Disorders of the Groin and Hip: Lateral and Posterior

Introduction

Lateral and posterior hip pain may be due to variety of intra- and extraarticular conditions. Ultrasound is a useful image modality for rapid assessment of extraarticular soft tissue abnormalities, many of which are tendon or muscle related. Certain specific soft tissue mass lesions occur around the lateral aspect of the hip, and may or may not be associated with pain.

Common conditions include:

• greater trochanteric pain syndrome

• iliotibial band (ITB) snapping

• lateral hip masses

• tensor fasciae latae (TFL) tendinopathy and hypertrophy

• hamstring tendinopathy

• sciatic nerve compression and piriformis syndrome.

Greater Trochanter Pain Syndrome

Abductor tendon abnormalities are a common cause of the so-called greater trochanter pain syndrome:

• abductor tendinopathy

• abductor tendon tears

• gluteal bursitis

• abductor calcific tendonitis.

Patients present with a dull, aching pain over the lateral and posterior aspect of the greater trochanter, often with focal tenderness on palpation. Pain usually occurs while walking or lying on the affected side. However, in the majority of patients there is no limitation of movement. Pain is mostly unilateral, but sometimes bilateral. Middle aged and elderly women are commonly affected, where a wider pelvis is thought to be a contributory factor. Symptoms are often accredited to trochanteric bursitis, but it is more frequently due to gluteus medius and minimus tendinopathy associated with subgluteus medius and minimus bursitis. The aetiology of abductor tendinopathy is unknown, but it is thought that microtrauma causes tendon degeneration and tearing at the tendon insertion.

Tendon insertion abnormalities are readily amenable to sonographic evaluation. Anisotropy may be encountered on longitudinal scanning due to the oblique course of gluteus medius tendon fibres, which may mimic a tear or tendinopathy.

Tendon thickening and diffuse hypoechogenicity are the hallmarks of gluteal tendinopathy. The anterior fibres of gluteus medius are most commonly involved ( Fig. 19.1 ), and may extend into the gluteus minimus tendon. Isolated involvement of gluteus minimus is not common. Subgluteus minimus and medius bursitis may coexist, seen as fluid-filled structures deep to the associated tendon with gluteal tendinopathy ( Fig. 19.2 ). Bony irregularity of the greater trochanter due to entheseal bone formation is frequently encountered but does not correlate with disease severity. Increased tendon vascularity on Doppler imaging representing neovascularization is less common than in other tendon groups. End stage tendinopathy may result in abductor tendon tears.

Partial thickness tears usually involve the deep and anterior fibres of the gluteus medius tendon. Partial tears appear as areas of tendon thinning or anechoic defects in the tendon substance.

Key Point

A ‘bald facet’ and absence of tendon fibres are consistent with a full-hickness tear ( Fig. 19.3 ).

In an acute full-thickness tear the tendon is retracted with haematoma and effusion adjacent to the greater trochanter. In chronic complete tears, muscle wasting may be evident with loss of muscle bulk and increased echogenicity due to fatty replacement. Ultrasound diagnosis of partial and complete gluteal tendon tears has a sensitivity of 90% and a specificity of 95% compared against surgery as a gold standard.

The trochanteric bursa, or subgluteus maximus bursa, is a crescenteric low-echo structure that lies lateral and superficial to the gluteus medius insertion, adjacent to the posterior facet of greater trochanter, and deep to the gluteus maximus muscle. Trochanteric bursitis is thought to be the result of an impingement phenomenon and may be present in up to 40% of patients with gluteus medius and minimus tendinopathy ( Fig. 19.4 ). If the hip abductors are weakened by tendinopathy, lateral subluxation of femoral head occurs, leading to impingement of the soft tissues between the greater trochanter and the iliotibial tract and development of bursitis. Therefore, trochanteric bursitis may be a sequela of hip joint instability, and hence the association with tendinopathy. Bursitis is commonest in the fifth and sixth decades but may be encountered in other age groups. Other less common causes of trochanteric bursitis are rheumatoid arthritis, tuberculosis and other systemic inflammatory conditions.

Calcification in the gluteal tendons has been reported in 10–40% of cases of gluteal tendinopathy. This can be linear or in the form of multiple small foci near the tendon insertion, and is often a result of degenerative tendinopathy. However, larger deposits of calcific tendinopathy may occur in hydroxyapatite deposition disease. The calcification appears as areas of increased echogenicity, which may or may not cast an acoustic shadow dependent on size and status of the calcification ( Fig. 19.5 ). Spontaneous resorption of the calcific deposits may occur. Calcific tendinosis may be associated with trochanteric bursitis.

Ultrasound-guided injection can be performed to treat greater trochanter pain ( Fig. 19.4 ). Peritendinous ultrasound-guided steroid and local anaesthetic injection is an effective method for the treatment of gluteal tendinopathy. In the study by Labrosse et al., there was a 55% average reduction of pain level after treatment. One month after treatment, 72% of the patients showed a clinically significant improvement in pain level, which was defined as a reduction in the visual analogue scale pain score of 30%. The long-term prognosis varies according to the evolution of the tendinopathy, the amount of functional use or overuse of the involved hip and treatments undertaken to improve the strength and range of motion of the hip. In trochanteric bursitis, a posterolateral approach is adopted for the accurate delivery of steroid and local anaesthetic into the bursa. In cases of calcific tendinosis of gluteal tendons, calcification may be aspirated and injected under ultrasound guidance. An anterolateral approach is preferred for injecting the subgluteus medius and minimus bursae to avoid transgressing the tendon.

ITB Snapping

Clinically, iliotibial snapping hip is similar to iliopsoas snapping but symptoms are present on the lateral aspect of the hip joint. Some patients may be completely pain-free. The snapping is due to intermittent impingement of the posterior border of ITB or anterior border of the gluteus maximus over the greater trochanter ( Fig. 19.6 ). Ultrasound may show thickening and low-reflective change within the ITB. Dynamic scanning demonstrates the sudden displacement of ITB over the greater trochanter associated with palpable snapping.

It may also be seen when an adducted and internally rotated hip is flexed and externally rotated with flexed knee. Patients will usually be able to voluntarily produce the snapping sensation, but sometimes only in standing position, which necessitates scanning in the erect position. ITB snapping is treated conservatively with nonsteroidal anti­inflammatory medicines, rest and physiotherapy. However, cases refractory to this treatment can be treated with ultrasound-guided steroid and local anaesthetic injection around the ITB.