Chapter 2: Understanding the Healing Process Through Rehabilitation

1. Chapter 2: Understanding the Healing Process Through Rehabilitation

2. Understanding the Healing Process • Programs must be based on healing process framework • Phases • Inflammatory • Fibroblastic-repair • Maturation-remodeling • No definitive beginning or end

3. The Primary Injury • Described as either chronic or acute • Macrotraumatic injuries • Result of acute trauma • Produce immediate pain and disability • Fractures, dislocations, sprains, strains • Macrotraumatic injuries • Overuse injuries, resulting from repetitive overload, incorrect mechanics • Tendinitis, tenosynovitis bursitis • Secondary injury • Inflammatory or hypoxia response

4. InflammatoryResponsePhase I • Injury results in altered cellular metabolism and chemical mediators • Macroscopic characteristics • Swelling • Tenderness • Redness • Increased temperature • Initial response is critical in healing process • An injury must cause the “Inflammatory Response”

5. Vascular Reaction • Involves vascular spasm, formation of clot and fibrous tissue growth • Vasoconstriction occurs 5-10 minutes following injury • Causes anemia followed by hyperemia due to dilation • Ultimately a slowing of blood flow occurs progressing to stasis and stagnation • Initial response lasts 24-48 hours

6. Chemical Mediators • Histamine • Vasodilation and increased cell permeability • Leukotaxin • Margination • Increased permeability • Necrosin • Phagocytic activity • Swelling is directly related to extent of vessel damage

7. Clot Formation • Disrupted vessel walls expose collagen within endothelium walls • Platlets adhere to vascular wall in conjunction with leukocytes forming a plug • Plug obstructs local lymphatic fluid drainage • Results in localization of the injury • Precipitated by fibrinogen  fibrin conversion • Cascade of events involving thromboplastin, prothrombin, and thrombin • Clot formation begins 12 hours after injury and is complete within 48 hours

8. Chronic inflammation • Occurs when acute inflammation does not eliminate injuring agents and restore normal physiological state • Leukocytes are replaced with macrophages, lymphocytes and plasma cells • Specific mechanism is unknown • Overuse and overload related • No specific time frame in which acute becomes chronic inflammation • Resistant to physical and pharmacological agents • Introduction of non-steroidal anti-inflammatory drugs (NSAID’s) some research indicates impedance of healing

9. Fibroblastic-Repair Phase II • Fibroplasia • Active scar formation • May last 4-6 weeks • Signs and symptoms will subside • Endothelial capillary buds develop allowing for aerobic healing • Increased blood flow for nutrient delivery

10. Fibroblastic-Repair (continued) • Granulation tissue develops with breakdown of fibrin clot • Granulation tissue composed of fibroblasts, collagen and capillaries • Fibroblasts synthesize extracellular matrix containing collagen and elastin • Proteoglycans • Glycosaminoglycans • Fluid • Collagen is deposited randomly at day 6 or 7 • Results in increased scar tensile strength • Persistent inflammatory response promotes extended fibroplasia, resulting in increased scarring

11. Maturation-Remodeling Phase III • Realignment of collagen • Continued breakdown and synthesis of collagen • Increased stress and strain results in increased collagen realignment • Nonvascular, contracted, strong, firm scar present after 3 weeks • Maturation may require several years to complete

12. Role of Progressive Controlled Mobility • Wolff’s Law • Bone and soft tissue will respond to physical demands placed upon them • Remodeling and realignment • Initial immobilization is necessary – what happens to: ligaments, tendons, bone? • Controlled mobilization enhances • Scar formation • Revascularization • Muscle regeneration and fiber reorientation • Tensile properties • Controlled activity allows for gradual return to normal levels of function

13. Extent of Injury Edema Hemorrhage Poor Vascular Supply Separation of tissue Muscle spasm Atrophy Corticosteroids Keloids and hypertrophic scars Infection Humidity, climate, and oxygen tension Health, age, and nutrition Factors that Impede Healing

14. Pathophysiology of Injury to Various Tissues • Epithelial Tissue • Covers internal and external surfaces • Skin, outer layer of organs, inner lining of blood vessels, glands • Purposes: • to protect and form structure for other tissues • Function in absorption and secretion • Relies on diffusion for fluid, oxygen, waste and nutrient transport • Injuries • Abrasions, lacerations, punctures, avulsions • Infection, inflammation or disease

15. Connective Tissue • Functions • Provides body framework, fill space, stores fat • Helps repair tissue, produces blood cells, protects against infection • Cell types • Defined by extracellular matrix (fibers, ground substance) • Macrophages, mast cells, fibroblasts • Collagen • Strong, flexible inelastic structure that holds connective tissue together • Enables tissue to resist mechanical deformation – oriented in direction of tensile stress • Mechanical properties • Elasticity, viscoelasticity, plasticity • Physical properties • Force-relaxation, creep response, hysteresis

16. Types of Connective Tissue • Fibrous • Dense – tendon, aponeurosis, fascia, ligaments, joint capsule • Loose – adipose • Cartilage • Rigid connective tissue composed of chondrocytes within a collagen, elastin, ground substance matrix • Poor blood supply slows healing • Hyaline, fibrocartilage and elastic • Reticular connective tissue • Composed of collagen and supports structural walls of organs • Elastic connective tissue • Composed of elastic fibers and found in blood vessels, airways and hollow organs

17. Bone • Consists of living cells and mineral deposits • Cancellous – spongy bone • Cortical bone – solid • Rich blood supply • Functions to provide support, movement and protection

18. Blood • Compose of various cells suspended in fluid intracellular matrix (plasma) • Plasma contains red blood cells, white blood cells and platelets • Essential for nutrition, cleansing, and physiology of the body

19. Ligament Sprains • Sprains involve damage to a ligament • Ligaments • Inelastic band of tissue • Provides joint stability, controls bone position during joint motion, provides proprioceptive input

20. Grades of Ligament Sprains • Grade I - some pain, minimal loss of function, no abnormal motion, and mild point tenderness • Grade II - pain, moderate loss of function, swelling, and instability • Grade III - extremely painful, inevitable loss of function, severe instability and swelling, and may also represent subluxation

21. Ligament Healing • Follows same course of repair events as with other vascular tissues • Ligaments sprained extra-articularly result in bleeding in the subcutaneous space • Intra-articular ligament sprains result in bleeding within the capsule • Vascular proliferation, fibroblastic activity and clot formation occur during the initial 6 weeks of recovery • Collagen and ground substance work to bridge torn ends of ligaments via scarring • Scar maturation will gradually occur and collagen tensile strength will increase

22. Factors Affecting Ligament Healing • Surgically repaired extra-articular ligaments • Heal with less scarring • Stronger than un-repaired ligaments • Non-surgically repaired ligaments • Heal via fibrous scarring resulting in ligament lengthening and increased joint instability • Intra-articular ligament damage • Results in synovial fluid presence, diluting hematoma, disrupting clot and healing • Ligament healing and immobilization • Muscle strength training can enhance joint stability

23. Fractures of Bone • Acute bone fractures - partial or complete disruption that can be either closed or open (through skin); serious musculoskeletal condition • Risk of infection is increased with open fractures • Type of fractures include: • greenstick, impacted, longitudinal, oblique, serrated, spiral, transverse, comminuted, blowout, and avulsion

24. A: Greenstick B: Transverse C: Oblique D: Spiral E: Comminuted F: Impacted G: Avulsion

25. Stress fractures- no specific cause but with a number of possible causes • Overload due to muscle contraction • Altered stress distribution due to muscle fatigue, changes in surface • Rhythmic repetitive stress vibrations • Signs and symptoms • Focal tenderness and pain • Pain with activity • Pain becomes constant and more intense, • Does not show up on X-ray until osteoblastic activity begins callus formation • Treatment • Removal from activity for at least 14 days • Does not usually require casting unless normal fracture occurs

26. Bone Healing • Significantly different from soft tissue healing • Additional functional elements associated with healing • Torsion • Bending • Compression • Trauma results in disruption of blood vessels, periosteal damage and clot formation • Fibrous collagen network is constructed after ~1 week -serves as framework for chondroblasts

27. Cartilage begins to infiltrate callus • Osteoblasts begin to proliferate, forming cancellous and trabeculae • Callus crystallizes – remodeling begins • Osteoclasts appear to resorb bone fragments and clean debris • Bone transition during remodeling • Fibrous cartilage  fibrous bone  lamellar bone • Osteoblasts and osteoclasts respond to stresses placed on bone • Immobilization is required for 3-8 weeks • Dependent on bone, severity, location, patient age

28. Cartilage Damage • Osteoarthritis • Arthritis is an inflammatory condition with secondary destruction • Arthrosis – degenerative process with cartilage destruction, bone remodeling and secondary inflammation • Cartilage fibrillates • Release of fibers and ground substance into joint • Often occurs in peripheral cartilage • Fibrillation – degenerative process associated with poor nutrition and disuse • Can extend to stressed areas and increase proportionally to stress applied

29. Osteophytosis • Attempt at increasing surface area to decrease contact force • Chondromalacia • Non-progressive cartilage transformation with areas of irregularity and softening • Begins in non-weight bearing areas and progresses to areas of stress • Use patterns, external force application, altered joint mechanics (laxity or trauma related) can serve as predisposing factors

30. Injuries conducive to osteoarthritic changes • Dislocations and subluxations • Osteochondritis dissecans • Recurrent synovial effusion and hemarthrosis • Ligament damage resulting in altered mechanics and cartilage damage • Additional factors • Loss of ROM, strength, power • Altered mechanics

31. Cartilage Healing • Limited healing capacity • Variable healing depending on damage to cartilage and or subchondral bone • Articular cartilage fails to undergo clot formation or cellular response • Defective region remains defective • When subchondral bone is involved the inflammatory process proceeds as normal

32. Injuries to Musculotendinous Structures • Skeletal muscle exhibits 4 traits • Elasticity • Extensibility • Irritability • Contractility • Muscle size and architecture often contribute to type and magnitude of motion (gross vs. fine, powerful vs. coordinated)

33. Muscle Strains • Strains occur when the musculotendinous unit is: • Overstretched • Forced to contract against too great a resistance • Damage occurs • Muscle • Tendon • Musculotendinous junction • Tendon-bone interface

34. Muscle Strain Classifications • Grade I : • some fibers have been stretched or actually torn resulting in tenderness and pain on active ROM, movement painful but full range present • Grade II: • number of fibers have been torn and active contraction is painful, usually a depression or divot is palpable, some swelling and discoloration result • Grade III: • Complete rupture of muscle or musculotendinous junction, significant impairment, with initially a great deal of pain that diminishes due to nerve damage

35. Muscle Healing • Similar healing to other soft tissues • Hemorrhaging and edema lead to phagocytosis • Fibroblasts and ground substance produce a gel-like matrix leading to fibrosis and scarring • Myoblastic cell infiltrate the region promoting myofibril regeneration • Collagen undergoes maturation – with active contractions being critical to apply tensile stress • Lengthy recovery for each grade • Patience is a must

36. Tendinitis • Term used to describe multiple pathological tendon conditions • Inflammation of tendon, with no involvement of paratenon • Paratenonitis • Inflammation of tendon outer layer • Friction injury • Tendinosis • Degenerative tendon changes with no clinical or histological signs of inflammation

37. Chronic Tendinitis • Tendon degeneration • Loss of normal collagen and cellularity • No inflammatory cellular response • Signs and symptoms • Pain with movement • Swelling • Crepitus • Key treatment = rest • Additional treatment options • NSAID’s and modalities • Alternative activities

38. Tenosynovitis • Due to friction and decreased space for sliding synovial sheaths are necessary in tendons • Overuse results in inflammation and development of sticky adhesions within the sheath • Signs and symptoms • Similar to tendinitis • Movement may be more limited with tenosynovitis • Treatment is the same as if the athletic trainer were treating tendinitis

39. Tendon Healing • Large amounts of collagen are required for adequate healing • However, collagen synthesis can become excessive resulting in fibrosis and interfering with tendon sliding action • Scar tissue will gradually elongate allowing for appropriate tendon motion • If a synovial sheath surrounds an injured tendon the injury could be devastating • Typical tendon healing may require 4-5 weeks before strong contractions can be imparted on tendon

40. Injury to Nerve Tissue • Generally involve contusion or inflammation • More severe injuries involve crushing or severing • Causes life-long disability • Paraplegia or quadriplegia

41. Peripheral nerves can regenerate if injury does not impact cell body • Slower regeneration with proximity to cell body • Regeneration requires an optimal environment • Degenerative changes occur • Increased metabolism and protein production for regeneration • While cell body contains genetic material necessary to maintain axon is does not transmit to distal segments of axon • Schwann cells • If cut contacts Schwann cells re-innervation of distal segments is more likely

42. New axon buds will develop on the proximal axon • One sprout will form new axon • Contact with Schwann cells will allow for Schwann cell proliferation = new myelin • Regeneration is slow • Occurs at a rate of 3-4 mm per day • Can be obstructed by scar formation • CNS nerves regenerate poorly due to lack of connective tissue support

43. Additional Musculoskeletal Injuries • Dislocations and Subluxations • Dislocations present with total disunion of bone apposition between articular surfaces- requiring manual or surgical realignment • High level of incidence in fingers and shoulder • Subluxations are partial dislocations causing incomplete separation of two bones • Reduction should not occur without and X-ray (necessary to rule out fractures) • Inappropriate reduction may complicate the injury • Return to play is largely governed by the degree of soft tissue injury

44. Bursitis • Result of excessive movement or trauma to bursa • Causes irritation, inflammation and increased synovial fluid production • May continue to become inflamed with repeat irritation with increasingly more pain • Commonly impacted bursa • Pre-patellar • Olecranon • Subacromial

45. Muscle Soreness • Overexertion in strenuous exercise resulting in muscular pain • Two types of soreness • Acute-onset muscle soreness • accompanies fatigue, muscle pain experienced immediately after exercise • Delayed-onset muscle soreness (DOMS) • pain that occurs 24-48 hours following activity that gradually subsides • Caused by slight microtrauma to muscle or connective tissue structures • Prevention and treatment • Gradual build-up of intensity • Some form of stretching

46. Contusions • Result of sudden blow to body • Can be both deep and superficial • Hematoma results from blood and lymph flow into surrounding tissue • Localization of extravasated blood into clot, encapsulated by connective tissue • Speed of healing dependent on the extent of damage • If muscle damage occurs ROM will be impacted • Incidents of repeated blows may result in myositis ossificans development • Prevention = rest and protection • Allow for calcium re-absorption

47. Managing the Healing Process Through Rehabilitation • Pre-Surgical Phase • Involves only those athletes requiring surgery • If surgery can be delayed, exercise may help to improve outcome • Maintaining or increasing strength, ROM, cardiorespiratory fitness, neuromuscular control may enhance the athlete’s ability to perform rehabilitation after surgery

48. Phase I: Acute Injury Phase • Initial swelling management and pain control are crucial • PRICE • If the athletic trainer is too aggressive during the first 48 hour the inflammatory process may not have time to accomplish what it needs to • Immobilization for 24-48 hours is a must • By days 3-4 the athlete should be engaged in some mobility exercises and should be encouraged to gradually bear weight if it is a lower extremity injury • Use of NSAID’s

49. Phase 2: Repair Phase • As the inflammatory process has subsided and pain decreases with passive ROM exercises should be added • Increase cardiorespiratory fitness • Restore full ROM • Restore or increase strength • Re-establish neuromuscular control • Continued modality use for pain modulation and swelling control • Cryotherapy • Electrical stimulation

50. Phase 3: Remodeling Phase • Longest phase with the ultimate goal being return to play • Continued collagen realignment • Pain continues to decrease with activity • Regain sports-specific skills • Dynamic functional activities • Sports-directed strengthening activities • Plyometric strengthening • Functional testing • Determine specific skill weakness