Sports — FRCS Quiz

66 slides

▸ Slide 636 · SportsSports · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

What is the topic of this section?
Which sports injuries are covered in this section?

Answers · Q & A

Q1.What is the topic of this section?

Sports (section slide); no speaker notes available

Q2.Which sports injuries are covered in this section?

Not covered in the speaker notes

▸ Slide 637 · Meniscal tearSports · 20 questions expand

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Q1-Q2020 questions — tap to reveal all answerslist

How does a meniscal tear present?
What is the differential diagnosis of acute haemarthrosis (Frank Noyes JBJS 1980)?
What MRI signal changes suggest a meniscal tear?
How do you describe a meniscal tear?
Which meniscal tears can heal by themselves?
Which meniscal tears should undergo meniscectomy (classical teaching)?
Which meniscal tears go for repair?
What other factors affect meniscal healing?
What disease and patient factors are considered when treating a meniscal tear?
Describe the inside-out meniscal repair technique.
What is the medial approach to the capsule for inside-out meniscal repair?
What is the lateral approach to the capsule for inside-out meniscal repair?
What are the advantages and disadvantages of outside-in meniscal repair?
What are the advantages and disadvantages of all-inside meniscal repair?
What are the generations of all-inside repair techniques?
What must be preserved during meniscectomy and why?
How can meniscal healing be improved?
What are the options if the meniscus is not repairable?
What is the definition of the red-red zone?
What are the pros and cons of acute one-stage bucket handle repair with ACL reconstruction?

Answers · Q & A

Q1.How does a meniscal tear present?

Presents as delayed swelling

Q2.What is the differential diagnosis of acute haemarthrosis (Frank Noyes JBJS 1980)?

ACL tear 72%
Meniscal injury 62%
Osteochondral fragment 20%
Patella dislocation

Q3.What MRI signal changes suggest a meniscal tear?

Globular signal is not specific
Linear signal is more suggestive of a tear

Q4.How do you describe a meniscal tear?

Timing
Morphology: radial, longitudinal, transverse, bucket handle, complex
Zone (RR 3-4mm from rim, RW, WW) from rabbit study
Site (root/body), stability, length
Partial thickness/ full thickness
These affect whether the tear can heal

Q5.Which meniscal tears can heal by themselves?

Stable longitudinal tear
RR zone
Partial thickness
<5mm

Q6.Which meniscal tears should undergo meniscectomy (classical teaching)?

Degenerative/complex/radial tear - radial tear breaks many longitudinal fibres
Chronic tear
WW zone
Irreducible tear
Leave a stable rim to maintain hoop stress (may not apply now)

Q7.Which meniscal tears go for repair?

Acute, traumatic tear
Vascular zone
Reducible and stable
Simple pattern (longitudinal/bucket handle)
Root tear

Q8.What other factors affect meniscal healing?

Age (young is <40 years old)
Smoking
Stability of the joint, malalignment

Q9.What disease and patient factors are considered when treating a meniscal tear?

Disease factors: chronicity (<8/52 better healing), size, shape, location, displacement, associated injury
Patient factors: age, functional demand, symptoms (pain/locking)
Aim: relieve symptoms, restore the meniscus as much as possible

Q10.Describe the inside-out meniscal repair technique.

Inside-out with nonabsorbable suture, vertical mattress = gold standard
Higher biomechanical strength
Problems: need an assistant, risk of needle stick injury and NV injury (saphenous, CPN)

Q11.What is the medial approach to the capsule for inside-out meniscal repair?

Incision posterior to the MCL at the level of the joint line (one third above and two thirds below), knee in 90 degrees flexion
Sartorial fascia incised, dissect anterior to semimembranosus, retract pes tendons anteriorly
Saphenous nerve and vein lie posterior to the incision in this position
Place a Henning retractor between the medial gastrocnemius and the capsule

Q12.What is the lateral approach to the capsule for inside-out meniscal repair?

Interval between the ITB and biceps femoris, just posterior to the LCL at the level of the joint line
Flex the knee to 90 degrees to allow the peroneal nerve to fall posteriorly
Then use the interval between the lateral head of gastrocnemius and the capsule

Q13.What are the advantages and disadvantages of outside-in meniscal repair?

For anterior 2/3 tears
Pros: no assistant, no posterior incision, no needle stick, no NV injury
Cons: Difficult reduction & oppose edge

Q14.What are the advantages and disadvantages of all-inside meniscal repair?

Pros: quick, easy, all arthroscopic, single surgeon
Cons: reduced strength, limited compression, variable resorption profile

Q15.What are the generations of all-inside repair techniques?

1st gen: described by Morgan - curved suture hooks through accessory posterior portals
2nd gen: T-fix - polyethylene bar with attached suture deployed through a sharp needle; inability to tension the knots
3rd gen: bioabsorbable meniscus repair device e.g. meniscus arrow
4th gen: Fastfix - 2 suture anchors connected by a nonabsorbable polyester suture with a pretied slip knot

Q16.What must be preserved during meniscectomy and why?

Keep the rim and root intact, otherwise there is no hoop stress
Meniscus functions = shock absorption, stability, load bearing, lubrication, proprioception - all affected
Medial side degeneration is more common due to roll back

Q17.How can meniscal healing be improved?

Trephination/shaving at the tear site to increase punctate bleeding; microfracture of the notch
PRP: CORR 2015 no difference in reoperation rate; Orth J Sport Med systematic review found lower failure rates but no difference in PRO
Exofibrin clot technique: chemotactic, mitogenic, acts as a scaffold to fill the defect -> inflammatory fibrovascular scar; 30-50ml blood stirred till clot, inserted under the repair site

Q18.What are the options if the meniscus is not repairable?

Allograft with bone graft
Artificial meniscus

Q19.What is the definition of the red-red zone?

3mm from the edge according to Warren and Arnoczky 1982 AJSM

Q20.What are the pros and cons of acute one-stage bucket handle repair with ACL reconstruction?

Pros: one OT
Biological: drilling of tunnels allows stem cells to seep into the joint -> good healing
Mechanical: stable environment for meniscal healing
Cons: contradictory rehab -> arthrofibrosis

▸ Slide 638 · Horizontal /cleavage tearSports · 2 questions expand

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Q1-Q22 questions — tap to reveal all answerslist

List the meniscal tear patterns shown.
What are the MRI findings of a radial tear of the medial meniscus body?

Answers · Q & A

Q1.List the meniscal tear patterns shown.

Horizontal/cleavage tear
Longitudinal/vertical tear
Radial tear of the medial meniscus (body)

Q2.What are the MRI findings of a radial tear of the medial meniscus body?

Sagittal: T2W signal change
Coronal: meniscal extrusion defined as 3mm
Axial: radial tear

▸ Slide 639 · T2W MRI right kneeSports · 5 questions expand

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Q1-Q55 questions — tap to reveal all answerslist

Describe the MRI findings of a meniscal root tear.
What is the definition and incidence of a meniscal root tear?
What is the Laprade classification of meniscal root tears?
How is a meniscal root tear repaired?
What are the consequences of meniscectomy?

Answers · Q & A

Q1.Describe the MRI findings of a meniscal root tear.

Coronal: extrusion of the medial meniscus (>3mm), vertical linear defect (truncation)
Axial: fluid interposition at the meniscus root and posterior horn (high signal cleft)
Sagittal: ghost sign - absence of the posterior horn of the meniscus

Q2.What is the definition and incidence of a meniscal root tear?

Avulsion of the meniscus insertion or radial tears within 9mm of the insertion
Incidence 7-13%

Q3.What is the Laprade classification of meniscal root tears?

1: partial stable root tear
2: complete root tear
3: bucket handle tear with complete root detachment
4: complex oblique or longitudinal tear with complete root detachment
5: bony avulsion of the root attachment

Q4.How is a meniscal root tear repaired?

Restore the root in anatomical position by suture anchor or drill bone tunnel

Q5.What are the consequences of meniscectomy?

Medial meniscectomy: contact area decreases 50-70%, contact stress increases 100%
Lateral meniscectomy: contact area decreases 40-50%, contact stress increases 200-300% (convex lateral tibial plateau)
So lateral meniscectomy has a much worse outcome
Lateral meniscus occupies ~80% vs medial ~60% of the articular surface
~70% of load in the lateral and 50% in the medial compartment is transmitted through the menisci

▸ Slide 640 · Young boy with knee slappingSports · 10 questions expand

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Q1-Q1010 questions — tap to reveal all answerslist

What is a discoid meniscus and how does it develop?
What is the common presentation of a discoid meniscus?
What are the X-ray findings of a discoid meniscus?
What are the MRI findings of a discoid meniscus?
What is the Watanabe classification of a discoid meniscus?
How is a discoid meniscus treated?
What are the meniscofemoral ligaments?
What are the dimensions and attachments of the meniscofemoral ligaments?
What is the function of the meniscofemoral ligaments?
What is a pseudotear and a Wrisberg rip?

Answers · Q & A

Q1.What is a discoid meniscus and how does it develop?

Abnormal development of the meniscus causing a thickened, discoid-shaped meniscus
Embryology: failed regression of tissue
25% bilateral

Q2.What is the common presentation of a discoid meniscus?

Often asymptomatic
When symptomatic, usually secondary to a meniscal tear
Knee clunk/click/lock after trivial trauma

Q3.What are the X-ray findings of a discoid meniscus?

Widened lateral joint space (11mm)
Squaring of the lateral femoral condyle
Hypoplastic lateral tibial spine
Cupping/ flattening of lateral tibial plateau

Q4.What are the MRI findings of a discoid meniscus?

Sagittal: consecutive 3 (5mm) cuts with continuous meniscus (bow tie sign)
Transverse: transverse diameter in the mid body >15mm
Coronal: medial-lateral height difference >2mm; meniscal width to maximal tibial width >20%
Sagittal: ratio of the sum of both lateral horns to maximal meniscal diameter >75%
R/O tear; +/- coronary ligament integrity

Q5.What is the Watanabe classification of a discoid meniscus?

Incomplete (type 2)
Complete (type 1)
Wrisberg type: absent meniscotibial ligament, only the meniscofemoral ligament remains; displaces into the intercondylar notch during extension
May alternatively be classified as stable or unstable

Q6.How is a discoid meniscus treated?

Surgery only for symptomatic patients
Partial meniscectomy / meniscal repair for a tear
Saucerization (5-8mm compared to the medial side) - reshapes to a semilunar shape, triangular cross-section, less click
Repair of the meniscotibial ligament for peripheral attachment
James Hui KSSTA 2021: meniscoplasty gives good mid- to long-term outcomes; concomitant repair/partial meniscectomy does not change outcomes

Q7.What are the meniscofemoral ligaments?

Anterior MFL (ligament of Humphrey) - anterior to the PCL
Posterior MFL (ligament of Wrisberg) - behind the PCL
70% of knees have either one, 6% have both

Q8.What are the dimensions and attachments of the meniscofemoral ligaments?

Anterior MFL is thinner (<one third the diameter of the PCL), from the posterior horn of the LM to the distal edge of the femoral PCL attachment; can be mistaken for the PCL at arthroscopy
Posterior MFL is usually larger (~half the diameter of the PCL), from the posterior horn of the LM to the medial femoral condyle, inserting near the posteromedial band of the PCL

Q9.What is the function of the meniscofemoral ligaments?

Stabilisers and protectors of the posterolateral femorotibial compartment
Increase congruity between the mobile lateral meniscus and lateral femoral condyle, protecting the posterior horn of the LM
Anterior MFL supplements the anterior band of the PCL; posterior MFL supplements the posterior band; they may act as a splint in PCL injuries
Anterior MFL is taut in flexion and lax in extension; posterior MFL is taut in extension and lax in flexion

Q10.What is a pseudotear and a Wrisberg rip?

Pseudotear: the posterior MFL commonly causes a pseudotear of the posterior horn of the lateral meniscus on imaging - a normal vertical/oblique signal at the junction of the ligament of Wrisberg with the posterior horn
Wrisberg rip: a longitudinal vertical tear of the posterior horn of the LM seen in association with ACL tears
It is frequently missed and may be used as a secondary sign of ACL disruption

▸ Slide 641 · ACLSports · 39 questions expand

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Q1-Q3939 questions — tap to reveal all answerslist

What is the X-ray finding of an ACL tear?
What are the sagittal MRI findings of an ACL tear?
What are the coronal MRI findings of an ACL tear?
What is the axial MRI finding of an ACL tear?
What are the physical examination findings of ACL deficiency?
Why examine the collateral ligaments at 30 degrees of flexion?
What injuries are associated with an acute ACL tear?
What is the anatomy and function of the anterolateral ligament (ALL)?
What is the biomechanical difference between ALL reconstruction and LET?
What are the results and downsides of the STABILITY trial (AJSM 2020)?
What are the indications for ALL reconstruction or LET?
What is the location of the ACL?
What are the dimensions and composition of the ACL?
What are the anteromedial and posterolateral bundles of the ACL?
What is the blood and nerve supply of the ACL?
What is the function of the ACL?
What is the mechanism of an ACL injury and what causes locking?
What is the natural history of the ACL-deficient knee (Frank Noyes JBJS 1983)?
When should ACL reconstruction be performed?
What factors determine whether to perform ACL reconstruction?
What are the graft options and their loads to failure?
What are the pros and cons of a BPTB graft?
What are the pros and cons of a hamstring graft?
What are the problems with allograft and artificial grafts?
What are the advantages of autograft versus allograft?
What do KT-1000 measurements show after ACL reconstruction?
Should single or double bundle ACL reconstruction be used?
What are the ideal properties of graft fixation?
What are the types of suspensory and aperture fixation and their pros and cons?
Which fixation is used in the femur, tibia and revision cases?
What are the key steps of ACL reconstruction?
Describe the operative details of ACL reconstruction.
What complications can occur according to time sequence?
Describe the phases of graft ligamentisation and healing.
What are the 4 zones of tendon-to-bone healing?
What are the phases of ACL rehabilitation?
What are the principles of ACL rehabilitation?
How is a dropped graft managed intra-operatively?
What are the pros and cons of one-stage versus staged meniscus and ACL surgery?

Answers · Q & A

Q1.What is the X-ray finding of an ACL tear?

Segond fracture on X-ray = ALL avulsion
Associated with ACL tear 75-100% of the time

Q2.What are the sagittal MRI findings of an ACL tear?

Discontinuity/waviness of fibres on T2
Abnormal orientation (too flat compared with Blumensaat's line)
PCL buckled
Anterior translation of the tibia

Q3.What are the coronal MRI findings of an ACL tear?

Discontinuity of fibres
Bone bruise in the LFC (middle 1/3) and lateral tibial plateau (posterior 1/3)
Effusion

Q4.What is the axial MRI finding of an ACL tear?

Fluid at the intercondylar notch = empty notch sign

Q5.What are the physical examination findings of ACL deficiency?

Palpate the bony prominence; feel step off bilaterally
Pivot shift (slide, jerk, clunk)
IR + valgus anterolaterally subluxes the tibia
Flexing the knee changes the ITB from extensor to flexor and reduces the tibia

Q6.Why examine the collateral ligaments at 30 degrees of flexion?

At 30 degrees of flexion the capsule and cruciate ligaments relax
This allows isolated assessment of the collateral ligaments

Q7.What injuries are associated with an acute ACL tear?

Lateral meniscal tear in 54% of acute ACL injuries
Unhappy triad = ACL + MCL + medial meniscus

Q8.What is the anatomy and function of the anterolateral ligament (ALL)?

Origin: anterior and distal to the femoral attachment of the LCL
Insertion: Gerdy tubercle on the tibia
Contributes to tibial internal rotation stability
Failure causes rotational instability; treated by ALL reconstruction or LET

Q9.What is the biomechanical difference between ALL reconstruction and LET?

ALL - non-isometric (tight in extension, slack in flexion), allowing physiological internal rotation at 90 degrees flexion
LET (modified Lemaire) - isometric, with a tendency to limit physiological internal rotation at 90 degrees flexion

Q10.What are the results and downsides of the STABILITY trial (AJSM 2020)?

Adding LET to single bundle ACLR in young high-risk patients results in a statistically significant, clinically relevant reduction in graft rupture and persistent rotatory laxity at 2 years
Downside: more pain and worse outcome scores in the first 3-6 months
Slower return to sport
Long-term studies suggest increased risk of lateral compartment OA

Q11.What are the indications for ALL reconstruction or LET?

2 of 3: Grade 2 pivot shift or greater
Desire to return to high-risk/pivoting sport
Generalised ligamentous laxity

Q12.What is the location of the ACL?

Intra-articular, extrasynovial - no haematoma formation; synovial fluid has a surfactant effect
From the medial surface of the LFC (bifurcate ridge) to the anterior tibia, just anterior and between the intercondylar eminences

Q13.What are the dimensions and composition of the ACL?

~33mm length, 11mm width
90% type 1 collagen, other type 3

Q14.What are the anteromedial and posterolateral bundles of the ACL?

AM bundle: more isometric, tight with the knee in flexion, controls AP translation more
PL bundle: tight in extension, controls rotation more

Q15.What is the blood and nerve supply of the ACL?

Blood supply: middle geniculate artery
Nerve supply: posterior articular branch of the tibial nerve

Q16.What is the function of the ACL?

Provides 85% of the stability preventing anterior translation of the tibia
Secondary restraint to valgus and varus stress and tibial rotation
2200N load to failure

Q17.What is the mechanism of an ACL injury and what causes locking?

Non-contact pivoting injury
Valgus + external rotation, partially flexed
Landing with the knee in extension
Cause of locking in an ACL tear: the stump

Q18.What is the natural history of the ACL-deficient knee (Frank Noyes JBJS 1983)?

1/3 have no/minimal symptoms in ADL or recreational activity
60% had repeated injury and meniscal/cartilage injury within 2 years
1/3 give up sport
1/3 deteriorate and require surgical stabilisation

Q19.When should ACL reconstruction be performed?

Delay around 6/52
Allow effusion and inflammation to subside
Regain good ROM and good quadriceps control
To avoid arthrofibrosis

Q20.What factors determine whether to perform ACL reconstruction?

Return to sports, especially pivot type
Prevent second injury - cartilage and meniscus
Theoretically reduces DJD, yet no concrete evidence (ACL deficiency puts more stress on the posterior horn of the medial meniscus)

Q21.What are the graft options and their loads to failure?

BPTB - 2600N, size 10mm
Hamstring - 4000N, size 7-8mm
Quadriceps tendon - 2500N, mainly for revision cases
Return to sport/repeat injury and ROM/failure rate are the same for BPTB and hamstring

Q22.What are the pros and cons of a BPTB graft?

Pros: early healing (animal study), bone-to-bone -> faster rehab
Cons: patella fracture (stellate) or PT rupture 0.5%, graft-tunnel mismatch
Anterior knee pain (15%)/PFJ OA - cannot kneel; patellar baja from retropatellar fibrosis; some flexion contracture

Q23.What are the pros and cons of a hamstring graft?

Pros: high tensile strength, easier/smoother passage
Cons: not used in generalised ligamentous laxity or complete MCL injury - do not jeopardise medial stability
Saphenous nerve injury during harvest, premature harvest, knee flexor weakness, graft attritional rupture

Q24.What are the problems with allograft and artificial grafts?

Allograft: fresh frozen risks infection; irradiation weakens the graft; quality not as good, not enough supply
Artificial: no incorporation, a lot of synovitis and pain, cannot absorb energy (stress-strain curve has no toe phase and is steep)

Q25.What are the advantages of autograft versus allograft?

Autograft: less immunogenicity, less disease transmission, faster incorporation, lower cost
Allograft: saves harvesting time, bigger graft for revision, no donor site morbidity
Grassi BJJ 2017: autograft has lower rates of postoperative laxity and fewer reoperations/complications; when irradiated grafts are excluded, outcomes are similar

Q26.What do KT-1000 measurements show after ACL reconstruction?

<3mm compared with the normal side is considered stable, and BPTB is more stable
If the difference is <5mm, BPTB and hamstring show no difference
Ligament has more elastin, is more viscoelastic and elongates less compared with hamstring

Q27.Should single or double bundle ACL reconstruction be used?

Meta-analysis: double bundle is better for rotational stability but clinical outcome is similar
Prerequisite: footprint at least 11mm
Freddie Fu CORR 2020: <14mm single, 14-18 controversial, >18 double

Q28.What are the ideal properties of graft fixation?

Strong enough to avoid failure
Stiff enough to restore load-displacement response
Secure enough to resist slippage under cyclic loading

Q29.What are the types of suspensory and aperture fixation and their pros and cons?

Suspensory: cortical (endobutton, staples, tie over post) or cancellous (transfix, rigidfix)
Pros: more healing surface, more rigid (fixed at closed loop), adjustable length
Cons: micromotion - bungee effect + windshield wiper effect -> tunnel widening
Aperture fixation: interference screw (depends on friction, longer = more pull-out strength)
Pros: fixation near the articular surface, less bungee effect; Cons: advancement of bone graft, graft/suture laceration, divergent -> less stability

Q30.Which fixation is used in the femur, tibia and revision cases?

Femoral: usually suspensory +/- double fixation
Tibial: usually aperture +/- double fixation
Revision: poorer bone quality -> double fixation
Reverse thread in the femoral tunnel of the right knee: the graft moves anteriorly and causes laxity (the isometric point is more posterior)

Q31.What are the key steps of ACL reconstruction?

Low morbidity harvest of a biologically active graft
Short arthroscopy time and prevent intra-articular injury
Accurate identification of the tibial and femoral footprints
Smooth passage of the graft through the tunnels
Robust fixation and tensioning of the graft
Appropriate rehabilitation

Q32.Describe the operative details of ACL reconstruction.

GA/SA with tourniquet; graft harvesting and preparation (preconditioning reduces stress relaxation)
Femoral tunnel: anatomical footprint, as posterior as possible but prevent blow out, coronally at 9-10 o'clock if done on the right knee
Tibial tunnel: anatomical footprint (centre 10-11mm in front of the anterior border of the PCL), trajectory <75 degrees from horizontal (55 degrees guide used)
Fixation: femoral endobutton, tibial interference screw
Graft tensioning: 40N with the knee at 20-30 degrees flexion

Q33.What complications can occur according to time sequence?

Intraoperative: graft harvest - BPTB patella fracture; hamstring infrapatellar branch of saphenous nerve injury, saphenous nerve injury, graft transection, contamination
Intraoperative: tunnel malposition, graft fixation problems (interference screw laceration/divergence, endobutton blow out at lateral cortex), poor tensioning, injury to secondary stabilisers
Postoperative: notch impingement (cyclops lesion around the tibial tunnel), stiffness/arthrofibrosis, infection, late patella fracture/anterior knee pain/patella tendon rupture (BPTB graft)

Q34.Describe the phases of graft ligamentisation and healing.

Early healing 0-6 months: inflammatory cytokines (IL6, TNF alpha, TGF beta, metalloproteinase 1 and 13) digest collagen; graft undergoes central avascular necrosis; maximum increase in anterior laxity at 6 months
Proliferation 6-12 months: Revascularization from the synovium, infrapatellar fat pad and pseudoligamentum mucosum, increased expression of the VEGF; Repopulation by progenitor cells from the autograft, bone tunnel and seeding fibroblasts from the residual stump lay down type III collagen
Maturation/ligamentisation >12 months: osseous integration by enchondral ossification; collagen remodelled to type I collagen

Q35.What are the 4 zones of tendon-to-bone healing?

Fibrous tissue surrounds the graft
Collagen grows into the fibrous tissue
Fibrocartilaginous tissue forms and then becomes bone
This is fibrocartilaginous healing

Q36.What are the phases of ACL rehabilitation?

Phase 1 (postop 1 week) [ROM + ADL]: cryotherapy for swelling and pain, obtain ROM 0-90 especially full extension, immediate weight bearing
Phase 2 (postop 2-8 weeks) [strengthening]: full ROM, isometric and isotonic exercise, commence close and open chain exercise
Phase 3 (postop 8-16 weeks) [functional]: isokinetic and endurance, increase resistance of OC/CC exercise from 9 weeks, plyometric exercise, normal running from 13 weeks
Phase 4 (postop 16-22 weeks) [sport specific + injury prevention]: Neuromuscle ex optimization, jumping, agility; return to sport when HQ ratio >0.8

Q37.What are the principles of ACL rehabilitation?

The cornerstone is ROM, strengthening, functional exercise and injury prevention, facilitating ligamentisation and graft healing
Avoid excessive stress on the graft: initial closed chain (open chain: distal limb unsupported -> increases shear force by gravity)
Eccentric quadriceps strengthening; isometric hamstring and quadriceps exercise
Avoid isokinetic quadriceps or open chain exercise in the early post-op period

Q38.How is a dropped graft managed intra-operatively?

Retrieve from the floor within 15 seconds
Remove all sutures; soak in saline
Soak in 2% chlorhexidine
Soak in triple antibiotics (gentamicin, clindamycin, polymyxin)
Minimise sutures in the graft, consider monofilament sutures; longer antibiotics and more frequent follow-up

Q39.What are the pros and cons of one-stage versus staged meniscus and ACL surgery?

One stage pros: one GA
Biological: drilling of tunnels provides MSC for meniscus healing
Mechanical: restores a stable environment for meniscus healing
Cons: contradictory rehab -> arthrofibrosis; for a locked knee go 2 stage (meniscus then early ACLR)

▸ Slide 642 · Principle: reduction of subluxed knee from IR + extension to valgus + flexionSports · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

Describe the technique and prerequisites of the pivot shift test.
What is the principle of the pivot shift?
What are the grades of pivot shift?
What does a high-grade pivot shift indicate?
What is a RAMP lesion and how is it classified (Thaunat)?

Answers · Q & A

Q1.Describe the technique and prerequisites of the pivot shift test.

IR tibia at knee extension
Valgus force + gradual knee flexion
Sudden glide/jump/clunk = reduction of the tibia relative to the femur
+ axial load to exaggerate
Prerequisites: intact MCL and intact ITB

Q2.What is the principle of the pivot shift?

IR of the tibia exaggerates ACL deficiency (especially the PL bundle)
Valgus stress tightens the MCL -> decreases medial tibial plateau movement -> lateral tibial plateau translates forward
Sudden reduction by the ITB on knee flexion (axis of pull posterior to knee COR/TEA -> ITB becomes a flexor)

Q3.What are the grades of pivot shift?

1: glide (may be physiological)
2: sublux with spontaneous reduction (jump)
3: subluxation +/- spontaneous reduction (clunk)

Q4.What does a high-grade pivot shift indicate?

Isolated ACL tear is unable to produce a high-grade pivot shift
Meniscus: LM root tear, ramp lesion, MM posterior horn tear
Anterolateral complex: ITB (superior and deep), ALL, AL capsule - secondary restraint to anterior translation and IR (with LM)
Generalised ligamentous laxity (Beighton score >=5/9)

Q5.What is a RAMP lesion and how is it classified (Thaunat)?

9-17% of ACL tears
1: capsulomeniscal junction lesions - very peripheral, low mobility at probing
2: partial superior lesions - stable, diagnosed only by the trans-notch approach (modified Gillquist manoeuvre)
3: partial inferior/hidden - not visible trans-notch, high mobility (meniscotibial ligament disruption)
4: complete tear in the red-red zone - very high mobility
5: double tear

▸ Slide 643 · 100 patients randomly assign OT/ conservative MxSports · 3 questions expand

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Q1-Q33 questions — tap to reveal all answerslist

What was the design of the study of operative versus conservative management?
What were the key findings of the study?
What happened to the conservatively managed patients?

Answers · Q & A

Q1.What was the design of the study of operative versus conservative management?

100 patients randomly assigned to operative (ACL reconstruction) or conservative management

Q2.What were the key findings of the study?

ACL reconstruction per se did not reduce risk of OA or improve outcome scores
ACL reconstruction can reduce risk of 2nd meniscal injury
Meniscal status is the most important predictor of OA

Q3.What happened to the conservatively managed patients?

1/3 of conservative patients later received ACL reconstruction due to instability

▸ Slide 644 · ACL complications and preventionSports · 6 questions expand

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Q1-Q66 questions — tap to reveal all answerslist

What are the intraoperative complications of ACL reconstruction related to graft harvest?
What complications can occur during tunnel placement in ACL reconstruction?
What complications can occur during graft passage in ACL reconstruction?
What complications can occur during graft fixation in ACL reconstruction?
What postoperative complications are related to ACL reconstruction?
How are postoperative complications of ACL reconstruction classified?

Answers · Q & A

Q1.What are the intraoperative complications of ACL reconstruction related to graft harvest?

Hamstring: premature harvest, deep MCL injury, hematoma, saphenous nerve injury
BPTB: fracture (patella or tibia)
Both grafts: dropped graft

Q2.What complications can occur during tunnel placement in ACL reconstruction?

MFC injury
Lateral wall blowout
Posterior wall blowout

Q3.What complications can occur during graft passage in ACL reconstruction?

Under-sized graft
Over-sized graft

Q4.What complications can occur during graft fixation in ACL reconstruction?

Late button flip
Screw breakage or slippage
Screw divergence
Graft laceration, advancement or rotation
Screw protrusion into the joint

Q5.What postoperative complications are related to ACL reconstruction?

Cyclops lesion
Arthrofibrosis
Septic arthritis
Prominent tibial screw

Q6.How are postoperative complications of ACL reconstruction classified?

Related to ACLR: cyclops, arthrofibrosis, septic arthritis, prominent tibial screw
Not related to ACLR (listed as a separate category by the lecturer; no examples given in the notes)

▸ Slide 645 · 10mm widthSports · 7 questions expand

Question list

Q1-Q77 questions — tap to reveal all answerslist

What are the dimensions and fixation of a BPTB graft?
What is the classical placement of a BPTB graft and why?
What is the problem if a BPTB graft is too long and how is the graft remedied?
What are the tunnel remedies if a BPTB graft is too long?
What is the problem if a BPTB graft is too short and how is it remedied?
What happens if a BPTB graft is too wide or too narrow?
How are patellar complications prevented during BPTB harvest?

Answers · Q & A

Q1.What are the dimensions and fixation of a BPTB graft?

10mm width, 90-100mm length
Rigidfix/interference screw (proximal) + interference screw (distal)

Q2.What is the classical placement of a BPTB graft and why?

Tibial bone --> femoral tunnel; patellar bone --> tibial tunnel
Because the tibial metaphysis is weaker, and there is increased bone contact if the intraop tunnel is too wide

Q3.What is the problem if a BPTB graft is too long and how is the graft remedied?

Too long: unable to use an interference screw
Graft remedy: trim and flip 180 degrees back
Graft remedy: self-twist 360 degrees to take up tension

Q4.What are the tunnel remedies if a BPTB graft is too long?

Femur: recess graft and secure at aperture with bioscrew
Tibia: secure bone plug in trough distal to tunnel

Q5.What is the problem if a BPTB graft is too short and how is it remedied?

Too short: fixation not cortical
Remedy: double fixation

Q6.What happens if a BPTB graft is too wide or too narrow?

Too wide: bone plug not through tunnel; remedy graft trimming +/- notchplasty
Too narrow: loosening; remedy alternative fixation

Q7.How are patellar complications prevented during BPTB harvest?

Patella fracture: trapezoidal/bevel cut to increase the cross-sectional area of bone at the donor site
Avoid transverse saw cut overruns
Burr to round off corners
Leave at least 1cm from the superior pole

▸ Slide 646 · Graft motion and fixationSports · 6 questions expand

Question list

Q1-Q66 questions — tap to reveal all answerslist

What types of graft motion occur after ACL reconstruction?
What are the consequences of graft motion greater than 3mm?
Compare the healing time of BPTB and hamstring grafts.
What are the types of aperture fixation and their pros and cons?
What are the types of suspensory fixation and their pros and cons?
How is the EndoButton loop length (EB-CL) calculated?

Answers · Q & A

Q1.What types of graft motion occur after ACL reconstruction?

Longitudinal motion: bungee effect
Horizontal motion: windshield wiper effect
Creep of graft: elongation

Q2.What are the consequences of graft motion greater than 3mm?

Delayed incorporation
Tunnel widening

Q3.Compare the healing time of BPTB and hamstring grafts.

BPTB: healing <8-10 weeks
Hamstring: tendon to bone >12 weeks

Q4.What are the types of aperture fixation and their pros and cons?

Aperture fixation: anatomical, at joint level (femoral subchondral, tibial cancellous), direct linkage
Pros: decrease graft motion, decrease widening of canal, decrease creep
Cons: lower margin of error, graft attrition during insertion

Q5.What are the types of suspensory fixation and their pros and cons?

Suspensory fixation: non-anatomical, distal level; mainly cortical (Endobutton, staple, tie on post) or cancellous (transfixation pin)
Pros: more versatile
Cons: increase graft motion

Q6.How is the EndoButton loop length (EB-CL) calculated?

Socket length is subtracted from total channel length and 6 or 7mm added for turning radius
If the number is a multiple of 5, that is the EB-CL; if not, select the next-largest multiple of 5
Example: channel 34mm, socket 27mm --> 7 + 6 = 13 --> 15mm EB-CL, so 34 - 15 = 19mm of graft in the femoral tunnel

▸ Slide 647 · Interference screwSports · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

How does an interference screw achieve fixation and how is interference defined?
What are the properties of bioabsorbable interference screws?
What screw size and position give the best fixation?
What is the purpose of reverse thread on an interference screw?
What are the complications of interference screw use?

Answers · Q & A

Q1.How does an interference screw achieve fixation and how is interference defined?

Relies on friction between graft and bone tunnel
Interference = amount by which the diameter of the screw exceeds the graft tunnel gap

Q2.What are the properties of bioabsorbable interference screws?

Biphasic CaPO4 (mixture of HA and tricalcium phosphate) + polylactide (more hydrophobic than polyglycolic)
Bioabsorbable over years; no need for removal; MRI compatible
Graft strength and stiffness decrease at 6 weeks
Titanium screws are also used; old material was stainless steel

Q3.What screw size and position give the best fixation?

1mm wider than tunnel
Longer screw gives better fixation but only engage bone plug in BPTB (20-30mm best)
Within 5mm proximal to joint; if too long may cause windswept effect

Q4.What is the purpose of reverse thread on an interference screw?

Reverse thread for less insertion torque

Q5.What are the complications of interference screw use?

Screw laceration of suture or graft
Screw divergence = difference between tunnel angle and screw direction; >20 degrees = less stability
BPTB only: bone plug advancement and plug cut off from graft
If plug cut off: intact side to interference screw, cut side to Krakow and fix with post/button/screw in tunnel

▸ Slide 648 · Description:Sports · 10 questions expand

Question list

Q1-Q1010 questions — tap to reveal all answerslist

What do you describe on an X-ray after ACL reconstruction?
What are the three reasons for ACL reconstruction failure?
What are the factors of recurrent or persistent instability (Pittsburgh classification)?
How does the lecturer classify ACLR failure according to time frame?
What do you look for on X-ray in a failed ACL reconstruction?
What history and risk factors are relevant in a failed ACL reconstruction?
What examination findings are relevant in a failed ACL reconstruction?
What is the preop workup before revision ACL reconstruction?
What are the intraoperative considerations in revision ACL reconstruction?
What are the expectations and postop plan for revision ACL reconstruction?

Answers · Q & A

Q1.What do you describe on an X-ray after ACL reconstruction?

Femoral and tibial tunnel position
Single or double bundle
Soft tissue or BPTB graft
Bone quality and mode of fixation

Q2.What are the three reasons for ACL reconstruction failure?

Recurrent instability
Recurrent pain
Loss of motion

Q3.What are the factors of recurrent or persistent instability (Pittsburgh classification)?

Mechanical/technical (majority): wrong patient choice (knee abuser, malalignment), graft choice, graft size, tunnel position, tension (3tension in the notes), graft fixation, graft impingement, secondary stabilisers (meniscus, peripheral ligament)
Failed graft incorporation: infection, immunological, avascularity, stress shielding
Traumatic: reinjury, aggressive rehab

Q4.How does the lecturer classify ACLR failure according to time frame?

Early (<3 months): failure of mechanical fixation or early biological problem (infection)
Midterm (3-12 months): technical problems - tunnel malposition, impingement, graft elongation, unrecognised ligamentous injury
Later (>1 year): trauma, underlying patient factor

Q5.What do you look for on X-ray in a failed ACL reconstruction?

Details of surgery (single/double bundle, graft and fixation type, graft size)
Tunnel position; tunnel widening >15mm may need 2-stage surgery; tibial slope; notch view for notch architecture
Complications: patella fracture, posterior blowout, endobutton position, interference screw divergence

Q6.What history and risk factors are relevant in a failed ACL reconstruction?

Age and premorbid status
Activity level (knee abuser)
Risk factors: ligamentous laxity, female, pivoting sports
Current symptoms: pain, instability, mechanical symptoms, reinjury

Q7.What examination findings are relevant in a failed ACL reconstruction?

Gait: varus thrusting
Generalised ligamentous laxity
Genu valgum
ROM and evidence of loss of secondary restraints
Position of previous scar

Q8.What is the preop workup before revision ACL reconstruction?

XR (AP/lat/tunnel/skyline/notch)
Scannogram for varus
CT and MRI: tunnel, graft, incorporation, bone stock; look for other concomitant injuries
Prerequisite: knee flexion >90 degrees, fixed flexion contracture <5

Q9.What are the intraoperative considerations in revision ACL reconstruction?

Choice of graft (BPTB, HS for widened tunnel, graft size suboptimal, quad, allograft)
Prepare screw/staple removal (revision ACL set)
Tunnel planning: use old tunnel if position okay, new tunnel if severe malposition, two stage if old and new are close with not enough bone stock (dilatation >15mm)
Revision notchplasty
Fixation: endobutton, interference screw, tie over post, over the top, double fixation
Send intraop culture if doubtful

Q10.What are the expectations and postop plan for revision ACL reconstruction?

Expectation mx: results inferior to primary ACLR (increase rerupture rate and rehab time)
One- vs two-stage operation
Postop: individualised, less aggressive rehab plan

▸ Slide 649 · ACL post reconstruction XraySports · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

What should be assessed on an X-ray after ACL reconstruction?
What is the optimal sagittal tunnel position after ACL reconstruction?
What is the coronal clock-face position of the femoral tunnel?
How can femoral tunnel position be predicted in transtibial versus transportal techniques?
What should be checked for fixation quality on a post-ACL reconstruction X-ray?

Answers · Q & A

Q1.What should be assessed on an X-ray after ACL reconstruction?

Details of surgery: number of tunnels, graft type (bone plug/harvesting) and fixation method
Complications: patella fracture, patella alta, posterior femoral blow-out, tunnel widening
Quality of reconstruction and tunnel position

Q2.What is the optimal sagittal tunnel position after ACL reconstruction?

Femur more posterior, tibia more anterior (to gain maximal AP length)
Femoral: Blumensaat line divided into 4 parts - tunnel at the posterior 4th quadrant, must not breach the posterior cortex
Tibia: plateau divided into 4 parts - tunnel at the anterior 2nd; too anterior causes notch impingement (double bundle can be more anterior)

Q3.What is the coronal clock-face position of the femoral tunnel?

10:30 and 1:30

Q4.How can femoral tunnel position be predicted in transtibial versus transportal techniques?

Transtibial: can use the tibial tunnel to predict the femoral tunnel
Transportal: by anteromedial portal

Q5.What should be checked for fixation quality on a post-ACL reconstruction X-ray?

Interference screw: divergence <15 degrees
Button: on cortex (may trap ITB / within bone)
Tunnel widening

▸ Slide 650 · Paeditric Acl tearSports · 6 questions 1 check expand

Question list

Q1-Q66 questions — tap to reveal all answerslist

When is surgery indicated in a paediatric ACL tear and what is the evidence on delay?
What are the surgical options for a paediatric ACL tear?
What is primary repair of a paediatric ACL tear and what is the evidence?
What type of intra-articular reconstruction is used according to growth remaining?
Why is a hybrid reconstruction used and how is growth considered?
What technical principles minimise physeal damage in paediatric ACL reconstruction?

Answers · Q & A

Q1.When is surgery indicated in a paediatric ACL tear and what is the evidence on delay?

Quoted evidence (Clin sport med 2021 metanalysis, PLUTO study group): delayed ACL reconstruction for more than 12 weeks significantly increases risk of meniscal injuries and irreparable meniscal tears
Take into account skeletal age, growth remaining, instability symptoms, aspiration for sport and associated injury

Q2.What are the surgical options for a paediatric ACL tear?

Primary repair (ongoing BEAR trial)
Extra-articular tenodesis
Intra-articular reconstruction: transphyseal, hybrid or physeal sparing

Q3.What is primary repair of a paediatric ACL tear and what is the evidence?

Primary repair is one option (ongoing BEAR trial)
Preliminary 2-year follow-up results promising

Q4.What type of intra-articular reconstruction is used according to growth remaining?

Transphyseal: <2 years of growth remaining
Hybrid: 2-5 years of growth remaining (femur spared)
Physeal sparing (over-the-top fixation): >5 years of growth remaining

Q5.Why is a hybrid reconstruction used and how is growth considered?

Femur is spared in hybrid as it contributes 40% of lower limb growth
Hybrid used when 2-5 years of growth remaining

Q6.What technical principles minimise physeal damage in paediatric ACL reconstruction?

Drilling damages the geminal layer ( 7-9% physis cross section); 7-9% of physis cross-section is sufficient to cause growth disturbance (germinal layer)
Aim tunnel size 3-4% of physis cross-sectional area
Soft tissue graft; centrally located vertical tunnels
Avoid transphyseal screws; avoid overtensioning the graft

Fact check

Clin Sport Med 2021 meta-analysis by the PLUTO study group shows delayed ACL reconstruction >12 weeks increases risk of meniscal injuries and irreparable meniscal tears — misattributed — PLUTO is a prospective multicentre descriptive epidemiology cohort of skeletally immature ACL tears, not a 2021 meta-analysis; evidence for irreparable medial meniscal tears shows risk rising by about 8 weeks (Everhart, AJSM 2019), and timing thresholds vary by study — medium confidence — source

▸ Slide 651 · BPTB graftSports · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

How do you recognise that a BPTB graft was used on a post-ACL reconstruction X-ray?
How do you describe tunnel position on the coronal view?
How do you describe tunnel position on the sagittal view?
What other findings should be commented on in this post-ACLR X-ray?

Answers · Q & A

Q1.How do you recognise that a BPTB graft was used on a post-ACL reconstruction X-ray?

Defect in the patella and tibial tuberosity
Bone inside the tunnel
Fixation by bioabsorbable screws on both sides

Q2.How do you describe tunnel position on the coronal view?

Graft position satisfactory; both tunnels obliquely aligned
Femoral tunnel w.r.t. notch is at 10 o'clock position
Tibial tunnel at 60 degrees w.r.t. knee joint (cf sagittally aligned)

Q3.How do you describe tunnel position on the sagittal view?

Tibial tunnel 40% from anterior (2nd quarter) with entry point posterior to Blumensaat line (ideally comment with knee in full flexion)
Femoral tunnel adequately posteriorly placed without posterior blow-out

Q4.What other findings should be commented on in this post-ACLR X-ray?

There is patella Alta with Insall salvati ratio > 1.2, but I will compare it with preop XR
No patellar fracture
Screw position is not divergent

▸ Slide 652 · Femoral tunnel positionSports · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

What does the position of graft fixation represent, and when is it usually tensioned?
What happens if the graft is fixed in extension with the femoral tunnel too anterior or too posterior?
What are the consequences of a femoral tunnel placed too anterior when fixed in flexion?
What are the consequences of a femoral tunnel placed too posterior when fixed in flexion?
What are the effects of tibial tunnel malposition?

Answers · Q & A

Q1.What does the position of graft fixation represent, and when is it usually tensioned?

Position of fixing the graft represents the affected motion
Usually tensioned in 20-30 degrees flexion and posterior drawer (maximum tension) --> most stable
If fixed in extension, ensure full extension postop

Q2.What happens if the graft is fixed in extension with the femoral tunnel too anterior or too posterior?

Too anterior: limit flexion
Too posterior: lax in extension

Q3.What are the consequences of a femoral tunnel placed too anterior when fixed in flexion?

Tight in flexion, lax in extension
Fails to clear the resident ridge
Physiologically not adequate flexion; graft gradually stretches out and becomes lax (biological problem)

Q4.What are the consequences of a femoral tunnel placed too posterior when fixed in flexion?

Lax in flexion, tight in extension
Rare

Q5.What are the effects of tibial tunnel malposition?

Anterior: notch impingement, limits extension
Posterior: impinges PCL, tight in extension
Medial: impingement on medial femoral condyle
Lateral: impingement on lateral femoral condyle

▸ Slide 653 · Tunnel malpositionSports · 6 questions expand

Question list

Q1-Q66 questions — tap to reveal all answerslist

What is the resident ridge and what does it mark?
What is the lateral bifurcate ridge?
How does the AM bundle position over the femur change with knee movement?
What is the optimal femoral tunnel position?
What are the pitfalls of femoral tunnel malposition?
What is the optimal tibial tunnel position and what are its pitfalls?

Answers · Q & A

Q1.What is the resident ridge and what does it mark?

Also called the lateral intercondylar ridge
Marks the anterior and superior border of the ACL insertion

Q2.What is the lateral bifurcate ridge?

Ridge located between the AM and PL bundles

Q3.How does the AM bundle position over the femur change with knee movement?

More posterior on flexion
More superior on extension

Q4.What is the optimal femoral tunnel position?

Coronal: right 10:30 / left 1:30
Sagittal: B line posterior 1/4, posterior to the resident ridge with 2 mm posterior cortex remained

Q5.What are the pitfalls of femoral tunnel malposition?

Too anterior: tight flexion if tightened in extension
Too posterior: blow out
Too vertical: rotational instability

Q6.What is the optimal tibial tunnel position and what are its pitfalls?

Sagittal: 2nd anterior 1/4 of the tibial plateau, 7 mm anterior to PCL
Coronal: between the tibial spines
Too anterior: notch impingement
Too posterior: PCL impingement + laxity?

▸ Slide 654 · Post ACLR stiffnessSports · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

What are the global causes of stiffness after ACL reconstruction?
What causes loss of knee flexion after ACL reconstruction?
What causes loss of knee extension after ACL reconstruction?

Answers · Q & A

Q1.What are the global causes of stiffness after ACL reconstruction?

Arthrofibrosis
Infrapatellar contracture syndrome (fibrous hyperplasia of anterior knee - loss of flexion + extension + patellar entrapment)
Infection

Q2.What causes loss of knee flexion after ACL reconstruction?

Femoral tunnel too anterior, tightened and fixed in knee extension
Excessively tensioned graft
Suprapatellar pouch scarring

Q3.What causes loss of knee extension after ACL reconstruction?

Tibial tunnel too anterior
Notch scarring
Cyclops lesion

▸ Slide 655 · ACL avulsionSports · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

Why does an ACL avulsion fracture occur rather than a midsubstance tear?
What is the Meyers and McKeever classification of ACL avulsion fracture?
How are ACL avulsion fractures treated?
What are the difficulties and complications of ACL avulsion treatment?
How is the knee immobilised and what fracture is associated with ACL avulsion?

Answers · Q & A

Q1.Why does an ACL avulsion fracture occur rather than a midsubstance tear?

Ligament stronger than physeal cartilage or cancellous bone
ACL fibres in continuity with perichondrium of tibial epiphysis/cartilage
Mechanism: hyperflexion or direct blow to flexed knee (e.g. fall from bicycle)

Q2.What is the Meyers and McKeever classification of ACL avulsion fracture?

Non-displaced
Minimally displaced with intact posterior hinge
Completely displaced

Q3.How are ACL avulsion fractures treated?

Long leg cast for types I and II
Type II: CR before casting by hyperextension to reduce
Treat early; arthroscopic or mini-open option
Fixation: screw (better x2), suture anchor (usually not enough strength) or pull-out suture through bone tunnel
Rehab similar to ACL reconstruction

Q4.What are the difficulties and complications of ACL avulsion treatment?

Reduction difficulty: interposition of intermeniscal ligament and meniscus
Recurvatum in children (fixation tethers anterior growth plate)
Remove metallic screw at 3-4 mths (3-4 months) to avoid articular cartilage damage (difficult)

Q5.How is the knee immobilised and what fracture is associated with ACL avulsion?

Cast in 20 degrees flexion to minimise distraction force; hyperextension increases tensile force and distracts the fragment
Position is controversial; some put in 0 degrees but usually better reduced
80% are type 1 or 2
Associated Segond fracture: disruption of meniscotibial portion of lateral capsule (direct evidence of lateral capsule, indirect for ACL)

▸ Slide 656 · PCL injurySports · 16 questions expand

Question list

Q1-Q1616 questions — tap to reveal all answerslist

What are the aims of assessing a PCL injury?
What are the usual injury mechanisms of PCL injury?
What positive physical signs should be elicited in PCL injury?
What tests indicate an associated PLC injury?
How is the reverse pivot shift performed and how does it work?
What imaging is used in PCL injury and how is stress view graded?
What associated injuries must be assessed in PCL injury?
Describe the anatomy of the PCL.
Why does the PCL heal better than the ACL?
What is the natural history of isolated PCL injury?
What is the rehab protocol for non-operative management of PCL injury?
What is the indication for surgery in PCL injury?
What factors are considered in PCL reconstruction?
Describe the all-arthroscopic transtibial PCL reconstruction technique.
What are the pros and cons of all-arthroscopic versus inlay PCL reconstruction?
What is the post-op rehabilitation after PCL reconstruction?

Answers · Q & A

Q1.What are the aims of assessing a PCL injury?

Assess severity
Rule out associated injury
Formulate management plan (also depends on patient's functional demand)

Q2.What are the usual injury mechanisms of PCL injury?

Hyperextension/hyperflexion
RTA dashboard injury (look for femoral neck fracture)
Varus force on a flexed knee
Fall onto the ground with a plantar-flexed foot

Q3.What positive physical signs should be elicited in PCL injury?

Loss of medial tibial step-off with knee 90 degrees flexion
Posterior sagging grading relative to medial femoral condyle: anterior, flush, posterior
Posterior drawer grading: <5mm, 5-10mm, >10mm with no endpoint; rule out PLC in high grade
Quadriceps active test: flex knee 60 degrees, stabilise foot and active extend knee

Q4.What tests indicate an associated PLC injury?

Dial test at 30/90 degrees (positive at 90 = combined injury, 30 only = PLC)
Recurvatum ER test: varus = LCL injury, ER = fabellofibular/popliteus tendon, recurvatum = PCL
Posterolateral drawer test
Reverse pivot shift - 26% sensitivity, 95% specificity
Gait: lateral thrust

Q5.How is the reverse pivot shift performed and how does it work?

Begins in flexion with ER and valgus stress applied, so tibia subluxes posteriorly
Knee is then brought to full extension (reverse)
ITB changes from flexor to extensor at ~30 degrees flexion, causing relocation (same principle)
Sensitivity 26%, specificity 95%

Q6.What imaging is used in PCL injury and how is stress view graded?

XR: avulsion fracture
Stress view (posterior tibial cortex to posterior end of Blumensaat line at knee flexion 70 degrees) with kneeling or Telos
3-8mm = partial, 8-12mm = complete, >12mm = PLC injury

Q7.What associated injuries must be assessed in PCL injury?

PLC injury
Multiple ligament injury
Knee dislocation
Posterior hip dislocation

Q8.Describe the anatomy of the PCL.

38x13mm, 30% larger than ACL; intracapsular, extrasynovial ligament
From MFC anterolateral surface (broad crescent-shaped footprint) to posterior tibial sulcus (1cm below joint line)
Bundles: AL (easier to rupture, tight at flexion) / PM; AL anterior to PM at femoral insertion
Meniscofemoral ligaments: Humphrey (anterior) and Wrisberg (posterior), contribute 20-30% stability
Type I collagen; blood supply middle geniculate artery; nerve supply posterior articular branch of tibial nerve
Primary restraint to posterior translation; secondary restraint to ER and varus; strength 2500-3000N

Q9.Why does the PCL heal better than the ACL?

Mechanical: increased stability from femoromeniscal ligaments
Biological: thick synovium sheath --> usually still extrasynovial after rupture (hematoma formation, no cytokine)
ACL is also an intracapsular, extrasynovial ligament

Q10.What is the natural history of isolated PCL injury?

Shelbourne 1999: 50% same sport, 30% lower level, 20% unable to play sport
Complication: anterior knee pain (PFJ arthritis)
Newer evidence: Agolley (prof Fares Haddad group) BJJ 2017 91.3% return to same level or higher

Q11.What is the rehab protocol for non-operative management of PCL injury?

Grade 1-2: PWB + quad strengthening
Grade 3: extension brace (Donjoy/posterior support) for 4-6 weeks, no flexion >50 degrees (PCL starts to take up tension around 50 degrees flexion)
PWB walking + quads isometric exercises

Q12.What is the indication for surgery in PCL injury?

Avulsion or peel-off lesion
Multiple ligament injury / concomitant PLC injury
Persistent symptoms (difficulty decelerating e.g. downstairs, PFJ pain) - observe 6-12 months

Q13.What factors are considered in PCL reconstruction?

Type of graft (hamstring / BPTB / quadriceps + bone)
Single/ double bundle: single bundle less demanding (reconstruct AL, tension at 90 degrees knee flexion)
Chahla Arthroscopy 2017 systematic review - double bundle better IKDC score and posterior tibial translation/knee stability
Inlay vs all-arthroscopic

Q14.Describe the all-arthroscopic transtibial PCL reconstruction technique.

Supine on tourniquet; harvest graft
Conventional portal + PM portal (injury to saphenous nerve)
PM portal dissection of posterior capsule (protect popliteal artery)
Drill tibial tunnel A to P, last few cm use hand drill, knee in 90 degrees flexion
Tibial tunnel 15mm distal to articular surface --> less killer turn
Femoral tunnel 7mm from articular surface at 1pm/11pm (shorter than ACL tunnel; consider aperture fixation if too short); tension at 90deg flexion with anterior drawer test

Q15.What are the pros and cons of all-arthroscopic versus inlay PCL reconstruction?

All-arthroscopic pros: single position, can use hamstring graft; cons: difficult to pass graft, killer turn
Inlay pros: avoid killer turn (less attrition), direct visualisation of NV bundle, better healing with bone union, biomechanically better
Inlay cons: floppy lateral position, less graft choice (BPTB or quadriceps tendon + patella bone with bone peg)

Q16.What is the post-op rehabilitation after PCL reconstruction?

Hinged knee brace locked in extension for ambulation and sleep for 6 weeks
Protect against gravity
Early motion in prone position
Quad strengthening; no open chain hamstring or isolated hamstring exercise for 3 months

▸ Slide 657 · PLC:Sports · 7 questions expand

Question list

Q1-Q77 questions — tap to reveal all answerslist

What are the static and dynamic structures of the PLC and their roles?
What is the layer arrangement of the PLC?
What is the anatomy of the fibular head insertion and structures to the fabella?
What are the common mechanisms, symptoms and physical signs of PLC injury?
What are the X-ray findings and varus stress grading in PLC injury?
What is the Fanelli classification and conservative management of PLC injury?
What are the indications for surgery, reconstruction options and evidence for repair vs reconstruction?

Answers · Q & A

Q1.What are the static and dynamic structures of the PLC and their roles?

Static (6): LCL, popliteus, popliteofibular ligament, fabellofibular ligament, arcuate ligament, capsule
Dynamic: ITB, biceps femoris, lateral gastrocnemius
Primary restraint to ER and varus; Secondary restrain to posterior translation

Q2.What is the layer arrangement of the PLC?

Layer 1: ITB/biceps femoris (CPN in between)
Layer 2: retinaculum
Layer 3 superficial: LCL/FFL/ALL (LGA in between)
Deep: arcuate/popliteal/PFL/capsule

Q3.What is the anatomy of the fibular head insertion and structures to the fabella?

Fibular head, anterior to posterior: LCL, biceps femoris (long then short), arcuate ligament, popliteofibular, FFL
Structures to fabella: capsular arm of short head of biceps, FFL, OPL, lateral gastrocnemius head, posterior lateral capsule

Q4.What are the common mechanisms, symptoms and physical signs of PLC injury?

Mechanism: blow to anteromedial knee, varus blow to flexed knee, hyperextension injury
Symptoms: instability in knee extension and upon pivoting
PE: dial test positive if >15 degrees difference, ER recurvatum, posterolateral drawer with foot 15 degrees ER, reverse pivot shift
(Peroneal nerve injury in 25% of patient with PLC injury)

Q5.What are the X-ray findings and varus stress grading in PLC injury?

Avulsion fracture (arcuate fracture) of fibula head
Varus stress (Laprade): <4mm = isolated PCL, 4-7mm = LCL + PCL, >7mm = LCL + PLC + XL
Long leg standing XR: malalignment, determine mechanical axis +/- need for HTO

Q6.What is the Fanelli classification and conservative management of PLC injury?

Fanelli A: increase ER only (PFL + popliteus)
Fanelli B: increase ER + varus laxity in knee flexion (above + LCL)
Fanelli C: increase ER + varus laxity in flexion and extension (above + ACL/PCL)
Conservative: isolated grade 1-2 injury - extension knee brace + protected weight bearing x2 weeks, then quad strengthening

Q7.What are the indications for surgery, reconstruction options and evidence for repair vs reconstruction?

Indications: bony avulsion, multiple ligament laxity, persistent symptoms, grade 3 injury (assess in MUA)
Unstable (varus stress >7mm) + within 2 weeks of injury --> early repair then later staged recon; stable --> brace 6 weeks then one-stage recon (Laprade favours single stage early recon of PCL and PLC)
Reconstruct LCL and popliteofibular ligament; graft: semitendinosus/achilles
Larson: non-anatomical fibular-based figure of 8; LaPrade anatomical recon with 2 soft tissue grafts (LCL+PFL and popliteus); transtibial double bundle fixation
CUHK arthroscopy paper: LaPrade technique gives better rotational stability
Recon better than repair: Stannard failure 37% vs 9%; Levy 40% vs 6%; Geeslin AJSM 2016 metanalaysis – recon better outcomes than repairs in acute PLC injuries (meta-analysis)

▸ Slide 658 · Stieda Pellegrini sign (few weeks after injury): ossified lesion signifying avulSports · 7 questions expand

Question list

Q1-Q77 questions — tap to reveal all answerslist

What is the Stieda Pellegrini sign?
What is the function of the MCL and the usual mechanism of injury?
What are the layers of the medial side of the knee?
How is MCL instability graded and where do tears most commonly occur?
When is operative management indicated in MCL injury?
How is a grade 3 MCL tear with ACL tear managed?
What are the classifications and reconstruction options for MCL tear?

Answers · Q & A

Q1.What is the Stieda Pellegrini sign?

Ossified lesion seen a few weeks after injury
Signifies avulsion injury of MCL at the medial femoral condyle

Q2.What is the function of the MCL and the usual mechanism of injury?

Primary restraint to valgus stress
Secondary restraint to ER, ant/ post translation (anterior/posterior translation)
Usual mechanism: valgus + ER

Q3.What are the layers of the medial side of the knee?

Layer 1: sartorius and fascia, patella retinaculum (gracilis, semitendinosus, saphenous nerve)
Layer 2: superficial MCL, POL, OPL, MPFL, semimembranosus
Layer 3: deep MCL, capsule

Q4.How is MCL instability graded and where do tears most commonly occur?

Medial gapping compared with opposite knee: <5mm, <10mm, >=10mm
Grade 1: stretch injury (no loss of ligamentous integrity)
Grade 2: incomplete tear (fibres opposed, endpoint at 30 degrees flexion valgus test)
Grade 3: complete tear (no endpoint)
Most common: femur side tear

Q5.When is operative management indicated in MCL injury?

All try conservative management (hinged brace) first
Grade III with: acute multiligamentous injury; acute displaced distal avulsion with Stener-like lesion (trapped torn end); subacute/chronic with persistent instability
Femoral origin tears have better healing potential

Q6.How is a grade 3 MCL tear with ACL tear managed?

Early MCL repair (within 2 weeks) + delay ACLR
Or conservative Mx for MCL + delay ACL reconstruction (MCL needs protection, which may cause stiffness)

Q7.What are the classifications and reconstruction options for MCL tear?

Taketomi (tibial side tear): under pes, Stener-like lesion, trapped inside joint
Nakamura: type 1 femoral, type 2 tibial (none in his study), type 3 femoral with extension below the joint line
Reconstruction: Bosworth (semitendinosus, distal intact, attached to femoral tunnel), Lind (gracilis looped over MCL), LaPrade
Acute reconstruction is controversial

▸ Slide 659 · Posteromedial cornerSports · 4 questions expand

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Q1-Q44 questions — tap to reveal all answerslist

What is the definition and what are the components of the posteromedial corner?
What is the role of the posteromedial corner?
What is anteromedial rotatory instability (AMRI)?
When is early repair of the posteromedial corner indicated?

Answers · Q & A

Q1.What is the definition and what are the components of the posteromedial corner?

From posterior margin of superficial MCL to PCL (does not include MCL)
Components (2nd layer): semimembranosus expansion (5 arms: capsular, anterior, inferior, distal, direct)
POL (ligament of Winslow), OPL, deep capsule, MM PH

Q2.What is the role of the posteromedial corner?

Dynamic
Secondary restraint to ER
Restraint to valgus stress in extension

Q3.What is anteromedial rotatory instability (AMRI)?

Medial tibial plateau anterior subluxation upon ER
Signs: valgus stress + at 30 degrees ER
Anterior drawer positive at 30 degrees ER

Q4.When is early repair of the posteromedial corner indicated?

In multiligament injury

▸ Slide 660 · Skeletally matureSports · 14 questions expand

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Q1-Q1414 questions — tap to reveal all answerslist

What are the differentials and how do you assess a suspected osteochondral lesion of the medial femoral condyle?
What imaging is used and what are the MRI criteria for instability?
What is the Clanton and Delee classification of OCD?
What is the Guhl arthroscopic classification and corresponding management?
What is the definition, epidemiology and prognosis of OCD?
What are the causes of OCD and the aim of management?
What is the Outerbridge classification of chondral lesions?
How is a sizable OCD flap repaired when the physis is open?
What are the three broad categories of resurfacing/reconstruction options for OCD?
What is the microfracture technique and what tissue does it produce?
What are the OAT (osteochondral autograft transfer) plug requirements?
How do ACI, MACI and AMIC differ?
What prognostic factors suggest a good outcome in OCD?
How is a high tibial osteotomy (HTO) performed?

Answers · Q & A

Q1.What are the differentials and how do you assess a suspected osteochondral lesion of the medial femoral condyle?

Differentials: osteonecrosis (SONK, post scope, secondary), osteoid osteoma, subchondral cyst, transient osteoporosis
History to rule out differentials: mechanical symptoms suggest displacement; trauma history
PE: Wilson's test (knee 30-90 degrees, pain with IR, relieved by ER); overall alignment; assess for instability. Gait: ER LL

Q2.What imaging is used and what are the MRI criteria for instability?

X-ray: weight bearing AP, lateral and notch view (flexed 30deg) to look for detached loose bodies; scannogram for overall alignment
MRI: position, size, attachment, displacement, loose body
Instability criteria: increased T2 signal >=5mm deep to lesion; focal defect >=5mm2 in articular surface

Q3.What is the Clanton and Delee classification of OCD?

1. Depressed
2. Connected by osseous bridge
3. Detached, undisplaced
4. Displaced

Q4.What is the Guhl arthroscopic classification and corresponding management?

1. Intact, 1-3cm (activity modification/retrograde drilling)
2. Stable flap (headless screw)
3. Partially displaceable flap (remove fibrous tissue, chondroplasty, fix)
4. Complete detachment (remove, chondroplasty +/- OC allograft, ACI, MACI)
Small (<2cm x 2cm) --> microfracture; large (>2cm x 2cm) --> chondroplasty

Q5.What is the definition, epidemiology and prognosis of OCD?

Definition: subchondral bone lesion with delamination + sequestration +/- articular involvement
Most common in knee (80% medial, 40% F, 20% bilateral, 10% patella); also talus and capitellum
70% resolve with conservative management
PAPPAS: I <12y, II 12-20y, III >20y (III usually OA)

Q6.What are the causes of OCD and the aim of management?

Constitutional: epiphyseal dysplasia with accessory nuclei separating from the epiphysis
Vascular: watershed region from attachment of the PCL
Traumatic: repetitive impingement of the tibial spine
Aim: relieve symptoms and improve function; always start conservative with protected weight bearing and NSAIDs
Surgery aims: restore joint congruity, increase local blood supply, address predisposing instability or malalignment

Q7.What is the Outerbridge classification of chondral lesions?

0 intact
1 softening
2 fissure not to subchondral bone
3 fissure to subchondral bone + diameter >1.5cm
4 subchondral bone exposed

Q8.How is a sizable OCD flap repaired when the physis is open?

Repair/fixation for sizable flap with open physis
Method of fixation: screw, bone peg, sutures
Rehab: PWB 6-8 weeks

Q9.What are the three broad categories of resurfacing/reconstruction options for OCD?

Resurfacing/ reconstruction options fall into three broad categories: MSC stimulation, substitution, cell-based biological replacement
MSC stimulation: microfracture, drilling, abrasion chondroplasty
Substitution options: OATS, osteochondral allograft
Cell based, biological replacement options: ACI, MACI, AMIC

Q10.What is the microfracture technique and what tissue does it produce?

OT x microfracture for fibrocartilage, others for hyaline
Microfracture 3-4mm apart, break surface till just across the tidemark with a chondral pick with low energy

Q11.What are the OAT (osteochondral autograft transfer) plug requirements?

Plugs should be cylindrical
At least 8mm long
4-12mm diameter

Q12.How do ACI, MACI and AMIC differ?

ACI: 2 procedures, expensive, can produce hyaline cartilage, not limited by size
MACI: similar to ACI but with a matrix
AMIC: one stage procedure

Q13.What prognostic factors suggest a good outcome in OCD?

Open distal femoral physis
Size <2cm
No sclerosis on XR
Location at medial femoral condyle posterolateral aspect
No synovial fluid behind lesion on MRI
High uptake on bone scan = good healing potential (grade II-IV, uptake at lesion, femoral, tibia)

Q14.How is a high tibial osteotomy (HTO) performed?

Approach: direct anteromedial
Identify the pes and release hamstrings
Release the distal MCL fibres subperiosteally in one layer until the posterior border of the tibia
Periosteal elevator to clear posterior structures off the tibia and place a radiolucent Homman retractor to protect the NV bundle
Mark out biplanar osteotomy either ascending or descending; trajectory of the saw cut guided by K wires
Apply Tomofix plate for FWB walking postop

▸ Slide 661Sports · 2 questions expand

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Q1-Q22 questions — tap to reveal all answerslist

What topic is covered in slide 661?
What are the key learning points from slide 661?

Answers · Q & A

Q1.What topic is covered in slide 661?

Not covered in the speaker notes

Q2.What are the key learning points from slide 661?

Not covered in the speaker notes

▸ Slide 662Sports · 5 questions expand

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Q1-Q55 questions — tap to reveal all answerslist

What are the four surgical options compared on the slide and their size indications?
How is fixation of an OCD performed and what are its limitations?
How is marrow stimulation performed and what are its advantages and disadvantages?
How is OAT/mosaicplasty carried out and what are its pros and cons?
What is the technique and the pros and cons of ACI on the slide?

Answers · Q & A

Q1.What are the four surgical options compared on the slide and their size indications?

Fixation: open physis, unstable OCD
Marrow stimulation: size <2cm2
OAT/mosaicplasty: size >2cm2
ACI: size >2cm2, contained defect

Q2.How is fixation of an OCD performed and what are its limitations?

Open or arthroscopic: 1. debride nonviable, 2. drill subchondral bone +/- bone graft, 3. absorbable/non-absorbable screw
Downside: lower healing rate in skeletally mature
May need removal of implant if a non-absorbable screw is used

Q3.How is marrow stimulation performed and what are its advantages and disadvantages?

Marrow stimulation by drilling/microfracture (2mm deep, 3-4mm apart) after debridement
Bleeding from subchondral bone, fibrin clot, formation of fibrocartilage; differentiation of mesenchymal stem cells into chondrocytes
Advantages: cost effective, single stage, arthroscopic
Disadvantages: replaced with fibrocartilage (type I), does not deal with the defect

Q4.How is OAT/mosaicplasty carried out and what are its pros and cons?

Replace cartilage defect with autologous cartilage and bone plug from a less weight bearing region (periphery of trochlea/notch)
Advantages: single stage, autologous, arthroscopic, cost effective
Disadvantages: donor site morbidity, difficult to match size and radius of curvature, prolonged rehab
Healing: medial > patella > lateral (worst)

Q5.What is the technique and the pros and cons of ACI on the slide?

Cell therapy aiming to produce hyaline-like cartilage
Arthroscopic harvest from a less weight bearing region, expand in culture, prepare defect, inject chondrocyst under periosteal patch
Advantages: large defect, may provide better histological tissue, autologous
Disadvantages: open, 2 stage, prolonged rehab, limited to contained defect; long term result comparable to microfracture

▸ Slide 663 · AP Xray of ankle, lesion over medial talar dome, well defined radiolucent rim anSports · 6 questions expand

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Q1-Q66 questions — tap to reveal all answerslist

What are the X-ray findings and additional view needed for osteochondritis dissecans of the talus?
What are the differential diagnoses for a talar dome lesion?
What are the classifications of talar OCD?
What history, examination and imaging are needed for talar OCD?
What is the conservative treatment and aims of surgery in talar OCD?
What determines the choice of surgery in talar OCD?

Answers · Q & A

Q1.What are the X-ray findings and additional view needed for osteochondritis dissecans of the talus?

Lesion over medial talar dome with well defined radiolucent rim
Fragmented bony lesion superficial to the rim, detached from talus but undisplaced
No subchondral cyst, no loose body, no degenerative change, no other signs of instability including talar tilt or avulsion fractures from fibula
Need Saltzman view (hindfoot alignment view, standing weight bearing, XR from behind 20 degrees caudally) to comment on hindfoot alignment
AL lesions: more associated with trauma, lower spontaneous recovery, usually displaced + symptomatic; PM: more common, larger and deeper

Q2.What are the differential diagnoses for a talar dome lesion?

Ddx: GCT (giant cell tumour)
Subchondral cyst
Osteoid osteoma (most common site for OO in the foot)

Q3.What are the classifications of talar OCD?

Berndt and Harty (XR): I small subchondral compression, II partial fragment detachment, III complete detachment undisplaced, IV complete detachment displaced
Frankel (CT): roof intact cyst, communication cyst, undisplaced lesion, displaced lesion
Hepple (MRI): cartilage edema, cartilage injury +/- bone edema, undisplaced lesion, displaced lesion, subchondral cyst

Q4.What history, examination and imaging are needed for talar OCD?

History: trauma, premorbid and sports, pain, functional limitations
PE: ankle ROM, tenderness, effusion, ligamentous stability (drawer test, syndesmosis), overall alignment
CT (Ferkel) + MRI (Hepple) to delineate size, bony component and overlying cartilage integrity
LL scannogram

Q5.What is the conservative treatment and aims of surgery in talar OCD?

Conservative: NSAID, rest, cast immobilisation and NWB 6 weeks (success rate 20-50%)
Aims: relieve symptoms and improve function
Aims of operation: restore joint congruity, increase local blood supply, Address predisposing factors such as malalignment and ligament instability
Technique: Diagnostic scope then decide whether to repair, resurface, reconstruct

Q6.What determines the choice of surgery in talar OCD?

Site and size, displacement, overlying cartilage integrity
Intact cartilage BH I or II --> retrograde drilling to stimulate growth
Large and fixable --> fix with absorbable pin/headless screws
Not fixable, cartilage not intact: contained --> chondroplasty/microfracture (cut off 2cm) +/- cartilage augmentation (AMIC/MACI/BMAC); uncontained --> OATS or mosaicplasty
Wener Cartilage 2021: small stable conservative; healthy fragment fixation; necrotic excision + BMS; medium/deep autograft, BMAC, AMIC, ACI; large bone graft/allograft; failed biological - mini metal implants
Overall quality of evidence poor: >90% of articles level III or IV

▸ Slide 664 · Xray showing laterally dislocated patella, no fracture seen, no loose body seenSports · 11 questions 2 check expand

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Q1-Q1111 questions — tap to reveal all answerslist

What is the immediate management of a first-time lateral patellar dislocation?
What history and examination findings are relevant to patellar instability?
What X-ray views and measurements are used in patellar instability?
How are CT and MRI used and what predicts recurrence risk?
What are the types and anatomical causes of patellar instability?
What are the surgical options for recurrent patellar dislocation and their complications?
What is the normal function of the patella?
What is normal patella movement during knee flexion and extension?
What are the details of MPFL reconstruction?
What are the types of trochleoplasty and their complications?
How do congenital/habitual patellar dislocation differ from traumatic instability?

Answers · Q & A

Q1.What is the immediate management of a first-time lateral patellar dislocation?

CR under sedation (knee extended with medially directed force); X-ray shows laterally dislocated patella, no fracture or loose body
First time: operate only if chondral lesion positive (with concomitant MPFL recon, Pedowitz AJSM 2019)
Otherwise conservative: donut bracing, physiotherapy (VMO strengthening), ITB stretching, closed chain exercises

Q2.What history and examination findings are relevant to patellar instability?

History: age at first dislocation, traumatic or atraumatic, associated bone or connective tissue dysplasias, mechanical symptoms
Owls eye patella, overall LL alignment, Q angle (M 8-10, F 15-20) vs carry angle of elbow (M 5-10, F 10-15)
Effusion, quad wasting, ROM
J sign (patella alta + maltracking), apprehension (push lateral at 20 degrees flexion), patella shift (>2 quadrants abnormal), patella tilt (should pass neutral), grinding test
Rotational profile and ligamentous laxity

Q3.What X-ray views and measurements are used in patellar instability?

Standing scannogram; lateral with knee flexed 30 degrees: Blumensaat line, Caton-Deschamps ratio 1.2, trochlear dysplasia signs (flat trochlea = crossing sign, convex = double contour + spur sign)
Merchant view (knee flexed 45 degrees, caudal directed beam 60deg from horizontal): sulcus angle (N=138), congruence angle (N=-6-16)
Laurin view (knee flexed 20 degrees, cephalad beam): lateral PFA (N = lateral opening 10)

Q4.How are CT and MRI used and what predicts recurrence risk?

CT: torsional malalignment, TTTG distance, trochlear dysplasia
MRI: OC fracture in 40%
Risk factors for recurrence: trochlear dysplasia, patellar alta, increased TTTG distance, patellar tilt
PIS score (patellar instability severity score) >4 = high risk (age, bilateral instability, patellar tilt, patellar alta, TTTG distance, trochlear dysplasia)

Q5.What are the types and anatomical causes of patellar instability?

Congenital
Acquired: acute, chronic, voluntary (party trick), habitual (dislocates every time with knee flexion within normal ROM, usually painless), recurrent (trivial sprain leads to dislocation with knee extension, painful)
Alignment (miserable malalignment): coronal Q angle, sagittal knee recurvatum/patella alta, axial femoral anteversion/tibial torsion
Bone: trochlear dysplasia, patella hypoplasia (Wiberg classification)
Soft tissue: weak VMO, tight lateral retinaculum, MPFL deficiency, weak hip abductors; general ligamentous laxity
TTTG 15mm in Asian, 20mm in Caucasian

Q6.What are the surgical options for recurrent patellar dislocation and their complications?

Principle: minimise destabilising forces while reconstructing bony and soft tissue restraints; recurrent --> MPFL reconstruction + correct risk factors
Proximal: MPFL reconstruction, medial plication +/- lateral release/lengthening, VMO advancement; trochlear dysplasia --> trochleoplasty
Distal: patella alta --> distal transfer of TT; increased TTTG --> medial transfer of TT; abnormal limb rotation --> derotational osteotomy
Roux-Goldthwait (transfer lateral half of patellar tendon medially), Elmslie-Trillat (TT medialization), Maquet (anteriorization), Fulkerson (anteromedial + distal transfer)
Complications: medial dislocation, medial PFJ arthritis, recurrence 5%, over-constraint leading to PFJ arthritis

Q7.What is the normal function of the patella?

Sesamoid bone
Increases moment arm of quadriceps
Aids cartilage nourishment
Protects knee joint

Q8.What is normal patella movement during knee flexion and extension?

Extended: not engaged, most unstable as knee is locked in screw home mechanism with tibia ER (increases Q angle)
Flexed 20 degrees: starts engagement, contact area moves proximal (increasing Q angle and stability)

Q9.What are the details of MPFL reconstruction?

The only anatomical option
Drill through patella or suture anchor
Interference screw to femur at the Schottle point (confluence of the posterior cortex extension line, blumensaat lines and the posterior curving line of the posterior femoral condyle)
Graft type: gracilis (size good) or semitendinosus (longer); latest study: semiT has better outcomes

Q10.What are the types of trochleoplasty and their complications?

Dejour trochleoplasty (thick flap, need split): creates a gap beneath the trochlea surface, trochlea split longitudinally, two flaps collapsed into the gap and held with staples/screws/sutures
Bereiter trochleoplasty (thin flap, no need split): elevates an osteochondral flap, thinned and moulded into a groove in the underlying bone created with osteotomes
Resection trochleoplasty
For Dejour B/D only; seldom done alone, technically demanding; complication: chondrolysis

Q11.How do congenital/habitual patellar dislocation differ from traumatic instability?

Pathology is lateral tightness and quadriceps contracture rather than a defective medial constraint
Treatment: early relocation to allow trochlear development, TT osteotomy, MPFL imbrication/recon
Extensive release of thick fibrous band tethering patella to lateral intermuscular septum; quadriceps VY plasty
Congenital: look for syndromes - arthrogryposis, nail-patella syndrome

Fact check

Merchant's view is taken with the knee flexed 45 degrees and the beam directed caudally 60 degrees from horizontal — error — Merchant's original technique inclines the beam 30 degrees from the horizontal (equivalent to 60 degrees from vertical), knee flexed 45 degrees — source

Normal congruence angle on the Merchant view is -6 to 16 — misleading — Normal mean congruence angle is -6 degrees; values greater than +16 degrees are abnormal (lateral subluxation), so -6 and 16 are not the ends of a normal range — source

▸ Slide 665 · TRUE LATERAL XRAYSports · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

How do you assess patella alta on a lateral X-ray?
What are the Dejour signs of trochlear dysplasia (based on CT)?
How is the Merchant's view taken and what do you measure?
How is the Laurin's view taken and what do you measure?
What do you look for on CT and MRI in patellar instability?

Answers · Q & A

Q1.How do you assess patella alta on a lateral X-ray?

Blackburne-Peel index: ratio of perpendicular distance of patella articular surface to tibial plateau and patella articular surface (a/b); normal 0.8, alta >1.0, baja <0.5
Caton-Deschamps: 0.6-1.3; >1.3 = alta, <0.6 = baja
Insall-Salvati: patella tendon length / patella length (LT/LP); normal 0.8-1.2; alta >1.2, baja <0.8 (affected by patella and tibial tuberosity morphology)
Blumensaat line: inferior pole of patella should sit on line drawn along superior aspect of intercondylar notch (rough guideline)

Q2.What are the Dejour signs of trochlear dysplasia (based on CT)?

A: crossing sign - sulcus too shallow and ended prematurely anterior to groove
B: supracondylar spur - flat trochlea with lateral condyle higher than medial
C: double contour due to lateral convex condyle
D: spur + double contour cliff

Q3.How is the Merchant's view taken and what do you measure?

Knee flexed 45 degrees, beam aimed caudal
Congruence angle: line connecting lowest pole of patella and lowest point of trochlear groove vs line bisecting the groove; normal should be negative 5 degrees (medial)
Sulcus angle: lines along medial and lateral trochlear ridges; normal 138 degrees

Q4.How is the Laurin's view taken and what do you measure?

Knee flexed 20 degrees, beam aimed cephalad
Lateral patellofemoral angle: line along top of femoral condyle and lateral facet of patella
Normal 10 degrees (tilt)

Q5.What do you look for on CT and MRI in patellar instability?

CT: femoral version, trochlear dysplasia, lateral patella tilt, TTTG (lateral offset of tibial tuberosity from trochlear groove)
MRI: MPFL injury (medial femoral epicondyle to superior medial patella)
MRI: chondral lesion (usual medial patella and lateral femoral condyle, injured during relocation)

▸ Slide 666 · Middle age, M = F Recurrent atraumatic haemarthrosisSports · 9 questions 1 check expand

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Q1-Q99 questions — tap to reveal all answerslist

What are the lateral knee X-ray findings in this patient with recurrent atraumatic haemarthrosis?
What is the differential diagnosis for recurrent atraumatic haemarthrosis with these X-ray findings?
What is pigmented villonodular synovitis (PVNS)?
How does the diffuse form of PVNS differ from the localized form?
What are the MRI and histological features of PVNS?
What is the management of PVNS?
How would you clinically assess a patient with recurrent atraumatic haemarthrosis of the knee?
What is the extra-articular equivalent of PVNS?
Describe the arthroscopic portals used for PVNS of the knee.

Answers · Q & A

Q1.What are the lateral knee X-ray findings in this patient with recurrent atraumatic haemarthrosis?

Increased radiopacity over the suprapatellar region and posterior to the femoral condyles
Well circumscribed, with no disruption of cortex, +/- nodular depression
Cystic lesion over the femoral condyle with a sclerotic margin
Mainly a soft tissue lesion

Q2.What is the differential diagnosis for recurrent atraumatic haemarthrosis with these X-ray findings?

PVNS (pigmented villonodular synovitis)
Haemophilia
Synovial chondromatosis
Inflammatory synovitis

Q3.What is pigmented villonodular synovitis (PVNS)?

Idiopathic monoarticular neoplastic synovial disease
Abundant proliferation of synovial villi and nodules
CSF1 gene, genetic locus at chromosome 5q33; pexidartinib
Can occur at any age; 50% have a history of trauma
Presents with swelling and limited ROM; intra-articular

Q4.How does the diffuse form of PVNS differ from the localized form?

Both forms are most common in the knee
Diffuse: more extra-articular involvement
Diffuse: more likely to be painful
Diffuse: less well circumscribed on MRI
Diffuse: higher recurrence (30% vs 8% after synovectomy)

Q5.What are the MRI and histological features of PVNS?

MRI: low signal on both T1 and T2
MRI: blooming artifact on gradient-echo sequences due to iron in hemosiderin (haemosiderin deposition)
Histology: haemosiderin-stained multinucleated giant cells
Mononuclear stromal cells; highly vascular villi with hyperplastic synovial cells
Pigmented foam cells (lipid-laden histiocytes)

Q6.What is the management of PVNS?

Nearly no role for conservative management
Total synovectomy (marginal excision): open, arthroscopic or combined
Arthroscopy: brownish or reddish inflamed synovium with frond-like papillary projections
+ Irradiation reduces recurrence to 10-20% (30-35Gy in 15 fractions, or 50Gy in 25 fractions)
+ TKI (e.g. imatinib)
Hip PVNS: joint damage occurs early, so perform synovectomy early

Q7.How would you clinically assess a patient with recurrent atraumatic haemarthrosis of the knee?

PE: confirm swelling, exclude a mass, document ROM
Examine the contralateral limb for involvement
Further imaging: MRI with gradient echo sequence
MRI shows blooming effect over the area of concern, also involvement posterior to the knee

Q8.What is the extra-articular equivalent of PVNS?

Giant cell tumour of the tendon sheath

Q9.Describe the arthroscopic portals used for PVNS of the knee.

Posteromedial portal: 1cm above the joint line behind the MCL
Posterolateral portal: 1cm above the joint line between the LCL and biceps tendon

Fact check

PVNS is linked to the CSF1 gene on chromosome 5q33 — wrong chromosome/locus — CSF1 is on chromosome 1p13; PVNS/TGCT is driven by t(1;2)(p13;q35) fusing CSF1 to the COL6A3 promoter on 2q35. Loci at 5q22-31 are only uncommon alternative translocation partners. — source

▸ Slide 667 · Clinical photo and Xray showing knee subluxationSports · 14 questions expand

Question list

Q1-Q1414 questions — tap to reveal all answerslist

What does the clinical photo show and what is the dimple sign?
How do you assess a knee dislocation acutely?
What associated injuries occur with knee dislocation and when is an ex-fix indicated?
Scenario 2: dislocated knee with an absent pulse - what is your management?
What signs suggest a knee dislocation that has spontaneously reduced?
Describe the definitive (staged) management of a multiligamentous knee injury.
Scenario 1: posterolateral dislocation with intact NV status - what is your management?
Scenario 3: dislocated knee with a palpable pulse - what is your management?
How do you classify a knee dislocation?
How do you reduce a knee dislocation other than posterolateral?
Why is a staged approach used in multiligamentous knee injury?
Compare the graft choices for multiligamentous knee reconstruction.
What are the controversies in operative treatment of knee dislocation?
Describe the posterior approach to the knee.

Answers · Q & A

Q1.What does the clinical photo show and what is the dimple sign?

Posterior displacement of the tibia with lateral translation
Dimple sign: puckering of anteromedial skin from the medial femoral condyle buttonholing through the medial retinaculum/capsule
Indicates a posterolateral dislocation
Contraindication to closed reduction (would cause skin necrosis)

Q2.How do you assess a knee dislocation acutely?

ATLS protocol, AMPLE history, primary survey
Local: rule out hip dislocation and open wound
Distally document pulse, CR, neurology and compartment syndrome
Systemic: secondary survey to rule out other injuries
Recheck pulse and document nerve status after any reduction
If stable, arrange CTA to look for an intimal tear

Q3.What associated injuries occur with knee dislocation and when is an ex-fix indicated?

Direct vascular injury in 10-30%
CPN injury in 10-40%, with complete recovery in only 20%
Ex-fix if fracture dislocation, significant soft tissue compromise/open injury, vascular compromise or compartment syndrome

Q4.Scenario 2: dislocated knee with an absent pulse - what is your management?

Analgesia, immediate closed reduction under sedation, splint with knee flexed 20-30 degrees, then recheck pulse
Pulse returns: CT angiogram or serial ABI monitoring
No return of pulse: vascular bypass, ex-fix knee, on-table angiogram, resect diseased segment and re-anastomose with reversed saphenous vein graft
Delay >8 hours gives >80% amputation rate
Prophylactic fasciotomy (EFFORT review 2020); Postop monitor CK for rhabdomyolysis and reperfusion syndrome

Q5.What signs suggest a knee dislocation that has spontaneously reduced?

20-50% reduce spontaneously before presentation
Hyperextension compared with the normal side
Popliteal ecchymosis
NV injury at presentation
Diffuse tenderness but NO effusion

Q6.Describe the definitive (staged) management of a multiligamentous knee injury.

Aim: stable painless knee, full ROM, return to pre-injury activity
Stage 1 at 2 weeks: PLC, PMC, MCL and LCL, meniscus +/- avulsion fracture fixation; hinged knee brace + NWB for 6 weeks
Stage 2: delayed simultaneous ACL and PCL reconstruction (PCL before ACL), after good ROM and muscle bulk restored
If vascular injury: no tourniquet, delayed surgery, inlay PCL

Q7.Scenario 1: posterolateral dislocation with intact NV status - what is your management?

Acute: analgesics, immobilise with a slab then proceed to open reduction
Medial parapatellar approach; reduce then check stability + NV condition
Then slab or external fixator
Avoid closed reduction in posterolateral dislocation (dimple sign - risk of skin necrosis)

Q8.Scenario 3: dislocated knee with a palpable pulse - what is your management?

Analgesia, immediate closed reduction under sedation + splint with knee flexed 20-30 degrees, then recheck pulse
Check symmetry of pulse and ABI
ABI >0.9: serial monitoring; ABI <0.9 and asymmetric: CTA
If CTA shows an intimal tear: anticoagulant, monitor, delayed OT for ligamentous reconstruction, no tourniquet, no tibial tunnel
+/- MRI to document ligamentous laxity; classify with Schenck

Q9.How do you classify a knee dislocation?

Kennedy: by direction - anterior/posterior/medial/lateral/rotational
Schenck: by number of ligaments involved + fracture
I = single cruciate; II = bicruciate; III = bicruciate + one collateral tear; IV = all 4; V = fracture

Q10.How do you reduce a knee dislocation other than posterolateral?

CR under sedation, stabilise the femur and pull the tibia opposite to the direction of displacement
Document NV status afterwards
Apply a slab in 20-30 degrees knee flexion or an ex-fix

Q11.Why is a staged approach used in multiligamentous knee injury?

Shorter OT time and each stage is simplified
Reduces the risk of arthrofibrosis
Delay definitive OT if vascular injury is present
Stage 1 addresses the capsular tear (risk of compartment syndrome) and soft tissue status

Q12.Compare the graft choices for multiligamentous knee reconstruction.

Autograft: no disease transmission, no added cost, documented healing/vascularisation; cons - donor site morbidity, longer OT
Allograft: no donor site morbidity, shorter OT, does not further destabilise the knee; cons - availability, disease transmission, cost, biomechanics
Synthetic: no donor site morbidity, shorter OT, readily available; cons - reactive synovitis, graft failure

Q13.What are the controversies in operative treatment of knee dislocation?

Timing: Hohmann Knee 2017 metanalysis - early surgery <3 weeks improved Lysholm scores compared with delayed surgery
Sheth 2019 ISAKOS J - early surgery may provide better functional outcomes without compromising ROM when using early postop mobilisation protocols
Mook 2009 systematic review JBJS - early <3 weeks vs staged: similar need for additional treatment for arthrofibrosis, both significantly higher than delayed; delayed >3 weeks had less residual instability and ROM deficit; staged had highest excellent/good outcomes
Jiang 2015 KSSTA - staged operation yields the best clinical results for KDIII; Marder 2021 - neither approach superior
Repair vs reconstruction: Stannard 2005 PLC repair failure 37% vs 9% with reconstruction; Levy 2010 40% vs 6%
Laprade AJSM 2019 –suggest single stage anatomic based recon of all ligament (single surgeon series); bicruciate reconstruction - simultaneous preferred at PWH

Q14.Describe the posterior approach to the knee.

Incision: lazy S, proximal limb lateral, distal limb medial
Open the popliteal fascia at opening of SSV and MSCN (small saphenous vein and medial sural cutaneous nerve), staying lateral to the MSCN
Trace the MSCN proximally to protect the popliteal AV bundle
Protect the common peroneal nerve along the posterior edge of biceps femoris
Retract popliteal vessels laterally; ligate superior medial and middle geniculate arteries; elevate popliteus +/- soleus

▸ Slide 668 · Knee dislocationSports · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

Define knee dislocation and explain why it is an orthopaedic emergency.
How is knee dislocation classified (Kennedy and Schenck)?
Which ligaments must be assessed in knee dislocation?
What are the key complications of knee dislocation?

Answers · Q & A

Q1.Define knee dislocation and explain why it is an orthopaedic emergency.

Not covered in the speaker notes - the slide image is the only source

Q2.How is knee dislocation classified (Kennedy and Schenck)?

Not covered in the speaker notes

Q3.Which ligaments must be assessed in knee dislocation?

Ligaments to assess: ACL, PCL, MCL, LCL, PLC

Q4.What are the key complications of knee dislocation?

Not covered in the speaker notes

▸ Slide 669 · When would you suspect knee dislocation?Sports · 8 questions 2 check expand

Question list

Q1-Q88 questions — tap to reveal all answerslist

When would you suspect a knee dislocation?
What are the common mechanisms of injury causing knee dislocation?
How do you classify knee dislocation?
Why is the popliteal artery prone to injury in knee dislocation?
How do you investigate for vascular injury in knee dislocation?
What is the timing of surgery for vascular injury and how is an intimal tear treated?
Describe the approach and key steps of the posterior approach to the knee.
What are the borders and contents of the popliteal fossa?

Answers · Q & A

Q1.When would you suspect a knee dislocation?

Multi-ligamentous injury (defined as two or more of ACL, PCL, PMC, PLC)
High energy trauma
Distal NV compromise
20-50% have spontaneously reduced by presentation

Q2.What are the common mechanisms of injury causing knee dislocation?

Usually high energy e.g. RTA; can occur with relatively low energy injury in athletes
Anterior (most common): LCP, intimal tear by traction
Posterior (2nd commonest): axial loading to flexed knee, complete tear of popliteal artery
Lateral: varus/valgus force, bicruciate tear + peroneal nerve
Medial: varus/valgus force, bicruciate tear
Rotational: irreducible

Q3.How do you classify knee dislocation?

Kennedy: by direction (anterior/posterior/medial/lateral/rotational)
Schenck: by number of ligaments involved + fracture
I = single cruciate; II = bicruciate; III = bicruciate + one collateral tear; IV = all 4; V = fracture

Q4.Why is the popliteal artery prone to injury in knee dislocation?

Incidence quoted as 20-60%
Tethered proximally by the adductor hiatus (trifurcation) and inferiorly by the soleus arch
Tied down medially and laterally by the geniculate arteries
Also tethered by the 5 geniculate arteries

Q5.How do you investigate for vascular injury in knee dislocation?

Document pulses; AAOS: ABI >0.9 admit + observe 24 hours, <0.9 angiogram, ischaemia explore
Pulse -ve -> reduce -> pulse returns -> CTA
Pulse -ve -> reduce -> pulse remains -ve -> vascular surgeon + OT
Pulse +ve -> ABI <0.9 -> CTA +/- explore
Pulse +ve -> ABI >0.9 -> serial monitoring for at least 72 hours
Notes state ABI 100% sensitive, NPV 100%

Q6.What is the timing of surgery for vascular injury and how is an intimal tear treated?

Emergency operation
Ischaemic time >8hr = 90% amputation rate; <6hr = 6%
Intimal tear: anticoagulation
Subsequent operation: pre-op no tourniquet, delayed surgery, no tibial tunnel
Nerve injury: ~30% peroneal nerve by traction, fair prognosis; explore if open wound, otherwise conservative first

Q7.Describe the approach and key steps of the posterior approach to the knee.

GA, prone with bony prominences padded
Lazy S incision with proximal limb lateral and distal limb medial to avoid the peroneal nerve
Distally find the small saphenous vein and medial sural cutaneous nerve
Trace proximally to reach the popliteal vein and tibial nerve in the popliteal fossa
Incise the popliteal fossa longitudinally lateral to the vein

Q8.What are the borders and contents of the popliteal fossa?

Diamond-shaped space over the posterior knee
Bounded by semitendinosus/semimembranosus, biceps femoris and the 2 heads of gastrocnemius
Floor is the posterior capsule of the knee; roof is the popliteal fascia
Most superficial structure is the tibial nerve

Fact check

ABI is 100% sensitive with a 100% negative predictive value for vascular injury after knee dislocation — overstated/contested — Mills et al (2004) reported 100%, but later cohort data show no single physical examination manoeuvre is 100% sensitive; a normal ABI can still miss intimal tears. Combine palpable pulses plus ABI >=0.9 and continue serial observation (48-72h). — medium confidence — source

Popliteal artery injury occurs in 20-60% of knee dislocations — imprecise range — Modern systematic reviews report weighted mean popliteal artery injury rates of about 8-18%; rates at the upper end (up to 60%+) are seen mainly in high-energy trauma and fracture-dislocations. — medium confidence — source

▸ Slide 670 · XR of the right proximal femur and right knee showing multiple well defined ossiSports · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

Describe the X-ray findings shown in this slide.
What is the differential diagnosis for periarticular ossification/calcification?
What is synovial chondromatosis?
How is synovial chondromatosis managed?

Answers · Q & A

Q1.Describe the X-ray findings shown in this slide.

Multiple well defined ossifications surrounding the right hip and knee joints
Calcifications are less well defined in the hip
No associated bone erosions

Q2.What is the differential diagnosis for periarticular ossification/calcification?

Dystrophic (vascular, tumour, infection, haematoma): synovial chondromatosis, synovial sarcoma, myositis ossificans
Metastatic: renal osteodystrophy
Calcinosis / tumoral calcinosis

Q3.What is synovial chondromatosis?

Proliferative disease of the synovium associated with cartilage metaplasia
Results in multiple intra-articular loose bodies
MRI: low T1, high T2

Q4.How is synovial chondromatosis managed?

Surgery as soon as possible
Removal of loose bodies
Synovectomy reduces recurrence rate
Approach: posterior knee portal or open

▸ Slide 671Sports · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

What is the clinical topic of this slide?
What are the key learning points from this slide?

Answers · Q & A

Q1.What is the clinical topic of this slide?

Not covered in the speaker notes - the slide image is the only source

Q2.What are the key learning points from this slide?

Not covered in the speaker notes

▸ Slide 672 · Shoulder stabilizerSports · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

What are the dynamic stabilizers of the shoulder?
What are the static stabilizers of the shoulder?
What are the roles of the glenohumeral ligaments?

Answers · Q & A

Q1.What are the dynamic stabilizers of the shoulder?

Rotator cuff
Biceps
Periscapular muscles

Q2.What are the static stabilizers of the shoulder?

Bony: osteotomy, version
Soft tissue: ligaments, labrum
Negative intra-articular pressure

Q3.What are the roles of the glenohumeral ligaments?

SGHL: inferior restraint at adduction
MGHL: AP restraint at 0-45 degrees abduction + ER
IGHL: AP + inferior restraint at 45-90 degrees abduction + ER
CHL: primary ER restraint

▸ Slide 673 · 50/F shoulder pain + weaknessSports · 21 questions expand

Question list

Q1-Q2121 questions — tap to reveal all answerslist

What are the functions of the rotator cuff?
What are the causes of rotator cuff tear?
What are the causes of impingement and what is Neer's staging?
What are the X-ray findings and special views in rotator cuff pathology?
What do you look for on MRI in a rotator cuff tear?
What are the indications for operative management of a cuff tear?
How would you assess a patient with a suspected rotator cuff tear?
How would you describe a rotator cuff tear on MRI and what associated findings do you comment on?
What is the natural history of symptomatic cuff tears (Kim KSSTA 2017)?
What conservative management is offered for a rotator cuff tear?
What is the principle of cuff repair and how is the tendon mobilised to the footprint?
How is a PASTA (partial articular supraspinatus tendon avulsion) tear repaired?
When is acromioplasty performed and how is it done safely?
What does double-row repair for massive cuff tears involve?
What are the partial repair options for a massive cuff tear?
What are the surgical choices for an irreparable cuff tear?
How is shoulder arthroscopy set up and performed?
What is the standard rehab protocol after cuff repair (<3cm tear/single cuff)?
How does rehabilitation differ after massive or multiple cuff repair?
Describe the footprint of the rotator cuff.
What is the definition of a massive cuff tear and what are the clinical clues?

Answers · Q & A

Q1.What are the functions of the rotator cuff?

Dynamic stabilizer of the shoulder
Force coupling to maintain a stable fulcrum for concentric rotation of the humeral head by neutralizing deltoid shear
Vertical: inferior cuff (IS, TM, subscap) counteracts the superior pull of deltoid so the GHJ rotates instead of migrating superiorly
Horizontal: IS + TM balanced by subscap

Q2.What are the causes of rotator cuff tear?

Impingement: subacromial -> SS, infraspinatus, teres minor (SIT); subcoracoid -> subscap
Trauma: middle-aged after shoulder dislocation -> SIT
Young patient after fall with hyperabduction/ER -> subscap

Q3.What are the causes of impingement and what is Neer's staging?

External: hooked acromion, ACJ arthritis/osteophytes
Internal: throwers with tight posterior and lax anterior capsule; anterior subluxation on abd + ER; GT with SS impinging on posterosuperior glenoid
Neer's staging: inflammation, fibrosis, tear with weakness
Type 1 collagen replaced by type 2 (better compression strength, less resistant to tensile strength)

Q4.What are the X-ray findings and special views in rotator cuff pathology?

AP: calcific tendonitis, cuff arthropathy, acromial sclerosis, GT cystic changes, Maloney's line
Critical shoulder angle (normal 30-35): increased in RCT, reduced in OA
Supraspinatus outlet view (Y view with 10 degrees caudal tilt) for Bigliani acromial morphology (flat, curved, hooked)
Also look for os acromionale (os acromiale) and ACJ osteophyte

Q5.What do you look for on MRI in a rotator cuff tear?

Number, size, retraction of tear; fatty infiltration/atrophy; bicep tendon pathology
Coronal: SS tear, Patte retraction, superior migration of humeral head
Sagittal: Goutallier fat atrophy 0-4 (0 normal, 1 fatty streak, 2 <50%, 3 50%, 4 >50%)
Axial: biceps tendon subluxation (medial), subscapularis and IF tendon
Ellman partial: I 3mm, II 3-6mm, III >6mm; A articular, B bursal, C intratendinous
Size: small <1cm, medium 1-3cm, large 3-5cm, massive = 2 or more cuffs involved or >5cm

Q6.What are the indications for operative management of a cuff tear?

Symptomatic failure of 6-12 months conservative management
Partial thickness >50% PASTA (Ellman 3A), or bursal side >3mm (Ellman 2B)
Full thickness + repairable
Young <60 with acute tear: repair within 6 weeks
Contraindications: irreparable tear, frozen shoulder
Irreparable: Goutallier IV, GHJ arthritis, advanced age; SS retraction beyond glenoid; cannot pull cuff beyond articular surface even at 60 degrees abduction

Q7.How would you assess a patient with a suspected rotator cuff tear?

Hx: history of injury, functional demand, symptoms (overhead activity, night pain) and functional limitation
PE: identify pathology (rule out other causes of weakness e.g. nerve palsy, identify which cuff), severity of weakness
Delineate cause (impingement) and complication (frozen shoulder)
First-line investigation: X-ray and MRI

Q8.How would you describe a rotator cuff tear on MRI and what associated findings do you comment on?

Morphology: crescent, U, L, massive
Delineate number, size and retraction of the tear; which cuff is involved
Comment on articular cartilage, associated ACJ arthritis, superior migration and the tangent line
Associated biceps tendon pathology

Q9.What is the natural history of symptomatic cuff tears (Kim KSSTA 2017)?

Symptomatic partial thickness: 26% progress at 2 years
Symptomatic full thickness: 82% progress at 2 years
Counsel the patient regarding the natural history

Q10.What conservative management is offered for a rotator cuff tear?

NSAID
Physio: strengthen periscapular muscles + deltoid recruitment exercises
Subacromial injection if impingement symptoms are severe
PRP: controversial; 2022 Bhandari meta-analysis showed better long-term pain relief than steroid

Q11.What is the principle of cuff repair and how is the tendon mobilised to the footprint?

Principle: anatomical, secure, tension-free repair to lower retear rate
Dissection between glenoid and cuff (not too medial 2cm or 1cm posterior - suprascapular nerve at risk)
Anterior interval slide (to coracoid, more anatomical) and posterior interval slide (to glenoid, less anatomical)
Release of the coracohumeral ligament

Q12.How is a PASTA (partial articular supraspinatus tendon avulsion) tear repaired?

If 25% SST remains - convert to full thickness
Small perforation - transtendinous repair
Young PASTA - transtendinous in situ repair
Old PASTA - complete the tear then repair

Q13.When is acromioplasty performed and how is it done safely?

Not to be done routinely
Indications: CA ligament fraying, bursal-side tear, anterolateral osteophyte, impingement on dynamic assessment
Avoid the anteromedial corner (thoracoacromial artery bleeding)
Together with bursectomy and biceps resection/tenodesis

Q14.What does double-row repair for massive cuff tears involve?

Chen 2013 meta-analysis: higher rate of intact tendon healing, especially for large tears, but no better clinical outcome
May not be possible with severe retraction
Conventional: tendon strangulation, worse footprint restoration, synovial fluid leakage
Transosseous: medial tendon strangulation, failure at musculotendinous junction, highest ultimate failure load
Knotless: lower structural strength, suture slippage

Q15.What are the partial repair options for a massive cuff tear?

Medialisation of footprint - no more than 10-12mm
Patch repair (fascia lata) to share tension
Augmentation with biceps
Marginal convergence no longer recommended (non-anatomical)

Q16.What are the surgical choices for an irreparable cuff tear?

Superior capsular reconstruction (>=6mm thick graft), medial anchor to superior glenoid
Muscle transfer: LD for posterosuperior SST/IST tear +/- simultaneous RSA to restore ER; TM for better strength; pec major for subscapular/anterosuperior defect
Old frail patient: debridement +/- balloon spacer (poly-L-lactide); START:REACTS (Lancet 2022) does not recommend the spacer
Reverse shoulder arthroplasty

Q17.How is shoulder arthroscopy set up and performed?

GA, lateral decubitus leaning 30 degrees posterior, parallel to the table; beanbag + correct head position
Arm draped hanging out, abducted with slight flexion to relax the brachial plexus
Landmarks: posterolateral corner of acromion and coracoid
Posterior portal 2cm medial and inferior to the posterolateral corner, directed at the coracoid; danger - too inferior = axillary nerve, too medial = suprascapular nerve
Rotator interval contents: coracohumeral ligament, SGHL, biceps; systematic view from anterior biceps, GHL, subscap, labrum, SS/IS
Cuff repair needs lateral portals for anchors; Bankart repair uses anterosuperior and anteroinferior portals

Q18.What is the standard rehab protocol after cuff repair (<3cm tear/single cuff)?

Phase 1 (first 6 weeks): muscle protection, swelling reduction, controlled mobilisation; abduction pillow, pendulum, scapular retraction exercises
PROM not beyond 90 degrees in the first 2 weeks, increase to 120 degrees by 4 weeks, then AAROM to 90 degrees
Phase 2 (up to 12 weeks): full AROM/PROM as tolerated, light isometric/isotonic exercises
Phase 3: intensive strengthening (theraband, pulleys, press-ups); Phase 4: endurance training (multi-push and lift machines)

Q19.How does rehabilitation differ after massive or multiple cuff repair?

Delay AROM and isotonic/isometric exercise until 10 weeks
Can start AAROM from 4 weeks onwards

Q20.Describe the footprint of the rotator cuff.

Overall dimension 20 x 25mm
SST at the anterosuperior greater tuberosity
Medial-lateral widths (SITS): SST 12mm, IST 13mm, TM 14mm, subscapularis 18mm
1.5-2mm from the articular cartilage
Anteroposterior 20mm (SST + anterior IST)

Q21.What is the definition of a massive cuff tear and what are the clinical clues?

>5cm (Cofield 4)
>1 tendon involved (Europe)
Retraction to the glenoid (Patte 3)
>50% fatty infiltration (Goutallier 4); AHI <6mm
Clinical clues: severe muscle atrophy, pseudoparalysis (active abduction <90 with full passive ROM and drop arm +), LHB rupture, ER lag or hornblower +

▸ Slide 674 · Suspension bridge theory (Burkhart)Sports · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

Describe the cable-crescent complex in the suspension bridge theory (Burkhart).
What is the clinical relevance of the suspension bridge theory?
What are the effects of rotator cuff deficiency?

Answers · Q & A

Q1.Describe the cable-crescent complex in the suspension bridge theory (Burkhart).

Cable- crescent complex
Cable: thickened part at the GT insertion of SST and IST, at the CHL avascular zone, running perpendicular to SST fibres and spanning SST and IST insertions
Crescent: thinner avascular zone of SST and IST distal to the cable (GT attachment)
Anterior post: LHB
Posterior post: behind IST

Q2.What is the clinical relevance of the suspension bridge theory?

Forces can be transmitted as long as the anterior and posterior posts are maintained
The cable can bypass the crescent and transfer load between the posts, shielding the crescent
Explains why partial repair is feasible

Q3.What are the effects of rotator cuff deficiency?

Loss of compressive centring forces
Superior migration of the humeral head
GHJ cartilage destruction; superior glenoid erosion
Synovial fluid leakage; osteoporosis
Humeral head destruction; articulation with acromion
CA ligament erosion; ACJ destruction

▸ Slide 675 · Nonoperative mx for cuff tearSports · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

What are the phases of physiotherapy for a rotator cuff tear?
What is the natural history of atraumatic rotator cuff tears (Moon group, JBJS 2014)?
What is the role of injections in cuff disease?

Answers · Q & A

Q1.What are the phases of physiotherapy for a rotator cuff tear?

Phase 1: pain relief + ROM maintenance (pendular, postural exercises, active-assisted ROM, flexibility)
Phase 2: strengthening
Phase 3: functional training +/- work hardening

Q2.What is the natural history of atraumatic rotator cuff tears (Moon group, JBJS 2014)?

75% do not require OT
Improvement occurs in 6-12 weeks
Beyond 3 months, likely to need OT

Q3.What is the role of injections in cuff disease?

Latest meta-analysis 2022 (Bhandari): steroid has short-term effects, PRP longer-term effects for the painful shoulder
Neither alters the disease course nor facilitates tendon healing

▸ Slide 676 · Subcoracoid impingementSports · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

Define subcoracoid impingement.
What are the clinical features of subcoracoid impingement and how is the impingement test performed?
Describe the Lafosse classification of subscapularis tears.
How is subcoracoid impingement managed?
What anatomy predisposes to subcoracoid impingement?

Answers · Q & A

Q1.Define subcoracoid impingement.

Impingement of the lesser tuberosity with attached subscapularis on the coracoid during adduction, IR and forward flexion
Similar pathology to subacromial impingement (type 1 replaced with type 2 collagen)
Coracohumeral distance <6mm
Related to subscapularis tear

Q2.What are the clinical features of subcoracoid impingement and how is the impingement test performed?

Posture: 90 degrees FF, adduction + IR
Impingement test: 90 degrees FF with forceful IR
Pain = SST/SSC
LA relief: subacromial -> SST; GHJ -> SSC
Associated with biceps tendinitis

Q3.Describe the Lafosse classification of subscapularis tears.

I: upper 1/3 partial
II: upper 1/3 complete
III: upper 2/3
IV: whole subscapularis, head centred, fatty infiltration 1-3
V: whole subscapularis, anterior subluxation, fatty infiltration 4-5

Q4.How is subcoracoid impingement managed?

Mostly conservative: stretching +/- steroid injection
OT indications: failure of conservative management; large subscapularis tear
Procedure: coracoplasty (7mm clearance between coracoid and subscap) + subscap repair
Open procedure requires reattachment of the conjoint tendon
Type I/II: posterior portal, 1 anchor, single row; III/IV: AL portal, 2-3 anchors, double row; V: salvage

Q5.What anatomy predisposes to subcoracoid impingement?

long/ too lateral coracoid
Post latarjet (lateralized coracoid)
Cuff tear with humeral head superior escape

▸ Slide 677 · Internal impingementSports · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

Define internal impingement of the shoulder.
What is the pathogenesis of internal impingement?
What are the associated lesions, clinical features and X-ray findings?
How is internal impingement managed?
What is GIRD and what are the throwing phases?

Answers · Q & A

Q1.Define internal impingement of the shoulder.

Impingement of the GT with attached SST on the posterosuperior glenoid during abduction, ER and extension

Q2.What is the pathogenesis of internal impingement?

Tight posterior capsule causes microinstability
GIRD (glenohumeral internal rotation deficit)
Humeral head translates posteriorly
Contact point shifts to the posterior and superior glenoid
Posterior articular-sided cuff impinges on abduction + ER (GT and posterosuperior labrum in contact)

Q3.What are the associated lesions, clinical features and X-ray findings?

Associated lesions: SLAP, GIRD
Clinical: same total arc but ER > IR
Posterior pain on apprehension test, relieved with relocated test
XR: Bennett lesion on axillary view; glenoid retroversion from posterosuperior bone loss

Q4.How is internal impingement managed?

Conservative: swimmer's stretch
OT: arthroscopic debridement
Posterior capsulotomy
Anterior plication

Q5.What is GIRD and what are the throwing phases?

GIRD: IR reduced by >25 degrees compared with the contralateral side (IR >25 reduction)
Throwing phases: wind up, early cocking, late cocking, acceleration, deceleration, follow through
In late cocking/acceleration, GIRD changes GHJ kinematics: tight posterior capsule, posterosuperior head shift, stretched anterior capsule, GT abuts posterosuperior labrum

▸ Slide 678 · Rotator cuff arthropathy loss of force couple and fixed fulcrumSports · 6 questions expand

Question list

Q1-Q66 questions — tap to reveal all answerslist

Describe the X-ray findings in rotator cuff arthropathy.
Describe the Hamada classification of rotator cuff arthropathy.
What imaging is needed to work up rotator cuff arthropathy?
What history is important in rotator cuff arthropathy?
What are the treatment options for rotator cuff arthropathy?
What did Gill et al (CORR 2021) conclude about aTSA vs rTSA for primary glenohumeral OA?

Answers · Q & A

Q1.Describe the X-ray findings in rotator cuff arthropathy.

Superior migration of the humeral head
Acetabularization / femoralization
Signs of loss of force couple in the shoulder

Q2.Describe the Hamada classification of rotator cuff arthropathy.

I: AHI >=6mm
II: AHI <=5mm
III: acetabulisation
IV A: GHJ narrow, no acetabulisation
IV B: GHJ narrow with acetabulisation
V: head collapse

Q3.What imaging is needed to work up rotator cuff arthropathy?

Ask for axillary view XR to better appreciate GHJ arthritis
MRI: massive rotator cuff tear with retraction of SS and fat atrophy
CT for glenoid bone stock and version

Q4.What history is important in rotator cuff arthropathy?

Pain
Stiffness
Patient expectations

Q5.What are the treatment options for rotator cuff arthropathy?

Conservative: NSAID, periscapular muscle strengthening, deltoid training
Arthroscopic debridement
Reverse arthroplasty (C/I: young, poor glenoid bone stock, non-functional deltoid)
Other: resection arthroplasty/shoulder fusion (salvage); hemiarthroplasty for pain, not function

Q6.What did Gill et al (CORR 2021) conclude about aTSA vs rTSA for primary glenohumeral OA?

No survivorship difference at 4 years between rTSA and aTSA
Differences exist in revision risk between men and women
Surgeons might select aTSA with an all-polyethylene glenoid to treat OA, despite the current popularity of rTSA

▸ Slide 679 · Classical indicationSports · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

What are the classical indications and prerequisites for reverse shoulder arthroplasty (RSA)?
What are Grammont's principles of RSA?
What are the keys to success and the key steps of RSA?
What are the complications of RSA and what is the Sirveaux classification?

Answers · Q & A

Q1.What are the classical indications and prerequisites for reverse shoulder arthroplasty (RSA)?

Elderly osteoporotic displaced 4-part fracture with comminuted tuberosities
Cuff deficient (even 2 or 3 part fracture)
Prerequisites: good glenoid bone stock, good deltoid power

Q2.What are Grammont's principles of RSA?

Medialised centre of rotation increases deltoid moment arm (effective lever arm from the start of movement) and recruits more deltoid fibres for FF/abduction; inferiorises to pretension deltoid
Fixed centre of rotation decreases shearing force to the glenoid
Reverse polarity has inherent stability: centripedal forces pass into the glenosphere; deltoid shear converted to compression
Maintenance of external rotation (LD transfer); subscapularis + pectoralis major preserve IR

Q3.What are the keys to success and the key steps of RSA?

Keys: good exposure, correct sizing and version, stable fixation, satisfactory soft tissue tension
Deltopectoral approach, biceps tenotomy, tag GT and LT fragments
Retrieve humeral head, expose glenoid, clear labrum, guide pin, ream and screw baseplate
Glenosphere with slight inferior overhang to prevent notching; trial
Humeral retroversion 10 degrees; 3rd generation cementation; suture cuff to implant

Q4.What are the complications of RSA and what is the Sirveaux classification?

General: bleeding, NV injury, infection, haematoma
Loosening (old lateral COR designs had high glenoid torque)
Inferior scapular notching - Sirveaux classification: pillar, reach lower screw, cross inferior screw, central peg
Dislocation; acromial fracture
Cosmesis - more squaring; lengthening of upper limb; cemented - more infection

▸ Slide 680 · Favard classifcation of glenoid bone erosionSports · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

Which classification is used for glenoid bone erosion in reverse shoulder arthroplasty?
What patient and surgical factors increase notching in RSA?

Answers · Q & A

Q1.Which classification is used for glenoid bone erosion in reverse shoulder arthroplasty?

The Favard classification

Q2.What patient and surgical factors increase notching in RSA?

Patient: rotator cuff arthropathy with a narrowed AHI (76% vs 38% in post-traumatic cases)
Glenoids with superior erosion (type E2 glenoid wear)
MRI grade 3 or 4 fatty infiltration of the infraspinatus
Surgical: anterosuperior approach higher than deltopectoral (86% vs 56%)
Neutral or superiorly tilted baseplates

▸ Slide 681 · Anterior shoulder dislocationSports · 14 questions expand

Question list

Q1-Q1414 questions — tap to reveal all answerslist

What history and examination findings are important in anterior shoulder dislocation?
Which X-rays should you take and how are the special views performed?
What soft tissue injuries are seen on MRI after anterior dislocation?
How do you reduce and immobilise an anterior shoulder dislocation?
Explain the glenoid track / on-off track concept and how it guides surgery.
Compare the Latarjet and Bristow procedures and describe screw fixation.
What are the principles of definitive management in anterior shoulder instability?
How is an arthroscopic Bankart repair performed and when is Latarjet indicated?
What is the remplissage procedure and what are its complications?
What other soft tissue and bony procedures are used for anterior instability?
What are the outcomes and indications after anterior instability surgery?
What is the Stanmore triangle classification of instability?
What are the quoted association rates in anterior dislocation?
What is the instability severity index score (Boileau JBJS 2007)?

Answers · Q & A

Q1.What history and examination findings are important in anterior shoulder dislocation?

Age - redislocation rate by Rowe: <20 years >90%, <30 60%, >40 20%
Cofield: 84% athlete vs 30% non-athlete
Times of dislocation, mechanism, occupation and sport, comorbid NM conditions
PE: direction of instability, generalized ligamentous laxity, associated injury (cuff tear, SLAP, axillary nerve palsy 5%), infraclavicular plexus injuries

Q2.Which X-rays should you take and how are the special views performed?

AP: fracture GT, Hill-Sachs lesion
Axillary view / Velpeau axillary view
Stryker notch (Hill-Sachs): supine, cassette under shoulder, palm on head, beam 10 degrees cephalic
West point (Bankart): prone, shoulder on 7.5cm pad, arm 90 abducted, beam centred 25deg down and 25deg medial
CT: glenoid inverted pear appearance, size of Hill-Sachs (70%), whether on or off track

Q3.What soft tissue injuries are seen on MRI after anterior dislocation?

Bankart (90%)
Labroligamentous complex + periosteal tear: Perthes, ALPSA (medial reattachment), GLAD
HAGL
Cuff tear (30-80% depending on age)
SLAP (7%)

Q4.How do you reduce and immobilise an anterior shoulder dislocation?

Reduction: traction-countertraction, Hippocratic, Stimson, Kocher (ER manoeuvre)
Immobilise in IR for 2 weeks
Itoi showed ER immobilisation decreased dislocation rate from 50% to 30%, but it could not be reproduced (compliance)
AJSM 2015 meta-analysis: ER immobilisation no improvement, duration does not matter
Cochrane review 2019: no difference

Q5.Explain the glenoid track / on-off track concept and how it guides surgery.

Glenoid track = contact point of glenoid and humeral head in functional abd + ER = 83% of glenoid width (0.83D - d)
Hill-Sachs interval (HSI) = distance from infraspinatus attachment to medial rim of the Hill-Sachs lesion
HSI larger than glenoid track = off-track (engaging) lesion
Bipolar bone loss concept predicts the risk of dislocation from pathological engagement of the hillsach lesion with the glenoid bone loss
Glenoid bone loss <25%: on track = Bankart; off track = Bankart + remplissage
Glenoid bone loss >25%: on track = Latarjet; off track = Latarjet +/- remplissage

Q6.Compare the Latarjet and Bristow procedures and describe screw fixation.

Size: Bristow = coracoid tip; Latarjet = entire coracoid (anterior to CC)
Position: Bristow <5mm from glenoid rim; Latarjet flush with rim
Orientation: Bristow not rotated; Latarjet rotated 90 degrees (concavity along glenoid)
Fixation: Bristow 1 screw; Latarjet 2 screws (4.0 cannulated or 4.5 cortical, below equator, <15 degrees divergent, within 5mm of rim)
Effect: Bristow = checkrein; Latarjet = triple block (bone, conjoint tendon sling, capsule repair)
Complications: nonunion, migration, cartilage injury, weak IR, stiff ER, lateral bone block -> OA

Q7.What are the principles of definitive management in anterior shoulder instability?

Definitive management depends on: patient's age and activity level, number of dislocations, and associated injury
Aim: restore the bony and soft tissue stabilizers of the shoulder, solid post-op rehab for early return to sport
C/I to surgery: multidirectional instability, uncontrolled epilepsy, voluntary dislocation

Q8.How is an arthroscopic Bankart repair performed and when is Latarjet indicated?

Arthroscopic Bankart repair restores the bumper + hammock effect of the labrum
Latarjet if bony Bankart >25%, as soft tissue Bankart repair alone has up to 70% failure with recurrent dislocation
Transfer coracoid with conjoint tendon (not CC ligament) through a vertical slit in subscap to the glenoid defect, fixed with screw anteroinferior

Q9.What is the remplissage procedure and what are its complications?

Indication: large (>25%) and engaging Hill-Sachs lesion
Suture infraspinatus and posterior capsule to the Hill-Sachs lesion, making the lesion extra-capsular
If >30%, may need bone graft or even osteotomy
Complications: loss of ER (especially with Latarjet), stiff IR (posterior tightness), dehiscence (partial filling)

Q10.What other soft tissue and bony procedures are used for anterior instability?

Capsular shift if ligamentous laxity: tighten the anterior capsule, less ER, reduces the chance to engage (indirect)
External osteotomy of the proximal humerus or fill with bone graft for a large Hill-Sachs lesion
Subscapularis operations: Putti-Platt (double-breast subscap and anterior capsule), Magnuson-Stack (lateral subscap shift)

Q11.What are the outcomes and indications after anterior instability surgery?

Young + male more recurrence, but symptom-free in between
If operated, recurrence 5%, may lose ER
No difference in outcome if operated early (after 1st time) or later (after 3-4th time)
Thus the common indications are apprehension and recurrent dislocation

Q12.What is the Stanmore triangle classification of instability?

1. Structural, traumatic
2. Structural, atraumatic
3. Non-structural, muscle patterning

Q13.What are the quoted association rates in anterior dislocation?

Bankart: acute 94%, chronic 49%
Hill-Sachs: 74%
Cuff tear: 30% (40s), 80% (60s)
Axillary nerve: 5%
Glenoid track (Yamamoto JBJS 2007); on/off track (Di Giacomo JARS 2014)

Q14.What is the instability severity index score (Boileau JBJS 2007)?

Patient <20 years: 0/2 points
Competitive sport, contact sport or forced overhead activity: 0/1 or 0/2
Shoulder hyperlaxity: 0/1
Hill-Sachs: 0/2, or loss of the sclerotic inferior glenoid contour: 0/2
>6/10 = recurrence risk of 70%, so Latarjet is needed

▸ Slide 682 · Bankart avulsion of IGHL anterior band + torn periosteumSports · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

What is a Bankart lesion?
What is a GLAD lesion?
What is an ALPSA lesion?
What is a Perthes lesion?

Answers · Q & A

Q1.What is a Bankart lesion?

Avulsion of the IGHL anterior band + torn periosteum

Q2.What is a GLAD lesion?

Glenoid labral articular defect
Shearing off of a portion of articular cartilage together with the labrum

Q3.What is an ALPSA lesion?

Anterior labral periosteal sleeve avulsion
Labrum-ligament complex detaches then reattaches medially and inferiorly

Q4.What is a Perthes lesion?

Labrum-ligament + periosteum stripped off in continuity and not reattached

▸ Slide 683 · AP Xray of shoulder:Sports · 8 questions expand

Question list

Q1-Q88 questions — tap to reveal all answerslist

Describe the AP X-ray findings in posterior shoulder dislocation.
What are the indications for open surgery and how is reduction performed?
What special tests and MRI findings relate to posterior instability?
What are the surgical options for posterior instability?
How is a chronic (delayed more than 2 weeks) posterior dislocation managed?
Describe the McLaughlin procedure and its modification.
What are the primary stabilizers against posterior dislocation?
How are posterior dislocations classified?

Answers · Q & A

Q1.Describe the AP X-ray findings in posterior shoulder dislocation.

Incongruent GHJ; disruption of Maloney's line (normal parabola)
Light bulb sign: internal rotation with loss of humeral head profile
Trough sign: impaction fracture over the anteromedial humeral head (reverse Hill-Sachs)
Vacant glenoid/rim sign: medial humerus to medial glenoid clear space >6mm
Reduced elliptical overlap; associated fractures; need scapular Y or axillary view to confirm
Causes: trauma 50% (fall on adducted IR arm), convulsion, electrical shock

Q2.What are the indications for open surgery and how is reduction performed?

Initial management: ATLS/associated injury; less likely axillary nerve or cuff injury; Plain CT to look for indications for open surgery
Major displaced LT fracture; large posterior glenoid fragment
Reverse Hill-Sachs (anteromedial) engaged with posterior glenoid or >20% humeral head involvement
Irreducible/impaction fracture
CR under GA (usually muscular man) by Delpalma method (in-line traction, adduct + IR, lateral lift + ER)
Intra-op check congruent reduction, stability and range; immobilise in ER and abduction
Convert to open via deltopectoral approach; may address bone defect at the same time

Q3.What special tests and MRI findings relate to posterior instability?

MRI: cuff, reverse Bankart, reverse HAGL, POLPSA
Kim test: seated, 90 abd + firm axial load, further 45 elevation with down/backward force; pain +/- clunk = posteroinferior labral tear
Jerk test: 90 abd + 90 IR, axial humeral force then adduction to FF; clunk = posterior labral or posterior subluxation
Posterior load and shift (under GA): 1 not to rim, 2 to rim, 3 beyond rim, 4 dislocation

Q4.What are the surgical options for posterior instability?

Indications: large bone loss, irreducible, unstable/recurrent instability
Soft tissue (reduce intracapsular volume): reverse Bankart repair, closure of rotator interval (reverse remplissage)/inferior capsule
Glenoid: bone graft if large reverse Bankart; posterior opening wedge osteotomy if excessive glenoid retroversion
Humerus <30%: disimpaction + bone grafting, modified McLaughlin, McLaughlin, rotational osteotomy
Humerus >30%: allograft, hemiarthroplasty

Q5.How is a chronic (delayed more than 2 weeks) posterior dislocation managed?

Pathology - bone: cartilage damage, bone loss, osteoporosis; soft tissue: capsulolabral injury, cuff tear, contracture, adherence to NV bundle
<4 weeks: try gentle CR; >4 weeks: OR
Humeral bone loss <40%: McLaughlin, cortical window to disimpact + bone graft, rotational osteotomy
Humeral bone loss >40%: young = bone graft; old = hemi or RSA
Glenoid loss >25%: reverse Bristow; redundant capsule: inferior/lateral capsular shift
During open reduction do not do subscap tenotomy - reserve for McLaughlin

Q6.Describe the McLaughlin procedure and its modification.

Classically via deltopectoral approach
A reverse remplissage: capsule + rotator interval + subscapularis filled into the defect
Modified McLaughlin adds LT transfer: better bone healing, more secure fixation

Q7.What are the primary stabilizers against posterior dislocation?

Posterior band of the IGHL
Subscapularis
Coracohumeral ligament (CHL)

Q8.How are posterior dislocations classified?

By timing: acute vs chronic
By underlying pathology: volitional, dysplastic, acquired

▸ Slide 684 · MechanismSports · 6 questions expand

Question list

Q1-Q66 questions — tap to reveal all answerslist

What is the mechanism of inferior shoulder dislocation (luxatio erecta)?
What are the clinical features of inferior shoulder dislocation?
What associated injuries must be assessed for in inferior shoulder dislocation?
How is closed reduction performed in inferior shoulder dislocation?
What is the management of inferior shoulder dislocation?
What is the outcome after inferior shoulder dislocation?

Answers · Q & A

Q1.What is the mechanism of inferior shoulder dislocation (luxatio erecta)?

Forceful abduction
Levering the humeral head against the acromion out inferiorly

Q2.What are the clinical features of inferior shoulder dislocation?

Salute position: locked humeral head at 110-160 degrees abduction
Palpable humeral head at lateral chest wall and axilla
May buttonhole through the inferior capsule, necessitating open reduction

Q3.What associated injuries must be assessed for in inferior shoulder dislocation?

Cuff / labrum / IGHL injury
Nerve: brachial plexus and axillary nerve injury
Vascular: axillary artery and DCT injury

Q4.How is closed reduction performed in inferior shoulder dislocation?

Traction and countertraction
Traction along the humeral shaft
Countertraction: bedsheet across the superior shoulder/neck
Gradual reduction with adduction

Q5.What is the management of inferior shoulder dislocation?

Mostly conservative
Surgery for subcutaneous humeral head, NV injury, or recurrent dislocation

Q6.What is the outcome after inferior shoulder dislocation?

Groh JSES 2010 / Malon 1990: 83% excellent/good for range and pain
NV injury NOT associated with outcome

▸ Slide 685 · Identify the structureSports · 7 questions expand

Question list

Q1-Q77 questions — tap to reveal all answerslist

Which structures should you identify on this arthroscopic view?
What is the anatomy and contents of the rotator interval?
What is frozen shoulder?
What are the associations of frozen shoulder?
What are the Reeves stages and MRI findings in frozen shoulder?
How is frozen shoulder managed and what did the FROST trial show?
Describe the Naviaser arthroscopic classification of frozen shoulder.

Answers · Q & A

Q1.Which structures should you identify on this arthroscopic view?

Long head of biceps and the biceps labral complex
Glenoid and anterior labrum
Subscapularis and the rotator interval
Humeral head

Q2.What is the anatomy and contents of the rotator interval?

Space between the supraspinatus and subscapularis
Contents: SGHL, coracohumeral ligament, long head of biceps, capsule
Diseases related to the rotator interval: frozen shoulder (tightening), LHB dislocation

Q3.What is frozen shoulder?

Adhesive capsulitis: global loss of active and passive ROM
Scarring and contracture of soft tissue (myofibroblast proliferation -> collagen type III), mainly involving rotator interval and coracohumeral ligament
Presents with pain and global stiffness, especially limited ER

Q4.What are the associations of frozen shoulder?

Immobilisation of the shoulder
Previous shoulder pathology (cuff tear, dislocation) or lung/breast/shoulder surgery
DM (poor prognosis)
Thyroid disease
Dupuytren contracture
Distal clavicle OT

Q5.What are the Reeves stages and MRI findings in frozen shoulder?

Painful phase: 3-9 months
Frozen phase: 4-9 months
Thawing phase: 5-26 months
MRI: thickened IGHL
Loss of joint volume (loss of axillary recess on arthrogram)

Q6.How is frozen shoulder managed and what did the FROST trial show?

Physio + injection (only in painful phase)
MUA (FEAR: flexion-extension-abduction-rotation); cons: labral injury, fracture
Arthroscopic capsular release after frozen phase: rotator interval release to gain ER, posterior capsule release to gain IR (270 degrees)
FROST trial (Lancet 2020): early structured PT, MUA and arthroscopic release - none superior for pain and function at 12 months
MUA is most cost effective; arthroscopic release carries increased risk

Q7.Describe the Naviaser arthroscopic classification of frozen shoulder.

Stage 1: erythematous/fibrinous synovium
Stage 2: red, angry, thick synovium; thick contracted interval; tight joint space; adhesions in the inferior fold
Stage 3: pink synovium
Stage 4: no evidence of synovitis but persistent tight inferior fold and joint

▸ Slide 686 · Histological layers of the cuffSports · 7 questions expand

Question list

Q1-Q77 questions — tap to reveal all answerslist

How many histological layers make up the rotator cuff and what is each layer?
Which layer of the cuff forms the rotator cable and what is it made of?
Which arteries supply the rotator cuff?
Between which layers of the cuff does the blood supply run?
What is the critical zone of Codman?
Which side of the rotator cuff is more vascular and which side is stronger?
On which side do most rotator cuff tears occur?

Answers · Q & A

Q1.How many histological layers make up the rotator cuff and what is each layer?

Layer 1: 1mm, coracohumeral ligament (CHL) fibres
Layer 2: 3-5mm, dense fibres parallel to the tendon
Layer 3: 3mm, loose fibres at 45 degrees to the tendon
Layer 4: thick collagen bands merging with CHL (rotator cable)
Layer 5: 2mm, shoulder capsule

Q2.Which layer of the cuff forms the rotator cable and what is it made of?

Layer 4: thick collagen bands that merge with the CHL
This structure is the rotator cable

Q3.Which arteries supply the rotator cuff?

Subscapular artery (Subscap A)
Suprascapular artery (Suprascap A)
AHCA and PHCA

Q4.Between which layers of the cuff does the blood supply run?

Between layers 2 and 3

Q5.What is the critical zone of Codman?

1cm from the humeral tuberosity insertion

Q6.Which side of the rotator cuff is more vascular and which side is stronger?

The bursal side is more vascular
The articular side has only half the strength of the bursal side

Q7.On which side do most rotator cuff tears occur?

Most tears are articular sided

▸ Slide 687 · Describe MRI:Sports · 12 questions expand

Question list

Q1-Q1212 questions — tap to reveal all answerslist

What did the MRI arthrogram show?
What does SLAP stand for and what is it associated with?
Describe the Snyder classification of SLAP lesions.
What is the history and what examination tests are used for a SLAP lesion?
Describe how the crank test is performed and what counts as positive.
What X-ray finding suggests internal impingement?
What is the function of the SLAP/biceps complex?
What are the normal labral variants and their frequencies?
What is the nerve supply of each rotator cuff muscle?
Where can the suprascapular nerve be compressed and what is the effect?
What will you look for on physical exam if there is a cyst at the spinoglenoid notch?
What is the treatment and rehabilitation after a SLAP lesion?

Answers · Q & A

Q1.What did the MRI arthrogram show?

Signal change/linear signal at the superior labrum, likely SLAP lesion
Cystic lesion at the spinoglenoid notch

Q2.What does SLAP stand for and what is it associated with?

Superior Labrum from Anterior to Posterior tear
Associations: cuff tear, shoulder dislocation
Internal impingement (frequent thrower), GIRD

Q3.Describe the Snyder classification of SLAP lesions.

I: fraying of superior labrum
II: biceps anchor detachment + labral fraying
III: superior labrum bucket-handle tear
IV: bucket-handle tear with extension into biceps
V: SLAP + Bankart; VI: SLAP + labral flap; VII: SLAP + extension into MGHL origin
Types 5-7 are the Maffet modification (total 7 types)

Q4.What is the history and what examination tests are used for a SLAP lesion?

Hx: deep shoulder pain, clicking; acute traction injury or recurrent throwing action
PE: O'Brien's test, crank test, anterior shoulder instability
SLAP lesion increases strain on the anterior band of IGHL
Scapular dyskinesia

Q5.Describe how the crank test is performed and what counts as positive.

Sitting, arm flexed to 90 degrees; examiner adjacent to affected shoulder holds the flexed elbow/forearm
Joint load applied along the axis of the humerus with one hand; the other hand performs humeral rotation while the shoulder is elevated in the scapular plane
Can be repeated supine
Positive if symptoms reproduced (usually pain), with or without a click, usually during external rotation

Q6.What X-ray finding suggests internal impingement?

Bennett lesion

Q7.What is the function of the SLAP/biceps complex?

Restraint to external rotation, anterior and inferior translation
Depresses the humeral head in abduction and external rotation

Q8.What are the normal labral variants and their frequencies?

Normal 85%
Sublabral foramen 12%: 1-3 o'clock, medial extension of contrast rather than lateral, smooth margin, <3mm, at biceps origin
Buford complex (absent labrum + cord-like MGHL) 1.5%
Sublabral foramen + cord-like MGHL 1%; meniscoid 1%

Q9.What is the nerve supply of each rotator cuff muscle?

Supraspinatus/infraspinatus: suprascapular nerve
Teres minor: axillary nerve
Subscapularis: upper and lower subscapular nerves

Q10.Where can the suprascapular nerve be compressed and what is the effect?

Suprascapular notch (suprascapular ligament): affects both SS and IS; suprascapular artery runs above the ligament; ganglion cyst from labral injury, fracture callus
Spinoglenoid notch (spinoglenoid ligament): affects IS only; paralabral ganglion cyst from SLAP/posterior labral tear, traction injury in volleyball players
Cyst at spinoglenoid notch: infraspinatus weakness (ER with arm at side) with no scar or winging
Ddx: C5 palsy, brachial plexus injury
Treatment: conservative; surgical excision of SOL/release of spinoglenoid ligament

Q11.What will you look for on physical exam if there is a cyst at the spinoglenoid notch?

Infraspinatus weakness (external rotation with the arm on the side) with no scar or winging
Ddx: C5 palsy, brachial plexus injury

Q12.What is the treatment and rehabilitation after a SLAP lesion?

Conservative or operation: type 1/3 debridement, type 2 repair
Type 4: debridement +/- biceps tenodesis if large biceps tendon involvement
Rehab: 1-4 weeks active + passive assisted flexion in scapular plane; 4-12 weeks active ROM and isometrics; 12 weeks onwards strengthening
Return to sports at 6 months

▸ Slide 688 · Humeral Avulsion of the Glenohumeral Ligament (HAGL)Sports · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

What is a HAGL lesion and why does it matter?
Which part of the IGHL is involved and what are the patterns of failure?
What is the association of HAGL with instability and failed stabilization?
What MRI sign is seen in HAGL and what is the West Point classification?
What is the management and rehabilitation of HAGL?

Answers · Q & A

Q1.What is a HAGL lesion and why does it matter?

Humeral Avulsion of the Glenohumeral Ligament
Injury to the inferior glenohumeral ligament causing instability/pain
Commonly a missed cause of recurrent shoulder instability

Q2.Which part of the IGHL is involved and what are the patterns of failure?

Anterior band most common (93%)
Medial (glenoid) versus lateral (humerus)
Failure at labral complex 40% > intrasubstance tear 35% > humeral insertion 25%

Q3.What is the association of HAGL with instability and failed stabilization?

10% of recurrent anterior shoulder dislocators
20% of failed anterior stabilization
30% of shoulder instability patients without a Bankart lesion

Q4.What MRI sign is seen in HAGL and what is the West Point classification?

MRI: J sign at the inferior pouch
West Point classification: posterior/anterior; bony/soft tissue; with or without Bankart

Q5.What is the management and rehabilitation of HAGL?

Conservative: 90% success
Open or arthroscopic repair: similar outcome
Rehab: anterior lesion limit ER; posterior lesion limit IR
Good prognosis

▸ Slide 689 · Which photo shows popeye sign?Sports · 14 questions expand

Question list

Q1-Q1414 questions — tap to reveal all answerslist

What does the popeye sign indicate?
What do you consider when managing a long head of biceps rupture?
What are the physical examination findings in a long head of biceps rupture?
What are the physical examination findings of a distal biceps rupture?
What factors are considered in managing a distal biceps tendon rupture?
What are the risk factors for distal biceps tendon rupture?
What investigations are performed for a distal biceps tendon rupture?
When is a distal biceps rupture treated conservatively versus operatively?
What are the treatment options for long head of biceps rupture?
How is distal biceps repair performed and what are the complications?
What fixation options are used for distal biceps repair?
What is the anatomy and blood supply of the biceps tendon relevant to rupture?
What are false positives for the hook test?
What are the biomechanical tolerances of the distal biceps tendon?

Answers · Q & A

Q1.What does the popeye sign indicate?

Left: long head of biceps rupture with Popeye sign
Right: reverse popeye sign = distal biceps tendon rupture

Q2.What do you consider when managing a long head of biceps rupture?

Age
Power (supination)
Pain due to biceps tendinitis
Cosmesis
Associated injury (rotator cuff tear)

Q3.What are the physical examination findings in a long head of biceps rupture?

Tenderness over the biceps groove
Assess cuff power
Elbow flexion and forearm supination power

Q4.What are the physical examination findings of a distal biceps rupture?

Hook test from lateral to medial (from medial blocked by lacertus fibrosis)
Ruland biceps squeeze test
Loss of biceps tracking with passive forearm rotation
Supination loss 50%, flexion loss 30%, endurance loss 80-90%

Q5.What factors are considered in managing a distal biceps tendon rupture?

Age and function
Power
Cosmesis
Chronicity of tear
Degree of tear

Q6.What are the risk factors for distal biceps tendon rupture?

Steroid use and smoking
Male, dominant hand
Prexisting pain (radiobicipital bursitis)

Q7.What investigations are performed for a distal biceps tendon rupture?

XR to rule out avulsion fractures
MRI: retraction and partial vs complete tear

Q8.When is a distal biceps rupture treated conservatively versus operatively?

Conservative in low functional demand (accepts 50% supination, 30% flexion loss, 80-90% endurance loss)
Operative in young and fit patients to regain supination power
Perform within weeks

Q9.What are the treatment options for long head of biceps rupture?

Tenodesis to proximal humerus (suture anchor/interference screw/keyhole procedure)
Tenodesis: improve ~10% flexion power only, improve cosmesis
Tenotomy for biceps tendinosis/subluxation with pain in a low-demand patient
Approach: arthroscopic or mini-open

Q10.How is distal biceps repair performed and what are the complications?

Single incision: cubital fossa transverse incision (BR/PT); protect LABCN (exits between biceps and brachialis) and PIN by lateral retraction + supination; ligate recurrent radial artery lying superficial to biceps tendon; locate radial tuberosity; incise radiobicipital bursa
Single incision: decreased risk of synostosis/HO but more LABCN injury
Two incision: posterior approach at PL elbow (ECU/EDC, between Kocher and Kaplan); less dissection to antebrachial fossa, less radial nerve/PIN injury but more synostosis (disrupts IOM + ulnar periosteum)
Complications: LABCN injury, SRN injury, PIN injury, synostosis, HO, proximal radius fracture

Q11.What fixation options are used for distal biceps repair?

Single incision: suture anchor / cortical button / bioabsorbable screw
JBJS 2014 systematic review: lower complication rate with cortical button
Double incision: pull-through suture

Q12.What is the anatomy and blood supply of the biceps tendon relevant to rupture?

LH biceps: further from the forearm rotational axis, supinator, inserts at proximal aspect of radial tuberosity
SH biceps: flexor, inserts at distal aspect of radial tuberosity
Blood supply: proximal brachial artery, distal posterior interosseous artery; watershed area at zone 2

Q13.What are false positives for the hook test?

False positive for positive hook test:
Bicipital aponeurosis
Partial tear
Underlying brachialis tendon

Q14.What are the biomechanical tolerances of the distal biceps tendon?

Elbow at 90 degrees, no load: distal biceps sustains 50N
Elbow at 90 degrees with 1kg load: 112N
Force to rupture 200N
Repair needs to withstand 50N

▸ Slide 690 · Shoulder arthrodesisSports · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

What is the goal of shoulder arthrodesis?
What are the indications and contraindications for shoulder arthrodesis?
What position is the shoulder arthrodesed in?
Describe the technique of shoulder arthrodesis.

Answers · Q & A

Q1.What is the goal of shoulder arthrodesis?

Stable base for the upper limb optimizing hand and elbow function
Rest at side without excess scapular winging
Reach head for combing, midline for dressing, back pocket

Q2.What are the indications and contraindications for shoulder arthrodesis?

Indications: stabilize paralytic disease (brachial plexus injury); recurrence of instability with multiple failed operations; irreparable deltoid and cuff arthropathy
C/I: advanced bilateral shoulder disease, contralateral arthrodesis, ipsilateral elbow arthrodesis
C/I: no scapulothoracic movement (need residual 60 degrees scapulothoracic movement)

Q3.What position is the shoulder arthrodesed in?

30 degrees abduction
30 degrees forward flexion
30 degrees internal rotation

Q4.Describe the technique of shoulder arthrodesis.

Cuff resected; LH biceps tenodesis; decortication
Extra-articular: 4.5mm recon plate from scapular spine/acromion to humeral shaft
Intra-articular: humeral head to glenoid neck; acromion to humeral head; clavicle to glenoid
Check intraoperatively able to reach mouth and adduction close to body

▸ Slide 691 · Calcified tendinitisSports · 4 questions expand

Question list

Q1-Q44 questions — tap to reveal all answerslist

What is the pathophysiology of calcific tendinitis?
Describe the Uhthoff classification of calcific tendinitis.
What is calcific tendinitis associated with and how is it investigated?
What is the treatment of calcific tendinitis?

Answers · Q & A

Q1.What is the pathophysiology of calcific tendinitis?

Local ischemia at codman zone -> fibrocartilaginous metaplasia -> CaHA deposition -> inflammation
Resorption phase: CaHA dissolution and engulfment by macrophages
HA - Alizarin red staining +

Q2.Describe the Uhthoff classification of calcific tendinitis.

Pre-calcific phase: fibrocartilaginous metaplasia leading to crystal deposition
Calcific phase: formative, resting, resorptive (phagocytic action, most painful)
Post-calcific phase: restoration of fibroblasts

Q3.What is calcific tendinitis associated with and how is it investigated?

Subacromial impingement, DM, hypothyroidism
MRI to look for a cuff tear

Q4.What is the treatment of calcific tendinitis?

Conservative: NSAIDs, physiotherapy, steroid
USG-guided aspiration and lavage (barbotage): 2 needles, one in one out
Surgical decompression

▸ Slide 692 · What does these photo shows and what are the underlying pathology?Sports · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

What do the photos show and what is the underlying pathology?
What are the causes and management of medial scapular winging?
What are the causes and management of lateral scapular winging?

Answers · Q & A

Q1.What do the photos show and what is the underlying pathology?

Left: lateral winging of scapula -> trapezius weakness due to accessory nerve palsy
Other cause of lateral winging: rhomboid weakness due to dorsal scapular nerve
Right: medial winging -> serratus anterior weakness due to long thoracic nerve palsy

Q2.What are the causes and management of medial scapular winging?

Causes: overhead activity with head tilted to the other side; iatrogenic during anaesthesia
Mx: observe for 6 months, then pect major transfer (pectoralis major transfer)

Q3.What are the causes and management of lateral scapular winging?

Causes: iatrogenic during lymph node dissection
Mx: observe; if failed, Eden-Lange levator scapulae and rhomboid transfer (medial border to lateral border)

▸ Slide 693 · Xray showing ACJ dislocation with marked superior displacement of the distal endSports · 7 questions expand

Question list

Q1-Q77 questions — tap to reveal all answerslist

What does the X-ray show and what must be considered?
How is an ACJ injury assessed?
How does the Rockwood classification guide management?
How does the surgical treatment differ between acute and chronic ACJ dislocation?
What is the modified Weaver-Dunn procedure?
What is done for isolated ACJ arthritis without instability, and what is the ACJ anatomy?
What happens if an ACJ dislocation is left untreated?

Answers · Q & A

Q1.What does the X-ray show and what must be considered?

ACJ dislocation with marked superior displacement of the distal clavicle
Associated fracture, especially floating shoulder
Will need further X-ray to classify; start with history and examination

Q2.How is an ACJ injury assessed?

Acute versus chronic (>3 weeks)
Compare contralateral side; axillary view (AP translation)
Zanca view: 10 degrees cephalic tilt (vertical translation); +/- stress view

Q3.How does the Rockwood classification guide management?

1-3: static stabilizers disrupted (AC sprain, AC torn, CC torn) -> conservative
4-6: dynamic (posterior through trapezius, deltoid + trapezius torn, inferior below coracoid) -> surgical
3 +/- operation

Q4.How does the surgical treatment differ between acute and chronic ACJ dislocation?

Acute – repair; CC fixation with Bosworth screw, CC sling, fibre tape or tightrope
ACJ fixation: hook plate
If associated arthritis: modified Weaver-Dunn
Chronic – reconstruct; with ACJ arthrosis, resect the distal clavicle

Q5.What is the modified Weaver-Dunn procedure?

Excision of distal clavicle
Transfer of the acromial end of the CA ligament to the distal clavicle
CC fixation
Repair of the deltotrapezial fascia

Q6.What is done for isolated ACJ arthritis without instability, and what is the ACJ anatomy?

Excision of 7-8mm (<1.5cm) of distal clavicle (too much jeopardizes capsule); can be done arthroscopically
ACJ is a diarthrodial joint with an articular disc connecting axial to appendicular skeleton
Stabilizers: superior (most important)/anterior/posterior/inferior; ~8 degrees rotation; Kenny Howard brace

Q7.What happens if an ACJ dislocation is left untreated?

The shoulder becomes protracted

▸ Slide 694 · GHJ arthritisSports · 7 questions expand

Question list

Q1-Q77 questions — tap to reveal all answerslist

What are the causes of glenohumeral arthritis?
What is the primary OA triad and X-ray finding?
What are the nonoperative and operative options for GHJ arthritis?
What are the contraindications, survival and complications of total shoulder arthroplasty?
When are hemiarthroplasty and reverse shoulder arthroplasty indicated?
When is arthroscopic debridement or a CAM procedure performed?
When is shoulder arthrodesis indicated in glenohumeral arthritis?

Answers · Q & A

Q1.What are the causes of glenohumeral arthritis?

More common in females
Primary osteoarthritis
Secondary: post-traumatic, arthritis of dislocation, inflammatory/crystalline arthritis, osteonecrosis, neuropathic (Charcot arthropathy)
Rotator cuff arthropathy

Q2.What is the primary OA triad and X-ray finding?

Anterior capsular contracture, posterior glenoid wear, posterior humeral subluxation
XR: osteophytes circumferentially at the humeral head, "goat's beard"

Q3.What are the nonoperative and operative options for GHJ arthritis?

Nonoperative: physical therapy, NSAIDs, intra-articular injections
Operative: total shoulder arthroplasty, hemiarthroplasty, reverse shoulder arthroplasty
Also arthroscopic debridement, CAM procedure, arthrodesis

Q4.What are the contraindications, survival and complications of total shoulder arthroplasty?

C/I: lack of deltoid or rotator cuff function, active infection, Charcot arthropathy
10-year survival 92-95%
Complications: glenoid/humeral component loosening, infection, fracture, nerve injury, cuff tear
Higher prosthetic joint infection risk within 3 months of prior arthroscopy

Q5.When are hemiarthroplasty and reverse shoulder arthroplasty indicated?

Hemi: younger patient, irreparable RC tear + insufficient bone stock, osteonecrosis without glenoid involvement
Ream-and-run over glenoid has early failure, not recommended, poorer outcomes
RSA: irreparable/large RC tear with intact deltoid; 10-year survival ~90-95%
RSA complications: scapular notching, infection, dislocation/instability, nerve injuries (higher than TSA)

Q6.When is arthroscopic debridement or a CAM procedure performed?

Debridement: mild-moderate OA without structural alteration; mechanical symptoms from loose bodies or small humeral head lesions due to AVN
CAM (comprehensive arthroscopic management): younger patient
Debridement, chondroplasty, synovectomy, loose body removal, humeral osteoplasty (goat's beard), capsular release, decompressions, axillary nerve decompression, biceps tenodesis

Q7.When is shoulder arthrodesis indicated in glenohumeral arthritis?

Paralysis, recurrent infection, severe soft tissue deficiency, failed replacement surgery

▸ Slide 695 · AVN of humeral headSports · 3 questions expand

Question list

Q1-Q33 questions — tap to reveal all answerslist

What is the most common initial site of avascular necrosis of the humeral head?
What is the nonoperative management of humeral head AVN?
What operations are used for humeral head AVN and when?

Answers · Q & A

Q1.What is the most common initial site of avascular necrosis of the humeral head?

Superior middle portion of the humeral head
Aetiology is similar to avascular necrosis of the hip

Q2.What is the nonoperative management of humeral head AVN?

Pain medications, activity modification, physical therapy
Operative treatment depends on the Cruess stage of disease

Q3.What operations are used for humeral head AVN and when?

Core decompression + arthroscopy (confirm cartilage integrity) for early disease (Cruess I-II)
Humeral head resurfacing for stage III with focal chondral defects and sufficient epiphyseal bone stock
Hemiarthroplasty for moderate disease (Cruess III-IV)
Total shoulder arthroplasty for advanced stage (Cruess V)

▸ Slide 696 · Femoral acetabular impingementSports · 9 questions 1 check expand

Question list

Q1-Q99 questions — tap to reveal all answerslist

What are the X-ray findings in femoroacetabular impingement?
What are the symptoms and signs of FAI?
Describe the alpha angle and its normal and abnormal values.
What other radiographic measurements are used in FAI?
What is the role of CT and MRI/MR arthrogram in FAI?
What are the treatment options and what does hip arthroscopy involve?
What are the indications for hip arthroscopy?
What are the compartments examined in hip arthroscopy and which require traction?
What are the portals used in hip arthroscopy?

Answers · Q & A

Q1.What are the X-ray findings in femoroacetabular impingement?

Cam lesion at the femoral neck: pistol grip appearance, decreased neck offset, aspherical head (SCFE, Perthes, fracture malunion)
Pincer lesion: anterosuperior acetabular rim overhanging
Retroversion: cross cover sign, posterior wall medial to femoral head centre, prominent ischial spine
Coxa profunda vs protrusio (head medial to ilioischial line); excessive CEA

Q2.What are the symptoms and signs of FAI?

Previous injury or childhood hip problems
Mechanical hip pain, difficulty sitting, pain in flexion and internal rotation
PE: limited flexion and IR; positive anterior impingement test (FADDIR)

Q3.Describe the alpha angle and its normal and abnormal values.

Angle between the central axis of the femoral neck and the line from femoral head centre to where the head loses sphericity
Normal <42 degrees; >42 degrees suggestive of head-neck offset deformity
>50-55 degrees indicates cam deformity

Q4.What other radiographic measurements are used in FAI?

Head-neck offset ratio: draw 2 lines parallel to neck central axis, one touching anterior head and one touching anterior neck, difference of the 2 lines divided by head diameter; >0.17 normal
CEA >40; anterior CEA >20; herniation pit
False profile view (pelvis 65 degrees from film) for anterior CEA
Dunn view (hip flexion 90, abduction 20, neutral rotation) for CAM

Q5.What is the role of CT and MRI/MR arthrogram in FAI?

CT: bony architecture, measure alpha angle
MRI/MR arthrogram: labral injury (more in pincer lesion), cartilage injury (more in cam lesion)
Countercoup lesion (unfavorable as difficult to attach posterior pathology)

Q6.What are the treatment options and what does hip arthroscopy involve?

Conservative: NSAIDs, physiotherapy
Operative: arthroscopic cam trim +/- labral debridement/repair; Ganz surgical dislocation; periacetabular osteotomy; THR
Hip arthroscopy: GA/SA on traction table, ~50 lb traction (pudendal nerve risk), X-ray guidance, 70 degree scope
Risks: direct cartilage injury, HO, instability from iatrogenic capsular deficiency (prevented by meticulous capsulotomy and closure/plication)
Nerve risks: pudendal (traction), superior gluteal (anterolateral portal), lateral cutaneous nerve of thigh/femoral vessels (anterior portal), sciatic (posterolateral portal), LFCA ascending branch

Q7.What are the indications for hip arthroscopy?

Intra-articular: FAI/labral lesion, chondral lesion, loose bodies, synovial disease
Extra-articular: AIIS impingement, capsular tear, iliopsoas pathology

Q8.What are the compartments examined in hip arthroscopy and which require traction?

Central (intra-articular): acetabular rim and fossa, femoral head, AIIS, capsule - requires traction
Peripheral (lateral to labrum): HN junction, iliopsoas, zona orbicularis, medial synovial fold - no traction needed
Lateral (peritrochanteric): ITB, trochanteric bursa - no traction
Deep gluteal: piriformis, ischial tuberosity (hamstring origin) - no traction

Q9.What are the portals used in hip arthroscopy?

Anterolateral portal first (primary viewing portal): 2cm anterior and superior to anterosuperior corner of GT
Anterior portal (central viewing): intersection of vertical line from ASIS and superior ridge of GT
Distal anterolateral (peripheral viewing): 3-5cm distal to anterolateral portal
Posterolateral (posterior viewing): 1cm posterior and superior to GT

Fact check

Alpha angle normal <42 degrees; >42 degrees is suggestive of a head-neck offset deformity — Misleading threshold: 42 degrees is the mean in normal controls, not a diagnostic cutoff — The usual diagnostic cutoff for cam morphology is >55 degrees (50 widely used); recent syntheses suggest 57-60 degrees and many normal hips exceed 42 degrees — source

▸ Slide 697 · False profile viewSports · 2 questions expand

Question list

Q1-Q22 questions — tap to reveal all answerslist

What is a false profile view used for?
What radiographic parameter is measured on the false profile view?

Answers · Q & A

Q1.What is a false profile view used for?

Not covered in the speaker notes
Slide title: False profile view

Q2.What radiographic parameter is measured on the false profile view?

Not covered in the speaker notes
Slide title: False profile view

▸ Slide 698 · Patient complaining of snapping sound upon hip flexionSports · 5 questions expand

Question list

Q1-Q55 questions — tap to reveal all answerslist

What is coxa saltans and who is affected?
What are the causes of external, internal and intracapsular snapping hip?
How do you examine a snapping hip?
What investigations are used for snapping hip?
What is the management of snapping hip?

Answers · Q & A

Q1.What is coxa saltans and who is affected?

Snapping sound on hip flexion
Common in athletes and dancers in their teens/20s
Usually the patient can reproduce the symptoms; +/- pain

Q2.What are the causes of external, internal and intracapsular snapping hip?

External: posterior IT band sliding over greater trochanter; glut max (gluteus maximus; repeated gluteus injections -> contracture/fibrosis); fibrotic bursa; exostosis
Internal: iliopsoas (prominent iliopectineal ridge, slide over femoral head, iliopsoas bursa, lesser trochanter exostosis)
Intracapsular: loose body, synovial chondromatosis, labral tear

Q3.How do you examine a snapping hip?

External: visible snap; pressing on the greater trochanter abolishes it; Ober’s +ve (limited adduction when hip placed in extension)
Internal: audible snap when hip moves from flexed + ER to extended + IR

Q4.What investigations are used for snapping hip?

X-ray (looking for chondromatosis)
USG (dynamic assessment)
MR arthrogram (rule out loose body/labral tear)
Iliopsoas bursography

Q5.What is the management of snapping hip?

Nonoperative: activity modification, physiotherapy, steroid injection
USG-guided injection (GT bursa, iliopsoas sheath, intra-articular)
Operative: excision of GT bursa with Z-plasty of ITB; release of iliopsoas tendon; resect lesser trochanter (distal part only); removal of loose body or labral repair

▸ Slide 699 · Stress fractureSports · 7 questions expand

Question list

Q1-Q77 questions — tap to reveal all answerslist

Define a stress fracture.
What is the difference between a fatigue and an insufficiency fracture?
What is the pathogenesis of a stress fracture?
What do X-ray, bone scan and MRI show in a stress fracture?
What are the high-risk sites for stress fractures?
What are the sport-specific stress fractures?
What is the Arendt grading and when is operative treatment indicated?

Answers · Q & A

Q1.Define a stress fracture.

A fracture occurring at a stress below the ultimate tensile strength

Q2.What is the difference between a fatigue and an insufficiency fracture?

Fatigue: repetitive stress under ultimate tensile strength and above endurance limit; normal bone; overuse history, insidious onset, prodromal pain, local tenderness/swelling
Insufficiency: normal stress, abnormal bone; sudden pain with no prodromal symptoms

Q3.What is the pathogenesis of a stress fracture?

1. Bone formation < bone resorption
2. Decrease in ultimate tensile strength with time
3. Microfracture, crack initiation and crack propagation

Q4.What do X-ray, bone scan and MRI show in a stress fracture?

X-ray normal in the initial 2-3 weeks; later lucent line with sclerotic edges and periosteal reaction
Bone scan sensitive but not specific
Acute: linear increase in uptake in all 3 phases; healing: normalises sequentially phases 1-3; soft tissue: only phases 1 and 2
MRI: STIR sequence

Q5.What are the high-risk sites for stress fractures?

Tibial anterior cortex
NOF (superolateral), medial malleolus, talus
2nd and 5th metatarsals, patella
Hallux sesamoids

Q6.What are the sport-specific stress fractures?

Runner: tibial shaft, NOF, 2nd metatarsal
Basketball: 5th metatarsal, navicular
Football: metatarsals, hallux sesamoids

Q7.What is the Arendt grading and when is operative treatment indicated?

Grading by Arendt (X-ray, bone scan, MRI)
High grade, high risk -> operative treatment

▸ Slide 700 · Tennis elbowSports · 6 questions expand

Question list

Q1-Q66 questions — tap to reveal all answerslist

What is lateral epicondylitis and what is the pathoanatomy?
What is the differential diagnosis of tennis elbow?
What are the physical examination findings in tennis elbow?
What conservative and operative treatment is used for tennis elbow?
How does the tennis elbow brace work?
What is the evidence for PRP versus corticosteroid in tennis elbow?

Answers · Q & A

Q1.What is lateral epicondylitis and what is the pathoanatomy?

Overuse injury from eccentric overload at the common extensor origin
Microtear begins at the ECRB origin
Histology: angiofibroblastic hyperplasia, disorganized collagen (degenerative process)

Q2.What is the differential diagnosis of tennis elbow?

Cervical radiculopathy
Radiocapitellar OA
Radial tunnel syndrome
PLRI of the elbow

Q3.What are the physical examination findings in tennis elbow?

Tenderness at the ECRB origin
Decreased grip strength (in entrapment syndromes)
Resisted wrist extension with elbow extended; resisted extension of long fingers
Maximum wrist flexion -> pain; passive wrist flexion in pronation -> pain

Q4.What conservative and operative treatment is used for tennis elbow?

Conservative: NSAIDs, physiotherapy, shockwave, brace worn 3-4cm distal to the common extensor origin, steroid/PRP injection
Operative: release and debridement of ECRB origin
Lift ERCL off ECRB (located deep and posterior to ECRL); excise degenerative tissue; decorticate epicondyle; repair capsule if breached; Side to side closure of the tendon

Q5.How does the tennis elbow brace work?

Inhibits the traction force by extensors on the common extensor origin
Inhibits full expansion of the muscle belly
Worn 3-4cm distal to the common extensor origin

Q6.What is the evidence for PRP versus corticosteroid in tennis elbow?

PM R 2020 Tang et al meta-analysis: PRP better long-term pain and function; corticosteroid most improvement short term
Latest Cochrane review 2021 does not support PRP: no evidence of benefit

▸ Slide 701 · Platelet rich plasmaSports · 6 questions 1 check expand

Question list

Q1-Q66 questions — tap to reveal all answerslist

What is PRP and how is it prepared?
What is the optimal platelet concentration in PRP?
What are the indications for PRP in orthopaedics?
What growth factors do platelets release and what is their proposed role?
What is the clinical evidence for PRP in soft tissue healing, OA and fracture healing?
What is the evidence for PRP in ACL reconstruction, meniscal repair, cuff repair and tendinopathy?

Answers · Q & A

Q1.What is PRP and how is it prepared?

Plasma from one's own blood enriched with autologous platelets
Centrifugation separates the platelet-rich layer from whole blood; calcium chloride used to initiate platelet activation
Spin twice: 3200RPM for 15minutes then 2 minutes at 2000RPM with calcium chloride
3 layers: lowest blood cells, middle PRP, top platelet-poor plasma

Q2.What is the optimal platelet concentration in PRP?

3-5x of whole blood
>5x will inhibit healing

Q3.What are the indications for PRP in orthopaedics?

Controversial use for possible stimulation of bone and soft tissue healing

Q4.What growth factors do platelets release and what is their proposed role?

PDGF, TGF-beta, VEGF, IGF-1, EGF, CTGF, FGF-2
Important role in the inflammatory cascade response after injury
Proposed: increase ECM deposition, Reduced pro-apoptotic signals, minimise joint inflammation

Q5.What is the clinical evidence for PRP in soft tissue healing, OA and fracture healing?

Soft tissue healing: no consensus for acute ligament, tendon or muscle injuries or chronic tendinopathies
OA: RESTORE trial (JAMA 2021) and PEAK trial (BJJ 2022) showed no difference vs saline
Fracture healing/fusion: limited evidence for bone formation

Q6.What is the evidence for PRP in ACL reconstruction, meniscal repair, cuff repair and tendinopathy?

ACL: does not support ligamentisation/graft maturation; may improve donor site outcomes and decrease patellar tendon gap
Meniscal repair: no clear evidence; rotator cuff repair: no benefit
Lateral epicondylitis: Cochrane review 2021 - no benefit; midsubstance Achilles: not supported
Patellar tendinopathy: AJSM 2016 Laprade group PRP vs saline, no difference

Fact check

Optimal PRP concentration is 3-5x whole blood and >5x will inhibit healing — Oversimplified: the exact inhibitory threshold is not established — Reviews commonly cite 3-4x (600,000-900,000/µL) as optimal and >1.2 million/µL unfavourable; in vitro studies show a plateau with reduced collagen synthesis at high concentrations — medium confidence — source

FRCS Quiz — private