sportEX medicine - Apr 09 by Tor Davies

ISSUE 40 april 2009

promoting

excellence in

sports

highlights n Chronic compartment syndrome n Femero-acetabular impingement syndrome n Grow your own knee cartilage n arterial compression syndromes at the shoulder - diagnostic arm manoeuvres

medicine

contents APRIL 2009 Issue 40 Publisher Tor Davies BSc tor@sportex.net Editor LYNN BOOTH MCSP lynn@sportex.net Art editor DEBBIE Asher debbie@sportex.net Advertising manager Paul Harris paul@sportex.net +44 (0) 20 8652 1906 Subscriptions Sandra Greatorex subs@sportex.net +44 (0) 845 652 1906

(Hons)

Technical advisors

Richard Bolton MCSP, MAPA Steve Aspinall BSc (BASRaT), MSc Sophie Cox BSc (podiatry), SRCh, MChS Dr Bryan English Dip Sports Med, DO Joanne Elphinston BPhty MA, MCSP Viv Lancey MCSP, SRP Dr Dylan Morrisey MCSP, MSc PhD Prof Graham Smith FCSP, SRP Joan Watt MCSP, SRP Dr Nick Webborn MRCGP, Dip Sports Med, MSC Dr Greg Whyte PhD, BSc (Hons

is published by Centor Publishing Ltd 88 Nelson Road Wimbledon, SW19 1HX

Welcome

Well this is quite literally an action packed issue and getting more active by the day! Our ever-popular ‘journal watch’ in the online version now hyperlinks directly to the individual research articles. Our first feature, written by Droitwich Knee Clinic orthopaedic surgeon, Mr Oliver Schindler covers the topic of cartilage regeneration and the online version links to a patient education animation as part of the SWARM interactive animations that sportEX purchases access to on behalf of our online subscribers. We then have an excellent article on chronic compartment syndrome by one of the UK’s most distinguished consultant podiatric surgeons, Dr Nat Padhiar. The online version of this article is supplemented by a playlist of YouTube videos. Finally the jewels in this issue’s crown in terms of interactivity are the two articles on femoral impingement and arterial compression syndromes in the shoulder (part 2). Both articles feature videos and animations that we hope significantly add to the practical application of the knowledge. We’d love to hear your feedback! Tor Davies, publisher tor@sportex.net

Tel: +44 (0)845 652 1906 Fax: +44 (0)845 652 1907 www.sportex.net other Titles in the SportEX range sportEX dynamics - ISSN 1744-93838 Written specifically for professionals working with a wide variety of athletes and sports people to help them get the most out of their athletic performance - personal annual subscription £30, practice subscription £55 sportEX health - ISSN 1471-8154 For people working in the physical activity health promotion sector, health and fitness industry as well as in primary care and occupational health - annual subscription £35 for individuals, £60 for departments

Contents

compartment syndrome of the leg 3 Journal watch 16 Chronic 6 Grow your own cartilage Arterial compression syndromes at the shoulder 22 Femero-acetabular inpingement 10 A look at some of the latest research

A look at one of the major advances in orthopaedic surgery for decades

FAI is on the rise - this article explains the, pathology, clinical presentation and rehabilitation and suggests a series of rehabilitative exercises (videos in the online version)

A detailed exploration of chronic compartment syndrome in the leg

Following on from the previous issue this article focuses on diagnostic arm manoevres used in physical examination, discusses diagnostic dilemmas and highlights areas that require further research

DISCLAIMER While every effort has been made to ensure that all information and data in this magazine is correct and compatible with national standards generally accepted at the time of publication, this magazine and any articles published in it are intended as general guidance and information for use by healthcare professionals only, and should not be relied upon as a basis for planning individual medical care or as a substitute for specialist medical advice in each individual case. To the extent permissible by law, the publisher, editors and contributors to this magazine accept no liability to any person for any loss, injury or damage howsoever incurred (including by negligence) as a consequence, whether directly or indirectly, of the use by any person of any of the contents of the magazine. Copyright subsists in all material in the publication. Centor Publishing Limited consents to certain features contained in this magazine marked (*) being copied for personal use or information only (including distribution to appropriate patients) provided a full reference to the source is shown. No other unauthorised reproduction, transmission or storage in any electronic retrieval system is permitted of any material contained in this publication in any form. The publishers give no endorsement for and accept no liability (howsoever arising) in connection with the supply or use of any goods or services purchased as a result of any advertisement appearing in this magazine.

sportEX medicine 2009;40(Apr):2

online

Click on the title to go to the abstract

Journal Watch KNEE IMMOBILIZATION FOR PAIN CONTROL AFTER A HAMSTRING TENDON ANTERIOR CRUCIATE LIGAMENT RECONSTRUCTION. Hiemstra LA, Heard SM, Sasyniuk TM, et al. American Journal of Sports Medicine 2009;37:56–64 A total of 102 patients aged 18–40 years were enrolled; 88 patients were randomised, and 14 were excluded intraoperatively. The patients were randomised (immobiliser or no immobiliser) after wound closure. The immobiliser used was a soft, unhinged brace with Velcro®. The primary outcome was patient self-assessed pain using a 0–100 mm visual analogue scale on day 2 after surgery. Secondary outcomes included pain and analgesic use in the first 14 days after surgery, complications, and range of motion (approximately 3 weeks postoperatively). A sample size estimate was calculated and resulted in the need for 44 patients per group. Results: There was no difference in mean visual analogue scale pain scores 2 days after surgery between immobilised and non-immobilised patients. There were no differences between groups in medication consumed, range of motion or complications. Pain and analgesic use were the same for both groups at 7 and 14 days postoperatively.

sportEX comment There is a constant stream of research papers into all aspect of anterior cruciate ligament reconstruction, which is creating a substantial knowledge base on what is and, more importantly, what is not effective. This paper shows that there is no difference in pain or analgesic use between immobilised and non-immobilised patients, so it is safe to spare the trouble and expense of a brace.

INCIDENCE OF SUBSEQUENT INJURY TO EITHER KNEE WITHIN 5 YEARS AFTER ANTERIOR CRUCIATE LIGAMENT RECONSTRUCTION WITH PATELLAR TENDON AUTOGRAFT. Shelbourne KD, Gray T, Haro M. American Journal of Sports Medicine 2009;37:246–251 A 5-year follow-up was obtained on 1,415 patients after primary anterior cruciate ligament (ACL) reconstruction. Subsequent injury was evaluated based on sex, age and activity level. Seventy-five patients (5.3%) had an injury to the contralateral knee, and 61 patients (4.3%) suffered an injury to the reconstructed knee. Women suffered more injuries (7.8%) to the contralateral normal knee than men (3.7%), but not more injuries to the reconstructed knee (4.3% v. 4.1%). The risk of subsequent injury to either knee was 17% for patients under 18 years of age, 7% for patients aged 18–25 years, and 4% for patients older than 25 years. There was no difference in injury rate between patients

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who returned before and after 6 months postoperatively.

sportEX comment The incidence of injury to either knee after reconstruction is associated with younger age and higher activity level, but returning to full activities before six months postoperatively does not increase the risk of subsequent injury. Women have a higher incidence of ACL injury to the contralateral knee than men after reconstruction. The question is, why? Another paper (Varus alignment leads to increased forces in the anterior cruciate ligament. Van de Pol GJ, Arnold MP, Verdonschot N, van Kampen A. Journal of Sports Medicine 2009;37:481– 487) published in the same journal concludes that there is a direct relationship between varus alignment and ACL tension. This is a small study using cadavers, but it might point towards the role of knee alignment strategies in the prevention of ACL injury.

online

Click on the title to go to the abstract

MEDIAL COLLATERAL LIGAMENT INJURIES AND SUBSEQUENT LOAD ON THE ANTERIOR CRUCIATE LIGAMENT. Battaglia MJ 2nd, Lenhoff MW, Ehteshami JR, et al. American Journal of Sports Medicine 2009;37:305–311 Ten human cadaveric knees were sequentially tested by a robot with the medial collateral ligament intact, in a partial injury model, and in a complete injury model with a universal forcemoment sensor measuring system. Tibial translation, rotation and anterior cruciate ligament (ACL) load were measured under three conditions – anterior load, valgus load and internal–external rotation torque – all at 0° and 30° of flexion. Anterior and posterior translation did not statistically increase with a partial or complete medial collateral ligament injury at 0° and 30° of flexion. In response to a 125-N anterior load, at 0° the ACL load increased by 8.7% in the partial injury and by 18.3% in the complete injury. At 30° the ACL load was increased by 12.3% in the partial injury and by 20.6% in the complete injury. In response to valgus torque at 30°, ACL load was increased by 55.3% in the partial injury model and by 185% in the complete injury model. In response to internal rotation torque at 30°, the ACL load was increased by 29.3% in the partial injury model and by 65.2% in the complete injury model. The amount of internal rotation at 30° of flexion was increased significantly in the complete injury model (22.8°) versus the intact state (19.5°).

sportEX comment Partial and complete medial collateral ligament tears significantly increased the load on the ACL. Patients may need to be protected from valgus and internal rotation forces after ACL reconstruction in the setting of a concomitant partial medial collateral ligament tear.

THE EFFECT OF ANKLE TAPING ON DETECTION OF INVERSION–EVERSION MOVEMENTS IN PARTICIPANTS WITH RECURRENT ANKLE SPRAIN. Refshauge KM, Raymond J, Kilbreath SL, et al. American Journal of Sports Medicine 2009;37:371–375 The threshold for movement detection was measured in 16 participants with recurrent ankle sprain under two conditions: with the ankle taped or untaped. The threshold for movement detection was examined at three velocities (0.1°/s, 0.5°/s, 2.5°/s) and in two directions (inversion, eversion). Results: application of tape significantly decreased the ability to detect movements at the ankle. For example, at 0.5°/s, the 70% detection threshold was 3.40° in inversion and 3.49° in eversion at the untaped ankle, and 4.02° in inversion and 4.04° in eversion at the taped ankle.

sportEx comment Taping is often used to counter the proprioceptive deficit after joint injury such as ankle sprain, but the effect of taping on proprioceptive acuity at the ankle is unclear, with studies producing conflicting findings. The findings here suggest that the efficacy of taping is unlikely to be explained by an enhanced ability to detect inversion or eversion movements. This should not stop clinicians taping in order to reduce the likelihood of re-sprain, as other studies suggest a prophylactic effect of taping.

DIFFERENCES IN ANKLE RANGE OF MOTION BEFORE AND AFTER EXERCISE IN two TAPE CONDITIONS. Purcell SB, Schuckman BE, Docherty CL, et al. American Journal of Sports Medicine 2009;37:383–389 This was a controlled laboratory study. Twenty volunteers participated in testing procedures on three separate days, one for each taping condition (selfadherent, white cloth, no tape). The participant’s ankle range of motion was measured with an electrogoniometer before application of the tape, immediately after application of the tape, and after 30 minutes of physical exercise. Range of motion was measured in two planes of motion: inversion to eversion, and dorsiflexion to plantar flexion. White cloth tape and self-adherent tape both restricted inversion to eversion range of motion immediately after application, but with 30 minutes of exercise only the self-adherent tape maintained the decreased range of motion. For dorsiflexion to plantar flexion range of motion, the white tape and self-adherent tape both significantly decreased range of motion immediately after application and after the exercise protocol.

sportEX comment Athletic tape has been used on the ankle to decrease range of motion and to prevent injuries. Results from previous research found that with physical exercise athletic tape loses some of its restricting properties. Self-adherent tape maintained range of motion restriction both before and after exercise and performs better than the white cloth tape, so although it may be more expensive the self-adhesive stuff is worth it.

sportEX 2008:40(April):3-5

Journal watch

THE INTERNATIONAL CLASSIFICATION OF FUNCTIONING, DISABILITY AND HEALTH: RELEVANCE AND APPLICABILITY TO PHYSIOTHERAPY. Sykes C. Advances in Physiotherapy 2008;10:110-118 This article focuses on the International Classification of Functioning, Disability and Health (ICF) and the role of the World Health Organization in maintaining and updating it. The ICF is an important tool that can augment physical therapy practice by providing a framework and common language. It can aid the collection of consistent and reliable information with which to appraise physical therapy practice, facilitate communication across settings and disciplines, and select or develop consistent outcomes measures.

sportEX comment Physical therapy in sport is a highly specialised branch of medicine and good communication is essential not only between disciplines but also between countries. Think of the number of international players. Their medical advisors often need to liaise with colleagues in other counties. The ICF framework provides a valuable role in this.

ELITE MALE ADOLESCENT GYMNAST WHO ACHIEVED UNION OF A PERSISTENT BILATERAL PARS DEFECT. Vrable A, Sherman AL. American Journal of Physical Medicine and Rehabilitation. 2009;88:156–160

An adolescent 15-year-old male competitive gymnast presented to a university-based multidisciplinary spine institute with a persistent lower back pain for 18 months. Although the results of X-rays were negative, his pain rendered him unable to compete in his sport any longer. A computed tomography (CT) scan was performed, which showed a bilateral pars fracture at L5, without spondylolisthesis. A nuclear medicine bone scan revealed negative findings, confirming chronic non-union. The patient completed a 4-week course of physical therapy for 6 months, without any relief of pain or radiological evidence of healing. He was subsequently treated with a bone stimulator for 4 hours/day and was recommended to wear a warm-and-form-type brace. Isometric core trunk exercises were also initiated. After 6 weeks of treatment, the subject showed clinical improvement at the follow-up visit. A CT scan performed 12 weeks after the initial scan showed complete union of the fracture, correlating with clinical improvement. Two years later, the athlete remains completely pain-free, is training regularly, and is able to compete on a national and, possibly, international level.

sportEX comment Many people working in sports medicine will have had similar patients who present with lower back pain and produce negative X-rays results and yet fail to improve with conservative treatment. The CT scan may answer the diagnostic problem. Bone growth stimulation is the technique of promoting bone growth in difficult-to-heal fractures by applying a low electrical current or ultrasound to the fracture. The theory behind this is based on the fact that the concave side of the bone becomes negatively charged and the convex side is positively charged. It is believed that artificially encouraging this by charging with an electric current will speed healing.

PHYSICAL ACTIVITY HABITS OF DOCTORS AND MEDICAL STUDENTS INFLUENCE THEIR COUNSELLING PRACTICES. Lobelo F, Duperly J, Frank E. British Journal of Sports Medicine 2009;43:89–92 Doctors are a respected source of health-related information and can provide continuing preventive counselling and follow-up; they may have ethical obligations to prescribe PA. Several barriers to PA counselling exist, including insufficient training and motivation of doctors Rates of exercise counselling

by doctors remain low; only 34% of US adults report exercise counselling at their last medical visit. Research shows that clinical providers who themselves act on the advice they give provide better counselling and motivation of their patients to adopt such health advice. There is compelling evidence that the health of doctors matters and that doctors’ own PA practices influence their clinical attitudes towards PA.

sportEX comment This essay is a warning: practise what you preach. The evidence is that physicians’ own attitudes are passed on to patients. It is reasonable to extrapolate the evidence to include the practices of all health professional rather than only doctors.

Part-time online distance education Enjoy Masters level study whilst still working and experience world class teaching relevant to your practice. Whether you are looking for recognised specialist qualification or continuing professional development our postgraduate programmes combine distance learning with face to face teaching and clinical skills practice. Apply now for 2009!

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Sport and Exercise Medicine

Sports Physiotherapy

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Growing your own cartilage By Oliver S Schindler, MD MFSEM(UK) ÖFD(Orth) FRCS(Orth)

HISTORICAL DEVELOPMENTS Opposing joint surfaces are covered with hyaline cartilage, the lining responsible for smooth and frictionless movement. The word “cartilage” originates from the Greek hyalo, meaning “glass”, and the Latin cartilage, meaning “gristle”. When we talk about cartilage we often refer erroneously to the soft cartilage or meniscus, a crescent-shaped structure that is located between the femur (thigh bone) and tibia (shin bone). Through being triangular in cross-section, the meniscus functions as a knee-joint stabiliser and stress dissipater. Even as far back as the eighteenth century, surgeons were aware that surface cartilage, once damaged, had little ability to heal. William Hunter, a British surgeon, was quoted as saying “From Hippocrates to the present age it is universally allowed that ulcerated cartilage is a troublesome thing and that once destroyed it is not repaired” (1). Since the days of Hunter, it has become apparent that joint surface damage, if left untreated, invariably deteriorates and eventually spreads to surrounding areas. The end result of such a process is often the development of debilitating osteoarthritis (2). Many clinicians have engaged in a desperate attempt to find ways to facilitate durable cartilage repair (3,4). Treatment of articular cartilage defects in the knee has been at the centre of attention over the past few years, as the number of young adults with joint injuries continues to grow. It has been estimated that in the UK 10,000 patients each year suffer cartilage damage, most often caused through sporting activities, which warrant repair (5). In a high proportion of these patients, the treatment opportunity is lost either through delay in diagnosis or through failure to recognise the condition altogether (5). Damage to articular cartilage may

Due to a lack of blood supply, articular cartilage, the lining of the joints, has a limited capacity for natural healing. Once damaged through injury or repetitive strain, cartilage becomes degenerate, eventually leading to osteoarthritis. Early treatment is therefore essential, particularly in young and active individuals. The ability to regenerate surface cartilage is one of the major advances in orthopaedic surgery for decades. Gene technology has allowed the growth of harvested cartilage cells outside the human body. Once re-implanted, autologous chondrocytes have the potential to improve the repair of cartilage defects. The most advanced of these techniques is matrix-guided autologous chondrocyte implantation (MACI), which has been shown to provide histologically and functionally normal articular cartilage.

Identification of surface cartilage damage represents a major challenge 6

be related to acute trauma, overuse, ligament instability, leg mal-alignment (bowed or knocked knees), menisectomy (removal of shock absorber cartilage) or osteochondritis dissecans (6). Acute cartilage defects may arise from a fall or a direct blow, but more often they occur as a result of twisting forces while the knee is exposed to full load-bearing. In such an environment, shear forces combined with joint compression forces create a build-up in tension between the surface cartilage and the underlying bone. As a result, the surface cartilage may delaminate from its under-surface, creating a “full-thickness” cartilage defect (see Fig. 1). Symptoms may be apparent immediately but often do not occur for many months or even years after the primary insult. If the damage to the articular surface remains untreated, it will lead to fibrillation and fragmentation of the damaged area, which in turn will affect the opposing surface. Over time, cartilage degeneration and osteoarthritis will develop.

STRUCTURE OF SURFACE OR HYALINE CARTILAGE Surface or hyaline cartilage is a material that consists of a mixture of substances. Apart from water, which represents almost 75%, the principle components are collagen fibrils and the gel-like hydrated glycoproteins creating the cartilage matrix. Encased within this matrix are relatively few highly specialised cartilage cells, known as chondrocytes (7). Chondrocytes have the ability to renew matrix elements

throughout life and hence play a vital role in maintaining joint homeostasis (8). Mechanically, cartilage represents a fluid-filled permeable porous structure, providing slipperiness, resilience, durability and strength (9). It also acts as a shock absorber, cushioning the bone from forces greater than five times body weight. Under normal circumstances, and in the absence of joint trauma or deformity, surface/hyaline cartilage allows for frictionless and painless movement throughout life.

DOES CARTILAGE NOT HEAL? Spontaneous healing of all musculoskeletal tissues begins with an inflammatory response, which is dependent on the tissue’s blood supply. Blood carries the vital ingredients to facilitate tissue repair. Surface cartilage, however, lacks both a blood supply and lymphatic drainage, making it ill-equipped to instigate a satisfactory repair process by producing new cartilage. If blood vessels were present in cartilage, it would significantly weaken the matrix and subsequently impair its mechanical properties (7).

SYMPTOMS The identification of surface cartilage damage represents a major challenge as there are no specific signs or symptoms that the injured person may present with. It is of paramount importance that the clinician, general practitioner (GP) or physiotherapist expresses a high degree of suspicion if the patient fails sportEX medicine 2009;40(Apr):6-9

orthopaedic orthopaedicmedicine medicinecartileage cartilage regeneration regeneration inconspicuous or overshadowed by adjacent fat tissues and hence may not be easily identifiable. If symptoms do point towards the pathology, then the clinical suspicion should be high, and a diagnostic arthroscopy (keyhole procedure) should be considered.

REPAIR OF DAMAGED CARTILAGE

to improve with conservative measures and if the mechanism of injury would be in keeping with a potential internal knee derangement. A large proportion of patients suffer acute stabbing pain immediately after the injury, while swelling often occurs several hours later. If knee swelling develops almost instantaneously, damage to internal ligaments such as the anterior cruciate ligament (ACL) is likely and needs to be ruled out. Weight-bearing may be painful and difficult during the first few days. Thereafter, patients may suffer from locking or giving-way of the knee, particularly when twisting, turning or descending stairs. If the surface cartilage is fissured during the initial injury, it may take several days or even weeks before a cartilage flap develops and breaks off. Under these circumstances, a loose body forms in the joint, which may subsequently impinge and cause locking of the knee. Once the damage has occurred, almost all patients describe a localised, toothache-like discomfort, particularly after any type of physical activity. Rest usually helps to ameliorate symptoms.

DIAGNOSIS

Figure 1: Large full thickness surface cartilage defect in the weight bearing zone of the knee

Traditional cartilage repair techniques are all based on stimulating the bone marrow below the joint surface. This can be facilitated by abrading the surface using a burr (abrasion arthroplasty) or through producing little indentations with a metal awl or spike (microfracture). In both cases the clinician injures the subchondral surface, creating a temporary blood supply and subsequent development of fibrous cartilage (11,12). The technique is not new and was first described by Kenneth Hambden Pridie from Bristol in 1959, but it has re-emerged through

the ability to perform the procedure arthroscopically (3). Unfortunately fibrous cartilage is mechanically inferior to hyaline cartilage and hence more likely to wear. A breakthrough in the creation of hyaline cartilage came in the 1970s, when Bentley and Greer observed that transplanted chondrocytes (cartilage cells) enhanced the healing of cartilage defects in rabbits (4). Two Swedish orthopaedic surgeons took up the idea and were able to report on their first series of chondrocyte implantation performed on humans in 1994 (Figs. 2 and 3) (13). They called their technique “autologous chondrocyte implantation” (ACI). The basic principles of this operation have not changed since its inception and are based on obtaining a small sample of the patient’s own (autologous) cartilage, which is cultured in the laboratory and later reimplanted into the surface defect (14–19). Thereafter, the implanted chondrocytes set in motion a complex process of matrix regeneration, which eventually leads to the development of tissue closely resembling hyaline cartilage (8).

THE PROCEDURE

Figure 2: First stage procedure: arthroscopic assessment of exact size and location of surface cartilage defect combined with cartilage biopsy. Cartilage may be harvested from non weight bearing areas in the joint periphery or from loose cartilage flaps within the lesion. (Image provided courtesy of Genzyme Therapeutics, Oxford, UK)

Unless a preoperative MRI has confirmed the patient’s suitability for chondrocyte implantation, the final decision must rest with the clinician, who will have a much better appreciation of the damage when looking inside the joint. The surgery is performed in two stages. During the first operation, a keyhole procedure, the surgeon obtains a cartilage biopsy, mostly taken from loose cartilage flaps in the periphery of the defect or from non-weightbearing aspects of the joint (Fig. 2). The biopsy is immediately sent to a laboratory in Denmark or Germany, where the cells are cultured over a

Figure 3: Autologous

Most clinicians examine the knee and chondrocyte implantation may raise the suspicion of cartilage technique (ACI): A damage but are unable to confirm membrane is sutured this unless further investigations are onto the defect and sealed using fibrin undertaken. Magnetic resonance imaging glue. Cartilage cells (MRI) has been the investigation of are then injected choice as it allows visualisation of all into the space beneath it. soft-tissue structures, including ligaments, menisci and surface cartilage, with high accuracy (10). Standard radiographs fail to demonstrate cartilage, which is radiolucent, and merely show the bony structure of the knee joint. MRI should, however not be considered the panacea Patient in the diagnostic process, as many education animation cartilage defects are small and somewhat

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period of 5–7 weeks to increase the number to approximately 2–5 million (13). Once the cell-culturing process is complete, only a very small window of time exists for the implantation process to be performed, as freezing affects the cells’ viability. In the second operation, the clinician makes a small incision into the knee to visualise the damaged area, which is cleaned thoroughly. A collagen membrane is then sutured on to the defect and the chondrocytes injected beneath (Fig. 3). Over several months, these cells create a matrix to reestablish the articular surface to the level of the surrounding cartilage. However, technical difficulties and problems with cell leakage and delamination and graft overgrowth (hypertrophy) have been reported (14,18–21). The implantation of cultured chondrocytes in suspension has led to concerns about the uneven distribution of chondrocytes within the defect and the potential for cell leakage (21). In order to avoid such problems, and to simplify the implantation process, biodegradable scaffolds seeded with chondrocytes have been developed. The second-generation technique now allows for chondrocytes to be cultured within a collagen matrix. This matrix is then glued directly on to the defect, allowing for a much smaller incision and reduced surgical time. The technique has become known as “matrix-guided autologous chondrocyte implantation” (MACI) (Figs. 4,5) (15,16). A further advantage of this method of cell delivery is that the scaffold may act as a barrier to invasion of the graft by fibroblasts, which may otherwise induce fibrous repair (22). By far the best results have been achieved in localised and confirmed defects surrounded by otherwise healthy surface cartilage (Figs. 5,6). The success is reduced in so-called bipolar lesions where defects are present on opposing surfaces, and those located in the patellofemoral joint (14,15). Many people are still under the misapprehension that ACI or MACI may facilitate the reconstruction of joints affected by osteoarthritis. Unfortunately, however, this is not feasible with the currently available technologies, primarily due to the fact that in osteoarthritis the whole joint is affected by changes in biomechanics and biochemistry, creating an environment unsuitable for cartilage implantation (7). 8

POSTOPERATIVE REHABILITATION The first week after surgery is usually spent with the leg in an elevated position, with regular ice applications and some isometric muscle exercises. Physical therapy usually commences once wound healing is complete. Motion is important to prevent formation of adhesions (tissues that grow together during the healing process) and stiffness following surgery. The continuous passive motion (CPM) machine will help to restore movement to the knee without requiring muscle activity (23,24). In addition to CPM, manual manipulation and massage around the scar and particularly mobilisation of the kneecap are also recommended to help prevent the formation of adhesions. The rehabilitation process after cartilage cell transplantation is critical to the healing process and the success of the procedure. Although the recovery period can be extensive and needs commitment, most patients can perform necessary low-impact activities such as walking and driving relatively early in the programme. Defects on the weightbearing surface (tibiofemoral joint) need to be offloaded, and patients usually stay on crutches for up to 3 months. Physiotherapy is particularly important during the initial postoperative period and should focus on maintaining muscle function and joint flexibility. Hydrotherapy, including underwater jogging, has proved to be very popular at this stage. Return to work depends on the demands placed on the knee. Patients may resume desk jobs at around 6–8 weeks, while physically demanding activities should be refrained from for at least 12 weeks. Recovery depends on the size, severity and location of the cartilage injury, the patient’s age and physical condition, and any additional surgery performed at the time of the implantation (eg. ACL reconstruction, high tibial osteotomy). Depending on the size and location of the cartilage injury, low-impact activity such as swimming and cycling may be resumed as early as 3 months following treatment. Higher-impact sports such as jogging, running and aerobics, however, should be refrained from for at least 9–12 months. Most surgeons verify cartilage integrity by obtaining an MRI scan during the rehabilitation period. In some cases, a second-look arthroscopy may be necessary, especially if the patient complains of mechanical symptoms such as locking or clicking. Return to a full level

Figure 4: Chondrocytes are loaded onto a collagen scaffold (membrane) and delivered in a sterile medium for implantation Figure 5: Minimally invasive opening of the knee joint and implantation of MACI type membrane

Figure 6: Pre- and postoperative MRI scan demonstrating a large full-thickness chondral defect treated with MACI. At 9 months the lesion is almost completely filled with newly grown surface cartilage

of sporting activities, especially those involving twisting and turning (e.g. football, rugby, tennis, squash), may compromise the durability of the repair and generally should not be considered until 12–18 months after surgery. It is important, however, to realise that sporting activities do enhance the outcome of the procedure, as Kreuz et al. have pointed out (25). They saw significantly better results at 36 months after surgery in patients performing sport at least one to three times per week compared with those with rare sports involvement of no more than three times a month. The authors concluded that “Physical training improves long-term results after autologous chondrocyte implantation of the knee and should be carried out for at least 2 years after surgery” (25). sportEX medicine 2009;40(Apr):6-9

orthopaedic medicine cartilage regeneration

CLINICAL RESULTS Patients need to be aware that the technique may not be successful in everyone for a variety of reasons. It is generally expected that 80–90% of patients undergoing either ACI or MACI will experience significant functional improvements. The relative effectiveness and durability of ACI compared with other cartilage repair techniques still remain somewhat inconsistent, which is due mainly to a lack of long-term follow-up studies (15,26). Poor preoperative function and a long history of symptoms with numerous previous surgical procedures have shown to be poor prognostic indicators. It is therefore of paramount importance that the clinician recognises these factors when providing the patient with treatment advice and prognosis. A limited number of long-term studies with up to 9 years follow-up have, however, confirmed good or excellent results in 82–92% of patients (5,14,27). Complications included superficial wound infections, postoperative haematomas, intra-articular adhesions and periosteal hypertrophy, while complete graft failure was reported in up to 16% of cases. Minas reported on a group of 169 patients with large cartilage lesions of up to 12 cm2 treated with ACI. Overall, 87% of patients showed significant improvement after a minimum follow-up of 24 months, while 13% were considered failures (28). Similarly good results have also been reported by Behrens et al. (29) using the second-generation MACI technique (Figs. 4-6) (29,30). References 1. Hunter W. On the structure and diseases of articulation cartilage. Philosophical Transactions. Royal Society (Great Britian) 1743;9:267–271 2. Bentley G. Repair of articular cartilage. In: Owen R, Goodfellow J, Bullough PG (eds) Scientific foundations of orthopaedics and traumatology. Heinemann 1980. ISBN 0433243201 3. Pridie KH. A method of resurfacing osteoarthritic knee joints. Journal of Bone and Joint Surgery 1959;41B:618–619 4. Bentley G, Greer RB III. Homotransplantation of isolated epiphyseal and articular cartilage chondrocytes into joint surfaces of rabbits. Nature 1971;230:385–388 5, National Institute of Health and Clinical Excellence. The use of autologous chondrocyte implantation for the treatment of cartilage defects in knee joints. Technology Appraisal 89. National Institute of Health and Clinical Excellence 2008. www.nice.org.uk 6. Schindler OS. Osteochondritis dissecans of the knee. Current Orthopaedics 2007;21:47– 58 7. Mankin HJ, Grodzinski AJ, Buckwalter JA. www.sportEX.net

Articular cartilage and osteoarthritis. In: Einhorn TA, Buckwalter, JA, O’Keefe RJ, American Academy of Orthopaedic Surgeons (eds) Orthopaedic basic science. American Academy of Orthopaedic Surgeons 2007. ISBN 9780892033577 8. Briggs TWR, Mahroof S, David LA, Flannelly J, et al. Histological evaluation of chondral defects after autologous chondrocyte implantation of the knee. Journal of Bone and Joint Surgery 2003;85–6:1077–1083 9. Armstrong CG, Mow VC. Friction, lubrication and wear of synovial joints. Owen R, Goodfellow J, Bullough PG (eds) Scientific foundations of orthopaedics and traumatology. Heinemann 1980. ISBN 0433243201 10. Teller P, König H, Weber U, Hertel P. MRI atlas of orthopedics and traumatology of the knee. Springer 2003. ISBN 3540440348 11. Steadman JR, Briggs KK, Rodrigo JJ, Kocher MS, et al. Outcomes of microfracture for traumatic chondral defects of the knee: average of 11 year follow-up. Arthroscopy 2003;19:477–484 12. Clarke HD, Scott WN. Alternatives in the treatment of knee arthritis: arthroscopy and cartilage restoration. In: Barrack RL, Hip Society, Knee Society, American Academy of Orthopaedic Surgeons, et al. (eds) Orthopaedic knowledge update: hip and knee reconstruction American Academy of Orthopaedic Surgeons 2006. ISBN 0892033487 13. Brittberg M, Lindahl A, Nilsson A, Ohlsson C, et al. Treatment of deep cartilage defects in the knee with autologous chondrocyte implantation. New England Journal of Medicine 1994;331:889–895 14. Peterson L, Minas T, Brittberg M, Nilsson A, et al. Two-to nine-year outcome after autologous chondrocyte transplantation of the knee. Clinical Orthopaedics and Related Research 2000;374:212–234 15. Bentley G, Biant LC, Carrington RW, Akmal M, et al. A prospective, randomised comparison of autologous chondrocyte implantation versus mosaicplasty for osteochondral defects in the knee. Journal of Bone and Joint Surgery 2003;85B:223–230 16. Haddo O, Mahroof S, Higgs D, David L, et al. The use of chondroguide membrane in autologous chondrocyte implantation. Knee 2004;11:51–55 17. Gillogly SD. Autologous chondrocyte implantation: complex defects and concomitant procedures. Operative Techniques in Sports Medicine 2002;10:120–128 18. Minas T, Peterson L. Advanced techniques in autologous chondrocyte transplantation. Clinical Sports Medicine 1999;18:13–44 19. Micheli LJ, Browne JE, Erggelet C, Fu F, et al. Autologous chondrocyte implantation of the knee: multicentre experience and minimum 3-year follow-up. Clinical Journal of Sport Medicine 2001;11:223–228 20. Ueno T, Kagawa T, Mizukawa N, Nakamura H, et al. Cellular origin of endochondral ossification from grafted periosteum. Anatomical Record 2001;264:348–357 21. Sohn DH, Lottman LM, Lum LY, Kim SG, et al. Effect of gravity on localization of chondrocytes implanted in cartilage defects.

Clinical Orthopaedics and Related Research 2002;394:254–262 22. Frankel SR, Toolan B, Menche D, et al. Chondrocyte using a collagen bilayer matrix for cartilage repair. Journal of Bone and Joint Surgery 1997;79B:831–836 23. Salter RB. The biological concept of continuous passive motion of synovial joints: the first 18 years of basic research and its clinical application. In: Ewing JW (ed.) Articular cartilage and knee joint function. Raven Press 1990. ISBN 0881675423 24. Rodrigo JJ, Steadman JR, Silliman JF, et al. Improvement of full thickness chondral defect healing in human the knee after debridement and microfracture using continuous passive motion. American Journal of Knee Surgery 1994;7:109–116 25. Kreuz PC, Steinwachs M, Erggelet C, Lahm A, et al. Importance of sports in cartilage regeneration after autologous chondrocyte implantation. American Journal of Sports Medicine 2007;35:1261–1268 26. Knutsen G, Engebretsen L, Ludvigsen T, Drogset JO, et al. Autologous chondrocyte implantation compared with microfracture in the knee. Journal of Bone and Joint Surgery 2004;860A:455–464 27. Brittberg M, Tallheden T, SjögrenJansson E, Lindahl A, Peterson L. Autologous chondrocytes used for articular cartilage repair. Clinical Orthopaedics and Related Research 2001;391S:S337–S348 28. Minas T. Autologous chondrocyte implantation for focal chondral defects of the knee. Clinical Orthopaedics and Related Research 2001;391(Suppl. 1):349–361 29. Behrens P, Bitter T, Kurz B, Russlies M. Matrix-associated autologous chondrocyte transplantation/implantation (MACT/MACI): 5-year follow-up. Knee 2006;13:194–202 30. Ronga M, Grassi FA, Manelli A, Bulgheroni P. Tissue engineering techniques for the treatment of a complex knee injury. Arthroscopy 2006;22:576

The author Oliver Schindler is a consultant orthopaedic surgeon who joined the team at the Droitwich Knee Clinic in 2001. He is one of only a few surgeons who have embraced the stateof-the-art concept of biologic knee resurfacing which in conjunction with knee re-alignment (osteotomy) can prevent the need for joint replacement surgery especially in the young and active patient group. In 2002 he was awarded the Ilizarov Fellowship in Russia and in 2006 he represented the British Orthopaedic Association as their ASG Travelling Fellow in Europe. The American Knee Society elected him for the 2007 Insall Travelling Fellowship, which allowed him to visit a number of renowned knee specialist units in North America. Since 1999 his orthopaedic practice has specialized exclusively in lower limb and knee surgery. He carries out well over 300 operations per annum most of which are either keyhole or minimally invasive procedures.

Femoro-acetabular impingement The aim of this article is to increase the awareness and understanding of therapists in the pathology involved in femoroacetabular impingement (FAI). FAI is not a cause of hip pain but is a morphological condition that predisposes the hip to intra-articular pathology, which is a precursor of hip osteoarthritis. Over the next few years, due to the inability of the human body to attenuate the forces directed through the hip joint, the number of cases of FAI secondary to trauma, repetitive micro-trauma and instability is likely to increase significantly. By David Binningsley BSc (HONS) MCSP SRP Consider the following questions: n When diagnosing labral lesions, is this the primary or secondary pathology? n Was it direct trauma that damaged the labrum, which then altered the biomechanics and caused the resulting damage to the bearing surfaces? Or was it a very subtle change in the bony contours at the femoral headâ&#x20AC;&#x201C;neck junction at a young age that resulted in labral pathology caused by repetitive microtrauma? n Does the amount of sport played by children, especially in professional teams, increase the amount of repetitive trauma in skeletally immature individuals?

INTRODUCTION Femoro-acetabular impingement (FAI) was first described in the literature in 1990s by Rhienhold Ganz. It is known to result from structurally distinct abnormalities, which include pincer- and cam-type FAI, acetabular retroversion, lack of femoral neck anteversion and coxa profunda, the clinical presentation of which is in common with developmental hip dysplasia (2). FAI is not a cause of hip pain. Rather, it is a morphological condition that predisposes the hip to intraarticular pathology, which then becomes painful and is a precursor of hip osteoarthritis (OA) (3). 10

RELEVANT ANATOMY The labrum is made of dense type II collagen (4), forming a triangular rim attached to the acetabulum. It consists of alternating layers of hyaline cartilage matrix and thick layers of collagen fibres, all oriented in the direction of functional stresses. The integrity of cartilage is maintained by chondrocytes, which are embedded in the extracellular matrix. Cartilage in the superior and posterior regions is considerably thicker, with a higher glycosaminoglycan content, and lower water and collagen content, than in its periphery (5). Aydingoz and Ozturk found a 15% variation in labral shape and 25% size variation, even in asymptomatic individuals (6). Tan et al. found that the labrum increases the surface area of the acetabulum by approximately 28% and deepens it by 21% (7). A double-layered synovial membrane surrounds the joint, the external membrane communicating with the capsule and the internal membrane helping to narrow the acetabulum. The importance of the labrum is shown by the contact stresses between the joint surfaces, which creates a sealing effect. Following the removal of the labrum, the frictional force between the femoral and acetabular surfaces is increased by up to 92% (8). The centre of contact sportEX medicine 2009;40(Apr):10-15

rehabilitation hip impingement also shifts towards the acetabular rim, proving that the labrum provides both structural resistances to lateral movement of the femoral head and joint congruity (9,10). It is important to note that labrum tears are uncommon (11). Therefore, it is also important to consider differential diagnosis in athletes with groin pain. There are many papers that very effectively describe groin pain in athletes (8,12,13) and offer a number of alternatives that must be considered before surgery (Table 1). Blood vessels penetrate the labrum from the outermost layer of the capsule to a depth of only 0.5 mm, leaving most of the labrum avascular, and hence any healing is minimal (14). Vascularity is seen as an influential factor in labral tears. The most vascularised area, which is also the most common site of pathology, is a zone encompassing the anterior, posterior and inferior parts of the labrum (15). This is also the area that encounters the highest mechanical stresses. Free nerve endings have also been identified in labral tissue (16).

HISTORY Over the past 10 years, as our understanding of intra-articular hip pathology has increased, patients are referred more frequently for investigation specifically of the hip joint. Most of these patients have seen a number of practitioners over a prolonged period. The average time to diagnosis is 8 months (17), with the vast majority having had previous surgery, ranging from inguinal hernia repair to lumbar disc surgery. The increasing frequency is supported in a recent paper by Bradshaw et al., who looked at 218 consecutive patients with groin pain and found that 50.4% had hip-based pathology following further investigations (18). The pistol grip deformity has, over the years, been correlated with idiopathic osteoarthritis. Subclinically, slipped capital femoral epiphysis has been suggested as a possible cause of this deformity and thus of secondary OA. Other authors have disputed this, suggesting instead that the deformity is secondary remodelling of the proximal femur as a result of idiopathic OA itself (19). The predisposing factors leading to the development of hip pain are unclear, although the pattern of chondral www.sportEX.net

damage is well documented.

PATHOLOGY To put this into perspective, a cadaveric study (mean age 78 years) showed 96% of the 55 hips studied had labral lesions, of which 74% were located in the anterosuperior quadrant (20). These occur commonly on the articular non-vascular edge of the tissue. This was further confirmed by Blankenbaker and Tuite, who found that 94% of the 61 subjects had labral damage in the anterior quadrant, of which 40% extended to more than one quadrant (21). Kelly et al. reviewed 300 arthroscopies and found that 90% had labral tears (22). They broadly classified five causes of labral tears: n Trauma n FAI n Capsular laxity/hip hypermobilty n Dysplasia n Degeneration. Labral lesions tend not to occur in isolation: 55% of labral injuries have associated articular cartilage lesions of either the acetabulum or the femoral head (23). Tannast et al. performed a computer simulation, showing that the damage caused to the labrum and acetabulum was caused at the zone of the FAI, causing early OA and labral changes (24). Clinically, impinging joints, labrum degeneration and cartilage

Figure 1: The Faber test

online Video

delamination occur in the anterior superior region of the acetabulum (25). Similar patterns of pathology were reported in elite handball players (26). There are both cam and pincer impingements. Beck et al. reported that 80% of patients with FAI have a combination of both pincer and cam lesions (25). Pincer-type lesions are more common in women due to the excessive femoral head coverage (27). Pincer lesions are thought to be more common in Asia due to the nature of work and cultural differences in the west (28). James et al. concluded that any evidence of fibrocystic changes at the anterosuperior femoral neck with or

With thanks to Youtube user jschuber

Table 1: Hip pain differential diagnosis Extra-articular

Intra-articular

Infection

Acetabular labral tears

Iliopsoas bursitis

Capsular sprain

Avulsion injuries

Chondral injuries

Rectus femoris tendonitis

Developmental dysplastic hip

Stress fracture of the lesser trochanter

Femoral neck stress fracture

Adductor strains

Inflammatory arthritis

Gluteus medius strain

Instability

External rotators tendonitis

Leggâ&#x20AC;&#x201C;Calveâ&#x20AC;&#x201C;Perthes disease

Myositis ossificans

Loose bodies

Gracilis strain

Osteoarthritis

Hamstring strains

Osteonecrosis

Iliopsoas tendon strain

Post-traumatic arthritis

Greater trochantic bursitis

Ruptured ligamentum teres

Ischial bursitis

Slipped capital femoral epiphysis

Sacroiliac joint strain

Transient synovitis

Hip pointer Obturator neuropathy Inguinal/femoral hernia (35)

without bone marrow oedema (BMO) should prompt the search for FAI (29). Despite a small sample size, they found that all had fibrocystic changes; the average cyst size was 9 mm (5–14 mm), and the size of the cysts and multiple cysts did not correlate with BMO. They concluded that BMO and cystic changes relate to the ongoing impaction between the femoral head and the acetabulum. An increasing number of golfers suffer from FAI. Biomechanical studies have shown that during the downswing of a right-handed golfer, the right hip is forced into external rotation (ER) during axial loading, forcing the femoral head anteriorly. The repetitive nature of golf leads to focal anterior capsule laxity with stretching of the iliofemoral ligament and subsequent increased translation (3). Injury to the ligamentum teres must also be considered, as this is the third most common finding during arthroscopy. Philippon reports an incidence of 8% of 1000 scopes (30). It becomes taut during adduction, flexion and lateral rotation. Its pathology can be classified into complete, partial and degenerative. In patients with hip instability, it is commonly found to be hypertrophic.

CLINICAL PRESENTATION The clinical presentation was evaluated by Neumann et al., who found that 48% had groin pain, 7% had groin/buttock pain, 56% described a “catching” sensation, 23% “clicking” and 7% “giving way” (31). In terms of range of movement, 62% had reduced range, with 81% of those being restricted in medial rotation; 68% had reduced flexion and 37% lateral rotation. The restricted medial rotation at 90o hip flexion is due to the osseous impingement of the anterolateral femoral head/neck junction with the acetabulum (31). Patients classically describe the “C sign” by cupping the thumb and first finger over the greater trochanter. There are a number of tests described in the literature, the main ones being the FABER (flexion/abduction/external rotation) and the impingement test. It is vital to feel both the amount and the quality of all hip ranges, especially noting whether during passive flexion the hip drifts into abduction at terminal flexion. If so, assess whether the 12

patient is able to adduct to neutral and beyond and whether the end feel is solid or springy.

CLINICAL TESTING Clinically, patients may describe the hip as being “tight”. This may be due to guarding by the iliopsoas and quadratus lumborum (30). The presence of hip instability must be addressed. A number of collagen disorders, such as Ehlers–Danlos, Marfan and Down syndrome, must be ruled out. Assessing elbow extension and wrist and finger laxity will give an indication. The log-roll test has been advocated by the Philippon group to assess hip capsule laxity, although no research has been published (30). Intra-articular anaesthetic injection can be used as a diagnostic. This has been shown to be 90% accurate (34). Field-based assessment can be performed post-injection if required. The FABER test (Fig. 1) is performed by crossing the foot of the affected side on to the opposite leg. This is a good objective marker for measuring range, taking the lateral joint line to the bed; this is then compared with the contralateral limb. The impingement test (Fig. 2), involves taking the hip to 90o, adducting and then medially rotating the hip. If the patient is acute and may have an acute capsulitis, then they may be positive even in this position. If not, then gently take the patient’s leg into the closed pack position and slowly extend the hip. You may feel a small clunk at a specific point in the range, which the patient may describe as their pain. If this is consistent, then by applying an axial load through the femur – try to imagine gapping the

Figure 3: 3D CT Image – showing CAM on femoral head-neck junction

anterior aspect of the joint – you should be able to offer temporary relief, giving further support to your diagnosis.

IMAGING Standard magnetic resonance imaging (MRI) produces both false positive results and an underestimation of labral pathology and has only a 30% sensitivity and a 36% accuracy (9). A magnetic resonance arthrogram produces better results, with reported accuracies as high as 91% (32). More recently, advanced techniques such as T2 mapping have allowed us to get a clearer picture of the quality of the articular cartilage (Fig. 3). Normal acetabular anatomy can be confirmed by measurement of the centre edge angle (CE) (33). An X-ray alpha angle of greater than 50.5o is quoted as a cut-off for diagnosis of cam-type FAI. The exact plane of measurement on MRI is unclear (3).

SURGERY The debate of how to deal with intraarticular hip pathology is beyond the scope of this article. However, surgical options include an open procedure called the mini-open, as described by Ganz (38), and the arthroscopy. Dienst has produced an excellent article on the technique and anatomy involved in hip arthroscopy, which is well worth reading (39). The type of surgery performed is dependant on the surgeons personal preference or if capsular restriction limit access.

online Figure 2: Impingement test

Video

CHONDROPLASTY Chondroplasty or osteoplasty involves removing the area of impingement on sportEX medicine 2009;40(Apr):10-15

rehabilitation hip impingement the femoral head–neck junction. The area of resection is marked with a radiofrequency probe; a burr is used to cut through about 5 mm deep. The bone resection is then carried out laterally on to the femoral neck to reshape the head–neck junction. It is important that the hip is assessed dynamically in order to ensure adequate clearance has been obtained.

CHONDRAL LESION Andreas Fontana found that the average chondral defect in a group of 30 patients (average age 36.8 years) was 2.6 cm2 (40). The severity of cartilage abnormality correlated with the severity of BMO (32). Patients with degenerative labral pathology are 2.9 times more likely to have a large femoral head chondral defect. Significantly, hips with cam impingements are 7.5 times more likely to have acetabular chondral defect.

Figure 4: Passive external rotation stretch – it is vital to block the knee and the foot. Be aware of any previous knee pathology which maybe stressed. I try to avoid adducting the hip as this is the position of impingement

Figure 5: Seatbelt lateral distraction – I use many seatbelt techniques, this being one of the most powerful. In side lying, place the belt high up in the groin. Fix the iliac crest and the knee, whilst laterally distracting the hip

www.sportEX.net

Microfracture to treat chondral defects of the hip is seen as safe and effective. Early results show significant improvement in functional outcomes and decreased pain in the majority of patients (42). Marc Philippon showed seven of nine patients with 100% fill and that average fill on second-look arthroscopy following microfracture is 91% (45). The quality of the literature assessing clinical outcome after open or arthroscopic treatment of FAI is limited. Historically, the open surgical dislocation with osteoplasty has been the gold standard. The scientific data do not show that this has superior outcomes to arthroscopic techniques (46).

REHABILITATION Thomas Byrd, one of the forefathers of hip arthroscopy, said recently that the “best operation will fail with poor rehab but an average surgery will turn out pretty well with good, structured, supervised rehab” (44). Philippon et al. (45) showed a strong correlation between time from injury to surgery and return to full playing: less than 1 year – 3 months, and more than 1 year – 4.8 months. The period of rehabilitation postsurgery is dependent on the type and amount of work performed. Generally, a hip arthroscopy without microfracture will be weight-bearing immediately. If the acetabulum or the femoral head has required microfracture, then the patient is flat-foot weight-bearing (10kgs) for 6–8 weeks. Continous Passive Motion (CPM) is preferred and can be prescribed for 8–12 hours a day for a 4-week period in some cases. This gives the newly recruited mesenchyme stem cells the optimal physical environment (47). Early passive motion is essential for all patients. It is worth noting, especially in patients who have had labral repair, that certain ranges do not put any stress on the anterosuperior labral, which covers the majority of lesions: n Flexion: 0–90o n Abduction: 0-25o n Lateral rotation: 0-25o. Daily cycling with no resistance is started on the day of surgery. Aquatic walking begins on day one. Chondroplasty requires avoidance of impingement of the hip while restoring full range. It is also important to limit

impact work for 8 weeks in order to minimise the risk of femoral neck fracture. At the Sports Hip Surgery meeting in 2008, only one of the experienced surgeons there had had a case of femoral neck fracture postchondroplasty. During the non-weight-bearing stage, the psoas can cause discomfort due to the isometric contraction required to support the limb during ambulation. Its distal attachment into the lesser trochanter can develop a typical tendinopathy pattern, occasionally needing infiltration. There area number of techniques such as seatbelt lateral distraction and passive external rotation than help maintain range and prevent adhesions forming post-arthroscopy (figures 4 and 5). Lewis et al. report that when patients with anterior hip and subtle hip instability perform prone hip extension, only minimal contraction of the gluteal muscles is noted (48). In contrast, significant contraction of the hamstring muscles, especially medially (mainly semimembranosis), is noted. They also suggest that during supine hip flexion the hip medially rotates due to the dominant action of tensor fascia lata (TFL) over the iliopsoas, increasing the anterior glide of the femoral head. Once the patient is able to bear weight, general conditioning to allow the patient to return to full function is progressed gradually. It is essential to maintain a leg-strength programme throughout, ideally alternating running and strengthening in the process.

THE FUTURE It is important that we continue to develop the rehabilitation protocols, as surgical procedures that advance the athletes we deal with are already pushing the limits of the protocol to enable them to return to competition. As with our understanding of the knee joint, preservation of labral tissue may improve the overall integrity of the joint and prevent early OA (12). Surgery for FAI is continually evolving, with surgeons now frequently performing iliotibial band (ITB) labral reconstructions and autologous chondrocyte implantations. Although the bony structure of the acetabulum may be able to withstand forces up to four times body weight, the soft tissue structures of the anterior hip joint may become injured at much 13

lower force levels, especially when the force is applied repeatedly. The critical threshold for injury to these tissues is not yet understood (48). The presence of a cam lesion alone does not predict injury, as there are many examples of bilateral pathology but only one symptomatic hip. It is therefore unclear at what point this continuum of injury progresses beyond a recoverable joint. We know that the presence of a large cam lesion creates an atrisk hip, but a number of factors, such as size of cam, previous injury, duration of symptoms, level of activity and resilience of the patient’s cartilage, must be considered. Further research is required to determine the prevalence and natural history of asymptomatic cam lesions and the relative contribution of these variables to the development of intra-articular hip damage (49). Over the next few years, due to the inability of the human body to attenuate the forces directed through the hip joint, the number of cases of FAI secondary to trauma, repetitive microtrauma and instability is likely to increase significantly.

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FAI is a morphological condition that predisposes the hip to intra-articular pathology 8. Ferguson SJ, Bryant JT, Ganz R, Ito K. The influence of the acetabular labrum on hip joint cartilage consolidation: a poroelastic finite element model. Journal of Biomechanics 2000;33:953–960 9. Czerny C, Kramer J, Neuhold A, Urban M, et al. MR imaging and MR arthrography of the acetabular labrum: comparison with surgical findings. Fortschritte auf dem Gebiete der Röntgenstrahlen und der Nuklearmedizin 2001;173:702–707 10. Edwards DJ, Lomas D, Villar RN. Diagnosis of the painful hip by MRI and arthroscopy. Journal of Bone and Joint Surgery 1995;77:374–376 11. Eriksson E, Arvidsson I, Arvidsson H. Diagnostic and operative arthroscopy of the hip. Orthopaedics 1986;10:392–399 12. Espinosa N, Rothenfluh DA, Beck M, Ganz R, Leunig M. Treatment of femoroacetabular impingement: preliminary results of labral refixation. Journal of Bone and Joint Surgery. American Volume 2006;88:2537 13. Fitzgerald RH Jr. Acetabular labral tears: diagnosis and treatment. Clinical Orthopaedics 1995;311:60–68 14. McCarthy JC, Noble PC, Schuck MR, Wright J, Lee J. The Otto E. Aufranc Award: the role of labral lesions to the development of early degenerative hip disease. Clinical Orthopaedics and Related Research 2001;393:25–37 15. Conn KS, Villar RN. Labrum lesions from the viewpoint of arthroscopic hip surgery. Orthopaedics 1998;27:699–703 16. Lephart SM, Ferris CM, Riemann BL, Myers JB, Fu FH. Gender differences in strength and lower extremity kinematics during landing. Clinical Orthopaedics and Related Research 2002;401:162–169 17. Stubbs A. Course notes: sports hip surgery, 2008 18. Bradshaw CJ, Bundy M, Falvey E. The diagnosis of longstanding groin pain: a prospective clinical cohort study. British Journal of Sports Medicine 2008;42:551–554 19. Seldes RM, Tan V, Hunt J, Katz M, et al. Anatomy, histologic features, and vascularity of the adult acetabular labrum. Clinical Orthopaedics and Related Research 2001;382:232–240 20. Hoaglund FT, Steinbach LS. Primary osteoarthritis of the hip: etiology and epidemiology. Journal of the America Academy of Orthopedic Surgery 2001;9:320–327 21. Blankenbaker DG, Tuite MJ. The painful hip: new concepts. Skeletal Radiology 2006;35:352–370 22. Kelly BT, Weiland DE, Schenker ML, Philippon MJ. Arthroscopic labral repair in the hip: surgical technique and review of the

literature. Arthroscopy 2005;21:1496– 1504 23. Byrd JW, Jones KS. Arthroscopic femoroplasty in the management of cam-type femoroacetabular impingement. Clinical Orthopaedics and Related Research 2009;467:736–746 24. Tannast M, Goricki D, Beck M, Murphy SB, Siebenrock KA. Hip damage occurs at the zone of femoroacetabular impingement. Clinical Orthopaedics and Related Research 2008;466:273–280 25. Beck M, Kalhor M, Leunig M, Ganz R. Hip morphology influences the pattern of damage to the acetabular cartilage: femoroacetabular impingement as a cause of early osteoarthritis of the hip. Journal of Bone and Joint Surgery. British Volume 2005;87:1012–1018 26. L’Hermette M, Polle G, Tourny-Chollet C, Dujardin F. Hip passive range of motion and frequency of radiographic hip osteoarthritis in former elite handball players. British Journal of Sports Medicine 2006;40:45– 49 27. Hunt D, Clohisy J, Prather H. Acetabular labral tears of the hip in women. Physical Medicine and Rehabilitation Clinics of North America 2007;18:497–520 28. Pfirrmann CW, Mengiardi B, Dora C, Kalberer F, et al. Cam and pincer femoroacetabular impingement: characteristic MR arthrographic findings in 50 patients. Radiology 2006;240:778– 785 29. James SL, Connell DA, O’Donnell P, Saifuddin A. Femoroacetabular impingement: bone marrow oedema associated with fibrocystic change of the femoral head and neck junction. Clinical Radiology 2007;62:472–478 30. Philippon M. Course notes: sports hip surgery, 2006 31. Neumann M, Cui Q, Siebenrock KA, Beck M. Impingement-free hip motion: the ‘normal’ angle alpha after osteochondroplasty. Clinical Orthopaedics and Related Research 2009;469:699–703 32. Nötzli HP, Wyss TF, Stoecklin CH, Schmid MR, et al. The contour of the femoral head-neck junction as a predictor for the risk of anterior impingement. Journal of Bone and Joint Surgery. British Volume 2002;84:556–560 33. Philippon M. ESSKA presentation, 2006 34. Byrd JW, Jones KS. Diagnostic accuracy of clinical assessment, magnetic resonance imaging, magnetic resonance arthrography, and intra-articular injection in hip arthroscopy patients. American Journal of Sports Medicine 2004;32:1668–1674 35. Van den Berg JC. Inguinal hernias: MRI and ultrasound. Seminars in Ultrasound, CT, and MR 2002;23:156–173 36. Leunig M, Podeszwa D, Beck M, Werlen S, Ganz R. Magnetic resonance arthrography of labral disorders in hips with dysplasia and impingement. Clinical Orthopaedics and Related Research 2004;418:74–80 37. Saw T, Villar R. Footballer’s hip a report of six cases. Journal of Bone and Joint Surgery. British Volume 2004;86:655– 658 38. Ganz R, Parvizi J, Beck M, Leunig M, sportEX medicine 2009;40(Apr):10-15

rehabilitation hip impingement et al. Femoroacetabular impingement: a cause for osteoarthritis of the hip. Clinical Orthopaedics and Related Research 2003;417:112–120 39. Dienst M. Hip arthroscopy: technique for positioning and distraction. Orthopade 2006;35:33–40 40. Fontana A. Course notes: sports hip surgery, 2006 41. Crawford K, Philippon MJ, Sekiya JK, Rodkey WG, Steadman JR. Microfracture of the hip in athletes. Clinics in Sports Medicine 2006;25:327-0-3 42. Philippon M. Unpublished data, AANA, 2006 43. Bedi A, Chen N, Robertson W, Kelly BT. The management of labral tears and femoroacetabular impingement of the hip in the young, active patient. Arthroscopy 2008;24:1135–1145 44. Byrd T. Course notes: sports hip surgery, 2008 45. Philippon MJ, Briggs KK, Yen YM,

online

Kuppersmith DA. Outcomes following hip arthroscopy for femoroacetabular impingement with associated chondrolabral dysfunction: minimum two-year follow-up. Journal of Bone and Joint Surgery. British Volume 2009;91:16–23 46. Johnston TL, Schenker ML, Briggs KK, Philippon MJ. Relationship between offset angle alpha and hip chondral injury in femoroacetabular impingement. Arthroscopy 2008;24:669–675 47. Stalzer S, Wahoff M, Scanlan M. Rehabilitation following hip arthroscopy. Clinics in Sports Medicine 2006;25:337– 357 48. Lewis CL, Sahrmann SA, Moran DW. Anterior hip joint force increases with hip extension, decreased gluteal force, or decreased iliopsoas force. Journal of Biomechanics 2007;40:3725–3731 49. Lewis CL, Sahrmann SA. Acetabular labral tears. Physical Therapy 2006;86:110–121

THE AUTHOR David Binningsley is employed by Sunderland Football Club as a senior physiotherapist. Originally from Durham, he graduated from the University of Teesside in 1998 with a BSc(Hons) in physiotherapy. After a brief spell working for the NHS at the University Hospital of North Durham, he joined the medical team at Middlesbrough Football Club, where he worked for the highly successful academy for three years. In 2002, David was recruited by Sunderland Football Club. His role is to provide assessment, treatment and rehabilitation for the first-team playing staff. David has a special interest in the hip pathologies of young athletes. He has developed a strong working relationship with the world’s leading hip surgeons and has overseen a great many hip surgeries.

Launch the videos by clicking on the images below

Videos and animations n Chondroplasty procedure video – an edited video showing a right hip CAM lesion. The surgeon removes the articular cartilage layer as well as subchondral bone. The normal procedure takes up to one hour. The camera is from a posterior portal and the femoral head and labrum are to the left. The hip is assessed dynamically throughout the process to check for impingement. n Hip ROM movie courtesy of Primal Pictures Ltd. – showing the bony articlulations of the hip joint online

Launch the videos by clicking on the images below

SuggeSted exerciSeS for femoro-acetabular impingement

1. Bosu lunge – work on strength and balance whilst stepping onto a upside down BOSU. A progression is to add in a medicine ball and/or bungee cord to add resistance. The drill can also be performed laterally.

2. Box step down – to facilitate gluteal muscles. Ensure the ASIS remain level and touch the heel onto the floor. The height of the box can be increased as the patient progresses.

5. Romans – begin in a standing position and lean forward and raise the leg behind you. The aim is to keep everything as flat as possible. This exercise is fantastic for recruiting both the gluteals and hamstrings, working on Vleemings sling principle. You can also progress this exercise with weights.

6. Split lunge – start with one foot on a raised surface (a box or stairs). Explode up, using the arms for propulsion. Change feet, with only the forefoot contacting the box. Four sets of four repetitions on each leg is a good starting point. Progression would include using a weighted vest or Vertimax.

3. Cable MR – to isolate the medial rotators of the hip, lie prone with a cable attached to the ankle. The knee is flexed to 90°. Add resistance as appropriate, rotate the hip across the body from full medial rotation. This can also be performed for lateral rotators. I prefer to do four sets to fatigue instead of a set number of repetitions.

4. Mirror drill – set up two boxes (approx 10m2) one person leads the other has to follow. It is best performed as a timed drill and jumps, forward rolls and slide tackle can be added. It can also be performed in opposite direction.

7. Squat hurdle – after performing a squat, immediately go into a series of explosive jumps over hurdles. Ideally to speed up the process, have two spotters take the Olympic bar after the squats have been performed.

8. Sidewinder (sw.mpg) – using an SAQ sidewinder attached to the ankles. Step forward and laterally, tapping the opposite foot on the swing through phase. The drill can be done purely laterally, or as if they were walking on a tightrope.

n Exercise movies - the online version of this article allows you to play individual movie clips of all the rehabilitation exercises above

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n Animation on arthroscopic surgery for femoroacetabular impingement (go to the sportex.net website>e-content>Animations>for clients>SWARM animations and choose Orthopaedics/Hip)

Chronic compartment syndrome of the leg The article defines acute and chronic compartmental syndrome of the leg and discusses the incidence, pathophysiology, aetiology and signs and symptoms of chronic compartmental syndrome. The value of specific investigations and of surgical or conservative treatment are discussed. By Dr Nat Padhiar, MSc PhD FCPodS

INTRODUCTION Pain in the lower leg brought on by exercise but relieved by variable periods of rest is a common complaint among athletes, particularly after an unaccustomed increase in activity or at the start of the season. The term “shin splints” or “fresher’s leg” is often used by athletes, trainers and doctors to describe the condition. These are non-specific terms and, although the history and symptoms have long been recognised, the term itself has never been defined restrictively. In 1966 the American Medical Association (AMA) published The Standard Nomenclature of Athletic Injuries (1). This was prepared by a subcommittee of the Committee on Medical Aspects of Sports and after extensive canvassing of the opinions of physicians, trainers, physical educators and other interested parties in sports medicine. They defined shin splints as “pain and discomfort in the leg from repetitive running on hard surfaces or forcible, excessive use of the foot flexors” and stated that “diagnosis should be limited to musculotendinous inflammations, excluding fracture or ischaemic disorders”. There was a mixed response to this definition, but in the main it was criticised widely. If nothing else, however, the AMA definition created enough interest in the subject for each author to express a preference for their own classification. There is now a broad agreement that most exercise-induced leg pain falls into one of the following 16

categories: n Pain of bony origin, eg. focal stress fracture and diffuse microfracture of stress reaction n Pain of osteofascial origin usually along the medial border of the tibia, eg. periostitis (often referred to as medial tibial stress syndrome; MTSS) n Pain of muscular origin, eg. exertional compartment syndrome (acute and chronic); the chronic form is commonly referred to as chronic compartment syndrome (CCS) n Pain due to compression of a nerve, eg. compression of the superficial peroneal or tibialis posterior nerve n Pain due to regional compression of a nerve at spinal and pelvis level, eg. radicular leg pain n Pain due to temporary vascular compromise, eg. popliteal artery entrapment syndrome.

COMPARTMENT SYNDROME Compartment syndrome is defined as a condition in which the circulation and function of tissues within a closed space are compromised by increased pressure within that space (2). The term “compartment syndrome” usually refers to localised myoneural ischaemia and occurs in acute and chronic forms with regards to aetiology, time sequence and reversibility.

Acute compartment syndrome Richard Volkmann first described the ischaemic contracture that followed the application of tight dressings: “Sciatic paralyses and contractures which have sportEX medicine 2009;40(Apr):16-22

diagnosis Chronic compartment syndrome Table 1: Various names given to acute compartment syndrome n Volkmann’s ischaemia

n Compartment syndrome

n Impending ischaemia

n Rhabdomyolysis

n Crush syndrome

n Exercise ischaemia

n Local ischaemia

n Traumatic tension ischaemia in muscles

n Acute ischaemia infarction

n Ischaemic necrosis contracture

n Anterior tibial syndrome

n Peroneal nerve palsy

n Calf hypertension

n Phlegmasia cerulean dolens

identical characteristics can be caused by bandages which are too tight, and thus cause constant constriction of the limbs” (3). He was defining the acute form of compartment syndrome. Acute compartment syndrome (ACS) is a significant clinical problem, causing major functional losses following a wide variety of traumatic, vascular, neurological, surgical, pharmacological, renal and iatrogenic conditions. When it occurs, it is a surgical emergency. Initially, confusing terminology was used to describe various sub-entities (Table 1) of ACS, masking the common aspects of the acute syndrome. Increased tissue pressure is the central pathogenic factor in compartment syndrome. This may result either from a decrease in the size of the compartment or from an increase in the volume of its contents (Table 2).

Table 2: Aetiological factors in compartment syndrome Decreased compartment size n Closure of fascial defects n Tight dressings n Localised Increased compartment content n Bleeding: major vascular damage n Bleeding disorder n Increased capillary permeability n Post-ischaemic swelling n Exercise (seizures, eclampsia) n Trauma (other than vascular) n Burns n Intra-arterial drugs n Orthopaedic surgery n Increased capillary pressure n Exercise n Venous obstruction (long leg brace) n Muscle hypertrophy n Infiltrated infusion n Nephrotic syndrome

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Childs collected 14 cases of acute forms of compartment syndromes from the literature, added one of his own and published the finding in the Annals of Surgery (4). This prompted several authors in the mid- and late 1940s to report on ACS. It is now a welldocumented condition.

Chronic compartment syndrome Although ACS was relatively well known, the chronic form was overlooked. Edward Wilson, a medical officer to Scott’s Antarctic expedition in 1912, unwittingly gave the first account of what was probably an exertion-related anterior compartment syndrome. The account of his own and Scott’s diary was written in 1910 and recovered from the expedition in which he perished (5). It was not until 1956 that Mavor first reported on the chronic form of compartment syndrome (6). This was in a young professional footballer who presented with a 2-year history of pain in the front of both legs, mainly occurring on exercise. Having exhausted all the conservative means, Mavor performed a successful fasciectomy of the fascia overlying the anterior tibial muscle. The postoperative phase was uneventful and the footballer returned to a successful career in the First Division. Since the 1960s there has been a steady flow of cases reported in the world literature coinciding with an upsurge of interest in this field. Reneman reported 61 cases in his series (7). Before this, nine other cases were reported in the literature. In addition, there was a significant development in the techniques for measuring intracompartment pressure (ICP). Thus, laboratory documentation of the diagnosis and pathophysiology of CCS became established. Matsen is worthy of note here, 17

as his classical article gave a unified concept of compartment syndrome (2). He observed that the unified concept proposes that the underlying features of all compartment syndromes are the same, irrespective of aetiology or location. Increased tissue pressure is by definition the central pathogenic factor in compartment syndrome. Compartment syndrome is a significant clinical problem.

DEFINITION Chronic compartment syndrome is “a reversible rise in tissue pressure to abnormal levels brought on by exertion and relieved by rest ... an increase in pressure within an enclosed space with potential to threaten perfusion and tissue viability” (8). It is a condition in which increased pressure within a closed anatomical space compromises circulation and the tissues within the space. It is due primarily to a relative inadequacy of musculoskeletal compartment size that is compounded further by an increase in muscle volume with activity. It is estimated that skeletal muscles increase in volume during exercise by as much as 20%. The patient typically presents with pain on exercise, which is relieved by rest. The condition is also known as “recurrent compartment syndrome”, “exercise-induced

compartment syndrome”, “subacute compartment syndrome” and “exertional compartment syndrome”. Mubarak and Hargens prefer to describe it as “chronic compartment syndrome”, a term that is universally accepted and in common use (9).

INCIDENCE Chronic compartment syndrome is much more common than the acute form, according to current literature. Several authors have reported a large series of patients with CCS: Reneman reported 61 patients (7), Sudman 51 patients (10), Detmer et al. 100 patients (11), and Allen and Barnes 110 patients (12). It occurs predominantly in soldiers and individuals involved in sporting activities. The condition is frequently bilateral and is predominant in males, and people involved in running sports are widely represented. The syndrome is common in the four lower leg compartments (Fig. 1), but it can also occur in compartments of the forearm and foot. Increasingly, other muscle compartments are involved and are reported as case histories.

PATHOPHYSIOLOGY All theories concerning the pathophysiology of CCS propose an increase in tissue pressure to a level that results in a compromise of muscle perfusion. This may be due to either excessive swelling of the muscles or insufficient compliance of the surrounding fascia.

Normal situation In normal exercising muscle, the capillary bed undergoes an increase in both surface area and filling pressure, causing an increase in resorption, with the result that the muscle increases in volume – by as much as 20% during vigorous exercise. Active muscle is not perfused during contraction. Relaxation allows adequate perfusion during the relaxation phase. Perfusion and function can be compromised if the pressure fails to fall to resting levels between contractions or the contraction is sustained.

Abnormal situation Figure 1: Cross-section of the leg, showing the four compartments

In symptomatic situations, the factors responsible for an abnormal increase in pressure following exercise remain

speculative. Theories suggest that the elevated intramuscular pressure is initiated by arterial or venous occlusion or is due to increased interstitial fluid as a result of increased hyperosmolarity. Tissue pressure Increased tissue pressure may result from the following: n Limited or decreased compartment volume, as a result of tight, thickened fascia, arteriovenous (AV) fistula or constitutionally small space. This may mean a loss of elasticity and decreased compliance of the fascia, implying a greater resistance to the volume change required for exercising skeletal muscle, thus resulting in a tissue pressure rise. Detmer et al. published results of fasciotomies performed on 100 patients with CCS and at the time of surgery took 36 fascial biopsies (11). Fascial thickness was measured and found to be greater than 600 microns in 25 of the 36 patients; in some it was greater than 1200 microns. The significance of this is unconfirmed, as no information is available regarding the normal thickness of the fascia at this site. n Increased compartment content/ volume, due to muscle swelling, hypertrophy or anomalous muscle insertion. The increase in muscle volume produces a sufficient increase in pressure within the small unyielding compartments to limit venous outflow by a collapsing of the veins. This increases capillary resistance, induces arterial vasospasm, decreases capillary perfusion, and triggers extravasation of fluid into the compartment, which further increases compartment pressure and creates ischaemic pain and/or tissue destruction. Hargens et al., in their canine study, infused autologous plasma into the compartment in 1-ml aliquots and plotted the pressure change (13). They revealed a direct correlation between pressure and volume, depending largely on the initial compartment volume. They also showed that little, if any, fluid permeated the osseofascial boundaries in the lower leg and that hydrostatic pressures within one compartment are not transmitted to adjacent compartments. General principles suggest that the pressure and volume within a compartment are dependent on the compliance of sportEX medicine 2009;40(Apr):16-22

diagnosis Chronic compartment syndrome the fascia. Qvarfordt et al., in a study of 15 patients with CCS, showed that there was a pronounced increase in lactate concentration immediately post-exercise in the same patients before fasciectomy (4.9 +/- 0.6 mmol/ kg) compared with post-exercise after fasciotomy (3.1 +/- 0.7 mmol/kg) (14). They also observed an increase in post-exercise water content both before and after fasciectomy, confirming understood physiology in exercising muscle. Wallensten and Eriksson also showed an increase in muscle water content in the anterior compartment following exercise but reported no obvious increase in the lactate concentration (15). n Externally applied pressure, eg. taping, bracing and casts. Tissue perfusion There are several theories that attempt to explain how the rise in intramuscular pressure causes a compromise in tissue perfusion: n Arterial spasm: this is thought to be mediated by a non-sympathetic antidromic reflex. n Critical closure theory: if tissue pressure rises significantly or if arteriolar perfusion pressure drops, then the gradient across the vessel wall drops below the critical closing pressure necessary to keep the vessel patent (law of Laplace). n Microvascular occlusion theory: rising tissue pressure causes passive collapse of soft-walled capillaries, resulting in a reduced flow. n AV gradient theory: increase in tissue pressure increases the local venous pressure, reducing the local AV gradient. This results in reduced blood flow and oxygenation, which impairs muscle function and viability. Whiteside et al. published the results of a large series, using a dog as a model for CCS. They showed that tissue injury increased as the duration of ischaemia increased (16). As the pressure within a closed compartment rises, the perfusion of tissue within that compartment declines progressively until it becomes significantly hampered at a level about 10–20 mmHg below the diastolic pressure. When the pressure within the closed compartment rises equals the diastolic pressure, tissue perfusion ceases, even though distal pulses may still be present. When the pressure www.sportEX.net

approaches systolic pressure, there is no tissue perfusion and the distal pulses disappear. Heppenstall et al. put forward the concept of perfusion index (Delta-P) (17). This was the difference between mean arterial blood pressure and ICP. Heppenstall et al. proved that the patient’s blood pressure was an important factor and that ICP was only an indirect indicator of muscle viability.

Summary of pathophysiology Increased tissue pressure is a prerequisite for the development of both the acute and chronic forms of compartment syndrome. The syndromes differ only in their degree of severity. In susceptible individuals, the fascial compartment is too small to accommodate the 20% increase in size of the muscle mass that typically occurs with heavy exercise.

AETIOLOGY Chronic compartment syndrome commonly affects young, active individuals who participate in endurance and high-impact sports. The symptoms are often related to running and it is therefore seen in many sports, as running forms part of many training programmes. Beckham et al. compared the anterior compartment pressure in asymptomatic competitive runners and cyclists (18). The results showed that there was no significant difference in the resting pressures, but the pressures were significantly higher in runners after maximal exercise (P=0.016). Unaccustomed increase in activity or symptoms occurring at the start of the season was reported by Allen and Barnes (12) as being relevant and significant. Others have reported symptoms occurring after: n an increase in activity, training and intensity n a change of training or playing surface n a change of footwear n a combination of some of the above. Abnormal biomechanical factors are considered widely to be predisposing factors. The exact aetiology and the reason why some individuals are susceptible to CCS remain unknown, but a pattern is emerging as larger series are reported.

The cardinal feature of CCS is pain on exertion that is relieved with rest CLINICAL SYMPTOMS The cardinal feature of CCS is pain on exertion that is relieved with rest. Wallensten and Eriksson described this pain as “claudication-like” (15). Mavor described his patients’ symptoms as “tightness” rather than a cramp, increasing in severity with exercise and always forcing them to rest (6). The description of the symptoms, however, is not consistent, as shown by Reneman, whose subjects used the terms “piercing”, “contracting”, “cramplike” and “burning” (7). Medial-sided tibial pain is usually described as “soreness” or a “dull ache”, often as deep pain in the calf. The lateral-sided tibial pain may be more aching and cramping in quality

Figure 2: Bilateral anterior and deep posterior compartments cannulated, catheterised and linked to pressure transducers

Figure 3: Online dynamic intracompartmental pressure (ICP) tracing of bilateral anterior and deep posterior compartments

Figure 4: Superficial fasciotomy of the anterior compartment

The amount of exercise required to bring on pain varies greatly between individuals. Usually for an individual the amount of exercise required to provoke symptoms is constant. The pain of CCS usually forces the individual to stop. The pain is usually well-localised, but it may radiate down the foot or be associated with paraesthesia. In these cases, the pain is probably due to neural compression. Wiley et al. describe the location of pain associated with individual compartments (19). It is evident that there is no “usual” location of pain, as there are large variations in the description and site of pain.

CLINICAL SIGNS ON EXAMINATION

Figure 5: Danger of wound dehiscence and infection when a long incision is performed during a fasciectomy

but is extremely variable. Detmer et al., in his series of 100 consecutive patients, described the following symptoms and their prevalence (11): n consistent history of pain with exercise n progressive worsening with continuing exercise (94%) n reduction/cessation of exercise reduced the pain (85%) n aching pain (85%) n tightness/cramps (81%) n bilateral symptoms (82%). Pain from CCS is not present at rest and is rarely provoked by walking, except in severe cases, where pain may occur on walking or even at rest.

It is generally accepted that surgery (fasciotomy and fasciectomy) provides the only effective treatment for this condition 20

Passive examination is essential, even though physical examination is unlikely to be helpful. The examination may reveal bulky muscles, tense muscle compartment(s), a fascial defect or hernia, and sometimes bruising. Physical examination following provocative exercise may reveal tenderness over the affected muscle compartment, but this is variable. As there are few signs associated with the condition, negative findings are definitely the most useful. However, some authors have reported the following: n slight oedema and thickening of the subcutaneous border of the tibia n highly developed musculature and tension over the associated compartment n small fascial defects and muscle hernias (incidence 20–60%) n neurological symptoms, with occasional pain and weakness on passive stretch of the muscles involved n vascular disturbances (rare).

Summary of clinical symptoms and signs Clinical findings are considered by some to be the most important feature, but others challenge their reliability. Amendola and WebsterBogaert correlated clinical features with pressure measurements and discovered that the most important criteria for CCS were (20): n age under 30 years n reproducible pain with exercise n no tenderness on palpation n bilateral symptoms n activity profile such as running,

where there is repetitive loading of the lower extremity. Wiley et al. used clinical criteria to select 16 patients for fasciotomy and reported good results in 14 of them (19). Several studies, however, have shown that not all patients suspected of having CCS entirely on clinical grounds have elevated ICPs. In nearly all cases, the findings of physical examination are decidedly unimpressive and unlikely to be helpful. History may be helpful but investigations are necessary for two main reasons: n to carry out a differential diagnosis n to confirm the diagnosis of CCS objectively.

INVESTIGATIONS Intracompartment pressure measurement Intracompartment pressure (ICP) measurement remains the mainstay of objective diagnosis of CCS. Several methods of direct measurement of ICP have been developed. Styf neatly classifies them as follows (21): n Injection technique: French and Price were the first to measure ICP on two patients using the needle manometer technique (22). There was criticism of this technique: it was highlighted that the ICP could not be determined during active muscle contraction and that long-term continuous monitoring was impossible. This is the main disadvantage and limitation of this technique when dynamic monitoring is required. n Infusion technique: this technique is suitable for recording both the dynamic and the resting pressures. This method reduces the problem of catheter blockage, but care has to be taken to reduce infusion of saline below 3 ml/h in order to prevent a local rise in tissue pressure. A multi-holed Teflon™ catheter allows infusion rates as low as 0.2 ml/h. n Non-infusion technique: this technique is ideal, but it is not readily available. The occlusion of the catheter by muscle fibres and blood clots remains a problem but can be alleviated by using Rorabeck™ slit catheters and repeated flushing with 0.1 ml of heparinised saline. The technique involves cannulating a slit catheter that is primed with heparinised saline via a 17g Medicut™ needle. The catheter is linked to a pressure transducer (Fig. 2) sportEX medicine 2009;40(Apr):16-22

diagnosis Chronic compartment syndrome and a recording system, which displays online information (Fig. 3). The main advantage of this technique is that it allows the ICP to be measured in the patient’s physical activity that provokes the symptoms and, often, the rise in ICP is exercise-specific (23). n Micro-tip transducer technique: this is the latest development in recording pressures utilising solid-state intracompartment transducers (STIC). Recent advances in technology have led to a quest for alternative methods that are non-invasive or less invasive than ICP studies.

Magnetic resonance imaging Magnetic resonance imaging (MRI) provides a non-invasive method of investigation that has been adapted mainly for research purposes in CCS. Proton-density MRI scans have shown specific changes after exercise, and these are believed to be due to increased extracellular water content, which correlates with previous histochemical studies. At this stage, MRI remains a research technique and its role in clinical diagnosis is yet to be established.

Nuclear magnetic resonance spectroscopy Phosphorous-31 nuclear magnetic resonance (NMR) spectroscopy provides a method to assess the physiological and metabolic characteristics of exercising skeletal muscle without ionising radiation or an invasive procedure. The initial studies were performed on the dog models of ACS and involved arterial occlusion for 6–8 hours. These methods involved assessment of the ratio of phosphocreatine to one of its metabolic products (inorganic phosphate) and muscle pH, which represents the commencement of anaerobic metabolic in response to inadequate oxygenation. NMR spectroscopy presents exciting opportunities to understand the pathophysiological processes involved in CCS. Its role in clinical diagnosis, however, is severely limited by cost and availability.

Nuclear medicine Nuclear medicine proposes techniques to assess local blood flow using www.sportEX.net

133-xenon or 99-technetium-MIBI, but its application in CCS is very much in its early stages. Styf et al., using 133-xenon, found that the decreased blood flow during exercise correlated well with the pathological increase of muscle relaxation pressure in symptomatic legs and suggested that blood flow may be impeded at intramuscular pressures between 30 mmHg and 50 mmHg (24). In Amendola et al.’s MRI study, an assessment of blood flow was made using nuclear medical techniques (99-Tc-MIBI) (25). There was evidence to suggest a direct correlation with local blood flow; however, no consistent ischaemic changes were found, despite pressure and MRI changes. Preliminary studies with a similar technique have shown some changes in CCS, but the most dramatic result has been shown by Jenner in a case of popliteal artery entrapment syndrome (26).

Quantitative hardness Palpatation has long been part of the clinician’s armamentarium, and hardness of the anterior compartment post-exercise has been described by some authors as a sign in chronic compartment syndrome. A recent study proposes a technique similar to ophthalmic tonometry, which assesses pressure in the anterior chamber of the eye, developed by Von Graefe in 1862. An experimental piston probe indents the muscle compartment by an amount called “quantitative hardness”, and this is correlated with ICP. Preliminary laboratory studies show a promising correlation. The main attraction is that the technique is simple and non-invasive. Further studies are required, however, to establish its reliability and role in diagnosing CCS.

Ultrasound Ultrasound has a great advantage in imaging soft tissue structures. It is dynamic and inexpensive, gives rapid online assessment, is radiation-free, and maintains high resolution. The use of ultrasound in sports medicine practice has a great potential as experience with its application increases. Recently ultrasound has been used as a technique to examine the crosssectional area of muscle compartments

(27,28). Its use is limited by the fact that CCS is a dynamic condition and that patients are usually examined while resting on a couch.

TREATMENT Surgery Once the diagnosis of CCS is confirmed with dynamic intracompartment pressure study, it is generally accepted that surgery (fasciotomy and fasciectomy) provides the only effective treatment for the condition. The main aim of the fasciotomy (Fig. 4) is to increase the compartment volume by dividing the entire length of the fascia through a short skin incision. The outcome of surgery is usually very good, but it varies between surgeons and compartments decompressed. Abramowitz and Schepsis (29) found that, in their series, patients with anterior compartment decompression had a better outcome than patients with deep posterior compartment decompression. Fasciectomy (removing a ribbon of fascia) is usually performed as an open procedure and requires a longer incision. It is usually performed when fasciotomy has failed. Turnispeed and Detmer carried out decompression in 209 patients (100 fasciotomy, 109 fasciectomy) and found a higher success rate with fasciectomy (98%) compared with fasciotomy (89%) (30). This was partly because better decompression is achieved by direct visualisation, but this requires a longer incision, which increases the risk of infection and dehiscence (Fig. 5). The success of surgery also depends on postoperative rehabilitation. It is generally agreed that patients should be weight-bearing as soon as possible in order to keep the compartment open and bigger. Surgery carries the usual risk factors, such as neuropraxia, infection, dehiscence, haematoma, deep vein thrombosis (DVT), and arterial and venous damage.

Conservative treatment The condition is self-limiting, as pain occurs mainly with exercise and is better with rest, so giving up the activity that causes the pain is an effective treatment. This is usually not acceptable to most athletes, however, and is not the advice that clinicians should offer. Various conservative treatment 21

measures have been implemented, but only with short-term benefit (31) and in most cases never achieving the ultimate goal. Conservative treatment may address the following: footwear, training surface, intensity and level of activity, abnormal biomechanics, core stability issues, neuromuscular involvement and training errors. As part of conservative management, non-steroidal antiinflammatory drugs (NSAIDs), analgesics, heat, ice, rest, ultrasound, physiotherapy, acupuncture, steroid injections, foot orthoses, osteopathy, deep massage, trigger point work and homeopathy have been used, but they have been found to have only short-term benefits and poor long-term success.

CONCLUSION Chronic compartment syndrome is a physiological condition that is relatively common among endurance athletes. Diagnosis is based on detailed history and supported by elevated intracompartment pressure study. The most definitive treatment is surgical decompression allowing a better prognosis for the athlete to return to sport. References 1. Rachun A, Allman FL, Blazina ME, Cooper DL, Schneider RC, Clarke KS. Standard nomenclature of athletic injuries. American Medical Association 1966 2. Matsen FA. Compartmental syndrome: a unified concept. Clinical Orthopaedics and Related Research 1975;113:8–14 3. Volkmann R. Die ischamischen Muskallahmangen und Kontrakturen. Centralblatt fur Chirugerie 1881;51:799– 803 4. Childs CG. Non-infective gangrene following fractures of the lower leg. Annals of Surgery 1942;116–721 {Note to Tor: page range OK?} 5. Freedman BJ. Dr Edward Wilson of the Antarctic. Proceedings of the Royal Society of Medicine 1953;47:7–13 6. Mavor GE. The anterior tibial syndrome. Journal of Bone and Joint Surgery 1956;38B:513–517 7. Reneman RS. The anterior and lateral compartmental syndrome of the leg due to intensive use of muscles. Clinical Orthopaedics and Related Research 1975;113:69–80 8. Black KP, Taylor DE. Current concept in the treatment of common compartment syndromes in athletes. Sports Medicine 1993;15:406–418 9. Mubarak SJ, Hargens AR. Exertional compartment syndromes. Presented at the AAOS Symposium on the Foot and Leg in Running Sports, 1982, St Louis, MO, USA 10. Sudman E. The painful chronic anterior 22

lower leg syndrome. Acta Orthopaedica Scandinavica 1979;50:573–581 11. Detmer DE, Sharpe K, Sufit RL, Girdley FM. Chronic compartment syndrome: diagnosis, management and outcomes. American Journal of Sports Medicine 1985;13:162– 170 12. Allen MJ, Barnes MR. Exercise pain in the lower leg. Journal of Bone and Joint Surgery 1986;68B:818–823 13. Hargens AR, Akeson WH, Mubarak SJ, Owen CA, Evans KL, Garetto LP, Gonslave MR, Schmidt DA. Fluid balance within the canine anterolateral compartment and its relationship to compartment syndrome. Journal of Bone and Joint Surgery 1978;60A:499–505 14. Qvarfordt P, Christenson MD, Eklof B, Ohlin, Saltin B. Intramuscular pressure, muscle blood flow and skeletal muscle metabolism in chronic anterior compartment syndrome. Clinical Orthopaedics and Related Research 1983;179:284–290 15. Wallensten R, Eriksson E. Intramuscular pressures in exercise induced lower leg pain. International Journal of Sports Medicine 1984;5:31–35 16. Whiteside TE, Hirada H, Morimoto K. The response of skeletal muscle to temporary ischaemia: an experimental study. Journal of Bone and Joint Surgery 1971;53A:1027 17. Heppenstall R, Sapega I. Compartment syndrome: a quantitative study of high energy phosphorous compounds using magnetic resonance spectroscopy. Journal of Trauma 1989;29:1113–1119 18. Beckham SG, Grana WA, Buckley P, Breazile JE, Claypool PL. A comparison of anterior compartment pressures in competitive runners and cyclists. American Journal of Sports Medicine 1993;21:36– 39 19. Wiley JP, Clement DB, Doyle DL, Miller SD. A primary care perspective of chronic compartment syndrome of the leg. The Physician and Sportsmedicine 1987;15:111–120 20. Amendola A, Webster-Bogaert S. Diagnostic criteria for the exertional compartment syndrome. Presented at the Annual Meeting of the American Academy of Orthopaedic Surgeons, 1995, Orlando, FL, USA 21. Styf J. Chronic exercise induced pain in the anterior aspect of the lower leg: an overview of diagnosis. Sports Medicine 1989;7:331–339 22. French EB, Price WH. Anterior tibial pain. British Medical Journal 1962;2:1290– 1296 23. Padhiar N, King JB. Exercise induced leg pain: chronic compartment syndrome. Is the increase in intra-compartment pressure, exercise specific? British Journal of Sports Medicine 1996;30:360–362 24. Styf J, Korner L, Suurkula M. Intramuscular pressure and muscle blood flow during exercise in chronic compartment syndrome. Acta Orthopaedica Scandinavica 1987;58:139–144 25. Amendola A, Rorabeck CH, Vellett D, Vezina W, Rutt B, Nott L. The use of MRI in exertional compartment syndromes. American Journal of Sports Medicine

online

Youtube playlist on compartment syndrome 1990;18:29–34 26. Jenner J. Personal communication, 1994, Cambridge, UK. 27. Martinson H, Stokes MJ. Measurement of anterior tibial muscle size using real time ultrasound imaging. European Journal of Applied Physiology 1991;63:250–254 28. Young D, Hughes I, Russell P, Parker MJ, Nicholls PJR. Measurement of quadriceps muscle wasting by ultrasonography. Rheumatology and Rehabilitation 1980;19:141–148 29. Abramowitz AJ, Schepsis AA. Chronic exertional compartment syndrome of the leg. Orthopaedic Review 1994;23:219– 226 30. Turnispeed W, Detmer DE, Girdley. Chronic compartment syndrome: an unusual cause of claudication. Annals of Surgery 1989;210:557–563 31. Styf JR, Korner LM. Diagnosis of chronic anterior compartment syndrome in the lower leg. Acta Orthopaedica Scandinavica 1987;58:139–144

Videos

The Authors Dr Nat Padhiar, MSc PhD FCPodS, graduated in podiatry from Chelsea School and pursued a career in podiatric sports medicine and podiatric surgery. In 1989 he was awarded a research-based MSc. In 1993 he became fellow of the Surgical Faculty, College of Podiatrists. In 1999 he was awarded a PhD in the field of orthopaedics and sports medicine from St Bartholomew’s and the Royal London School of Medicine and Dentistry, Queen Mary College, London University. In 1997 he was given a gold award for his presentation at the Scientific Meeting of British Association of Sports and Exercise Medicine. The presentation was in the field of chronic compartment syndrome, which was the basis of his PhD thesis. He holds a dual consultant podiatric surgeon post at the Royal London Hospital (BLT) in the Musculoskeletal and Surgical Directorate and also at the Mile End Hospital (THPCT) in the Foot Health Department. He was recently made an honorary member of the European College of Sport and Exercise Physicians.

sportEX medicine 2009;40(Apr):16-22

diagnosis arterial compression

Arterial compression syndromes at the shoulder part 2: diagnostic arm manoeuvres By Claire Stapleton, MCSP

INTRODUCTION Part 1 of this article (sportEX medicine 2009;39:22-25) presented a description of arterial compression syndrome at the shoulder. In brief, two compression sites at the subclavian artery and two compression sites at the axillary artery were described, as well as compression of the posterior humeral circumflex artery. This part of the article continues the theme of arterial compression syndrome at the shoulder but focuses on diagnostic arm manoeuvres used in the physical examination, discusses some diagnostic dilemmas, and highlights some areas that require further research. Upper-limb manoeuvres such as Adsonâ&#x20AC;&#x2122;s test (1), the hyperabduction manoeuvre (2), the elevated arm stress test (EAST) (3) and the costoclavicular manoeuvre (4) aid the diagnosis of arterial compression syndromes, either with or without advanced imaging techniques such as computed tomography (CT), magnetic resonance imaging (MRI), angiography and ultrasonography. It is assumed that these manoeuvres stress the vasculature to accurately reproduce the signs (eg. radial pulse disappearance, visible restriction or occlusion of blood flow, reduction in vessel diameter, doubling of or dampened peak systolic velocity (PSV) response) and symptoms (eg. ischaemic pain, paraesthesia, anaesthesia, heaviness) of vascular compromise. Alternatively, reproducing the arm position (usually an overhead-throwing arm position) that a specific athlete performs repeatedly is used as a diagnostic test position while pulse, blood pressure and blood flow are monitored. Unfortunately, in clinical practice, the diagnosis of vascular compromise remains a difficult challenge due to poor sensitivity and specificity of tests (5).

DIAGNOSIS WITHOUT ADVANCED IMAGING TECHNOLOGY Descriptions of these tests vary throughout the literature in terms of the movements incorporated and the terms used. However, most of the manoeuvres utilise several components that are capable of causing compression at more than one of the vulnerable sites (scalene triangle, costoclavicular space, retro-pectoralis minor space, anterior to the humeral head and the quadrilateral space syndrome), making localisation of the specific anatomical site of arterial compression difficult (Table 1). As has been reported, compression at the subclavian artery in particular is thought to result from bony anomalies such as cervical ribs and anomalous first ribs. However, symptoms do www.sportEX.net

This article covers one aspect of upper-limb vascular assessment. The outcome of diagnostic arm manoeuvres with or without advanced imaging equipment must be interpreted with the subjective history and other physical findings in order to exclude differential diagnoses and to determine whether a positive result should be considered clinically significant. The article focuses on diagnostic arm manoeuvres used in the physical examination, discusses some diagnostic dilemmas, and highlights some areas that require further research. not present in these individuals early in life, suggesting that other factors are contributory to the condition. In addition, many patients benefit from conservative measures such as muscle stretches, soft-tissue releases, manual therapy, posture correction, acupuncture and taping to relieve symptoms from neurovascular compression syndromes, again suggesting that factors other than bony anomalies are at fault. It would, therefore, be valuable to physiotherapists to be able to locate the specific site of arterial compression in order to achieve effective results by targeting treatment at specific anatomical borders. With knowledge of the vulnerable sites for arterial compression and their respective anatomical borders, a stepby-step approach to diagnosis may prove more useful than a single â&#x20AC;&#x2DC;catch-allâ&#x20AC;&#x2122; diagnostic arm manoeuvre. The author recommends assessing the effects of (1) deep inhalation, (2) scapula retraction and (3) cervical rotation/extension, in isolation and held for 10 seconds, and then (1) and (2) in combination, before undertaking any manoeuvre involving abduction. Abduction over 40o becomes problematic as the clavicle starts to elevate and rotate posteriorly, producing a scissor-like motion with the first rib; this results in less space for the underlying structures, such as the subclavian artery. As a consequence, when the arm is abducted, compression at the costoclavicular space cannot be differentiated from any other site. However, the performance of deep inhalation and scapula retraction in isolation, early in the assessment, would give a better indication of whether the site is the cause of symptoms. 23

Figure 1: Duplex ultrasound image of the axillary artery, with the arm in a rested neutral position

Figure 2: Duplex ultrasound image of the axillary artery, with the arm in a hyperabducted position

DIAGNOSIS WITH ULTRASOUND

as PSV, to be calculated. Figure 2 shows a doubling of the PSV compared with Fig. 1 (see the spectral waveform scale) as well as obvious changes in the artery diameter. It is speculated that these changes resulted from movement of the humeral head. Spencer and Reid (7) proposed a theoretical model that described an increase in PSV simultaneously with a reduction in vessel diameter. Their model predicts that diameter reductions have to be greater than 50% before PSV changes will occur. As a result, studies and clinical assessments use a doubling of PSV in the stress manoeuvre compared with the neutral arm position to identify a clinically significant arterial narrowing (this refers to cases where the measurement is obtained within the narrowed segment) (8). Where the measurement site is distal to the narrowed segment, a non-quantified dampened PSV with spectral broadening of the Doppler waveform indicates clinically significant compression (8). This classification is used as the standard clinical criteria for diagnosis of clinically significant arterial compression.

Due to recent advancements in technology, ultrasound is now the preferred imaging choice for suspected vascular compression syndromes. When assessing for an upperlimb arterial compression syndrome, sonographers use the same arm manoeuvres, ie. costoclavicular manoeuvre and hyperabduction manoeuvre, as we have discussed already (6). With increasing numbers of physiotherapy departments and practices having access to diagnostic ultrasound machines for musculoskeletal assessment and biofeedback, the use of ultrasound to assess the vasculature and confirm diagnoses of suspected arterial compression syndromes has the potential to be a valuable tool for all physiotherapy clinics. It should be noted, however, that the success of using ultrasound for vascular assessment is operator-dependent and requires substantial training and practice. Figures 1 and 2 demonstrate the assessment of the third portion of the axillary artery with duplex ultrasound (combined B-mode and Doppler), with the arm in a neutral position (approximately 40o abduction) and in the hyperabduction manoeuvre (120o abduction, 30o horizontal extension, 90o external rotation), respectively. The splitscreen facility allows simultaneous viewing of the artery in B-mode ultrasound and the spectral waveform. The latter allows an estimation of the blood-flow characteristics, such

DIAGNOSTIC DILEMMAS Generally, therapists without access to advanced imaging equipment use a reduction of the radial pulse pressure or pulse disappearance (comparing the at-rest arm position with the diagnostic arm manoeuvre) as indicative of a positive

Table 1: Diagnostic arm manoeuvres for upper limb arterial compression syndromes, their component parts and the anatomical sites compressed Deep Scapular Cervical Cervical Cervical Abduction Glenohumeral Glenohumeral Exercise Site of (hand inspiration retraction extension rotation rotation external horizontal arterial gripping) (towards (away from rotation extension compression affected side) affected side) Adsonâ&#x20AC;&#x2122;s

Modified Adsonâ&#x20AC;&#x2122;s 3 3 3 3 3

3 AER 3 3

Costoclavicular

ST, CC ST, CC, RPM, HH, QSS CC, (ST) CC, RPM, HH,

QSS EAST QSS

Hyperabduction 3 3 3 3

CC, RPM, HH, ST, CC, RPM, HH, QSS

CC, costoclavicular space; HH, humeral head; QSS, quadrilateral space syndrome; RPM, retro-pectoralis minor; ST, scalene triangle. 24

sportEX medicine 2009;40(Apr):23-26

diagnosis arterial compression

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and haemodynamically significant (8,12); however, this figure test. However, an investigation to determine the false positive does not take into account changes in orthostatic pressure. rates of vascular thoracic outlet syndrome (vTOS) diagnostic To date, no published studies have investigated the effect of arm manoeuvres reported pulse alteration to be an unreliable changing posture on upper-limb blood-flow characteristics, measure (9). The reported lack of reliability for such tests such as pulse pressure, blood pressure or PSV, during highlights the importance for clinicians to use reproduction diagnostic arm manoeuvres. It would be beneficial for of the patient’s symptoms, in addition to pulse and blood clinicians to know the most appropriate subject positioning pressure measurements and advanced imaging technology, for sensitivity and specificity of the test manoeuvre, or at to confirm a positive test. least to have available a diagnostic criteria for blood-pressure However, the use of advanced imaging technology in changes that take into account the effects of orthostatic diagnosis is not without error. Diagnostic tests for vascular pressure. compression shown to reproduce vascular By Author have namebeen caps Finally, the criteria used to detect clinically significant occlusion notexonly in symptomatic patientsambut also in reet, si exerosto odolortin henim arterial compression with ultrasound are based on the asymptomatic individuals. ipit luptatue erilis at. Previous research by our team vascular demands of activity levels in the average individual. revealed that approximately 20% healthy asymptomatic In hent nonsecte ea adipisi eaoffeu It should be noted that athletes demand much more than individuals demonstrate clinically significant (more than 50% facipsustie voluptatum vel ex exeraesto their sedentary counterparts from the vascular system; diameteradreduction and/or a doubling of PSV)ercompression conulla molendrem zzriuscilis nim erosto therefore, smaller limitations to blood flow become more of theeuis thirdnulla portion of the axillary sum at, corerciduis aliquiartery esto with del ilthe arm significant during high-intensity activity, presenting as positioned at 120 degrees abduction, 30 degrees horizontal ullam ipit praessed eumsandre vel dolessequi symptom production or deterioration of performance (8). extension andvel 90dunt degrees external rotation (10). This was in et ulluptatum amcon ero odolorperate Schep et al. suggested that a 10–30% reduction in the vessel keepingnos with the findingsdionsed of Mochizuki et al., who investigated exerit endreraestis dionsed diameter the false-positive hyperabduction diagnostic modolor peraessitrate inisi oftethe commolo reetum qui esectetum et lor sum dion esequatue dolut may prove to have significant implications on an elite athlete’s performance (13). However, smaller limitations manoeuvre with sum magnetic resonance (MR) angiograms bla consequam, delessis autpat velismod dolore ent non utat praese min ut aliquamet to blood flow may not be detected at rest. As with the for alit occlusion theelit posterior humeral circumflex artery tis am nimofalis lorting ea commy niam digna(afeui blan hendionse dolupta tumsandre detection of external iliac artery endofibrosis in the lower branch of the axillary artery) and found occlusion induisi. 80% venisi. limb (14), the addition of exercises (eg. handgrip or elbow (eight shoulders) of healthy asymptomatic controls (5). Scum zzrit nim dolorem voloboreet exercises) may be required to increase blood flow Similarly, Rohrer et al. measured axillary artery compression praesto euguer sum dolendit deliquisflexion at Subheading 1 one here and,niam, therefore, to increase the blood pressure drop should and systolic blood pressure placed er iureet, quatuer aeseniatet Subheading 2 two here change with shoulders accumsan in throwing abduction and external velit ulla augiamet dunt iril ipit augue an minarterial lesion exist (15). Roos and Owens suggested the l the Heading to position go here(extreme Pute dolut am velisi. addition of handgrip exercises to the abducted, externally rotation) in baseball pitchers, lore athletes and non-athletes (11). autem illuptat lum ip ea consequ esequis Ignisl ut accum quisissequat modolore Caption to go here to here to fill range left or right rotated arm position (16); however, as yet, there is no Out of 92 tested, a reducedissecte internalcor alit euisit niate eummy non magnis nimshoulders do odolobor alit, 83% quis showed dolore conse. diameter of the artery ultrasound, 56% ullummod tie modolore magna coreetstandard nullamet,protocol for blood pressure or ultrasound that l Heading to axillary go here dipison ateduplex dolortie tat exercise, standardises the workload of the showed a drop in blood pressure of 20mmHg commodolore velenim doloreet, quis incorporates nonsed venis nonulputpat illa feum dolor iusci eummy or greater upper when in theatis throwing in 13% blood tie tatetum vel ute tem adit alit wis eu feu limb muscles, or provides a criterion for diagnosis. nonullaplaced feum nos exeriureposition, duis alit,and conse It should be highlighted that this article covers only one pressure was siundetectable. These results indicate that facipsu msandipit ilit lorero dionull umsandre exer seniam, eriliquat luptat et alisi. aspect of upper-limb vascular assessment. The outcome normal asymptomatic subjects reactdolobor to the test in feuis such augueros a doloreet ilisi ullutem nonse Ipismodit in ut ipiscilit ut nonum of diagnostic arm manoeuvres with or without advanced manner couldcor clinically be et defined It is feum eumsan henit wis nonsequis deliquis eu senissimthat quamet, si tincip ex et falsely luptat. as positive. uncertain whether this sumsandiam, induced intermittent a ut vel ut ulla consequate imaging faccumis vel tat nos equipment must be interpreted with the subjective Duismod olumsandrer quating compression history and other physical findings in order to exclude true positive be considered incidental feuisci duisci tisi. eugaitfalse loreet wisimand quatshould vel dolobore doloreetas an nulla differential diagnoses and to determine whether a positive and innocuousmodoloreet finding or whether is has pathological wis niamcom nullametiteratue result should be considered clinically significant. significance could predisposedotheeaindividual References digna con utthat augait nullamconse feugiat. to arterial 1. Department of Health. At least 5 a week: Evidence In summary, arterial compression syndromes affecting injury the veniam future. enismodignim doloboreet Rud teincon relationship subclavian artery, axillary artery and posterior humeral Another dilemma for diagnosis concerns patienton the impact of physical activity and its the at lore molobore molorem in et, verosto to health. A report from the Chief Medical Officer. circumflex artery have been identified in young, fit and healthy positioning. It is unclear whether the patient should Department be odiam, sequamet, veliquisi. of Health 2004 athletes. In order to aid localisation of the specific anatomical positioned in a seated quat. or supine posture during performance Obore consectem Suscidunt of arterial compression, suggestions were made to of these manoeuvres. Textbook descriptions ulluptatet lor in eros nonulpu tpatetum exerosand illustrations 2. Stratton G, Ridgers ND, Gobbii R et al. site Physical separate of the various manoeuvres dignim in volorediagnostic commodoarm lendre mincilit for arterial Activity Exercise, Sport and Health: Regional Mappingthe component parts of common diagnostic arm manoeuvres. However, diagnosis has proved difficult, with compression syndromes in the a North-West 2005 nim quisciliquam velisit ullahave condepicted velismo the subjectfor seated position, with the therapist detecting changes in dolore volumsan hendiate core volutpatisim www.nwph.net/pad/accessed 13/3/07)clinically significant levels of arterial compression recorded for both healthy, asymptomatic individuals and patients pulse pressuretatetuer or blood However, del doluptate sit pressure. utatet aliqua tum the positioning 3. Ridgers ND and Stratton G. Physical activity with proven vascular injury, inconsistent patient positioning of patients studies zzriliq using uipisi ultrasound or MR angiography acipsum doindolutem te feugiamet during school recess - The Liverpool Sporting to blood-flow in patients Playgrounds with aditinvestigate lum iure con vent ea characteristics faci euguerc ilismodit Project. Pediatric Exercise affecting Science arterial pressures, and reports of unreliable clinical measures. Many questions remain unanswered, and thoracic syndrome are do inconsistent, la adignitoutlet lute tin hent ut wis consequat,utilising either 2005; 17:281-290 thus more research into these areas would develop our the supinedel position the seated position. consecte utat. Utoraugait nulla con utpat.The problem with understanding and enhance our clinical practice. positioning the patient in the el seated Tat. Ro consecte dolesequip iusto position er se is that, as the arm is elevated above the level of the heart, due to changes The Authors tet aliquam commodionum zzriusc illuptatue References in orthostatic commy nisi. pressure, pulse pressure and blood pressure Bor sim ing eu facidunt pratum am, veliquisl incil eui blan heniat, seniat dunt 1. Fechter nos JD, Kuschner SH. Theconsenim thoracic outlet syndrome. Orthopedics diminish slightly, even ifipsusto no arterial compression Borperit, consend doloreet pratum exists. veniate tis amet, sim velenis nullaorpero dolor alit Scum zzrit 1993;16:1243–1251 However, the seated/upright posturedoloreet is a more functional velit ad dolorem zzrilit augiamcore nim dolorem voloboreet praesto euguer sum dolendvolesequis nit amcore 2. Wright I. The neurovascular syndrome produced by hyperabduction position and therefore likely toconsequat reproduce the subject’s dolore doloreet, quat. ofing lum nonullam velis nos more alit praesto eu facidunt pratum am, veliquisl incil eui blan the arm. American Heart Journal 1945;29:1–19 symptoms. detectconsequ clinicallyatuero significant arterial narrowing, vel do eum To ametue dip esto heniat ing eu facidunt pratum am, veliquisl incil eui blan heniatoutlet in am, veliquisl 3. Roos DB. New concepts of thoracic syndrome that incil explain aeugiam, difference of more in brachial vulluptat numthan iliqui15mmHg tat irit adiat. Duisit bloodeui.blan heniat etiology, symptoms, diagnosis, and treatment. Vascular Surgery 1979;13:313–32 pressure is classified as clinically doloborperbetween autat exarm ex positions ea feuisl ut el in

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www.sportEX.net

4. Baker CL, Liu SH. Neurovascular injuries to the shoulder. Journal of Orthopaedic and Sports Physical Therapy 1993;18:360–364 5. Mochizuki T, Isoda H, Masui T, Ohkawa Y, et al. Occlusion of the posterior humeral circumflex artery: detection with MR angiography in healthy volunteers and in a patient with quadrilateral space syndrome. American Journal of Roentgenology 1994;163:625–627 6. Thrush A, Hartshorne T. Peripheral vascular ultrasound: how, why and when? Churchill Livingstone 1999. ISBN 0443060495 7. Spencer MP, Reid JM. Quantitation of carotid stenosis with continuous-wave (C-W) Doppler ultrasound. Stroke 1979;10:326–330 8. Strandness D. Hemodynamics of arterial stenosis and occlusion. In: Strandness D (ed.) Duplex scanning in vascular disorders, 3rd edn. Lippincott Williams and Wilkins 2002. ISBN 078172631X 9. Plewa MC, Delinger M. The false-positive rate of thoracic outlet syndrome shoulder maneuvers in healthy subjects. Academic Emergency Medicine 1998;5:337–342 10. Stapleton C, Herrington L, George K. Sonographic evaluation of the axillary artery during simulated overhead throwing arm positions. Physical Therapy in Sport 2008;9:126–135 11. Rohrer MJ, Cardullo PA, Pappas AM, Phillips DA, Wheeler HB. Axillary artery compression and thrombosis in throwing athletes. Journal of Vascular Surgery 1990;11:761–768 12. Ouriel K. Noninvasive diagnosis of upper extremity vascular disease. Seminars in Vascular Surgery 1998;11:54–59 13. Schep G, Schmikli SL, Bender MHM, Mosterd WL, et al. Recognising vascular causes of leg complaints in endurance athletes. Part 1:

online

validation of a decision algorithm. International Journal of Sports Medicine 2002;23:313–321 14. Abraham P, Bickert S, Vielle B, Chevalier EM, Saumet JL. Pressure measurements at rest and after heavy exercise to detect moderate arterial lesions in athletes. Journal of Vascular Surgery 2001;33:721–727 15. Le Faucheur A, Noury-Desvaux B, Jaquinandi V, Louis Saumet J, Abraham P. Simultaneous arterial pressure recordings improve the detection of endofibrosis. Medicine and Science in Sports Exercise 2006;38:1889–1894 16. Roos DB, Owens JC. Thoracic outlet syndrome. Archives of Surgery 1966;93:71–74.

THE AUTHOR Claire Stapleton is a chartered physiotherapist currently completing her PhD at Liverpool John Moores University. Her research focuses on the mechanisms and diagnosis of vascular compression syndromes at the shoulder. In addition, Claire maintains a clinical caseload with the English Institute of Sport and sport scholarship students at the university. Before undertaking her PhD, Claire lectured in sports therapy and sports science at the University of Hertfordshire and worked at the Commonwealth Games and the World Transplant Games in 2002.

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Videos and animations

Step 1: Deep inhalation - closing down the costoclavicular space

Step 2: Scapula retraction - further compression of the costoclavicular space

Step 4: The Hyperabduction manoeuvre

Step 4: Hyperabduction manoeuvre in quadrilateral space syndrome

Step 3: Combined cervical rotation and extension - targets the scalene triangle

sportEX/Primal Pictures: Anatomy of compression syndrome animations

sportEX medicine 2009;40(Apr):23-26

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+44 (0)845 652 1906 www.sportex.net www.sportEX.net

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Knee articular cartilage repair and athletes

Click on the images below to see the videos

on: 2line Ref

Autologous chondrocyte transplantation (note: animation only covers first generation procedure)

Cartilage repair - (note: animation only covers first generation procedure)

Microfracture drilling procedure for isolated chondral defect (microfracture drilling)

OAtS cartilage repair surgery (OAtS)

The Rol PReven e of exeRcise Tion of in hamsTR The ing inj

Click on the pict ures

or links to see the interactive

extras

tel +44(0)845 652 1906 email: subs@sportex.net web: www.sportex.net

see videos

www.youtube.com/isportex

1) Nordic hamstring

uRy

2) Anima tion review hamstring ing anatomy

exercise

3) Anima ted patient lea hamstring flet

http://www.slideshare.net/sportEX tel +44(0) 84

5 652 19 06 email : subs@s po

rtex.net

Unfortunate ly to leave for our animator had Africa for before this two weeks sequence animations of was com pletely finished. By mid-Feb we something considerab will have so come ly improve back soo d n!

web: ww w.sporte

x.net