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What is scapholunate dissociation?
The scapholunate interosseous ligament (SLIL) is a C-shaped structure which connects the scaphoid and the lunate and is important for carpal stability. Most injuries are degenerative in nature, occurring in patients over 80 years of age with arthritis but acute injuries are associated with FOOSH style injuries.
What are the clinical features to make me concerned for acute scapholunate dissociation?
A patient presenting with dorsal and radial-sided wrist pain with after a FOOSH, specifically with the wrist in extension and ulnar deviation. Typically, pain will be increased with pressure applied to the carpal bones (ex. push up position), clicking or catching of the wrist, “giving way” with lifting or grasping, and instability or weakness. Tenderness may occur just distal to Lister’s tubercle or in the snuffbox. There may also be swelling on the dorsum of the wrist, pain (worse with extension and radial deviation) and a positive Watson’s test. Watson’s test is performed by grasping the patient’s thumb with the 1st and 2nd digits over the scaphoid. The scaphoid is dorsally subluxed by bringing the thumb in a volar and opposed direction. A positive test is dorsal wrist pain or a clunk which indicates scapholunate instability.
AP and lateral views of the wrist are a start but the clenched fist view is the best radiograph. A gap between the scaphoid and the lunate greater than 3mm is called the Terry Thomas sign and is positive for SL dissociation. MRI can be considered but is considered to have a low sensitivity. Arthroscopy is the gold standard.
Non-operative management is appropriate for acute and undisplaced SLIL injuries. Requires casting or approximately 8weeks with periodic imaging and follow up. Operative management is required for any form of malaligment, failure to improve after 18 months, SL dissociation due to scaphoid fracture, presence of associated arthritis or other complicating factors. This can be achieved in multiple ways such as K-wire fixation, direct repair of the ligament or tendinous grafting, depending on injury.
A failure to adequately identify and appropriately managed SLIL injuries can lead to scaphoid lunate advance collapse (SLAC) which causes progressive degeneration of the radiocarpal and midcarpal joints and has a significant effect on function in the hand and wrist.
FOOSH without obvious fracture; consider ligamentous injury, especially SLIL injury. Normal xrays will not adequately assess, always order clenched fist view. Most cases treated with casting but some will require surgical management. Lack of management can lead to progressive degeneration of the wrist and serious functional impairment.
Anthony Caragianis, PGY3 SEM, University of Ottawa
Landry, C.H., Allan, K.S., Connelly, K.A., Cunningham, K., Morrison, L.J., and Dorian, P. (2017). New England Journal of Medicine, 337(20): 1943-53.
Family practitioners are frequently tasked with assessing fitness, such as for driving, work duties, and (return to) sport participation. In the sport setting, although many competitive athletes have dedicated physicians to perform Pre-Participation Examinations (PPEs), this responsibility frequently falls to their family physician. Reasons for this are varied, and include the lack of a physician associated with a competitive youth team, or “clubs” rather than “varsity” designated teams at the post-secondary level, for instance. Investigations as a part of this evaluation can be hard to determine, and this is especially true with respect to the cardiac system, given the potentially serious complications (e.g. sudden cardiac arrest (SCA), in the otherwise generally healthy competitive athlete.
This NEJM article “sought to identify all sudden cardiac arrests that occurred during participation in sports activities within a specific region of Canada to determine their cause.” From this arose a discussion of which causes may have been identifiable, to estimate the efficacy of screening systematically during a PPE.
SCA was defined as an abrupt loss of vitals resulting in death or successful resuscitation. It was considered “during sport participation”, if the event occurred during or within 1 hour following an activity estimated to have involved exerting at >3 METS. “Competitive” was defined as an organized or sanctioned event certified by an official, whereas it was classified as “non-competitive” if it was not formally organized/sanctioned. Presumably, competitive athletes were the focus, as they are the individuals who would present for a PPE.
The authors used the Rescu Epistry registry – a prospective, comprehensive registry of all EMS attended (via 911) cardiac arrests that occurred out-of-hospital. They obtained information from multiple sources (e.g. ER reports, discharge summaries, autopsies, etc.). It is unclear why events occurring in private were excluded, with inclusion criteria specifically identifying public locations only, when such events did not need to be witnessed. That is, 1681/3825 cases of out-of-hospital SCAs were excluded for “location”, which would seem to miss individuals who could have had an SCA at home within 1 hour following sport participation, for example. This region in Ontario had a population of 6.6 million, including urban and rural regions. The study period was 2009 to 2014, and individuals aged 12-45 were included in an attempt to catch young athletes potentially eligible for screening, as well as the maximum number of individuals with heritable cardiac syndromes, while reducing the overlap with SCA secondary to coronary artery disease (CAD).
Results: 74 cases of SCA in a public space occurred (as defined above) during sports; 16 during competitive and 58 during non-competitive sports. Focusing on competitive athletes (again, as defined above), there were 9 deaths and 7 survivors (43.8% survival) and sufficient data to determine the cause of the SCA in 10/16 cases. Similar survival was seen in the non-competitive category (44.8%). The incidence of SCA in competitive athletes was 0.76 cases per 100,000 athlete-years (highest rate: 1.17 for ages 12-17, lowest rate: 0.41 for ages 35-45). This rate has been reported as 4.84/100,000 person-years in the general population, of the same age range, according to the authors.
On autopsy of 2 competitive non-survivors and 4 competitive survivors, there was no identifiable cause, and they were considered primary arrhythmias. That is, these 6 cases were found to have either a normal cardiac structure at autopsy, or in the case of the survivors, normal echo or cardiac catheterization. Interestingly, most SCAs in competitive athletes were race events and soccer events (4 each). The gym (12) and running (9) were the most common activities in the non-competitive. For both competitive and non-competitive, the predominant cause varied by age: <35, structural and primary arrhythmia; 35-45, CAD. Also of note, hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy were uncommon causes.
Perhaps most importantly, two competitive athletes had structural abnormalities (i.e. hypertrophic cardiomyopathy) that were likely to have been identified during a PPE with an ECG or echo. However, one of these individuals had actually been previously assessed for presyncope, and was found to have a normal ECG and echo. Amongst competitive survivors, none had a condition likely to have been identified with cardiac screening. The authors also use a broad definition of “competitive” – one that would include “beer league” hockey, university intramural or “community sport and social league” participants, for example, which frequently are organized events with referees – and exclusion of these participants (who are unlikely to present for PPE) perhaps would change these figures.
This study indicates that SCA in competitive athletes is rare, and raises questions about systematic screening for cardiac conditions in athletes, as a part of PPEs. There is a great deal of controversy ongoing and no clear consensus, and although this interesting study adds to the current knowledge, I eagerly await the forthcoming Canadian guidelines on the subject, to help inform my decision making in regards to investigations to pursue!
Alison Bagg MD, CCFP
PGY3, Sport & Exercise Medicine
University of Ottawa
Advisor: Dr. Taryn Taylor BKIN, MSc, MD, CCFP (SEM), Dip Sport & Exercise Medicine
Carleton Sport Medicine Clinic
Don’t have to see it to believe it – The Effect of Magnetic Resonance Imaging Scans on Knee Arthroscopy
Don’t have to see it to believe it:
The Effect of Magnetic Resonance Imaging Scans on Knee Arthroscopy: Randomized Controlled Trial Arthroscopy. 2007 Nov;23(11):1167-1173.e1
Multiple pathologies of the knee cannot be picked up on x-ray and ultrasound. Increasing prevalence of MRI has led to increased use. We as physicians may not see the bill for these investigations but they are still a considerable expense for our system. Due to long wait times, the National Health Service (UK) has started to perform MRIs to try and reduce the number of patients that will actually require surgery while in the US, they are questioning whether MRI will actually add value.
A randomized control trial was performed using 252 patients on a waiting list for knee arthroscopy. All patients had an MRI of their knee performed. They were then randomized into two groups; one had their MRIs read by their surgeons prior to surgery and the other did not. Even though the group whose MRIs were read had a diagnosis change in 47% of cases, compared to 1% in the control group, ultimately, the rate of surgery was the same.
Important to highlight that this is American data and they may be more likely to proceed with arthroscopy than their Canadian colleagues. Important to note that a diagnosis change occurred in 47% meaning information from MRI was still of value.
Take away message to consider: Don’t wait for an MRI report to refer to orthopaedics because it is unlikely to change the management plan in patients you suspect will require arthroscopy but still order the MRI as it can provide valuable information for operative planning.
Anthony Caragianis, PGY3
Advisor Dr. Taryn Taylor BKin, MSc, MD, CCFP (SEM), Dip Sport Med
Falls are a leading cause of injury among seniors. 20-30% of seniors (age 65+) experience one or more falls each year and 85% of seniors’ injury-related hospitalizations are due to falls.
The Champlain LHIN IMPACTT Centre is conducting a research project supported with Ontario Centres of Excellence funding from the MOHLTC Ontario Chief Innovation Strategist.
This project will ddetermine the value of a falls prediction model that leverages a new technology; QTUGTM and uses trained technicians (non-professionals such as personal support workers) to engage seniors that are normally not being actively screened for falls, and to identify those at higher risk of falling prior to their first fall.
If a senior has been identified with a moderate to very high falls risk, we are suggesting they take the handout materials and speak with their physician or other healthcare professionals to better understand what may be contributing to their risk of falls and what they can do to help prevent falls.
What is QTUGTM?
The “Timed Up and Go” or TUG test is one tool that health professionals use during a falls assessment. It consists of the person getting up from a chair walking 3 meters, turning around, walking back the 3 meters and sitting down while the professional monitors the time it takes, the gait, steadiness, etc.
The QTUGTM uses sensors worn on the shins (over clothing) and a hand-held tablet to track the person during the TUG test. With proven qualitative input, analytical data and algorithms it produces a Falls Risk Score.
First, the person is asked a few questions about age, weight, height, recent falls, any problems with mobility, medications, blood pressure, dizziness and/or vision. The sensors and tablet then measure the time taken to stand, average stride time, average stride velocity, step time variability, time taken to turn, number of steps in turn and time to complete the test. The sensor information combined with the short falls questionnaire determines your risk of falling.
For more information contact the IMPACTT Centre.
Email: Judy Marshall-Brunke
Tel: 613-745-8124, ext. 5879 | Toll Free: 1.800-538-0520
Ryan C. Xiao, Kempland C. Walley, Joseph P. DeAngelis, Arun J. Ramappa. Clinical Journal of Sports Medicine, May 2017, Volume 27, Issue 3, 308-320.
Adhesive capsulitis (AC) is a relatively common condition that can have a significant impact on function and quality of life. Briefly, it consists of three phases: pain at rest and progressive loss of range of motion (“freezing” stage), stiffness without pain at rest (“frozen” stage), and gradual return of range of motion (“thawing” stage). It is classified as Primary AC (idiopathic) and Secondary AC (following trauma or with diabetes, for example). It is thought to be due to chronic inflammation and (subsequent) fibrosis, though uncertainty remains regarding underlying pathophysiology. It is self-limiting, usually lasting 2-3 years (or longer) before resolution is achieved. Individuals experiencing AC often seek treatment options to manage the pain and hasten recovery. Corticosteroid injection is commonly offered.
The purpose of this review was to evaluate corticosteroid injection effectiveness, in terms of disease duration and recovery. Sixteen randomized prospective studies involving corticosteroid injection for the treatment of AC compared with a control/comparison group were included in the review. Comparison group treatments included stretching, home exercises or (multi-modal) physiotherapy; injection with normal saline or lidocaine; corticosteroid or lidocaine bursal or subacromial injection; oral NSAIDs; as well as a combination of one or more of the aforementioned treatments, including corticosteroid injection. A few studies investigated the effect of corticosteroid injection dosing (three studies), injection location (glenohumeral versus subacromial) (three studies), and the effectiveness of using ultrasound guidance (one study). Finally, two studies specifically looked at corticosteroid injections in diabetics with AC.
Notably absent in this review was hydrodistension as a comparator treatment modality. Follow-up began as early as one-week post-treatment initiation, and the length of follow-up ranged from 6 weeks to 12 months.
Nine of 12 studies found a significant benefit of corticosteroid injection in terms of short-term pain reduction and mobility restoration compared to control group(s), with effects lasting between 2 and 24 weeks. The three studies that failed to find a significant benefit had comparison groups that received formal physical therapy.
With respect to corticosteroid dosing, 2 out of 3 studies did not find a significant difference between 20 mg and 40 mg of triamcinolone for pain relief or improved function. The third study used 3 injections spaced 1 week apart, and 40 mg doses were more effective than 10 mg injections. This review concluded that an injection of 20 mg of triamcinolone seemed to be as effective as 40 mg injections. Further research would be helpful in determining if there is an optimal dosing and injection frequency that provides the most benefit.
In terms of location, the three studies suggest that subacromial injections are just as effective in reducing pain and improving function, contrary to the common belief that glenohumeral injections are superior. Furthermore, one study that examined the effect of using ultrasound guidance (versus landmarked “blind”) injections for AC over a 6 week period, found that the only significant difference was during the 2 weeks post-corticosteroid injection, with significantly improved pain, range of motion and function when ultrasound was used. This study also involved weekly follow-up hyaluronate injections, however, which makes it difficult to evaluate the effect of the corticosteroid and use of ultrasound itself.
Remarkably, as diabetics are widely recognized as being at a significantly greater risk of developing AC, there is a paucity of research specifically investigating this population in the setting of AC. One study compared corticosteroid injection with NSAIDs, and another study compared corticosteroid injection with home exercises. Interestingly, the first study reported no difference in outcome at 24 weeks, and the second found reduced pain at, but not beyond 4 weeks, and improved function at, but not beyond 12 weeks. This suggests that diabetics may benefit less from corticosteroid injection for AC, than their nondiabetic counterparts.
In terms of adverse effects of corticosteroids injected into various joints in the body, the most common are injection-related pain and injection site skin discolouration. Transiently increased blood glucose levels in diabetics have also been noted. There is the possibility of weakening tendons in the shoulder, especially with repeated injections or those that are improperly placed, and the risk of tendon rupture exists, although reportedly this is a small risk when done infrequently. Finally, the authors note that antiretroviral therapy (i.e. protease inhibitors) can interact with corticosteroids that are injected, resulting in an iatrogenic Cushing syndrome via respective inhibition of, and metabolism by, the P450 CYP(34A) pathway.
Overall, the authors of this review conclude that corticosteroids injected for AC can provide significant short-term pain reduction, with evidence of effect for at least 2 weeks, but up to 24 weeks post-injection. The evidence suggests that these injections can be intra-articular or subacromial and that 20 mg may be as effective as 40 mg when triamcinolone is used. At this time, there is insufficient evidence to suggest the superiority of ultrasound-guided versus landmarked injection. As well, formal physical therapy may be as effective as an injection. Unfortunately, diabetics may not benefit as much from such injections for AC and they can experience transiently raised blood sugar. Caution should be used when protease inhibitors are being taken, as an iatrogenic Cushing syndrome can develop.
This review certainly adds to the current knowledge regarding treatment and use of corticosteroid injections for AC. The conclusions can be used to more accurately discuss the potential benefits of injections, with special consideration for diabetics, and perhaps set more realistic expectations of the improvement they can expect. Furthermore, given the range in costs associated with different treatments, when funds and insurance coverage are limited, these conclusions can also help guide treatment decisions (i.e. physiotherapy versus injection, use of ultrasound guidance, etc).
Alison Bagg MD, CCFP
PGY3, Sport and Exercise Medicine
University of Ottawa
Supervisor: Dr. Taryn Taylor BKin, MSc, MD, CCFP (SEM), Dip Sport & Exercise Medicine
In October 2016, world leaders in the field of sport-related concussion (SRC), of which a large proportion are Canadian, met in Berlin to develop the latest statement on our current knowledge of the science of SRC. As a quick review, an SRC is a traumatic brain injury induced by biomechanical force transmitted to head causing functional disturbance. It does not require a direct blow to the head. Some of the new developments and highlights from the statement include:
– Assessment of mental status, cognitive functioning, sleep/wake disturbance, ocular function, vestibular function, gait, and balance is recommended
– Insufficient evidence for investigations such as EEG or MRI
– A new Sports Concussion Assessment Tool Version 5 (SCAT) was developed
– A brief period (24–48 hours) of cognitive and physical rest is appropriate for most patients
– Subsymptom threshold activities and submaximal exercise are encouraged (as long as symptoms are not exacerbated)
– Cervical spine rehab is recommended for neck pain/headaches
– Vestibular rehab is recommended for dizziness
– Return-to-play and return-to-school/work protocols can advance in parallel
– Children and adolescents should not return to sport until they have successfully returned to school
– Physiological dysfunction may be delayed relative to clinical recovery, suggesting that using a ‘buffer zone’ of a graduated return to activity/return to play progression before full return to contact risk may be appropriate
– Preinjury mental health problems and prior concussions appear to be risk factors for persistent symptoms.
– Greater acute and subacute symptoms are a consistent predictor of worse clinical outcome.
– The teenage years might be a particularly vulnerable time for having persistent symptoms—with greater risk for girls than boys.
– Strongest evidence exists for disallowing body checking in youth ice hockey
– Strong recommendations to mandate helmet use in skiing/snowboarding
– Mixed evidence for mouthguard but there may be an overall protective effect
The top 5 key messages from the 5th International Consensus Statement on Concussion in Sport
- McCrory P, Meeuwisse W, Dvořák J, et al. Consensus statement on concussion in sport—the 5thinternational conference on concussion in sport held in Berlin, October 2016. Br J Sports Med 2017;51:838-847.
- Shields, MD, CCFP, Sport and Exercise Medicine Fellow, University of Ottawa
Advisor: Taryn Taylor, MD, CCFP (SEM), Dip Sport Med
Tom A Ranger, Andrea M Y Wong, Jill L Cook, Jamie E Gaida
Ranger TA et al. Br J Sports Med 2016; 50: 982-989
The prevalence of Diabetes in our population is increasing, as is the morbidity and mortality associated with this chronic disease. As a primary care provider, we are well aware of the role ‘lifestyle’ plays in the development and control of Type 2 diabetes mellitus. For this reason, the guidelines recommend exercise and diet as first line treatment for this condition. It has been shown that up to 50% of participants who quit exercise as part of their management do so because of musculoskeletal symptoms. So the question arises: Does tendinopathy, a condition that reduces exercise tolerance, have a role to play in lack of adherence to an exercise program in diabetics?
Earlier studies have shown that hyperglycemia does change the collagen cross-linking of tendons and reduced their proteoglycan content (Reddy, 2003) leading to weakened tendons and predisposing them to tendinopathy. This study investigated the potential association between diabetes and tendinopathy by systematically reviewing and meta-analysing case control, cross sectional, and studies that considered both of these conditions. In total 31 studies were selected for the final analysis with good attention paid to exclusion criteria and reduction of bias. Confounding variables were identified: age, sex, adiposity, statin use and hyperglycemia. There is observational evidence that statins may induce tendinopathy (Marie I, Arthritis Rheum 2008;59:367-72) as well as an association between adiposity and tendinopathy (Gaida, Arthritis Rheum 2009; 61 840-9).
This systematic review showed that “diabetics had greater than three times the odds of tendinopathy compared to controls; and people with tendinopathy had 1.3 times increased odds of diabetes compared to controls. Therefore there is evidence of a strong link between diabetes and tendinopathy however cause and effect cannot be established even though there are plausible biological pathways by which high blood glucose can affect tendon structures.” It was also shown that those diabetics with tendinopathy have had a longer duration of diabetes.
Regardless of the cofounders that may exist, the compelling evidence supports the link between diabetes and tendinopathy. This has important clinical implications such as careful monitoring and structuring of load progression when initiating exercise to prevent the development of tendinopathy. A slower, more graduated approach would be crucial for these patients. As well, those who have tendinopathy and require rehabilitation should ensure tight glycemic control to speed resolution.
“Co-management by medical and allied health practitioners may be indicated for people with tendinopathy and long standing diabetes.”
Keith Morgan BSC, MD, CCFP, Sport Medicine Fellow February 2017
Advisor: Dr. Taryn Taylor BKin, MSc, MD, CCFP (SEM), Dip Sport & Exercise Med
Tendon disorders are often some of the most difficulty presentations to treat when it comes to musculoskeletal complaints. This is evident from the various modalities that are proposed to help in the healing process of tendinopathies, including physiotherapy, dry needling, active release therapy (ART), extracorporeal shockwave therapy (ESWT), platelet-rich plasma (PRP), and nitroglycerin patches. Stem cells are often touted as the next frontier in medical therapy given their potency to become multiple cell types in the right environment, so it is no surprise that stem cell therapy research has begun for tendinopathies.
Chronic tendon disorders have histological findings of necrotic and apoptotic tenocytes, neovascularisation and collagen disarray. The proposed mechanisms of repair through stem cells involve the cells’ differentiating capabilities into new tenocytes to generate new tendon tissue and their modulation of the local immune response and stimulation of repair in the surrounding cells by the production of growth factors and cytokines.
This systematic review focused on the efficacy of stem cell therapy for pain and functional outcomes in the treatment of tendon disorders in humans. Seven articles were selected for inclusion in the study, but data was only available for four. Three of the studies were case series and one was a matched non-randomized study. Conditions studies included lateral epicondyle, patellar, and rotator cuff tendinopathies. 3 out of 4 studies used bone marrow cells (from anterior iliac crest) and one used adipose tissue derived cells. The 2 studies on the rotator cuff evaluated post-surgical response to bone marrow-derived stem cells. While the studies generally found improvements in pain scores and lower re-tear rates of the rotator cuff, all of the studies were level 4 evidence, so a conclusion about stem cell efficacy cannot be confidently drawn. Furthermore, only 1 study reported adverse events, none of which were serious.
In summary, there is a lack of any evidence for stem cell therapy for tendon disorders and the safety of these procedures cannot be determined. Patients should be made aware of these facts if they are seeking therapy for their tendinopathies.
- H Pas, MH Moen, HJ Haisma, M Winters. No evidence for the use of stem cell therapy for tendon disorders: a systematic review. Br J Sports Meddoi:10.1136/bjsports-2016-096794
Dr. Ryan Shields (PGY3 Sport Medicine, University of Ottawa)
Advisor: Dr. Taryn Taylor BKin, MSc, MD, CCFP(SEM), Dip Sport Med
Article: Brison RJ, Day AG, Pelland L, et al. Effect of early supervised physiotherapy on recovery from acute ankle sprain: randomised controlled trial. BMJ 2016;355:i5650
Lateral ankle sprains are one of, if not the most common musculoskeletal injuries and account for approximately 14% of sports injuries. Resulting from inversion of the ankle after quick changes in direction or awkward landings, most ankle sprains are grade 1 (mechanically stable) or grade 2 (some joint laxity) ligament sprains of the anterior talo-fibular ligament (ATFL). These can be graded by performing the anterior drawer test and comparing side to side, with the optimal time to test at day 5 post injury. If there is any pain in the malleolar zone, bone tenderness at the posterior edge or tip of either malleolus, or inability to bear weight for four steps immediately after the trauma and in the ED, then radiographs are indicated as per the Ottawa ankle rules.
Like everything MSK related, physical therapy is recommended for the rehabilitation process, however the evidence for supervised physiotherapy (PT) is limited in terms of breadth and quality. Principles of PT in ankle sprains include early weightbearing as tolerated, range of motion exercises (drawing out the alphabet with the foot), strengthening of lateral stabilizers (peroneals) using resistance bands, and proprioceptive training (standing on one leg/BOSU ball/mini trampoline/wobble board). It takes 8-12 weeks for complete neuromuscular retraining so bracing or taping for at least this period of time is recommended.
Recently, an article was published out of Kingston which is the largest randomised controlled trial (RCT) to have evaluated the therapeutic benefits of supervised physiotherapy in the treatment of acute ankle sprains. In this study, patients who presented to the ED in Kingston were randomized to either the usual care or physiotherapy arms. The usual care arm included medical assessment and a one-page written summary of instruction for basic management of the injury at home, including ankle protection, rest, ice, compression, elevation, use of analgesics as necessary, graduated weight bearing activities, and information about expected recovery. Participants assigned to the physiotherapy arm were provided with usual care (as above) plus a regimen of supervised physiotherapy. They received a maximum of 7 treatment sessions of 30 minutes in length (maximum 210-minute dose) and treatment was augmented by standardised home exercise programs. Ankle function reported by patients, re-injury, clinical measures, and laboratory based assessments of ankle strength were recorded at one, three, and six months.
Groups were similar at baseline and showed that ~40% of sprains were sport-related and ~60% had previous sprains, highlighting the recurrent nature of these injuries. Except for seeing a benefit for physiotherapy at three months in the subgroup of patients aged <30yo, there were no significant differences between groups. These results are in contrast to a recent meta-analysis which indicated rehabilitative exercises were associated with significant improvements in self reported function and reduced risk of recurrent injury, which was lowest with a cumulative dose of >900min of therapeutic exercise. Compliance of with appointments and home exercises in the Kingston study was recorded but unfortunately not included in the results, which hinders our ability to judge the dose of exercise received.
In summary, this trial can be interpreted in a couple of ways. First, it suggests that supervised physiotherapy may not reliably improve clinical outcomes post low-grade ankle sprain within 6 months, and therefore maybe we don’t need to push supervised PT as much in the general population given that it also comes with significant financial cost. Secondly, it could also suggest that a dose of greater than 210 min of therapeutic exercise may be required to see improved clinical outcomes, so if you’re going to do PT, you might need to err on the side of being more aggressive with the volume of rehab. And considering that less than half of participants had excellent outcomes by 6 months, further investigation to reduce morbidity would be prudent.
- Brukner & Khan’s Clinical Sports Medicine, 4th ed. Peter Brukner, Karim Khan Sydney: McGraw-Hill Australia; 2012.
- Doherty C, Bleakley C, Delahunt E, Holden S. Treatment and prevention of acute and recurrent ankle sprain: an overview of systematic reviews with meta-analysis. Br J Sports Med 2016 doi:10.1136/bjsports-2016-096178
Ryan Shields, MD, MSc, CCFP
PGY-3 Sport and Exercise Medicine
Advisor: Dr. Taryn Taylor, BKin, MSc, MD, CCFP (SEM), Dip SPort & Exercise Medicine
Zellers JA, Carmont MR, Silbernagel KG (2016) Return to play post-Achilles tendon rupture: a systematic review and meta-analysis of rate and measures of return to play. Br J Sports Med. 2016;50:1325-1332
Achilles tendon ruptures are relatively common in the middle-age male “weekend warrior” population, and present a significant obstacle to maintenance of health and prevention of morbidities related to inactivity. Muscle weakness, decreased endurance, and fear of re-rupture may cause an individual to avoid the sports activity during which injury occurred, and resulting altered biomechanics may induce other MSK problems like knee injuries and contralateral Achilles tendinopathy.
Achilles tendon ruptures are caused by rapid and forceful contraction, often in the eccentric loading phase (forced dorsiflexion). Risk factors include preceding tendinopathy, intermittent activity, recent changes in athletic training schedule, poor warm-up, and fluoroquinolone or corticosteroid use. Patients present with acute onset of localized pain associated with hearing or feeling a pop. There may be a prodrome of muscle pain prior to event. On physical exam, the injured leg may be more dorsiflexed when prone, have a palpable gap and be weak in plantar flexion. Lack of plantar flexion when the calf is squeezed is considered a positive Thompson test. Ultrasound may be used to determine complete vs. partial ruptures. Urgent referral to orthopedics should be considered as operative treatment should occur within 6 weeks to avoid tendon retraction, especially in young sprinting athletes. However, non-operative management involving functional rehabilitation and casting in resting plantar flexion is becoming more common in most patients as new evidence emerges. Re-rupture rates and plantar flexion strength have been shown to be not significantly different when comparing non-operative to operative management. Also, studies have consistently shown increased complications rates with operative management.
Traditional recommendations are that jogging can be started after 12-16 weeks, return to non-contact sport after 16- 20 weeks. and to contact sports after 20- 24 weeks. In this article, return to play (RTP) rates were close to 80% and average time to RTP was 6 months, ranging from 3 to 10.4 months. However, it did not differentiate between surgical and non-surgical management. Functional criteria to consider prior to RTP, as always, include range of motion, strength (using single-leg heel raises), and sport-specific movements.
Ryan Shields, MD, MSc, CCFP
PGY-3 Sport and Exercise Medicine, University of Ottawa
Advisor: Dr. Taryn Taylor BKin, MSc, MD, CCFP (CAC SEM), Dip SPort & Exercise Medicine