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KINI MEMORIAL ORATION Table of Contents   
Year : 2003  |  Volume : 37  |  Issue : 2  |  Page : 2
Osteonecrosis of the femoral head (in young individuals)


Sushrut Hospital, Research Centre and Post Graduate Institute of Orthopaedics, Nagpur, Former Professor of Orthopaedics, Indira Gandhi Medical College and Mayo General Hospital, Nagpur, India

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How to cite this article:
Babhulkar SS. Osteonecrosis of the femoral head (in young individuals). Indian J Orthop 2003;37:2

How to cite this URL:
Babhulkar SS. Osteonecrosis of the femoral head (in young individuals). Indian J Orthop [serial online] 2003 [cited 2019 Sep 18];37:2. Available from: http://www.ijoonline.com/text.asp?2003/37/2/2/48500
Osteonecrosis of the femoral head, also known as avascular necrosis or aseptic necrosis is now recognised as a major musculo-skeletal problem mostly affecting the young people in their productive years of life. It is often characterised by relentless progression despite treatment.

Osteonecrosis (ON) is known to affect multiple locations in the axial and appendicular skeleton and is associated with diverse medical conditions and injury. The true prevalence of the disease is difficult to ascertain. In 5 to 18% of total patients undergoing total hip replacement in the US, the indication was reported to be advanced osteonecrosis with secondary osteoarthritis.[1],[2]

Historical Perspective [3] :

The earliest documentation and probably one of the first reports of `aseptic necrosis' of the femoral head was by James Russel, Professor of Clinical Surgery in Edinburgh in the year 1794. The gross appearance of bone necrosis was clearly described by James Paget in 1860. In 1888, the first description of necrosis in a femoral head associated with Caisson's disease was published by Twynham. Another landmark paper was by Phemister in 1915, who described the microscopic findings in necrotic bone, comparing the changes in bone dying as result of infection (septic necrosis) with those resulting from a circulatory disturbance (aseptic necrosis). The earliest reports of ON with common associated conditions like alcoholism and steroids were published by Axhausen (1922) and Pietrogrande and Mastromarino (1957) respectively. In 1948, Chandler postulated that occlusion of posterolateral retinacular artery leads to ischaemic infarction and eventual collapse of anterolateral area of femoral head producing typical wedge shaped deformed femoral head on plain radiograph, like the process of coronary artery disease. He coined the term `Coronary disease of hip' which was widely accepted.

Types of ON:

Broadly two types of ON are recognised: Traumatic and Nontraumatic.

Traumatic ON:ON can occur in a bone with vulnerable vascular supply with or without associated risk factors. The incidence of traumatic ON is known to vary with the location and severity of injury, type and timing of treatment and associated injuries. [4],[5],[6]

Although the hip is the most common anatomic location for traumatic ON, other vulnerable sites include the scaphoid, talus and the proximal humerus.

Nontraumatic ON:This is usually a disease of the young people. The average age of patients in a large series was found to be 38 years, with only 20% of patients being older than 50 years of age [2] . In another study, the mean age was reported to be 34 years.?

Factors associated with high risk:

Nontraumatic ON is usually associated with one or more risk factors. In the western literature, approximately two thirds of this is related to alcohol abuse and corticosteroid intake. The remaining third are associated with diverse conditions like decompression sickness, sickle cell haemoglobinopathy, storage disorders like Gauchers disease, pregnancy and coagulopathies. Other groups of patients prone to develop ON include organ transplant recipients, inflammatory bowel disease, lupus erythematosus.

In Central India, sickle cell disease has a very high prevalence and is the most common associated condition with osteonecrosis followed by alcohol abuse and corticosteroid use. The various causes of nontraumatic osteonecrosis studied over a period of 25 years and with a minimum follow up of 10 years is given in [Table 1].

The Silent Hip:The difficulty in estimating the prevalence of ON arises because the condition is aymptomatic in the early stages. The term 'Silent Hip' is applied to the asymptomatic hip in patients who present for the management of the contralateral painful hip. The reported incidence of bilaterality ranges from 6 to 72%. [8],[9],[10] Despite a high incidence of bilaterality only about 15% of patients report bilateral symptoms on initial presentation. [10]

Theories of causation of osteonecrosis:

A number of different theories have been proposed for the causation of osteonecrosis. These include: the microembolisation theory, the intraosseous hypertension theory, intravascular coagulation and multifactorial causation of osteonecrosis.

It is observed that anterosuperolateral segment of the femoral head undergoes necrosis first. This is obviously because of occlusion of posterolateral retinacular vessels or by emboli from various sources finding their way through the microcirculation into the subchondral zone of femoral head. This results into weakening of trabecular structure leading to multiple micro-fracture and finally collapse in weight bearing portion of the femoral head. This is the 'Micro-embolization theory' for the pathogenesis of avascular necrosis of femoral head. [11]

There is another concept for the formation of avascular necrosis of femoral head: 'Intraosseous hypertension theory'. According to this theory the femoral head bone functions as a closed compartment and the eventual infarction of weight bearing bone is the end stage of progressive compartment syndrome produced by increased intraosseous pressure. [12] The findings of increased bone marrow pressure at all stages and even in early pre-radiologic stage supports this theory.

It is presumed that there could be combination of both the theories. [11]

'Intravascular coagulation' was proposed by Jones as the missing link joining several unrelated risk factors that result in nontraumatic osteonecrosis. [13] It was proposed that the coagulopathy was not the cause of ON but only an intermediary event initiated by an underlying etiologic factor, The thrombotic threshold may be decreased in the various hypercoagulable patients with hereditary thrombophilia, hyperlipemia or antiphospholipid antibodies. Subsequent exposure to one or more additional risk factors facilitates thrombosis and bone infarction. Intravascular lipid has been observed in histologic studies of the femoral heads from osteonecrosis patients with alcoholism and hypercortisonism. [14] Jones has proposed that fat emboli arising from different sources like fatty liver, destabilization and coalescence of plasma lipoproteins and disruption of bone marrow trigger a thrombotic process of focal intravascular coagulation resulting in osteonecrosis. [13]

Imaging of osteonecrosis:

Osteonecrosis is a disease characterized by ischaemic death of bony and marrow tissues. Different imaging modalities provide different information on the mineralized and non-mineralised component of the bone. Early diagnosis and proper staging of the disease are important for planning the treatment and improving clinical outcome. [2],[15],[16] The advent of Magnetic resonance imaging (MRI) has dramatically improved the diagnosis of ON.

Radiography :The standard technique should include antero-posterior (AP) of the pelvis and frog leg lateral views of both hips. The plain radiographs are of limited use in the early stages but plain radiography findings are characteristic in stage 3 and 4 and any additional imaging modality is not required for final diagnosis. [17],[18] Plain radiography is unable to detect changes during the ischaemic stage and changes become apparent only after the process of repair has started. Another limitation of plain radiographic findings is poor inter- and intra-observer correlation. [19],[20] Despite this plain radiographs remain the first imaging step as it can help in differentiating ON from a number of other causes of painful hip joint and is also useful for staging of the disease. The Steinberg staging is still useful in taking management decisions and hence is given in the later section on staging.

Computed tomography :CT is particularly useful in detecting subtle collapse of the femoral head when conventional radiographs appear normal. [21] Additional multiplanar two dimensional reconstruction in the coronal and sagittal planes are helpful for ARCO staging and surgical planning. The complex architecture of the trabeculae in the femoral head allows early recognition of the patchy repair process on CT. This so called 'asterisk sign' represents an early but nonspecific ON pattern. [18],[22] The main advantage of CT compared to other imaging modalities is the accurate detection of subchondral fracture or early femoral collapse.

Bone scintigraphy:The standard technique should include three phase scintigraphy and anterior and posterior planar scans. Bone scintigraphy can visualize the regional blood flow, but is not able to measure the efficiency of the vascular supply or repair mechanism. The interruption of blood supply, detected as cold spot, is an nonspecific pattern and can be found in several other bone marrow processes. [18] The repair process with revascularisation, detected as a hot spot is the most common finding but is nonspecific. Only a combination of cold in hot spot represents a diagnostic pattern for ON. [21] Thus bone scan is highly sensitive for detection of early ON changes but the specificity is low to allow a definitive diagnosis of ON. Bone scintigraphy in ON is indicated for patients with risk of multifocal lesions when MRI is not available or for patients at high risk for ON who have persistent pain despite negative MRI. [21]

Magnetic resonance imaging (MRI):MRI is the most accurate imaging modality for the diagnosis of ON of femoral head, especially in the early stages when there are only bone marrow changes. Conventional MRI studies may be false negative in evaluating the earliest lesions in which the cellular integrity of the necrotic fatty marrow is intact or when the lesion is very small and under the resolution of MRI. An accuracy of more than 90% is reported with routine MRI techniques. [2],[8],[21],[23]

The preferred equipment and imaging technique should include at least 0.5 Tesla units, 3mm slice thickness, body coil with coronal sections of both hips, and T1- and T2 weighted images. An additional fat suppression sequence will increase the accuracy of MRI. [21] Characteristic MRI signal alterations in the anterosuperior portion of the femoral head surrounded by a band of low signal intensity on T1- and T2 weighted images represent the diagnostic criteria of ON on MRI [Figure 1]. The occurrence of a double-line sign on the T2-weighted image represents a pathognomonic ON sign, but its absence does not eliminate the diagnosis of ON. [21] An additional MRI finding in ON is a joint effusion, which can be graded on T2 weighted images. [23]

The limitation of MRI in ON is indicated by the lack of clear prognostic criteria for the signal alterations. [24],[25] Furthermore, MRI is less sensitive than radiography and, especially CT in detecting subchondral fractures or early femoral flattening. [18],[21],[26]

Additional imaging studies:

Digital Substraction Angiography:With the use of this technique Wheeless et al [27] have demonstrated vessel abnormalities in 31% of control hips compared to 94% of osteonecrosis hips. The vessel abnormalities were significantly higher in subgroups with additional risk factor. Their results may indicate that there is a population that is at risk for ON as a result of anomalies of the macrovascular circulation to the femoral head.

Staging of osteonecrosis:

There are a number of staging systems for osteonecrosis, but with inherent problems of poor reliability.

Neel Marcus et al (1973) - Florida system [28]

Steinberg et al (1984) - Philadelphia system [29]

Ficat & Arlet (1985) - French system [30]

ARCO Classification (1993) [31]

The Steinberg staging given below [Table 2] is widely accepted and is used in planning the treatment.

ARCO classification

The Association Research Circulation Osseous (ARCO) has proposed a new international classification system including radiographs, computed tomography (CT), bone scans, and MRI. [2],[31] This classification system incorporates the Pennsylvania system based on lesion size and the Japanese system based on lesion location. [32] Quantitation (% area involvement of femoral head, length of crescent sign, % surface collapse, and dome depression) and location of the lesion (medial, central or lateral) represent important prognostic factors. The ARCO classification has been proposed as the preferred system. [2],[33],[34]

The new ARCO classification is based on newer imaging techniques and is expected to correlate with histomorphologic findings. [2],[17],[35] The ARCO classification is therefore given here in detail [Table 3].

Diagnostic criteria:

The diagnosis of avascular necrosis should be considered as established if any of the following are found:

  1. Pathognomonic radiographic changes (collapse of the femoral head, anterolateral sequestration, crescent sign)
  2. A double line on T2 weighted MRI.
  3. Increased uptake surrounding a photopenic area of bone scan (cold in hot)
  4. Positive finding on bone biopsy- showing empty lacunae involving multiple adjacent trabeculae.


Treatment

Rationale for the treatment of osteonecrosis of femoral head requires a lot of consideration. [2],[36] Prime importance in this is the age of patients, whether both hips are affected, etiology of the associated diseases, demands and requirement of the patients, and the stage of the disease when the patient presents for treatment is equally important. The treatment should be planned according to ARCOs classification and Steinberg staging. Non-weight bearing conservative management of ischaemic necrosis has not been proved to be beneficial and hence various operative procedures are done depending upon the stage of necrosis of femoral head.

Observation and protected weight bearing:More than 85% patients had collapse of femoral head at two years when symptomatic hips with stage I and II were left untreated. More studies have shown that non-operative treatment yields poor results. The only condition for which the protected weight bearing might be effective is a type A lesion - involvement of medial aspect of femoral head. No drugs have been useful and specific in the treatment of osteonecrosis

Electrical stimulation:Experimentally electrical stimulation has shown to enhance neovascularisation, as well as alter the osseous turnover. Three different methods have been used.

  • Non-invasive pulsed electromagnetic field stimulation.
  • Direct current stimulation of necrotic area through electrode after core decompression.
  • Non-invasive direct current stimulation after core decompression.


Aaron et al [37] reported good to excellent results in 68% after pulsed electromagnetic field. Electrical stimulation still remains experimental for Osteonecrosis of femoral head in most of the patients and our institute has no experience of this method.

Operative Treatment

Prophylactic treatment (Stage O and I)

Whenever possible one must prevent the disease from occurring altogether. This can be very well achieved partially in the cases of osteonecrosis of femoral head following alcohol abuse, dysbarism and by avoiding the use of corticosteroids in condition like renal transplantations, skin manifestations, ulcerative colitis etc. Sickle cell patients are monitored closely and at the earliest hint of a crisis they are hydrated and oxygenated properly and acidosis is corrected. Control of alcoholism will definitely reduce the incidence of osteonecrosis of femoral head.

The patient with proven unilateral osteonecrosis of femoral head should be observed closely since 50% to 80% of the patients develop bilateral affection. [38],[39] Any symptoms in untreated hip should be taken as high risk suspicious of osteonecrosis of femoral head. If there are no radiographic changes, MRI or bone scanning should be done. If the bone scan is negative, patient should be closely observed and followed. May be sequential MRI has a place in this group of patients for early diagnosis and treatment.

Treatment before collapse (Stage II &III)

Aim of the treatment at this stage is to reduce the intraosseous tension and perform the procedure, which will cause early revascularization of ischaemic head. In the patients where changes are evident radiologically before the collapse (II and III) core decompression and various bone grafting procedures are advised. Vascular pedicle grafting, muscle pedicle grafting or free fibular grafting after core decompression are commonly indicated depending upon the stage of the disease. Core decompression and free bone grafting using long cortical graft from fibula or core decompression and bone grafting using cancellous bone graft from iliac crest of the same side is advocated in early stages. It is observed that cortical graft adds both to the biomechanical and biological advantages during the process of revascularization. Whenever the crescent sign had appeared without any collapse, it was taken as the indication of vascular or muscle pedicle grafting in addition to core decompression for early revascularisation. Meyer's (Quadratus femoris muscle pedicle graft) procedure by posterolateral approach and Sartorius muscle pedicle grafting by anterolateral approach in addition to forage was done previously. But routinely now we use TFL-tensor fascia lata graft [Figure 2a],[Figure 2b]. [40],[41] However use of vascularised pedicle graft is more advantageous since high percentage of marrow and osteogenic cells survive within a living graft, which helps for early vascularisation. This is done by anterior approach by using part of iliac crest with deep circumflex iliac vessels.

Personal experience of head preserving surgeries in stage II and III of osteonecrosis is summarized in [Table 4].

Results of Core Decompression and Bone Grafting:

The results obtained in my personal series of patients are summarized in [Table 5].

In 1995, Mont and associates [42] reported the results of a literature search of core decompression. They found 42 reports involving 2025 hips treated by either core decompression (1206 hips) or nonsurgical management (819 hips). In the 24 reports of core decompression, 63.5% of the hips had a satisfactory clinical result, compared to only 22.7% of the hips in the 21 studies reporting on non-surgical treatment.

There are only two prospective randomised studies on this subject. [43],[44] Robinson [43] reported 4/19 radiographic failures noted as progression of the disease and 15/19 clinical successes in the cored group compared to 10/16 radiographic failures and 7/16 clinical successes in the non-surgically managed group. In the cored group, three had proceeded to THR compared to 7 in the non-surgical group.

Stulberg and associates [44] reported similar results with 8/28 cored hips (stage I to III) progressing to THR compared to 20/22 conservatively managed hips.

Treatment following Collapse (Stage IV)

It is believed that once crescent sign appears and there is a collapse of necrotic bone segment, even if it is minimal on X-ray, further collapse is inevitable and hip joint is likely to disintegrate. [11] Any procedure likes core decompression and bone grafting which is likely to revascularise the dead segment is not going to be useful once the collapse of segment occurs. Hence at this stage the procedure to change the weight bearing necrotic segment to non-weight bearing portions by different osteotomies are performed. [45],[46] This is to eliminate from the necrotic focus of shear forces that impede the reparative process and also restore the joint alignment as the femoral head is subluxated secondary to collapse of the articular process.

Transtrochanteric ventral rotational osteotomies [Figure 3a],[Figure 3b] in stage IV are done primarily in cases with collapse of femoral head without any degenerative changes. [45],[46] At times instead of ventral rotation, flexion osteotomies are done. Basically in both these osteotomies the weight bearing superolateral segment is rotated anteromedially in non-weight bearing region. Valgus / varus osteotomy [47],[48] is also advised depending upon the situation of collapsed femoral head segment, for proper containment of undamaged femoral head underneath the acetabulum for weight bearing [Figure 4a],[Figure 4b]. McMurray's osteotomy frequently done in earlier days is not considered presently as a suitable operation for osteonecrosis of femoral head. In all these operated patients early mobilization is done but non-weight bearing is maintained for 4-5 months.

I have no experience of osteochondral allograft [49] , spongioplasty, vascular bundle transplantation or electrical stimulation. [29]

Results of Proximal Femoral Osteotomy:

The results of proximal femoral osteotomies performed at our center are summarized in [Table 6].

Although few authors have reported results of either varus or valgus intertrochanteric osteotomy in osteonecrosis [47],[48], Sugioka and associates advocate rotational osteotomy.

Hosokawa et al [50] reported results of 136 rotational osteotomies in 98 patients followed up for at least 10 years. Satisfactory clinical results were obtained in 85% of the hips with stage II osteonecrosis. Hips that underwent surgery in early stages showed better results than the hips operated on in late stages. The incidence of prosthetic replacement after rotational osteotomy also increased with the advanced stage of the disease with 6.8% in stage 2 and 24.1% for stage 4 osteonecrosis.

Treatment in Late Stages (Stage V and VI)

If the patient came very late in stage V and VI after degenerative changes have started one is left with no other choice than to do hemiarthroplasty; total hip joint replacement, rarely arthrodesis or Girdlestone operation.

It has been observed that there is an early failure of total hip replacement in osteonecrosis than in age-matched patients with other diagnosis because of abnormal remodeling of bones, and subsidence of prosthesis because of poor quality of proximal femoral bone. Other contributory factors are- ongoing systemic disease, defects in mineral metabolism, use of steroids, high level of activity in young patients and increased body weight. Hence we prefer to delay or eliminate the need for hip replacement by performing head preserving surgeries.

Results of total hip replacement in osteonecrosis:

It is my preference to use hybrid THR in young patients with osteonecrosis. Though long term results are not available, early results at 2 years follow up have showed a remarkable change in the Harris hip score in these patients.

Early reports on the use of total hip replacement for osteonecrosis showed a high incidence of unsatisfactory results. Stauffer [51] reported a 50% failure with a follow up of 10 years whereas Cornell and Salvatti [52] reported a 37% failure with 8 years of follow up. In both of these studies, cemented prostheses were used.

The results using cementless prostheses have been mixed. Brinker and associates [53] reported 80% excellent results at a follow up of 4 - 6 years with a revision rate of 10%. The revision rate in patients younger than 35 years of age was 24%. Thigh pain was noted in 25% of patients after THR using PCA prostheses at a follow up of 4 - 6 years. [54] Another study using porous coated THA in 78 cases reported a failure rate of 20.5% and an incidence of acetabular and femoral osteolysis of 20.5% at a follow up of 7.2 years. My personal approach to the management of osteonecrosis in young adults can be summarized in [Table 7].

 
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47.Saito S, Ohzono K, Ono K. joint preserving operations for idiopathic avascular necrosis of the femoral head: Results of core decompression, grafting and osteotomy. J Bone Joint Surg [Br] 1988;70-B:78-84.  Back to cited text no. 47    
48.Meyers MH. The treatment of osteonecrosis of the hip with fresh osteochondral allografts and with the muscle-pedicle graft technique. Clin Orthop 1978; 130: 202-209.  Back to cited text no. 48  [PUBMED]  [FULLTEXT]
49.Hosokawa A, Mohtai M, Hotokebuchi T, Jingushi S, Sugioka YL. Transtrochanteric rotational osteotomy for idiopathic and steroid-induced osteonecrosis of the femoral head: Indiacations and long-term followup. In Urbaniak JR, Jones JP (eds) Osteonecrosis: etiology, diagnosis, and treatment. American Academy of Orthopaedic Surgeons,1 st ed., 1997.  Back to cited text no. 49    
50.Stauffer RN. Ten-year follow up study of total hip replacement. J Bone Joint Surg [Am] 1982;64-A:983-990.  Back to cited text no. 50    
51.Cornell CN, Salvati EA, Pellicci. Long term follow-up of total hip replacement in patients with osteonecrosis. Orthop Clin North Am 1985;16:757-769.  Back to cited text no. 51    
52.Brinker MR, Rosenberg AG, Kull L et al. Primary total hip arthroplasty using uncemented porous-coated femoral components in patients with osteonecrosis of the femoral head. J Arthroplasty 1994;9:457-468.  Back to cited text no. 52    
53.Lins RE, Barnes BC, Callaghan JJ et al. Evaluation of uncemented total hip arthroplasty in patients with avascular necrosis of the femoral head. Clin Orthop 1993;297:168-173.  Back to cited text no. 53    
54.Kim YH, Oh JH, Oh SH. Cementless total hip arthroplasty in patients with osteonecrosis of the femoral head. Clin Orthop 1995;320:73-84.  Back to cited text no. 54  [PUBMED]  [FULLTEXT]

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Correspondence Address:
Sudhir S Babhulkar
Sushrut Hospital, Research Centre and Post Graduate Institute of Orthopaedics, Nagpur, Former Professor of Orthopaedics, Indira Gandhi Medical College and Mayo General Hospital, Nagpur
India
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Source of Support: None, Conflict of Interest: None


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