Adductor strains are generally referred to as a “pulled groin” and are a common cause of hip and groin pain in athletes. The adductor longus, adductor magnus, adductor brevis, adductor minimus, pectineus, and gracilis muscles are all adductors of the hip, contribute to hip flexion and extension, and contribute to internal and external rotation of the hip. In sport, the adductor longus is the most often injured, and may comprise up to 10 % of all athletic injuries [1, 2].

An acute adductor strain is caused by a sudden change in direction, sprinting, forced external rotation of an abducted leg, or powerful abduction stress during simultaneous adduction. Acute adductor strains are commonly seen in the sports of hockey and soccer because of the frequent cutting and frequent eccentric contraction of the adductors in these sports [2, 3]. Adductor tendinopathy is a mechanical enthesopathy generally due to repetitive strain injuries [4].

The differential diagnosis includes avascular necrosis of the femoral head, femoral neck stress fracture, iliopsoas bursitis, osteitis pubis, obturator nerve entrapment, osteoarthritis, pelvic stress fracture, inguinal hernia, and athletic pubalgia.

With an acute injury, athletes will complain of immediate pain piercing into the groin and an inability to continue activity. Delayed ecchymosis and soft tissue swelling may also occur. In chronic injury, athletes will report an insidious onset of groin pain, possibly starting after a change in training that is worse at the start of exercise. Severe pain and dysfunction that occur after a “pop” may suggest adductor tendon avulsion.

Physical examination will reveal tenderness to palpation along the subcutaneous border of the pubic ramus and along the involved adductor muscles and tendons. The patient will have pain with resisted adduction and with passive stretching.

The diagnosis of an adductor strain is usually made clinically. Plain radiographs can be helpful in excluding fractures or avulsions of the hip and pelvis. If the diagnosis is in question, musculoskeletal ultrasonography (Fig. 6.1) or magnetic resonance imaging (MRI) can be used to confirm the diagnosis and fully evaluate the degree of injury [4, 5].

Eccentric strengthening of the adductor muscles is an established preventative measure to protect against groin injuries in soccer players [6]. However, after the injury occurs, treatment depends on the severity of the symptoms. Initially, rest from aggravating factors for 1–2 weeks with ice and oral analgesics provides symptomatic relief. Athletes can begin a stretching program after the inflammation subsides. The goal of physical therapy is to prevent atrophy and to regain strength, flexibility, and endurance. Rehabilitative therapy should be instituted as soon as pain allows and should include isometric contractions without resistance followed by isometric contractions against resistance. Prevention and correction of predisposing biomechanical factors should be included in the rehabilitation program. Return to play may take 4 weeks to 6 months depending on the extent of injury. Shorts with directional compression may aid in preventing adductor strains and these shorts may reduce demand during rehabilitation after strains [7]. Athletes with chronic adductor longus strains that have failed several months of conservative therapy may be considered for platelet-rich plasma injection (PRP) [8]. Athletes with adductor avulsion injuries or with chronic tendinopathy that has failed more conservative measures should be referred to orthopedics for consideration for possible surgical intervention .

The quadriceps muscles are the rectus femoris, vastus lateralis, vastus medialis, and vastus intermedius. The main action of the rectus femoris is to flex the hip and extend the knee, and it is the most commonly injured of the quadriceps muscles [9]. The quadriceps are heavily recruited and frequently overused during jumping, sprinting, cutting, skating, bicycling, and during other explosive movements. Injuries usually occur as a result of a heavy eccentric load. Quadriceps injuries are twice as common in the dominant leg, and risk factors for quadriceps injuries include short height and heavy weight, lack of flexibility, dry field conditions, and a history of quadriceps injuries [10]. The differential diagnosis includes femoral shaft stress fracture, acute compartment syndrome of the anterior thigh, meralgia paresthetica, and femoral nerve injury.

Athletes may report a sensation of “pulling” or “tearing” in the anterior hip with acute injury. Onset of pain is typically after forceful contraction of the quadriceps muscles. The pain is in the anterior thigh and occurs with knee extension or hip flexion. The pain often radiates down the thigh and into inguinal area. Physical examination may reveal pain with resisted hip flexion or resisted knee extension. There is often tenderness to palpation of the quadriceps muscles and a palpable defect or mass.

A rectus femoris strain is diagnosed clinically, but if an avulsion injury to the anterior inferior iliac spine is suspected then plain radiographs should be ordered . Ultrasonography (Fig. 6.2) and MRI can aid in the diagnosis and be used to determine severity.

Initial treatment consists of rest, ice, compression, oral analgesia, protected weight bearing, gentle range of motion, and quadriceps exercises. Ice massage and therapeutic ultrasound should be started early in the rehabilitation course. Rehabilitation strengthening exercises are initially concentric and progress to eccentric. An example of this progression is to start the athlete with backward walking, progress to backward running, and later transitioning to forward running. The athlete can return to running when his or her knee range of motion is 80 % that of the unaffected side. Depending on the severity of the injury, return to play may take 2–6 weeks. Data is currently lacking on evidence-based return to play protocols following quadriceps injury.

Contusions of the quadriceps muscles are a common injury in contact sports including football, rugby, hockey, and martial arts. Quadriceps contusions are caused by direct trauma to the anterior thigh. The differential diagnosis includes femoral shaft fracture, acute compartment syndrome of the anterior thigh, meralgia paresthetica, and quadriceps strains.

Athletes will generally be able to give a history of trauma to the anterior thigh and will describe pain with passive knee flexion and active extension at the knee. Examination often reveals tenderness, swelling, and a hematoma on the anterior thigh. Pain with knee flexion and a loss of range of motion at the knee is often present on exam. If necessary, the diagnosis can be confirmed with musculoskeletal ultrasound, which will show disruption of the normal muscle fibers and hematoma formation.

Initial treatment is essentially the same as with quadriceps strains including rest, oral analgesia, elevation, and intermittent application of ice with a compression wrap. Keeping the muscle in a lengthened and flexed position for the first 24 h after injury can help maintain flexibility, decrease bleeding, and may shorten the time required for return to play [6]. The athlete should be allowed to weight bear as tolerated. Deep massage and ultrasound should be avoided, as these can increase muscle bleeding. Active flexio n should be encouraged and continued frequently. Heat and cold contrasts and strengthening exercises are initiated after the swelling begins to decrease. Return to play may be allowed after the athlete regains quadriceps flexibility and strength equal to 90 % of the unaffected side.

Myositis ossificans is a pseudosarcomatous lesion that is characterized by bone formation in or adjacent to muscle and can be a post-traumatic complication of a quadriceps contusion [11]. Post-traumatic myositis ossificans occurs after initial muscular bleeding leads to the formation of a hematoma, which later calcifies within the muscle. This process causes pain and reduced flexibility. The incidence of myositis ossificans following muscle contusion is 9–17 % [12]. Although occurrence after a contusion is the most common scenario reported by athletes, myositis ossificans can also develop in an athlete with a history of repetitive minor trauma.

The differential diagnosis includes hematoma, abscess, focal rhabdomyolysis, and malignant primary or secondary soft tissue tumors [13]. Post-traumatic myositis ossificans will become clinically suspected when an athlete does not respond to conservative interventions within 3–4 weeks after a contusion. The usual symptoms include a painful and palpable mass with progressive loss of range of motion.

On examination, the athlete may have an antalgic gait and a tender anterior leg mass. Plain radiographs are performed to evaluate the femur for fracture. A bone scan is often used to track myositis ossificans formation. Radiographic evidence of calcification due to myositis ossificans may not be present for weeks following injury and, therefore, a presumptive diagnosis of myositis ossificans is often made after a severe contusion does not show rapid improvement. To help differentiate late presenting myositis ossificans from a sarcoma, computed tomography (CT) scan or MRI is often utilized. Sonographic findings in myositis ossificans have also been described [14] (Fig. 6.3).

Treatment of myositis ossificans is similar to that of a quadriceps strain. The goals of therapy are to restore strength and range of motion. Placing and holding the knee in end of range of flexion immediately after a significant contusion to the quadriceps may shorten the time to return to unrestricted full activity [10]. Early administration of indomethacin may aid in prevention of myositis ossificans; however, this concept is extrapolated from indomethacin’s use in prevention of heterotopic ossification following hip arthroplasty. At this time, it is uncertain if indomethacin has a substantial impact on the prevention of heterotopic bone formation following quadriceps contusion. Treatment with short term use of bisphosphonates has been suggested in the literature [15]; however, its use is limited by tetratogenicity. Additionally, once the drug is discontinued, the mineralization process appears to resume [16].

Early rehabilitation should include active stretching and strengthening exercises. Extracorporeal shock wave therapy may be considered in the treatment of myositis ossificans [17]. Surgical treatment generally is not indicated, but if necessary, it should be delayed until the mass has matured. Radiographic resolution is not necessary for return to play. However, rehabilitation to achieve full strength and flexibility is mandatory. Wearing protective padding over the affected area should be considered as well.

The iliopsoas muscle is a strong flexor of the hip and can be acutely injured when the hip is forced into extension or is blocked during active flexion. This injury is commonly called a hip flexor strain. Tendinopathy may also occur with overuse. It often occurs in soccer players who are hit as they flex at the hip and extend at the knee to kick the ball. It also occurs in weightlifting, uphill running, and with sit-ups. The differential diagnosis includes adductor strains, quadriceps strains, femoroacetabular impingement, osteitis pubis, and athletic pubalgia.

Athletes present with a complaint of sharp, deep groin pain that worsens with active hip flexion or passive hip extension. Physical examination reveals tenderness to palpation in the femoral triangle and increased pain with resisted hip flexion and passive external rotation or extension. The diagnosis is made clinically and imaging is rarely needed. When the diagnosis is not clear, plain radiographs followed by MRI can help establish a diagnosis, with MRI able to distinguish between abnormalities of the involved bones, tendons, and muscles.

Initial treatment involves rest, protection, and oral analgesia followed by rehabilitation. In adults, this injury may result in a partial or complete tear at the musculotendinous junction and these tears take longer to rehabilitate. Corticosteroid injection and surgery may be considered in refractory cases [18].

The iliopsoas tendon results from the joining of the iliacus and psoas muscles and inserts onto the lesser trochanter of the femur after passing over the protective iliopsoas bursa. The iliopsoas bursa is the largest bursa in the body and communicates with the hip joint in 15 % of athletes [19]. This bursitis is associated with sports requiring extensive use of the hip flexors (i.e., soccer, ballet, uphill running, hurdling, jumping) and may be particularly disabling for athletes. It is also associated with degenerative or inflammatory arthritis, infections, trauma, osteonecrosis, and hip replacement [20].

The differential diagnosis includes iliopsoas tendinopathy, FAI and labral tears, athletic pubalgia, AVN, and stress fractures of the femur and pelvis.

Athletes may present with severe, acute, deep groin pain radiating to the anterior hip or thigh. The pain may be great enough to disrupt ambulation. It is often associated with a snapping sensation caused by the iliopsoas tendon snapping over the iliopectineal eminence.

Athletes will assume a position of hip flexion and external rotation to obtain relief [21]. The musculotendinous junction of the iliopsoas lies in the femoral triangle, and deep palpation of the femoral triangle may elicit pain [19]. Pain may be exacerbated by passive hip extension or when the supine athlete raises his or her heels off the table approximately 15°, thereby isolating the iliopsoas [22]. Musculoskeletal ultrasonography will demonstrate an enlargement of the iliopsoas bursa [20] (Fig. 6.4), and MRI reveals a collection of fluid adjacent to the muscle in iliopsoas bursitis [23].

Treatment is almost always nonoperative and consists of rest, ice, nonsteroidal anti-inflammatories (NSAIDs), and stretching of the iliopsoas. If symptoms are recalcitrant to conservative therapy, corticosteroid injection with ultrasonographic (Fig. 6.5) or fluoroscopic guidance, release of the iliopsoas tendon near its insertion on the lesser trochanter, or excision of the bursa may be considered [19].

The rectus abdominis originates on the pubis adjacent to the origin of the adductor longus . As such, injury to the rectus abdominis may easily be confused or coexist with an adductor injury.

The differential diagnosis includes intra-abdominal pathology, sexually transmitted diseases, inguinal hernia, adductor strain, and osteitis pubis.

Athletes typically report deep groin pain that is worsened by tightening or stretching of the rectus abdominis muscle. On physical examination, pain is elicited on palpation of the superior aspect of the pubic ramus, and is exacerbated in the supine patient by a bilateral straight leg raise or resisted sit-up. Imaging is generally not needed to make the diagnosis; however, if necessary, musculoskeletal ultrasound or MRI may demonstrate the injury.

Treatment includes relative rest and oral analgesia followed by activity modification with a physical therapy program that includes core stabilization. Local injection of anesthetic and corticosteroid can be considered in particularly painful cases or in recalcitrant cases, which the authors prefer to perform under ultrasound guidance [24].

The symphysis pubis plays a key role in energy dissipation and cushioning of impact forces during the human gait, and those forces multiply during sport causing biomechanical strain on the pubic symphysis [2]. Chronic pain at the pubis symphysis results from joint instability. This injury typically occurs in sports where high-speed cutting activity is common and is often present concurrently with an adductor strain. The disorder can also be seen in pregnancy, with widening of the pelvic joints occurring to allow passage of the infant through the pelvis during delivery [25].

The differential diagnosis of pubic symphysis pain includes osteitis pubis, inguinal hernia, athletic pubalgia, and pubic ramus stress fracture.

Athletes may complain of suprapubic pain that is worsened with walking, climbing stairs, turning in bed, getting up from a chair, or lifting. They may report suprapubic pain radiating to the groin or to the sacroiliac region and pain with urination.

The physical examination includes evaluation of the position of the pubic tubercles by palpating their borders to assess right-to-left variation in the frontal plane. Pubic symphysis dysfunction is present if the pubic bones are not level and tension of the two inguinal ligaments is asymmetric. Pain is also evoked by a lateral compression test. Rarely, a palpable groove at the level of the symphysis is detected. Conventional plain radiographs of the pelvis are often helpful in assessing pathologic widening of the symphysis. Flamingo view radiographs may aid in making the diagnosis and should be considered along with conventional plain radiographs. MRI will demonstrate soft tissue injuries and osseous edema and is the imaging study of choice [26].

Treatment i s traditionally conservatively with rest, oral analgesia, and pelvic support and compression. A graded exercise program including pelvic stabilization should be initiated as the patient tolerates. Symphyseal injections have also been shown to relieve pain. Referral for surgical intervention is appropriate if there is failure to improve with these conservative measures.

Osteitis pubis is a painful condition, generally caused by overuse in athletics , which affects the pubic symphysis and surrounding tendinous attachments. More recently, experts have differentiated osteitis pubis into three clinical entities specified as “pubic bone stress injury,” “symphysis pubis stress injury,” and “traumatic osteitis pubis.” [27] Osteitis pubis is commonly reported in sports requiring cutting, twisting, pivoting, excessive side-to-side motion, or multidirectional motions with frequent acceleration and deceleration [28]. For these reasons, osteitis pubis is common in athletics, and it is also common in pregnant and postpartum women, after urologic and gynecologic procedures, and in degenerative and rheumatologic conditions [29]. Athletes with reduced total hip range of motion, reduced hip abduction and adduction strength, and reduced trunk control may be at increased risk for the development of osteitis pubis [30].

The differential diagnosis of osteitis pubis includes pubic ramus stress fracture, pubic symphysis dysfunction, inguinal hernias, athletic pubalgia, proximal adductor pathology, and osteomyelitis.

Athletes describe a gradual onset of pain in the pubic region, which may radiate to the hip, groin, abdomen, proximal medial thigh, testes, and scrotum. The pain is often described as sharp, stabbing, or even burning. Athletes may report worsened pain with striding, pivoting, twisting, climbing stairs, kicking, sit-ups, leg raises, or Valsalva maneuvers. Athletes may also describe an audible or palpable clicking sensation at the symphysis [28].

Physical examination often reveals tenderness over the pubic symphysis and adductor origins of the inferior pubic ramus. Pain may be exaggerated with passive hip abduction, active hip flexion, or active adduction. The lateral pelvic compression and cross-leg tests are often positive. Trendelenburg’s test is often positive indicating weak hip abductors, and in severe cases, the athlete may have an antalgic gait with partially flexed hips and knees [28].

Plain radiographs of the pelvis should be obtained. It is important to note that radiographs can lag behind clinical symptoms by as much as 4 weeks. As the disease progresses, reactive sclerosis of the adjacent pubic bones, erosion and resorption of the symphysis margins, and widening of the joint space may appear on the radiographs [28]. If instability is suspected, one-legged standing flamingo views should be performed. Instability is defined as greater than two millimeter height difference between the superior rami of the symphysis [28]. MR I of the pelvis is the most detailed study and can be used to identify acute, subacute, and chronic osteitis pubis. However, marrow edema may be seen in asymptomatic patients, so clinical correlation is necessary to make the diagnosis [1, 27].

Various treatment options for osteitis pubis have been suggested, but most programs start with rest and pharmacologic pain reduction. The goal is to reduce inflammation and remove the provocative activity by modifying training. Athletes should decrease mileage, prevent over-striding, and eliminate downhill running. Oral corticosteroids can be used if the athlete demonstrates intense pain that is limiting their ability to participate in a rehabilitative program [28]. Ultrasound or fluoroscopic guided corticosteroid injection into and around the pubic symphysis may be considered in athletes with refractory symptoms [29]. However, prior to injection, laboratory evaluation should be performed to evaluate for osteomyelitis as a possible cause [27]. A structured physical therapy program should begin when pain and inflammation are reduced. Modalities such as ultrasound and phonophoresis may assist with pain reduction. Leg length discrepancy should also be corrected if found. A graduated exercise program should be utilized with the goal of returning the athlete to a preinjury level of participation. However, patience is required, as this may take 3–6 months or longer, and time to return to play correlates well with the athlete’s experienced level of dysfunction [30]. Compression shorts may reduce pain during and after the rehabilitation program. Surgical interventions may be considered if the athlete fails to improve after a long trial of conservative interventions [29]. As some cases take longer than 9 months to improve and there is a high recurrence rate, surgery may also be considered if there is a desire for earlier return to sport or if femoroacetabular impingement coexists [31].

Stress fractures are common in athletes and military personnel . Pubic ramus stress fractures account for a small percentage of the stress fractures and are considered to be a low risk stress fracture. The etiology of pubic ramus stress fractures has not been fully elucidated, but one common thought is that it often starts with a periosteal reaction at the adductor muscle origin on the pubis as a result of the tensile forces. In general, risk factors for stress fractures include female sex, amenorrhea, smoking, poor nutrition, valgus knee alignment, and leg length discrepancy [32]. Stress fractures are usually seen in distance runners with recent increases in distance or speed as well as in military personnel who enter basic combat training with poorer indices of physical fitness [33].

The differential diagnosis includes femoral neck stress fracture, osteitis pubis, pubic symphysis dysfunction, athletic pubalgia, inguinal hernia, adductor tendinopathy, or referred pain from the genitals or pelvic organs.

Athletes complain of an insidious onset of groin pain that is exacerbated by weight bearing and relieved by rest. It may be localized to the inguinal, peroneal, or adductor regions [34]. Physical examination reveals tenderness of the inferior aspect of the pubic rim, an antalgic gait, and a positive standing sign (frank pain or inability to stand unsupported on the affected leg). Plain radiographs may not be positive for several weeks after the initial injury but are still the preferred initial study due to cost and availability [33]. If the plain radiograph is negative and a stress fracture is still suspected, then advanced imaging with MRI is indicated [32].

Treatment consists of avoiding pain-inducing activities for 4–6 weeks. The athlete should focus on non-weight-bearing activities and stretching of the adductor muscle group and hip joint capsule. This is followed by a gradual functional progression to activity. Most athletes will show a response to treatment in 3–5 months. In addition, evaluation of the athlete’s nutritional intake, estrogen status, and training program is warranted.

Femoral neck stress fractures account for approximately 10 % of stress fractures, but these injuries can be a potentially career-ending with complications that include avascular necrosis, nonunion, and varus deformity [33]. As such, the clinician needs to maintain a high index of suspicion for this injury. Femoral neck stress fractures are classified as tension or compression, with tension side fractures much more likely to become a displaced fracture, but with compression side stress injuries being more common. Like pubic ramus stress fractures, stress fracture of the femoral neck often occur in distance runners and is usually preceded by a recent change in mileage or intensity. Both intrinsic characteristics of an individual’s body and extrinsic factors can precipitate a stress injury. Risk factors include training errors, inadequate footwear, inadequate nutrition, amenorrhea, running on poor surfaces, coxa vara, and femoroacetabular impingement [32, 35, 36].

The differential diagnosis includes avascular necrosis, transient osteoporosis, hip flexor tendonitis or bursitis, hernia, osteitis pubis, and neoplasm [37].

The athlete may describe an aching in the groin, hip, thigh, or knee, which abates shortly after cessation of activity. Nocturnal pain is also common. Pain is associated with exertion and weight-bearing. The athlete often notes a progressive limitation of activity because of the pain.

On physical examination , the athlete may have a positive log roll, a positive FABER test, and the Stinchfield test will cause groin pain [24]. There may also be pain with axial compression and pain with percussion over the greater trochanter. A walking evaluation may reveal an antalgic gait or painful Trendelenburg gait. The single leg hop test will likely be positive, but many feel the hop test should not be performed in patients suspected of having a femoral neck stress fracture for fear of completing the fracture.

If a femoral neck stress fracture is suspected and physical exam findings are suggestive, then it should be considered to be present until proven otherwise. Distinct radiographic findings may not develop until weeks after the initial injury (Fig. 6.6). MRI is used to localize the injury and grade its severity [38]. Additionally, studies have found MRI for the diagnosis of femoral stress fracture to be both 100 % sensitive and specific [39, 40].

The primary goal in management of femoral neck stress fractures should be to prevent complications through early diagnosis and careful treatment. If a stress fracture is suspected, the athlete should remain non-weight-bearing on the affected leg until a full evaluation for a stress injury is completed. Return to play following a stress fracture can take as long as 4–5 months.

Tension side stress fractures , also known as distraction fractures , are more common in older patients and occur on the superolateral side of the femoral neck. These should be referred immediately to an orthopedic surgeon as the preferred treatment is surgical fixation of the fracture.

Compression side stress fractures are more common in younger patients and occur on the inferomedial side of the femoral neck. Compression side femoral neck stress fractures involving more than 50 % of the width of the femoral neck should be referred to an orthopedic surgeon for consideration of operative management. If the fracture involves less than 50 % of the width of the femoral neck, there is low risk for displacement, and it can be treated with prolonged non-weight-bearing until pain-free. Some patients require a short time on bed rest. The athlete should not bear weight until there is evidence of radiographic healing. Frequent radiographs should be performed until complete healing is documented. Supervised gradual return to activity can then occur. Recurrence of pain requires rest for 2–3 days, and then resumption of activity at the last tolerated level of activity. Progression of the fracture and other failures of nonoperative management are indications for immediate orthopedic surgical referral.

A displaced fracture is a combination of both tension and compression fractures, which results in displacement of the femoral head. This type of femoral neck stress fracture is an orthopedic emergency requiring immediate surgical reduction and internal fixation. Exact time lines for return to activity depend upon the nature of the fracture, type of fixation utilized, and surgeon’ s preference.

A trauma with high energy directed along the axis of the femur when the hip is in the extremes of its normal range of motion is required to cause a hip dislocation. Hip dislocations can be anterior, posterior, or central. Posterior dislocations account for 90 % and anterior dislocations account for much of the remainder [41, 42]. The clinician must maintain a high index of suspicion for associated injuries including fractures of the femoral neck, femoral head, and acetabulum.

When a hip dislocation occurs, the athlete is immediately disabled and complains of extreme pain. Attempts to move the hip will increase discomfort. Posteriorly dislocated hips are characteristically held in adduction, internal rotation, and slight flexion. The femoral head may be palpable posteriorly.

A hip trauma series of plain radiographs should be obtained in the emergency room . CT scans are not routinely obtained prior to reduction because of the need for rapid treatment but are usually obtained after the reduction.

Hip dislocations are orthopedic emergencies . Attempts at reduction should not be performed on the playing field. However, it is critical to perform an on-field neurovascular examination, because sciatic nerve injury is observed in 10–14 % of patients with posterior dislocations. The athlete should be immobilized and transported to the emergency room for definitive evaluation and treatment [42, 43]. Prompt reduction using proper technique is important in decreasing the incidence of avascular necrosis of the femoral head, sciatic nerve injury, degenerative joint disease, and chondrolysis. The blood supply to the femoral head reaches a minimum level after 24 h after injury, and reduction after 24 h has been shown to cause an increase in osteonecrosis and post-traumatic arthritis. A reduction within 6 h enhances early recovery of the vascularity to the femoral head [44].

Avascular necrosis of the femoral head (AVN) is a cause of pain and loss of function. The pathophysiology of this disease is poorly understood, but it involves thrombus formation in the microvasculature of the bone followed by endothelial cell dysfunction and a disruption of normal angiogenesis [45]. There are both traumatic and atraumatic causes of AVN. Traumatic causes include displaced fractures of the femoral neck and hip dislocation. Atraumatic causes are not as well defined but include systemic corticosteroid use and heavy alcohol intake [46]. The majority of cases of AVN will be diagnosed in persons between the ages of 30 and 60 years and will be males [47].

The differential diagnosis includes osteoarthritis, iliopsoas bursitis, femoroacetabular impingement, and femoroacetabular labral tears.

Athletes usually present with nonspecific groin or hip pain that is worse with weight-bearing and nonspecific hip motion. Pain at rest and night pain also occur. On physical examination, hip range of motion and gait are usually normal except in advanced disease. Plain radiographs of both hips are essential in making the diagnosis. Osteopenia or a mottled appearance with patchy areas of sclerosis and lucency of the femoral head are the earliest radiographic findings but may not be present until 3 months after the inciting injury. As the disease progresses, there is collapse of the involved segment and degenerative change. If AVN is suspected and radiographs are normal, MRI can be used to make the diagnosis and to stage severity. The use of gadolinium increases the likelihood of detection early in the course of the disease.

Management depends on the stage of the disease and should be coordinated with an orthopedic surgeon. Goals of treatment include pain control and improved function. Bone marrow transplants have shown promise in the treatment of AVN [48], but core decompression a nd arthroplasty are the mainstays of treatment .

Osteoarthritis of the hip is the end stage of many different disorders and the prevalence is on the rise as the population ages. It is the main cause of anterior hip pain in patients over 50 years of age [49]. Patients will complain of hip and groin pain with weight bearing that is relieved by rest. Plain films are helpful in confirming the diagnosis and will show joint degeneration. The disease process is irreversible and the mainstays of treatment are analgesia and surgery. For a more complete discussion of osteoarthritis, see Chap. 14.