This case study highlights the influence that abnormal joint positioning and altered postural states have on musculoskeletal pathology. It describes a goal-kicking rugby player suffering from a recalcitrant internal snapping hip. The associated pathology with this particular problem is clearly evident. However, what is initially missed is the aberrant musculoskeletal cause.
As therapists we often encounter patients who show up with clear postural abnormalities, but it is sometimes harder to work out the relationship between cause and effect. It is the proverbial chicken v egg argument: is the postural muscle change a result of the offending pathology or is it causing the pathological insult?
In this instance the outcome justified the philosophical approach which advocates treating an abnormal musculoskeletal issue when the therapist encounters it, whether or not you believe it is the cause of the problem, or simply an effect.
A 24 year old left-footed rugby player presented to the clinic, referred from an independent sports physician after two months of failed treatment for an internal snapping left hip.
The patient recalled that before he had been to see the sports physician his hip had being giving him pain for two months, with an associated ‘snapping’ sensation when performing hip rotation drills as part of his individual goal-kicking sessions. He had at the time also been undergoing a lot of speed and agility training involving hurdling and rotational movements over hurdles.
He continued to train with this discomfort for a number of weeks but it gradually worsened until he could no longer perform the warmup drills necessary for his goalkicking sessions – although running and sprinting were painless. At this point he sought medical treatment.
His sports physician says that on initial physical examination, his client demonstrated a palpable ‘snapping’ sensation in the hip as it was brought from a flexion-abductionexternal rotation (FABER) position to extension-adduction-internal rotation (EADDIR). Initial X-rays proved unremarkable. The doctor referred the patient on for an MRI to exclude labral injuries to the hip and loose bodies. The findings from the MRI were as follows:
The sports doctor initially prescribed a course of oral non-steroidal anti-inflammatories, with cessation of hip rotation drills in warm-up. The player was referred to a physiotherapist for psoas lengthening and strengthening exercises. The pain quickly settled and three weeks later he recommenced hip rotation drills. The pain and snapping recurred almost immediately.
The sports doctor was again consulted and recommended an ultrasound-guided local anaesthetic and hydrocortisone injection. The iliopectineal bursa and iliopsoas tendon sheath were injected, with immediate relief of pain but with continued snapping of the hip. For the next three weeks the athlete excluded hip rotation exercises from his warm-up with continued treatment to the psoas muscle. During this time the hip was pain-free and the snapping had almost completely resolved.
He recommenced rotation drills three weeks after injection, which initially was pain-free. However, within two weeks the snapping and pain had returned. That’s when the frustrated player was referred to the clinic for evaluation of mechanical faults that might be predisposing him to internal snapping hip syndrome.
After a thorough discussion of the history of the problem, we undertook a physical evaluation. The most striking initial feature of the player’s posture in standing was an externally rotated left lower limb. This was present both in neutral stance and walking. He was able to squat pain-free and kick pain-free. Of real interest was the fact that he had changed his squat technique three months previous to the onset of symptoms.
He was finding it more comfortable to squat heavy with a wider and more externally rotated stance. It is commonly known in strengthtraining circles that this technique places more load on the external rotators of the hip, in particular the piriformis.
In supine the left lower limb continued to demonstrate an externally rotated position. The pelvis also demonstrated a posterior rotation of the left ilium with restricted antero-posterior glide of the ilium on the left, indicating a blocked left sacroiliac joint (SIJ).
Left hip flexion-abduction-external rotation to extension-adductioninternal rotation reproduced the internal painful snapping. Hip quadrant (combined forced flexion/ adduction/internal rotation) also reproduced internal hip pain. Muscle length testing proved unremarkable (including psoas muscle) except for the left piriformis. This was more evident in prone when the hips were internally rotated whilst in neutral. On palpation the piriformis demonstrated increased tone and a ‘thickened and woody’ feel.
We agreed with the initial sports doctor’s diagnosis of internal snapping hip with inflamed iliopectineal bursa and psoas tendon sheath. However, it was felt that the offending mechanical cause was the piriformis.
It was hypothesised that the tight hypertonic piriformis was causing the femoral head to assume a more anterior translated and externally rotated position, similar to how a hypertonic infraspinatus can cause an anteriorly translated humeral head in the shoulder. We believed that this was causing the iliopsoas tendon to be more disposed to friction and movement across the femoral head as the hip went from FABER to EADDIR. With the anterior femoral head position, the tendon was always going to suffer from friction and a snapping sensation as it moved over the femoral head. Direct medical intervention in the form of cortisone injection would resolve inflammation in the tendon and bursa, but the irritation would tend to recur once the rotational movement was reintroduced.
Initial treatment was directed at myofascial therapy to the left piriformis muscle. This consisted of direct ischaemic pressure type therapy (direct pressure which is held) and pressure with combined passive hip internal rotation as a myofascial release technique. Remarkably the patient’s internal snapping with FABER to EADDIR completely resolved within the first treatment session, as did the painful quadrant.
Obviously encouraged by the sudden improvement, the patient was warned that it was likely the piriformis would ‘re-tone’ in the next few days and cause problems again. Progression with this sort of treatment can result in a ‘two steps forward, one step back’ improvement. It is important to avoid the offending movements such as hip rotation and externally rotated squat positions.
Treatment continued thus for the next two sessions (all within seven days). We also felt that the thickened anterior capsule evident on the MRI would cause problems with the position of the femoral head, so we started antero-posterior glides of the femoral head to improve hip joint mobility. This was performed in prone lying with the hip in a neutral position. A seat belt was placed around the upper thigh and a posterior directed force was applied to induce posterior translation. This was done both as a mobilisation oscillation and as a sustained stretch.
The patient was treated for the next month, with squatting and hip rotation movements re-introduced. He was shown self management techniques for the piriformis and hip joint capsule. He was completely pain-free within a month and suffered no exacerbations of the pain or internal clicking.