It was the young tennis player’s friends who spotted what the therapists and textbooks could not work out. By Sean Fyfe
One of the elite tennis players I look after recently presented with a puzzling knee injury. After returning from a reasonably successful and injury-free overseas tour, Matt had enjoyed a well earned two-week rest. Upon recommencing his training regime, however, he began to develop a niggling pain over his left tibial tuberosity whenever he was forced to load that leg while pushing wide out to the forehand side. Matt is a left-hander, so when he sets up for a shot on that side, he places his left leg out wide (known as open stance) under weight with the knee bent, eccentrically loading the quadriceps mechanism.
Matt, one of Australia’s leading juniors, is at a crucial point in his career. He is 18 years old and just starting out on the gruelling ATP Tour. Over the past 12 months, he has worked hard to develop his game and has seen his world ranking improve accordingly. When he first developed the tibial tuberosity pain, Matt had approximately eight weeks to go before his next competition phase, in which he was intending to increase his year-on-year haul of ATP points. Rankings don’t just work to motivate players, they also determine which tournaments they get to take part in, and how much training and travel funding the national body gives them. Serious injury to players at this stage of their careers can be devastating.
Having reviewed Matt’s previous injury history, alarm bells began to ring. Matt has a definite propensity to bone stress related injuries. At age 14 he suffered a lumbar spine stress fracture which required a lengthy reha bilitation; then at 16 he developed bone stress to the lateral tibial plafond. The latter injury was managed poorly and he continued to play on it, leading eventually to an acute frac ture which knocked him out of the game for quite a while.
There have been other non-bony injuries, too. You can imagine how hard Matt’s team has been working to keep him on court for an extended run. So when he started devel oping more bony pain, we needed to jump on the problem.
An MRI scan showed bone marrow oedema within the tibial tuberosity – in effect, another bone stress-related problem. We defi nitely didn’t want a repeat of the ankle scenario, so in conjunction with the sports physician, we put in place a management plan. The first step was rest. The inflamma tion needed to settle and Matt was also put on anti-inflammatories and told to ice reli giously.
The initial assessment also revealed significant tightness through Matt’s tensor fascia lata, iliotibial band, quadriceps and gluteals, so we incorporated daily soft-tissue work and/or stretching. Matt began a daily strengthening regime on that leg (as well as doing strength work on the other leg), which covered everything that didn’t place load on the injured structure. This included:
* open-chain quadriceps
* lateral hip stabilises
* glute max and hip flexors in open chain
* bridging work for more glute max strength
* calf raises
* gentle hamstring curls.
No pain was to be felt during or after the exer cises. Matt also began a rigorous core stability, upper-body strength programme and cardio vascular work in the pool (swimming and water running). As the pain started to settle, he began a graduated eccentric loading regime and the stationary bike was included to increase the cardiovascular effort.
To be honest, both I and other members of the medical team were still perplexed at the problem. None of us had seen this injury or had read any literature on it. We expected that eccentric overload of the quadriceps mecha nism would have manifested in a patella tendon, patello-femoral, fat pad or even quadriceps tendon injury, but not inflam mation in the marrow of the tibial tuberosity. We had, of course, considered Osgood Schlatter’s but Matt was a physically mature 18-year-old and hadn’t grown in a couple of years, so we could consider the apophysis at the tibial tuberosity to be fused and strong.
As the inflammation and pain settled, we progressed Matt’s rehabilitation. He started proprioception/balance work on the mini trampoline, a gentle eccentric loading programme, bodyweight squats and very small inner range single-leg squats. He also started work back on court in a controlled way that avoided his having to move and load the leg. He began rolling his serve over without using his legs, and hitting returns of serve.
The exercises then progressed to single leg press, squatting with weight and full single-leg squats. Again, there was to be no pain during or after exercising. The rehabil itation was going well, Matt was getting stronger, maintaining his fitness, strength and core and was starting to hit the ball well. The final ingredient to be added was his full movement on-court.
It was then that Matt walked into the clinic and announced, ‘I’ve grown again’. I was stunned. Friends had been telling Matt that he looked taller and so he decided to measure himself and discovered he had grown half an inch.
Suddenly this put everything into perspec tive. I think we could pretty much safely say that at the age of 18 he was suffering from Osgood-Schlatter’s (see box, above). I have come across players who suffered some ongoing pain in the region of the tibial tuberosity at this age, having previously had a severe case of Osgood-Schlatter’s as a younger player. But I have never seen nor read of a player with an acute flaring at the age of 18, with no previous history.
Many young men are still growing at the age of 18, but they tend to be late developers, not men who have had such a long period without growth. Matt, by contrast, had been quite an early developer. So why did he not grow for a couple of years and then grow again at this age?
In reviewing the literature, most of the studies dealing with delayed growth relate to gymnastics. In a 2004 article, Georgopoulos et al(1)point to delayed puberty in athletes involved with sports that require a strict control of energy input in the pres ence of high-energy output, such as artistic gymnastics. Nothing similar is reported as an issue in sports that don’t involve a control on energy input.
There is also a phenomenon known as ‘late catch-up growth’ in which people grow later after having had their genetic potential for growth during the main pubertal years interrupted by extrinsic factors such as hormonal dysfunction or malnutrition. Although there is definitely no answer for Matt’s unusual growth pattern, we needed to be aware of the possibilities.
Now that we understood Matt to be suffering Osgood Schlatter’s rather than bone stress at the tibial tuberosity, we could alter our management. We had to accept that this problem could be around for a while – until Matt finishes his belated growth spurt. Previously we didn’t want him playing with any discomfort, because of the risk of further injury. Now he would be able to play his intended tournament schedule – but was going to have to manage the problem himself, probably over a number of months.
The enforced rest and rehabilitation would have been needed anyway, to get the acute pain to settle, but at least Matt could increase his training schedule, two weeks out from the first tournament. One positive was that his first two tournaments were on clay (a much softer surface than hard court) and so we ensured his training was taking place on clay. We continued to limit him to one on-court session a day, with every third or fourth day off and a strict icing regime.
By the time Matt departed for his first two tournaments, he had been playing sets, was physically fit, pain free and confident. If he hadn’t undertaken such a rigorous rehabil itation and maintenance programme, things would have been quite different, not just physically but also psychologically. During his first tournament back, he had only mild discomfort, made the quarter finals and was well on the way to accumulating more ATP points then he gained last year.
1. Georgopoulos, NA, Markou, KB et al (2004) ‘Growth, pubertal development, skeletal maturation and bone mass acquisition in athletes’. Oct-Dec;3(4):233-43.