The document outlines the types of soft tissue, including skin, ligaments, tendons, fascia, and skeletal muscle, and describes common injuries such as sprains, strains, and contusions. It details the four overlapping phases of soft tissue healing: inflammatory, proliferative, maturation, and remodeling, highlighting key processes like clot formation, granulation tissue development, and collagen organization. Additionally, it presents a five-phase rehabilitation protocol aimed at restoring function and preventing reinjury after muscle injuries.
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Soft Tissue Healing
The document outlines the types of soft tissue, including skin, ligaments, tendons, fascia, and skeletal muscle, and describes common injuries such as sprains, strains, and contusions. It details the four overlapping phases of soft tissue healing: inflammatory, proliferative, maturation, and remodeling, highlighting key processes like clot formation, granulation tissue development, and collagen organization. Additionally, it presents a five-phase rehabilitation protocol aimed at restoring function and preventing reinjury after muscle injuries.
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Soft Tissue Healing
What is Soft Tissue?
• Skin • Ligaments – connects bones at joints • Tendons – attaches muscle to bone • Fascia – dense connective tissue • Skeletal Muscle – usually attached to bone and moves parts of the skeleton • So, tissue that has not hardened into bone and cartilage What are the Type of Injuries? • Sprain ligaments are • Intramuscular hematoma commonly caused by is confined to the muscle indirect impact, over- compartment which fills stretching (twisting) up with blood. Is more • Muscle strains – painful and restrictive of pulling action, over ROM stretching, rupture or • Intermuscular hematoma direct trauma / is when the blood overuse. Includes escapes through the tendons fascia and so becomes • Contusions (bruise) – distributed, thus bruising Soft Tissue Healing from Injury • Healing is a natural restorative response to injury. • systemic process has got 04 overlapping classic phases: haemostasis / inflammatory / proliferation / maturation or remodelling phases. • Platelets play a crucial role in clot formation during haemostasis, inflammatory cells debride injured tissue during the inflammatory phase. • Epithelialisation, fibroplasias, and angiogenesis occurs during the proliferative phase. Meanwhile, granulation tissue forms and the wound begins to contract. • Maturation phase, collagen forms tight cross links to other collagen and protein molecules, increasing the tensile strength of the scar. Early vs cellular phase
3. Remodelling phases (3 to 4weeks to 3 months or more)
1. Inflammatory phase (0-6days • The acute phase involves three mechanisms that act to stop blood loss from the wound:
• 1). Local vasoconstriction occurs, lasting a few seconds to as long as 10
min. Larger constrict due to the influence of serotonin and catecholamines released from platelets. The resulting reduction in the volume of blood flow in the region promotes increased blood viscosity or resistance to the flow, which further reduces blood loss at the injury site.
2). The platelet reaction provokes clotting as individual cells irreversibly
combine with each other and with fibrin to form a mechanical plug that occludes the end of a ruptured blood vessel. The platelets also produce of chemical mediators in the inflammatory phase: serotonin, adrenaline, noradrenaline, and histamine. Also ATP is use for energy in the healing process. • 3). Fibrinogen molecules are converted into fibrin for clot formation through two different pathways. Following vasoconstriction, vasodilation is brought on by a local axon reflex and approximately 20 proteins that normally circulate in the blood in inactive form become active to promote variety of activities essential for healing.
• Phagocytosis- is the activation of neutrophils and
macrophages to rid the injured site debris and infectious agents. As the blood flows to the injured area slows, these cells are redistributed to the periphery, where they begin to adhere to the endothelial lining. • Mast cells and basophils are also stimulated to release histamine, further promoting vasodilatation. • Bradykinin also promotes vasodilation and increase blood vessel wall permeability, contributing to the formation of tissue exudates • .The acute inflammatory response is of relatively brief duration and involves activities that generate exudates- plasma like fluid that exudes out of tissue or its capillaries and is composed of protein and granular leukocytes (white blood cells). • In the Chronic inflammatory response is of prolonged duration and involves the presence of nongranular leukocytes and the production of scar 02. Proliferative phase • Formation of granulation tissue is a central event during the proliferative phase. Its formation occurs 3-5 days following injury and overlaps with the preceding inflammatory phase. Granulation tissue includes inflammatory cells, fibroblasts, and neovasculature in a matrix of fibronectin, collagen, glycosaminoglycans, and proteoglycans. A. Epithelialisation
• Epithelialisation is the formation of epithelium over a
denuded surface. It involves the migration of cells at the wound edges over a distance of less than 1 mm, from one side of the incision to the other. Incisional wounds are epithelialized within 24-48 hours after injury. This epithelial layer provides a seal between the underlying wound and the environment. • The process begins within hours of tissue injury. Epidermal cells at the wound edges undergo structural changes, allowing them to detach from their connections to other epidermal cells and to their basement membrane. • When epithelialisation is complete, the epidermal cell assumes its original form. B. Fibroplasia
Fibroplasia is the process of forming fibrous tissue.
• The fibroblast is a critical component of granulation tissue. Fibroblasts are responsible for the production of collagen, elastin, fibronectin, glycosaminoglycans, and proteases Fibroblasts grow in the wound as the number of inflammation cells decrease.
• Fibroplasia begins 3-5 days after injury and may
last as long as 14 days. Skin fibroblasts and mesenchymal cells differentiate to perform migratory and contractile capabilities. C. Angiogenesis
• The macrophage is essential to the stimulation of angiogenesis and
produces macrophage-derived angiogenic factor in response to low tissue oxygenation. This factor functions as a chemoattractant for endothelial cells. Basic fibroblast growth factor secreted by the macrophage and vascular endothelial growth factor secreted by the epidermal cell are also important to angiogenesis. • Angiogenesis results in greater blood flow to the wound and, consequently, increased perfusion of healing factors. Angiogenesis ceases as the demand for new blood vessels ceases. • Contraction • Contraction results in a decrease in wound size, appreciated from end to end along an incision; a 2-cm incision may measure 1.8 cm after contraction. Depends on the degree of tissue laxity and shape of the wound. 03. Maturation and remodeling(WEEKS TO MONTHS) • The ultimate endpoint following remodeling depends on the tissue type. This phase is focused on increasing cellular organisation of the collagen fibers. • healing, in contrast, involves fiber alignment and contraction to reduce the wound size and to reestablish tissue strength. Complete recovery of original tissue strength is rarely obtained in secondary healing because repaired tissue remains less organized than noninjured tissue, which results in scar formation. The Healing Process • The healing process after a muscle injury: • This classification is based on a treatment protocol . But is not indifferent from other classifications. It is possible that some phases overlap, dependable on the individual response to healing and the type of injury. Not every patient undergoes all phases to achieve a full rehabilitation • 1. PHASE 1: Acute phase: ( 1 to 7 days) In this phase treatment exists out of the RICE- method. This method exists of Rest, Ice, Compression and Elevation. The main goal of this method is to minimize inflammation and pain. During the treatment with ice, a flexion and extension exercises are important but must be pain free (to prevent further injury). • 2. PHASE 2: Subacute phase: (Day 3 to < 3 weeks) This phase starts when signs of inflammation begin to reduce. Inflammation signs are heat, swelling, redness and pain. Muscle action is important to prevent muscle atrophy. When the patient has a full range of motion without any pain during this movement, concentric strength exercises can be done. When there is pain, the intensity must be immediately decreased. • 3. PHASE 3: Remodeling phase: ( 1 to 6 weeks ) In this phase, the patient can begin with stretching exercises to avoid a decrease in flexibility of the hamstrings. Eccentric strengthening exercises can also be done in this stage. These exercises are heavier than concentric exercises. Therefore it is important that the muscle is already regenerated because otherwise, reinjury is possible. • 4. PHASE 4: Functional phase: ( 2 weeks to 6 months) The main goal in this stage is to return to sport without a reinjury. To accomplish this goal, the patients need to increase their strength, endurance, speed, agility, flexibility and proprioception until the normal values of patient. Sport specific activities are the best indicators for a patient who returns to his sport. • 5. PHASE 5: Return to competition phase: ( 3 weeks to 6 months) When a patient returns to the competition, it is important that he can avoid a reinjury. Only when the patient has a full range of motion, strength, coordination and psychological readiness, he is allowed to return to competition. A study reveals that a program consisting of progressive agility a trunk stabilization is effective in promoting return to sports and in preventing for reinjury. This program turned out to be less risky for acute reinjury than isolated stretching and strengthening exercises. [2]
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