Traumatology Topic 1-3 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.