EXAMINER: This is a radiograph of a 72-year-old lady complaining of pain and gradual deformity of her left knee (Figure 4.1a and 4.1b). She has been referred to your clinic to be considered for total knee arthroplasty. What can you see?

CANDIDATE: This is a weight-bearing AP radiograph of a 72-year-old female demonstrating severe osteoarthrosis of the left knee with moderate valgus deformity. The cardinal features of osteoarthritis are demonstrated here, which include loss of joint space, subchondral sclerosis, osteophyte formation and subchondral cysts.

EXAMINER: How will you manage this patient?

CANDIDATE: Firstly, I would establish what are the symptoms the patient is suffering from. I would focus on pain, loss of function and severity of symptoms. I would like to know the exact location of the pain, alleviating and relieving factors, and where the pain is radiating to. How the pain is affecting activities of daily living such as cutting toenails, putting shoes and socks on, how easy it is to go up and down stairs are all questions I would ask. Treatment to date is also important; has the patient had any physiotherapy/rehabilitation, trialled any analgesics? Previous surgical procedures need to be established. Assessment of the effect of osteoarthritis on the patient’s function, quality of life, occupation, mood, relationships and leisure activities is also important. Clinical examination findings such as assessment of the soft tissue envelope is also important. Severity of the deformity in the coronal plane will need to be established. A fixed flexion deformity should also be noted. The competency of the knee collateral ligaments and degree of deformity correction should be assessed in order to plan the type of implants.

EXAMINER: OK, after the history and examination, what are you actually going to do?

CANDIDATE: The management should commence with non-surgical options and generally should be exhausted before surgical options are explored. As per the NICE guidelines, strengthening, low-impact aerobic exercise and neuromuscular education should all be recommended. Acetaminophen and NSAIDS and Tramadol should be the first analgesics offered. Interventions to lose weight, as there is moderate evidence that this will influence osteoarthritis of the knee. Obese patients generally have an increased risk of infection and tend to have an earlier onset of symptoms [1]. Other non-pharmacological treatments include education, social support, physical therapy, exercise and orthotics devices. Acupuncture and herbal remedies have limited evidence; however, they are still popular methods of treatment.

EXAMINER: What conditions are associated with this pattern of joint disease?

CANDIDATE: The valgus deformity of the knee with arthritis is commonly seen in women and in inflammatory joint conditions such as rheumatoid arthritis. It can also occur in primary osteoarthritis, overcorrection of high tibial osteotomy (HTO), post-traumatic arthritis following lateral meniscectomy and osteonecrosis of the lateral femoral condyle.

EXAMINER: What are your technical goals of treatment?

CANDIDATE: My aims are the following:

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  Restoring neutral mechanical axis of 0° (±3°).

  
  
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  Balancing the flexion/extension gap.

  
  
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  Ensuring the joint line perpendicular to the mechanical axis.

  
  
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  Preserving the joint line height.

  
  
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  Balancing ligaments (2–3 mm symmetrical opening).

  
  
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  Restoring normal joint alignment and Q angle.

EXAMINER: How would you restore the mechanical alignment?

CANDIDATE: The bony cuts of the femur and tibia should both be made perpendicular to the mechanical axis of the limb. The mechanical axis is a line bisecting the centre of the hip, knee and ankle. This is to ensure equal loading and even contact pressure of both medial and lateral compartments. The natural tibia has 3° of natural varus to the mechanical axis; however, we do cut perpendicular to the anatomical/mechanical axis. Deformity within the tibia needs to be taken into consideration and the cut should be made perpendicular to the mechanical axis and not the anatomical axis. Long leg mechanical axis views can be helpful for preoperative planning. The mechanical and anatomical axes of the femur are different, and it is this difference which creates the distal femoral valgus angle. This is usually 5–7°. The femoral component must be externally rotated by 3° with respect to the femoral neutral axis to create a rectangular flexion gap with the tibia. As the tibia was cut perpendicular to the mechanical axis, hence in 3° of valgus relative to the native plateau, the femoral component rotation will create a rectangular flexion gap.

EXAMINER: Tell me more about the intraoperative considerations.

CANDIDATE: In valgus knees the lateral femoral condyle is often deficient. This is important to remember because if you perform posterior femoral condylar referencing for femoral component rotation the resultant position of the femoral component will be internally rotated with reference to the transepicondylar axis. In this situation, the AP axis (Whiteside line) can be used to prevent malrotation in the form of internal rotation. The medial structures are stretched while lateral and posterior structures are contracted. The vastus lateralis acts as a subluxing or dislocating force to patella. In severe valgus deformity (7–10°) a distal femoral cut of 5 or 6° can improve patella tracking and avoid the need for lateral retinacular release. Patients with severe valgus deformity may require a lateral retinacular release to achieve normal patella tracking. Excessive PCL release usually requires cruciate-sacrificing implants in order to balance the knee. With correction of significant valgus deformity, one has to be cautious of the common peroneal nerve palsy in the postoperative period. It may be wise to identify the nerve to ensure no increased tension or damage occurs.

EXAMINER: OK, so what will be your choice of implant?

CANDIDATE: I would use a cemented implant. From the latest report of our National Joint Registry, over 84% of the primary TKA procedures performed are cemented, with less than 5% being uncemented and the remaining being a hybrid fixation. The advantages are that the cemented knee is less prone to aseptic loosening. There is, however, growing evidence for the use of uncemented knees [2]. There is an association with higher failure rates of cemented TKR in younger, heavier men. There are theoretical advantages of mobile bearing devices over fixed bearing devices, such as reduction in shear stresses and subsequent wear as the tibial insert will be able to rotate on a smooth tibial platform. However, I would use a fixed bearing insert; the Knee Arthroplasty Trial Group, after a large multicentre RCT, concluded that there is no advantage with the mobile bearing designs [3–5]. There are advantages and disadvantages of both cruciate-retaining and posterior stabilized knee replacements; however, I use a posterior stabilized knee, i.e. a cruciate-sacrificing knee replacement. There are many advantages, such as this implant design will facilitate deformity correction and provide anterior posterior stability with the CAM-post mechanism. I find it is technically easier to balance a PCL-sacrificing TKR and the results are more consistent. It can also be used in patients with previous patellectomy.

EXAMINER: How would you manage gap imbalance?

CANDIDATE: Ligament balancing is essential for proper knee stability and range of movement. When both the flexion and extension gaps are tight, options would be to reduce the polyethylene thickness or resect proximal tibia as this will equally alter both the flexion and extension gaps. If the extension and flexion gap are both equally loose, a larger polyethylene insert can be used. A tight flexion gap with a normal extension gap would require downsizing of the femoral component or shifting of the femoral component anteriorly [6,7]. With normal knee flexion, a flexion contracture would indicate a tight extension gap and may be an indication of an overstuffed extension spacer. Options of management would be to remove posterior osteophytes initially and release some posterior capsule. If the knee is still tight in extension the next step would be to resect some distal femur. Again, a normal flexion gap but a loose extension gap would indicate excessive distal femoral resection and distal femoral augmentation would be required. Flexion instability results when the flexion gap is larger than the extension gap and is often a result of undersized implants, incompetent PCL or excessive tibial slope. When the extension gap is normal the femoral component can be shifted posteriorly or one can augment the posterior condyles. It is imperative to ensure there is no anterior femoral cortex notching as a result of this shift.

EXAMINER: This young gentleman sustained a varus type injury to the knee and there is a suspected posterolateral (PLC) injury. Can you describe the lateral structures of the knee by layers (Figure 4.2)?

CANDIDATE: The lateral side of the knee comprises three main layers. Layer one, i.e. the most superficial layer, consists of the iliotibial tract and biceps femoris. The patella retinaculum is the primary constituent of the second layer. The common peroneal nerve lies between layers one and two. Layer three is split into superficial and deep layers. The lateral collateral ligament (LCL), fabellofibular ligament and anterolateral ligament (ALL) lie superficially. Within the deep layer are the arcuate ligament, coronary ligament, popliteus tendon and popliteofibular ligament. The lateral genicular artery lies between the deep and superficial layers.

EXAMINER: How about the medial side of the knee?

CANDIDATE: The medial side of the knee, similarly to the lateral side of the knee, is split into three layers. Layer one, most superficial, contains the sartorius and patella retinaculum. Layer two contains the semimembranosus, superficial MCL and the MPFL. The deepest layer consists of the deep MCL, capsule and the coronary ligament. Gracilis, semitendonosis and the saphenous nerve run between layers one and two.

EXAMINER: So, what is the function of the PLC and how commonly is it injured?

CANDIDATE: The role of the PLC is to resist external tibial rotation, varus and posterior tibial translation. The integrity of varus and external rotation stability ultimately depends on the integrity of the fibular collateral ligament (FCL), popliteus, the popliteofibular ligament and the lateral capsule. The PLC is rarely injured in isolation and is often associated with multiligament knee injuries; the PCL is injured less often than the ACL.

EXAMINER: Are you aware of any clinical tests to detect a PLC injury?

CANDIDATE: Hyperextension of the limb on passive extension testing can indicate a PLC injury. Initial gait examination may reveal a varus thrust. Lateral compartment gapping is assessed and compared with the contralateral side. If there is more gapping of the lateral compartment in flexion, then injury to the secondary stabilizers such as popliteus should be suspected. The dial test essentially measures external rotation of the tibia relative to the femur. I place the patient prone, and flex both knees to 30°. If there is more than 10° external rotation compared with the normal side, a PLC injury is diagnosed. I then flex both knees to 90° and repeat this manoeuvre. An increase in external rotation would suggest a combined PCL and PLC injury. I also use the reverse pivot shift test. I place the patient supine with the knee flexed to 90°. A valgus load is applied through the knee joint as well as an external rotation moment around the tibia. The knee is then brought out into extension. If the posteriorly subluxed tibia reduces at 40° of extension, this is interpreted as a positive result. The tibia reduces as a result of the ITB changing from a knee flexor to a knee extender.

EXAMINER: What investigations would you perform?

CANDIDATE: A routine radiograph work up should be performed including anteroposterior (AP), lateral and axial views. Mechanical axis long leg views should also be performed to assess the lower limb alignment. If there is any malalignment, an osteotomy should be performed prior to or at the time of reconstruction. These should be done to exclude fractures. Varus and PCL stress radiographs are reliable to assist in PCL and PLC injuries respectively.¹ Lateral compartment varus gapping of 2.7–4 mm is consistent with isolated FCL injuries, whereas more than 4 mm indicates a severe-grade PLC injury. Kneeling stress radiographs are best to assess PCL injuries and an opening of 4–12 mm would indicate an isolated PCL injury. Arthroscopy and MRI also have a role to assess for associated chondral, ligamentous and meniscal pathology. Double varus injuries can lead to a varus thrust as the LCL is injured. A triple varus can also lead to hyperextension and recurvatum, indicating a PLC injury.

EXAMINER: What are the options of management?

CANDIDATE: PLC injuries are usually part of a multi-ligament injury spectrum. It is rare to sustain an isolated PLC injury; however, if this were expected, the majority can be managed non-operatively.² If part of a multi-ligament injury, the PLC should be addressed. Patients with ACL ruptures should be assessed for PLC injuries and, depending on the grading of injury, should have a reconstruction to assess this deficiency. Grade 3 injuries are a different entity and there is good evidence to suggest poor functional outcomes and degenerative changes if non-operative measures are pursued. Options of operative approaches for grade 3 PLC injuries include acute repairs, which generally are reserved for bone or soft tissue avulsion injuries such as fibular head avulsions. This is normally done within 2–3 weeks and offers the advantage of fixing avulsed bony fragments and other structures anatomically. The ACL and PCL will need to be reconstructed acutely. Delayed reconstruction involves reconstruction of all structures including the PCL, ACL and PLC. Earlier evidence by Levy and Stannard et al. have both demonstrated higher failure rates with repair compared to delayed reconstruction.^3,4 However, more recent evidence by Westermann et al. has suggested good outcomes can be achieved with both repair and reconstruction of PLC injuries treated concurrently with ACL reconstruction at 6-year follow-up.⁵ Anatomical reconstruction using tendon allograft and all three static stabilizers has been shown biomechanically to restore native knee biomechanics with improved outcomes. The common peroneal nerve needs to be identified and protected. I would use a modified Larson’s technique for a grade I associated PLC injury, an Arciero for grade II and a LaPrade PLC reconstruction for a grade III injury.

EXAMINER: Tell me about the anatomy and function of the meniscus.

CANDIDATE: The menisci are crescentic cartilaginous structures interposed between the tibia and femoral condyles. They are triangular in cross-section. The peripheral borders are attached to the joint capsule. The medial meniscus is nearly semicircular with a wider posterior than anterior horn. This is attached anterior to the ACL insertion while the mid aspect is firmly attached to the deep MCL. The lateral meniscus is circular with a larger surface than the medial meniscus. The posterior horns of both menisci attach to the posterior intercondylar eminence. The attachment of the lateral meniscus to the capsule is interrupted by the popliteus tendon. Due to the loose attachment to the capsule, the lateral meniscus has twice the excursion to that of the medial meniscus. The anterior horns of both menisci are connected by intermeniscal ligaments. Histologically, the menisci have an extracellular matrix composed mainly of water (70%) and primarily type 1 collagen fibres (60%), proteoglycans, elastin and glycoproteins. The main cellular component is the fibrochondrocytes that synthesize and maintain extracellular matrix. The blood supply to the meniscus comes from the lateral, middle and medial geniculate vessels with 20–30% of the peripheral portion being vascular. The main functions of the menisci are load transmission with estimated 50% in extension and 85% in flexion, joint conformity and articular congruity, distribution of synovial fluid aiding nutrition and joint lubrication. The menisci also have proprioceptive function, act as shock absorbers and prevent soft tissue impingement during joint motion.

EXAMINER: What are the vascular zones of meniscus?

CANDIDATE: The menisci are relatively avascular structures with peripheral blood supply from the premeniscal capillary plexus formed by branches from lateral and medial geniculate vessels. Studies have shown that the degree of peripheral vascular penetration is 10–30% of medial meniscal width and 10–25% of lateral meniscal width. This gives rise to the three zones of meniscal vasculature from peripheral to central, namely red–red, red–white and white–white. Therefore, peripheral tears are suitable for repair while central tears may not be suitable due to lack of healing capacity.

EXAMINER: These are the images which belong to a young professional footballer (Figures 4.3b and 4.3c). What can you see?

CANDIDATE: The first is a sagittal T1 MRI image and the second is a T2-weighted image. The coronal image does not show any medial meniscal tissue indicating a peripheral detachment. There is a ‘double PCL sign’ on the sagittal image suggestive of bucket handle tear of the medial meniscus.

EXAMINER: How would you manage this patient?

CANDIDATE: I would start by taking a detailed history and clinical examination … [ EXAMINER interrupts].

EXAMINER: How would you treat this patient? [ EXAMINER getting impatient]

CANDIDATE: I would offer this patient EUA, arthroscopy, repair or excision of bucket handle tear.

EXAMINER: Good. What factors affect the prognosis following meniscal repair?

CANDIDATE: Firstly, the patient’s age dictates what I would do for the bucket handle tear. As he is a young professional footballer I would do my best to preserve the meniscus. Older patients have less cellularity and decreased healing response. Re-tears are common in patients above the age of 30. Location of the tear and the tear pattern are also important factors. The chronicity of the tear will also dictate what I do. I am also much more inclined to preserve the lateral meniscus than the medial meniscus. Other factors include location and pattern, and associated pathology, i.e. ligamentous malalignment and pre-existing arthritis.

EXAMINER: Are you aware of any meniscal repair techniques?

CANDIDATE: The four main meniscal repair methods are open repair, inside out, outside in and all inside. The ‘outside in’ method is versatile and safe but is reserved for anterior horn tears. [ EXAMINER interrupts again]

EXAMINER: Let’s move on …

EXAMINER: This gentleman had a TKA performed 3 months ago. Ten days after surgery he developed a large blister that was drained on the ward. Two weeks later he developed a draining abscess at the proximal aspect of the wound. He was taken to theatre and the abscess was washed out. The skin was debrided and closed primarily. Have you got any concerns?

CANDIDATE: This patient has a periprosthetic joint infection (PJI) until proven otherwise. He clearly developed an acute infection following the surgery. An acute infection is defined by the American Academy of Orthopaedic Surgeons and the International Consensus on PJI as infection within 3 weeks of the procedure, or in the case of late haematogenous infection, within 3 weeks of development of symptoms. Any infection developing after this time is considered as late. This is irrespective of bone stock and stability of the components.

EXAMINER: These are the most recent radiographs and there are no other postoperative radiographs available (Figures 4.4a and 4.4b). What would you like to do for this patient?

CANDIDATE: I would start by taking a detailed history of the perioperative events, general health as well as current problem. I would like to know the date of index operation, if there was prolonged discharge from the wound, redness or persistent swelling in the immediate postoperative period. A pain-free interval after the operation followed by sudden deterioration may be suggestive of haematogenous spread precipitated by bacteraemia from UTI, URTI or dental procedure.

EXAMINER: Are you aware of any staging systems with the use of periprosthetic joint infection?

CANDIDATE: McPherson advocated the concept of staging, which consists of timing of infection, i.e. early, acute haematogenous or late. The systemic medical and immune status of the patient is used. Systemic compromising factors include excessive alcohol, diabetes, smoking, liver, renal and lung failure. Immune status assessment includes CD4 count and neutrophil counts. Local compromising factors are also recorded and include whether active infection is present, synovial cutaneous fistula presence and a subcutaneous abscess of more than 8 cm². Each category has different grades according to what they score.¹

EXAMINER: So how would you diagnose a periprosthetic joint infection?

CANDIDATE: I would always start with the history and clinical examination of the patient. I would focus on the events around the procedures this gentleman has had. Even without signs of infection, a painful TKR can manifest as a low-grade infection. I am aware of the AAOS clinical guideline practice summary for diagnosis of periprosthetic joint infection of the knee. The working group strongly recommend:

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  Testing ESR and CRP.

  
  
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  Joint aspiration.

  
  
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  The use of intraoperative frozen sections.

  
  
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  Obtaining multiple intraoperative cultures, against initiating antibiotic treatment until after cultures and against the use of intraoperative Gram stain.

  
  
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  Nuclear imaging was weakly recommended as an option in patients in whom diagnosis of periprosthetic joint infection has not been established and who are not scheduled for reoperation.²

I refer to the diagnostic criteria set out by the workgroup of the MSK infection society. The major criteria include either a sinus tract communicating with the prosthesis or if a pathogen is isolated by culture from at least two separate tissue or fluid samples obtained from the affected prosthetic joint, or four of the following six minor criteria: (a) elevated CRP and ESR, (b) elevated synovial leucocyte count, (c) elevated synovial neutrophil percentage, (d) presence of purulence in the affected joint, (e) isolation of a microorganism in one culture of periprosthetic joint fluid or tissue and (f) > 5 neutrophils per high power field observed at ×400 magnification.³ The isolation of the infecting organism and the corresponding antibiotic profile are essential.

EXAMINER: Anything else?

CANDIDATE: Analysis of the joint fluid which should include a leucocyte esterase assessment …

EXAMINER: Anything more recent in the literature?

CANDIDATE: The alpha-defensin test, which is an immunoassay, has recently been shown to have a sensitivity and specificity of 100% in the diagnosis of PJI. Advantages include the specimen could also be assessed when blood was in the synovial fluid.⁴

EXAMINER: So how are you going to manage this case?

CANDIDATE: It is unfortunate, but I think this gentleman cannot be treated as an acute infection. He has missed the window of opportunity of debridement, antibiotic treatment and implant retention. He has already undergone a soft-tissue debridement and I am worried about the soft tissue envelope. It may require a plastic surgeon to review the wound. I would offer this patient a revision knee arthroplasty.

EXAMINER: And how would you do this?

CANDIDATE: It can be done over a one-stage or two-stage procedure. One stage has many advantages including low treatment costs and shorter hospital stays. The infecting organism and its sensitivity should be established preoperatively. There are, however, contraindications to this, including infection with a highly virulent organism, sepsis with substantial systemic manifestations and culture-negative PJI where appropriate antibiotic treatment cannot be determined.

EXAMINER: So … ?

CANDIDATE: I would plan for a two-stage exchange procedure where I would remove all the material, including the cement, and perform an aggressive debridement of the soft tissues and bone. I would insert an antibiotic-loaded dynamic cement spacer. This should preserve the joint space, reduce soft-tissue contractures, and provide better ROM and knee function scores while eluting high doses of IV antibiotics.⁵ Debridement is the most essential part of the procedure with meticulous handling of soft tissues to remove all septic membranes.