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Groin Injuries and Groin Pain in Athletes: Part 2
Prim Care Clin Office Pract 32 (2005) 185–200
Groin Injuries and Groin Pain in Athletes: Part 2 Vincent Morelli, MDa,*, Luis Espinoza, MDb a
Primary Care Sports Medicine Fellowship, Louisiana State University Health Sciences Center, 200 West Esplanade Avenue, Suite 412, Kenner, LA 70065, USA b Orthopaedic Residency Program, Health Sciences Center, Louisiana State University, 671 West Esplanade Avenue, Suite 100, Kenner, LA 70065, USA
Sports injuries to the hip and groin region have been noted in 5% to 9% of high school athletes [1,2]. These injuries occur most commonly in athletes participating in sports involving side-to-side cutting, quick accelerations and decelerations, and sudden directional changes. Symptoms may range from intermittent episodes of mild discomfort to severe and chronic career-ending pain. Groin injuries may result from a variety of causes. Although this article deals mainly with athletic etiologies, the physician must keep in mind that many other medical conditions may also affect the groin. Differential diagnosis of nonathletic causes of groin pain is outlined below: Intra-abdominal disorders (eg, aneurysm, appendicitis, diverticulosis, inflammatory bowel disease) Genitourinary abnormalities (eg, urinary tract infection, lymphadenitis, prostatitis, scrotal and testicular abnormalities, gynecologic abnormalities, nephrolithiasis) Referred lumbosacral pain (eg, lumbar disc disease) Hip joint disorders (eg, Legg-Calve-Perthes disease, synovitis, slipped femoral capital epiphysis in younger patients and osteochondritis dissecans of femoral head, osteoarthritis) Because of these overlapping medical conditions and because the anatomy of the region is so complex, a team approach is optimal. In the National Institute for Groin Injuries, primary care sports physicians coordinate input from a team of urologists, neurologists, radiologists,
* Corresponding author. E-mail address: [email protected] (V. Morelli). 0095-4543/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.pop.2004.11.012 primarycare.theclinics.com
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interventional radiologists, orthopedists, general surgeons, gynecologists, physical therapists, and gastroenterologists. The primary care physician, in addition to performing a focused history and physical examination, should have an understanding of the diagnostic imaging available and a working knowledge of the sensitivities and specificities of each test. After generating a complete differential diagnosis, appropriate referral when needed, and formulation of a treatment plan, the coordinating physician must diligently maintain oversight of the athlete’s response to initial conservative management. This is paramount not only because of the difficulty of diagnosis, but also because 27% to 90% of patients presenting with groin pain have more than one coexisting injury [3,4]. As the authors will illustrate, these coexisting injuries are thought to arise due to the close proximity of anatomical elements in the region, predisposing one insult to naturally involve adjacent structures. Alternatively, an initial injury may alter the delicate biomechanics of the hip and groin, leading to secondary overuse injuries. Whatever the reason, it is common for one injury to be properly diagnosed and be improving with treatment, while at the same time a concomitant injury may have gone entirely undiagnosed and untreated, leaving both the athlete and physician frustrated if proper monitoring and re-evaluation are not done. In the second of this two-part series, disorders of the os pubis, stress fractures and various hip pathologies are reviewed as causes of groin pain. Disorders of the os pubis Osteitis pubis, or inflammation of the symphysis pubis, is seen commonly in runners [1], hockey players [2], and soccer players. In this condition, shearing forces across the pubic symphysis may result in symphysis inflammation or even joint disruption [3]. Repetitive adductor pull on the symphysis has also been proposed as one of the etiologic mechanisms [2]. Cutting and twisting forces may transmit even greater forces to the pubic symphysis in athletes lacking ideal ranges of hip flexibility [4]. Although no published studies have addressed the role that biomechanical abnormalities of the lower limb (eg, leg-length discrepancies, excessive pronation) play in the genesis of osteitis pubis, it is intuitive that such abnormalities might increase forces acting across the os pubis, and thus increase susceptibility to the condition. Osteitis pubis has been found in some sports medicine clinics to be the most common cause of chronic groin pain [5]. It may be difficult to distinguish from adductor strains, because the origin of the adductors lie in such close proximity to the symphysis (see Fig. 1. Groin Injuries and Groin Pain in Athletes: Part 1 elsewhere in this issue). Also one must keep in mind that the two conditions may occur concomitantly, and that distinguishing among osteitis pubis, adductor strain, obturator entrapment, and posterior abdominal wall abnormalities is usually difficult.
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The symptoms of osteitis pubis are usually gradual onset of exerciseinduced pain in the lower abdomen and medial thighs [5]. The symptoms may be initially indistinguishable from adductor strain, and may be aggravated by kicking and running. Symptoms may increase in severity if athletic activity is not curtailed. A clinical review [2] noted that in athletes who have documented osteitis pubis, adductor pain occurred in 80%, pain around the pubic symphysis in 40%, lower abdominal pain in 30%, and hip pain in 12%. Referred scrotal pain, previously described as a classic complaint, was found in only 8%. Physical examination usually reveals tenderness over the pubic symphysis, and lack of such tenderness usually excludes the diagnosis [6]. Pain can often be provoked by active adduction if the distal symphysis is involved, or by sit-ups if the proximal portion is involved. Plain film may show widening of the pubic symphysis, irregular contour of articular surfaces, or periarticular sclerosis; however, in early or mild disease, radiographic findings may be normal [7]. Plain-film interpretation in adolescents may be particularly difficult, due to the overlap in the appearance of normal ossification patterns and the changes characteristic of osteitis pubis. To make matters more confusing, some adult athletes who have no symptoms of osteitis pubis may have plain-film radiographic changes characteristic of osteitis pubis. In one study of professional soccer players, radiographic changes around the symphysis were found in 76% of asymptomatic players [8]. Bone scan in patients who have osteitis pubis may demonstrate diffuse increased uptake in the area of the pubic symphysis; however, some athletes who have classic clinical symptoms fail to show abnormal uptake, and thus clinicians are helped only by a positive scan [9]. In a recent review of osteitis pubis, it was noted that the correlation between symptoms and isotope bone scan findings is difficult [7]. MRI shows marrow edema in the pubic bones early in the course of the condition, followed by low signal on T1- and T2-weighted images as the disease progresses [9]. This modality is becoming increasingly useful in the diagnosis of osteitis pubis [7]. MRI performed in a series of 25 Italian athletes who had unexplained groin pain for over 6 months revealed osteitis pubic in 14 cases, an impressively high yield [10]. Treatment begins with reassurance that the condition is usually selflimited [7]; however, osteitis pubis can take more than a year to resolve, and one study of 59 patients found that the average time to healing was 9 to 10 months [2]. Following reassurance, physical rehabilitation is the cornerstone of treatment. Pain-producing activity should be avoided and pain-free exercise should be maintained in the interest of general fitness [11]. Therapy should progress in the usual stepwise fashion (restoring range of motion exercise, then strength exercise, and finally sport-specific exercise) with particular attention to hip range of motion and adductor stretching and strengthening. Biomechanical abnormalities should also be corrected in
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order to minimize their contribution to shearing stresses placed on the pelvis. The use of steroid injections in osteitis pubis is controversial. A 1995 series [12] of 11 patients who had osteitis pubis concluded that steroid injections were more helpful in athletes who had acute symptoms of less than 2 weeks duration than in patients who had chronic symptoms. Those athletes in whom symptoms were present for greater than 16 weeks needed an additional 11 to 16 weeks for symptomatic improvement. This benefit seen in acute athletic injuries is probably clinically useless information, because most primary care sports physicians would not undertake injection in patients who have symptoms of such short duration. Although case reports and small series have shown some benefit of steroid injection in the treatment of osteitis pubis [1,12], the authors could find no rigorous trials substantiating these findings, and consequently no proper patient selection criteria. Recently, case studies have reported that a 3- to 6-month course of biophosphonate therapy has been a beneficial treatment option [13]. Surgical treatment for recalcitrant cases of osteitis pubis has been reported to be beneficial. Wedge resection of the symphysis pubis has been used in the treatment of osteitis pubis that is nonresponsive to conservative treatment [14,15]; however, this procedure has commonly been associated with postoperative instability and continued symptoms [15,16]. Although still controversial, surgical treatment may be more beneficial when chronic osteitis pubis exhibits vertical instability (greater than 2 mm) of the symphysis pubis, as demonstrated on flamingo view radiographs [17]. In a study of seven rugby players who had chronic osteitis pubis, arthrodesis of the pubic symphysis by bone grafting and compression plating was noted to have excellent results in all patients at a follow-up of 22 to 166 months. All returned to full match fitness within 9 months, with no limitation of hip range of motion and no need for oral analgesics.
Osteomylitis of the pubic symphysis Another condition that must be kept in the differential diagnosis of osteitis pubis is osteomyelitis, or bacterial infection of the pubic symphysis or adjacent bone. This condition is usually seen following surgical procedures in the area, but has also been seen after childbirth [18], and has been reported to occur spontaneously in athletes [19–21]. A recent review of 100 cases reported that 24% of cases occurred after female incontinence surgery, 19% occurred spontaneously in athletes—most often soccer players, 17% occurred in pelvic malignancy, and 15% occurred in intravenous (IV) drug use [22]. Staphylococcus aureus was the major pathogen in athletes, and Pseudomonas was the main causative agent in IV drug abusers. In the authors’ National Institute for Groin Injuries, we have
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noted this condition in only one patient presenting with chronic groin pain (authors’ early unpublished data). Clinically, patients present with fever in 74% of cases, pubic pain in 68%, antalgic gait in 59%, and groin pain in 41% [22]. Interestingly, some patients complain only of pain that is present during exercise, and are symptom-free when at rest [21]. Although bone scan and MRI are helpful in making the diagnosis, distinguishing between osteitis pubis and osteomylitis can be difficult, and can often require biopsy and culture to make a definitive diagnosis [21]. Most experts recommended a 6-week course of antibiotics, beginning with 10 to 14 days of IV therapy, followed by at least 4 weeks of oral medication. In addition, reviews have noted that as many as 55% of patients will eventually needed surgical debridement as definitive therapy [21,22]. Stress fractures The two most common stress fractures of the groin region are femoral neck stress fractures and pubic ramus fractures. They are caused by repetitive overuse and overload, and are usually seen in distance runners or military recruits. Additional risk factors include relative osteoporosis in young female athletes who have nutritional or hormonal imbalances, muscle fatigue (which may reduce shock-absorbing abilities), changes in foot gear or training surface, and sudden increases in intensity or duration of training regimens [23,24]. Presenting complaints are similar to those of stress fractures seen in other parts of the body. Athletes present with medial thigh and groin pain that is exacerbated by exercise and relieved by rest. Pain at rest represents advanced disease. Physical examination In reference to femoral neck stress fractures pain on physical examination is usually difficult for patients to localize, but painful internal rotation of the hip and inability to hop on the affected limb should raise the clinician’s index of suspicion. In the case of pubic ramus fractures, pain on direct palpation over the ramus is usually present. As above, pain will be elicited by one legged standing or jumping. Diagnostic imaging Radiographic evaluation with plain film has shown limited usefulness, because bony changes (periosteal reaction, cortical breaks, and so forth) normally lag behind the onset of symptoms by 2 to 4 weeks. In addition, it must be remembered that 50% of patients who have stress fractures never exhibit changes on plain film [25]. Bone scan is usually positive within 72
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hours of skeletal injury [9], but has been reported to be falsely positive in as high as 32% of patients presenting with hip/groin pain. This is presumably due to high osteoblastic activity in the area, because of high stress loads and constant remodeling [26]. MRI is currently the diagnostic imaging modality of choice when evaluating for femoral neck or other stress fractures of the groin region. Because groin pain suggestive of stress fracture may arise from the femoral neck, the pubic ramus, acetabulum, and sacrum, MRI should encompass a wide enough field to visualize all of these areas [27]. It should be performed early in order to make an early definitive diagnosis and implement proper treatment [23]. MRI showing early pre-fracture findings of marrow edema allows the sports physician to impose a period of relative rest to let repair strengthening occur [28]. Treatment Patients who have stress fractures of the inferior femoral neck (compression side) (see Fig. 1) can be treated conservatively with activity restriction and gradual return to activity. Follow-up imaging helps to ensure healing before return to activity. A return to sport can usually be anticipated in 2 to 3 months [11]. In contrast to inferior femoral neck stress fractures, stress fractures of the superior femoral neck (traction side) are more problematic, and must be treated with open reduction and internal fixation in order to prevent risk of progression to complete fracture, displacement, and subsequent avascular necrosis [24]. Less worrisome are stress fractures of the inferior pubic ramus [7]. These injuries usually occur in female distance runners and military recruits, and are comparatively easy to diagnose on physical examination. The diagnosis can be confirmed by a bone scan or MRI. Four to 6 weeks of relative rest can be followed by gradual return to sport, with most athletes regaining their prior level of sport within 3 to 5 months [29].
Fig. 1. Stress fractures of the femoral neck: (A) traction, (B) compression, (C) complete.
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As with any injury, treatment of femoral neck and pubic ramus stress fractures would be incomplete without also addressing and modifying risk factors. Risk factors that should be addressed include biomechanical contributors, maintenance of hormonal and nutritional balance, modification of foot gear and training surface, and most important, a conscientious review of the athlete’s training program.
Disorders of the hip When evaluating groin pain in the athlete, the physician must remember that hip pathology can refer pain to the groin region. Acetabular labral tears, articular cartilage defects of the femoral head or acetabulum, loose bodies, capsular laxity, and injuries to the ligamentum teres all may present as groin pain. Other less common presenting conditions include osteonecrosis of the femoral head, slipped capital femoral epiphysis, gout, pseudogout, synovial chondromatosis, and infection [30]. Labral tears Acetabular labral tears are increasingly being recognized as a source of groin pain in athletes. In one prospective study of patients presenting to a sports medicine center with chronic groin pain, 22% were found to have labral tears [31]. Labral tears have been found by several investigators to be associated with developmental dysplasia [32,33]. Anatomical considerations The cartilaginous acetabular labrum has little vessel penetration except into the peripheral margins [34]. This relative avascularity leads most experts to conclude that there is limited ability for healing after injury. Two types of labral lesions have been noted in cadaver studies: fraying of the labral-articular cartilage junction, and actual tears of the labrum. Lage et al [35] divided labral tears into four descriptive categories: (1) radial free margin flap tears (57%), (2) radial fiberlated labrum (22%), (3) longitudinal tears located along the peripheral margins (16%), and (4) ‘‘abnormally mobile’’ tears (5.4%).Tears occurring in athletes as a result of minimal or no trauma as are usually seen in the anterior/superior aspect of the labrum, a place postulated to be developmentally weak and thus more prone to injury and overload stresses [36]. Indeed, in most US series, about two thirds of labral tears are located in this position [37,38]. Labral lesions have been found in high association with adjacent articular cartilage damage, and thus are thought to contribute to progressive degenerative joint disease of the hip. It is theorized that tears disrupt the usual stabilizing function of the labrum, resulting in instability and increased wear-and-tear damage to the adjacent articular cartilage [39,40].
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History and physical One third of athletes recall a specific traumatic event as the cause of symptom onset. The remainder of tears are caused by relatively atraumatic mechanisms, such as twisting or pivoting during athletic endeavor, or by chronic degenerative disease [39]. Presenting symptoms include diffuse poorly localized groin pain and mechanical symptoms in the hip/groin area. Some patients may present with a painful snapping hip syndrome (see below). In one study, a clicking sensation of the hip was both sensitive (100%) and specific (85%) in predicting labral tears. On physical examination, the internal rotation/flexion/axial compression maneuver was 75% sensitive but only 43% specific [31], and the flexion/ abduction/external rotation (FABER) test was found to be 88% sensitive [41]. The sports physician must keep in mind that these physical maneuvers are imperfect, and must maintain a high index of suspicion for such injuries.
Diagnostic imaging Plain films are not helpful in diagnosing labral tears, though they may help in ruling out other hip abnormalities (osteonecrosis of the femoral head, slipped capital femoral epiphysis, osseous loose bodies, and so forth). MRI arthrography for diagnosing labral tears and associated articular cartilage damage is the current imaging technique of choice. It has been shown to have a sensitivity of 50% to 77%, and a specificity of 77% to 84% [36]. The imprecision in diagnosing associated articular cartilage defects is in part caused by the relative thinness of the articular cartilage in the hip (as compared with the knee), which makes femoral and acetabular cartilages difficult to visualize separately on MRI arthrography.
Treatment Conservative treatment is usually tried for at least 6 weeks before definitive surgical intervention. This is done to insure that mechanical symptoms are not due to snapping hip syndrome (see below), and that any associated injuries are given a chance to heal. In one study (N = 436) [40], surgical treatment was considered for patients presenting with painful mechanical symptoms, localization of pain to the groin, no success with conservative treatment after 6 months, reproduction of symptoms on physical examination, McCarthy sign, positive flexion/abduction/internal rotation test, and MRI or MRI arthrogram confirming a labral lesion or loose body. In this study, 55% were found to have labral tears, and 35% had labral fraying at the labral chondral junction. As above, 86% of labral tears were located anteriorly, and all were at the labral-articular cartilage junction, none at the periphery. Seven percent were noted to have multiple tears, and 74% of those with fraying or tears also had associated femoral or acetabular articular cartilage damage.
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Treatment of labral tears by careful debridement has been noted to eliminate both painful and mechanical symptoms. Results of intervention vary depending on pathology present. Pathology is summarized by stages below: Stage 1—discrete labral free margin tear with intact articular cartilage of both the femoral head and acetabulum Stage 2—labral tear with articular damage to adjacent femoral head but not to acetabulum Stage 3—labral tear with acetabular articular cartilage damage, with or without femoral head articular cartilage damage Stage 4—extensive acetabular tear with associated arthritic changes of the hip In one study [39], stage 1 and 2 lesions responded to surgical intervention with 80% to 90% good-to-excellent results. Stage 3 lesions were less responsive, achieving good-to-excellent results in only 17% to 40%. Stage 4 hips fared even worse, with 78% achieving poor results. Forty-three percent of these patients eventually needed total hip arthroplasty. Articular cartilage injuries of the hip Articular cartilage lesions of the acetabulum or femoral head are generally felt to be the result of trauma. Injuries ranging from hip dislocation [42] to subclinical shearing or minor ‘‘routine’’ hip impact have been noted to cause these lesions [43]. Presenting complaints are nonspecific, and may include diffuse groin pain with or without mechanical symptoms. Physical examination maneuvers are neither sensitive nor specific, but pathologic symptoms may be elicited with logrolling of the affected extremity, flexion with internal rotation, and abduction with internal rotation [44]. An intra-articular diagnosis may be confirmed if symptom relief occurs with a guided injection of anesthetic into the joint [44]. MRI may be used both to diagnose and grade osteochondral lesions of the hip [27]. MRI arthrography is generally thought to be superior (50%–68% sensitive, 77%–84% specific) to noncontrast MRI for identifying chondral defects, but is still poor at detecting partial thickness lesions, small lesions, and loose bodies [27,45]. Again, the shortcomings of MRI in these conditions is caused in part by the relative thinness of the articular cartilage in the hip (as compared with the knee), making femoral and acetabular cartilages difficult to visualize separately. Also, loose bodies may imbibe gadolinium contrast, rendering them nondetectable. CT arthrography has been stated to be superior at detecting loose bodies [44]. One added advantage of performing arthrography is that if anesthetic is added to contrast material at the time of injection, the diagnosis may be definitively localized as intra-articular.
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Surgical treatment is contemplated for any partially or completely detached lesions (Grade II, III, and IV), whereas conservative management is reserved for Grade I lesions (intact articular cartilage with changes in subchondral bone) [46].
Injuries to the ligamentum teres Injuries to the ligamentum teres are relatively uncommon, accounting for only 8% of pathologic lesions found at hip arthroscopy [47]. These lesions may be traumatic or degenerative in origin. As above, traumatic injury may be the result of a substantial impact (motor vehicle accidents, falls, football dislocations, and the like) or of relatively minor twisting injuries. Patients usually present with longstanding deep groin pain, and many experience mechanical locking, popping, or giving way as well [48]. Complete rupture of the ligament is usually traumatic in origin and is often (roughly two thirds of the time [48]) associated with other concomitant hip injuries (eg, labral tears, articular cartilage damage) [30]. Partial tears usually present with long-standing, ill-defined groin pain, and are less likely to have mechanical symptoms These lesions have been noted to have a high incidence in ballet dancers [30]. Degenerative tears are usually noted in elderly patients who have concomitant osteoarthritis. Diagnostic imaging is notoriously poor for detecting ligamentum teres lesions. One study noted that only 2 of 23 arthroscopicaly documented lesions (12 complete ruptures, 11 partial tears) were detected by MRI, MRI arthrogram, or CT [48]. Treatment consists of arthroscopic debridement, and results are usually best when there are no associated acetabular or femoral chondral defects.
Avascular necrosis of the hip Avascular necrosis (AVN) of the hip is a progressive debilitating lesion that usually affects people in the third and fourth decades of life. The incidence has been estimated to be between 10,000 and 20,000 cases per year in the United States, with a mean age at presentation of 38 years [49]. Although the pathogenesis is still not entirely understood, it is generally agreed that an initial disruption of circulation to a portion of the femoral head occurs. This insult leads to localized cell death and bone necrosis, eventually followed by more widespread necrosis, and ultimately by bony collapse and progressive arthritis of contiguous joints [50]. The initial disruption of blood flow may result from a single traumatic event, from repetitive minor damages, or from various nontraumatic causes. Femoral neck fractures and hip dislocations are the most common traumatic causes. In 1991, a case of AVN of the hip in a professional football player who sustained a traumatic hip subluxation was reported [51].
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Ninety percent of nontraumatic causes of AVN have been associated with either systemic corticosteroid use or heavy alcohol consumption [52]. Numerous case reports have noted an association of AVN with corticosteroids used in treating asthma, chronic obstructive pulmonary disease (COPD), autoimmune diseases, leukemia, or psoriasis, and when used as an immunosuppressive agent after transplant surgery [53]. Both short-term steroid ‘‘bursts’’ and long-term use have been implicated, as has the use of unusually high doses [54]. The exact way in which corticosteroids lead to AVN is unknown; however, it is currently thought that steroids induce a hypercoaguable state, with subsequent impaired fibrinolysis, and eventual venous thrombosis and bone infarct [55,56]. The use of anabolic steroids has also been associated with AVN in athletes. In one case report, a weight lifter with an 8-year history of ergogenic steroid use and no other predisposing risk factors developed bilateral femoral head avascular necrosis [57]. Most other risk factors and disease states associated with atraumatic avascular necrosis have systemic effects that alter circulating lipids or disrupt coagulation pathways. Such conditions include smoking, sickle cell anemia, coagulopathies, lupus, hypercholesterolemia, organ transplantation, Gaucher disease, and hypertriglyceridemia. Despite a large number of risk factors that can be directly linked with the incidence of AVN of the hip, approximately 10% to 20% of cases have no clearly identifiable risk factor and are classified as idiopathic [58].
Clinical presentation and diagnosis A high index of suspicion and awareness of the predisposing factors mentioned above is critical. Athletes who have avascular necrosis of the femoral head typically complain of groin pain. Occasionally, nonspecific hip pain that may affect the buttock or knee region may be described as well. On physical examination in the early stages, hip range of motion and gait are normal; however, as the disease progresses, internal rotation becomes restricted, and passive rotation of the hip (especially internal rotation) generally reproduces the pain. In addition to evaluating the symptomatic hip, a complete examination of the contralateral hip should also be performed, because 40% to 80% of patients have bilateral involvement [59]. Initially, antero-posterior and antero-lateral radiographs of both hips should be obtained. Among the earliest radiographic changes that occur are osteopenia, or patchy areas of sclerosis and lucency. As necrosis progresses, the crescent sign appears, representing collapse of the trabecula beneath the subchondral bone. Because radiograph changes are not apparent until 3 months after the initial insult, MRI of the hip should be obtained if the disease is suspected despite normal plain films. MRI is the imaging modality of choice in identifying early AVN, and is both sensitive and specific (88%–100%) [58].
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Management If this entity is recognized early, proper treatment may have a beneficial effect on outcomes. Unfortunately however, the majority of cases are recognized only in the advanced stages, when treatment options are limited. No single surgical or medical method has been demonstrated to universally prevent disease progression. Treatment depends on the stage of the disease. In the past, early disease was thought best treated by simple restricted weight bearing and symptom control. Currently however, although at least one randomized trial still finds no difference between surgical and conservative management [60], other prospective trials come down clearly on the side of early surgical core decompression [61,62]. Other surgical treatments that seek to promote vascular ingrowth in the compromised femoral head include cortical or vascularized bone grafting [63,64]. In the late stages of disease, the accompanying femoral head collapse and altered mechanics obviate the possibility of performing any of these femoral head ‘‘sparing’’ procedures, and usually necessitate total hip arthroplasty for restoration of function and relief of symptoms. Prompt recognition of this disease is critical for the best clinical outcome. If diagnosed early with a good history and physical and ancillary studies such as an MRI, an athlete who has avascular necrosis of the hip can be surgically managed, and has the best chance of avoiding catastrophic disease progression and permanent disability. Snapping hip syndromes Snapping hip syndrome refers to a snapping sensation felt or about the hip with movement. Less than one third of these patients will experience pain with snapping, and it is only in these cases that treatment need be initiated. Snapping hip syndrome may be classified as intra-articular and extraarticular. The more common lateral extra articular type of snapping hip syndrome occurs when the iliotibial band, tensor fascia lata, or gluteus medius tendon slides back and forth across the greater trochanter. This normal action becomes a snapping hip syndrome when one of these connective tissue bands thickens and catches with motion. The underlying bursa may also become inflamed, causing a painful external snapping hip syndrome. The medial extra-articular type of snapping hip syndrome results from the iliopsoas tendon catching on the anterior inferior iliac spine (AIIS), the lesser trochanter, or the iliopectineal ridge during hip extension, as the tendon moves from an anterior lateral to a posterior medial position. With overuse, the resultant friction may eventually cause painful symptoms, resulting in muscle trauma, bursitis, or inflammation in the area [65]. The intra-articular type of snapping hip syndrome results from labral tears, articular cartilage damage, ligamentum teres tears, or loose bodies.
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The physician should attempt to identify the source of the symptomatic clicking on physical examination, with directed testing as noted above for iliopsoas involvement, ranging the hip while palpating over the greater trochanter for lateral symptoms, and employing the physical examination maneuvers noted above when trying to detect intra-articular pathology. Ultrasound during hip motion may visualize tendon subluxation and any concomitant bursitis when evaluating for iliopsoas involvement in medial extra-articular snapping [66]. As stated above, MRI can sometimes identify intra-articular causes of snapping hip syndrome. Treatment of the condition requires elucidation of the underlying pathology and tailoring therapy to the inciting cause. Correcting any contributing biomechanical abnormalities and stretching tightened muscles (eg, iliopsoas muscle, iliotibial band) are important. Corticosteroid injections can be useful if bursitis is present. Surgical treatment is rarely indicated unless intra-articular pathology is present, or in patients who have persistently painful iliopsoas symptoms. In the latter case, surgical tendon lengthening has been described as a beneficial procedure [67].
References [1] Koch RA, Jackson DW. Pubic symphysitis in runners. A report of two cases. Am J Sports Med 1981;9(1):62–3. [2] Fricker PA, Taunton JE, Ammann W. Osteitis pubis in athletes. Infection, inflammation or injury? Sports Med 1991;12(4):266–79. [3] Renstroem AF. Groin injuries: a true challenge in orthopaedic sports medicine. Sports Medicine and Arthroscopy Review 1997;5:247–51. [4] Williams JG. Limitation of hip joint movement as a factor in traumatic osteitis pubis. Br J Sports Med 1978;12(3):129–33. [5] Ekberg O, Persson NH, Abrahamsson PA, et al. Longstanding groin pain in athletes. A multidisciplinary approach. Sports Med 1988;6:56–61. [6] Westlin N. Groin pain in athletes from Southern Sweden. Sports Medicine and Arthroscopy Review 1997;5:280–4. [7] Fricker PA. Management of groin pain in athletes. Br J Sports Med 1997;31:97–101. [8] Harris NH, Murray RO. Lesions of the symphysis in athletes. BMJ 1974;4:211–4. [9] Karlsson J, Jerre R. The use of radiography, magnetic resonance, and ultrasound in the diagnosis of hip, pelvis, and groin injuries. Sports Medicine and Arthroscopy Review 1997;5: 268–73. [10] Barile A, Erriquez D, Cacchio A, et al. Groin pain in athletes: magnetic resonance imaging evaluation. Radiol Med (Torino) 2000;100(4):216–22. [11] Lynch SA, Renstrom PA. Groin injuries in sport: treatment strategies. Sports Med 1999;28: 137–44. [12] Holt MA, Keene JS, Graf BK, et al. Treatment of osteitis pubis in athletes. Results of corticosteroid injections. Am J Sports Med 1995;23(5):601–6. [13] Maksymowych WP, Aaron SL, Russell AS. Treatment of refractory symphysitis pubis with intravenous pamidronate. J Rheumatol 2001;28(12):2754–7. [14] Coventry MB, Mitchell WC. Osteitis pubis: observations based on a study of 45 patients. JAMA 1961;178:898–905.
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[15] Grace JN, Sim FH, Shives TC, et al. Wedge resection of the symphysis pubis for the treatment of osteitis pubis. J Bone Joint Surg Am 1989;71(3):358–64. [16] Moore RS Jr, Stover MD, Matta JM. Late posterior instability of the pelvis after resection of the symphysis pubis for the treatment of osteitis pubis. A report of two cases. J Bone Joint Surg Am 1998;80(7):1043–8. [17] Williams PR, Thomas DP, Downes EM. Osteitis pubis and instability of the pubic symphysis. When nonoperative measures fail. Am J Sports Med 2000;28(3):350–5. [18] Eskridge C, Longo S, Kwark J, et al. Osteomyelitis pubis occurring after spontaneous vaginal delivery: a case presentation. J Perinatol 1997;17(4):321–4. [19] Combs JA. Bacterial osteitis pubis in a weight lifter without invasive trauma. Med Sci Sports Exerc 1998;30(11):1561–3. [20] Hedstrom SA, Lidgren L. Acute hematogenous pelvic osteomyelitis in athletes. Am J Sports Med 1982;10(1):44–6. [21] Pauli S, Willemsen P, Declerck K, et al. Osteomyelitis pubis versus osteitis pubis: a case presentation and review of the literature. Br J Sports Med 2002;36(1):71–3. [22] Ross JJ, Hu LT. Septic arthritis of the pubic symphysis: review of 100 cases. Medicine (Baltimore) 2003;82(5):340–5. [23] Roos HP. Hip pain in sport. Sports Medicine and Arthroscopy Review 1997;5:292–300. [24] Rolf C. Pelvis and groin stress fractures: a cause of groin pain in athletes. Sports Medicine and Arthroscopy Review 1997;5:301–4. [25] Ohashi K, Brandser EA, el-Khoury GY. Role of MR imaging in acute injuries to the appendicular skeleton. Radiol Clin North Am 1997;35(3):591–613. [26] Shin AY, Morin WD, Gorman JD, et al. The superiority of magnetic resonance imaging in differentiating the cause of hip pain in endurance athletes. Am J Sports Med 1996;24(2): 168–76. [27] Bencardino JT, Kassarjian A, Palmer WE. Magnetic resonance imaging of the hip: sportsrelated injuries. Top Magn Reson Imaging 2003;14(2):145–60. [28] Lee JK, Yao L. Stress fractures: MR imaging. Radiology 1988;169(1):217–20. [29] Hill PF, Chatterji S, Chambers D, et al. Stress fracture of the pubic ramus in female recruits. J Bone Joint Surg Br 1996;78(3):383–6. [30] Kelly BT, Williams RJ 3rd, Philippon MJ. Hip arthroscopy: current indications, treatment options, and management issues. Am J Sports Med 2003;31(6):1020–37. [31] Narvani AA, Tsiridis E, Kendall S, et al. A preliminary report on prevalence of acetabular labrum tears in sports patients with groin pain. Knee Surg Sports Traumatol Arthrosc 2003; 11(6):403–8. [32] Ikeda T, Awaya G, Suzuki S, et al. Torn acetabular labrum in young patients. Arthroscopic diagnosis and management. J Bone Joint Surg Br 1988;70(1):13–6. [33] McCarthy JC, Noble PC, Schuck MR, et al. The watershed labral lesion: its relationship to early arthritis of the hip. J Arthroplasty 2001;16(8 Suppl 1):81–7. [34] Lage LA, Patel JV, Villar RN. The acetabular labral tear: an arthroscopic classification. Arthroscopy 1996;12(3):269–72. [35] Schmid MR, Notzli HP, Zanetti M, et al. Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology 2003;226(2):382–6. [36] Baber YF, Robinson AH, Villar RN. Is diagnostic arthroscopy of the hip worthwhile? A prospective review of 328 adults investigated for hip pain. J Bone Joint Surg Br 1999;81(4): 600–3. [37] Farjo LA, Glick JM, Sampson TG. Hip arthroscopy for acetabular labral tears. Arthroscopy 1999;15(2):132–7. [38] McCarthy J, Noble P, Aluisio FV, et al. Anatomy, pathologic features, and treatment of acetabular labral tears. Clin Orthop 2003;(406):38–47. [39] McCarthy JC, Noble PC, Schuck MR, et al. The Otto E. Aufranc award: the role of labral lesions to development of early degenerative hip disease. Clin Orthop 2001;(393): 25–37.
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[40] Mitchell B, McCrory P, Brukner P, et al. Hip joint pathology: clinical presentation and correlation between magnetic resonance arthrography, ultrasound, and arthroscopic findings in 25 consecutive cases. Clin J Sport Med 2003;13(3):152–6. [41] Laorr A, Greenspan A, Anderson MW, et al. Traumatic hip dislocation: early MRI findings. Skeletal Radiol 1995;24(4):239–45. [42] Weaver CJ, Major NM, Garrett WE, et al. Femoral head osteochondral lesions in painful hips of athletes: MR imaging findings. AJR Am J Roentgenol 2002;178(4):973–7. [43] Byrd JW. Lateral impact injury. A source of occult hip pathology. Clin Sports Med 2001; 20(4):801–15. [44] Edwards DJ, Lomas D, Villar RN. Diagnosis of the painful hip by magnetic resonance imaging and arthroscopy. J Bone Joint Surg Br 1995;77(3):374–6. [45] Dipaola JD, Nelson DW, Colville MR. Characterizing osteochondral lesions by magnetic resonance imaging. Arthroscopy 1991;7(1):101–4. [46] Rao J, Zhou YX, Villar RN. Injury to the ligamentum teres. Mechanism, findings, and results of treatment. Clin Sports Med 2001;20(4):791–9; vii. [47] Byrd JW, Jones KS. Traumatic rupture of the ligamentum teres as a source of hip pain. Arthroscopy 2004;20(4):385–91. [48] Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am 1995;77(3):459–74. [49] Assouline-Dayan Y, Chang C, Greenspan A, et al. Pathogenesis and natural history of osteonecrosis. Semin Arthritis Rheum 2002;32(2):94–124. [50] Cooper DE, Warren RF, Barnes R. Traumatic subluxation of the hip resulting in aseptic necrosis and chondrolysis in a professional football player. Am J Sports Med 1991;19(3): 322–4. [51] Noccion SL, Hunter DM, Finerman GAM. Hip and pelvis. In: DeLee JC, Drez D Jr, editors. DeLee and Drez’s orthopaedic sports medicine: principles and practice. 2nd edition. Philadelphia: Saunders; 2003. p. 1443–79. [52] Reichert-Penetrat S, Trechot P, Barbaud A, et al. Bilateral femoral avascular necrosis in a man with psoriasis: responsibility of topical corticosteroids and role of cyclosporine. Dermatology 2001;203(4):356–7. [53] Knight A. Corticosteroids and avascular necrosis of the femoral head. CMAJ 2001;165(4): 397; 399. [54] Glueck CJ, Freiberg R, Glueck HI, et al. Hypofibrinolysis: a common, major cause of osteonecrosis. Am J Hematol 1994;45(2):156–66. [55] Glueck CJ, Freiberg R, Glueck HI, et al. Idiopathic osteonecrosis, hypofibrinolysis, high plasminogen activator inhibitor, high lipoprotein(a), and therapy with stanozolol. Am J Hematol 1995;48(4):213–20. [56] Pettine KA. Association of anabolic steroids and avascular necrosis of femoral heads. Am J Sports Med 1991;19(1):96–8. [57] Lavernia CJ, Sierra RJ, Grieco FR. Osteonecrosis of the femoral head. J Am Acad Orthop Surg 1999;7(4):250–61. [58] Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg Br 1995;77(1):34–41. [59] Koo KH, Kim R, Ko GH, et al. Preventing collapse in early osteonecrosis of the femoral head. A randomised clinical trial of core decompression. J Bone Joint Surg Br 1995;77(6): 870–4. [60] Stulberg BN, Davis AW, Bauer TW, et al. Osteonecrosis of the femoral head. A prospective randomized treatment protocol. Clin Orthop 1991;(268):140–51. [61] Steinberg ME, Larcom PG, Strafford B, et al. Core decompression with bone grafting for osteonecrosis of the femoral head. Clin Orthop 2001;(386):71–8. [62] Ishizaka M, Sofue M, Dohmae Y, et al. Vascularized iliac bone graft for avascular necrosis of the femoral head. Clin Orthop 1997;(337):140–8.
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[63] Rijnen WH, Gardeniers JW, Buma P, et al. Treatment of femoral head osteonecrosis using bone impaction grafting. Clin Orthop 2003;(417):74–83. [64] Johnston CA, Wiley JP, Lindsay DM, et al. Iliopsoas bursitis and tendinitis. A review. Sports Med 1998;25(4):271–83. [65] Janzen DL, Partridge E, Logan PM, et al. The snapping hip: clinical and imaging findings in transient subluxation of the iliopsoas tendon. Can Assoc Radiol J 1996;47(3):202–8. [66] Jacobson T, Allen WC. Surgical correction of the snapping iliopsoas tendon. Am J Sports Med 1990;18(5):470–4. [67] Dorrell JH, Catterall A. The torn acetabular labrum. J Bone Joint Surg Br 1986;68(3):400–3.
Groin Injuries and Groin Pain in Athletes: Part 2 Vincent Morelli, MDa,*, Luis Espinoza, MDb a
Primary Care Sports Medicine Fellowship, Louisiana State University Health Sciences Center, 200 West Esplanade Avenue, Suite 412, Kenner, LA 70065, USA b Orthopaedic Residency Program, Health Sciences Center, Louisiana State University, 671 West Esplanade Avenue, Suite 100, Kenner, LA 70065, USA
Sports injuries to the hip and groin region have been noted in 5% to 9% of high school athletes [1,2]. These injuries occur most commonly in athletes participating in sports involving side-to-side cutting, quick accelerations and decelerations, and sudden directional changes. Symptoms may range from intermittent episodes of mild discomfort to severe and chronic career-ending pain. Groin injuries may result from a variety of causes. Although this article deals mainly with athletic etiologies, the physician must keep in mind that many other medical conditions may also affect the groin. Differential diagnosis of nonathletic causes of groin pain is outlined below: Intra-abdominal disorders (eg, aneurysm, appendicitis, diverticulosis, inflammatory bowel disease) Genitourinary abnormalities (eg, urinary tract infection, lymphadenitis, prostatitis, scrotal and testicular abnormalities, gynecologic abnormalities, nephrolithiasis) Referred lumbosacral pain (eg, lumbar disc disease) Hip joint disorders (eg, Legg-Calve-Perthes disease, synovitis, slipped femoral capital epiphysis in younger patients and osteochondritis dissecans of femoral head, osteoarthritis) Because of these overlapping medical conditions and because the anatomy of the region is so complex, a team approach is optimal. In the National Institute for Groin Injuries, primary care sports physicians coordinate input from a team of urologists, neurologists, radiologists,
* Corresponding author. E-mail address: [email protected] (V. Morelli). 0095-4543/05/$ - see front matter Ó 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.pop.2004.11.012 primarycare.theclinics.com
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interventional radiologists, orthopedists, general surgeons, gynecologists, physical therapists, and gastroenterologists. The primary care physician, in addition to performing a focused history and physical examination, should have an understanding of the diagnostic imaging available and a working knowledge of the sensitivities and specificities of each test. After generating a complete differential diagnosis, appropriate referral when needed, and formulation of a treatment plan, the coordinating physician must diligently maintain oversight of the athlete’s response to initial conservative management. This is paramount not only because of the difficulty of diagnosis, but also because 27% to 90% of patients presenting with groin pain have more than one coexisting injury [3,4]. As the authors will illustrate, these coexisting injuries are thought to arise due to the close proximity of anatomical elements in the region, predisposing one insult to naturally involve adjacent structures. Alternatively, an initial injury may alter the delicate biomechanics of the hip and groin, leading to secondary overuse injuries. Whatever the reason, it is common for one injury to be properly diagnosed and be improving with treatment, while at the same time a concomitant injury may have gone entirely undiagnosed and untreated, leaving both the athlete and physician frustrated if proper monitoring and re-evaluation are not done. In the second of this two-part series, disorders of the os pubis, stress fractures and various hip pathologies are reviewed as causes of groin pain. Disorders of the os pubis Osteitis pubis, or inflammation of the symphysis pubis, is seen commonly in runners [1], hockey players [2], and soccer players. In this condition, shearing forces across the pubic symphysis may result in symphysis inflammation or even joint disruption [3]. Repetitive adductor pull on the symphysis has also been proposed as one of the etiologic mechanisms [2]. Cutting and twisting forces may transmit even greater forces to the pubic symphysis in athletes lacking ideal ranges of hip flexibility [4]. Although no published studies have addressed the role that biomechanical abnormalities of the lower limb (eg, leg-length discrepancies, excessive pronation) play in the genesis of osteitis pubis, it is intuitive that such abnormalities might increase forces acting across the os pubis, and thus increase susceptibility to the condition. Osteitis pubis has been found in some sports medicine clinics to be the most common cause of chronic groin pain [5]. It may be difficult to distinguish from adductor strains, because the origin of the adductors lie in such close proximity to the symphysis (see Fig. 1. Groin Injuries and Groin Pain in Athletes: Part 1 elsewhere in this issue). Also one must keep in mind that the two conditions may occur concomitantly, and that distinguishing among osteitis pubis, adductor strain, obturator entrapment, and posterior abdominal wall abnormalities is usually difficult.
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The symptoms of osteitis pubis are usually gradual onset of exerciseinduced pain in the lower abdomen and medial thighs [5]. The symptoms may be initially indistinguishable from adductor strain, and may be aggravated by kicking and running. Symptoms may increase in severity if athletic activity is not curtailed. A clinical review [2] noted that in athletes who have documented osteitis pubis, adductor pain occurred in 80%, pain around the pubic symphysis in 40%, lower abdominal pain in 30%, and hip pain in 12%. Referred scrotal pain, previously described as a classic complaint, was found in only 8%. Physical examination usually reveals tenderness over the pubic symphysis, and lack of such tenderness usually excludes the diagnosis [6]. Pain can often be provoked by active adduction if the distal symphysis is involved, or by sit-ups if the proximal portion is involved. Plain film may show widening of the pubic symphysis, irregular contour of articular surfaces, or periarticular sclerosis; however, in early or mild disease, radiographic findings may be normal [7]. Plain-film interpretation in adolescents may be particularly difficult, due to the overlap in the appearance of normal ossification patterns and the changes characteristic of osteitis pubis. To make matters more confusing, some adult athletes who have no symptoms of osteitis pubis may have plain-film radiographic changes characteristic of osteitis pubis. In one study of professional soccer players, radiographic changes around the symphysis were found in 76% of asymptomatic players [8]. Bone scan in patients who have osteitis pubis may demonstrate diffuse increased uptake in the area of the pubic symphysis; however, some athletes who have classic clinical symptoms fail to show abnormal uptake, and thus clinicians are helped only by a positive scan [9]. In a recent review of osteitis pubis, it was noted that the correlation between symptoms and isotope bone scan findings is difficult [7]. MRI shows marrow edema in the pubic bones early in the course of the condition, followed by low signal on T1- and T2-weighted images as the disease progresses [9]. This modality is becoming increasingly useful in the diagnosis of osteitis pubis [7]. MRI performed in a series of 25 Italian athletes who had unexplained groin pain for over 6 months revealed osteitis pubic in 14 cases, an impressively high yield [10]. Treatment begins with reassurance that the condition is usually selflimited [7]; however, osteitis pubis can take more than a year to resolve, and one study of 59 patients found that the average time to healing was 9 to 10 months [2]. Following reassurance, physical rehabilitation is the cornerstone of treatment. Pain-producing activity should be avoided and pain-free exercise should be maintained in the interest of general fitness [11]. Therapy should progress in the usual stepwise fashion (restoring range of motion exercise, then strength exercise, and finally sport-specific exercise) with particular attention to hip range of motion and adductor stretching and strengthening. Biomechanical abnormalities should also be corrected in
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order to minimize their contribution to shearing stresses placed on the pelvis. The use of steroid injections in osteitis pubis is controversial. A 1995 series [12] of 11 patients who had osteitis pubis concluded that steroid injections were more helpful in athletes who had acute symptoms of less than 2 weeks duration than in patients who had chronic symptoms. Those athletes in whom symptoms were present for greater than 16 weeks needed an additional 11 to 16 weeks for symptomatic improvement. This benefit seen in acute athletic injuries is probably clinically useless information, because most primary care sports physicians would not undertake injection in patients who have symptoms of such short duration. Although case reports and small series have shown some benefit of steroid injection in the treatment of osteitis pubis [1,12], the authors could find no rigorous trials substantiating these findings, and consequently no proper patient selection criteria. Recently, case studies have reported that a 3- to 6-month course of biophosphonate therapy has been a beneficial treatment option [13]. Surgical treatment for recalcitrant cases of osteitis pubis has been reported to be beneficial. Wedge resection of the symphysis pubis has been used in the treatment of osteitis pubis that is nonresponsive to conservative treatment [14,15]; however, this procedure has commonly been associated with postoperative instability and continued symptoms [15,16]. Although still controversial, surgical treatment may be more beneficial when chronic osteitis pubis exhibits vertical instability (greater than 2 mm) of the symphysis pubis, as demonstrated on flamingo view radiographs [17]. In a study of seven rugby players who had chronic osteitis pubis, arthrodesis of the pubic symphysis by bone grafting and compression plating was noted to have excellent results in all patients at a follow-up of 22 to 166 months. All returned to full match fitness within 9 months, with no limitation of hip range of motion and no need for oral analgesics.
Osteomylitis of the pubic symphysis Another condition that must be kept in the differential diagnosis of osteitis pubis is osteomyelitis, or bacterial infection of the pubic symphysis or adjacent bone. This condition is usually seen following surgical procedures in the area, but has also been seen after childbirth [18], and has been reported to occur spontaneously in athletes [19–21]. A recent review of 100 cases reported that 24% of cases occurred after female incontinence surgery, 19% occurred spontaneously in athletes—most often soccer players, 17% occurred in pelvic malignancy, and 15% occurred in intravenous (IV) drug use [22]. Staphylococcus aureus was the major pathogen in athletes, and Pseudomonas was the main causative agent in IV drug abusers. In the authors’ National Institute for Groin Injuries, we have
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noted this condition in only one patient presenting with chronic groin pain (authors’ early unpublished data). Clinically, patients present with fever in 74% of cases, pubic pain in 68%, antalgic gait in 59%, and groin pain in 41% [22]. Interestingly, some patients complain only of pain that is present during exercise, and are symptom-free when at rest [21]. Although bone scan and MRI are helpful in making the diagnosis, distinguishing between osteitis pubis and osteomylitis can be difficult, and can often require biopsy and culture to make a definitive diagnosis [21]. Most experts recommended a 6-week course of antibiotics, beginning with 10 to 14 days of IV therapy, followed by at least 4 weeks of oral medication. In addition, reviews have noted that as many as 55% of patients will eventually needed surgical debridement as definitive therapy [21,22]. Stress fractures The two most common stress fractures of the groin region are femoral neck stress fractures and pubic ramus fractures. They are caused by repetitive overuse and overload, and are usually seen in distance runners or military recruits. Additional risk factors include relative osteoporosis in young female athletes who have nutritional or hormonal imbalances, muscle fatigue (which may reduce shock-absorbing abilities), changes in foot gear or training surface, and sudden increases in intensity or duration of training regimens [23,24]. Presenting complaints are similar to those of stress fractures seen in other parts of the body. Athletes present with medial thigh and groin pain that is exacerbated by exercise and relieved by rest. Pain at rest represents advanced disease. Physical examination In reference to femoral neck stress fractures pain on physical examination is usually difficult for patients to localize, but painful internal rotation of the hip and inability to hop on the affected limb should raise the clinician’s index of suspicion. In the case of pubic ramus fractures, pain on direct palpation over the ramus is usually present. As above, pain will be elicited by one legged standing or jumping. Diagnostic imaging Radiographic evaluation with plain film has shown limited usefulness, because bony changes (periosteal reaction, cortical breaks, and so forth) normally lag behind the onset of symptoms by 2 to 4 weeks. In addition, it must be remembered that 50% of patients who have stress fractures never exhibit changes on plain film [25]. Bone scan is usually positive within 72
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hours of skeletal injury [9], but has been reported to be falsely positive in as high as 32% of patients presenting with hip/groin pain. This is presumably due to high osteoblastic activity in the area, because of high stress loads and constant remodeling [26]. MRI is currently the diagnostic imaging modality of choice when evaluating for femoral neck or other stress fractures of the groin region. Because groin pain suggestive of stress fracture may arise from the femoral neck, the pubic ramus, acetabulum, and sacrum, MRI should encompass a wide enough field to visualize all of these areas [27]. It should be performed early in order to make an early definitive diagnosis and implement proper treatment [23]. MRI showing early pre-fracture findings of marrow edema allows the sports physician to impose a period of relative rest to let repair strengthening occur [28]. Treatment Patients who have stress fractures of the inferior femoral neck (compression side) (see Fig. 1) can be treated conservatively with activity restriction and gradual return to activity. Follow-up imaging helps to ensure healing before return to activity. A return to sport can usually be anticipated in 2 to 3 months [11]. In contrast to inferior femoral neck stress fractures, stress fractures of the superior femoral neck (traction side) are more problematic, and must be treated with open reduction and internal fixation in order to prevent risk of progression to complete fracture, displacement, and subsequent avascular necrosis [24]. Less worrisome are stress fractures of the inferior pubic ramus [7]. These injuries usually occur in female distance runners and military recruits, and are comparatively easy to diagnose on physical examination. The diagnosis can be confirmed by a bone scan or MRI. Four to 6 weeks of relative rest can be followed by gradual return to sport, with most athletes regaining their prior level of sport within 3 to 5 months [29].
Fig. 1. Stress fractures of the femoral neck: (A) traction, (B) compression, (C) complete.
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As with any injury, treatment of femoral neck and pubic ramus stress fractures would be incomplete without also addressing and modifying risk factors. Risk factors that should be addressed include biomechanical contributors, maintenance of hormonal and nutritional balance, modification of foot gear and training surface, and most important, a conscientious review of the athlete’s training program.
Disorders of the hip When evaluating groin pain in the athlete, the physician must remember that hip pathology can refer pain to the groin region. Acetabular labral tears, articular cartilage defects of the femoral head or acetabulum, loose bodies, capsular laxity, and injuries to the ligamentum teres all may present as groin pain. Other less common presenting conditions include osteonecrosis of the femoral head, slipped capital femoral epiphysis, gout, pseudogout, synovial chondromatosis, and infection [30]. Labral tears Acetabular labral tears are increasingly being recognized as a source of groin pain in athletes. In one prospective study of patients presenting to a sports medicine center with chronic groin pain, 22% were found to have labral tears [31]. Labral tears have been found by several investigators to be associated with developmental dysplasia [32,33]. Anatomical considerations The cartilaginous acetabular labrum has little vessel penetration except into the peripheral margins [34]. This relative avascularity leads most experts to conclude that there is limited ability for healing after injury. Two types of labral lesions have been noted in cadaver studies: fraying of the labral-articular cartilage junction, and actual tears of the labrum. Lage et al [35] divided labral tears into four descriptive categories: (1) radial free margin flap tears (57%), (2) radial fiberlated labrum (22%), (3) longitudinal tears located along the peripheral margins (16%), and (4) ‘‘abnormally mobile’’ tears (5.4%).Tears occurring in athletes as a result of minimal or no trauma as are usually seen in the anterior/superior aspect of the labrum, a place postulated to be developmentally weak and thus more prone to injury and overload stresses [36]. Indeed, in most US series, about two thirds of labral tears are located in this position [37,38]. Labral lesions have been found in high association with adjacent articular cartilage damage, and thus are thought to contribute to progressive degenerative joint disease of the hip. It is theorized that tears disrupt the usual stabilizing function of the labrum, resulting in instability and increased wear-and-tear damage to the adjacent articular cartilage [39,40].
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History and physical One third of athletes recall a specific traumatic event as the cause of symptom onset. The remainder of tears are caused by relatively atraumatic mechanisms, such as twisting or pivoting during athletic endeavor, or by chronic degenerative disease [39]. Presenting symptoms include diffuse poorly localized groin pain and mechanical symptoms in the hip/groin area. Some patients may present with a painful snapping hip syndrome (see below). In one study, a clicking sensation of the hip was both sensitive (100%) and specific (85%) in predicting labral tears. On physical examination, the internal rotation/flexion/axial compression maneuver was 75% sensitive but only 43% specific [31], and the flexion/ abduction/external rotation (FABER) test was found to be 88% sensitive [41]. The sports physician must keep in mind that these physical maneuvers are imperfect, and must maintain a high index of suspicion for such injuries.
Diagnostic imaging Plain films are not helpful in diagnosing labral tears, though they may help in ruling out other hip abnormalities (osteonecrosis of the femoral head, slipped capital femoral epiphysis, osseous loose bodies, and so forth). MRI arthrography for diagnosing labral tears and associated articular cartilage damage is the current imaging technique of choice. It has been shown to have a sensitivity of 50% to 77%, and a specificity of 77% to 84% [36]. The imprecision in diagnosing associated articular cartilage defects is in part caused by the relative thinness of the articular cartilage in the hip (as compared with the knee), which makes femoral and acetabular cartilages difficult to visualize separately on MRI arthrography.
Treatment Conservative treatment is usually tried for at least 6 weeks before definitive surgical intervention. This is done to insure that mechanical symptoms are not due to snapping hip syndrome (see below), and that any associated injuries are given a chance to heal. In one study (N = 436) [40], surgical treatment was considered for patients presenting with painful mechanical symptoms, localization of pain to the groin, no success with conservative treatment after 6 months, reproduction of symptoms on physical examination, McCarthy sign, positive flexion/abduction/internal rotation test, and MRI or MRI arthrogram confirming a labral lesion or loose body. In this study, 55% were found to have labral tears, and 35% had labral fraying at the labral chondral junction. As above, 86% of labral tears were located anteriorly, and all were at the labral-articular cartilage junction, none at the periphery. Seven percent were noted to have multiple tears, and 74% of those with fraying or tears also had associated femoral or acetabular articular cartilage damage.
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Treatment of labral tears by careful debridement has been noted to eliminate both painful and mechanical symptoms. Results of intervention vary depending on pathology present. Pathology is summarized by stages below: Stage 1—discrete labral free margin tear with intact articular cartilage of both the femoral head and acetabulum Stage 2—labral tear with articular damage to adjacent femoral head but not to acetabulum Stage 3—labral tear with acetabular articular cartilage damage, with or without femoral head articular cartilage damage Stage 4—extensive acetabular tear with associated arthritic changes of the hip In one study [39], stage 1 and 2 lesions responded to surgical intervention with 80% to 90% good-to-excellent results. Stage 3 lesions were less responsive, achieving good-to-excellent results in only 17% to 40%. Stage 4 hips fared even worse, with 78% achieving poor results. Forty-three percent of these patients eventually needed total hip arthroplasty. Articular cartilage injuries of the hip Articular cartilage lesions of the acetabulum or femoral head are generally felt to be the result of trauma. Injuries ranging from hip dislocation [42] to subclinical shearing or minor ‘‘routine’’ hip impact have been noted to cause these lesions [43]. Presenting complaints are nonspecific, and may include diffuse groin pain with or without mechanical symptoms. Physical examination maneuvers are neither sensitive nor specific, but pathologic symptoms may be elicited with logrolling of the affected extremity, flexion with internal rotation, and abduction with internal rotation [44]. An intra-articular diagnosis may be confirmed if symptom relief occurs with a guided injection of anesthetic into the joint [44]. MRI may be used both to diagnose and grade osteochondral lesions of the hip [27]. MRI arthrography is generally thought to be superior (50%–68% sensitive, 77%–84% specific) to noncontrast MRI for identifying chondral defects, but is still poor at detecting partial thickness lesions, small lesions, and loose bodies [27,45]. Again, the shortcomings of MRI in these conditions is caused in part by the relative thinness of the articular cartilage in the hip (as compared with the knee), making femoral and acetabular cartilages difficult to visualize separately. Also, loose bodies may imbibe gadolinium contrast, rendering them nondetectable. CT arthrography has been stated to be superior at detecting loose bodies [44]. One added advantage of performing arthrography is that if anesthetic is added to contrast material at the time of injection, the diagnosis may be definitively localized as intra-articular.
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Surgical treatment is contemplated for any partially or completely detached lesions (Grade II, III, and IV), whereas conservative management is reserved for Grade I lesions (intact articular cartilage with changes in subchondral bone) [46].
Injuries to the ligamentum teres Injuries to the ligamentum teres are relatively uncommon, accounting for only 8% of pathologic lesions found at hip arthroscopy [47]. These lesions may be traumatic or degenerative in origin. As above, traumatic injury may be the result of a substantial impact (motor vehicle accidents, falls, football dislocations, and the like) or of relatively minor twisting injuries. Patients usually present with longstanding deep groin pain, and many experience mechanical locking, popping, or giving way as well [48]. Complete rupture of the ligament is usually traumatic in origin and is often (roughly two thirds of the time [48]) associated with other concomitant hip injuries (eg, labral tears, articular cartilage damage) [30]. Partial tears usually present with long-standing, ill-defined groin pain, and are less likely to have mechanical symptoms These lesions have been noted to have a high incidence in ballet dancers [30]. Degenerative tears are usually noted in elderly patients who have concomitant osteoarthritis. Diagnostic imaging is notoriously poor for detecting ligamentum teres lesions. One study noted that only 2 of 23 arthroscopicaly documented lesions (12 complete ruptures, 11 partial tears) were detected by MRI, MRI arthrogram, or CT [48]. Treatment consists of arthroscopic debridement, and results are usually best when there are no associated acetabular or femoral chondral defects.
Avascular necrosis of the hip Avascular necrosis (AVN) of the hip is a progressive debilitating lesion that usually affects people in the third and fourth decades of life. The incidence has been estimated to be between 10,000 and 20,000 cases per year in the United States, with a mean age at presentation of 38 years [49]. Although the pathogenesis is still not entirely understood, it is generally agreed that an initial disruption of circulation to a portion of the femoral head occurs. This insult leads to localized cell death and bone necrosis, eventually followed by more widespread necrosis, and ultimately by bony collapse and progressive arthritis of contiguous joints [50]. The initial disruption of blood flow may result from a single traumatic event, from repetitive minor damages, or from various nontraumatic causes. Femoral neck fractures and hip dislocations are the most common traumatic causes. In 1991, a case of AVN of the hip in a professional football player who sustained a traumatic hip subluxation was reported [51].
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Ninety percent of nontraumatic causes of AVN have been associated with either systemic corticosteroid use or heavy alcohol consumption [52]. Numerous case reports have noted an association of AVN with corticosteroids used in treating asthma, chronic obstructive pulmonary disease (COPD), autoimmune diseases, leukemia, or psoriasis, and when used as an immunosuppressive agent after transplant surgery [53]. Both short-term steroid ‘‘bursts’’ and long-term use have been implicated, as has the use of unusually high doses [54]. The exact way in which corticosteroids lead to AVN is unknown; however, it is currently thought that steroids induce a hypercoaguable state, with subsequent impaired fibrinolysis, and eventual venous thrombosis and bone infarct [55,56]. The use of anabolic steroids has also been associated with AVN in athletes. In one case report, a weight lifter with an 8-year history of ergogenic steroid use and no other predisposing risk factors developed bilateral femoral head avascular necrosis [57]. Most other risk factors and disease states associated with atraumatic avascular necrosis have systemic effects that alter circulating lipids or disrupt coagulation pathways. Such conditions include smoking, sickle cell anemia, coagulopathies, lupus, hypercholesterolemia, organ transplantation, Gaucher disease, and hypertriglyceridemia. Despite a large number of risk factors that can be directly linked with the incidence of AVN of the hip, approximately 10% to 20% of cases have no clearly identifiable risk factor and are classified as idiopathic [58].
Clinical presentation and diagnosis A high index of suspicion and awareness of the predisposing factors mentioned above is critical. Athletes who have avascular necrosis of the femoral head typically complain of groin pain. Occasionally, nonspecific hip pain that may affect the buttock or knee region may be described as well. On physical examination in the early stages, hip range of motion and gait are normal; however, as the disease progresses, internal rotation becomes restricted, and passive rotation of the hip (especially internal rotation) generally reproduces the pain. In addition to evaluating the symptomatic hip, a complete examination of the contralateral hip should also be performed, because 40% to 80% of patients have bilateral involvement [59]. Initially, antero-posterior and antero-lateral radiographs of both hips should be obtained. Among the earliest radiographic changes that occur are osteopenia, or patchy areas of sclerosis and lucency. As necrosis progresses, the crescent sign appears, representing collapse of the trabecula beneath the subchondral bone. Because radiograph changes are not apparent until 3 months after the initial insult, MRI of the hip should be obtained if the disease is suspected despite normal plain films. MRI is the imaging modality of choice in identifying early AVN, and is both sensitive and specific (88%–100%) [58].
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Management If this entity is recognized early, proper treatment may have a beneficial effect on outcomes. Unfortunately however, the majority of cases are recognized only in the advanced stages, when treatment options are limited. No single surgical or medical method has been demonstrated to universally prevent disease progression. Treatment depends on the stage of the disease. In the past, early disease was thought best treated by simple restricted weight bearing and symptom control. Currently however, although at least one randomized trial still finds no difference between surgical and conservative management [60], other prospective trials come down clearly on the side of early surgical core decompression [61,62]. Other surgical treatments that seek to promote vascular ingrowth in the compromised femoral head include cortical or vascularized bone grafting [63,64]. In the late stages of disease, the accompanying femoral head collapse and altered mechanics obviate the possibility of performing any of these femoral head ‘‘sparing’’ procedures, and usually necessitate total hip arthroplasty for restoration of function and relief of symptoms. Prompt recognition of this disease is critical for the best clinical outcome. If diagnosed early with a good history and physical and ancillary studies such as an MRI, an athlete who has avascular necrosis of the hip can be surgically managed, and has the best chance of avoiding catastrophic disease progression and permanent disability. Snapping hip syndromes Snapping hip syndrome refers to a snapping sensation felt or about the hip with movement. Less than one third of these patients will experience pain with snapping, and it is only in these cases that treatment need be initiated. Snapping hip syndrome may be classified as intra-articular and extraarticular. The more common lateral extra articular type of snapping hip syndrome occurs when the iliotibial band, tensor fascia lata, or gluteus medius tendon slides back and forth across the greater trochanter. This normal action becomes a snapping hip syndrome when one of these connective tissue bands thickens and catches with motion. The underlying bursa may also become inflamed, causing a painful external snapping hip syndrome. The medial extra-articular type of snapping hip syndrome results from the iliopsoas tendon catching on the anterior inferior iliac spine (AIIS), the lesser trochanter, or the iliopectineal ridge during hip extension, as the tendon moves from an anterior lateral to a posterior medial position. With overuse, the resultant friction may eventually cause painful symptoms, resulting in muscle trauma, bursitis, or inflammation in the area [65]. The intra-articular type of snapping hip syndrome results from labral tears, articular cartilage damage, ligamentum teres tears, or loose bodies.
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The physician should attempt to identify the source of the symptomatic clicking on physical examination, with directed testing as noted above for iliopsoas involvement, ranging the hip while palpating over the greater trochanter for lateral symptoms, and employing the physical examination maneuvers noted above when trying to detect intra-articular pathology. Ultrasound during hip motion may visualize tendon subluxation and any concomitant bursitis when evaluating for iliopsoas involvement in medial extra-articular snapping [66]. As stated above, MRI can sometimes identify intra-articular causes of snapping hip syndrome. Treatment of the condition requires elucidation of the underlying pathology and tailoring therapy to the inciting cause. Correcting any contributing biomechanical abnormalities and stretching tightened muscles (eg, iliopsoas muscle, iliotibial band) are important. Corticosteroid injections can be useful if bursitis is present. Surgical treatment is rarely indicated unless intra-articular pathology is present, or in patients who have persistently painful iliopsoas symptoms. In the latter case, surgical tendon lengthening has been described as a beneficial procedure [67].
References [1] Koch RA, Jackson DW. Pubic symphysitis in runners. A report of two cases. Am J Sports Med 1981;9(1):62–3. [2] Fricker PA, Taunton JE, Ammann W. Osteitis pubis in athletes. Infection, inflammation or injury? Sports Med 1991;12(4):266–79. [3] Renstroem AF. Groin injuries: a true challenge in orthopaedic sports medicine. Sports Medicine and Arthroscopy Review 1997;5:247–51. [4] Williams JG. Limitation of hip joint movement as a factor in traumatic osteitis pubis. Br J Sports Med 1978;12(3):129–33. [5] Ekberg O, Persson NH, Abrahamsson PA, et al. Longstanding groin pain in athletes. A multidisciplinary approach. Sports Med 1988;6:56–61. [6] Westlin N. Groin pain in athletes from Southern Sweden. Sports Medicine and Arthroscopy Review 1997;5:280–4. [7] Fricker PA. Management of groin pain in athletes. Br J Sports Med 1997;31:97–101. [8] Harris NH, Murray RO. Lesions of the symphysis in athletes. BMJ 1974;4:211–4. [9] Karlsson J, Jerre R. The use of radiography, magnetic resonance, and ultrasound in the diagnosis of hip, pelvis, and groin injuries. Sports Medicine and Arthroscopy Review 1997;5: 268–73. [10] Barile A, Erriquez D, Cacchio A, et al. Groin pain in athletes: magnetic resonance imaging evaluation. Radiol Med (Torino) 2000;100(4):216–22. [11] Lynch SA, Renstrom PA. Groin injuries in sport: treatment strategies. Sports Med 1999;28: 137–44. [12] Holt MA, Keene JS, Graf BK, et al. Treatment of osteitis pubis in athletes. Results of corticosteroid injections. Am J Sports Med 1995;23(5):601–6. [13] Maksymowych WP, Aaron SL, Russell AS. Treatment of refractory symphysitis pubis with intravenous pamidronate. J Rheumatol 2001;28(12):2754–7. [14] Coventry MB, Mitchell WC. Osteitis pubis: observations based on a study of 45 patients. JAMA 1961;178:898–905.
198
MORELLI & ESPINOZA
[15] Grace JN, Sim FH, Shives TC, et al. Wedge resection of the symphysis pubis for the treatment of osteitis pubis. J Bone Joint Surg Am 1989;71(3):358–64. [16] Moore RS Jr, Stover MD, Matta JM. Late posterior instability of the pelvis after resection of the symphysis pubis for the treatment of osteitis pubis. A report of two cases. J Bone Joint Surg Am 1998;80(7):1043–8. [17] Williams PR, Thomas DP, Downes EM. Osteitis pubis and instability of the pubic symphysis. When nonoperative measures fail. Am J Sports Med 2000;28(3):350–5. [18] Eskridge C, Longo S, Kwark J, et al. Osteomyelitis pubis occurring after spontaneous vaginal delivery: a case presentation. J Perinatol 1997;17(4):321–4. [19] Combs JA. Bacterial osteitis pubis in a weight lifter without invasive trauma. Med Sci Sports Exerc 1998;30(11):1561–3. [20] Hedstrom SA, Lidgren L. Acute hematogenous pelvic osteomyelitis in athletes. Am J Sports Med 1982;10(1):44–6. [21] Pauli S, Willemsen P, Declerck K, et al. Osteomyelitis pubis versus osteitis pubis: a case presentation and review of the literature. Br J Sports Med 2002;36(1):71–3. [22] Ross JJ, Hu LT. Septic arthritis of the pubic symphysis: review of 100 cases. Medicine (Baltimore) 2003;82(5):340–5. [23] Roos HP. Hip pain in sport. Sports Medicine and Arthroscopy Review 1997;5:292–300. [24] Rolf C. Pelvis and groin stress fractures: a cause of groin pain in athletes. Sports Medicine and Arthroscopy Review 1997;5:301–4. [25] Ohashi K, Brandser EA, el-Khoury GY. Role of MR imaging in acute injuries to the appendicular skeleton. Radiol Clin North Am 1997;35(3):591–613. [26] Shin AY, Morin WD, Gorman JD, et al. The superiority of magnetic resonance imaging in differentiating the cause of hip pain in endurance athletes. Am J Sports Med 1996;24(2): 168–76. [27] Bencardino JT, Kassarjian A, Palmer WE. Magnetic resonance imaging of the hip: sportsrelated injuries. Top Magn Reson Imaging 2003;14(2):145–60. [28] Lee JK, Yao L. Stress fractures: MR imaging. Radiology 1988;169(1):217–20. [29] Hill PF, Chatterji S, Chambers D, et al. Stress fracture of the pubic ramus in female recruits. J Bone Joint Surg Br 1996;78(3):383–6. [30] Kelly BT, Williams RJ 3rd, Philippon MJ. Hip arthroscopy: current indications, treatment options, and management issues. Am J Sports Med 2003;31(6):1020–37. [31] Narvani AA, Tsiridis E, Kendall S, et al. A preliminary report on prevalence of acetabular labrum tears in sports patients with groin pain. Knee Surg Sports Traumatol Arthrosc 2003; 11(6):403–8. [32] Ikeda T, Awaya G, Suzuki S, et al. Torn acetabular labrum in young patients. Arthroscopic diagnosis and management. J Bone Joint Surg Br 1988;70(1):13–6. [33] McCarthy JC, Noble PC, Schuck MR, et al. The watershed labral lesion: its relationship to early arthritis of the hip. J Arthroplasty 2001;16(8 Suppl 1):81–7. [34] Lage LA, Patel JV, Villar RN. The acetabular labral tear: an arthroscopic classification. Arthroscopy 1996;12(3):269–72. [35] Schmid MR, Notzli HP, Zanetti M, et al. Cartilage lesions in the hip: diagnostic effectiveness of MR arthrography. Radiology 2003;226(2):382–6. [36] Baber YF, Robinson AH, Villar RN. Is diagnostic arthroscopy of the hip worthwhile? A prospective review of 328 adults investigated for hip pain. J Bone Joint Surg Br 1999;81(4): 600–3. [37] Farjo LA, Glick JM, Sampson TG. Hip arthroscopy for acetabular labral tears. Arthroscopy 1999;15(2):132–7. [38] McCarthy J, Noble P, Aluisio FV, et al. Anatomy, pathologic features, and treatment of acetabular labral tears. Clin Orthop 2003;(406):38–47. [39] McCarthy JC, Noble PC, Schuck MR, et al. The Otto E. Aufranc award: the role of labral lesions to development of early degenerative hip disease. Clin Orthop 2001;(393): 25–37.
GROIN INJURIES AND PAIN 2
199
[40] Mitchell B, McCrory P, Brukner P, et al. Hip joint pathology: clinical presentation and correlation between magnetic resonance arthrography, ultrasound, and arthroscopic findings in 25 consecutive cases. Clin J Sport Med 2003;13(3):152–6. [41] Laorr A, Greenspan A, Anderson MW, et al. Traumatic hip dislocation: early MRI findings. Skeletal Radiol 1995;24(4):239–45. [42] Weaver CJ, Major NM, Garrett WE, et al. Femoral head osteochondral lesions in painful hips of athletes: MR imaging findings. AJR Am J Roentgenol 2002;178(4):973–7. [43] Byrd JW. Lateral impact injury. A source of occult hip pathology. Clin Sports Med 2001; 20(4):801–15. [44] Edwards DJ, Lomas D, Villar RN. Diagnosis of the painful hip by magnetic resonance imaging and arthroscopy. J Bone Joint Surg Br 1995;77(3):374–6. [45] Dipaola JD, Nelson DW, Colville MR. Characterizing osteochondral lesions by magnetic resonance imaging. Arthroscopy 1991;7(1):101–4. [46] Rao J, Zhou YX, Villar RN. Injury to the ligamentum teres. Mechanism, findings, and results of treatment. Clin Sports Med 2001;20(4):791–9; vii. [47] Byrd JW, Jones KS. Traumatic rupture of the ligamentum teres as a source of hip pain. Arthroscopy 2004;20(4):385–91. [48] Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am 1995;77(3):459–74. [49] Assouline-Dayan Y, Chang C, Greenspan A, et al. Pathogenesis and natural history of osteonecrosis. Semin Arthritis Rheum 2002;32(2):94–124. [50] Cooper DE, Warren RF, Barnes R. Traumatic subluxation of the hip resulting in aseptic necrosis and chondrolysis in a professional football player. Am J Sports Med 1991;19(3): 322–4. [51] Noccion SL, Hunter DM, Finerman GAM. Hip and pelvis. In: DeLee JC, Drez D Jr, editors. DeLee and Drez’s orthopaedic sports medicine: principles and practice. 2nd edition. Philadelphia: Saunders; 2003. p. 1443–79. [52] Reichert-Penetrat S, Trechot P, Barbaud A, et al. Bilateral femoral avascular necrosis in a man with psoriasis: responsibility of topical corticosteroids and role of cyclosporine. Dermatology 2001;203(4):356–7. [53] Knight A. Corticosteroids and avascular necrosis of the femoral head. CMAJ 2001;165(4): 397; 399. [54] Glueck CJ, Freiberg R, Glueck HI, et al. Hypofibrinolysis: a common, major cause of osteonecrosis. Am J Hematol 1994;45(2):156–66. [55] Glueck CJ, Freiberg R, Glueck HI, et al. Idiopathic osteonecrosis, hypofibrinolysis, high plasminogen activator inhibitor, high lipoprotein(a), and therapy with stanozolol. Am J Hematol 1995;48(4):213–20. [56] Pettine KA. Association of anabolic steroids and avascular necrosis of femoral heads. Am J Sports Med 1991;19(1):96–8. [57] Lavernia CJ, Sierra RJ, Grieco FR. Osteonecrosis of the femoral head. J Am Acad Orthop Surg 1999;7(4):250–61. [58] Steinberg ME, Hayken GD, Steinberg DR. A quantitative system for staging avascular necrosis. J Bone Joint Surg Br 1995;77(1):34–41. [59] Koo KH, Kim R, Ko GH, et al. Preventing collapse in early osteonecrosis of the femoral head. A randomised clinical trial of core decompression. J Bone Joint Surg Br 1995;77(6): 870–4. [60] Stulberg BN, Davis AW, Bauer TW, et al. Osteonecrosis of the femoral head. A prospective randomized treatment protocol. Clin Orthop 1991;(268):140–51. [61] Steinberg ME, Larcom PG, Strafford B, et al. Core decompression with bone grafting for osteonecrosis of the femoral head. Clin Orthop 2001;(386):71–8. [62] Ishizaka M, Sofue M, Dohmae Y, et al. Vascularized iliac bone graft for avascular necrosis of the femoral head. Clin Orthop 1997;(337):140–8.
200
MORELLI & ESPINOZA
[63] Rijnen WH, Gardeniers JW, Buma P, et al. Treatment of femoral head osteonecrosis using bone impaction grafting. Clin Orthop 2003;(417):74–83. [64] Johnston CA, Wiley JP, Lindsay DM, et al. Iliopsoas bursitis and tendinitis. A review. Sports Med 1998;25(4):271–83. [65] Janzen DL, Partridge E, Logan PM, et al. The snapping hip: clinical and imaging findings in transient subluxation of the iliopsoas tendon. Can Assoc Radiol J 1996;47(3):202–8. [66] Jacobson T, Allen WC. Surgical correction of the snapping iliopsoas tendon. Am J Sports Med 1990;18(5):470–4. [67] Dorrell JH, Catterall A. The torn acetabular labrum. J Bone Joint Surg Br 1986;68(3):400–3.