Differential diagnosis for trochanteric bursitis?

Trochanteric bursitis is a decently common PT script diagnosis, but I’ve been caught unsure of how to proceed in the absence of cardinal signs of bursitis (redness, warmth, swelling) or with unsuccessful local cortisone injection. Now that I have treated a few patients with this diagnosis, I have noticed that "trochanteric bursitis" can often be the default descriptor for the broader diagnosis of Greater Trochanteric Pain Syndrome. Structures that can contribute to this pain syndrome include the trochanteric bursa, subgluteus medius busa, subgluteus minimus bursa, proximal IT band, and glueus medius and minimus tendons. Because PT treatment may vary depending on the source of pain, further testing can help allow more targeted intervention.

In my residency program this week, I learned a special test that I hadn’t seen before in school/practice called The Gluteal Derotation Test. The PT places the patient into supine with test hip flexed to 90 deg and externally rotated to end-range. From here, the patient activates the gluteus medius and minimus muscles by internally rotating the hip back to neutral against PT resistance. A positive test will reproduce lateral hip pain (Sensitivity 88%, Specificity 97%). Following a negative test, examiners in the study then repeated the test in prone with the hip extended, which was only evaluated as an adjunct to the initial positioning (rather than a stand-alone test) but which did increase sensitivity to 94%. The likely advantage this test holds over resisted testing is the standardization of testing position. Additionally, the test begins in a traditional position of symptom provocation for greater trochanteric pain syndrome: the glut med and min are on stretch, and the compressive forces of the ITB also increase with hip flexion.

Diagnostic accuracy may improve with corroboration using the single leg stand test during which a patient with greater trochanteric pain syndrome will likely have reproduction of lateral hip pain if instructed to stand on one foot for 30 seconds. The duration of time balancing does not affect interpretation of this test (Sensitivity 100%, Specificity 97.3%).

These different potential sources of nociception are grouped into one pain syndrome because of the close relationship of structures in the lateral hip area, and the the above tests have not been assessed regarding the differentiation between a tendinopathy versus bursitis alone. Rather, the addition of these standardized tests to our arsenal may help us identify pain patterns which can help shape treatment.

Besides pain provocation, in the above tests we may gain valuable information by paying attention to the timing of pain in relation to the position of the hip/pelvis. For example, it is worth noting that in the starting position of the gluteal derotation test, maximal hip ER, compresses the region and is likely not much more sensitive than manual pressure to the lateral hip. I wonder if it would be more clinically useful to resist IR in different ranges of hip ER to determine if pain is more related to compression of the area or related to contraction of the tendon. Then again, the pre-stretched test position may be selected to bias the muscles of interest or avoid compensatory muscles masking the symptoms. I have been meaning to do a deeper dive into the differential assessment of hip rotators, so this gives more more motivation to revisit those questions.

When a patient reports pain during the single-leg stand test, we may be able to assess if the pain is more related to the duration of glut med activation, or if the pain report is more consistent with visual pelvic drop creating compression in the lateral hip region. Interestingly, in the study I reviewed for these tests, most of the subjects had partial tendon tears identified on MRI however testers claim that they did not observe trendelenburg signs (frontal plane pelvic drop) in the subjects during the single-leg stand test. While this was not a primary outcome measure, but rather a quick note in the write-up, the main take-away is that partially torn gluteal tendons are often still capable of maintaining pelvic stability in single-leg stance for 30 sec. On the other hand, (as we see in the clinic) plenty of intact tendons lack the motor control for frontal plane stability. Observation for a trendelenburg sign, trendelenburg gait, or compensated trendelenburg posture can help us identify modifiable risk factors to address in PT sessions.

As physical therapists, we have an awesome advantage in that we are working with patients consistently over time, and we may be able to take note of and interpret these patterns during their sessions so as to better treat our patients!

I learned something new today, so just thought I’d share!

Dr. Mary Kate Halligan, PT, DPT

Lequesne M, Mathieu P, Vuillemin‐Bodaghi V, Bard H, Djian P. Gluteal tendinopathy in refractory greater trochanter pain syndrome: diagnostic value of two clinical tests. Arthritis Care & Research. 2008 Feb 15;59(2):241-246.

Bird PA, Oakley SP, Shnier R, Kirkham BW. Prospective evaluation of magnetic resonance imaging and physical examination findings in patients with greater trochanteric pain syndrome. Arthritis Rheum. 2001; 44: 2138–2145.

Grimaldi A, Mellor R, Hodges P, Bennell K, Wajswelner H, Vicenzino B. Gluteal Tendinopathy: A Review of Mechanisms, Assessment and Management. Sports Med. 2015;45(8):1107-1119.