A modular femoral head–neck junction has practical
advantages in total hip replacement. Taper fretting and corrosion
have so far been an infrequent cause of revision. The role of design
and manufacturing variables continues to be debated. Over the past
decade several changes in technology and clinical practice might
result in an increase in clinically significant taper fretting and
corrosion. Those factors include an increased usage of large diameter
(36 mm) heads, reduced femoral neck and taper dimensions, greater
variability in taper assembly with smaller incision surgery, and
higher taper stresses due to increased patient weight and/or physical
activity. Additional studies are needed to determine the role of
taper assembly compared with design, manufacturing and other implant
variables. Cite this article:
Since 1996 more than one million metal-on-metal
articulations have been implanted worldwide. Adverse reactions to
metal debris are escalating. Here we present an algorithmic approach
to patient management. The general approach to all arthroplasty
patients returning for follow-up begins with a detailed history,
querying for pain, discomfort or compromise of function. Symptomatic
patients should be evaluated for intra-articular and extra-articular
causes of pain. In large head MoM arthroplasty, aseptic loosening
may be the source of pain and is frequently difficult to diagnose.
Sepsis should be ruled out as a source of pain. Plain radiographs
are evaluated to rule out loosening and osteolysis, and assess component
position. Laboratory evaluation commences with erythrocyte sedimentation
rate and C-reactive protein, which may be elevated. Serum metal
ions should be assessed by an approved facility. Aspiration, with
manual cell count and culture/sensitivity should be performed, with
cloudy to creamy fluid with predominance of monocytes often indicative
of failure. Imaging should include ultrasound or metal artifact
reduction sequence MRI, specifically evaluating for fluid collections
and/or masses about the hip. If adverse reaction to metal debris
is suspected then revision to metal or ceramic-on-polyethylene is indicated
and can be successful. Delay may be associated with extensive soft-tissue
damage and hence poor clinical outcome.
Biochemical markers of bone-turnover have long been used to complement the radiological assessment of patients with metabolic bone disease. Their implementation in daily clinical practice has been helpful in the understanding of the pathogenesis of osteoporosis, the selection of the optimal dose and the understanding of the progression of the onset and resolution of treatment. Since they are derived from both cortical and trabecular bone, they reflect the metabolic activity of the entire skeleton rather than that of individual cells or the process of mineralisation. Quantitative changes in skeletal-turnover can be assessed easily and non-invasively by the measurement of bone-turnover markers. They are commonly subdivided into three categories; 1) bone-resorption markers, 2) osteoclast regulatory proteins and 3) bone-formation markers. Because of the rapidly accumulating new knowledge of bone matrix biochemistry, attempts have been made to use them in the interpretation and characterisation of various stages of the healing of fractures. Early knowledge of the individual progress of a fracture could help to avoid delayed or nonunion by enabling modification of the host’s biological response. The levels of bone-turnover markers vary throughout the course of fracture repair with their rates of change being dependent on the size of the fracture and the time that it will take to heal. However, their short-term biological variability, the relatively low bone specificity exerted, given that the production and destruction of collagen is not limited to bone, as well as the influence of the host’s metabolism on their concentration, produce considerable intra- and inter-individual variability in their interpretation. Despite this, the possible role of bone-turnover markers in the assessment of progression to union, the risks of delayed or nonunion and the impact of innovations to accelerate fracture healing must not be ignored.
The management of patients with a painful total knee replacement requires careful assessment and a stepwise approach in order to diagnose the underlying pathology accurately. The management should include a multidisciplinary approach to the patient’s pain as well as addressing the underlying aetiology. Pain should be treated with appropriate analgesia, according to the analgesic ladder of the World Health Organisation. Special measures should be taken to identify and to treat any neuropathic pain. There are a number of intrinsic and extrinsic causes of a painful knee replacement which should be identified and treated early. Patients with unexplained pain and without any recognised pathology should be treated conservatively since they may improve over a period of time and rarely do so after a revision operation.
A comprehensive review of the literature relating to the pathology and management of the diabetic foot is presented. This should provide a guide for the treatment of ulcers, Charcot neuro-arthropathy and fractures involving the foot and ankle in diabetic patients.
Chronic patellofemoral instability can be a disabling condition. Management of patients with this condition has improved owing to our increased knowledge of the functional anatomy of the patellofemoral joint. Accurate assessment of the underlying pathology in the unstable joint enables the formulation of appropriate treatment. The surgical technique employed in patients for whom non-operative management has failed should address the diagnosed abnormality. We have reviewed the literature on the stabilising features of the patellofemoral joint, the recommended investigations and the appropriate forms of treatment.
