Cricket Sports HASSAN M Y, HELEN

Introduction: Sports medicine is a broad and complex branch of the health care profession. It is a demanding field in medicine providing the health care professional with challenges both on and off the field. The principles of treatment include the maintenance of euphysiological benefits of exercise while attending to the with specificity. It is important to treat to the biological as well as the psychological component of the injured athlete. Successful management include early and correct diagnosis, rehabilitation and compliance of the athlete and sports administrators. Despite the advent of technology, a small percentage of athletes are unable to return to sports medicine and it is for this reason that primary prevention is imperative to reduce the incidence of injuries where possible.

INJURY PREVENTION Injury prevention can be caused by intrinsic or extrinsic causes. Intrinsic causes include anatomical dysfunction while extrinsic causes are environment factors. Addressing both factors is imperative in reducing injury rates in sports medicine. Categorization of prevention into primary, secondary and tertiary structures is possible. Primary prevention: Primary prevention deals with direct or indirect prevention on an individual basis. An example would be correction of muscle imbalances of the shoulder structure of a bowler in an attempt to prevent shoulder dysfunction. Secondary prevention: Secondary prevention deals with preventing injury on a group basis. An example would be educating cricketers to the benefits of warm up, stretching and cooling down in an attempt to reduce musculotendinous injuries. Tertiary prevention: Tertiary prevention is efforts undertaken by the sports governing bodies in the field of cricket with initiation and implementation of strategies to reduce injuries at a club, provincial and national level. An example include the United Cricket Board of South Africa initiating the production of a proactive guideline policy on educating cricketers, coaches and governing bodies on injury prevention.

Preventing Cricket Injuries: Medical screening Attention to Footwear Orthotics Conditioning Training Technique Training Hydration Nutrition Playing environment Warm up/Cool down/stretching UV protection Game rules Coach education Environmental factors Protective equipment: visors, padding, helmets

SCREENING OF THE ATHLETE MUSCULOSKELETAL EVALUATION: General Health Previous injuries Postural and biomechanical assessment Spinal movements Strength/flexibility Muscle imbalances Proprioception Neurodynamic tests Special sport/position tests Level of fitness Other activities: gym

ISOKINETIC TEST EXAMPLE OF A NATIONAL CRICKETER:

INTERPRETATION:

SHOULDER VALUE INTERPRETATION

EXTERNAL ROTATION Bilateral differences 11.9 R weakness – Slight imbalance concentric (%) Bilateral differences 18.2 L weakness – Slight imbalances eccentric (%) Concentric/eccentric L: -13.0 Severe eccentric weakness (Nm) R: 16.6 Moderate eccentric weakness INTERNAL ROTATION Bilateral differences 7.1 L weakness – Slight weakness concentric (%) Bilateral differences 16.7 L weakness – moderate imbalance Eccentric (%) Concentric/Eccentric L: 1.4 Severe eccentric weakness (Nm) R: -10.0 Severe eccentric weakness

LOWER LIMB INJURIES

HIP AND PELVIS INJURIES

(1) FEMORAL NECK STRESS FRACTURES  Overuse injuries of the femoral bone may occur at the neck of the femoral bone. The SA fast bowler NGAM was diagnosed with stress fracture of femoral neck.  Risk factors include muscle fatigue, training errors, and poor training surfaces or poor shock absorption. Symptoms  Anterior thigh or groin pain.  Pain becoming progressively worse nocturnal pain relieved by rest. Examination  Antalgic gait with pain produced with axial compression.  X-rays may be normal. Diagnosis with bone scan / G / MRI. Management  Depends on site of fracture and severity. Compression fracture Non-displaced: Bed rest, progressive WB Displaced: ORIF Tension fracture Non-displaced: Bed rest, progressive WB. Consideration of ORIF Displaced: ORIF OSTEITIS PUBIS Osteitis pubis is an inflammatory condition of the symphysis pubis resulting from activities that cause acute or continuous shearing forces across the pubic symphysis. Repetitive micro trauma evokes an inflammatory response. Symptoms  Insidious pain becoming progressively worse in the inguinal or groin area. The pain is sharp, stabbing or burning and twisting movements aggravates it. A click if present represents assign of instability. Resting relieves the pain.  Signs:  Tenderness localized to pubic symphysis with .  Painful passive hip abduction  Resisted adduction painful.  Positive lateral pelvic compression or cross-leg tests.  Associated abnormal biomechanics such as weak abductor muscle may be present. X- rays: Radiographic imaging may lag behind by as much as 4 weeks in confirming the diagnosis. Radiographic findings include: Unilateral or bilateral fraying of the periosteum, bone resorption of adjacent pubic bones and widening of the symphysis space. Residual osteophyes with sclerosis and cystic changes may occur. Pubic symphysis shifting of greater than 2mm indicates instability.

Bone scan: Increased isotope with symmetric involvement of the pubic symphysis in the area. Treatment: Rest, NSAIDs. Oral corticosteroids recommended by some authors. Physical therapy includes therapeutic ultrasound. Localized injection using steroid is controversial. Progressive strengthening program and return to competition. Duration varies 3 to 6 months. is considered as a last resort and only after nonoperative measures have deemed to fail. Arthrodesis of the pubic symphysis has a definite role to play in patients with proven osteitis pubis recalcitrant to nonoperative management and in whom instability is clearly demonstrated.

SPORTS HERNIA A sports hernia is result of disruption of the posterior inguinal wall structures. It occurs in twisting sports and results from injury to the inguinal wall structures viz. transverses abdominus, conjoint tendon, internal oblique muscle and external oblique aponeurosis. Symptoms Unlike the classical hernia it does not present with a bulge representing a hernia. It presents with pain in the groin. On examination localized tenderness and increased sensitivity of related structure with straining. Investigation Ultrasound useful for diagnosis however user dependent MRI useful. Treatment Surgery for repair and stabilization.

MUSCLE STRAINS Thigh muscle strains Acute muscle injuries in the thigh area include injuries to flexor, abductor and adductor compartments. (i) Adductor muscle strain  The adductor longus muscle is the commonest adductor muscle to be involved.  Pain and swelling localized to injured site.  Painful passive abduction with resisted, adduction causing pain.  Ultrasound useful in grading injury. (i) Rectus femoris muscle strain  Localized or pain at injured site with painful resisted hip flexion and extension. (iii) Iliopsoas muscle strain  Pain on resisted hip flexion with hip 90° flexion as starting point. Lower abdominal wall injuries  Pain in proximity of pubic bone.  Resisted leg eleration or resisted sit up will reproduce the pain.  Lateral abdominal strain muscle injury seen with fast bowlers.

LOWER LIMB INJURIES Acute injuries KNEE

OVERVIEW OF ACUTE KNEE INJURIES  Acute injuries include injuries to the muscles and crossing the knee joint.  Intra articular injuries include cruiate and meniscal injuries. Acute : The anatomical structures that may be injured on the medial side include the medial collateral ligament, , and proximal tibialfibular joint and medial plica. Medial collateral ligament sprains: The medial collateral ligament is the result of a vulgas force to the knee joint. Injury is graded according to the severity of the injury. Isolated Grade 1 is treated conservatively with early mobilization and strengthening exercises. Medial knee strapping is recommended for support and for proprioception. Isolated grade 2 sprains requires some degree of immobilization with the aid of a knee brace limiting knee flexion to 20 to 30 degrees of flexion for 4 to 6 weeks depending on the severity of the injury. Grade 3 degree injury is usually associated with associated cruciate or meniscal tears. Management depends on the nature and severity of the associated injuries. Medial plica syndrome: The medial plica is a medial synovial fold that may become symptomatic. The management is conservative with pain control and surgery is indicated if symptomatic after failed conservative treatment. Meniscal tears: Meniscal tears will present with knee swelling. Associated knee locking and giving way may be present. Diagnosis is confirmed with MRI or at arthroscopy. Ultrasound of the knee is an inexpensive, non-invasive modality that is user dependent and is useful for diagnosis of meniscal tears and also for the staging of concomitant ligament sprains. Meniscal staging by identifying location from the meniscosynovial junction allows preoperative assessment to definite intra- operative management. The management depends on the location from the meniscosynovial junction. The tears located in the vascular peripheral area may heal spontaneous or with suturing while tears in the avascular zone requires partial meniscectomy.

ULTRASOUND IMAGE OF MENISCUS: Longitudinal view of meniscus, demonstrating possible staging of meniscus tear from the meniscosynovial junction.

Cruciate ligament injuries: Cruciate ligament injuries are assessed and treated according to an individualized assessment approach. Lateral collateral knee injuries: Lateral collateral ligament sprains are caused by a varus strain on the knee joint. The principles of management are similar to medial collateral ligament injuries.

OVERUSE INJURIES

Infrapatellar tendinopathy: Musculoskeletal injuries are common in cricket. The infrapatella tendon of bowlers is subjected to forces, which may exceed the tensile strength of the tendon. It is important to make the diagnosis as patellar tendinopathy may become progressive and result in a chronic condition. Pathogenesis: Microscopic tearing at the tendon bone attachment with inflammation, swelling, myxoid degeneration, fibrinoid necrosis of the tendon and infrapatellar insertion erosion. The incidence of patellar tendinopathy is found to be dependent on training frequency and volume. Decreased quadriceps and muscle strength is associated with patellar tendinopathy. Symptoms: The pain is often insidious anterior knee pain. Signs : Painful isometric contraction of the quadriceps muscle against resistance and painful passive maximal stretching of the quadriceps muscle. Diagnosis: Ultrasound will confirm the diagnosis. Management: Rest, ice, compression and NSAID. Identify and correct intrinsic and extrinsic causes. In the early stages, physical therapy and cryotherapy is effective. Local corticosteroid injection is not recommended. Initially eccentric loading of the quadriceps such as squatting and climbing should be avoided. Prolonged stretching caused by sitting with knee flexed more than 90 degrees must be avoided. Strengthening of the quadriceps muscle with gentle eccentric exercises to allow adaptation to greater loads is necessary. Quadriceps, hamstring , adductor and abductor muscle stretching and isometric contractions initially. Eccentric quadriceps program is introduced later in progression.

Surgery is only indicated when failed conservative management of 6 months rehabilitation. Arthroscopic resection of the lower pole with excision of the degenerative area, stripping of the paratendon, multiple longitudinal tenotomies and drilling of the bone-tendon junction has been performed.

Iliotibial band syndrome  The ilistibial band lies, lateral to the knee and attaché to Gerdy’s tubercle on the .  It is an overuse injury aggravated by specific bio kinetic abnormalities.  Lateral knee pain aggravated by 30° knee flexion when the ITB rubs against the femoral condyle. Treatment  Initially rest, stretching of lateral structures and correcting the specific biomechanical abnormalities.  Localized steroid injection may be used.

Patellofemerol syndrome  Patelofemoral syndrome is an overuse injury of the infrapatellar cartilage.  Anterior knee pain with crepitations.  Treatment, include correction of biomechanical aggravating factors.

Lower limb “shin pain”:  Lower limb ‘shin’ pain is a term often used by athletes to describe lower limb pain. The term is not a diagnosis but represents a colloquial term with a specific underlying medical condition. The cause of pain may result from injuries to the bone, periosteum or muscle/muscle compartment. Bone stress injury Tibia bone stress injury presents within pain becoming progressively worse with exercise. Night pain with bony percussion tenderness.  X-rays may be normal  Diagnosis made with bone scan or MRI Treatment  Depends on grade of injury. Principles include rest with immobilization 6-8 weeks. Tibia periostalgia  Tibia periostalgia is an injury of the tibia periostlgia presenting with pain aggravated with exercise and subsides with progression of exercise duration.  Pain at the periostum aggravated by passive dorsi flexion.  Diagnosis: Bone scan/ MRI when early. 

 Treatment, include stretching of posterior calf muscles and strengthening exercises.  Compartment syndrome  The lower limb consists of 5 compartments (Retmed) when the compartment pressure exceeds, diastolic blood pressure – 30mm HY, muscle perfusion is affected.  Pain occurs with / without neurological symptoms and signs if related nerves are compressed.  Pain becomes progressively worse with exercise and a ‘bursting’ sensation felt in the respective compartment. Anterior compartment  Weak dorsi flexion with decreased sensation between 1st and 2nd toes. Lateral compartment  Weak foot eversion with sensory changes at lateral aspect of lower limb. Posterior compartment superficial  Weak foot plantar flexion with sensory changes at the dorsum of the foot. Posterior tibialis muscle compartment  Weakness with plantar flexion and foot inversion. Diagnosis  Pressure measurements of compartment at rest, exercise and post exercise. Treatment  Treat aggravated factors  Surgery includes fasciotomy

ANKLE INJURIES Anatomy: The ankle joint is a hinge joint and stability is dependent on the congruity of the joint with the supporting ligaments. Dynamic stability is dependent on the ankle position. Injury is most likely when the ankle joint is in the position of plantarflexion i.e. the toe touching the ground. The lateral stabilizing ligaments of the ankle joint includes the anterior talofibular ligament, calcaneofibular ligament and the posterior talofibular ligament. The medial stabilizing ligament is the superficial and deep deltoid ligament. Ankle sprains usually involve the lateral ligament.

Acute ankle injuries  Medical or lateral ankle sprain are common injuries.  The most common injury is a lateral ankle sprain.  Lateral ankle Sprain:

  Lateral ankle sprain injury takes place when landing on a plantar flexed and inverted foot. The mechanism is plantar flexion, inversion and internal rotation. The first ligament to tear is the anterior talofibular ligament followed by calcaneo fibular ligament and then the position talofibular ligament.  Symptoms:  The symptoms include pain, swelling and limitation of movement. Skin discoloration may be present due to the underlying bleeding. A Cricketer presenting after a right lateral ankle injury. Note the swelling on the lateral aspect of the ankle joint.

Clinically: The extent of the injury is dependent on a detailed assessment of the integrity of the involved ligaments. Clinical tests for ligamentous stability include the anterior draw test, inversion stress test and the suction sign test. Testing for syndesmotic and other associated injuries is mandatory. Investigations: X-rays are warranted when an associated fracture is suspected. Stress radiographs are functional radiographic assessment of ligamentous instability. Ultrasonography enables definitive ligamentous assessment and staging. Principles of treatment: Acute: Rest, ice and compression. Treat associated injuries accordingly. Grade 1 injuries requires approximately 10 to 14 days of treatment before return to sport, Grade 2, 2 to 6 weeks and Grade3 4 to 26 weeks. Surgical versus non-surgical treatment for grade3 injuries are debatable however studies have shown that functional rehabilitation has a favourable outcome and role to play in management. Duration of rehabilitation is an individualized assessment and time frames are mere guidelines of estimation. Functional rehabilitation and stability is imperative before return to competition as the risk for recurrence is higher in a previously injured ankle. Rehabilitation principles:  Progressive range of motion  Strengthening progresses from isometric, isotonic and isolcinetic.  Strengthening of foot muscle and eversion muscles  Bracing of the injured ankle.  Prophylactic ankle strapping. Ankle taping is an efficient way of protecting the ankle by reduced inversion amplitudes, reducing tilting angular velocities and enhancement of proprioception.

DIAGRAM OF RIGHT ANKLE STRAPPING.

Persistent ankle pain post ankle injury: Some athletes may complain of persistent ankle pain after an ankle injury. The possible causes include a missed fracture, osteochondral lesion of the talus, subtalar joint instability, ankle impingement, and peronei subluxation and sinus tarsi syndrome. Ankle instability: Repeated episodes of recurrent ankle joint sprains or history of “giving way” signify ankle instability. Stress radiograph demonstrates joint laxity and mechanical instability. Functional instability in the presence of normal radiographic assessment may be present. Correction of the functional instability, which includes correction of deficient neuromuscular control, impaired proprioception or peroneal muscle weakness, is necessary. Other causes of instability with normal radiographs include subtalar joint instability, rotational instability of the talus, syndesmotic instability and hindfoot varus malalignment. Surgery is indicated for failed conservative treatment. Surgical intervention is designed to tighten up the anterior talofibular and calcaneofibular ligamnents. Return to sport after 3 months of rehabilitation.

Ankle overuse injuries: Anterior impingement syndrome:

Anterior impingement syndrome is a condition where the anterior structures of the ankle i.e. the anterior tibia and talus impinges during dorsiflexion (upward foot motion). The imposing structures may be soft tissues or bony osteophytes. Entrapment of the chronically swollen and hypertrophied synovium causes anterior pain. Predisposing factors include previous or repeated ankle injuries, ankle instability and muscle weakness. Symptoms and signs: Progressive pain aggravated by ankle dorsiflexion. Forceful dorsiflexion reproduces anterior ankle pain. In long standing cases limitation of ankle dorsiflexion occurs. Investigations: X-rays changes include osteophytic changes. Ultrasonogrphy will demonstrate impingement. Management: Conservative management is attempted to alleviate symptoms. Topical corticosteroid injection has been advocated. Failed conservative management is followed by arthroscopic surgical debridement. Other sites of impingement include anterolateral impingement and posterior impingement syndromes.

X-RAY OF ANTERIOR IMPINGEMENT SYNDROME: Note the anterior osteophyte of the tibia causing the anterior impingement.

Posterior impingement syndrome:

Posterior impingement syndrome occurs when the posterior ankle structures impinges with plantarflexion. The posterior tibia and the posterior talus cause impingement of the synovium and soft tissue structures. The impingement may be caused by soft tissue structures (posterior tibial nerve), tendons (flexor hallucis longus), osteophytes or by os trigonum. Os trigonum is a secondary ossification area that persists in some individuals. It is situated posterior to the talus and may cause or aggravate posterior impingement of the ankle joint. Management: Acute inflammation is treated with rest, ice and NSAID. Conservative treatment is attempted and local infiltration with local anaesthetic and corticosteroids is useful. Failed response requires surgical arthroscopic debridement or removal of Os trigonum when present.

LOW BACK PAIN IN CRICKETERS Backache is a common presenting complaint for athletes and it is often the result of muscle strains or discogenic in origin. In adults treatment can be initiated on the basis of history and physical examination, with further diagnostic work-up if persistent symptoms or if clinically sinister from the onset of assessment. Backache in children is considered pathological until proven otherwise requiring full clinical workup. Primary prevention of back pain includes implementation of stability exercises as part of preseason exercise program. Pelvic stability, abdominal stability and flexibility form the basis of effective management. ANATOMY:

 There are 24 free vertebrae in the vertebral column with 5 fused sacral and 4 fused coccygeal vertebrae: 7 cervicle, 12 thoracic and 5 lumber vertebrae  Vertebral bodies are bound together anteriorly by intervetebral discs and posterior are united by synovial between known as facet joints.  Motion segment is defined as two vertebral bodies.

DIAGRAM OF TWO VERTEBRAL BODIES (MOTION SEGMENT) OF LUMBAR SPINE

Predisposing factors for backache: 1) Hereditary factors: there are genetically predisposing egg such as spinal stenos is. 2) Biomechanics of fast bowling: Rotation, hyper flexion, and side flexion. 3) Technique: Side on, front on, mixed action. 4) Age: Immature musculoskeletal system 5) Ground reaction force: 3.8-6.4 X Body weight at front foot strike Vertical>horizontal Front footRear foot 6) Knee Angle: Straight vs. bent 7) Overuse: longer seasons, more matches, start earlier, number of seasons bowling during growing period 8)Poor preparation 9) Decreased flexibility: Entire kinetic chain 10) Decreased pelvic stabilization 11) Decreased strength 12) External forces: surface, divets, and boots 13) Other factors: release height, arch of foot, other sports, off-season activities

POSSIBLE CAUSES OF LOWER BACKACHE IN CRICKETERS

(1) Disc Pathology  The vertebral disc is kidney shaped in the lumbar spine.  The consist of a central nucleus pulposus supported by the annulus fibrosis.  Injury to the disc causes disc degeneration  Disc degeneration occurs in bowlers and batsman.  Complications of disc degeneration include disc termination which may cause Compression of nerve roots or spinal cord.  Clinical presentation includes and backache aggravated by flexion

MRI SCAN OF ACUTE DISC: MRI scan demonstrating acute disc L4/L5 lumbar vertebra. Hypertranslucent area representing Swelling in disc.

Diagram of MRI of Acute disc injury  Management includes stabilization.

(2) Spondylolysis  Spondyloysis is a defect or fracture of the pars interarticalaris.  Clinical presentation includes backache that becomes progressively worse. Nocturnal pain present. The site of the injury is the contra lateral facet joint to the bowling arm.  Clinically:  Palpation of the Para vertebral areas, usually L5 will cause discomfort. The pain is aggravated by back extension. The single-leg standing hyperextension test will produce pain on the affected side. PREDISPOSING FACTORS FOR SPONDYLOLYSIS (STRESS

FRACTURES) (1) Exercise load / volume  Excessive bowling overs is an important cause for spondylolysis  Strict guidelines to age specific bowling overs is important as a primary prevention (2) Technique  Mixed bowling action has the highest incidence of stress fractures (3) Weak stabilizers  The back is supported by the anterior abdominal wall and posterior by the back musculature.  Flexibility of hip musculature reduces the stress on the back.  Stabilization as a primary intervention is mandatory and the incorporation of latter should be included in routine exercise program. (4) Age  Adolescents are more prone to stress fractures than adult cricketers (<18years)  Backache in an adolescent is pathological until proven otherwise and a full clinical workup is necessary with a definite diagnosis. (5) Training surfaces  Hard training surfaces increases the likelihood of stress fracture  Correct footwear with adequate shock absorption is necessary  Specific orthosis may be necessary depending on the biomechanical behaviour of the athlete’s feet.

 Athletes with flat feet require arch supports

 Investigations:  Radiographic imaging may be negative in the early stages. If positive, the findings include the classical “Scotty dog” appearance on oblique views.  Bone scans are highly sensitive for diagnosis but not specific.  Single-photon emission computed tomography (SPECT) increases specificity in diagnosis.  Magnetic resonance imaging (MRI) is also used in diagnostic imaging.

FIGURE OF BONE SCAN AND CT OF STRESS FRACTURE: Increase uptake on bone scan in posterolateral aspect of L5 lumbar vertebra.

FIGURE DEMONSTRATING BILATERAL STRESS FRACTURE: Bilateral stress fractures of pars interarticularis of Left and Right lumbar vertebra.

FIGURE DEMONSTRATING PROGRESSION OF STRESS FRACTURE: In figure1, L and R bilateral stress fractures of pars interarticularis of L4 lumbar vertebra. Figure 2 taken 2 months after initial diagnosis, R stress starting to heal while L still ununited. . Figure 3, 7 months later, healed right pars interarticularis stress fracture while left pars still ununited.

FIGURE DEMONSTRATING STRESS FRACTURES AT MULTIPLE LEVELS IN A FAST BOWLER OCCURRING SIMULTANEOUSLY: Figure1, stress fracture of pars interarticularis of L3. Figure2, partially ununited fracture of left L4 with partial union of right L4.Figure 3, healed right L5 stress fracture with non bony union of left pars interarticularis.

MRI SCAN OF STRESS FRACTURE: Stress fracture of pars interarticularis of left L4 shown by arrow.

Diagram of MRI of Spondylolysis

Treatment  Initial treatment includes rest, ice and NSAIDs. Pain is an important indicator of activity restriction. Rest includes restricting of running, jumping and bowling. For a minimum period of 4 to 6 weeks. Hyperextension should be restricted. Initiation of hamstring flexibility and abdominal stabilization may commence. After the initial phase activity level is progressively increased under medical supervision. Stabilization commences. Treat underlying abnormal biomechanical abnormalities.  Bracing: Some authors recommend bracing while others advocate usage to those athletes that have persistent pain despite activity modification.  Stabilization includes: abdominal wall muscle and back muscle strengthening together with hip flexibility. (3) Spondylolithesis  Spondylolithesis is a condition where one vertebral body slips forward over another.

FIGURE OF SPONDYLOLITHESIS: Lumbar vertebral body L3 slides over L4 vertebral body producing a step in the anterior spinal line.

(4) Soft tissue injuries  The back muscles of the spine may be injured and present with muscle spasm  It is important to exclude motion segment disorder as cause for the muscle spasm  Principle treatment of muscle strains include rest, ice compression.

BACK STABILIZATION: LOW BACK PAIN

ABDOMINAL STABILISATION The concept of functional pathology of the neuro-motor system of the lumbar spine has been advocated by researchers and clinicians such as Alexander, Kendall, Janda, Schmidt, Sahrmann, Vleeming, Richardson, Jull, Hodges, Hides and Comerford over the past decade. Therefore the aim with abdominal stabilisation is: To obtain good quality muscle contraction with correct sequence of activation of individual muscles during a particular movement. This will ensure strength and therefore maximal joint and muscle protection, as well as maximal motor efficiency. Thus correct synergy (co contraction of muscle) and synchronisation (timing of muscle recruitment) is vital to prevent injuries of the lumbar spine, as well as enhancing performance. Lumbar spine segmental stability is based on:  Passive stabilisation = Osseous and ligament restraints  Dynamic stabilisation = Neuromuscular control Movement dysfunction may present as: 1. LOCAL (postural, tonic) e.g. lumbar multifidi, psoas major, quadratus lumborum, lumbar parts of iliocostalis and longissimus, transverse abdominus, the diagphragm and the posterior fibres of internal oblique. These provide segmental stability and control the lumbar segments during movement. 2. GLOBAL (dynamic, phasic) e.g. rectus abdominus, external oblique and the thoracic part of lumbar iliocostalis which links the pelvis to the thoracic cage. These provide pelvic stabilisation as well as movement. The correct functioning of the recruitment and motor control of these muscle actions are of major importance. The loss of ideal or normal local or global control results in abnormal stresses and strains being imposed on joints, supporting soft tissue, related myo-fascial tissue and neural tissue. Pain and pathology may result from this dysfunction. Some muscles may be overactive and tight, whilst others may be inhibited and present with functional weakness. 3 Basic dysfunctions:  MUSCLE WEAKNESS (strength / length) Inhibited – pain ; spasm; atrophy  MUSCLE TIGHTNESS / SHORTNESS a. Muscle tightness Overuse / tightness = strength b. Increased muscle tone Spasm / TPs in response to pain and injury = weak  ABNORMAL MVT PATTERNS (Janda) Involves whole neuromuscular system. i.e. Motor cortex ------Controlling active movement Limbic systems------controlling muscle tone Muscle------Physiological changes. Principles of Treatment: O’Sullivan P, 2000 Stage 1 = Cognitive stage (isolate TA and multifidus; neutral lordosis) Stage 2 = Associative stage ( retraining movement patterns with low load and high reps) Stage 3 = Autonomous stage (dynamic stabilisation with high load activation of global muscles and leading to skilled activities) Therefore management: (Sahrman’s movement balance system)  Maintenace of precise movement of rotational parts  Correct muscle length  Correct motor control  Correct relative stiffness of both contractile and non-contractile tissue.  Correct kinetics i.e. Poor muscle control: motor skill – functional skill – sport specific / position skill Train stabilisers Static – Dynamic stabilisation Proximal - Distal 1. Train prime movers 2. Train assistors 3. Train neutralisers 4. Train antagonists 5. Correct abnormal movement patterns  Identify cause of inury  Address extrinsic factors (technique, surfaces, divets, boots,etc)  Address intrinsic factors (biomechanical abnormalities including posture and ADL; age; other sports; overuse etc.)  Identify any sacro iliac dysfunction

BACK STABILIZATION PROGRAM

SHOULDER INJURIES IN CRICKET

Acute shoulder injuries in cricket are most likely during fielding with driving during fielding. Injury to the various anatomical shoulder structures may occur. Common shoulder injuries will be discussed. SHOULDER ANATOMY AND FUNCTION: SHOULDER STABILITY STATIC FACTORS Labrum The glenoid labrum is a fibrocartilagenous structure that attaches circumferentially to the glenoid rim. It offers stability by reducing shoulder translation, increasing surface area of articulation and allows attachment for the glenohumeral ligaments. Shoulder capsule and glenohumeral ligaments The glenohumeral ligaments include the superior, middle and inferior glenohumeral ligaments. The superior glenohumeral ligament limits external rotation of the adducted shoulder and prevents posterior translation of the flexed, adducted and internally rotated shoulder. Anterior translation is limited during 60 to 90 degrees of abduction by the middle ligament. The inferior ligament consists of three parts viz. anterior, ininferior and posterior parts. It limits anterior translation of the shoulder during movements of shoulder abduction and external rotation. DYNAMIC FACTORS: Rotator Cuff Rotator cuff provides a compressive load in joint stability throughout the range of shoulder motion, a phenomenon described as “concavity compression”. Biceps tendon: The long head of the biceps tendon contributes to anterior shoulder stability during movements of shoulder abduction and external rotation such as the cocking phase of throwing. The protective role includes stress reduction on the inferior glenohumeral ligament. Anterior joint stability occurs with internal rotation while posterior stability occurs with external rotation. Shoulder proprioception: There are mechanoreceptors and neural structures in the capsule and glenohumeral ligaments that play an important role in joint stabilization Scapular stabilizer musculature The scapular musculature attaching the scapular to the thorax allows the scapular to serve as a stabilizing platform for glenohumeral movements.

Biomechanics of throwing: The throwing mechanism is divided into different phases. Windup phase: Windup is a preparative phase during which the arm is brought into a pre cocking position. The arm is brought into a position of abduction and external rotation. While the trunk rotates, the scapular is brought into position over the thorax in a position of scapular retraction.

Wind up: Muscles involved include deltoid, external rotator cuff muscles, stabilizing muscles of the thoracoscapular region

Cocking phase: During the cocking phase the shoulder is brought into extremes of external rotation in a 90 degree abducted position. The external humeral rotators are responsible for the latter movement. The stored energy is then translated into kinetic energy and movement signifies the onset of the acceleration phase.

Cocking phase: Muscles involved include the deltoid, supraspinatus, infraspinatus and teres minor followed by subscapularis. Subscapularis activated eccentrically before the acceleration phase. Greatest strain on the superior labrum during late cocking phase.

Acceleration phase: The acceleration phase consists of medial humeral rotation and forward movement of the arm with lateral flexion of the trunk until the ball leaves the hand.

Acceleration phase: Muscles involved include the internal rotators for acceleration of the arm. Lattissimus dorsi and pectoralis major and subscapularis for medial rotation. The external rotators works eccentrically for stabilization. The infraspinatus and teres minor, with some support from supraspinatus muscle stabilize the humerus. Scapular stabilization is from the serratus anterior muscle. Other muscle involvemed include triceps muscle.

Release phase: Maximal power occurs when the release point f the ball occurs when the arm is parallel with the shoulder line and 40-60 degrees of lateral rotation (Pappas et al 1985). Follow through phase:

Follow through phase:

Muscles involved include the humeral muscles that include the deltoid, the

external rotator muscles and the rotator cuff muscles for stability. Scapular

stabilization includes the serratus anterior and trapezius muscle.

Follow through occurs after the ball is released. After the action of the internal rotators, the external rotators then act to counteract internal rotation. Continual trunk flexion and rotation allows transferral of the energy and weight of the body to be transferred anterior to the body. The energy is transferred to the leading hip and knee. Kinematics and kinetic changes in throwing with volume of throwing: Increased volume of throwing results in a decrease in joint range of motion at the shoulder and knee joints. Forces and torques at the elbow and shoulder joint also decreases. This seems to relate to muscle fatigue during excessive bowling and throwing and therefore demonstrates the point that excessive volume of training may predispose to abnormal biomechanics putting the athlete at risk to injuries.

(1) Acromioclavicular joint sprain (AC)

AC joint sprains occur in throwing sports and collision sports. Acute injuries to the accromioclavicular joint arise when falling onto the shoulder. The magnitude of the force will determine the severity of AC joint. Degeneration and instability injuries may result from training errors. Degenerative changes may follow previous AC joint sprains.

Clinical presentation:  Superior shoulder pain aggravated by shoulder abduction and flexion, most prominent at extreme range of latter motion. Symptoms most pronounced during the follow-through stage of throwing.  Localized tenderness at AC joint. AC compression test positive.

AC COMPRESSION TEST: Positive test if pain or discomfort elicited.

Treatment:  Grade Ι and П sprains are treated with rest in a sling, ice and nonsteroidal anti- inflammatory medications. Local steroid injection is useful. Local steroid injection may provide symptom relief for 20 days to 3 months. Recommended dosage includes 3 injections over 3 to 6 months when indicated. Failed conservative management can be treated with surgical excision of the distal clavicle either open or arthroscopicalyl.  Grade Ш controversial conservative or surgical management depends on individualized assessment.

(2) Clavicle fracture The clavicle fracture occurs when the athletes falls with the arm in an outstretched position: Presentation:  Pain at fracture site  Swelling  Palpable fracture Diagnosis: X-rays will confirm diagnosis. Treatment: Figure of 8 sling and limb supported in sling for 3 weeks.

(3) Shoulder Dislocation The humerus may dislocate anteriorly or posterioly depending on the mechanism of injury. Anterior dislocation is the commonest form. Anterior dislocation Presentation  Falling with outstretched arm  Pain and loss of function  Limitation of movement, the injured arm is usually supported by contralateral arm  Step deformity Treatment:  X-ray will confirm the diagnosis  Important to assess neurovascular status, specifically assessing C5 (axillory) nerve pre and post reduction.  Shoulder reduction using iatrogenic weight traction of the arm or manipulative procedures such as Kochers or Hippocratic methods.

(4) Subacromial bursitis

Mechanism: Fall to outstretched arm Presentation: Painful shoulder abduction  Typical painful area 60 - 120°  Localized tenderness  Abduction painful area  Specific tests for will elicit painful obstruction egg. Neers test for impingement. Management:  Rest, ice and compression  Sling

Shoulder Impingement Syndrome Shoulder impingement syndrome occurs when impingement occurs underneath the coracoacromial complex. The acromion complex the coracoacromial complex is formed by the acromion and the coracoacromial ligament interiorly forms the coracoacromial complex. Predisposing factors include congenital abnormalities of the acromion such as ‘beaking acromion’, shoulder joint laxity, muscle imbalance and overuse that occurs with repetitive bowling and throwing.

Supraspinatus tendinopathy presents with painful abduction during inititiation phase of abduction and resisted abduction. Shoulder impingement syndrome is graded (Neers) according to pathological changes. Early detection has a good outcome, as it is reversible with correct rehabilitation.

Supraspinatus testing: Centenella/Open can test: Positive test produces pain or discomfort.

Clinical symptoms include shoulder pain that becomes progressively worse with activity as the staging progresses. Clinical examination will demonstrate impingement with the aid of impingement shoulder evaluation tests.

IMPINGEMENT TEST: Positive test if pain or discomfort Elicited.

X-rays will not demonstrate any pathology in the early stage however it may demonstrate abnormalities with the acromial shape. Osteophytic changes will be detected later in the disease process.

Ultrasonography is useful in demonstrating subacromial bursitis, rotator cuff tendinopathy with early sclerotic changes. Management: In the acute stage treatment include rest, ice, compression and anti-inflammory medication. Correct scapular, shoulder and spinal dysfunction.

SHOULDER JOINT SPRAIN: A) ANTERIOR CAPSULE SPRAIN: The mechanism of an anterior shoulder capsule sprain is loading of the shoulder joint in abduction and external rotation. The injury can be graded as mild, moderate or complete anterior shoulder dislocation. With mild anterior capsular sprains the capsule and ligaments remain intact. The clinical symptoms include painful shoulder movements during abduction especially with abduction and external rotation. Moderate anterior capsular sprains produces capsular disruption and therefore the potential for anterior subluxation with functional anterior instability may occur if it treated incorrectly. The shoulder pain is severe and clinical evaluation will demonstrate painful active and passive range of movements with shoulder abduction. The presence of a click may indicate an associated labral tear. Management: Rest, ice, compression, allow adequate time for healing (3weeks). Conservative treatment is important because of the progression to functional anterior instability. Complication: Anterior Shoulder Instability- Anterior instability may result from poorly rehabilitated anterior capsule sprain. Pain is exacerbated during overhead throwing as the arm is in abduction and external rotation. The pain may be anterior or posterior due to eccentric loading of the posterior structures. The symptoms include intermittent and may present as impingement rotator. Rotator cuff muscle wasting may result. Treatment includes rehabilitation and surgical stabilization for failed conservative management.

ANTERIOR APPREHENSION TEST: Positive test confirmed with pain or discomfort with abduction and external rotation.

NONOPERATIVE MANAGEMENT OF SHOULDER INSTABILITY: The goals of treatment include pain elimination, restoration of movement, correction of predisposing abnormal biomechanical abnormalities allowing the athlete to return to a premorbid level of function. Wilk and Wilk et al recommends a four-phase rehabilitation program. Phase 1:Reduction of pain and inflammation by resting the injured shoulder and the use of anti- inflammatory medication Phase 2: Progressive range of motion and strengthening. Phase3: Advanced strengthening program. Phase4: Return to completion.

DIAGRAM OF SHOULDER STRAPPING:

Strapping of right shoulder for mechanical and neurological stabilization.

SURGICAL TREATMENT: Surgery is indicated for failed conservative treatment. The challenge of repair is to establish physiologic and pathological capsule laxity in a symptomatic athlete and correction of the instability. Capsulorrhaphy using either the medial or superior shift. The superior shift has a more profound effect on global laxity reduction while at the same time has less loss of external rotation. Thermal heating using laser, radio frequency energy and standard electrocautery energy on glenohumeral joint capsule laxity has been recently defined and used by surgeons. Thermal capsulorrhaphy results in capsular changes. It is the heat and not the mode of energy that results in structural changes. The capsule of the joint is made predominantly of type 1 collagen that has a highly ordered triple helix formation. Disruption of the bonds by thermal heating results in a phase transition in which the collagen contracts into a random coil with resultant formation of a shortened collagen fibril. . B) POSTERIOR CAPSULE SPRAINS: The mechanism includes indirect force applied to the shoulder in a position of flexion, medial rotation and adduction. The posterior capsule sprains usually heal without residual problems if treated correctly. Management follows the same principles as for anterior shoulder instability.

Scapulothoracic Bursitis: Adventitious bursa around the scapular includes bursa between serratus anterior and subscapularis muscle, serratus anterior and the thoracic wall and the bursa between the inferior angle of the scapular and the thorax. This bursa may become inflamed and the athlete will complain of insidious onset of pain that is worse during the cocking phase of throwing. Crepitus may be present. On clinical examination the crepitus may be present and palpable swelling may be felt at the bursa sites. Radiographs are normal. The diagnosis can be made with the aid of CT or MRI scans. The latter scan can exclude osteochondromas as a possible cause. Treatment includes rest, ice and anti- inflammatory medication. Persistent symptoms require surgical excision of the inflamed bursa.

Quadrilateral Space Syndrome: The axillary nerve supplies the deltoid muscle and the teres minor muscles. Entrapment of the axillary nerve by fibrous bands in the quadrilateral space causes quadrilateral space syndrome. The symptoms include pain in the posterior shoulder area that is worse during the cocking phase of throwing. The signs include weakness of the teres minor muscle with pai at the site of the quadrilateral space. The posterior humeral circumflex artery branch will occlude with shoulder abduction and external rotation and this will be demonstrated on arteriograhy. The management includes rest, nonsteroidal anti-inflammatory medication, and scapular and rotator cuff stabilization.

SHOULDER STABILIZATION MANAGEMENT OF SHOULDER INJURY AIM: Prevent recurrence of injury Maximise shoulder function. Optimise performance. GENERAL: 1. Identify exact cause of injury. a) Identify local anatomical deficits including any force couple imbalances. b) Identify regional deficits especially scapula (position, motion and strength of muscles) c) Identify distant (global) deficits e.g. Thoracic, Lumbar spine, hip inflexibility, previous injuries, muscle imbalances etc. 2. Have a working diagnosis. 3. Address any predisposing factors – extrinsic and/or intrinsic. 4. Knowledge of biomechanics of all disciplines – batting, bowling, fielding, keeping. 5. Activities of daily living. 6. General posture. SPECIFIC: Decrease pain and inflammation. 1. Mobilisation of the joints contributing to the disorder.

2. Mobilisation of the neural structures 3. Proximal stability before distal mobility 4. Scapula stabilisation 5. Rotator cuff stabilisation 6. Training of neuro-motor control. This should include the trunk, scapula, rotator cuff (+scapulo humeral rhythm) i.e. entire kinetic chain Further, PNF rhythmic stabilisation of the rotator cuff in different positions; progressive closed chain exercises; eccentric and plyometric exercises should be included. 7. Endurance exercises. 8. Increase speed, load and complexity of training. 9. Sport and specific discipline rehabilitation. Note: 1. The rehabilitation should start as soon as possible. 2. The sequence of rehabilitation should always address functional deficits in association with shoulder abnormalities 3. When re establishing the kinetic chain, always: - simulate the patterns of cricket - emphasise eccentric muscle work - combined patterns of movement - endurance activities - aerobic endurance - anaerobic endurance including agility and power. 4. Different goals for each phase of rehabilitation i.e.  Acute phase  Recovery phase  Functional phase

SHOULDER STABILIZATION PROGRAM:

SUPRASCAPULAR NERVE ENTRAPMENT: The suprascapular nerve supplies the supraspinatus and infraspinatus muscle. Dysfunction occur secondary to supraspinatus nerve entrapment. The nerve may be compressed at the suprascapular notch or at the entry of the nerve to the infraspinatus muscle. Symptoms: Suprascapular notch entrapment produces posterolateral shoulder pain. Clinically: Weakness and wasting of the supraspinatus and infraspinatus muscles. The second site of entrapment may present asymptomatically with infraspinatus muscle wasting and weakness without functional impairment The mechanism include nerve entrapment at the medial tendinous margin between the infraspinatus and supraspinatus muscle against the scapular spine with the infraspinatus branch being compressed in the process EMG analysis will demonstrate nerve denervation. Management includes conservative treatment with activity modification, rest strengthening of rotator cuff, and deltoid and scapular stabilizing muscles. Surgery advocated for failed favourable outcome.

ELBOW INJURIES

Radio-capitella Joint: Overuse injuries of the elbow joint in throwing sports include proximal radio-capitella joint degeneration. Repetitive trauma to the articular surfaces of the joint results in cartilaginous injury with osteoarthritis. Symptoms include painful elbow movement relieved with rest, decrease elbow extension; swelling and obstructive symptoms of locking may be present. Diagnosis: X-rays of the elbow joint may show degeneration.

Treatment: Restriction of activity until pain free with progressive graded return to sports activity.

Ulnar Collateral ligament injuries: Anatomy: The medial elbow structures include the ulnar collateral ligament, which consists of the anterior, posterior and transverse bands. The anterior band is the primary stabilizer for vulgas stress at the elbow joint. The medial elbow ligament complex is placed under stress during throwing and repeated stress may produce injury. Stresses occur during the late cocking and acceleration phases of throwing. There is rapid acceleration of the ball as the elbow extends from 120 degrees to 60 degrees during which time the medial elbow complex is vulnerable to injury. If the force exceeds the tensile strength the structures will sustain microscopic tears. The cumulative effect will produce inflammation with medial elbow pain.

Treatment: Rest, ice compression and NSAIDs. Non-operative management includes muscle strengthening , the outcome in one recent study (Arthur C et al 2001) allowed athletes to return in an average period of 24 weeks without requiring surgery. Where surgery has been indicated the ulnar collateral ligament reconstruction of the elbow using palmaris longus, plantaris or toe extensor autografts has yielded favourable results with athletes returning to sport at the same level or even better.

Lateral Tennis Elbow: Lateral elbow anatomy:

Tennis elbow is an overuse injury caused by repetitive overloading of the origin of the extensor muscle groups. Symptoms: Pain on the outside (lateral) side of the elbow joint aggravated by throwing and relieved by rest. Treatment: Decrease the magnitude of training load, counterforce bracing, and local steroid injection useful if concretive treatment fails.

Golfers elbow: Golfers elbow is an overuse injury of the medial side of the elbow joint. Symptoms: Progressive pain on the medial side, swelling and weakness. Treatment: Rest, stretching and strengthening program.

Olecranon Bursitis:

DIAGRAM OF OLECRANON BURSITIS AND ULTRASOUND CLIP: Picture of a left olecranon bursitis with the bursa swollen demonstrated on ultrasound. The ultrasound clip shows the hypoechoic cystic swelling of the bursa.

The olecranon bursa lies superficial to the triceps muscle insertion over the olecranon. The bursa may become inflamed acutely after a single episode of trauma or secondary to repeated grazing or weight bearing over the area. The clinical presentation includes localized swelling. Management includes ice, compression and anti-inflammatory medication. Failed conservative treatment requires aspiration of fluid with topical injection of local anaesthetic and corticosteroids. It is important to assess for symptoms and signs of , as this is a serious condition requiring urgent aspiration and treatment with antibiotics.

Triceps tendinosis: The triceps muscle attaches to the olecranon of the ulnar bone. Triceps tendinosis is an overuse injury similar to that of infrapatellar tendinopathy. The treatment follows the same principles, which include rest, activity modification and recommendation for the usage of glucosamine and hyaluronic acid combination. Stretching and strengthening program is important.

Posterior impingement syndrome: Posterior impingement syndrome of the elbow joint is the result of excessive extension loading of the elbow causing compression between the olecranon trochlea and fossa. The synovitis and hypertrophy causes articular cartilage damage and may result in degenerative joint changes with loose body formation. The symptoms include painful elbow extension at extremes of elbow extension. The symptoms are reproducible during examination. Treatment includes rest, compression and anti-inflammatory medication. Local steroid injection may be necessary. Rehabilitation includes strengthening of local musculature and identifying any abnormal biomechanics with correction.

HAND INJURIES IN CRICKET

Mallet finger  Mallet finger is an injury to the terminal extensor tendon of the finger.  There may be an associated distal phalangeal bone fracture.

FIGURE OF MALLET INJURY: Injury sustained to 1st left finger.

Treatment  Splint the finger in extension for 6-8 weeks  A mallet splint may be used

FIGURE OF MALLET SPLINT: Mallet splint on the 3rd finger.

 If the finger is securely immobilized the athlete may return to sport provided there is no stress to the injured area. Rehabilitation post splintage  After wearing the splint, active and passive range of motion exercises is done for the 1st week.  If there is no flexion lay of 5-10° of the distal interptral angeal joint strengthening exercise is continued.

BOUTONNIÈRE DEFORMITY  A boatonnière deformity of the finger results from an injury to the central slip of the extensor mechanism as it inserts onto the base of the second phalanx. Treatment  Boutonniere splint 6 weeks Post splintage  Active exercises are initiated 5-6 times / day with splintage continue at all times between exercises  Once extension of the finger is maintained, the splint may be discontinued  Passive range of motion exercises followed by strengthening exercise then follows.

FINGER DISLOCATION  Dislocated finger joints are relocated immediately  Rest, ice and compression is important to minimize swelling Proximal interphalangeal joint dislocations (PIP)  Pip may be dorsal, volar or lateral  Dorsal dislocation is the most common  With dorsal dislocation the volar plate is injured and an associated phalangeal fracture may occur  Reduction of the dislocation then follow specific management

Treatment: (A) Stable injury  Digital extension splintage for / week with the proximal interphalangeal joint in 30° of flexion  Active extension / week followed by:  Passive range of motion exercises / week past splintage  Buddy tapping for 3 weeks (B) Unstable injury  If the injury involves >50% of articular phalangeal bone or is unstable in extension then surgery is required  Surgery done include open reduction and internal fixation with kischner wires. FINGER COLLATERAL LIGAMENT SPRAINS (1) Metacarpahalangeal (MCP) collateral ligament sprain Mechanism: Either radial or ulnar stress to the flexed MCP joint. Treatment: Stable (Grd1)  Buddy strapping

DIAGRAM OF BUDDY STRAPPING: Buddy strapping of left 2nd and 3rd fingers. Note that the strapping does not cross the proximal and distal interphalangeal joints.

Unstable (Grd11 / 111)  Splintage in 70% flexion of MCP in a hand based splint (2) Proximal interphalangeal joint collateral ligament sprains:  Treat with buddy strapping

PHALANGEAL FRACTURES (A) PROXIMAL PHALANGEAL FRACTURES (1) Base fractures:  If stable it is treated with an orthosis  For unstable basal fractures surgery may be required with fixation with the aid of kirshner wires (2) Diaphyseal fractures:  Stable fracture treated with buddy strapping  Displaced fractures are reduced and the position maintained with an orthosis (3) Distal neck fractures:  Usually unstable and treated with surgical fixation with kirshner wires. (B) MIDDLE PHALANGEAL FRACTURES (1) Proximal middle phalangeal fractures:  If non-displaced it is treated with buddy strapping  Displaced fractures are reduced and the position maintained with wrist-based orthosis for 3 weeks, then followed by buddy strapping for 3 weeks.

(2) Distal middle phalangeal fractures:  Angulation of greater than 30° must be corrected and position maintained with wrist based orthosis for 3 weeks followed by gutter splintage for 3 weeks.

(3) DISTAL PHALANGEAL FRACTURES (1) Proximal distal phalangeal fractures  Non –displaced fractures treated with gutter splint for 3 weeks  Displaced fractures treated with external splint or surgical fixation with kirshner wires  (2) Distal distal phalangeal fractures  Non-displaced fractures treated with protective splintage for 3 weeks  Nail bed injuries require surgical treatment