CHAPTER SYNOPSIS
The initial chapter in the series on hip arthritis and arthroplasty focuses on the varying causes and symptoms of hip arthritis. Arthritis of the hip joint can lead to debilitating quality of life from both physical and psychological aspects of patients’ lives. Different etiologies are explored that lead to the same basic end point: degenerative joint disease of the hip.
IMPORTANT POINTS:
- 1
Osteoarthritis is not an inflammatory condition; rather, it is a wear-and-tear disease with a predisposition in patients with a high body mass index.
- 2
Femoroacetabular impingement has become a well-known entity in the etiology of mechanical hip degeneration. Today’s arthroplasty surgeons should dedicate much focus to the early recognition of the femoral neck abutting the acetabular rim.
- 3
Late diagnosis of congenital dysplastic hip can lead to increased difficulty in total hip replacement from femoral head articulation with a false acetabulum and subsequent shortening of hip musculature.
- 4
Periarticular hip fractures should be monitored closely for early signs of degenerative joint disease.
- 5
Many etiologies can lead to osteonecrosis of the femoral head, including slipped capital femoral epiphysis, Legg-Calvé-Perthes disease, and iatrogenic causes. Again, early recognition of chondral collapse and subchondral fracture is pivotal to the early intervention in this typically younger population.
- 6
Inflammatory arthropathies require specific diagnoses to maximize treatment effectiveness.
- 7
Septic arthritis is a unique form of arthritis because of its potential infectious complications in the setting of hip arthroplasty.
INTRODUCTION
Arthritis of the hip joint can be a debilitating disease. It can also be a subclinical entity that rarely causes symptoms. It encompasses a wide range of etiologies, with the common end point being degeneration of the hip joint. This chapter focuses on those etiologies and the mechanisms for the development of arthritis.
With an aging population in North America, the prevalence of arthritis and the resulting need for total hip replacement is expected to rise. In 2003 data from the American Academy of Orthopaedic Surgeons, primary total hip arthroplasty procedures numbered 234,000, up from 117,000 in 1991. Furthermore, the number of hip revision surgeries has also increased, from 23,000 in 1992 to 46,000 in 2004. Average length of hospital stay for primary hip replacement has been dramatically reduced. In 1990, the average hospital stay was approximately 11 days. This number was just over 4 days in the most recent data in 2004. The decreased length of hospitalization is mirrored in partial and revision hip procedures (from 14 to 6 days for each). Interestingly, hospital costs for these procedures have strikingly increased. In 1990, both partial and total hip procedure hospital costs were $23,000 per procedure. By 2004, both procedures, on average, cost $35,000. Revision hip procedures saw similar increases, from $31,000 in 1990 to $45,000 in 2004. This equates to a dramatic increase in total hospitalization costs to our health care system, from $7.02 billion for all three procedures in 1990 to $12.01 billion in 2004, with the greatest percent change in primary total hip arthroplasty procedures.
A study published in 2007 lends strong evidence to the continued increase in total hip arthroplasty. The study projects primary total hip procedures to increase from 209,000 in 2005 to 572,000 by the year 2030, an increase of 174%. Revision total hip surgeries also are expected to continue their rise in number, from 40,800 in 2005 to 96,700 by 2030 (a 137% increase).
MECHANICAL ETIOLOGIES
Mechanical etiologies of arthritic hips are progressive processes from either frank or more insidious causes of joint abnormalities. Below is a brief review of some of the more commonly encountered causes and how their disease processes lead to an arthritic hip joint.
Osteoarthritis
Arthritis of the hip has multiple etiologies, with osteoarthritis being the most prevalent. In data from 2004 to 2005, a reported one in five Americans had a physician diagnosis of arthritis. This number is expected to increase to 67 million by the year 2030. Most cases are osteoarthritic in nature and often involve the lower extremity, either the hip or knee. Osteoarthritis is one of the most debilitating diseases in the United States, accounting for 36 million ambulatory care visits and $128 billion in total costs annually.
Nearly all persons older than 70 years will exhibit imaging evidence, either on magnetic resonance images or plain radiographs, of osteoarthritic changes. However, symptomatic hip arthritis is present in only 3% of elderly people. Several etiologic factors lead to symptomatic hip osteoarthritis without a definable cause or predisposition. Some risk factors associated with hip osteoarthritis include age, sex, family history, and possibly race. Other risk factors, deemed potentially modifiable, include obesity, lack of physical activity or exercise, muscle weakness, and joint injury.
Persons with higher bone density are actually at an increased risk for osteoarthritis; thus the prevalence of osteoporosis and osteoarthritis is inversely related. Because it is a large weight-bearing joint, the hip would seem to be strongly affected by obesity, leading to higher bone density and higher osteoarthritis rates. However, the evidence has been inconsistent. One theory holds that adiposity below the hip joint does not directly contribute to loading of the hip joint, and that by its ability to distribute weight loads in a broader fashion, the hip joints self-protect from the effects of obesity. However, other studies indicate a relation between being overweight or obese and increased risk of hip osteoarthritis.
Links between high body mass index (BMI) and hip osteoarthritis have been made both in the United States and abroad. In a 2003 article, Karlson et al discovered that BMI was associated with an increased risk of osteoarthritis and proved that a patient’s recalled BMI at 18 years of age had an effect on later risks. The study showed a high BMI at age 18 years greatly increased risk estimates more than recent BMI reported after symptoms were well established. Another article estimated that hip osteoarthritis would decrease by 25% if obesity could be eliminated. More recently, a study from the United Kingdom showed that middle-aged women were at increased risk of hip osteoarthritis with increased BMI. Women with BMI of 30 kg/m 2 or greater, when compared with women with BMI levels less than 22.5 kg/m 2 , had a relative risk of 2.47 kg/m 2 for hip replacement. In another study examining the risks of more than 300,000 male construction workers in Stockholm, BMI also correlated to an increased risk of hip osteoarthritis. The relative risks of hip osteoarthritis more than doubled for participants with a BMI between 20 and 24 versus those with BMI from 17 kg/m 2 to 19 kg/m 2 . Even within normal-range BMI this study shows that BMI is an important predictor and risk factor for the development of hip osteoarthritis.
The development of idiopathic osteoarthritis is not one of inflammation, but rather a wear-and-tear disorder. Fibrillation and cracking of matrix soften the cartilage, leading to a fluid influx. Subsequent subchondral cysts can result, which typically are simply a sign of the disease and do not cause symptoms. Eburnation of bone, cartilage microfracture, and loose bodies in the joint space can cause pain and contribute to the progression of hip joint degeneration ( Fig. 1-1 ).
Femoroacetabular Impingement
The increasing awareness of subtle, underlying hip joint changes causing future degenerative joint pathology has been extensively studied. One of these causes, femoroacetabular impingement (FAI), has been found to cause degenerative changes such as labral tears, acetabular articular cartilage damage and, ultimately, global arthritic changes ( Fig. 1-2 ). Several factors are believed to be causative in FAI, such as Legg-Calvé-Perthes disease, slipped capital femoral epiphysis, developmental hip dysplasia, posttraumatic changes, and osseous malformations, such as the pistol grip deformity of the femur and several acetabular bony abnormalities. As a corollary, slipped capital femoral epiphysis (SCFE) and later development into arthrosis has been postulated to be attributable to an impingement-type etiology. One study identified lack of range of motion in flexion and internal rotation was from a mechanical jamming, caused by a prominent femoral metaphysis abutting against the acetabular labrum and cartilage. This report postulates that even slight degrees of SCFE, asymptomatic in nature, may be a strong negative prognostic factor in future development of arthrosis.
FAI is a distinct entity in which the proximal femur abuts against the acetabular rim. This occurs either from a widening of the femoral neck or a decreased offset at the anterolateral head-neck junction. As a result, the joint has a decreased ability for clearance and restriction of motion can occur, especially in flexion with adduction and internal rotation. This typically affects young, active adults who present clinically with the chief complaint of joint pain exacerbated by activity or prolonged sitting.
FAI has two distinct variants, although they rarely occur singly in patients. Cam impingement typically results from a portion of the femoral head that is nonspherical, resulting in abutment against the acetabular rim, most significantly in flexion and internal rotation. It is more often seen in young, athletic men. Damage from repetitive motion typically is found in the acetabular cartilage in the anterosuperior acetabulum. Pincer impingement is more commonly found in middle-aged athletic women and occurs as a result of the femoral head-neck junction making contact with the acetabular rim, often because of excessive acetabular coverage. Typical pincer-type damage results in labral changes, often ossification.
As stated above, these changes rarely occur as a single entity. One study of 302 hips showed only 26 isolated cam and 16 isolated pincer impingement cases. However, each has a different pathologic mechanism of damage. In cam impingement, the eccentric femoral head shears the cartilage from the labrum in the anterosuperior area of the acetabulum. This differs from pincer impingement, which typically results from a deep-pocketed acetabulum, as seen in the prototype aberration, coxa profunda, and limited range of motion from an overlying acetabular rim. This causes the acetabular rim to abut the femoral neck at the limits of motion, causing a narrow strip of degeneration in the labrum surrounding the entire acetabulum. These changes typically present as a varying ratio of cam/pincer combination of damage.
The study by Beck et al gives a mechanism for the pathologic basis of previously described idiopathic osteoarthritis. Many structural abnormalities linked with osteoarthritis coexist in FAI, such as the aforementioned coxa profunda, the common pistol grip abnormality, and acetabular retroversion and protrusio. In their study linking FAI to degenerative hip disease, 57 of 149 hips studied showed pistol grip deformity, with 31 of these hips having coexisting acetabular bony abnormalities (coxa profunda, protrusio, retroversion, and coxa vara). Furthermore, Tanzer and Noiseux specifically analyzed the role of the pistol grip deformity in subsequent labral pathology and arthritis development. In an arthroscopic labral tear study, they showed 37 of 38 hips having the pistol grip deformity preoperatively. The study also examined idiopathic cases of hip arthritis in 200 patients receiving total hip arthroplasty. Excluding 75 hips in which slip angle could not be determined, the remaining 125 hips examined showed a radiographic pistol grip deformity.
Identifying these subtle bony abnormalities in the young patient with hip pain is becoming increasingly important for orthopedists. It allows earlier intervention to relieve symptoms and possibly prevent long-term sequelae of end-stage hip arthritis. Current nonoperative treatment regimens include activity modification that avoids excessive hip motion along with nonsteroidal antiinflammatory medication. However, this typically only temporizes symptoms and surgical intervention becomes the next option. Further discussion of these procedures is found in later chapters of this text.
Congenital Hip Dysplasia
Congenital dysplasia or dislocation of the hip presents its own unique complexities to arthroplasty surgeons. Disrupted anatomy, leg-length discrepancies, and postoperative neuropathies are a few of the difficulties this problem presents. Developmental dislocation of the hip is cited to occur at a rate of 1 to 1.5/1000 live births, with 80% of cases occurring in females and a significantly higher rate in some ethnic groups, such as Native Americans. Osteoarthritis secondary to congenital hip dysplasia presents a further challenge by the typically younger age of presentation of these patients at end-stage disease. Although many cases are diagnosed on routine clinical and sonographic examinations shortly after birth, many patients do not respond to early treatment or are diagnosed later in life. The following section deals with the osteoarthritic hip caused by such developmental dysplasia.
The term hip dysplasia denotes an abnormality in the femoral head and/or acetabulum regarding its shape, orientation, and size. Several factors contribute to this condition. For one, the dislocated femoral head remains in an anteverted, valgus position and is pulled proximally and laterally by hip abductors. Furthermore, the femoral head becomes misshapen and flattened. Without the femoral head located in the native acetabulum, the acetabulum becomes flattened ( Fig. 1-3 ). The femoral head’s normal location in the native acetabulum stimulates the contouring of the acetabulum around the head. The acetabular labrum also becomes enlarged around the superior, posterior, and inferior rim. The labrum may even become inverted into the joint, called an inverted limbus , which can block reduction of the hip joint. The hip joint fills with pulvinar, or fibrofatty debris. Hip abductors, hamstrings muscles, and the psoas become shortened and contracted, further complicating reduction. All these features can lead to the development of a femoral head in a “false acetabulum,” which degenerates into end-stage osteoarthritis, commonly at an early age.
Posttraumatic Hip Arthritis
Disruption of the hip joint’s congruity, whether through femoral head dislocation or fracture of the proximal femur or acetabulum, often can lead to progressive degenerative hip joint disease years later. Once the structural integrity of the hip joint is disrupted, permanent persistent mechanical irregularities often exist, insidiously traumatizing the joint to the point of pain and limitation of activity. In a study of hip and knee injuries in medical students at Johns Hopkins Medical School, Gelber et al found a threefold increase in the likelihood of developing hip arthritis in participants who reported a history of a hip injury.
Traumatic hip dislocations typically occur in younger adults in the setting of high-energy injuries, such as motor vehicle accidents. Upadhyay and Moulton in a 14-year follow-up study of 74 patients with isolated, uncomplicated hip dislocations without associated fractures, found posttraumatic hip arthritis in 16% of the patients. Another 8% of these patients had arthritis develop as a result of eventual femoral head necrosis. Other authors have cited fair or poor results in 33% to 50% of patients who sustained anterior dislocations. Although expedient reduction of hip dislocations to avoid sciatic nerve palsy is standard of care, one retrospective study of 50 patients with hip dislocations and no fractures found no significant data that early reduction improves long-term outcomes in the development of arthritis. In this study 12 and anterior and 38 posterior hip dislocation cases were reviewed and placed into timelines of less than 1 hour to reduction and reduction within 1 to 6 hours. This study and others reported the severity of injury, secondary injuries, and direction of the dislocation as better indicators of long-term prognosis.
Other prognostic factors associated with posttraumatic hip arthritis include associated femoral head fractures, acetabular fractures, residual joint incongruity, and secondary osteonecrosis of the femoral head.
Different risk factors are involved in anterior and posterior dislocations. Anterior dislocations are at higher risk of osteoarthrosis as a result of indentation fractures more than 4 mm in depth, transchondral fractures, and osteonecrosis. Posterior dislocation risk factors include nonconcentric reduction, time delay between injury and reduction, higher energy injuries, and osteonecrosis.
In a nontraumatic hip joint, the cartilage is able to withstand normal loading involved with hip joint function. However, despite its ability to withstand long-term stress of ambulation and activity, death of chondrocytes from energy yields too high for them to withstand have been cited as a possible reason for the increased incidence in posttraumatic hip osteoarthritis. Further complications in chondrocyte death, joint incongruity from femoral head lesions, and acetabular fracture also hasten the joint degeneration process and coxarthrosis ( Fig. 1-4 ). The complication of osteonecrosis from loss of blood supply as a result of fracture and/or dislocation also leads to joint degeneration and is addressed in a different section in this chapter.
