Traumatology Topic 1-3-2 PDF

TOPIC 1: MUSCLE INJURY GENERALITIES Introduction Skeletal muscle (striated muscle) Facilitates movement through active contraction and is composed of long cells called muscle fibers. These fibers vary in length from a few mm to a maximum of 50cm in the sartorius muscle and have diameters ran...

TOPIC 1: MUSCLE INJURY GENERALITIES Introduction Skeletal muscle (striated muscle) Facilitates movement through active contraction and is composed of long cells called muscle fibers. These fibers vary in length from a few mm to a maximum of 50cm in the sartorius muscle and have diameters ranging from 10 to 100 micrometers, influenced factors such as age and gender. Each muscle fiber contains nuclei at its periphery and is filled with contractile proteins arranged in myofibrils, where actin and myosin alternate. Muscle fibers Type I (Slow-Twitch, red fibers), which utilize oxygen for energy and are resistant to fatigue, making them dominant in postural and antigravity muscles. Type II (Fast-Twitch, white fibers), primarily rely on anaerobic metabolism and are prevalent in muscles responsible for quick propulsion. -They can be further divided into IIa and IIb, based on their oxidative capacity. Appearance of muscle fibers The striated appearance of muscle fibers is due to dark A bands, made of myosin and actin, alternating with lighter I bands, which contain actin. The central area of the A band is known as the M line, while Z line separates actin filaments. Muscle contraction occurs as actin fibers slide over myosin, causing the bands to come closer together and shortening the fiber. Organization Connective tissue in skeletal muscle is organized into three layers: Epimysium -Which encases the entire muscle. Perimysium -Which surrounds groups of muscle fibers known as fascicles. Endomysium -Which encircle individual muscle fibers. -Interacts with the sarcolemma and contains blood vessels, lymphatics and nerve endings. In the event of muscle injury, satellite cells, vestigial embryonic cells with differentiation potential reside in the basement membrane and play a crucial role in repair, aided by growth factors stored in the membrane. Muscle related injuries The myotendinous junction Is the area where the muscle transitions into tendon and is responsible for the transfer of forces generated by muscle contractions to the tendon and to the bone. This region endures significant mechanical stress, making it frequent site for injuries. The junction features invaginations, enhancing the contact surface and load distribution, which can improve the distribution of the load.  The enthesis Is where the tendon attaches to bone, and it be fibrous or fibrocartilage out. Injuries typically occur near this junction rather than within it. Muscle storage Muscles can store mechanical energy, functioning like elastic systems when properly stretched. Their efficiency is enhanced when an eccentric contraction occurs before a concentric contraction, allowing for the release of stored energy. This principle is often applied in activities such as running, jumping, throwing and kicking. Additionally while muscles can absorb energy, their capacity diminishes when fatigued or damaged. Muscle injury repair process * The repair of a muscle injury is a known process split into different phases. However, these phases are not sequential independent stages, but rather overlap each other in continuity. In general, soft tissue injuries resolve by repair mechanisms, but length of the phases is different between muscle and tendon. In bone, on the contrary, the same tissue that was injured regenerates. In muscle injuries are described 3 phases: Destruction, Repair and Remodelling. * 1. During muscle tear, the fascia and muscle are broken and therefore this causes bleeding, where the first thing that must be done is the Platelet Growth Factor (PGF) will activate and lead platelets to the site of injury to form a clot. 2. Fibroblasts then make their way to arrange the debris, this is done through the activation of the growth factor Fibroblast Grwoth Factor (FGF). 3. Later inflammation occurs, histamine is released into the site of injury and attracts the macrophages to clean the debris, cytokines (interleukin 1) will also be released to ask for the back up of neutrophils, basophils, leukocytes. 4. After, angiogenesis will take place as it will be activated by the growth factor Vascular Growth Factor (VGF) to form new capillaries in order to provide blood. (After 1 day) 5. After 1 week, satellite cells will be activated to get into the middle to transform into sarcoblasts where they will transform into myoblasts through myogenesis. 6. Myoblasts will turn into myocytes who will then create new muscle fibers. 7. After 2-4 weeks, more innervation, more blood and perfecting fascia formation. 8. 1-2 months the wound has 80% strength. 9. A year later the wound is fully healed. MUSCLE PATHOLOGY Causes of muscle injury Physical Examinations Fatigue ① Inspection Dehydration ② Palpation Lack of potassium, sodium, fibre ③ Examination monovers How to prevent muscle injuries? Hydration Oral hygiene Warming up Stretching -Dynamic exercises with ↑ ROM —> Specific sport movements (short increasing intensity) -Dynamic stretching ↑ Performance, static stretching ↓ performance (decrease tension —> less benefit of elastic energy and ↓ coordination) Supplements (Na, K, Ca, Mg) Training load control Classification * While assessing the severity of an injury is important, classification also needs to consider the injury’s site, mechanism, and any underlying conditions to effectively guide treatment. Mechanism of Injury Classification 1A: Minor muscle problem * Distension: Excessive elongation muscle * No fibers tear Pain + Functional deficit Palpation: increased local muscle tone. Painful mobilization (but complete ROM). No haematoma Usually a couple of days and its finished. Strain (Overuse Syndrome): * Muscle soreness beginning (leisure, work). NO prevent activity. Palpation: Tense + Pain. Increased muscle contraction Treatment: Rest + Ice (acute phase) + Kinesiotherapy Grade I strains heal within a few weeks. Grade II strains can take up to 3 months or longer. Grade III strains require surgery and months of rehabilitation. Cramps - Muscle Spam (contracture, tense bands) * Structural abnormality: A and Z band tears. Myofibril disruption (especially IIb) Increased creatine kinase, myoglobin and LDH. Also urinary hydroxyproline (no contractile connective tissue destruction) Acute onset, Short duration Muscle spam: Hard mass and palpable. Relief by stretching muscle. 1B DOMS * Physiopathology: Interstitial Oedema + Pain Unknown Aetiopathogenesis (overuse involvement) Variable symptomatology (Common: Strength loss). Usually 24-72h after eccentric exercise following a resting period. Self resolves in 1-2 weeks. 3A Minor partial muscle tear * Tear with a maximum diameter of less than muscle fascicle. Sharp, needle-like or stabbing pain at time of injury. Palpable defect in fiber structure within a firm muscle band. Stretch-induced pain aggravation. Primarily muscle-tendon junction (specially in eccentric contraction) 3B Moderate partial muscle * Tear with a diameter of greater than a fascicle. Stabbing, sharp pain, often noticeable tearing at time of injury. Palpable defect in muscle structure, often haematoma, fasciae injury. Stretch-induced pain aggravation. Primarily muscle-tendon junction. 4 Total muscle tear * Tear involving complete muscle diameter injury involving the bone-tendon junction. Dull pain at time of injury, noticeable tearing. Large defect in muscle haematoma, palpable gap, muscle retraction, pain with movement, loss of function Primarily at muscle tendon junction Contusion * Direct injury Direct muscle trauma, caused by blunt external force, leading to diffuse haematoma within the muscle causing pain and loss of motion. Dull pain at time of injury, possibly increasing due to increasing haematoma. Tenderness to palpation depending on the severity of impact, swelling and decreased pain. Any muscle, mostly Vastus intermedius and Rectus femoris. Muscle tear Classification Grade I: Soreness after physical activity. -Distension fibril tear. Might follow capillary tears. Grade II - III: Sharp pain -Grade II: Moderate tear muscle +/- tendon. -Grade III: Complete tear muscle belly, myotendinous injury or tendon. Treatment * 1st Phase (Inflammatory Phase) = 0-24/48h. Objective Reduce. Unanimity (100%) * Cryotherapy: Ice 10-15 min/ 30 mins-1hr in the 1st 24h -In excess will decrease cell metabolism (decrease healing) Elevation * No immobilization: * -Activitation of cell-regeneration processes and enhancement of extracellular matrix production. -No splints -No raised insoles- Orthotics: Muscle shortening and subsequent muscle repair complications. -Decrease protein synthesis No NSAIDS: Analgesics (Paracetamol, Metamizol) * -Reduce muscle regeneration -Produces fibrosis 1-2 weeks 2 - 4 weeks Always use POLICE (minor impry) (major injury) P-Protection 1-2 n Flexoextension Sports drills: Upon tolerance, avoiding as possible affected area. No massage No RICE No NSAIDS: ANALGESICS (Paracetamol, Metamizol) -Reduce muscle regeneration + produces fibrosis. Strongly recommended (75-99%) * Vascular Physiotherapy (95%) Enzyme therapy -Increasing the degradation of damaged extracellular fibers and matrix. Vasoactive medication -Problems: Dizziness, headache, cough. Recommended (55-75%) * Thermotherapy Stem cells - Satellite stem cell stimulating drugs (PRP, platelet rich plasma) Massage Increase oxygen supply techniques. 3rd phase (Cell stimulating, Proliferative, and Fibrotic or Fibrogenesis Phase) Unanimity * Painfree stretching Increased aerobic —> Sport drills: Upon tolerance -Isometric —> Concentric —> Eccentric (beware of load angle, eccentric with different loads) Strongly Recommended (75-99%) * USS control Antifibrotic therapy +drugs (Curcumin) Increase protein intake (especially Alanine, Glutamine and BCAAs) Metabolic supplement 4th Phase (Remodelling Phase) * Unamity * Painfree stretching + Exercises + sports skills Return competition # Basic sports technique movements in absence of pain Stretching in absence of pain Contractions in absence of pain Complications * Relapse: Same site and type injury -Early: 1 year Complementary * 80-85% Strength vs non affected limb TOPIC 2: FASCIA Histology Collagen type I. -Dense -Unidirectional -Types of Union= Resistance to traction. Dynamic Mainly proprioception (also nociceptors): Responsible for joint stability. Transmit tension forces + present muscle insertions (abdomen muscle, head and neck) Collagen Type I and III (most common collagen types in body) -Fascicular = Muscle, Tendon, Bones, Vessels, Nerves. -Movement control, Protection, Nutrition. Rich in mechanoreceptors and nociceptors -Responds to pressure, temperature, vibration. Receptors Paccini: Vibration + sudden muscle changes. Ruffini: Sustained slow pressure forces, responsible of the relaxing effect associated to sustained pressure by reducing CNS activity. Muscular interstitial: Type III and IV: Drives sensory from fascia to CNS, response to pain, pressure and light touch. Function Mechanical Enhance muscle mechanical efficiency. Increase muscle strength: influencing sarcomere length. Improves muscle action efficacy -Muscle Contraction: maintains tendon position. Contracts in response to tension: produces 30-40N (by myofibroblasts) Muscle action + Coordination + Proprioception + Joint stability. Connects agonist Muscle groups: forming functional unit, myofascia, part body tension (forces) transmission system. -Depends: Age, mechanical stress, diseases. -Controls Synergy: Regulates Agonist and Antagonist action. Protection: Transmits forces supported by muscles to surrounding tissues. -DOES NOT increase resistance to trauma. Reduces muscle mechanical stress, preventing muscle tear. Trauma absorption, preserving muscle integrity: By proteoglycans. -Endogenous: Genetic -Exogenous: Trauma, Stress, Infection, Malnutrition. Types Superficial Collagen fibers intertwined, mixed w/ elastic fibers. Function Coordination w/ musculoskeletal myofascial system. Protection + Support Trunk + Limbs, related to fat. Deep Groups of 2-3 parallel layers collagen fibers separated by lax conductive tissue. Resist tension forces. -Myofascial injury: Loss of sliding capacity. Causes: Overload, Trauma. Function Strengthening ligaments around joints. Support, Integrity, Maintenance joints, muscles, bones. Helps venous return. Diseases Controls body movements control + Adequate body posture causing a fasciae system imbalance produce posture compensation Pathology: Related Diseases Iliotibial Band Syndrome,Fibromyalgia, CLBP, Myofascial pain. Higher concentration myofibroblasts in fascia: Frozen shoulder, Ledderhose Disease (plantar fascia issue). Chronic lumbar pain: Increased Connective tissue surrounding spinal muscles + Reduced mobilitgy. -Especial chronic lumbar pain w/o remarkable abnormalities. Myofascial Pain Syndrome Main reason for chronic pain and disability. Typical: Referred Pain because Pain —> trigger points —> Distal Pain +Tense bands. -Active trigger point: Area of extreme tenderness usually within the skeletal muscle and asocies with local or regional pain. -Latent trigger point: Dormant (inactive) area that has the potential to act like a trigger point, may cause muscle weakness or restriction of movement. Fascia involvement: By rich proprioception innervation. Tissue aggression Triggering Factors: Nutrition (mineral and vitamin deficits) = important for myofascial tissue, thyroid pathology (endocrine dysfunction) Hyalauronic acid: Allows sliding collagen fibers form fascia + involved in viscoelastic properties. -Loss in viscoelastic properties activate nociceptors = might trigger myofascial pain. TREATMENT: -NSAIDs (antidepressants, sleep medication) -“Cooling” trigger point + Slow stretching muscle. -Massage -Trigger point infiltration. Diseases (SHORT QUESTIONS) Fibromyalgia Aetiology Unknown, hereditary? Brain and spinal cord pain processing disorder (increased pain signalling). Factors: women aged between 20-50, arthritis, infection, anxiety-depression, sedentary. Clinic General muscle and joint pain + intense fatigue Pain: burning, twitching, tightness. Low pain threshold or tender points. “Fibro fog”: Memory and concentration loss. Insomnia Fibro Symptoms: headaches, dry mouth, numbness, tingling in arms and feet. Treatment Medication: analgesia, antidepressants, muscle relaxants. -Specially: Duloxetine, Pregabalin. -Opiods: no good results. Exercise: low-impact activities, walking. -Endorphin release: improves pain. Dupuytren contractrion Are hard lumps of connective tissue under skin palm. Aeitiology Associated to alcoholism, seizures. Clinic Asymptomatic lumps under skin palm —> fibrous beans extending to fingers (usually 4th to 5th) —> fingers contracture in flexion. Can affect other parts: Knuckle pads, soles of the feet and penis. Diagnosis “table top test” = impossibility of flattening hand placed (palm down) on a table. Treatment: NONE Stretching (mild) Infiltration: -Corticosteroids: No correction of contracture. Slows evolution. -Enzyme (collagenase): 2-3 injections. Softens bands —> Posteriorly stretching +straightening fingers. Surgery Splint after surgery. Full recovery= 2-3 months. Fasciotomy: Open wounds heals by its own. Recently: Needle aponeurotomy. Iliotibial Band syndrome (runners, cyclists) Aetiology Iliotibial tract friction on lateral epicondyl. Factors: Running downhill, uneven surfaces, no previous stretching. Clinic Lateral knee pain, just above joint line. Diagnosis Pain palpation lateral epicondyle in knee flexo-extension. Renne Test: Pain lateral epicondyle at 30-40 degrees flexion in monopodal standing. Noble Test: Pain lateral epicondyle in knee extension in lateral decubitus non injured side. Treatment Proper warm up, Cryotherapy. Proper stretching Iliotibial band. Infiltration: Good results Surgery: Iliotibial band enlargement + Lateral epicondyle osteoporosis. Full recovery: 6 weeks. Plantar fasciitis * Aetiology Track and field. Hard surface. Traction Plantar fascia: Pes cavum (high arch) - flat feet, hyperpronation, high heel shoes. Clinic Foot sole pain (especially after rest). Heel spurs= RESULT of plantar fasciitis, no cause of pain. Diagnosis Clinic, USS, MRI. Treatment NSAIDs, cryotherapy, orthotics (insole, heel support pads) Plantar fascia stretching Infiltrations: Good results. Surgery: Plantar fasciotomy