint lines are fairly well maintained and
the normal anatomy is essentially resurfaced.
• Femur is usually resected first
• It is very important in PCL retaining; as slight elevation of the joint line in
PCL-retaining designs can have adverse effects on knee kinematics
• Advantages:
o Close matching of the AP dimension of femur
o Preserve femoral rollback without the “booking” phenomenon
o Avoids 􀁹 post stresses
o Avoids limited flexion associated é tight PCL
o Avoids excessive translation é loose PCL
o Whiteside line ......................... not for big anterior osteophytes
[Knee Disorders] Page | 67
Preparation of Femoral Cut
• The distal level of the femoral implantation is critical to preserve the proper level of JL
• The flexion and extension gap must be equal.
• The coronal alignment and proper ER are critical.
1].Anterior and Posterior Sizing
• After the distal femoral cut is made and the ER has been determined, make the anterior and
posterior femoral cuts. In general, there are two references:
1]. ANTERIOR REFERENCING technique, where the anterior cut is made first by referencing
from the anterior cortex. This approach ensures no femoral notching
2]. CALIPER TECHNIQUE (Jig system technique, mostly used): measure the distance bet post
condyles & ant cortex. If size is bet 2 sizes, take the smaller one to avoid overstuffing
• OVERSTUFFING is a phenomenon that occurs when too large femoral component is placed. If
the component is placed posterior 􀃆 tight flexion gap & 􀁺 flexion. If an oversized component
is placed too far anterior 􀃆 extensor mechanism impinge on the femoral flange 􀃆 tight knee.
• In the so-called “GREYHOUND KNEE,” named for its resemblance to canine anatomy, there is
large AP diameter & narrow medial-lateral diameter 􀃆 medio-lateral over hanging femoral
component. Proper implant system selection 􀁺 this phenomena
• Restoration of the proper posterior translation of the femoral component 􀃆 􀁹 flexion; this is
reproduced by High-Flexion Designs in 􀔅 there is 􀁹 in the thickness of the posterior
condyle 􀃆 delay of the tibial impingement during flexion
• Lastly, check the bone cuts for:
1]. Appropriate rotations.
2]. MATTERHORN SIGN (after a mountain) = longer lateral
condylar ant cut than the medial one
3]. Posterior cuts should show asymmetry, é more medial
> lateral bone in most cases.
2].Removing the Posterior Osteophytes
• Remove posterior osteophytes after the chamfer and other finishing cuts. The posterior
osteophytes do not act as a mechanical block to limit flexion only, but also tent the posterior
capsule and limit full extension.
• With the knee held in extreme flexion, retract the femur superiorly with a blunt bone hook
placed in the notch. Use a 1-inch sharp, curved osteotome to resect posterior osteophytes
• Remove adherent capsular attachments by either curettage or rongeur. A soft sulcus should
result behind the posterior condyles
• This approach will maximize the potential extension and flexion of the knee
Check for pitfalls:
1]. Oversized femoral component
2]. Improper ER
3]. Notching of the femur
4]. Improper axial alignment
5]. Flexion & extension gaps: this can be a guide to
the amount of tibial cut needed
68 | Page [Knee Disorders]
Tibial Resection
• Tibia is resected to its long axis. The anatomic axis is in 3° varus.
• Implant systems initially attempted to replicate this slight varus profile 2°
to 3° varus that produced 5-6° varus cut 􀃆 early component loosening.
• Therefore, attempt a cut with the knowledge that a slight varus cut 2-
3° should not alter clinical results. We prefer extramedullary technique.
Multidirectional orientation of tibial cut:
[1]. ROTATION
• This is best determined by sighting down “bird's-eye view” relying on:
a- Tubercle line (most reliable): keep the profile centred on the
medial third of the tubercle
b- Posterior condylar axis
c- Transcondylar line
[2]. CORONAL ALIGNMENT
• Secure the yoke of the tibia cutting guide at 2/3 of the way down the
tibia above the ankle; not at the ankle joint, as the fibula widens it 􀃆
produce a lateral offset 􀃆 varus angularion.
• Place the proximal jig of the tibia cutting guide right over the center of
the tibial tubercle. The bulk of the patellar tendon may bias the cutting
jig medially 􀃆 varus angulation, so a smaller footprint cutting block is
better
• Distally, place the guide // to the chin of the tibia / its tip over TA tendon
/ pointing to 2nd ray
• Always, place the distal tip of the guide medially (over the anterior tibialis
tendon) 􀃆 􀁺 varus risk
[3]. HEIGHT
• Variety of height guides are available:
1]. Curved wing-shaped device
2]. Measuring Jigs that measure from the cutting surface to fixed points above the tibial
surface
• In general, it is prefered to take 10 MM OFF THE “NORMAL” SIDE 􀃆 slight subchondral resection
on the “abnormal” side.
[4]. POSTERIOR-TIBIAL TILT
• AP Caudal downslope of the tibia ≈ 5º (most systems have it built in i.e. use a neutral cut)
• Avoid putting the tibia in extension 􀃆 tight flexion gap & 􀁺 motion
[5]. TIBIAL COMPONENT SIZE
• The largest size is used to 􀁺 force/area unit
• Avoiding overhang of the tibial plateau, particularly posterolaterally.
Resection
􀂃 Resect the proximal tibia, protecting the medial collateral ligament on the inside of the
knee, the patellar tendon on the outside of the knee, and the posterior vascular
structures.
􀂃 Then lift off the plateau one piece after releasing it from soft-tissue
Saving the PCL
• Make a slot ant to PCL by a saw, then place a
rectangular osteotome into that slot.
• Start to do tibial cut é that osteotome in place
Check for pitfalls
1]. Varus alignment caused by:
o Patellar tendon bias
o Medial ankle offset
2]. Mal-rotation
3]. Over hang tray
4]. Elevation of joint line
5]. Reversed tilt 􀃆 tight flexion
When to sacrifice PCL
1]. Bowstring tension of PCL
2]. Incomplete flexion or forced flexion
3]. Excess rollback at >90º flexion
4]. Anterior lift off ð tight flexion gap
5]. Femoral sublux ð tight flexion gap
[Knee Disorders] Page | 69
Seven points of ligamentous balance
1]. Achieve full extension of the knee
2]. Achieve full flexion é out excessive rollback of femur
3]. Achieve good medio-lateral balance at full extension
4]. Achieve good medio-lateral balance at full flexion
5]. Track the patella over a full arc of motion é no thumb
6]. Good rotational balance in full extension
7]. Good varus-valgus must be correct
Balance of the Knee
• Perform rigorous medial and lateral ligament balancing, and flexion and extension gap
balancing using appropriately sized blocks.
• If femoral preparation is completed, trial components are inserted & lig balance checked
• In general, balance the knee with soft-tissue releases rather than by bony cuts.
1]. Ligament Balancing
• Lig balancing can be straightforward or complex
• Plan to have more constrained implants available if the deformity is severe e.g. > 15° of varus
or valgus, but remember that constrained knee implants have poor longevity
• There are 7 points of lig balancing that
must be achieved
• At this point, balancing may require
conversion from PCL retaining 􀃆 PCL–
substituting, as PCL may contribute to
the deformity esp if severe
2]. Varus Deformity
• Is the commonest & usually the simplest deformity to correct by cutting the tibial to the axis.
• However, commonly there is still medial tightness in extension, after appropriate cuts.
3]. The Valgus Knee
• Technically is more difficult to realign
• The tightest structure is usually the ITB with the knee in full extension. Release this from
inside out to ITB long axis at the joint line.
* If tight in extension only (14%) ♠ If tight in flexion only (1%) If both are tight do both (85%)
• Combined deformity; valgus flexion are the most challenging
• Valgus + flexion deformity = tight in extension
• Bony lateral release (lateral femoral sliding osteotomy) & fibular head decompression could
be done as an alternative to LCL release
• Steps To Correct Varus Deformity:
1]. Remove medial OSTEOPHYTES on the femur and tibia
2]. Release the MEDIAL CAPSULE with care to MCL
3]. Release DEEP MCL subperiosteally
4]. Release SUPERFICIAL MCL subperiosteally (é break SHARPEY frs.)
5]. Release PES ANSERINA as a secondary constraint medially.
6]. Release the POSTERIOR CAPSULE and PCL
7]. Release MEDIAL GASTROC
• Steps To Correct Valgus Deformity:
1]. Release ITB at the joint line .................... *
2]. Release popliteus tendon ...................... ♠
3]. Femoral attachment of the LCL .......... ♠
4]. Release fibular attachment of LCL....... ♠
5]. Release PLC .................................................. *
6]. PCL Is Resected Routinely
7]. Biceps tendon is transected from fibular insertion
8]. Consider other implant system
70 | Page [Knee Disorders]
1]. Sagittal balance (Flexion and Extension Gap)
2]. Coronal balance
VARUS DEFORMITY (medial release) VALGUS DEFORMITY (lateral release)
1]. Osteophytes 1]. Osteophytes
2]. MCL deep (coronary) then superficial 2]. Lateral Capsule
3]. Postero-medial corner + semi-membranosus 3]. ITB If Tight In Extension
4]. Pes Anserinus 4]. Popliteus If Tight In Flexion
5]. PCL in rare cases 5]. LCL
Patella (follows femoral & tibial components, & ligament balancing)
• Indications:
i. Inflammatory arthritis
ii. Severe OA
iii. Patellar deformity & insufficiency
iv. Some do it routinely
• PF articulation is the source of the MAJORITY OF COMPLICATIONS IN TKA due to:
i. Boxier femoral components
ii. Inadaquate patellar tracking
• PATELLAR CLUNK results from fibrosis on
quadriceps tendon that catches on the anterior
aspect of the femoral component. The
offending fibrous tissue may be resected
arthroscopically
Patellar maltracking etiology and prevention
ISSUE GUIDE LINE PROBLEM SOLUTION
1]. Femoral rotation Never IR femur beyond
neutral axis
Lateral patellar
tilt & lat sublux
Slight ER of femoral
component
2]. Femoral position Never medialize femur 􀁹 Q angle Centralize or even lateralize
3]. Tibial rotation Never IR tibia past med side
of tibial tubercle (TT)
􀁹 ER of TT
􀁹Q angle
Tibia is centered bet centre &
med border of TT
4]. Leg alignment Never leave excess valgus 􀁹 Q angle Revise bone cuts
5]. Patella position Avoid lateralization 􀁹 Q angle Centre or slight medialize
Avoid inferiorization Patella baja Centre or slight sup
6]. JL position Never raise joint line level Patella baja Normal or lower JL if pat baja
[Knee Disorders] Page | 71
• Reflect the fat pad & remove all osteophytes til you see patellar margin all around é out
compromizing quadriceps tendons.
• Cut the patella flat to give symmetric cut & drill the peg holes
• Most components are pegged
• Check PF tracking by “NO THUMB” or touch-free tech
• Tracking & lateral retinacular tension is controlled by:
i. Subvastal approach is better for tracking
ii. Appropriate ER of femoral & tibial components
iii. Appropriate alignment
iv. Lateralization of femoral and tibial components 􀁺 retinacular tension & improve tracking
v. Never lateralize the patella usually lateralize every thing except patella
vi. If still there is mal tracking ............................ do lateral retinacular release (5%)
vii. Distal realignment procedures or medial capsulorraphy, μß needed in extreme cases
• Pitfalls:
i. Under resection .......................................... overstuffed PF joint
ii. Too much resection .................................. patellar fracture
iii. Lateralized patella ...................................... maltracking
iv. Asymmtrical cut .......................................... patellar tilt
Cementation
• Remove the trial components 􀃆 lavage the bone surfaces é normal saline 􀃆 Clear the debris
• Drill sclerotic bone small shallow holes, to 􀁹 cement interdigitation (avoid many holes in 1
line)
• Mix the cement 􀃆 pressurize some cement into the plateau 1st 􀃆 add another 1-mm cement
layer on plateau 􀃆 gives adequate cement mantle in spite of bone irregularity
• Apply the tray and impact it. Vigorous impaction improve pressurization, but may #
• Remove excess cement, particularly posterior to the tibial tray.
• 2nd apply a donut-shaped piece of cement to femur &pressurize it into a uniform thickness
• Place a small amount of cement on the posterior rails of the femoral component
• Impacat the femoral component neither in flexion nor in extension.
• Always remove excess cement before and after every component cementation
• Place a trial insert and extend the knee fully till the cement sets.
• Patellar cementation is done é a cut insulin syringe used to pressurize the cement into holes
• Apply the patellar component onto the three holes &pressurize é the patella clamp.
• After the cement has hardened, verify the seven points of ligament balancing
Wound Closure
• Irrigate all of the soft tissue, and prosthetic and bony surfaces of the knee joint vigorously.
• Now close extensor mechanism watertight, with monofilament resorbable suture.
• Distal seal is difficult but imp (that’s why distal incision incoorprating the patellar tendon is VIP)
• Close the deep fat layer, peritenon, and the skin with staples 􀃆 dress the wound.
Tibial Tubercle Osteotomy
• Indications:
i. Difficult exposure
ii. Severe angular deformity
iii. Bone deficiency
iv. Prior surgery
v. Obese patients
vi. Associated patellar disorders
• Place the oscillating saw // to the tibia and make a 1cm thick, 8cm long cut from medial to lat
• Keep the lateral periosteal hinge intact laterally.
• Make a 2nd cut // to JL and 2 cm distal to it, at a 45° angle to meet the initial osteotomy site.
POSTOPERATIVE CARE
• Begin early motion according to your preferences and the clinical situation
• Early motion can improve recovery and shorten the hospital stay.
• CPM is useful for obtaining early motion (achieve extension early and advance CPM by 10°/d)
• WB allowed on the first postoperative day
• Discharge from the hospital at 90° in an immobilizer until sufficient quadriceps control
72 | Page [Knee Disorders]
PITFALLS AND COMPLICATIONS
Long-lasting complications of TKA are rare, and long-term success is generally the rule.
NONMECHANICAL COMPLICATIONS
The most common nonmechanical complications of TKA are thromboembolism and anemia.
1- THROMBOEMBOLISM
o 50% of pts mainly at or below knee; 10% are proximal to the knee; < 2% pulmonary
o Pulmonary emboli may be fatal esp if large
o Dx:
􀂃 Contrast venography: gold standard, sensitive, specific, nepphrotoxic
􀂃 B-mode duplex: not for iliac or deep vv, technician dependant
􀂃 Other: clinical (Homann, Hoffman,..), I131 labeled fibrinogen scan,
plethysmography
􀂃 No test yet proven to be effective as a postop screening test to pick risky pts
o Prophylxis:
􀂃 For those reasons; most surgeons favor chemical, mechanical, or both
􀂃 Mechanical: all may prevent leg DVT but not the serious higher embolism
1- elastic calf
2- thigh hose
3- sequential intermittent pneumatic compression stockings
4- Plantar foot compression pumps
5- Early mobilization
6- CPM
7- Inferior vena caval filters; but invasive, expensive, hazardous contrast
􀂃 Chemical:
1- Continuous IV heparin
2- LMWt heparin sc
3- Oral warfarin
4- IV dextran
5- Aspirin
6- All predispose to bleeding, hematomas, hemarthrosis, GI & CNS
bleeding
o Treatment:
􀂃 Immediate IV heparin infusion (keep PTT 1.5-2 times the control)
􀂃 Discontinue heparin and replace by warfarin (the same level) till 6wk-6mo
􀂃 Discontinue afterward
􀂃 Continuously monitor the patient for bleeding (40%)
2- NEUROLOGIC INJURY after knee arthroplasty is
o most common in valgus deformity ± flexion deformity of severe rheumatoid arthritis
o Mainly peroneal nerve (1/3 complete, and 2/3 incomplete)
o Due to:
􀂃 Traction upon the nerve during surgery after realignment of the deformity
􀂃 Compression by a tourniquet
􀂃 Compression by a tight bandage or orthosis
o Prognosis
􀂃 ½ recover and ½ would have partial recovery
o Treatment:
􀂃 Prophylactic decompression is not recommended
􀂃 Remove all the tight bandages
􀂃 Flex the knee
􀂃 Conservative ttt + rehabilitation
􀂃 AFO
􀂃 Surgery after several months of no improvement 􀃆 decompression
[Knee Disorders] Page | 73
3- VASCULAR INJURY:
o Most common vessels to be injured:
􀂃 Superficial femoral
􀂃 Popliteal
􀂃 Genicular
o Type of injuries:
􀂃 Direct lacerations
􀂃 Late AV fistulae
􀂃 Aneurysm
􀂃 Thrombosis: esp in predisposed pt é peripheral vascular disease
o Dx: diminished pulses (esp é lacerations)
o Treatment:
􀂃 Prophylaxis: consultation of vascular surgery – non use of tourniquet in risky pt
􀂃 TTT:
4- FAT EMBOLISM SYNDROME (FES)
o Mainly occur with trauma; but also é joint replacements (3% of TKA)
o Pathogenesis:
􀂃 Incompletely understood
􀂃 Introduction of BM elements into the systemic circulation
􀂃 Eventually deposited in the pulmonary vv 􀃆 liberates inflammatory mediators
􀂃 Mediators cause compromised gas exchange and respiratory failure
o PDF:
1- Intramedullary drills
2- Guide rod system
3- Stemmed prosthesis
4- Sudden release of the tourniquet
o Clinically: (usually mistaken as narcotic sequelae, or senile sundowning)
􀂃 Respiratory insufficiency
􀂃 Mental confusion and agitation
􀂃 Petechae (trunk, axilla, conjunctiva)
􀂃 Fever & tachycardia
􀂃 Retinal changes
o Prophylaxis:
1- Use of fluted IM guides
2- Lavage the IM marrow fat
3- Over drilling of the guide holes
4- Slow advancement of the IM guides and stems
o Treatment: (mainly supportive)
􀂃 Mechanical ventilation
􀂃 IV fluids & glucose
􀂃 Heparin, Aspirin, Dextran, Ethanol (proven to have no effect)
􀂃 Steroids may be effective if given early
74 | Page [Knee Disorders]
5- WOUND PROBLEMS:
o More in obese, DM, Poor nutritional status, RA, Multiple scars
o 􀁹 é hematoma formation, clumsy technique, inadequate tight closure of all layers
o No relation to tourniquet deflation time or to CPM usage had been attributed
1- Prolonged Drainage:
o Expected for several days. After 7-10 days considered prolonged
o ð incomplete closure, poor superficial healing
o the problem is that it promotes bacterial contamination of sc tissues
o ttt: immobilization till closure 􀃆 explore 􀃆 irrigation 􀃆 close in layers
2- Superficial necrosis:
o Uncommon
o ttt; do not overlook and do gastroc rotational flap
3- Wound dehiscence:
o Rare
o Usually 2ry to trauma, obesity, patellar instability, premature stitch removal
o ttt: as a surgical emergency, copious lavage, Broad AB, closure é 2ry sutures
MECHANICAL COMPLICATIONS
• The majority of the mechanical complications of TKR can 􀁺 é careful attention to proper softtissue
balance in all planes. Patients é more challenging preop deformity or motion restriction
should be counseled about possible postoperative complications
1- ASEPTIC LOOSENING
• Typically is different from aseptic loosening of the total hip arthroplasty. Polyethylene debris–
induced, macrophage-initiated osteolysis is considerably more rare. This problem is thought to
be due to the different wear environment of the TKA. Threefold larger wear particles are
produced in a shearing, less-conforming environment. These larger particles are less likely to
induce a macrophage response and lead to a lower rate of aseptic loosening. Malalignment,
especially of the tibial component in varus, can lead to mechanical subsidence of tibial
component & loosening.
2- INFECTED TKA:
• Costly complication that occurs in approximately 1% of all knees
PDF:
• EXOGENOUS: in the surgical technique
• ENDOGENOUS: in the patient e.g. DM, poor nutritional status, steroid, immunocompromized
Bacteriology
• Low virulent organisms:
o Staph epidermidis (methicillin sensitive, non glycocalyx forming)
o Staph aureus (methicillin sensitive, non glycocalyx forming)
o ß hemolytic strept
o Anerobic strept
• High virulent organisms:
o Gram negative organisms E. coli, Pseudomonas, Proteus, & Entero-cocci
o Staph epidermidis (methicillin resistant, glycocalyx forming)
o Staph aureus (methicillin resistant, glycocalyx forming)
• Others: Corynobacterium, Group B strep, Strep faecalis
Sources
Intra-operative:
• Sampling of theatre air identified the same organisms & same proportions
• Contamination with the surgeons gloves, gowns, light handles, skin blades and needles
mainly affected. 76% of the organisms grown were coagulase-negative staphylococcus.
Post-operative:
• Drains left for 48 hours allow ingrowth of organisms (Willett et al. JBJS 1988)
• Haematogenous spread: Most common source is skin(46%), mouth(15%), UTI(13%)
[Knee Disorders] Page | 75
Organism Virulence
1]. ORGANISM RESISTANCE TO AB:
[i]. Altered target: altered DNA gyrase (Quinolones)
[ii]. Detoxyfying enzymes: ß lactamase (penicillins)
[iii]. 􀁺 uptake: membrane transport (erythromycin & tetracyclin)
2]. RACE FOR SURFACE THEORY
• When a total joint prosthesis is placed into the human body, the body's cells hurry to get hold
on the surface of the prosthesis.
• Once the body cells colonize the surface of the total joint prosthesis they can protect this non
living surface against the bacterial colonization.
• If any bacteria (usually skin bacteria) are present in the operation wound, they hurry to get
hold on the prosthesis surface too, racing the body cell to colonize the surface.
• If bacteria win, thet evolve the capability to adhere to surfaces for their survival, by secretion
of a glyco-protien cell wall called GLYCOCALYX:
i. Very strong adhesive
ii. Mask the bacterial antigens
iii. Colonize inside this biofilm away
from immune system
iv. Invite other types of bacteriae to
trick the immune system
v. When they adhere to the inert
implant surface, bacteria are
protected by the antiphagocytic
effect of biomaterial.
• All these factors will create a very
powerful resistance 100 to 1000 times
against AB & immune system.
Classification
1]. Stage 1= immedialte postoperative:
o Staph-aureus /ß hemolytic strept
o Usually needs irrigation, unless glycocalyx forming organism is identified
2]. Stage 2 = 6-24 mo
o Methicillin resistant staph epidermidis
o Usually needs staged operation
3]. Stage 3: after 2y
o Hematogenous spread from other septic focus
New Classification
1]. Type I Early < 6wk
2]. Type II Late > 6wk
3]. Type III Hematogenous
4]. Type IV Incidental +ve culture
76 | Page [Knee Disorders]
PREVENTION
Pre-operative:
1. All septic lesions must be identified & treated (feet, dental, urinary, prostate)
2. Admit patient as late as possible & into a clean ward
3. Shave in the anaesthetic room
Intra-operative:
[1]. Surgical Technique:
1. Careful tissue handling & Haemostasis
2. Length of procedure
3. Wound lavage - mechanical effect more important than type of fluid used.
[2]. Antibiotic prophylaxis
• Systemic antibiotics: methicillin-realated penicillin or cephalosporin
• Antibiotic Loaded Cement: reduces risk of infection by 11 fold
[3]. The team: keep the operating team as small as possible
[4]. Movement: shed up to 10 000 skin scales/min
[5]. Theatre gowns.
• Standard Gowns are permeable to organisms when wet “moist bacterial strike through”
• Weaved Gortex & disposable non-woven 'paper' gowns are preferred
• Body Exhaust Suits (Charnley): maintain –ve pressure, cool surrounding (􀁺shedding)
[6]. Footwear: no evidence that outdoor shoes are a source of infection; but overshoes wearing
can result in the contamination of the hands of the clinicians.
[7]. Headgear.
[8]. Face masks.
[9]. Gloves and hands: scrub in a separate area, wear 2 gloves, change the outer after prepping.
[10]. Sterile drapes
[11]. Drainage of wound has 􀁹 risk of becoming infected than closed wound (only when sure)
[12]. Transporting the patient to operating theatre on a separate clean trolleys in the induction zone
[13]. Theatre equipment & instruments
[14]. Ventilation System: Vertical Laminalr Air Flow is recommended for arthroplasties
[15]. Ultra-violet Light: bacteriocidal; but not commonly used, ð potential dangers to staff
Post-operative:
• In the early post-op phase - antibiotic cover for urethral catheterisation (Gentamycin IM)
• AB cover for all GI & UTI & skin & Dental lesions é antistaphylococcal agent
DIAGNOSIS
• You must suspect infection all the time & use every tool to reach the final diagnosis
1- Clinically
• History of pain, swelling, erythema, fever problems post-op
2- Radiology:
• Need serial radiographs (get original post-op films)
• Osteolysis around the components
• Periosteal reaction
3- Blood: WBC, ESR, CRP usually not helpful (usually –ve or irrelevant) except if strongly suggestive
4- Bones scans (incl. white cell scan):
• usually unable to differentiate septic from aseptic loosening
• Indium111 may be helpful
5- Aspirates:
• CELL COUNT .................................. >25.000/MM3 (May be helpful 85%)
• DIFFERENTIAL COUNT..................... >75% PNL
• Gram stain ............................................ +ve 25%
• Glucose .................................................. 􀁺
• Protein .................................................... 􀁹
• PCR ......................................................... Newly introduced to diagnostic tools
• IL6 serum level ................................... Newly introduced to diagnostic tools
6- Open biopsy:
• Often identifies organism & sensitivities.
[Knee Disorders] Page | 77
TREATMENT
1- Antibiotic suppression
• Antibiotics alone will not eradicate deep sepsis so it is rarely indicated alone
• Considered in:
o Elderly, unfit for surgery.
o Early infection
o Single organism
o Low virulent
o Gram +ve organism
2- Debridement alone:
• 20% success rate in TKR.
• Considered in the same conditions but can combat also virulent organisms
3- Resection arthroplasty:
• for the unfit or unwilling to have revision surgery & severe RA
• not good for knee
4- Arthrodesis:
• Remain a last resort especially for young active patients
5- Amputation:
• for knee - High functional cost - end of line.
6- Revision Arthroplasty:
• 75% success is achievable
• Pre-requisites:
o Healthy individuals who can stand long treatment
o Organism sensitive to AB
o Adequate bone stalk
One Stage Two Stage
Advantages: 1. single operation
2. quicker return to normal function
probably safer & more successful
Disadvantages: 1. Prolonged procedure
2. AB sensitivity must be known pre-op
3. Can't use cementless prosthesis (lose
benefit of antibiotic in cement)
1. two procedures
2. prolonged bed rest betw. stages
Contraindicated: 1. If AB sensitivities not known pre-op
2. Mixed infection
3. Gram –ve organism
4. bone loss requiring allograft
5. Doubt about debridement adequacy
6. Failure of previous one stage revision
Two stage Revision:
• First stage:
o Debridement (Capsule, prosthesis, inf tissues, Cement, & cement restrictor) & lavage
o Tissues must be sent for microbiology (even if organism is diagnosed pre-op)
o Insert AB loaded cement beads or a ab cement spacer
• Between stages:
o Continue iv antibiotics
o Traction if beads used (or ext fix)
• Second stage:
o Timing:
􀂃 Early at 3wk
􀂃 Late: after 6 wk, more effective (the wound would have healed & -ve CRP); but
more tissue scarring that’s why many surgeons use AB spacers (AB-PMMA)
o Continue antibiotics for 3 months.
78 | Page [Knee Disorders]
3- PERIPROSTHETIC FRACTURE
o Is the fracture that occurs éin 15cm of the prosthesis; or adjacent to prosthesis stem
o 1%, more in femur > in tibia, more in Revision & osteoporosis
o Ætiology:
􀂃 Traumatic
􀂃 More in poor bone quality
􀂃 Intraop during impaction, during trailing
􀂃 Post op ð anterior femoral notching 􀃆 fatigue fracture
o Treatment:
􀂃 Conservative as long as the alignment is preserved
􀂃 Operative ORIF with plate and screws or IMN
4- TIBIAL FRACTURE is associated with malalignment or component loosening. The fracture
may be bypassed with a stemmed prosthesis.
5- PATELLAR FRACTURE:
• Well known complication that may occur with or without resurfacing of the patella
• Ætiology:
o Direct trauma
o Under resection (marked stresses over the patella)
o Over resection (weak patella)
o Patellar pegs create stress risers (some use multiple small rather than one large peg)
6- PROSTHETIC FAILURE
• In contemporary arthroplasties is limited to delamination or fracture of tibial polyethylene
components or failure of metal-backed patellae. In the compromised environment with either
mechanical imbalance or secondary to polyethylene failure, a tibial metal backing may rarely
crack. This type of failure may often lead to particulate-induced synovitis & mechanical
symptoms.
7- PATELLAR INSTABILITY:
• Ætiology:
o Excessive internal rotation of the tibial or femoral components
o Over sized or overhang patellar component
o Lateral placement of the patellar component
o Avoid thick patellar component 􀃆 tight patellar tracking
o More to occur é valgus deformities é tight lat retinaculum ± medial reefing of the VMO
• Treatment:
o Revision arthroplasty
o If sure about the rotation of the major components 􀃆 proximal of distal realignment
o are the most common reason for revision knee arthroplasty. These complications
were addressed in the technique section.
8- AVN PATELLA
• May predispose to patellar fracture
• Ætiology:
o ð sacrifice of the supero medial genicularte and inferior medial geniculate vv in medial
parapatellar approach
9- PATELLAR LOOSENING
• Uncommon event
• More é patellar maltracking
• Require revision of the patellar component
• If no bone stalk; retain unsurfaced patella or do the hated patellectomy
[Knee Disorders] Page | 79
10- PREMATURE FAILURE É METAL BACKED PATELLA
• Previously used to improve the stress transfer from the implant of the bone and consequent
decrease in deformation and shear rate on PE. More with patellar maltracking
• Failure modes:
o PE wear
o PE metal dissociation
o Peg failure
• Dx:
o Anterior knee pain and swelling
o PXR: Ficat views metal to metal articulation / AP metal debris
o Aspiration: drak + metallic debris
• Treatment:
o Patellar revision ± total synovectomy
o Some times tricompartmental TKA revision
11-DISRUPTION OF THE EXTENSOR MECHANISM: (rare but distastrous)
• Ætiology:
o After difficult exposures and over release of the tendon
o Tibial tuberosity osteotomy
o After revision TKA
o É limited ROM
o Poor bone stalk
• Prophylaxis:
1- Thorough lateral gutter debridement
2- Cut Patellofemoral ligament
3- Lateral retinacular release
4- Quad snip
5- Quad V-Y turn down
6- Distal tibial osteotomy
• Treatment:
o Immediately postop:
􀂃 Immediate reattachment ± screw fixation
o Later postop
􀂃 Autograft or allograft reconstruction of the patellar tendon
• Prognosis:
o persistent extension lag 􀃆 abnormal gait and walking stairs
o Rerupture
12- CATASTROPHIC WEAR: is the premature failure of prosthetic implants
FACTOR PROBLEM SOLUTION
1]. PE thickness PE < 8 mm 􀃆 past the yielding
strength
Thinnest PE portion must be >8mm
Thicker tibial cut
All PE tibia
2]. Articular design Flat PE
Low contact surface area
High contact stress load
Congruent articular surface design
High contact surface design
Low contact stress load
3]. Kinematics Femoral role back
PCL retained design
Posterior slope to improve flexion
4]. Kinematics Diskinetic sagittal motion
Sliding wear
PCL substituting design
5]. PE sterilization PE chain session
Subsurface delamination
Vacuum PE γ irradiation
Vacuum packing
Metal-on-metal / ceramic-on-ceramic
6]. PE machining PE stretching at subsurface
zone 􀃆 delamination
Direct compression molding instead of surface
machining
80 | Page [Knee Disorders]
CONTROVERSIES IN TKA
Cementless Vs cemented:
• ð the brittle nature of the PMMA and its association é osteolysis sight was aroused towards
cementless TKA
• Porous coating provides biological interlock
• Disadvantages:
o Radiolucent lines
o Tibial subsidence
o Loose beads
o More pain and patellar failure and inadequate bone ingrowth
• Some suggested hybrid cementless femur + cemented tibia
• Till now the cemented TKA remain the gold standard procedure
Retaining vs substituting:
• Retaining Rational:
o Normal knee kinematic
o Preserve proprioception
o Minimal constraint
o Preserve femoral bone stalk
o Normal gait
• Substituting Rationale:
o PCL even if present never normal 􀃆 alter the normal kinematics
o Difficult balance with PCL sparing
• Almost same clinical outcome and scores are noticed for both
Obesity
• Was considered to be a relative contraindication for TKA
• Associated é high rate of complications, PE wear & hospital stay
Age
• Young age has been a relative contraindication for TKA
• But if the conservative ttt fail to control the condition 􀃆 make the pt is candidate for surgery
• Surgery start é arthroscopic debridement 􀃆 realignment osteotomies 􀃆 arthrodesis
• If all fail é pain persistence + functional limitations 􀃆 TKA
• Long term results shown 94% results é PE wear being the major failing factor
Hemophilia
• Recurrent hemarthrosis 􀃆 articular degradation and severe arthritis 􀃆 Ankylosis
• Pathogenesis of arthritis: free radical formation 2ry to hemoglobin breakdown 􀃆 synovitis &
cartilage damage
• Knee is the most common affect joint
• Arthrodesis is an option; but UCR and osteotomies are contraindicated
• Treatment:
o Prevent bleeding: Factor VIII (may secrete anti F VIII make things worse)
o Preserved joint space ................................................. Splintage for rest followed by
physiotherapy
o Narrowed joint space ............................................... TKA
o Synovitis .......................................................................... synovectomy
o Any surgery require F VIII monitoring:
􀂃 > 100% ............................................................. till 3rd day postop
􀂃 > 50% ................................................................ till 3rd week
􀂃 30-50% ............................................................. till 6th week
• Prognosis there is a high level of adverse effects & HIV transmission is common
Paget’s
• Not uncommon disorder in UK and USA; and usually asymptomatic & discovered accidentally
• Most symptomatizing patients are ð DJD of the knee
• TKA results are satisfactory
[Knee Disorders] Page | 81
Revision TKA
• Rationale:
o Done when it is expected to achieve a good function
o Can neutralize minor deficiencies (major bone deficiencies call for arthrodesis)
• Indications:
1- Aseptic loosening
2- Prosthesis failure
3- Severe pain
• Contraindications:
1- Active infection
2- Marked bone deficiency
3- Severe ligamentous laxity and subluxation
4- Extensor mechanism insufficiency
5- Bad general condition
• Preoperative Planning:
o Address cause of failure (pt selection, implant failure, malalignment, instability)
􀂃 Poor pt selection: young, active, heavy wt
􀂃 Failures are common with the old constrained designs
􀂃 Alignment, rotation, and soft tissue balance are crutial
• Exposure:
o Through the previous planes
o New incisions 􀃆 hinders the superficial blood supply 􀃆 sloughing
o If previous transverse incision 􀃆 crossed at right angle
o Usually median parapatellar incision is used
o Care should be taking during eversion of the patellar tendon
o Thorough synovectomy, lateral release, and lateral gutter release for better exposure
o Quad snip or turndown may be needed
o Remove the components and the cement anchor
• Implantation:
o Coronal orientation is adjusted ...................... 7º valgus
o Femoral cut is done using IM guide & keep it at minimum (usually augments needed)
o Rotational orientation is difficult ð absent reliable bony land mark; but depend on
epicondyles; the medial being more anterior
o Tibial cut is a straight forward procedure .. ⊥ to the anterior tibial border
o JL should mimic the normal for better flexion extension balance and PF tracking
o Normal joint line is determined by ............... Preop AP view (1.5cm above fibular head)
• Implant size:
o Difficult ð bone loss; so preoperative planning and templating is mandatory
o Intraoperative posterior augments are the key for proper sizing é the best balance
o Tibial size is selected as in primary
o If upper tibial deformity 􀃆 custom tibial component é asymm stem orientation is used
o Usually CEMENTED UNCONSTRAINED STEMMED PCL SUBSTITUTING device is used
􀂃 Unconstrained ......................................... 􀁺 stressed across the joints
􀂃 Stemmed ................................................... stresses distribute away from bone interface
􀂃 PCL ............................................................... usually scarred and un physiologic
􀂃 Cemented ................................................. Immediate strong fixation
• Bone deficiency:
o Central ........................................................................ cementation or BG (acc to age, size of loss)
o Peripheral .................................................................. bone or metal wedge, custom implant
• Patella:
o Revise only if maltracking + good bone stalk
o Rule of thumb; at least 10mm is needed as a stalk for revision
• Results: up to 75% with semiconstrained & 90% é unconstrained
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• Complications:
o PF malalignment
o Slough
o Wound problem
o Sepsis
• The modern TKA has instrumentation that facilitates reproducible alignment and proper
ligament balance, and materials and design that permit functional and durable recovery of
motion. When implanted in closely monitored and maintained surgical and rehabilitation
environments, it has a remarkable and predictable record of success. Most of the mechanical
and some of the nonmechanical complications of knee replacement are preventable by
meticulous surgical technique with careful cross checking of anatomic landmarks and softtissue
tensions with appropriate jigs