Lateral Hip Pain: Mechanisms and Management

 

This article was published in In Touch magazine, a resource exclusive to members of Musculoskeletal Physiotherapy Australia, a National Group of the Australian Physiotherapy Association. For more information on the exercise apparatus pictured in this article, Physiotec's TWS Slider, click here

This article was published in In Touch magazine,
a resource exclusive to members of
Musculoskeletal Physiotherapy Australia,
a National Group of the Australian Physiotherapy Association.

For more information on the exercise apparatus pictured in this article,
Physiotec’s TWS Slider, click here

History and prevalence

Lateral hip pain (LHP) has traditionally been referred to as trochanteric bursitis. More recent evidence has demonstrated that bursal distension is an inconsistent feature of lateral hip pain (Connell et al. 2003—15%; Bird et al. 2001—8%). Furthermore, histological studies of the bursa in such cases have found no signs of acute or chronic inflammation (silva et al. 2008). radiological and surgical studies have now shown that bursal distension is almost always a secondary finding associated with a primary pathology of gluteus medius or minimus tendinopathy (Bird et al. 2001, Cvitanic et al. 2002, Connell et al. 2003, dwek et al. 2005, Kingzett-taylor 1999, Kong et al. 2007, Pfirrmann et al. 2005, Woodley et al. 2008).

Prevalence studies suggest that degenerative tears of the gluteus medius or minimus tendons occur in 20% of patients with osteoarthritis of the hip (Howell et al. 2001). Prevalence of tendinopathy that has not yet progressed to a tear is therefore likely to be much higher. Gluteus medius tendinopathy (GMt) also occurs in 20–35% of patients with low back pain (Collee et al. 1991, tortolani et al. 2002). due to the pseudoradicular referral pattern from the greater trochanter down the lateral thigh, it is often misdiagnosed as lumbar pathology. this may lead to years of inappropriate and ineffective treatment, including laminectomy (tortolani et al. 2002). GMt is much more common in females than males, with a ratio of 3–4:1, peaking in the perimenopausal period. However, this condition may also occur in young athletes, particularly runners or those involved in step training.

Mechanisms

While aetiological mechanisms for tendinopathy continue to be explored, compression is thought to be a key factor in the development of insertional tendinopathies (Cook & Purdam 2009; almekinders et al, 2003). Consideration of this mechanism in exercise prescription has been shown to be integral to positive program outcomes in insertional achilles tendinopathy (Jonsson et al. 2008). similarly, identification and control of compressive mechanisms in normal daily life, and in exercise prescription, are central to optimal short and long-term outcomes for the management of GMt.

Compression of the insertions of the gluteus medius and minimus tendons into the lateral and anterior facets of the greater trochanter occurs beneath the iliotibial band (itB). any increases in tension in the itB will increase compressive loading. tightness and overactivity of muscles of the superficial lateral stability system—tFL, upper gluteus maximus, and vastus lateralis—will directly impact on this tension, and therefore tendon compression. those who stand and sit in abduction, which is more common in males, may develop functional tightness over time. the use of saddle chairs tends to promote excessive static abduction and subsequent soft tissue tightness of the lateral structures. this will be particularly so for those working in seated occupations over many years.

On rising from static abduction, the hips will be brought into relatively more adduction for dynamic function, resulting in significant increases in compressive loading of the gluteus medius and minimus tendons.
Birnbaum et al. (2004) demonstrated that rapid increases in compressive loading occur

Beneath the ITB at the level of the greater trochanter as the hip is moved into adduction. While in neutral hip adduction, the ITB exerts only four newtons (N) of pressure over the greater trochanter. this has risen to 36N by 10 degrees adduction and continues to rise to 106n by 40 degrees adduction. if the lateral structures are tighter than normal, these loads are likely to be reached even more rapidly. it is more common, however, that those suffering from LHP have normal or even excessive length in the lateral soft tissues. in this situation it is the frequency and degree of functional adduction that has the most important role to play in aetiological mechanisms.

Increases in functional adduction, and therefore compression, appear to be linked to poor postural and movement habits. standing ‘hanging on one hip’ in hip adduction is a common postural habit as it requires less energy to hang passively on the itB. sitting with the legs crossed in adduction, and sleeping in sidelying with the uppermost hip positioned in flexion/adduction will also add significantly to time spent in a position of compression. it is also known that prolonged positioning of a muscle in a lengthened position results in structural change by which there is a shift in the optimal position of function to the new, lengthened position (Goldspink 1977, Kendall & McCreary 1983, Williams & Goldspink 1978). subsequent to this shift in the length–tension relationship, dynamic function such as walking and stairclimbing will also occur in relatively greater degrees of hip adduction. Furthermore, functioning in hip adduction will favour greater recruitment of the superficial over the deeper members of the hip abductor synergy (Kumagai et al. 1997), adding to compressive loading of the deepest and most commonly affected portions of the trochanteric tendons.

fig1Other factors that may impact on degree of functional adduction include leg length differences, pelvic obliquity such as that associated with scoliosis, hip flexor dysfunction resulting in midline or cross-midline striking (foot placement in a position of greater hip adduction), inadequate distal shock absorption at foot strike, and training errors such as running on the camber of a road, the camber of the beach, or the same direction around a track. Bony factors may also contribute to pathoaetiological mechanisms due to impacts on the relative association between the greater trochanter and the itB. For example, femoral offset will affect prominence of the greater trochanter, while genu valgum, and femoral anteversion will affect orientation of the itB. other factors such as abdominal girth, systemic disease, and hormonal profile may also play a role, but they are beyond the scope of this short report.

There are little other than anecdotal descriptions of physical therapy approaches for lateral hip pain in the literature. treatments that have been mentioned for trochanteric bursitis or ‘greater trochanteric pain syndrome’ have been ice, ultrasound for the anti-inflammatory effects and stretching of the itB, which involves placing the hip frequently and often forcefully into end-range hip adduction. With current knowledge of the pathoanatomy and proposed pathomechanics of the situation, there is little sound rationale for this approach. the contemporary approach to management of GMt is based on a clearer under•standing of mechanisms and contributing factors. education, tendon decompression strategies and therapeutic exercises aimed at reducing excessive functional hip adduction are the core elements of contemporary management. the identification and management of predisposing factors is extremely important for the long-term control of symptoms.

Education on the condition, its mechanisms, and the natural time course of tendon recovery can empower the patient and reduce fear and catastrophisation. Better understanding will also improve compliance with decompression and exercise programs, and reduce frustration associated with unrealistic expectations of time to full recovery.

Tendon decompression strategies aim to minimise the amount of compressive loading that may occur over a 24-hour period. this is the key to early symptom control. increasing awareness of negative postural habits and controlling them are critical. Positions to avoid include standing hanging on one hip in adduction, sitting with legs crossed, or sitting with the feet wide and knees together, which is a common female trait. due to the connection of the fascia lata into the gluteal and thoracodorsal fascia, sitting in more than 90-degree hip flexion for prolonged periods can also be a problem. sitting in low lounges and car seats, which generally slope backwards, often results in ‘start up’ pain on rising to stand. avoiding low chairs and using a wedge cushion to bring the hips higher than the knees can be very beneficial.

Night time is the other major issue, as it represents a significant portion of the 24-hour period. eight hours of either lying on the symptomatic side (direct compression against bed), or lying with the symptomatic hip in flexion/ adduction will significantly add to the cumulative compressive load. Patients may be most painful at night, particularly lying on their side, or when initiating a rolling manoeuvre, similar to the sit-to•stand ‘start up’ pain. sleeping in supine with a pillow under the knees to offload the hips and lumbar spine minimises compressive loading. Many patients, however, find it difficult to sleep in this position. to reduce compression for the side-sleeper, an appropriate recommendation would be to add an eggshell mattress overlay to the bed, and sleep with a pillow, or pillows, between the knees and ankles that preferably approximates a horizontal position of the uppermost lower limb.

For the patient who has tightness and overactivity of the superficial soft tissues, stretching, while a common strategy, will only aggravate the situation due to the associated compressive loading. Massage, self-trigger point releases, acupuncture, dry needling and heat will all be more appropriate. But this should never be an isolated management approach. Long-term positive outcomes will only be achieved by addressing poor postural and movement habits, and active correction of muscle dysfunction.

Therapeutic exercise should be directed towards techniques that aim to recruit the muscles of the abductor synergy in a way in which:

  • there is adequate recruitment of the deep abductors, gluteus minimus and the deep fibres of gluteus medius;
  • there is consistency with the natural function of these muscles; and
  • compressive loading is minimised by avoidance of repetitive or loaded hip adduction.

Real-time ultrasound presents the best opportunity in a clinical situation to assess and retrain the deeper hip abductors. once appropriate recruitment strategies have been elicited, graduated strengthening should occur wherever possible in a weightbearing environment. sidelying ‘clams’ (abduction/ external rotation to adduction/ internal rotation) and sidelying leg lifts are often provocative due to repetitive compressive loading on return to adducted start positions. these exercises should therefore be avoided.

Furthermore, open chain exercise is unlikely to replicate closely enough the natural proprioceptive stimulus and balanced abductor activation of weightbearing function. sliding platforms (e.g. Pilates reformers) that allow resisted abduction in standing provide both a low compression exercise alternative and a situation more consistent with natural functioning in these antigravity muscles. Further bias for the deeper abductors can also be achieved via targeted inner range abductor strengthening on these sliding platforms. the primary focus during other functional weightbearing tasks such as single leg stance, lunges and step work should be on minimising hip adduction, which may require hand support (stick, back of chair, wall) in the early phases. Higher level exercises should be progressed as appropriate for the patient’s needs. a graduated return to activity should also be instituted to avoid rapid changes in tendon loading which may be provocative.

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