A 22-year-old rugby footballer who played as a flanker (weighing in at 113kg) and a 29-year-old prop forward 115kg) both sustained minor ankle injuries during the same match. The dysfunction was not significant enough in either player to have stopped them from playing.
After the match, they both presented with clinical Grade 1 ATFL anterior talo-fibular ligament) inversion sprains, with pain over the anterior-inferior fibula and associated swelling. No laxity was present, but passive talocrural dorsiflexion was limited at the end of range of movement, with a ‘blocked’ feel to passive posterior talar glides.
We applied the usual ice and elevation treatment alongside antiinflammatory medication (NSAIDs), talocrural dorsiflexion mobilisations, posterior talo-fibular capsule releases and peroneal/calf and proprioception exercises. Both players commenced straight-line running four days post-injury and played seven days after injury with no ill effects. Both were strapped with supportive zinc oxide tape to train and play, and we continued to manage them in the same way after they resumed playing.
But all was not well. First, the prop (about two weeks post-injury) and then the flanker (a week later) started noticing heel pain that was initially worse in the mornings and with warming-up for training. They both felt that perhaps the pressure on the heel from the taping of the sprained ankle was responsible for the symptoms. This is a common complaint with protective ankle taping, and we took particular care to ensure the ‘locking’ tape was not encroaching on the medial arch.
On examination, pain was focused around the medial calcaneal origin of the plantar fascia, with tenderness extending into the mid-portion of the plantar fascia and underlying flexor hallucis brevis muscle. Pain was also reproducible with passive ankle dorsiflexion and big toe flexion. The players were treated for mild plantar fascia strain/irritation.
This can happen after ankle sprains. Increased anterolateral gutter ankle swelling and anterior positioning of the talus because of the ‘stretched’ ATFL, commonly leads to reduced dorsiflexion. In turn this can cause excessive pronation and increased plantar fascia stretch. In essence, less motion in one articular complex (the ankle) leads to increased motion in another (subtalar joint/midfoot).
Treatment consisted of soft-tissue massage to the plantar fascia and gastro-soleus complex, intrinsic muscle rehabilitation (short flexor group and interossei muscles), periodic stretching of gastro-soleus/flexor hallucis longus and brevis/plantar fascia, self-massage over a golf ball or can of tinned fruit and continuation of talo-crural dorsiflexion mobility. The medial longitudinal arch was supported with taping that effectively off-loaded the plantar fascia. The symptoms were never severe enough to prevent either player from training or playing, so both continued like this for the next two weeks. Neither player had any injections to the plantar fascia.
About two weeks after the onset of plantar fascia symptoms, on the recommendation of a podiatrist, the players were given sleeping socks. Sleeping socks are designed to help treat plantar fasciitis by holding the ankle in an almost plantar grade position with the big toe in 5 to 10 degrees of dosiflexion during the night. The socks are very comfortcorrecting able and both players felt they were very effective in relieving morning pain and pain with warm-up. The players continued to rehabilitate the intrinsic muscles, stretch all involved myofascial groups and have their feet taped to support the medial longitudinal arches.
About a week and a half after they’d started wearing the socks, the flanker was warming up during a game, when he felt an acute ‘pop’ at the calcaneal insertion of his plantar fascia. He had started the match as a reserve and was performing routine warm-up drills about 10 minutes into the second half. He felt the ‘pop’ whilst accelerating from a crouched position, and told the touchline medical staff about it. A rupture of the plantar fascia was immediately suspected. The player’s foot was further strapped to support the medial arch in case he was required to play. He did in fact play for the last 10 minutes of the match quite effectively, but all the time he was on the field he was aware of pain and swelling in the arch.
After the match the foot was assessed: there was noticeable swelling at the calcaneal origin and in the soft tissue of the medial arch. Walking was acutely painful. On passive dorsiflexion of the ankle and big toe, the plantar fascia was unable to be palpated, heightening our suspicions of a complete plantar fascia rupture.
Four days later an MRI scan described an incomplete plantar fascia rupture. However, based on the rapid resolution of symptoms and rapid progression of function we suspected that the MRI was incorrect and a complete rupture had occurred. This was confirmed clinically by a sports physician and supported by diagnostic ultrasound nine days after the original MRI.
The second player (the prop) suffered a similar fate two weeks after his colleague. He had aggravated an old thoracic spinal injury a few weeks previously, which had kept him out of playing and training for a week and a half. During this recovery time he was continuing to selfmanage his plantar fascia with exercises and the sleeping sock. He was happy that the plantar fascia felt quite good with the sock and he believed the problem was almost completely resolved.
Included as a reserve for a match, the prop was called upon to play the last five minutes of the game. As he joined the play, he had to accelerate rapidly to take part in a ruck. He felt a ‘pop’ and acute pain in his heel and the arch of his foot. He went down and complained to the medical team of his problem, but insisted that he carry on as the game was almost over. He played that five minutes in obvious discomfort.
After the match the prop’s foot was assessed, revealing the same telltale swelling at the calcaneal origin and in the soft tissues of the medial arch. On passive dorsiflexion of the ankle and big toe the plantar fascia was unable to be palpated. Once more, we suspected a complete plantar fascia rupture.
A diagnostic ultrasound was ordered three days post-injury and this described a complete rupture of the medial band of the plantar fascia with about 10% of the lateral band still intact on the calcaneum. Like his team-mate, the prop enjoyed a rapid resolution of symptoms and rapid progression of function postinjury.
Both players were treated with aggressive intrinsic muscle rehabilitation to train these muscles to support the medial longitudinal arch; temporary orthotics were made to support the medial arches and off-load the calcaneal origins, which were still quite tender.
Both players commenced training at 16 days post-injury, full training at 23 days, and were declared fit to play after 26 days. They both missed three games. They continued to manage their respective problems with muscle rehabilitation and protection through orthotics and taping. They both continue to suffer mild symptoms of heel pain and arch swelling from time to time, but never enough to affect playing or training.
Data to be published shortly on injury rates in the English Zurich Premiership shows that in two full seasons (with more than 200 players followed each season), there were two reported cases of plantar fascia irritation/ strain – and none involving rupture. These cases resulted in a maximum of three weeks away from playing and training.
So plantar fascia problems would seem to be pretty rare. However, the study did not include complaints by players of low level symptoms where the player carried on training and playing, so it may be giving us a slightly distorted picture.
It is perfectly plausible that elite level rugby players (particularly forwards) would suffer from symptoms of plantar fascia irritation and soreness. The nature of the game requires players to spend a lot of time in a forward lean position up on the toes, such as in scrums and rucks/mauls, in effect, winding up the ‘windlass mechanism’ of the foot.
The ‘windlass mechanism’ can be described as the tensioning of the plantar fascia/aponeurosis as the foot pushes off. This is caused by dorsiflexion of the great toe which applies tension to the plantar fascia and causes the medial longitudinal arch to be elevated and supported as the foot pushes off. The repeated pushing-off that rugby players have to do in scrums, mauls/rucks and sprints could potentially load the plantar fascia excessively. If you add to this pattern the poor medial arch support afforded by rugby boots and soft playing grounds (such as commonly found in the English Premiership), you can appreciate why players might experience plantar fascia problems.
My estimate based on personal experience with rugby squads is that up to four players from a squad of 40 (10%) will be suffering plantar fascia symptoms at any time. But they will rarely miss games or training time because of these symptoms, and the symptoms are easily managed with stretching and muscle control.
As noted above, the forthcoming injury incidence study recorded zero cases of rupture among the English Zurich Premiership players. There are many accounts of complete ruptures of the plantar fascia in older athletes linked to degenerative fascial tissue and overzealous corticosteroid use in the management of plantar fasciitis. But in elite rugby union, complete plantar fascia ruptures are almost unheard of.
It does seem odd, then, that one club manages to suffer two complete ruptures in the space of two weeks. Why is it so?
It is just possible that the answer lies in the sock, and, intrigued by this possibility, I have sought extensive discussions with sports physicians, other physiotherapists and podiatrists to try and get to the bottom of it. I feel we have arrived at a consensus regarding the possible pathomechanical relationship between the sock and the ruptures experienced by my rugby players, with the most likely explanations being tissue ‘creep’ of the plantar fascia/aponeurosis and muscle inhibition.
Tissue ‘creep’ refers to the phenomenon whereby tissues lose elasticity if held in a sustained position for a long period (similar to how an elastic band loses its recoil properties if held in a stretch position for a long time). You can imagine how the sock may cause a ‘creep’ response in the plantar fascia if used repeatedly for long periods. Because the sock’s design ensures that most of the dorsiflexion force is directed at the great toe, the greatest ‘creep’ may be in the medial band of the plantar fascia from the calcaneal origin through to the first toe. This could lead to a weakening of collagen tissue and cross-links in tissue structure, resulting in a weakened plantar fascia.
In this context sustained stretching of the plantar arch may make matters worse, as the short intrinsic muscles of the plantar arch will also be excessively stretched. These muscles are quite important in providing dexterity for the toes, as well as adding active support to the medial longitudinal arch as the foot pronates during weight-bearing and then re-supinates as the foot goes to push off.
Arguably, a prolonged and sustained stretch on these muscles may change the length-tension relationship and influence force production and recruitment of these muscles during the gait cycle, particularly while running. It has been shown that sustained and prolonged stretching that increases muscle length will also affect muscle recruitment patterns as the contracting tissue needs to deal with the ‘slack’ caused by elongated connective tissue(1). Furthermore, it has been shown that altered force-length properties may change the neural activation patterns of muscle(2). Thus, because of the elongated muscle tissue, the medial arch may be operating with no muscular protection for short periods of time. This may cause the plantar fascia to become excessively loaded to create a medial arch during the push-off phase of the gait cycle. The short amount of time spent with protective strapping of the medial arch (1-2 hours for training) may not be enough to counteract the change in muscle function caused by the prolonged time (8 hours) spent in stretch.
Before raising undue alarm, we need to be cautious about this hypothesis, not least in terms of its wider applicability. Indeed, there are good reasons to believe that our unusual injuries may also be highly specific.
As mentioned earlier, rugby players experience abnormally high forces across the midfoot and forefoot because of the unique positions and skills involved in performance of the sport. What’s more, elite level rugby players are much heavier than the general population or most other sportspeople, leading to greater forces acting over the midfoot. These factors, combined with the ‘creep’ and inhibition factors mentioned above, may provide a plausible explanation to this rare and odd coincidence of injuries.