Structured Oral Hip Examination Question 4

EXAMINER: These are the radiographs of a 78-year-old lady who has been referred to the orthopaedic clinic by her GP because of increasing pain in her right hip. Would you care to comment on the radiographs? (Figure 2.7.)

CANDIDATE: This is an AP radiograph, demonstrating lower lumbar vertebrae, both hips and proximal femur. The most obvious features in the right hip are loss of joint space, osteophytes, sclerosis and bone cysts. The radiographic features are highly suggestive of osteoarthritis (OA) of the hip. EXAMINER: How is osteoarthritis classified?

CANDIDATE: OA is classified into primary OA when obvious cause can be identified and secondary OA caused by such conditions as avascular necrosis, DDH, post traumatic, Paget’s disease, slipped capital femoral epiphysis, protrusio acetabuli, Perthes’ disease.

EXAMINER: What are the percentages of each type of OA?

CANDIDATE: Various studies have suggested that almost 90% of cases of OA are secondary.

EXAMINER: How are you going to manage this patient?

CANDIDATE: I would take a full history and examination from the patient, specifically I would want to know the location of pain, exclude referred pain from the spine. Hip pain is

Figure 2.7 Anteroposterior (AP) radiograph demonstrating severe osteoarthritis of the left hip.

classically located in the buttock or groin radiating to the knee. Pain radiating below the knee to the foot is strongly suggestive of radicular type pain from the spine. I would inquire whether the patient had difficulty putting shoes and socks on, tying shoe laces, bending to pick up an object from the floor, getting in and out of a car [Examiner interrupts]

EXAMINER: The patient struggles to walk a quarter of a mile. She has typical symptoms of advanced OA. What are you going to do?

CANDIDATE: Assuming that all conservative options had been tried and have been unsuccessful I would offer her THA.

EXAMINER: What type of hip arthroplasty would you perform?

CANDIDATE: I would perform a cemented Exeter THA.

EXAMINER: Why this particular implant?

CANDIDATE: The Exeter THA has excellent peer-reviewed longterm data. It has a 10A ODEP rating for clinical use. It is an implant that I am very comfortable using, I have been trained to use this implant by my consultants, the instrumentation is straightforward and simple to use, the neck cut is not critical and the introducer allows for even pressure when inserting the implant.

EXAMINER: What are the design principles of the Exeter Stem?

CANDIDATE: The Exeter implant is a loaded taper model and becomes lodged as a wedge in the cement mantle during axial loading, reducing peak stresses in the proximal and distal

cement mantle. The stem is allowed to subside initially until radial compressive forces are created in the adjacent cement and transferred to the bone as hoop stresses.

EXAMINER: What approach would you use to the hip?

CANDIDATE: I am happy to use either the Hardinge or posterior approach to the hip.

EXAMINER: Make up your mind. Which one are you going to do?

CANDIDATE: For the majority of cases I would prefer to use the posterior approach to the hip. In rare instances I would use a Hardinge anterolateral approach if the risk of dislocation was high such as neurological or muscular weakness around the hip (Parkinson’s disease/CVA), early dementia or substance abuse.

The posterior approach is considered easier to perform and is generally a quicker procedure, limiting operative complications such as blood loss and anaesthetic issues.

The abductor muscles are not disturbed significantly so there is generally no gait abnormality but the acetabulum is more difficult to see and can make prosthesis positioning difficult, possibly causing an increased dislocation rate due to component malpositioning. The sciatic nerve is at slightly more risk of being injured as well.

EXAMINER: There is approximately double the risk of sciatic nerve injury using the posterior approach. Most surgeons would say that there is no significant difference in surgical time between the two approaches; the posterior approach can take just as long as the anterolateral approach. The posterior approach is marginally technically easier than the anterolateral approach but this also depends on surgeon training, experience with using either approach and personal preference. I would argue about the acetabulum being less easy to visualize posteriorly as most surgeons believe the posterior approach provides better acetabular visualization especially for revision cases. The pelvis tends to tilt more and so the degree of cup anteversion is usually underestimated leading to an increased risk of dislocation. Where I think the posterior approach does make a difference is a reduced incidence of Trendelenberg gait postoperatively and improved Harris hip scores compared with the anterolateral approach. Whilst results have been a bit contradictory the risk of posterior dislocation is slightly higher posteriorly even with a careful repair of the soft tissues. Larger head sizes are being used now so this is becoming less of an issue.

EXAMINER: Talk me through the posterior approach to the hip.

CANDIDATE: Assuming full informed consent has been obtained, all relevant case notes and radiographs have been obtained, the leg has been marked and she has been suitably anaesthetized I would position the patient laterally, affected leg uppermost, with hip supports. I would then prepare and drip the patient and make an incision centred over the greater trochanter, approximately 15 cm in length.

I would cut through the skin, subcutaneous tissue, and open up the fascia lata, splitting the gluteus maximus along the line of muscle fibres, and then release the short external rotators from the greater trochanter. Finally, I would perform a capsulectomy and then dislocate the hip.

I would protect the sciatic nerve being aware of its position and avoid dissecting too near to it.

EXAMINER: What are the pathological processes involved in the development of osteoarthritis of the hip?

CANDIDATE: Disruption of the integrity of the collagen network occurs early in OA allowing hyperhydration. The increased water content of cartilage causes softening, decreases Young’s modulus of elasticity and reduces its ability to bear load.

Initial changes in OA involve damage to the tangential zone immediately below the articular surface, with disorganization of the collagen network, loss of proteoglycans and swelling. This leads to a hypertrophic repair response with increased synthesis and accumulation of proteoglycan. However the repair process fails with loss of surface integrity, and fibrillation parallel to the surface. In regions of severe damage, there is a loss of cellularity and sporadic formation of cell clusters or clones.

Normal cartilage metabolism is a highly regulated balance between synthesis and degradation of the various matrix components. With OA the equilibrium between anabolism and catabolism is weighted in favour of degradation.

Cartilage catabolism results in release of breakdown products into synovial fluid, which then initiates an inflammatory response by synoviocytes.

These breakdown products include: chondroitin sulphate, keratan sulphate, PG fragments, type II collagen peptides and chondrocyte membranes.

Activated synovial macrophages then recruit PMNs establishing a synovitis. They also release cytokines, proteinases and oxygen free radicals (superoxide and nitric oxide) into adjacent synovial fluid. These mediators act on chondrocytes and synoviocytes modifying synthesis of PGs, collagen, and hyaluronan as well as promoting release of catabolic mediators.

Cartilage changes in osteoarthritis are characterized by increases in:

 Water content.

 Chondrocyte activity and proliferation.

 Stiffness of articular cartilage.

 Interleukin-1.

 Metalloproteinase levels.

 Cathepsins B and D levels. and decreases in  Quality of collagen.

 Proteoglycan quality and size.

Histology classically demonstrates:

 Loss of superficial chondrocytes.

 Replication and breakdown of the tidemark.

 Fibrilation.

 Cartilage destruction with eburnation (polished, shiny smooth with an appearance like ivory) of subchondral bone.

EXAMINER: Is OA simply an ageing process of cartilage?

CANDIDATE: Several differences between ageing cartilage and OA cartilage have been described suggesting a separate disease entity. For example OA and normal ageing cartilage differ in the amount of water content and in the ratio of chondroitin sulphate to keratin sulphate constituents.

EXAMINER: [Interrupting] That’s fine that’s okay.¹ What molecules are responsible for degrading the cartilage matrix?

CANDIDATE: The primary enzymes responsible for the degradation of cartilage are the matrix metalloproteinases (MMPs). These enzymes are secreted by both synovial cells and chondrocytes and are categorized into three general categories:

(a) collagenases, (b) stromelysins and (c) gelatinases.

In OA, synthesis of MMPs is greatly enhanced and the available inhibitors are overwhelmed, resulting in net degradation. Interestingly, stromelysin can serve as an activator for its own proenzyme, as well as for procollagenase and prostromelysin, thus creating a positive feedback loop of pro-MMP activation in cartilage.

EXAMINER: What factors are responsible for inducing metalloprotease synthesis?

CANDIDATE: IL-1 is a potent pro-inflammatory cytokine that, in vitro, is capable of inducing chondrocytes and synovial cells to synthesize MMP. In addition IL-1 suppresses the synthesis of type II collagen and proteoglycans. Therefore in OA, IL-1 actively promotes cartilage degradation and may also suppress attempts at repair.

CANDIDATE 1

The most obvious abnormality is patchy diffuse sclerosis with increased density in the superolateral aspect of the right femoral head (Ficat 2).

The left femoral head has a possibly minimal osteoporosis and/or blurring and poor definition of the bony trabeculae (Ficat 1). The radiograph is suspicious of bilateral AVN. I would like to obtain a frog-leg lateral radiograph of both hips. I would look for the crescent sign, indicating subchondral fracture, a feature of AVN that is more obvious on a frog-leg lateral than AP projection. This is because the anterior and posterior margins of the acetabulum on the AP projection are superimposed over the superior portion of the femoral head, the usual location of the sign. When AVN is bilateral, it usually occurs in each hip at different times, and the staging of disease in each hip is often different.

[Candidate score 7–8]

CANDIDATE 2: This is an AP pelvic radiograph showing both hips. There is nothing very obvious staring at me. There are no features of osteoarthritis such as joint space narrowing, osteophytes or sclerosis.¹ [Candidate score 4]

EXAMINER: What do you mean by AVN?

CANDIDATE: Avascular necrosis occurs due to interruption of the blood supply to the femoral head leading to ischaemia and cellular death.

EXAMINER: What is the aetiology of AVN?

CANDIDATE: A number of conditions are associated with AVN. The most common cause is trauma secondary to fracture and/or dislocation of the femoral head. Other conditions include:

 Corticosteroid use.

 Alcohol abuse.

Figure 2.8 Anteroposterior (AP) radiograph of bilateral avascular necrosis.

 Smoking.

 Coagulopathies.

 Sickle cell anaemia.

 Caisson disease.

 Hypercholesterolaemia.

 Organ transplantation.

 Systemic lupus erythematosus.

 Gaucher’s disease.

 Hypertriglyceridaemia.

 Intramedullary haemorrhages.  Chronic pancreatitis.

AS IT GRIPS 3Cs (mnemonic)

Alcohol

Steroids

Idiopathic

Trauma

Gout, Gaucher’s

Rheumatoid/radiation

Infection/increased lipids/inflammatory arteritis

Pancreatitis/pregnancy

SLE/sickle cell/smoking

CRF/chemotherapy/Caisson disease

In approximately 10–20% of cases no cause can be identified. EXAMINER: What is the pathophysiology of AVN?

CANDIDATE: Aetiological factors in AVN are usually related to underlying pathological conditions that alter blood flow, leading to cellular necrosis and ultimately to collapse of the femoral head. This damage can occur in one of five vascular areas around the femoral head: arterial extraosseous, arterial intraosseous, venous intraosseous, extravascular intraosseous and extravascular extraosseous.

1.      Extraosseous arterial factors are the most important. The femoral head is at increased risk because the blood supply is an end-organ system with poor collateral development. Blood supply can be interrupted by trauma, vasculitis (Raynaud’s disease), or vasospasm (decompression sickness).

2.      Intraosseous arterial factors may block the microcirculation of the femoral head through circulating microemboli. These can occur in sickle cell disease (SCD), fat embolization or air embolization from dysbaric phenomena.

3.      Intraosseous venous factors affect the femoral head by reducing venous blood flow and causing stasis. These factors may accompany conditions such as Caisson disease, SCD or enlargement of intramedullary fat cells.

4.      Intraosseous extravascular factors affect the hip by increasing the pressure, resulting in a femoral head compartment syndrome. For example: fat cells hypertrophy after steroid administration or abnormal cells, such as Gaucher and inflammatory cells, can encroach on intraosseous capillaries, reducing intramedullary circulation and contributing to compartment syndrome.

5.      Extraosseus extravascular (capsular) factors involve the tamponade of the lateral epiphyseal vessels located within the synovial membrane, through increased intracapsular pressure. This manifests as trauma, infection and arthritis, causing hip effusion that may affect the blood supply to the epiphysis.

EXAMINER: Specifically how do steroids cause AVN?2

CANDIDATE: The mechanism postulated for steroid-induced AVN is still unclear.

Johnson proposed that fat cell hypertrophy within the bone marrow increases femoral head pressure resulting in sinusoidal vascular collapse and necrosis of the femoral head.3 The exact mechanism of fat cell hypertrophy remains obscure but a disorder in fat metabolism is implicated.

Jaffe et al. believe patients undergoing steroid treatment are in a hyperlipidaemic state, which can increase the fat content within the femoral head and raise intracortical pressure producing sinusoidal collapse and finally necrosis.4 Other investigators have proposed that this hyperlipidaemic state leads to fat embolism occluding the femoral head microvasculature, which initiates the pathophysiological process.5 A recent study in rabbits suggests that the use of steroids can also damage endothelial and smooth muscle cells within the vasculature. This may result in interruption of the venous drainage from the femoral head, leading to blood stasis, an increase in intraosseous pressure and AVN.6 Other studies suggest primary osteocyte cell death without any other features. This is seen with steroid use, in transplant patients and those who consume significant amounts of alcohol.

EXAMINER: How common are steroids as a cause of AVN?

CANDIDATE: High-dose corticosteroids are the most common cause of non-traumatic AVN accounting for 10–30% of cases. However only 10% of patients exposed to corticosteroids may develop AVN. Dosage is typically steroids > 2 g of prednisone, or its equivalent, within a 2–3-month period.

The period from the start of corticosteroid treatment to the diagnosis of AVN ranges from 1–16 months (mean 5.3 months), and the majority of patients are diagnosed within 1 year.

EXAMINER: You mentioned the crescent line, what is its significance?

CANDIDATE: Therapeutic interventions are less likely to halt progression of the disease once this sign appears.

EXAMINER: How does AVN of the hip present?

CANDIDATE: Although AVN can be clinically silent typically a patient complains of pain, usually localized to the groin area but occasionally to the ipsilateral buttock and knee. It is usually a deep intermittent, throbbing pain, with an insidious onset that eventually occurs at rest and may be present or even worsen at night. Physical examination reveals pain with both active and passive range of motion, especially with passive internal rotation. Range of motion is important as this helps determine the extent of the disease. In general, more limited flexion and abduction indicate more extensive articular damage, whereas limited rotation alone may indicate less destruction. A careful examination of the contralateral hip should always be undertaken as AVN is bilateral in 40–80% of cases.

EXAMINER: How is AVN classified?

CANDIDATE: Several classification systems for AVN exist. Ficat and Arlet is the most commonly known and consisted of four stages.⁷ Hungerford and Lennox later added a fifth stage (Stage 0) when MRI became available.⁸

Stage 0 (preclinical). Suspected disease in the contralateral hip when the index joint has definitive findings. No clinical symptoms. MRI non-diagnostic.

Stage I (pre-radiological). Normal findings on radiographs and positive findings on MRI or bone scan. The MRI shows a doubleline sign, consistent with a necrotic process.

Stage II (pre-collapse). Osteopenia, demineralization, sclerosis or cysts. A late finding is the crescent sign, a linear subcortical lucency, situated immediately beneath the subcortical bone, representing a fracture line and impending femoral head collapse.

Stage III (collapse). The femoral head is flattened and collapsed with the presence of sequestration manifested by a break in the articular margin without acetabular involvement.

Stage IV (progressive degenerative disease). Severe collapse and destruction of the femoral head, acetabular osteophytes.

Osteoarthritis superimposed on a deformed femoral head.

EXAMINER: Any other classification systems?

CANDIDATE: Steinberg (Table 2.6) expanded the staging system into seven stages and quantified the amount of involvement of the femoral head into mild (< 15%), moderate (15–30%) and severe (> 30%), based on radiographs.⁹ It is considered more useful than Ficat because it grades the severity and extent of the involvement, both of which are thought to affect prognosis.

EXAMINER: Any others?

CANDIDATE: Other classification systems include the ARCO (Association Research Circulation Osseous) classification, University of Pennsylvania system and the Mitchell MRI classification.

EXAMINER: What is the Kerboull necrotic angle and its importance?

CANDIDATE: The Kerboull necrotic angle is used to calculate the size of the necrotic segment. It is the sum of the angle of the necrotic segment as measured on both the anteroposterior and frog-lateral radiographs. Patients with a Kerboull angle > 200 more commonly have poor results with certain bonepreserving procedures.

EXAMINER: How are you going to manage this patient?

CANDIDATE: I would perform bilateral core decompression. The AVN is still at an early stage where it may be successful (Ficat stage I and II AVN). The procedure has no role in the management of Ficat stage III or IV disease. Results have been satisfactory when core decompression is combined with either non-vascularized or vascularized fibular grafts in patients with Ficat stage II lesions.

EXAMINER: What are the prerequisites for performing a free vascularized fibular graft (VFG)?

Table 2.6 Staging system of Steinberg et al.

CANDIDATE: VFG for AVN is a major operative procedure with a long rehabilitation time and therefore patient selection to minimize the potential for an unsuccessful operation is critical.

McKee from Toronto suggests the operation should be limited to patients:¹⁰

1.      With 2 mm or less of femoral head collapse as measured on plain radiographs.

2.      Who are 45 years of age or younger (and have a reasonable life expectancy).

3.      Have had withdrawal of an identified aetiological agent.

4.      Have no contractures about the hip.

5.      Have a supple joint.

These are obviously general guidelines that may be adjusted somewhat depending on the individual patient.

EXAMINER: What are the advantages of performing a free vascularized fibular graft (VFG)?

CANDIDATE: Advantages of vascularized fibular grafting include:  Being able to perform a core decompression of the femoral head.

 The ability to perform curettage and removal of the osteonecrotic focus.

 Impaction of autogenous cancellous graft to fill the defect created by removal of the osteonecrotic bone.

 The structural support of the subchondral surface provided by the fibular graft.

 The addition of vascularized bone and blood supply to the area of osteonecrosis enhances the revascularization process.

EXAMINER: What complications can occur with a free vascularized fibular graft?

CANDIDATE: Gaskill et al. from a tertiary centre in North Carolina performing a large volume of VFG reported a 16.9% complications rate, 4.3% of complications require reoperation or chronic pain management.^11,12 Donor site morbidity

 Great-toe flexion contracture (4.3%). Majority asymptomatic noticeable only on clinical examination with the ankle fully dorsiflexed. Occasionally requires z-lengthening of the FHL tendon at the level of the medial malleolus. Flexion contracture of the second and third toes may co-exist in a small number of patients.

 Persistent weakness in the operated extremity (0.6%) either long toe flexors or peroneal group.

 Mild persistent pain and tenderness at the ankle or distal osteotomy site (4.1%) usually after prolonged standing or moderate activity such as jogging.

 Sensory deficits (1.7%). The sensory deficit was not always consistent with peripheral nerve or dermatomal distributions.

 Superficial infection.

Graft site complications

 Symptomatic lateral pin migration (2.4%). A Kirschner wire was used routinely to secure the fibular graft in its final position after placement in the femoral head.

 Symptomatic heterotopic ossification (1.4%).

 Femoral fracture (0.7%). All occurred in the intertrochanteric and subtrochanteric region after a fall.

 Deep venous thrombosis (0.3%).

 Superficial infection (4%).

 Deep infection (4%).

 Haematoma (1%).

 Trochanteric bursitis (1%).

EXAMINER: What are the other techniques that can be used to manage AVN hip?

CANDIDATE: The trapdoor procedure is performed with an arthrotomy to dislocate the hip anteriorly, followed by curettage of the necrotic segment of the head and packing of the defect with iliac crest bone graft through a cartilage window in the femoral head. This can be used for Ficat stage III and early Ficat stage IV and reasonable results reported.

EXAMINER: You have to be more specific than that – what do you mean by reasonable results?¹³

CANDIDATE: Michael Mont reported on a series of 30 hips Ficat stage III/IV at 5 years with 73% having good to excellent

results.¹⁴

EXAMINER: Any other options?

CANDIDATE: Osteotomy has been used to treat Ficat stage III and IV disease but results have been variable because it is difficult to rotate the necrotic segment out from the weightbearing area, especially when the lesion is large. Sugioka et al. reported good to excellent results at 3 to 16 years of follow-up in 78% of 229 hips treated with the transtrochanteric anterior rotational osteotomy.¹⁵ Their results with this technically demanding procedure have not been reproduced by others.

A success rate of approximately 30% at 5 years is common, with the best results reported in patients whose lesions do not result from trauma and who have less than 30% of the head involved.

EXAMINER: Any new technique that has emerged in the last 2 or 3 years?

CANDIDATE: Stem cells have been used to manage AVN.

EXAMINER: Go on – do you know about the technique or results? CANDIDATE: Sorry that’s all I know.

EXAMINER: Two techniques are being promoted. One is a threestage procedure and the other is a single-stage procedure. The first method is by stem cell culture in the lab to multiply the number of cells several million fold. These cultured stem cells are reinjected into a previous core decompression site.

In the second method, bone marrow obtained from the pelvis is centrifuged in the operating room to yield a bone marrow concentrate rich in stem cells. The patient is supine on a traction table with a C arm image intensifier. Percutaneous core decompression drilling with a Kirschner wire (diameter 2.7 mm) is performed to perforate the interface between the necrotic lesion and healthy bone. Following this concentrated autologous bone marrow aspirate is slowly transplanted into the necrotic area under fluoroscopic control. This is still an experimental procedure but early results seem promising for early disease.

EXAMINER: The patient had surgery on both hips. These are his postoperative radiographs.

CANDIDATE: The AP radiograph demonstrates a metal core rod in the right hip. (Figure 2.9.)

EXAMINER: What do we call this?

CANDIDATE: The patient has had a tantalum rod inserted into the femoral head. The implant achieves decompression, supports the subchondral plate of the necrotic areas and probably induces bone regeneration.

EXAMINER: Anything else?

CANDIDATE: The use of a trabecular metal ‘AVN rod’ has a number of attractive theoretical advantages, including no donor site morbidity, improved rehabilitation, structural support of the femoral head and the potential for

‘osseointegration’ of the biologically friendly material.

EXAMINER: The patient had core decompression performed on the left hip and a core decompression with tantalum rod inserted in the right hip. He initially got good pain relief from the procedures for about a year or so but he returns to the orthopaedic clinic complaining both hips are now painful. The left side is worse than the right. What do you think of the radiographs?

CANDIDATE: The AP radiograph suggests AVN has progressed. EXAMINER: What will you do?

CANDIDATE: I would offer him bilateral hip arthroplasty, the left one being more symptomatic first.

EXAMINER: What type of hip replacement would you use?

CANDIDATE: In view of his relatively young age I would perform an uncemented THA with a ceramic bearing surface.

EXAMINER: What are the advantages of using a ceramic bearing surface?

CANDIDATE: The advantages of using a ceramic bearing surface include superior lubrication, friction, and wear properties compared with other bearing surfaces in clinical use. Specifically it is an extremely hard material, very resistant to wear, with a low coefficient of friction, excellent abrasive resistance and excellent wettability properties for

Figure 2.9 Anteroposterior (AP) radiograph pelvis with tantalum rod inserted into the right hip.

improved lubrication. It is presumed that the lower wear rates lead to a lower rate of aseptic loosening and the need for revision surgery.

Disadvantages include potential for catastrophic fracture, squeaking, chipping on insertion and reduced range of implant sizes.

EXAMINER: What is the incidence of squeaking?

CANDIDATE: The reported incidence of squeaking with alumina ceramic bearings varies widely from 0.45% in a series of 2716 ceramic implants to 7.0% in a series of 159 ceramic implants. Most reported series note that squeaking is rare and without clinical significance; however, on rare occasions, major squeaking has led to revision surgery.¹⁶

EXAMINER: Will there be any special issues removing the tantalum rod and performing THA?

CANDIDATE: I would contact the manufacturers of the implant as there is a special implant removal kit. Otherwise not using the removal kit makes the surgery much more difficult. I would use a Gigli and reciprocating saw to section the head, implant removal corer to take out the tantalum rod and then perform a conventional uncemented THA.

EXAMINER: Are there any worries with tantalum material?

CANDIDATE: Studies suggest a trend towards an poorer outcome in patients following conversion of tantalum rod to THA.¹⁷

Figure 2.10 Anteroposterior (AP) radiograph left metal-on-metal (MOM) hip and right ceramic large jumbo hip arthroplasty.

There is also concern of tantalum residue within the joint space found in the majority of conversions. Although there is no catastrophic wear seen in studies there is the potential for accelerated joint damage in the medium to long term.

EXAMINER: These are his radiographs. He had a large jumbo head MOM performed on the left side and a large ceramic jumbo head THA performed on the right side. Do you have any worries? (Figure 2.10.)

CANDIDATE: The BOA released a statement after the annual conference at Torquay in 2011 reporting a higher than anticipated early failure rate for large jumbo head MOM hips. Concern was expressed regarding the trunnion at the ‘Morse’ taper where the large diameter metal head attaches to the stem. Various examples were shown of damage from either wear or corrosion or both resulting in either loosening of the acetabular component, loosening of the femoral component or a metal reaction with necrosis and soft tissue damage. As such its use should now be avoided. Excluding the ASR implant theses devices have a reported revision or impending revision rate of 12–15% at 5 years.

EXAMINER: What about follow-up?

CANDIDATE: This should be as per BHS guidelines for MOM bearing surfaces, yearly for the first 5 years and probably for life. Pain in this group of patients should be taken seriously and investigated appropriately with cobalt chromium levels and an MRI scan of the hip looking for any local reaction/ tissue necrosis/presence of pseudotumour.

EXAMINER: What about the other ceramic hip?

CANDIDATE: There are some worries again regarding the trunnion, where the large ceramic head attaches to the stem which may be the source of excessive wear or corrosion, leading again to early failure, although the evidence is not as strong.

 

Endnotes

1.       If you initially miss a subtle AVN spot diagnosis it is extremely difficult to recover the viva especially if the candidates before and after you spot it without prompting.

2.       Take your pick. On the day steroids but you may be asked about alcohol, smoking, Caisson disease, sickle cell anaemia and transplant recipients etc. A few buzzwords may be sufficient to bluff your way through although it’s more likely the examiner will want a more detailed explanation.

3.       Johnson LC. Histiogenesis of Avascular Necrosis. Presented at the Conference on Aseptic Necrosis of the Femoral Head. St Louis, 1964.

4.       Jaffe WL, Epstein M, Heyman N, Mankin HJ. The effect of cortisone on femoral and humeral heads in rabbits. An experimental study. Clin Orthop Relat Res 1972;82:221–228.

5.       Jones JP Jr. Fat embolism, intravascular coagulation, and osteonecrosis. Clin Orthop Relat Res 1993; 292:294–308.

6.       Nishimura T, Matsumoto T, Nishino M, Tomita K. Histopathologic study of veins in steroid treated rabbits. Clin Orthop Relat Res 1997;334:37–42.

7.       Ficat RP. Idiopathic bone necrosis of the femoral head. Early diagnosis and treatment. J Bone Joint Surg Br 1985;67(1):3–9.

8.       Hungerford DS, Lennox DW. The importance of increased intraosseous pressure in the development of osteonecrosis of the femoral head: implications for treatment. Orthop Clin North Am 1985;16(4):635–654.

9.       Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg Br 1995;77:34–41. (Level 2/3 evidence).

10.     McKee MD, Waddell JP, Kudo PA, Schemitsch EH, Richards RR. Osteonecrosis of the femoral head in men following short-course corticosteroid therapy: a report of 15 cases. Can Med Assoc J 2001;164:205–206.

11.     Gaskill TR, Urbaniak JR, Aldridge JM 3rd. Free vascularized fibular transfer for femoral head osteonecrosis: donor and graft site morbidity. J Bone Joint Surg Am 2009;91-A:1861–1867.

12.     Standard protocol is that Gaskill should be mentioned as the first author when quoting papers in the exam. Rules sometimes need to be bent and as Urbaniak is a recognized world expert in VFG the examiners may be more familiar with his research and therefore mentioning him as the lead author may be tactically more astute. There were 215 complications (a 16.9% rate) at the time of follow-up, at an average of 8.3 years, after the 1270 procedures. Quote papers and results but be sensible about it.

13.     Sometimes you will get away with that type of general statement regarding results, other times the examiners may press you.

14.     Mont MA, Einhorn TA, Sponseller PD, Hungerford DS. The trapdoor procedure using autogenous cortical and cancellous bone grafts for osteonecrosis of the femoral head. J Bone Joint Surg Br 1998;80:56–62.

15.     Sugioka Y, Hotokebuchi T, Tsutsui H. Transtrochanteric anterior rotational osteotomy for idiopathic and steroid induced necrosis of the femoral head: indications and longterm results. Clin Orthop 1992;277:111–120.

16.     Jarrett CA, Ranawat A, Bruzzone M et al. The squeaking hip: a phenomenon of ceramic-on-ceramic total hip arthroplasty. J Bone Joint Surg Am 2009;91-A:1344–1349.

17.     Lewis P, Olsen M, McKee M, Waddell J, Schemitsch E. Total

Hip Arthroplasty Following Failure of Core Decompression and Tantalum Rod Insertion for Femoral Head Avascular Necrosis. 11^th Congress Effort E poster content. 2–5 June 2010 Madrid, Spain.