Classification of Injuries Sports Injury Classification Acute / Traumatic • extrinsic causes: direct blow, collision, impact • intrinsic causes: muscle forces, joint loadings Acute vs Overuse Injuries v increasing frequency of overuse injuries v acute injuries: high velocity uncontrolled impacts macro-trauma Muscle Strains v among most common sporting injuries v muscle fibres fail under imposed demands v recurrent (particularly hamstrings) Muscle Strains Grade I small # fibres ruptured, pain localised, no strength loss Grade II large # fibres ruptured, reduced strength, swelling & pain limited movement Grade III complete tear of muscle, muscle-tendon junction, significant strength loss, obvious visual defect Biomechanical & Anatomical Factors in Muscle Strains v sudden acceleration or deceleration v neural innervation Biomechanical & Anatomical Factors in Muscle Strains v eccentric action mode ² force velocity curve v biarticular muscles pre-disposed ² hamstrings ² rectus femoris ² medial gastrocnemius Applying Exercise Physiology Knowledge Draw a Force-Velocity Curve on the Graph below Contraction Force 200% 100% Sarcomeres shortening under load Sarcomeres lengthening under load eccentric 0 concentric Contraction Velocity Biomechanical & Anatomical Factors in Muscle Strains v agonist-antagonist imbalance (e.g., quad - ham ratio) v muscle-tendon interfaces (e.g., semitendinosus) v elasticity (cc, sec, pec) Muscle Contusions “Corks” v forceful impact v localised (blunt) trauma v “common” (superficial) sites v vastus lateralis / biceps brachii v “other” (medial) sites v thigh adductors / med. gastroc Muscle Contusions “Corks” v mild - severe bruising v local fibre damage & bleeding v edema & hematoma v ICE not HARM v myositis ossificans Tendon Rupture v Partial Rupture Small to large # ruptured fibres, pain and limited function (equivalent to Grade I / II sprain) v Complete Rupture Total rupture of tendon, pain and non-function of specific muscletendon unit (Grade III equivalent) Biomechanics & Anatomy in Tendon Rupture v sudden acceleration v jumping / landing v unexpected loading v stretch-shortening action Biomechanics & Anatomy in Tendon Rupture v in vivo loading pattern v excessive stiffness v muscle-tendon “imbalance” (e.g., Achilles tendon) Tendon “Avulsions” v detachment of tendon v mallet finger (extensor mechanism) v jersey finger (flex digit profundus) Ligament Sprains Grade I Grade II pain on stressing ligament no increased joint laxity pain increased joint laxity with definite end point Grade III pain + / - gross joint laxity without a firm end point Ligament Sprains v Clinical continuum based on ligament stress-strain curve ² Stress-Strain curve v Grade I - III “overstretching” fibre model ² mild, moderate, severe Stress - Strain Curve Classic Ankle Inversion Sprain Rupture of Joint Capsule / Ligaments (AC Injury Examination under Anesthesia) v AC Injuries: Type I - VI (Rockwood classification) v joint capsule v acromioclavicular lig’s v coracoclavicular lig’s trapezoid conoid Ligament Sprains v single, debilitating episode ² e.g., Knee ² ACL ² ACL + L/MCL ² ACL + L/MCL + Meniscus ² ACL + PCL Ligament Sprains v multiple, debilitating episodes (chronic on acute) ² e.g., Ankle ² ATFL ² ATFL+CFL+PTFL ² Syndesmosis ² ATFL+CFL+PTFL+Deltoid Joint Dislocations & Subluxations v Clinical premise -“hypermobility”, assessed by multi-joint “laxity”, predisposes to subluxation / dislocation injuries Beighton Score Joint Action ROM Elbow extension > 10° Knee extension >10° Thumb apposition to ant forearm 5th finger ext >90° Forward flexion Palms flat on floor / knees straight Total maximum possible score 9 Score 1 1 1 1 1 1 1 1 1 Joint Dislocations & Subluxations v dislocation: complete dissociation of the articulating joint surfaces v subluxation: articulating surfaces remain partially in contact Biomechanics & Anatomy in Joint Injuries v direct impacts v distracting forces Biomechanics & Anatomy in Joint Injuries v injury to surrounding joint capsule and structures with luxations v luxation / laxity predispose to impingement (e.g., acromion process) and recurrent injury Biomechanics & Anatomy in Joint Injuries v “unstable” joints / structures more likely to dislocate ² shoulder (anterior) ² acromioclavicular joint ² fingers (PIP joints) ² patella (lateral) v “stable” joints however do dislocate ² hip ² elbow Acute Meniscus Injuries v Joint line pain v +ve McMurray’s test v Joint effusion / swelling v Popping or clicking within joint v Giving way sensation / locking v Arthroscopic surgery Acute Joint Injuries – Joint Effusion v increased intra- articular fluid v traumatic ligament, bone or meniscal injuries Acute Joint Injuries – Joint Effusion v synovial fluid v bloody effusion: hemarthrosis Acute Articular Cartilage Injuries v fragments sheared from articular surfaces (luxations) v chondral & osteochondral fractures common v osteoarthritis link v typical changes seen on X-ray include: joint space narrowing, subchondral sclerosis, subchondral cyst formation, and osteophytes v better detection (MRI, CT) v arthroscopic surgery Bone Fractures v common sporting injury v direct trauma ² blow / collision v indirect trauma ² twisting v splint / stabilize v medical referral Bone Fractures v closed fractures v open fractures ² (compound) v nerve damage v vessel damage v bleeding / shock v infection Simple & Complex Fractures Peak Fracture Prevalence in Adolescence Collés Fracture Biomechanics & Anatomy in Fractures Avulsion fractures Greenstick fractures l internal forces l incomplete break l younger athletes l younger athletes Stress fractures l repetitive forces l pars interarticularis Bone Bruising • Microtrabecular fracture /haemorrhage / oedema in bone following traumatic insult • MRI shows bone marrow oedema • Evident for 12 - 14 weeks • Subperiosteal hematoma - bleeding beneath periosteum. • Interosseous bruise - bleeding inside bone marrow is located. • Subchondral bruise – between cartilage and bone beneath, causing cartilage to separate from bone. Growth Plate Injuries Type I - epiphysis (E) completely separated from metaphysis (M) Type II - E + growth plate (GP) separated from metaphysis M Type III - Fx thru E separates part of E & GP from M Type IV - Fx thru E, across GP and into M Type V - GP compressed / crushed (prognosis poor) Salter & Harris Overuse Injuries v repetitive microtrauma exceeds tissue repair capacity v ⇑ prostaglandin E2 in tissues - ⇑ collagenase, ⇓ collagen synthesis v upregulation of genes for cartilage, down-regulation of genes for tendon (rat) ⇒ tendon morphology alters to more cartilaginous. Overuse Injuries v important to identify / consider risk factors (RF) v addressing intrinsic / extrinsic RF may help prevent re-injury v often recalcitrant to treatment (months to resolve) Overuse Risk Factors v Extrinsic Factors ² Training Errors Errors ² Surfaces ² Shoes ² Equipment ² Technique Overuse Risk Factors v Intrinsic Factors ² Previous Injury of Flexibility ² Leg Length Discrepancy ² Malalignment tibial torsion / vara genu valgum / varum ² Lack Overuse Risk Factors v Intrinsic Factors ² Malalignment patella alta pes planus / cavus ² Muscle Imbalance ² Muscle Weakness In the News Tendinopathies (Overuse) v pathology is tendon (collagen) degeneration (tendinosis) not inflammation v surrounding structures may have inflammation (paratendinitis) Normal → Abnormal Pathological Findings Multiple tendons (Supraspinatus, ECRB, Achilles) v Collagen disarray v Absent cells, prolific cells v Abnormal vessels & nerves v Abnormal extracellular matrix Dealing with Tendinopathies (Overuse Injuries) v History (onset, nature, potential causes) v Examination (anatomical structure, reproduce pain) Diagnosis required! v Treatment Relative rest / maintain fitness Avoid aggravating activities v Pharmacology (NSAIDs??, GTN) v Rehab (eccentric strengthening) Try to find intrinsic / extrinsic causes! v v Removing Abnormal Vessels & Nerves Joint “Diseases” in Children / Adolescents (Chronic??) v Osteochondritis (apophysitis / enthesopathy) Articular Non-articular Physeal v Osgood-Schlatter (tibia) v Sever’s (calcaneus) Articular Cartilage Injuries / OA v Many alternative medicines purported to decrease pain. v little supporting evidence for: vitamin A, C, and E, ginger, turmeric, omega-3 fatty acids, chondroitin sulfate and glucosamine. v Glucosamine - 2010 meta-analysis found no better than placebo. v S-Adenosyl methionine may relieve pain similar to NSAIDs. v electrostimulation techniques - no evidence it reduces pain or disability in knee OA Chondral Defects v Perera et al. 2012 - isolated chondral defects of knee (>1,000 cases) Autologous chondrocyte implantation, following conclusions: v Smaller (<1cm2), well contained lesions may be suitable for microfracture v larger defects – ACI satisfactory procedure in 70–80% of cases. v Motivated patients (15–55 yrs) with single lesion & short (<1 yr) history and no previous procedures have best outcome. v ACI - statistically significant improvement in objective and patient reported clinical outcome scores with durable outcome for as long as 10years. v clinical results of ACI and MACI techniques comparable and percen hyaline cartilage (biopsy) appears to improve with time. v Lesions of the femoral condyles have superior results to those in the patellofemoral joint. microfracture Osteochondral autograft/ allograft transfer (mosaicplasty) – cartilage plugs ACI “tidemark” show filling Stress Fractures (Reactions) v Bone failure v (repetitive microtrauma) v Repetitive stresses ² Bending (muscle action) ² Compression (calcaneum) ² Tension (femoral neck)*** v Fatigued muscle ⇓ stress absorb Stress Fracture Risk Factors Intrinsic v Sex / Age v Menstrual irregularities v Decreased tibial bone width v Increased ext rot of the hip v Extrinsic v Training change (type, frequency, intensity) v Footwear / Training surface v Equipment Stress Fractures v Onset usually insidious v Initially pain during exercise v Relieved by rest v Symptoms occur one month after change in training regime v Prolonged pain as condition worsens Imaging of Stress Fractures Bone Scans v excellent sensitivity / poor specificity v 50% athletes increased uptake in asymptomatic sites v non-visualization of fracture CT v visualise fracture MRI (best performed within 3 weeks) v differential diagnosis (e.g., infection) v fracture lines appear as low signal intramedullary bands Stress Fractures v Modified rest v Avoid precipitating activity v Minimal weightbearing activity v Modify biomechanics v Orthotics v Avoid risk factors v Avoid ultrasound v Most heal ~6 weeks v Healed when ² Absence of local tenderness precipitating activity without pain ² Perform
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