I was flattered Glenn Ruscoe took the time to read my blog and kindly responded:
DAMNIT! That was my favorite line of the whole blog! Seriously?? And while I thought to myself, ‘now THAT sounds good’… I was taken aback by Glenn’s comment. How IS that different? He challenged me to expand on that statement and so here it goes.
Who are we?
According to Wikipedia, Physical therapy (PT), also known as physiotherapy, is a physical medicine and rehabilitation specialty that, by using mechanical force and movements, remediates impairments and promotes mobility, function, and quality of life through examination, diagnosis, prognosis, and physical intervention. It is performed by physical therapists (known as physiotherapists in many countries).
Nothing in the definition says anything about EDUCATING, ADVISING, REASSURING, FOSTERING SELF-EFFICACY. Our profession is one of “doing”. And as said before, the “doing” part varies from therapist to therapist. Compare to a dentist– If you have a cavity, your treatment will likely be a filling and will be consistent from dentist to dentist. If you have anterior knee pain, your treatment provided by a physical therapist will include or by limited to ___________ (fill in your favorite “tool”).
We are defined by what we DO.
The definition of insanity is: doing the same thing over and over and expecting a different result. Am I implying we are all insane? Yes. Read on.
So, WHO are we?
Our degrees have advanced from certifications to doctorates. How much of our education has advanced? A lot, I presume. We expect to have more credibility, autonomy, and HECK, more pay (which is total bullshit, right?) because we have ‘higher’ degrees, yet, our profession, by definition, is not a whole lot different than it was from its inception. We are not applying our knowledge base. We are a far cry from our potential, yet we are our own road block.
We are still a profession that carries out a treatment plan from someone else. And those various treatments are vastly different and some even total crap. Even worse, our explanations for someone’s complaints are different. But we all received the same education, right? I don’t look at what the referrals say, diagnosis, or even surgical protocols. It is my responsibility, if to be viewed as a professional, to know exactly what the procedure entails. If not, I discuss with the surgeon. By that, I don’t mean ask for the protocol. You can watch any surgical procedure (Arthrex website is a good source) and figure out what needs to be protected and apply healing times. Armed with that knowledge we can talk shop about how hard it is to pull out anchors, and other fun stuff. Trust me, they haven’t thought about any of the questions you might have.
In all fairness, I do work at a POPTS (go ahead! Come at me!) and have easy access to physicians. My referral sources know me very well. I am treated as an equal colleague. I know this because often times a patient comes to me and says “Dr. Baker wants to get your opinion on me. He said you’d figure it out.” THAT is going to a physical therapist. I strongly believe, we should all work for these relationships and not expect them because we are now Doctors of Physical Therapy. If you want the respect, you have to earn it. Apply your knowledge and critical reasoning!
The challenge: don’t be insane. You are the expert. Promote yourself to your patients and your non-therapist colleagues. Take the focus off the “doing” and act like an autonomous professional. Therapeutic alliance. Simplify an explanation. Reassurance. Pass the baton to the patient. Self-efficacy. It’s up to them now.
Every Christmas eve, my Sweden-born grandmother would prepare an authentic Scandinavian dinner, complete with a variety of meticulously made cookies that only a grandmother could bake. It was a tradition that my entire family eagerly awaited each year. Although I didn’t care for some of the items on the menu—pickled herring on rye cracker hors devores–and others I did not even try until I was much older—kaldomar, for one, if a single item was changed, or heaven forbid omitted, there would be a general discourse from the entire familj.
Traditions are not only events that occur within families. Traditions can be habits, belief systems, religious practices, and even standard practices in medicine. Traditions can be accepted as ‘the way’ or rejected as ‘the highway’. Which ‘way’ you go depends on your own biases, boredom or even resistance to change— how many times have you heard “that is how we have always done it”?
Assuming you, the reader, follow Twitter. One frequently occurring topic Is the identity crisis within physical therapy. Who are we and what is it we do? Impossible to define, because we all “do” different things… and bicker about it endlessly! “Physio Will Eat Itself”, a tongue in cheek reponse by Roger Kerry @rogerkerry1 to another good read by Dave Nicholls entitled “Should we give up physiotherapy?” If you haven’t read them, do it now!
Identity is not our biggest problem. What about resistance to change?
A recent RCT on total hip replacements and a systematic review on total knee replacements both conclude “we” are not necessary for a good outcome. Unless this is your entire caseload, keep calm and move on. If it is your caseload, you can keep calm and move on too. Traditionally, we have seen many of these cases. And many of us would agree we helped them. For those of us that have been around a long time, remember when there was no Medicare Cap, no pre-authorization, and endless amounts of insurance funds available to us at our disposal. When Medicare added a cap, we all gasped with despair—“how can we get this poor person better after such a major surgery on only $1800? Damn you, Medicare!” But really, it ended up not being a big deal. We adjusted. And now, we might not even be necessary beyond setting patients up with a good home program.
In our desperation to find our place, we are MAKING ourselves needed. Whether it be offering an outrageous explanation for someone’s assumed dysfunction—“well, Mr. Jones… it seems that your foot pain is caused by a facilitated segment at L5 and a manipulation to this joint will restore your gluteus medius’ ability to control your pelvis. Because it can’t control your pelvis, you laterally lean and force your uncompensated rearfoot varus into a zone it can’t go and– voila!–your foot hurts!”—or even the trending “tool” of the year, often proprietary to a physical therapist that believes in blowing up balloons, cups, needles, scraping, taping, and more, all the while making a shit ton of money.
We might even claim that we are BETTER than surgery. We are BETTER than opioids. We should be CHOSEN first! Not only does it somewhat demonize surgery and frankly, the hand that feeds us, it makes sense that we would be obvious choice when compared to something that most people don’t want. It’s like saying– “yes! I prefer the broccoli over dog food”. You get the picture.
Traditions need change.
My grandmother sadly passed away in 2001, shortly after I received my degree in physical therapy. My mom tried her best to keep the Christmas eve dinner alive, but it was just not the same. The single most important ingredient was no longer there—my grandmother. And so it was, we made new traditions, and as painful as it was, we moved on. While some may embrace this as a fresh start, many prefer to continue to do things as once was because doing otherwise defies the boundaries of their comfort zone. And perhaps, much of their money and time, even most of their career, was spent doing things the way they have always been done. Waiting for that return on a very large investment.
Our profession is scared to death of simplicity– we are smarter than that, aren’t we? While budgets are tighter and people are busier, it makes much better sense to offer simple, sound advice, even reassurance. Also offering an alternative—you CAN do nothing!—is accepted by patients. OMG! Did she really say that?
Why are we here?
It IS the advice we give. Simple to us? Yes. To others? Maybe not. Unless you under-load your patients, and give them shitty advice, like “don’t do that anymore” or “rest” or “sit up straight!” in addition to the extensive 45 page home program with 3 sets of 10 exercises that they will never do anyway, you are still needed! Much can be accomplished and not replaced, in the first and sometimes only encounter. Tendinopathy is a perfect example. This person is not likely to improve in the 2x/week, 4 week referral session. Manage their load, give 1-2 exercises, and follow up for a recheck in 1 month. Teach them how to take care of themselves.
We should spend less time “doing” and more time “educating” if we want people to say “I am going to a physical therapist” rather than “I am going to physical therapy”. Got it? If you don’t, read here. This is the change needed in our profession’s traditions. I have no problems with this. In fact, I find it much more satisfying to foster self-efficacy than anything else.
My mom continues to make fattigmann every year. I hate to admit it—never cared for fattigmann (mom, if you are reading this… sorry!). I always went for the Swedish Heirloom cookies, or even the krumkake. There was also a toffee-like cookie that was amazing. But, I am always willing to try a new cookie. I might even stop eating cookies all together.
Achilles rupture is one of the most common tendon injuries despite being the thickest tendon, affecting more men than women, during middle age. The common site for rupture is 2 to 6 cm from its insertion on the calcaneus, where the cross sectional area is the smallest.4 Unfortunately, most patients with an Achilles tendon rupture seldom achieve full function at 2 years after surgery; and, only minor improvements occur after the first year. Further, in a study of professional football players, 32% of players never returned to football following an Achilles tendon rupture.11 Of those who did return, there was an average reduction of 50% in performance level. In the NBA, 39% of athletes with Achilles rupture did not return to professional levels.16 While surgical techniques and rehabilitation protocols have not reached a consensus, we are understanding variables that can affect outcomes:
Early Weight bearing
Achilles tendon forces of approximately 1500 N have been recorded during walking in healthy subjects.3 C0mmon repairs can fail at forces from only 45 to 250 N. Strongest techniques are the “3-bundle” (453 N) and “augmented 4-strand Krackow” (323 N).4 Following Achilles repair, a period of immobilization and non-weight bearing precedes weight bearing in a walking boot, usually with heel lifts. Achilles tendon forces of 370 N have been estimated for healthy subjects walking with the ankle immobilized in neutral.2 The addition of a 1-in heel lift decreased the estimated force to 191 N.4 Therefore, immobilization and heel lifts are vital components during the early post-operative period.
In a meta-analysis, Brumann6 concluded that immediate FWB leads to significant higher patient satisfaction, earlier ambulation and returns to pre-injury activity including time to return to work and sports, with no evidence for increased re-rupture rate or tendon lengthening. Carvalho7 also reported better outcomes in regards to time to return to sports/work, return to normal range of motion, heel-raise ability, rates of re-rupture, major complications and minor complications when patients received early range of motion exercises and weight bearing.
Animal studies have demonstrated that early loading rehabilitation could improve tendon characteristics through the maturation and orientation of collagen fibers, synthesis of type III collagen, heightened activity of fibroblasts, as well as decreased muscle atrophy.8
Most commonly, with an open repair, the first 2 weeks are non-weight bearing with the foot splinted into equinus followed by 2 weeks 40% weight bearing with a dorsal blocking splint, custom made at 20 degrees plantar flexion. The next 4 weeks are in a walking boot, full weight bearing.
Avoid over lengthening
It is imperative that dorsiflexion ROM is controlled and closely monitored following Achilles tendon repair. Increased stress on the repair can result in loss of tendon stiffness and over-lengthening. Typically, stretching is not advised in the early weeks of rehabilitation. In my experience, after about 2-4 weeks of ambulating without the boot (8-10 weeks post-surgery for our repairs), DF normalizes to the contralateral side without stretching, provided the patient attempts to ambulate with normal gait. This is consistent with authors suggesting to wait until 12 weeks to stretch at all.1
Kangas et al9 found that elongation increased up to 6 weeks in both early motion and casted groups of patients, but the rise was somewhat steeper in the cast group. After 6 weeks, the AT preserved its length or even shortened a little in the early motion group between 24-60 weeks.
In my clinical practice, our repairs are knotless, augmented with a suture bridge. This allows FWB with heel lifts once the sutures are removed around 10 days post-operative. The lifts are made from orthopedic felt and vary in size depending on patient’s comfort. Ruptures that have retracted are typically tighter, and usually require more of a lift. Lifts are gradually removed until discontinued at 4 weeks from surgery.
Over-lengthened tendons adversely affect end range plantar flexion strength. Described by Mullanay et al1, over-lengthened tendon leads to greater muscle shortening during muscle contraction. With the ankle in plantar flexion, the muscle is already in a shortened position and below the angle for optimal force production. Based on the length-tension relationship, further muscle shortening due to tendon lengthening would decrease force production.
Early motion and loading
Early motion does not appear to affect re rupture rate when allowed free plantar flexion with restriction of dorsiflexion to 0 degrees no later than 3 weeks.6Once the post-operative dressing and/or splint is removed, allowing frequent active plantar flexion encourages tendon gliding and may reduce adhesions/scarring, reduce calf atrophy, and reduce edema.8 Interestingly, the same benefits are not apparent from range of motion exercises alone.7 In other words, beneficial early rehabilitation requires weight bearing.
Return of strength does not happen by daily activities alone. The patient must be encouraged to load the tendon in the form of sitting then standing heel raises, double to single, of both concentric and eccentric most days of the week. This does not mean 3 sets of 15 reps forever. Body weight alone will not be sufficient to restore pre-injury strength. In fact, during running, the peak muscle force on the Achilles tendon is 6.4x body weight.10 At some point, the patient should do heel raises on a leg press or with weighted vest, holding dumbbells, using barbell, etc. In my opinion, this is the most fun yet challenging part of the achilles repair rehabilitation. Loading progressions will be very patient specific and should be monitored closely to ensure the patient is progressing.
I heavily encourage a pool program beginning post operative week 4. Patients start in chest deep water (weeks 4-6) and progress to waist deep (6+). Activities include multi directional walking, walk/jog progression, heel raises (at week 5) and finally jumping/bounding (weeks 8+ in deep water). I do notice better outcomes in those that do an aquatic program in addition to clinical rehabilitation.
Compensations can occur following Achilles tendon repair. Weakness of the plantar flexors limits the ability to stabilize the rearfoot and likely results in greater demand on the posterior tibialis muscle.12 Increased demand on the knee extensor mechanism of the involved lower extremity may place this individual at greater risk for overuse injuries, such as patellofemoral pain syndrome or patellar tendinopathy.13 It is very important to address the entire kinetic chain as well as the non-affected side.
Considering changes in running biomechanics following Achilles repair that has healed in a lengthened position is also important. A case report by Silbernagel, Willy & Davis13 demonstrated peak rearfoot eversion and abduction during running was increased and plantar flexion and eversion moment and power generation are reduced compared to the non-affected side. Further, power absorption and power generation are increased at the knee of the involved side.
End Range Strength
A common weakness I’ve noted clinically in patients with previous Achilles repair, is poor end range strength. Weakness in end range plantar flexion can adversely affect the ability to jump, land, and sprint. Mullanay et al1 found significant plantarflexion weakness evident on the involved side at 20° and 10° of plantar flexion and concluded this was due to anatomical lengthening, increased tendon compliance, or insufficient rehabilitation.
I’ve found that working on end range strength is best accomplished using an adjustable decline board. Some of my patients have made their own. Once able to sustain an isometric at end range, toe walking is a great functional exercise that allows the patient to monitor improvements towards symmetry.
Plyometric training is essential to improve the load tolerance and power of the myotendinous unit. Is also improves tendon stiffness and elastic energy storage and recoil.15 Jumps should not be applied half hazard. Application should consider progressive loading; for example, beginning with two feet and progressing to one foot. Volume (number of jumps) and intensity (depth, height, speed) should also be carefully progressed so that loading is gradual. See the table below from Cuoco17 for a general plyometric guideline. Plyometric programs should allow 72 hours between sessions due to collagen response to heavy loading.14
Patient in clinic
Increase number contacts before intensity; 10-20% increases
Primarily low, increase to medium during mid-workout when not fatigued
Attempt high when not fatigued
Primarily medium and high
As early as 10 weeks, I allow patients to use a small trampoline and perform heel raise rebounders and light plyos. Around 12 weeks, beginning plyos can be performed on the ground if the patient is able to perform 5 single-limb heel raises. Of note, only 50% of patients are reported to be able to perform a single limb heel raise at 12 months post surgery18 so it is very important to follow a criterion based guideline. Plyometrics can also be performed in the pool. I typically allow 2 foot jumps in chest high water as early as 8 weeks. If the patient isn’t already doing an aquatic program and is having difficulty improving strength, now is the time to encourage use of the pool!
Achilles repair rehabilitation is one of the most fun and challenging diagnoses. A fundamental understanding of healing times, loading progressions, common problems such as over-lengthening and end range weakness is important to offer the patient the most robust program.
This post is not intended to replace current surgical protocols. Please follow your surgeon’s recommendations.
Mullaney M, McHugh M, Tyler T, et al. Weakness in end range plantar flexion after Achilles tendon repair. Am J Sports Med. 2006;34(7):1120-1125.
Akizuki KH, Gartman EJ, Nisonson B, Ben-Avi S, McHugh MP. The relative stress on the Achilles tendon during ambulation in an ankle immobilizer: implications for rehabilitation after Achilles tendon repair. Br J Sports Med. 2001;35:329-333.
Finni T, Komi PV, Lukkariniemi J. Achilles tendon loading during walking: application of a novel optic fiber technique. Eur J Appl Physiol. 1998;77:289-291.
Maquirrian, J. Achilles Tendon Rupture: Avoiding Tendon Lengthening during Surgical Repair and Rehabilitation. Yale J Biol Med. 2011 Sep; 84(3): 289–300.
Olsson N, Nilsson-Helander K, Karlsson J, Eriksson BI, Thomée R, Faxén E. et al. Major functional deficits persists 2 years after acute Achilles tendon rupture.Knee Surg Sports Traumatol Arthrosc.2011;19(8):1385–1393
Brumann M, Baumbach S, Mutschler W, Polzer H. Accelerated rehabilitation following Achilles tendon repair after acute rupture- development of an evidence-based treatment protocol. 2014;45(11): 1782-1790.
Carvalho F, Kamper S. Effects of early rehabilitation following operative repair of Achilles tendon rupture (PEDro synthesis). Br J Sports Med2016;50:829-830
Huang J, Weng C, Ma X,et al. Rehabilitation regimen after surgical treatment of acute achilles tendon ruptures. Am J Sports Med 2015;43:1008–16.
Kangas J, Pajala A, Ohtonen P, Leppilahti Achilles tendon lengthening after rupture repair: a randomized comparison of 2 post operative regimens. Am J Sports Med 2007;35(1):59-64.
Lenhart R, Thelen D, Wille C, Chumanov E, Heiderscheit B. Increasing running step rate reduces patellofemoral joint forces. Med Sci Sports Exerc. 2014;46(3):557-564.
Parekh SG, Wray WH, 3rd, Brimmo O, Sennett BJ, Wapner KL. Epidemiology and outcomes of Achilles tendon ruptures in the National Football League. Foot Ankle Spec. 2009; 2: 283– 286
Flemister AS, Neville CG, Houck J. The relationship between ankle, hindfoot, and forefoot position and posterior tibial muscle excursion. Foot Ankle Int. 2007; 28: 448– 455
Silbernagel K, Willy R & Davis I. Preinjury and post injury analysis with measurements of strength and tendon length in a patient with a surgically repaired Achilles rupture. J Ortho Sports Phys Ther. 2012;42(6): 521-529.
Langberg H, Skovgaard D, Petersen LJ, Bülow J, Kjaer M. Type I collagen synthesis and degradation in peritendinous tissue after exercise determined by microdialysis in humans. J Physiol. 1999; 521 pt 1: 299– 306.
Foure A, Nordez A, Cornu C. Plyometric training effects on Achilles tendon stiffness and dissipative properties. J Applied Phys. 2010;109(3): 849-854.
Amin N, Old A, Tabb L et al. Performance outcomes after repair of complete achilles tendon ruptures in national basketball association players. Amer J Sports Med. 2013;41(8):1864-1868.
Cuoco A. Principles of Strength and Conditioning. Sports Certified Specialist Exam Preparatory Course. Chapter 13.
Olsson N, Karlsson J, et al. Abilitytoperformasingleheel-riseissignificantlyrelatedto patient-reportedoutcomeafterAchillestendonrupture. Scand JMedSciSports2014:24:152–158.
Iliopsoas tendinopathy, iliopsoas bursitis, coxa saltans (“Internal Snapping Hip”) and iliopsoas impingement (IPI) are collectively described as iliopsoas syndrome because of the likelihood they coexist and the difficulty of discriminating one from another. Iliopsoas syndrome is also very difficult to discern from femoroacetabular impingment (FAI) and acetabular labral tears (ALT), and is a frequent complication post hip arthroscopy.
Pain presents insidiously in the anterior hip, though has been reported to occur in the ipsilateral lower back.2 Pain can be reproduced with running up hill, resisted hip flexion in the supine position, lifting the leg in and out of the car and in the forward plank position as the affected limb stabilizes. If the patient has “snapping hip”, this can be self-reproduced by having the patient move their hip from a flexed, abducted and externally rotated position to extension, adduction and internal rotation. Iliopsoas impingement can be reproduced with FADIR (Flexion, Adduction, Internal Rotation) testing, though this can also implicate intra-articular problems. Tenderness at the anterior hip and iliopsoas is likely found; however, this is very non-specific and not always present.
Anatomy of the Iliopsoas
The psoas muscle originates from the 12th thoracic and all five lumbar vertebrae. The iliacus muscle originates from the iliac crest and the inner table of the ilium. The two merge to form the iliopsoas muscle, which has a musculotendinous insertion on the lesser trochanter, although some muscle fibers of the iliacus attach directly on the lesser trochanter and proximal femur.3 The iliocapsularis, is found adjacent and lateral to the iliopsoas, originating from the inferior facet of the AIIS and the anteromedial hip joint capsule to insert 1.5cm distal to the lesser trochanter.4
The iliopsoas tendon directly overlies the anterior capsulolabral complex at the 3:00 o’clock position.5 Most acetabular labral tears occur in the 1:00 to 2:00 position which corresponds to the area of impingement in FAI when the hip is in flexion, adduction, and internal rotation. Domb et al6 believe the iliopsoas contributes to the pathogenesis of focal labral tears at the 3:00 position.
There has been much debate surrounding the primary function of the iliopsoas. The iliacus and psoas muscles are proposed to contribute to stability of the lumbar spine, pelvis and hip joint16 as well as contribute to stability of the femoral head in the acetabulum through the muscle belly and tendon of the iliopsoas muscle as it crosses the anterior hip joint.14 The iliopsoas complex likely has individual and task specific activations depending on the demand.16
In a passive kinetic experiment using cadavers, Yoshio et al8 concluded the psoas major functioned more as a stabilizer of the femoral head and erector of the trunk at smaller (0–45deg) hip flexion angles whereas its function as a hip flexor was only evident at 45-60 degrees.
During running, Lenhart et al1 found the iliopsoas functions to eccentrically control the hip in extension during terminal stance and concentrically to advance the hip forward in the initial swing phase.1 The psoas major has also been found to have a larger cross sectional area in a kicking limb compared to the contralateral leg in footballers15, indicating its function as a hip flexor. The iliacus has been found to stabilize the hip and pelvis in the stance limb while the contralateral limb extends.16
There is conflicting evidence in regards to the postural role of the iliacus and psoas.16 In contrast to other studies, Andersson et al.16 found no activity of the iliacus or psoas in normal standing; however, psoas activity is higher when sitting up straight versus in a forward flexed position.16 The psoas also assists in stabilizing the lumbar spine in the frontal plane when a heavy load is applied to the contralateral side.16
The psoas has been found to be hypertrophied Australian Rules footballers with low back pain and atrophied in non-athletes.15 An explanation is needed, but is postulated that athletes continue to train, while non-athletes are more likely to experience disuse atrophy or pain inhibition.15 My clinical observation is that hip flexors often compensate for weak trunk flexors, especially in athletes with lower back pain.
Snapping hip occurs in 5-10% of the population but is estimated to be more prevalent in the athletic population, to include dancers, runners, weightlifters and soccer players.9 It is important to note that snapping alone is not pathologic. A small femoral neck angle (coxa vara) or developmental dysplasia, may also contribute to snapping hip.9
Snapping occurs when the iliopsoas either “snaps” over the anterior aspect of the femoral head and associated joint capsule or the iliopectineal eminence as the tendon moves medial to lateral during hip extension.9 In contrast, a dynamic sonography study suggests that the snap is caused by movement of the iliacus muscle itself and not that of the iliopsoas tendon across bony structures.11 Deslandes et al observed abnormal movement of the iliacus muscle between the pubic bone and the iliopsoas tendon resulting in snapping of the tendon against the bone, when compared to the non-snapping hip.
Diagnosis of “Snapping Hip” is made with physical exam, anesthetic injection to the iliopsoas bursa, and dynamic sonography. Static images with ultrasound can reveal tendon thickening, an enlarged bursa, and peri-tendinous fluid collections.17 Snapping hip can lead to both iliopsoas impingement and iliopsoas tendinopathy.
The average age for IPI is 25-35 years old and over 80% of the patients participate in sports.6 Possible contributing factors to IPI are tightness of the iliopsoas in extension, scarring of the iliopsoas leading to traction injuries of the labrum as a result of chronic internal “snapping hip”, or hypertrophy of the iliopsoas or iliocapsularis tendon. Anatomical features which may create a predilection to IPI include abnormal angulation of the tendon, a large femoral head, or high femoral anteversion.6
Iliopsoas Impingement can also occur in patients following total hip arthroplasty with an incidence as high as 4.3%.7 The impingement occurs at the anterior rim and can be caused by an acetabular component that is too large, or malpositioned acetabular component, usually in a retroverted position. These patients often fail conservative management and require iliopsoas tenotomy or revision of the acetabular component.7
Overuse tendon injury occurs in tendons of the upper and lower extremities and results in pain and decreased exercise tolerance. Specific changes occur in tendon structure, resulting in a tendon that is less capable of sustaining repeated tensile load.13 Iliopsoas tendinopathy can occur as a result of Snapping Hip or IPI, as well as in isolation. Great research in the etiology and management of tendinopathy has emerged in the last few years. Cook & Purdam13 describe 3 phases of tendinopathy as a continuum: 1) Reactive Tendinopathy, 2) Tendon Dysrepair and 3) Degenerative Tendinopathy. To keep this blog simple, I will refer readers to this paper, as it is a worthwhile read.
Iliopsoas Tendinopathy Post Hip arthroscopy
One common complication following hip arthroscopy is iliopsoas tendinopathy. In my clinical experience, this usually occurs around the 6th post-operative week when activity increases, though it can occur earlier or later. In my opinion, I believe that the iliopsoas is inhibited in the early days following surgery due to its close proximity to the capsulotomy, labral repair, and femoroplasty. The rectus femoris, a synergist to the iliopsoas, compensates as a hip flexor, which is why it is typically very hypertonic following surgery.
I suspect one of two reasons for developing iliopsoas tendon pain post hip arthroscopy: 1)disuse atrophy and inhibition: the iliopsoas is not ready for the increased demand when the patient is allowed to do closed chain exercises and more walking, around 6 weeks post-operatively. 2) Chronically weak, inflamed, prior to surgery, especially in patients with a history of snapping hip.
Early iliopsoas isometrics after post-operative week 3 may assist in tissue adaptation. It is important to gradually load the tissues to facilitate adaptations to new demands.
Though issues involving the iliopsoas are collectively termed Iliopsoas Syndrome, the treatment is not a homogenous approach. Careful attention to the potential cause is vital for success in conservative management. Between 36% and 67% of patients diagnosed with snapping hip had reduction or resolution of symptoms with conservative measures.9 Patients with Iliopsoas Impingement due to structural abnormalities, as in malpositioned acetabular components of a total hip, may need iliopsoas tenotomy.7
Intra-articular injections may differentiate intra-articular problems from extra-articular issues involving the iliopsoas; however, this may not always be the case because of the close proximity and communication between the labrum, hip capsule and iliopsoas. Direct injections to the iliopsoas bursa or tendon can provide temporary relief, but does not offer long term solutions.10
In my opinion, irritated iliopsoas tendons respond well to gradual tendon loading programs as described by Malliaras, Cook, Purdam, & Rio.12
Stage 1 Isometric Loading
Goal: reduce pain, if having more than minimal pain during isotonic exercises
Isometric Performed at 70 degrees of hip flexion supine
45 second holds at 70% MVC, 5 repetitions with 2 minute rest between sets, up to 3x/day
Select Resistance that can be held for 45 seconds without shaking, Progress as Tolerated
Should Have Decrease in Pain Following
Stage 2 Isotonic Loading
Perform when only minimal pain (3/10) with isotonics
Pre Exercises: supine marching against wall with neutral pelvis, single to bilateral or mountain climbers (shown below). Patient should demonstrate ability to flex hip without compensation through the spine (ie flexion and posterior pelvic tilt).
Perform the below exercises: 3 to 4 sets of 15RM, progressing to 6RM, every other day; fatiguing load
Continue Stage 1 isometrics on off day
Psoas Marching Concentric
2. Reverse Psoas Marching Eccentric
In addition to load management of the iliopsoas, gluteal and core strengthening to create balance and control of the lumbopelvic complex is helpful. Chronically overloaded tendons are usually a combination of improper training, weakness of the iliopsoas or nearby muscles, and lack of rest/recovery. All of these factors should be addressed.
Mobility versus Stability… are the hip flexors tight?
The age old question. The first question to ask, is if the “tight” hip flexors make sense for the person. For example, a ballet dancer or gymnast who complains of chronically tight hip flexors, who clearly is very flexible, needs a thorough evaluation. More than likely, the hip flexors are in a protective mode of guarding due to instability of the hip or lumbar spine. Stretching will only make this scenario worse. In contrast, a person, who is grossly stiff, could simply have a true length problem, or stiffness in the hip joint.
The Thomas Test is a standard test to assess flexibility of the hip flexors. One way to determine if the hip flexor “tightness” is true length issue versus protective guarding, is to modify the position of the knee or hip to see if this allows the thigh to drop to the table. If the thigh reaches the table when the knee is straight or if the hip is adducted or abducted, it may indicate tight TFL, rectus femoris, or both. This should be compared to FABER testing (which also assess hip joint mobility and tissue extensibility) as well as prone passive hip extension ROM. A consistent loss of hip extension in various positions could be joint stiffness or a flexibility problem. In contrast, if you can improve the “length” by have the patient assist with their core (see below), the “tightness” is likely driven by poor core stability.
If the patient has poor core stability, assessment of a curl up or rolling patterns is useful to determine movement strategies.18 In the first set of pictures, she is unable to curl up without drawing in her hips, a compensation for trunk flexors. With core assist (2nd picture) to give her a bit of help into flexion, she can complete without excessive use of hip flexors. Similarly, assessing rolling (2nd set of pictures) to each side can give an idea of her coordination and muscle sequencing. Using PNF techniques with rolling patterns is effective to facilitate muscle sequencing and timing. This approach is beyond the scope of this blog. For further reading read this!
Iliopsoas Syndrome is a complex and often frustrating condition to address, particularly following hip arthroscopy. Proper management include a thorough evaluation and understanding of driving mechanisms, choice of interventions that properly load the tissues, education regarding tissue adaptation, and an understanding of the interaction between the spine, pelvis and hip joints. There is minimal research on conservative management, particularly physical therapy beyond passive modalities and stretching. The application of recent tendon research to iliopsoas syndrome is promising.
Lenhart R, Thelen D, Heiderscheit B. Hip loads during running at various step rates. J Orthop Sports Phys Ther 2014;44:766-774
Laible C, Swanson D, Garofolo G, et al. Iliopsoas syndrome in dancers. Orthop J Sports Med 2013;1:1-6
Blomberg JR, Zellner BS, Keene JS. Cross-sectional analysis of iliopsoas muscle-tendon units at the sites of arthroscopic tenotomies: an anatomic study. Am J Sports Med 2011; 39: 58S–63S
Philippon MJ, Michalski MP, Campbell KJ et al. An anatomical study of the acetabulum with clinical applications to hip arthroscopy. J Bone Joint Surg Am 2014; 96: 1673–82
Alpert JM, Kozanek M, Li G et al. Cross-sectional analysis of the iliopsoas tendon and its relationship to the acetabular labrum: an anatomic study. Am J Sports Med 2009; 37: 1594–8
Domb BG, Shindle MK, McArthur B, Voos J et al. Iliopsoas impingement: a newly identified cause of labral pathology the hip. HSSJ 2011;7: 145-150
Dora C., Houweling M, Koch P, Sierra R. Iliopsoas impingement after hip arthroscopy: results of non-operative management, tenotomy, or acetabular revision. J Bone Joint Surg [Br] 2007; 89-B(8):1031-1038
Yoshio M, Murakami G, Sato T et al. The function of the psoas major muscle: passive kinetics and morphological studies using donated cadavers. J Orthop Sci 2002; 7: 199–207
Lewis C. Extra-articular snapping hip: a literature review. Sports Health. 2010;2(3):186-190.
Deslandes M, Guillin R, Cardinal E, Hobden R, Bureau NJ. The snapping iliopsoas tendon: new mechanisms using dynamic sonography. AJR Am J Roentgenol. 2008;190(3):576-581.
Malliaras P, Cook J , Purdam C, Rio E. Patellar tendinopathy: clinical diagnosis, load management, and advice for challenging case presentations. J Ortho Sports Phys Ther. 2015;45(11):887-897
Cook J, Purdam C. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. Br J Sports Med. 2009;43: 406-416.
Lewis C, Sahrmann S, Moran D. Effect of position and alteration in synergist muscle force contribution on hip forces when performing hip strengthening exercises. Clinical Biomechanics. 2009;24:35-42.
Stewart S, Stanton W, Wilson S, Hides J. Consistency in size and asymmetry of the psoas major muscle among elite footballers. Br J Sports Med. 2010;44:1173-1177.
Andersson E, Oddsson L, Grundstrom H, Thorstensson A. The role of the psoas and iliacus muscle for stability and movement of the lumbar spine, pelvis and hip. Scand J Med Sci. 1995;5:10-16.
Falnum M, Keene J, Blankenbaker D, DeSmet A. Arthroscopic treatment of the painful internal snapping hip: results of a new endoscopic technique and imaging protocol. Am J Sports Med. 2007;35(5):770-779
Hoogenboom B, Voight M, Cook G, Gill M. Using rolling to develop neuromuscular control and coordination of the core and extremities. N Am J Sports Phys Ther. 2009;4(2):70-82.
Chronic Exertional Compartment Syndrome (CECS) is a cause of lower leg pain in young athletes, runners, and military recruits. It is extremely under recognized, with a 22-month delay in diagnosis1, even though it is responsible for 27% of anterior pain in the lower leg.2 CECS affects men and women equally. CECS occurs when there is increased intracompartmental pressure within one or more fascial spaces during exercise. Muscles can increase their volume up to 20% during exercise which can increase pressure within the compartment. This can be problematic if the fascia is unusually thick.11 There is no definitive answer as to why this causes pain.1 Some believe the increase in pressure causes ischemia, though there are no studies to support this theory.1 Other theories attribute pain to stimulation of sensory or intramuscular pressure fibers in the fascia from excessive stretch.2 Additional studies found evidence of low capillary supply in muscle6 and dysfunctional venous outflow10 in CECS.
The lower leg contains 4 compartments:
Anterior: contains tibialis anterior, long toe extensors, and deep peroneal nerve.
Lateral: contains peroneus longus and brevis, and superficial peroneal nerve.
Superficial Posterior: contains the gastrocnemius, soleus, plantaris and sural nerve.
Deep Posterior: contains the posterior tibialis, long toe flexors, peroneal artery, and tibial nerve.
As a physical therapist, CECS, should always be part of differential diagnosis when an athlete presents with lower leg pain. In my experience, CECS is often self-diagnosed as “shin splints” and I’ve seen CECS in long distance competitive and recreational runners, sprinters, dancers, skiers, soccer and basketball players. The patient’s history is extremely important. Athletes will usually describe their symptoms as heavy, “like feet stuck in cement”, aching, tight, pressure, burning, and/or numbness. In my clinical experience, many do not complain of numbness, and if they do, is typically superficial peroneal distribution from the lateral compartment. Symptoms seem to occur at the same time or distance during activity and often times the athlete is unable to continue their activity. After a brief period of rest, symptoms completely resolve. CECS occurs bilaterally 95% of the time.9 The anterior and lateral compartments of the leg are affected 95% of the time.3
A clinical exam is often benign, unless the athlete is asked to perform the activity, usually running, until they reproduce their complaints. Muscle herniation through defects in fascia can be palpated in 40–60% of patients with CECS. The herniated muscle is normally palpated over the anterior tibia. Fascial defects often occur at the sight of the peroneal nerve’s exit from the lateral compartment.1 There should not be a loss of arterial pulses, as CECS does not usually involve arteries. If decreased pulse is noted, one should rule out claudication, or popliteal artery entrapment syndrome (PAES). A doppler study is needed to confirm a vascular origin.
Other differential diagnoses include medial tibial stress syndrome (MTSS), stress fractures and peripheral nerve entrapment. Stress fractures and MTSS are fairly focal and the tenderness is on posteromedial tibia, rather than muscle. Tinnel’s at the site of entrapment of the peripheral nerve may reproduce symptoms. Numbness and weakness are not always present. Most common lower leg nerve entrapments involve the common peroneal, superficial peroneal, and saphenous nerves.8
If an athlete has reproduced their symptoms in the clinic with running, it may be possible to determine which compartments are involved. The compartment(s) will be very firm and may be tender. Numbness and weakness, if present, may also reveal the involved compartment(s):
Anterior Compartment: dorsiflexion weakness and numbness in 1st web space
Lateral Compartment: ankle eversion weakness and numbness dorsum of foot
Superficial Posterior Compartment: plantar flexion weakness and numbness along lateral foot
Deep Posterior Compartment: toe flexor and invertor weakness and numbness plantar surface of foot
If CECS is suspected, referral to a specialist is necessary to confirm the diagnosis by measuring the pressure in each compartment. Many times the resting pressure is high and exertional testing is deferred, but usually, the athlete is asked to run as part of the exam to obtain baseline and post-exertional measurements. A needle that includes a pressure scale is inserted into each compartment. A resting pressure >15 mmHg, >30 mmHg immediately post exercise and 5 min post-exercise pressures greater >20 mmHg are diagnostic of compartment syndrome.16 Both legs are typically tested, and all compartments should be tested.
Conservative management is scarce in the literature. Treatments including ice, medications, massage, orthotics, activity modification and physical therapy have been associated with inconsistent results and limited relief of symptoms.12, 13 Diebal et al14 found that altering running biomechanics in US military cadets from hindfoot to forefoot running in 10 runners improved running performance and decreased exercise induced pain after 6 weeks. Post exercise ICP also decreased from 78 mmHg to 32 mmHg and all cadets were able to avoid surgery. The underlying premise is that a forefoot running technique diminishes the increased ICP and eccentric activity of the anterior compartment while reducing ground-reaction forces.
Other methods, include a period of rest, followed by a very slow running progression, sometimes started in the pool, in addition to strengthening and soft tissue mobilization, either instrument assisted or foam rolling. I’ve had the opportunity to work with an athlete who refused surgery, and 4 months into rehab, is asymptomatic. This may be more realistic for athletes that are not necessarily endurance athletes, but have symptoms as part of conditioning for their sport, such as basketball players. The patient should be very compliant and it is very helpful to have a training staff that is on the same page so that the volume of exercise is monitored and gradually increased. Fortunately, this is the case for us.
If an athlete is unwilling to stop the aggravating activity or decrease the intensity to levels that don’t provoke symptoms, a fasciotomy is recommended. Fasciotomies can be performed with an open technique or subcutaneously. An 80% success rate is reported with anterior and lateral compartment releases and a 50% success rate with posterior compartment releases.3 Other authors report success rates from 80-90%.7 The rate of recurrent CECS is reported to be 6-11%.5
Physical therapy is usually started within the first 7-14 days to prevent post-operative scarring, improve soft tissue mobility and to gradually load muscles. Like conservative management, little research is available on ideal post-operative physical therapy protocols.
Schubert15 describes a 4 phase rehabilitation for anterior compartment release, though principles are applied to all compartments:
PHASE I: Protection and Mobility (2-3 weeks Post-operatively).
PHASE II: Light Strengthening (Begin after meeting Phase I criteria, approximately 3-4 weeks following surgery).
PHASE III: Progression of Strengthening (Begin after meeting Phase II criteria, approximately 4-6 weeks following surgery).
PHASE IV: Impact/Sport Training (Begin after meeting Phase III criteria, approximately 8-12 weeks following surgery).
A patient post bilateral 4 compartment fasciotomy, used with permission. Pictured: lateral incision on left leg access to anterior and lateral compartments; medial incision of right leg access to superficial and deep posterior compartments
Chronic Exertional Compartment Syndrome (CECS) is a common source of exercise induced leg pain in athletes and should be part of a physical therapist’s working diagnosis. History taking is of importance and the patient’s description of pain, provoking activities and behavior are usually enough to raise suspicion for CECS. More research is needed in the areas of conservative management as well as post-operative management for best outcome.
Tucker A. Chronic exertional compartment syndrome of the leg. Curr Rev Musculoskelet Med. 2010 Oct; 3(1-4): 32-37.
Blackman PG. A review of chronic exertional compartment syndrome in the lower leg. Med Sci Sports Exerc. 2000 Mar; 32(3 Suppl):S4-10.
Brennan FH Jr, Kane SF. Diagnosis, treatment options, and rehabilitation of chronic lower leg exertional compartment syndrome. Curr Sports Med Rep. 2003 Oct; 2(5):247-50.
Raikin SM, Rapuri VR, Vitanzo P. Bilateral simultaneous fasciotomy for chronic exertional compartment syndrome. Foot Ankle Int. 2005 Dec; 26(12):1007-11.
Englund J. Review Chronic compartment syndrome: tips on recognizing and treating. J Fam Pract. 2005 Nov; 54(11):955-60.
Edmundsson D, Toolanen G, Thornell . Evidence for low muscle capillary supply as a pathogenic factor in chronic compartment syndrome Scand J Med Sci Sports. 2010 Dec;20(6):805-13
George CA, Hutchinson MR. Chronic Exertional Compartment Syndrome. Clinics in Sports Medicine. 2012 Apr;31(2):307-319.
McCrory P, Bell S, Bradshaw C. Nerve entrapments of the lower leg, ankle and foot in sport. Sports Med. 2002; 32(6):371-91.
Touliopolous S., and Hershman E.B.: Lower leg pain. Diagnosis and treatment of compartment syndromes and other pain syndromes of the leg. Sports Med 1999; 27: pp. 193-204
Birtles D.B., Rayson M.P., Casey A., et al: Venous obstruction in healthy limbs: a model for chronic compartment syndrome? Med Sci Sports Exerc 2003; 25: pp. 1638-1644
Hurschler C., Vanderby R., Martinez D.A., et al: Mechanical and biochemical analyses of tibial compartment fascia in chronic compartment syndrome. Ann Biomed Eng 1994; 22: pp. 272-279
Packer J.D., Day M.S., Nguyen J.T., et al: Functional outcomes and patient satisfaction after fasciotomy for chronic external compartment syndrome. Am J Sports Med 2013; 40: pp. 430-436
Blackman P.G., Simmons L.R., and Crossley K.M.: Treatment of chronic exertional anterior compartment syndrome with massage: a pilot study. Clin J Sport Med 1998; 8: pp. 14-17
Diebal A.R., Gregory R., Alitz C., et al: Forefoot running improves pain and disability associated with chronic exertional compartment syndrome. Am J Sports Med 2012; 40: pp. 1060-1067
Schubert A.G.: Exertional compartment syndrome: review of the literature and proposed rehabilitation guidelines following surgical release. Int J Sports Phys Ther 2011; 6: pp. 126-141
Pedowitz R.A., Hargens A.R., Mubarak S.J., et al: Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am J Sports Med 1990; 18: pp. 35-40
Radiographs are used to diagnose femoroacetabular impingement (FAI) in addition to clinical exam and history. Three different views are generally used: AP Pelvis, Dunn Lateral, and False Profile. Proper interpretation is essential as it is necessary for accurate diagnosis, treatment planning, and surgical decision-making. Physical therapists do not typically have access to radiographs, let alone the training to interpret radiographs; however, understanding the report can be helpful in treatment planning and selection.
In this view, the hips and pelvis are viewed front to back. In this position the examiner can measure joint space, center edge angle, depth of acetabulum and presence of cross over sign.
Joint Space Width (JSW) is typically measured in mm from the head of the femur to the acetabulum at the superomedial hip joint. In patients with less than 2mm joint space, early conversion to total hip arthroplasty is likely.7 Joint space less than 2mm may be a contraindication to hip arthroscopy.
Lateral Center Edge Angle (LCEA) is formed by finding the center of the femoral head and drawing a line vertical and another line from the center of the femoral head and drawing a line to the lateral acetabulum. The normal range is from 25-39o. A center edge less than 20 degrees indicates hip dysplasia and above 40 degrees, over-coverage of the acetabulum.1 Mild acetabular dysplasia (LCEA <25o) has been associated with hip osteoarthritis.5
Depth of Acetabulum is normal when acetabular fossa is lateral to the ilioischial line. Protrusio acetabuli (overcoverage) occurs when femoral head is medial to the ilioischial line and coxa profunda occurs when the fossa acetabuli overlaps the ilioischial line medially.1 Protrusio acetabuli has been associated with worsening osteoarthritis among women.4
Cross Over Sign is when the anterior acetabular rim is lateral to the posterior rim, representing acetabular retroversion.1 This is important to note, because retroverted hips are likely to have less internal rotation. Further, true acetabular retroversion indicates a deficient posterior wall, while a crossover sign due to anterior overcoverage does not indicate deficient posterior wall.2
For this view, the patient is either standing or supine and the hip is flexed to either 45o or 90o and abducted to 20o with neutral rotation. The beam is directed between the anterior superior iliac spine and pubic symphysis. This view is used to identify pathology of the proximal femur.2
Alpha angle is the angle between the femoral neck axis and a line connecting the head center with the point of beginning aspheric of the head neck contour. Angles greater than 50o are abnormal and indicative of cam type deformity1, though angles less than 60o are less likely to develop hip pain.6 Alpha angles greater than 60o may be associated with the development of hip osteoarthritis4, and greater than 83o are considered pathological cam deformities especially in the presence of reduced internal rotation (<20o) of the hip.6
Head Neck Offset Ratio is determined by three lines: (1) a line through the center of the long axis of the femoral neck, (2) a line parallel to line 1 through the most anterior aspect of the femoral neck, and (3) a line parallel to line 2 through the most anterior aspect of the femoral head. The head-neck offset ratio is calculated by measuring the distance between lines 2 and 3, and dividing by the diameter of the femoral head. If the ratio is <0.17, a cam deformity is likely present.2
This view is obtained with the patient standing with the pelvis rotated to 65o. Anatomy of the acetabulum and joint space is appreciated with this view.2 This view provides a second view to assess OA or dysplasia from AP Pelvis.
Harris-Hayes M. Relationship of acetabular dysplasia and femoroacetabular impingement to osteo arthritis: a focused review. Phys Med and Rehab. 2011 ;3(11):1055-1067.
Head Neck Offset Image from:
Clohisy J et al. A systematic approach to the plain radiographic evaluation of the young adult. J Bone Joint Surg Am. 2008;90:47-66.
Llopis E et al. Anatomic and radiographic evaluation of the hip. Euro J Radiol. 2012;81:3727-3736.
Clohisy J et al. A systematic approach to the plain radiographic evaluation of the young adult. J Bone Joint Surg Am. 2008;90:47-66.
Harris-Hayes M. Relationship of acetabular dysplasia and femoroacetabular impingement to osteo arthritis: a focused review. Phys Med and Rehab. 2011 ;3(11):1055-1067.
Nelson AE et al. Measure of hip morphology are related to development of worsening radiographic hip osteoarthritis over 6 to 13 year follow up: the Johnston county osteoarthritis project. Osteoarthritis Cartilage. 2016; 24(3):443-450.
Agricola R et al. Pincer deformity does not lead to osteoarthritis of the hip whereas acetabular dysplasia does: acetabular coverage and development of osteoarthritis in a nationwide prospective cohort study (CHECK). Osteoarthritis Cartilage. 2013;21:1514-1521.
Agricola R et al. Cam impingement causes osteoarthritis of the hip: a nationwide prospective cohort study (CHECK). Ann Rheum Dis. 2013;72:918-923.
Philippon MJ et al. Hip arthroscopy for femoroacetabular impingement in patients aged 50 or older. Arthroscopy. 2012; 28(1):59-65.
Microinstability of the hip is a recently recognized source of hip pain in young patients and athletes. The etiology of hip microinstability includes bony abnormalities, residual laxity after traumatic dislocation, connective tissue disorders resulting in ligamentous laxity, repetitive microtrauma associated with athletic activities, iatrogenic injuries to the hip capsule and idiopathic.1 The pathomechanism begins with repetitive joint forces that include repetitive hip external rotation on an axially loaded limb in sports including golf, baseball, gymnastics, ballet, figure skating, football, soccer, tennis and martial arts in the presence of subtle anatomical abnormalities or inherent ligamentous laxity.2 It is important to note laxity and microinstability are not the same thing. Microinstability of the hip describes symptoms occurring in the presence of laxity.4
Because of the anterior orientation of both the acetabulum and the femoral head, the femoral head has the least bony constraint anteriorly and relies instead on the labrum, joint capsule, and ligaments for stability.5 The iliofemoral ligament (Y Ligament) makes up most of the anterior capsule and prevents anterior translation of the femoral head in extension and also limits external rotation.2 Ligamentum teres, recently described as the ACL of the hip, is thought to resist joint subluxation forces and when torn, can lead to microinstability.4 Interestingly, the ligamentum teres has been found to be thickened in people with developmental hip dysplasia, indicating an adaptation to resist hip dislocation.4 It has also reported to have a secondary role as a stabilizer to external rotation in a labral deficient hip.6 This ligament is often found partially or completely torn in individuals undergoing hip arthroscopy.
Repetitive joint forces, as described above, stress the anterior soft tissues, including the anterior labrum and capsuloligamentous complex as the femoral head is forced anteriorly. Anterior joint translation continues to increase, as the passive restraints can no longer tolerate the load, leading to tears of the anterior labrum and capsular ligament stretching. The result is symptomatic hip microinstability.1 These athletes may already have subclinical levels of laxity of their soft tissues which allows for extremes in hip range of motion needed for their sport, most notably in gymnastics and ballet.1 Once passive restraints are compromised, athletes rely on their dynamic stabilizers, such as the iliopsoas or tensor fascia latae, to provide hip stability. The psoas crosses the hip joint and can be subjected to very high loads in athletes. Consequently, these patients may present with hip flexor tendinitis, ITB syndrome or Coxa Saltans (Snapping Hip).4 These athletes may also complain of hip flexor or ITB “tightness”, though these muscles are more likely to be hypertonic than shortened.
There is no definitive diagnostic test, imaging or physical exam finding used to diagnose microinstability of the hip.1 Suspicion is raised with a patient’s history. Patients typically complain of hip pain, apprehension, or giving way episodes during specific activities or movements. Patients may also complain of mechanical symptoms, such as clicking, catching, popping, and snapping.2 It is not unusual that an athlete complains of “impingement” in the anterior hip, such as pain with deep hip flexion or stiffness after sitting, even in the absence of cam or pincer deformities typical of femoroacetabular impingement (FAI); however, microinstability can also occur in the presence of FAI, particularly of Cam type.
Assessment of global laxity can be assessed using Beighton Scoring.3 Excessive internal and external rotation (>60 degrees in either direction) and Dial Test may indicate increased hip joint laxity. The Dial Test is performed to assess capsular laxity. The examiner internally rotates the limb on a supine patient and releases, noting the spring back to external rotation. The test is positive If the spring back is greater than 45 degrees from the vertical axis. The Log Roll Test may indicate insufficiency of the iliofemoral ligament, especially if asymmetric. While supine, the examiner notes asymmetry in resting external rotation of the limb. Mechanical symptoms or pain is noted with rolling the limb into external and internal rotation. Patients with synovitis will not tolerate this test.
There are three tests typically utilized to assess a patient’s apprehension. To test anterior apprehension, the patient lies at end of bed with hip off of the exam table. The examiner extends hip and leg past neutral and the hip is externally rotated. Abduction-Extension-External Rotation Test also tests anterior instability. The patient is placed in the lateral decubitus position with the affected side up, abducted to 30° and externally rotated. An anteriorly directed pressure is placed on the posterior greater trochanter and the leg is slowly extended from 10° of flexion to full extension with a positive test reproducing the patient’s symptoms. To test posterior apprehension, the examiner flexes, adducts and internally rotates the hip and knee and applies force posteriorly through the femur. This is the same test as the Stoddard Test used for sacroiliac joint pain provocation, so careful interpretation of results is needed.
Labral testing is done by reproducing symptoms with the hip in 90 degrees of hip flexion and internally rotating the hip with overpressure (Flexion-Internal Rotation Test). Anterior impingement (FAI) testing, or FADDIR test, is essentially the above test with the addition of adduction. Both tests are better to rule out labral tears and FAI than to rule in given their high sensitivity and low specificity.9
Ober’s Test and Thomas Test are used to assess muscle length of the ITB and hip flexors, respectively, with careful interpretation of true muscle shortening versus hypertonicity or guarding.
Physical therapy management is typically the first line of treatment for these patients. Athletes may have poor control of their spine and pelvis and should improve this stability and strength through core, deep hip rotator, and gluteal muscle strengthening. A progression from unloaded exercises to weight bearing exercises help to isolate smaller stabilizing muscles prior to utilizing large muscle groups, that may be compensating. Further, many of these athletes appear strong in inner ranges, so it is imperative that they work on end range strength. Stretching is usually not indicated. I’ve found that improving stability though strengthening allows the “tight” muscles (actually hypertonic) to return to normal resting length.
One of my favorite exercises is neuromuscular rolling as described by Hoogenboom et al.7 I use this as both an assessment and early exercise as movement compensations can easily be uncovered and addressed. Progression may include assisted curl ups, during which a band is used to assist a curl up position with cueing to relax the hip flexors and adductors. Assistance is gradually removed as movement improves. Other exercises include those to isolate gluteus maximus in the prone position, such as heel kicks. The athlete is asked to extend from the hip (with knee at 90 degrees to shorten the hamstrings) without extending the spine. Gluteus medius can be strengthening with lateral leg raises, Comerford clamshell exercises or side planks.
Proprioceptive exercises may include small hip circumduction in side lying, focusing on precision of movement or PNF patterns. This can be progressed with weight bearing single limb balance once the athlete can demonstrate control of pelvis in all planes of movement. Single limb Romanian Dead Lifts are a great way to incorporate glute strengthening with proprioception.
Those patients presenting with painful tendinopathy of the hip flexors may benefit from isometrics to relieve pain. Isometrics have been documented to improve symptomatic patellar tendinopathy.8 Athletes are asked to perform an isometric in mid range to the hip flexors at 70% effort for 45 seconds, 3-5 repetitions with two minutes rest between each isometric. Athletes should have an immediate analgesic effect that may last several minutes. This can be performed throughout the day as needed for pain.
Further research is needed to describe microinstability of the hip. While surgical options, such as capsular plication or thermal capsulorrhaphy exist1,2, more research for conservative management is needed. Microinstability of the hip can prove to be a challenge for the physical therapist or athletic trainer, especially in athletes with high demand rotational activities.
Kalisvaart M, Safran M. Microinstability of the Hip—it does exist: etiology, diagnosis, and treatment. J Hip Preserv Surg. 2015; 2(2): 123-135.
Shu B, Safran M. Hip Instability: Anatomic and Clinical Considerations or Traumatic and Atraumatic Instability. Clin Sports Med. 2011; 30:349-367.
Beighton P. Hypermobility scoring. Br J Rheumatol. 1988; 27:163.
Cerezal L, et al. Emerging topics on the hip: ligamentum teres and microinstability of the hip. Eur J Radiology. 2012;81:3745-3754.
Lewis CL, Sahrmann SA. Acetabular Labral Tears. Phys Ther. 2006 Jan; 86(1):110-21.
Rao J, Zhou YX, Villar RN. Injury to the ligamentum teres: mechanism, findings, and results of treatment. Clin Sports Med. 2001;20:791-799.
Hoogenboom B, Voight M, Cook G, Gill M. Using rolling to develop neuromuscular control and coordination of the core and extremities. N Am J Sports Phys Ther. 2009;4(2):70-82.
Rio E, Kidgell D, Purdam C, Gaida J, Moseley GL, Pearce AJ, Cook J. Isometric exercise induces analgesia and reduces inhibition in patellar tendinopathy. Br J Sports Med. 2015 Oct:49(19):1277-83.
Reiman M, Mather R, Cook C. Physical examination tests for hip dysfunction and injury. Br J Sports Med. 2015;49:357-361.