Joint pain is an extremely common complaint with an almost intimidatingly broad differential diagnosis; a systematic approach is key to the proper workup of these patients. An essential first step is determining the exact joints which are involved; note that in this specific patient, the pain is localized to the large joints of the right lower limb. When assessing pain in the large joints of the lower limbs, a key point which should be kept in mind is that pain in the hip can be referred to the knee (and at times even perceived as only involving the knee). Evaluation of this patient's right knee joint reveals no evidence of inflammation or swelling, while all active and passive movements are unrestricted. This essentially rules out pathology of the knee. On the other hand, pathology of the hip joint is quite likely; in particular, anterior hip pain is classically associated with intra-articular pathology. Note also the coxalgic gait; this shifts the patient's center of gravity, so as to lessen the forces that act upon the acetabulofemoral joint; it is characteristic of hip pathology. Following identification of the specific joint involved, the next step should be close assessment of the specific characteristics of the pain, including the location, onset, and duration. This patient's pain is localized to the anterior hip; thus, key pathologies to consider include fractures of the proximal femur, iliopsoas bursitis, tendinitis of the hip flexors, acetabular labral tears, osteoarthritis, osteonecrosis (avascular necrosis), inflammatory arthritis, septic arthritis, and tuberculous arthritis. Note also that the pain was insidious in onset, and has persisted for an extended period of time; this argues against septic arthritis, where symptoms are typically florid and rapid in onset. The absence of previous trauma argues against a fracture, although stress fractures cannot be ruled out; iliopsoas bursitis, hip flexor tendinitis, and hip labral tears are typically encountered in athletes, as a consequence of overuse or sports injury. Inflammatory arthritis is also clinically less likely, as there is no pain at rest, or relief/reduction of pain with activity. Neither is tuberculous arthritis likely, as there is no history of immunocompromise, or a contact history with tuberculosis. However, osteoarthritis is a definite possibility (although this is less common in patients under the age of 40); this could either be primary, or secondary to another disease process. Note that when considering secondary osteoarthritis in a patient of this age, the possibility of old Legg-Calve-Perthes' disease should be kept in mind; this often causes only transient symptoms during childhood, which the patient may not recall unless explicitly prompted. Osteonecrosis (avascular necrosis) is an even stronger possibility; note in particular that alcoholism is a major risk factor for the condition. The next step in his workup should be targeted investigations, starting with plain radiographs showing an anteroposterior view of the pelvis and a frog-leg lateral view of the symptomatic hip; it would also be prudent to obtain an x-ray of the right knee as well. Note that the radiographs reveal sclerotic and lytic lesions of the right femoral head, along with partial subchondral collapse and narrowing of the joint space; this appearance is highly suggestive of osteonecrosis of the femoral head. A follow up magnetic resonance imaging (MRI) study confirms these findings; note also that this indicates stage V osteonecrosis, as per the Steinberg classification (i.e. early collapse of the femoral head). Once femoral head collapse has taken place, total hip arthroplasty (THA) is the preferred technique of management. Core decompression is mainly useful in early disease (i.e. before collapse has occurred). Glucocorticoid therapy is a risk factor for osteonecrosis, and is contraindicated here; nor is there any indication for immediate antibiotic therapy.
Osteonecrosis (which is also known as aseptic or avascular necrosis) is defined as death of bone cells and bone marrow secondary to the loss of blood supply. In the United States, between 10,000 and 20,000 cases are reported annually; the condition accounts for 5% to 12% of all total hip replacements performed each year. Overall, it is most common between the 3rd of 5th decades of life, with a male preponderance. Osteonecrosis can be associated with traumatic or non-traumatic insults to femoral head blood supply. Traumatic insults include displaced fractures and dislocations of the hip; the two most common risk factors for atraumatic osteonecrosis are corticosteroid therapy and alcohol consumption. The pathophysiology of alcohol-induced osteonecrosis is not completely understood as of writing. Proposed mechanisms include increased accumulation of lipids inside the osteocytes of the femoral head resulting in compression of their nuclei, and/or the direct toxic effects of alcohol on osteocytes causing chronic cellular lesions that are unable to heal. The ultimate outcomes are cell death and eventual collapse of the femoral head. The mechanism of steroid induced osteonecrosis is also believed to be due to changes in lipid metabolism within the femoral head. Note also that connective tissue disorders, vascular disorders, vasculitis and orthopedic conditions such as developmental dysplasia of the hip, congenital hip dislocation, hereditary dysostosis, Legg-Calve-Perthes' disease, and slipped capital femoral epiphysis may also cause osteonecrosis. Up to 10% to 20% of cases have no identifiable cause and are classified as idiopathic. Osteonecrosis can present with many different clinical manifestations; in some cases, it may be clinically silent. The chief presenting complaint is pain, often localized to the anterior hip or groin, and occasionally to the ipsilateral buttock or knee. Physical examination typically reveals pain with both active and passive motion of the affected hip, and a coxalgic gait. Pain with internal rotation, clicking of the hip, and a reduced range of motion are signs that the femoral head has collapsed. Note that a complete evaluation of the contralateral hip should always be undertaken, as 40% to 80% of cases are bilateral. Anteroposterior and lateral ('frog-view') hip x-rays are important first-line investigations. However, as bone remodeling is relatively slow, there may be no x-ray changes in early disease. Magnetic Resonance Imaging (MRI) is considered the current gold standard diagnostic study, and shows a sensitivity and specificity of 99%; it can detect changes as early as 5 days after the initial insult. Bone scans may also detect early remodeling, but can be misleading, with a 25% to 45% false negative rate. Over 16 major classification systems are used to stage osteonecrosis. These include the Ficat classification, which uses x-ray appearances; and the Steinberg system which also uses information from MRIs and bone scans. Treatment options for Osteonecrosis include medical and physical measures and operative techniques. In general, in the early stages of the disease, prophylactic measures are instituted to prevent further progression, while in the latter stages, a reconstructive procedure is the treatment of choice. Physical treatment options include the use of raised shoes, walking aids, the avoidance of squatting positions and preferable adoption of a sitting position. Medical treatment options include bisphosphonates to reduce osteoclast activity, lipid-lowering drugs to correct the altered lipid metabolism, and vasodilators to reduce intraosseous pressure. Other novel techniques which are still being evaluated include extracorporeal shock wave therapy, pulsed electromagnetic therapy, and administration of hyperbaric oxygen. The surgical management of osteonecrosis can be divided into head-preserving procedures (core decompression and resurfacing) and arthroplasty. Patients who are pre-collapse are generally treated with head-preserving procedures; these include core decompression, and limited femoral resurfacing. Core decompression involves drilling a single large hole in the femoral head. This reduces the intraosseous pressure in the femoral head and promotes new bone formation and angiogenesis. Limited femoral resurfacing can be used in late to mid collapse to salvage the femoral head provided there is no acetabular involvement. In younger patients, the above techniques have several potential advantages, including preservation of femoral bone stock, low dislocation rates, simplicity of revision, and deferral of total hip arthroplasty. In patients who have experienced collapse of the femoral head and/or arthritis arthroplasty is generally preferred. Total hip arthroplasty (THA) is the single treatment with the highest likelihood of providing excellent early pain relief and good functional outcome. However, it sacrifices more host bone and narrows future operative options. Relative contraindications to the procedure include the younger patient in whom head preserving options may be more appropriate, and individuals who may be at risk of recurrent dislocation, such as alcoholics. Note also that in all patients, modifiable risk factors, such as alcohol abuse, should be assessed and treated as appropriate.