♦ Types of injury—traumatic and overuse
♦ Importance of determining the energy involved in an injury
♦ The relevance of mechanical load curves
♦ Types of fracture healing—how and why they occur
♦ Healing in articular cartilage, tendon, ligaments, peripheral nerves, and brain tissues.
The musculoskeletal system (also known as the locomotor system) provides the supporting framework for the human body, protects vital internal organs, and enables us to move in space through an arrangement of bones, ligaments, and articulations. The system consists of the human skeleton, made by bones attached to other bones with joints, and skeletal muscle attached to the skeleton by tendons.
Injury is damage caused to the structure or function of the body by an outside agent or force, which may be physical or chemical. Injury occurs when an acting force exceeds the elastic, plastic (hard tissues), viscoelastic (soft tissues), or endurance limits (stress, overuse) of a particular tissue (Box 1.4.1).
In a traumatic injury, the acting internal force (e.g. a contracting hamstring muscle tearing in a sprinter) or external force (e.g. a fall from a height causing a vertebral compression fracture) exceeds the strength of a normal tissue. A pathological injury occurs when a force of ordinary magnitude damages a tissue weakened by a pathological process (e.g. tumour /bone cyst).
A stress or overuse injury occurs after ordinary forces act repeatedly on normal tissues. Microinjuries are produced which do not have sufficient time to heal prior to the next submaximal event. The tissue fails after its endurance limit has been exceeded. In an overuse injury, the repeated impact produces a chronic inflammatory response (e.g. a tenosynovitis) which may prevent ultimate tissue failure by temporarily limiting the further use of an extremity.
Mechanical trauma is the commonest cause of injury to the musculoskeletal system. These events are governed by Newton’s second law of motion. This states that the force acting on a body is proportional to the product of the mass of the body and its acceleration (or deceleration).
Energy transmitted to the body is absorbed and dissipated through the bone and soft tissue envelope. Kinetic energy (KE) equals mass (m) × velocity (v) squared divided by two: KE = mv2/2. Hence doubling the mass of a moving body will double its traumatizing kinetic energy, while doubling its velocity will quadruple the resulting traumatic impact. The kinetic energy imparted to an object can deform the object temporarily (elastic deformation) or permanently (plastic deformation), or cause its complete disruption (by exceeding the ultimate failure limit). A small part of the transmitted impact can be converted to thermal energy. If the impacting force exceeds the failure limit of the bone, it breaks.
Variables such as age and the rate at which loads are applied (strain rate) affect the resulting injury patterns. An example of how the relative strength of musculoskeletal tissues changes with age can be seen when a lateral force is applied to the knee joint in a child. This will most likely lead to a fracture through the epiphyseal plate or possibly a fracture of the adjacent tibial shaft. The same mechanism will tear the medial–collateral ligament in a young adult and cause a tibial plateau fracture in an older person. With higher loading rates, a bone appears stronger thus requiring more energy to fail. This also explains why a slowly applied load to a joint will probably lead to a bony avulsion, while at a faster loading rate an in-substance tear of the ligament is more common.
Injuries caused by firearms
Firearms can be divided into handguns, shotguns, and rifles. The barrels of most firearms have helical grooves imparting a spin to the bullet, which increases stability in flight and accuracy.
Velocity and kinetic energy
Velocity (distance divided by time) refers to the speed of a missile on exit. The muzzle velocity is the maximal velocity. Bullets with muzzle velocities below 1000 feet/s (305m/s) are considered ‘low velocity’. This includes most rifles and shotguns. Bullets with muzzle velocities more than 1000 feet/s are considered ‘high-velocity’ firearms. Velocity on impact is important since tissue damage is proportional to a missile’s KE. Because of its geometric progression, velocity is of greater importance than mass.
Ballistics is the science of the movement of a projectile through a firearm, the air, and into or through a target. The tissue destruction is determined by the dissipation of the energy upon impact (ΔKE). If the bullet or its fragments have remained within the target, the exit velocity is zero and complete energy transfer has occurred.
Maximizing tissue destruction
Secondary missiles are created when the KE is imparted to dense tissues (e.g. a tooth) which themselves become missiles. Cavitation is caused by the rapid expansion and elastic recoil of tissues impacted by a missile (Box 1.4.2). Cavitation is proportional to the density of the tissue, the velocity of the projectile, and KE on impact. The temporal cavity may exceed the missile diameter by a factor of five to ten, which may produce tissue destruction many centimetres beyond the missile path. One of the more harmful effects of cavitation is the resulting vacuum which sucks foreign bodies and organisms into the projectile’s tract, an ideal situation for infection.
When managing firearms injuries, ballistic information should be available (Box 1.4.3). A thorough physical evaluation with special focus on the neurovascular status must follow. Bullets may fragment and even change course in the body (for example, bouncing off the spine) so the search for injuries needs to be comprehensive. All firearm injuries involving vital structures and/or by high-velocity missiles must undergo evaluation and formal debridement in the operating room. This is frequently repeated at 24–48h.
Musculoskeletal tissues: basic repair mechanisms
Tissues respond to injury
Most musculoskeletal tissues heal using three common phases: inflammation, repair, and remodelling. However, some structures (e.g. tendons) can heal using tissue-specific healing mechanisms. In contrast, some tissues (e.g. meniscus with in situ tears in the white zone) are incapable of repair.
The standard healing model: inflammation–repair–remodelling
Soft tissue injury can initiate a complex pathway of physical and biochemical changes. Healing progresses typically in four stages: haematoma, to inflammation, to proliferation, and finally remodelling (Box 1.4.4) Healing is most effective in well-vascularized tissues, and usually initiated from the tissues surrounding the injury site.
During haemostasis a primary platelet plug usually forms shortly after the injury. Secondary clotting occurs using fibrin and the coagulation cascade. Platelets release mediators that stimulate the next phase of healing.
During inflammation, the non-viable tissue is phagocytosed by macrophages within the first week. The end result is the formation of granulation tissue. Prostaglandins are actively involved in mediating this stage. Activation of the coagulation system and cytokines released by injured tissues attract polymorphonuclear leucocytes, monocytes, and T lymphocytes which remove necrotic material. They also release vasoactive mediators and activate growth factors and cytokines such as fibroblast growth factor, platelet-derived growth factor, and transforming growth factor-β (TGFβ). These attract cell migration, proliferation, and matrix differentiation.
The granulation tissue is replaced by a tissue-specific matrix which facilitates the ingrowth of undifferentiated pluripotent mesenchymal cells from surrounding muscle, periosteum, and marrow. These differentiate into tissue-specific cells such as osteoblasts, chondroblasts, myoblasts, and fibroblasts which fill the injury site with material closely resembling the original tissue.
In this phase, the disorganized repair tissue is optimized over several months under the guidance of local mechanical stresses. The result is tissue approaching the pre-injury status both structurally and functionally. However, scar tissue filling large defects contracts and this can be cosmetically unattractive or limit the movement of a limb.
Fracture mechanics and new bone formation
Structure and mechanical properties of bone
Normal bone is lamellar and is divided into cortical and cancellous bone. The mechanical properties of bone and its failure mechanisms directly derive from its composition and three-dimensional structure (Figure 1.4.2). Bone is a viscoelastic material and fractures are subsequently related to the magnitude of the force applied and its rate of application. This force is stored until breaking point and subsequently dissipated resulting in soft tissue damage.
Cortical bone has a slow turnover rate, a relatively high Young’s modulus, and a higher resistance to torsion and bending than cancellous bone. Cortical bone is weakest in shear, weak in tension, and strongest in compression. Trabecular bone is less dense and undergoes increased remodelling related to the lines of stress (Wolf’s law). It has a higher turnover rate, a lower Young’s modulus, and a greater elasticity than cortical bone. Trabecular bone, with a much greater ability to deform plastically, is about four to 50 times weaker than cortical bone. By the fifth decade, progressive reduction in bone mass with changes in material properties reduces bone strength and modulus resulting in a greater susceptibility to fracture. This tendency is less severe in men because increased endosteal resorption is partially compensated by a concomitant subperiosteal expansion. The loss in bone material with increasing age is partially counteracted by improved structural properties (increased polar moment of inertia).
A fracture involves a breech in the continuity of bone. Injuries may be from indirect forces such as a twist. These are termed low-velocity injuries. With high-velocity injuries, the fractures may be highly fragmented and damage to the surrounding soft tissues much greater, compromising blood supply. The forces that bone has to withstand include compression, bending, and twisting. Bone is strongest in compression and weakest in tension. Compressive forces lead to fractures predominantly in cancellous bone (metaphysis). Transverse, oblique, and spiral fracture patterns primarily occur in diaphyseal bone. Failure commences with the formation of a small crack on the tension side. As this crack progresses to the neutral axis, and then to the convex side, a transverse fracture results (Figure 1.4.3).
Transverse fractures occur following a bending force and may be associated with a small extrusion wedge on the compression side. If the wedge is less than 10% of the circumference of the bone, the fracture is defined as simple transverse fracture. With larger extrusion fragments, the fracture is termed a wedge fracture. Oblique fractures are secondary to a bending force. The extrusion wedge remains attached to one of the main fragments. Spiral fractures result from indirect twisting injuries and may occur with a spiral wedge fragment.
Mechanisms of bone regeneration: overview
Fracture healing involves a complex series of events leading to restoration of bone to its pre-injury condition. Fracture repair is influenced by factors such as the mechanical and biological environment of the fracture site, motion at the fracture site, and stability.
Fracture healing and regeneration of new bone can principally occur by primary or secondary bone healing or distraction osteogenesis. The prerequisites for the type of fracture healing include the fracture gap size and the degree of motion between the two bone fragments.
Fracture healing is a continuous process progressing from the initial fracture haematoma to, ultimately, bone remodelling. The most important factor is adequate blood supply.
Inflammation—formation of granulation tissue
Bleeding from the fracture site and disruption of surrounding tissues (periosteum, blood vessels, and muscles) results in a haematoma which may expand into the surrounding tissues. Soon after fracture, the blood vessels constrict, stopping any further bleeding The haematoma provides a source of haematopoietic cells capable of secreting growth factors. The fibrillar network of the haematoma serves as a scaffold for invading fibroblasts which become part of a composite matrix called granulation tissue (Figure 1.4.4). In the fracture thrombus, platelet-derived growth factor (PDGF) is released. Necrotic material releases cytokines which attract macrophages. Osteoclasts (derived from circulating monocytes) and their marrow precursors resorb bony debris and avascular bone ends. Cytokines also encourage vascular buds to form and begin to invade the fracture site. Examples of cytokines involved include fibroblast growth factor (FGF) which stimulates angiogenesis and TGFβ which initiates chondroblast and osteoblast formation. The fibroblasts replicate and form a loose aggregate of cells, interspersed with small blood vessels, known as granulation tissue. This is the perfused, fibrous connective tissue that replaces a fibrin clot.
Repair—formation of the fracture callus
During the repair phase, the fracture haematoma is replaced by soft callus consisting of fibroblasts, chondroblasts, and osteoblasts. A few days following the fracture, cells from the periosteum are recruited, replicated, and transformed into specific cells. The periosteal cells proximal to the fracture gap develop into chondroblasts and form hyaline cartilage. The periosteal cells distal to the fracture gap develop into osteoblasts and form woven (immature) bone. The fibroblasts within the granulation tissue also develop into chondroblasts and form hyaline cartilage. This process forms the fracture callus. Eventually, the fracture gap is bridged by the hyaline cartilage and woven bone, restoring some of its original strength and stability. The callus strength and stiffness appears to be prerequisites for mineralization of the fibrocartilage and subsequent transformation to woven bone. Mineralization appears to be a two-step process. The glycosaminoglycans (inhibit mineralization) are counteracted by neutral proteoglycanases secreted by the chondrocytes. Calcium phosphate complexes released by chondrocytes and osteoblasts initiate callus mineralization.
The next phase is the replacement of the hyaline cartilage and woven bone with lamellar bone thereby restoring much, if not all, of the bone’s original strength. The replacement process is known as endochondral ossification with respect to the hyaline cartilage and ‘bony substitution’ with respect to the woven bone. The lamellar bone begins forming soon after the collagen matrix of either tissue becomes mineralized. Vascular channels and osteoblasts penetrate the mineralized matrix. The osteoblasts form new lamellar bone upon the surface of the mineralized matrix. This new lamellar bone is in the form of trabecular bone.
The fibrinous to osseous callus transformation closely resembles enchondral ossification and typically occurs in the central healing zone. More peripherally, the cambium layer of the elevated periosteum generates woven bone using intramembranous ossification (Figure 1.4.5). This develops a circumferential bone sleeve, hard callus, conveying early and progressive stability to the fracture site.
This process begins during the middle of the repair phase and continues long after the fracture has clinically healed (up to 7 years). The remodelling process substitutes the trabecular bone with compact bone and allows the bone to assume its normal configuration and shape based on the stresses to which it is exposed (Wolff’s law). The trabecular bone is first resorbed by osteoclasts, creating a shallow resorption pit known as a ‘Howship’s lacuna’. Then osteoblasts deposit compact bone within the resorption pit. Eventually, the fracture callus is remodelled into a new shape which closely duplicates the bone’s original shape and strength.
Type of bone formation
Bone is formed via endochondral, intramembranous, and appositional ossification. With endochondral ossification, bone replaces the cartilage model. With intramembranous ossification, a cartilage precursor is not present. Undifferentiated mesenchymal cells differentiate into osteoblasts and deposit an organic matrix that mineralizes to form bone. Finally, with appositional ossification, osteoblasts align on the bone surface and lay down new bone.
Primary cortical healing occurs with rigid immobilization and anatomic reduction. With closed treatment of the fracture, endochondral ossification with periosteal bridging callus occurs. With rigidly fixed fractures (compression plate), direct osteonal or primary bone healing occurs without visible callus.
Primary bone healing
Primary or direct bone healing is characterized by the absence of formation of callus (which would otherwise be visible on x-ray). The prerequisites include anatomical reduction, absolute rigidity, and interfragmentary compression. Typically, primary bone healing usually occurs with a fracture gap of less than 2mm and motion at the fracture site of less than 1mm. With the development of anatomic reduction and stable fixation with metal plates and screws, the primary fracture healing was seen for the first time. The stability provided by the fixation allows early motion of adjacent joints allowing accelerated rehabilitation.
Primary bone healing is a continuous process of coupled bone resorption and bone formation (Figure 1.4.6). Bone remodelling units form parallel channels to the longitudinal axis of the bone and contain cutting cones lined by multicellular osteoclasts. Behind the cutting cone, the walls of the osteon are lined by osteoblasts which circumferentially appose new osteoid at the rate of about 1µm per day. Completion of a new osteon will take approximately 3–4 months.
The fracture site regains immediate stability with plate fixation, but fracture union usually occurs at a slower rate than would be seen under conditions of secondary bone healing. When comparing two identical fractures, one healing by primary and the other by secondary bone healing, the fracture that heals by secondary bone healing will initially be 66% stronger and 100% more rigid.
Gap healing typically occurs with gap sizes less than or equal to 1mm. The process requires micromotion at the fracture site and occurs in three stages. In stage one, there is rapid filling of the gap with woven bone. Stage two involves Haversian remodelling of the avascular areas at the margins of the fracture edge. In stage three, remodelling of the woven bone to lamellar bone occurs and bridges the gap.
Plating of a fracture provides stability but does not guarantee a particular type of fracture healing. Tightly applied plates may lead to bone necrosis and/or stress shielding.
The bone necrosis directly underneath the implant is caused by the interruption of the periosteal blood supply and the plastic deformation distorting or obliterating the small intraosseous vessels. Plates remaining in place for prolonged periods alter the load-bearing requirements. The resulting stress-shielding effect is dependent on the rigidity of the construct and may lead to permanent reduction of bone cross-sectional area. For this reason, removal of a plate from a large bone should be managed by a period of partial weight bearing (Figure 1.4.7).
Neutralization plates protect the primary lag screw from bending, shear, and rotational forces.
A plate applied to the tension side of a bone achieves stability by axial compression, but also, because of its location on the tension side, bending forces are generated under load. This leads to increased axial compression. Such a plate is referred to as a tension band plate.
Secondary bone healing
Secondary bone healing is often seen with fractures managed with traction or cast. Secondary bone healing progresses through an inflammatory phase followed, within a few days, by a repair phase (several weeks to a few months), and finally a remodelling phase which may continue for several years.
Ilizarov invented the technique of distraction osteogenesis in the 1950s. The procedure describes a process of new bone formation after the creation of an osteotomy using controlled gradual distraction of the bone ends. Optimally, intramembranous bone develops. If the process is disturbed (e.g. lack of stability), cartilaginous tissue or fibrous tissue forms and non-union may develop. In addition to bone formation, there are effects on the muscles, vessel walls, and associated tendons. There are several prerequisites for successful distraction osteogenesis (Box 1.4.6).
The distraction period lasts until the desired length of new bone has been achieved. During the consolidation period, the newly formed bone matures. The fixators can be removed when the distraction gap has uniformly consolidated and at least three new cortices have formed (neocorticalization) as seen on orthogonal radiographs.
After initiation of distraction, trabeculae form on both sides of the osteotomy which are oriented in line with the distraction force. The outer surfaces of the trabeculae are covered by a layer of osteoblasts. While the interzone is relatively avascular, the regions between the trabeculae contain abundant capillary blood supply. It appears that the interzone consists of undifferentiated mesenchymal cells which, under optimal conditions, directly transform into osteoblasts (intramembranous bone formation). Under less optimal conditions, chondroblasts or fibroblasts emerge. Depending on the conditions, consolidation of the regenerate may still occur, by a process similar to enchondral ossification. Alternatively, a fibrous non-union may develop.
The Ilizarov fixator is primarily used for bone lengthening and is particularly useful where deformity correction may also be required. In addition, the fixator can be used for the management of non-unions using compression (instead of distraction) and the acute management of complex fractures (e.g. tibial pilon fracture). With optimal conditions, bone formation is principally by intramembranous ossification.
Ligaments: injury and repair
Ligaments are dense, highly organized connective tissue structures connecting bone to bone (Box 1.4.7) They are composed of cells (fibroblasts) and extracellular matrix principally of type I collagen (70% of the dry weight). They function by stabilizing joints and have embedded in them mechanoreceptors and free nerve endings. The sliding of collagen fibres over each other is key for changes in ligament length (growth and contracture). Compared with tendons, ligaments have a higher elastin content (e.g. ligamentum flavum). In contrast to tendons, they have a uniform microvascularity and receive their blood supply at the insertion site. Ligaments are arranged in progressively more complex structures from fibrils to fasciculi which have a predominantly parallel (collateral ligaments) or spiral (cruciate ligaments) organization.
Ligament insertion into bone represents a transition from one material to another and can be classified into two types: indirect insertion (more common) and direct insertion.
With indirect ligament insertion, superficial ligament fibres insert at acute angles into the periosteum and tend to be broader than direct insertions (e.g. tibial insertion of the medial collateral ligament of the knee). With direct insertions (e.g. femoral insertion of the medial collateral ligament of the knee), there are superficial and deep fibres. The deep fibres insert at right angles to bone and superficial fibres blend with the periosteum. The transition from ligament to bone occurs in four stages: ligament, to fibrocartilage, to mineralized fibrocartilage, to bone. Sharpey’s fibres cross all four zones.
The tensile properties of ligaments are similar to those of tendons, with an initial toe region produced by the non-linear straightening of the crimped fibres. As elongation progresses, fibres become more parallel to the load. Ligaments exhibit viscoelastic properties such as creep, hysteresis, and stress relaxation. Clinically, this becomes relevant in anterior cruciate reconstruction where stress relaxation of graft materials may be observed in the initial hours after tensioning, and preconditioning may be appropriate prior to final tensioning. Many ligaments, such as the cruciates, have multiple bands of collagen fibres attached at different points of the insertion. This allows different components of the ligament to tighten with varying joint position.
Mechanisms of injury
Ligament sprains are the most common joint injuries. Three grades of severity are usually differentiated.
♦ Grade I disruption implies pain with stress, but no increase in laxity
♦ Grade III injuries are complete disruptions of the ligament with significant laxity and an absence of a firm endpoint to stress.
In the knee, ligament injuries can be produced by contact (medial collateral disruption from a blow to the lateral aspect of the leg) or non-contact (anterior cruciate tears from varus internal rotation or valgus external rotation). The continued application of a deforming force will stress and injure secondary restraints, producing combined ligamentous disruptions. The most common mechanism of ligament failure is rupture of sequential series of collagen fibre bundles. Ligaments do not plastically deform. Mid-substance tears are more common in adults; avulsion injuries are more common in children. Avulsion typically occurs between the un-mineralized and mineralized fibrocartilage layers.
Healing of extra-articular ligaments
Healing occurs in three phases, a pattern similar to bone, and benefits from normal stress and strain across the joint. Immobilization adversely affects the strength (elastic modulus decreases) of an intact ligament and of a ligament repair. Immediately post injury, bleeding produces a fibrin clot. Within 3 days, macrophages, platelets, and neutrophils migrate to the injury site and release chemotactic, proteolytic and angiogenic factors. Early healing produces a disorganized cellular scar consisting primarily of type III collagen and proteoglycans. The proliferative scar formation slowly produces increased type I collagen. Remodelling takes place up to a year following injury. Mature ligament repair tissue only achieves 70% of the tensile strength of normal ligament tissue. The increased cross-sectional area of the repair tissue appears to compensate for this weakness. Increased tensile stress and early mobilization in the healing phase of a transected medial collateral ligament results in increased total collagen and improved histological organization. Therefore, operative repair is not always necessary.
Healing of intra-articular ligaments
Intra-articular ligaments do not display predictable healing. A fibrin clot is not produced after an anterior cruciate ligament injury, maybe because of synovial fluid interference. Repairs of mid-substance intra-articular ligament tears have rarely been successful and as a consequence such interventions have been replaced by primary or secondary reconstructions.
Injury and repair of articular cartilage
The varieties of cartilage include: growth plate (physeal), fibrocartilage at tendon and ligament insertions, elastic (e.g. trachea), fibroelastic (e.g. menisci), and articular cartilage. Articular cartilage functions to reduce friction and distribute loads across joints. It is classically described as avascular, aneural, and alymphatic. Chondrocytes receive nutrients and oxygen from synovial fluid via diffusion through the matrix.
The tissue predominantly consists of water (65–80% of wet weight). Shifts of the retained water in and out of cartilage allow for surface deformation secondary to the stresses applied. In osteoarthritis, the water content may increase to account for 90% of weight. Increased water content results in increased permeability, reduced strength, and decreased Young’s modulus of elasticity. In addition, water is involved in nutrition and lubrication. The primary mechanism responsible for lubrication during dynamic function is elastohydrodynamic lubrication. Here, deformation of articular surfaces and thin films of joint lubricates separates the surfaces. Other types of lubrication methods include: boundary, boosted, hydrodynamic, and weeping lubrication.
Collagen makes up 10–20% of the wet weight and type II collagen accounts for approximately 90–95% of the total collagen content. The cartilaginous framework which anchors the cartilage to the subchondral bone is responsible for tensile strength and shear stiffness. Cartilage consists of a limited number of chondrocytes (5% of wet weight) surrounded by extensive extracellular matrix consisting mainly of type II collagen and proteoglycans (10–15% of wet weight). Protein polysaccharides provide compressive strength. Proteoglycans are produced by chondrocytes and are composed of subunits of gylcosaminoglycans (GAGs). GAGs are bound to a protein core by a sugar bond to form an aggregan molecule. Charged hydrophilic groups on the proteoglycans hold water and produce the swelling pressure resulting in the ability of cartilage to resist compressive loads. Shear and compression squeeze water to the articular surface and thus diminish friction during joint motion. Other matrix components include adhesives (fibronectin, chondronectin) and lipids.
With aging, chondrocytes increase in size and no longer reproduce leading to a relative hypocellularity. Cartilage stiffness increases. The proteoglycans decrease in mass and size. Protein content increases and water content decreases. These changes lead to a reduced elasticity. The structure and layers of articular cartilage are described in Box 1.4.8.
Vascular–inflammatory tissue response to injury occurs only once the subchondral bone is penetrated, allowing distinction between superficial cartilage injuries which do not involve the subchondral bone and deep cartilage injuries which do (Box 1.4.9, Figure 1.4.8).
The stages of cartilage healing are summarized in Box 1.4.10. Deep injuries may heal with fibrocartilage which is produced by undifferentiated marrow mesenchymal stem cells that differentiate into cells capable of producing fibrocartilage. Type I collagen is in abundance at 1 year post injury. For deep injuries, most of our knowledge stems from techniques such as drilling and puncturing the bed of osteochondral defects and abrasion chondroplasty. Here the calcified cartilage is penetrated or removed down to bleeding subchondral bone which is initially covered by a fibrin clot. This is followed by formation of hyaline cartilage (type II collagen) and later fibrocartilage (type I collagen). Superficial lacerations cause chondrocytes to proliferate but do not heal because cartilage is avascular.
Injury and repair of tendons
Structure and anatomy
Tendons are densely arranged tissues that connect and transmit loads from muscle to bone. They are structurally organized in order to resist high tensile forces and are composed of groups of collagen bundles (fascicles—composed of fibrils), separated by endotenon with surrounding epitenon (Box 1.4.11). The predominant cell type is fibroblasts. They are arranged in parallel rows in fascicles with surrounding peritenon (areolar tissue). The spindle-shaped fibroblasts mainly produce type I collagen and synthesize the connective tissue matrix precursors including elastin, and proteoglycans. Elastin is a protein found in small quantities within tendons (less than 1% dry weight). It enables tendons to undergo large changes in length without any permanent structural change. The water-binding capacity of proteoglycans, glycoproteins, and glycosaminoglycans influences the viscoelastic properties of tendons.
The collagen contains a high concentration of the amino acids glycine (33%), proline (15%), and hydroxyproline (15%). All types of collagen consist of three particular chains covalently cross-linked and combined with globular and non-helical structural elements to form a rigid triple tropocollagen molecule. In the extracellular matrix, collagen molecules become aligned head-to-tail and side-by-side in a quarter-staggered array (Figure 1.4.9) leading to a highly ordered and stable unit of microfibrils and fibrils.
Tendons surrounded by paratenon are referred to as vascular tendons. Those surrounded by a tendon sheath are called avascular tendons. The avascular tendons contained within synovial sheaths have mesotenons that function as vascularized conduits called vincula. In addition, both types of tendons have additional blood supply from vessels originating in the muscle and bone attachments.
Tendons insert into bone via four transitional tissues: tendon, fibrocartilage, mineralized fibrocartilage (Sharpey’s fibres), and finally to bone. Tendinous structures orient themselves along stress lines and possess one of the highest tensile strengths of all soft tissues. However, because of the low amount of ground substance, tendons resist shear and compressive forces poorly.
Elongation of tendons is dependent on the force magnitude and the rate and duration of the force. With repetitive loading and unloading, their stress–strain curve moves to the right as the tendon becomes less stiff or more compliant. An increase in elongation, speed, and a higher strain rate moves the curve to the left, indicating increasing stiffness. This protects tendons from rupturing under very large eccentric forces. Tendons also exhibit creep. In an isometric contraction, tendon lengthening from creep allows the muscle to shorten over time. This increases muscle performance by decreasing fatigue.
Factors affecting the properties of tendons are described in Box 1.4.12.
Indirect or direct trauma may lead to tendon injury. The former commonly manifests as an intrasubstance rupture or bony avulsion. The injury is influenced by anatomic location, vascular supply, skeletal maturity, and the magnitude of the applied force. Most indirect injuries are at the bone–tendon or muscle–tendon interface. This is related to tendons’ ability to withstand high tensile forces. Mid-substance tendon rupture is often secondary to pre-existing pathological conditions and may be seen in chronic overuse injuries with repetitive microtrauma and incomplete healing. Common sites of degenerative change include the Achilles, patella, rotator cuff, and biceps tendons.
Tendons have extrinsic and intrinsic healing potential. The extrinsic theory hypothesises that an inflammatory response by the surrounding tissues is involved. The intrinsic theory maintains that tendons possess an intrinsic capability to heal.
Healing continues in three phases: inflammatory, reparative or collagen-producing phase, and a remodelling phase (Box 1.4.13).In the inflammatory phase, cells from the extrinsic peritendinous tissues (synovial sheath, deep fascia, and periosteum) and intrinsic tissue of the epitenon and endotenon move into the injured area (first 48–72h) and remove cellular debris and collagen remnants. Granulation tissue is produced to bridge the defect. In the inflammatory phase, tendon repair strength is almost entirely dependent on the suture strength. In the reparative stage, fibroblasts are actively involved in collagen synthesis and resorption. The remodelling phase results in increased mechanical strength. Tension on the granulation tissue results in remodelling of fibre architecture; similar to Wolff’s law for bone.
Methods of improving tendon repair
The most important factor appears to be postoperative mobilization of tendon repairs. Rapid commencement of tendon gliding provides the stimulus for cellular activation of the epitenon (intrinsic response). Continued immobilization stimulates ingrowth of cells from the surrounding tissues (extrinsic response) leading to adhesions. An ideal postoperative protocol is one providing the greatest tensile stress across a repair and preventing gap formation or rupture of the repair. The ultimate goal is to restore immediate motion and stress to a tendon repair. Limiting factors include the strength of the repair, which is a factor in all locations of injury. The benefits of passive mobilization are characterized in Box 1.4.14.
Following suture principles increases strength of the repair (Box 1.4.15).
Nerve injuries and repair
Peripheral nerve anatomy
The peripheral nerve is a highly organized structure made of nerve fibres, blood vessels, and connective tissue. They possess peripheral processes named axons which are covered with a fibrous tissue called endoneurium. The axons group into nerve bundles called fascicles (smallest unit of a nerve), covered by a connective tissue layer named perineurium. Schwann cells support and surround the axons. Groups of fascicles are bound together by the epineurium, which provides a gliding surface. Fascicles are vascularized segmentally by epineurial vessels and each fascicle has a longitudinally-oriented perineurial and endoneurial microvascular system. Myelinated axons conduct action potentials rapidly, facilitated by nodes of Ranvier (gaps between Schwann cells).
Classification of nerve injuries
Sharp lacerations result in nerve transactions whereas the energy transfer secondary to a blast, crush, or traction injury leads to unpredictable nerve damage. Neurological studies such as electromyography (EMG) and nerve conduction studies may be useful to document injury extent. Cortical evoked potential testing is the most accurate method. Seddon (1943) first described three types of nerve injury: neurapraxia, axonotomesis, and neurotomesis. Subsequently, Sunderland (1951) defined five severity degrees with two degrees lying between axonotomesis and neurotomesis (Box 1.4.16).
Healing of nerve injuries
Peripheral nerve injury results in death of the distal axons and Wallerian degeneration of myelin. Macrophages remove degraded myelin and axoplasm. Regeneration is dependent on nerve cell survival. The remaining Schwann cell tube serves as a guide for the sprouting axon. The distal nerve stumps and target organs facilitate axonal regeneration using neurotropic and adhesive factors. Within hours of injury, a regenerating axon produces multiple sprouts from the most distal intact node of Ranvier which enter the Schwann cell tubes. Eventually, only one axon is regenerated. Proximal axonal budding occurs approximately 1 month post injury and results in regeneration at a rate of about 1mm/day. Pain is the first modality to return. The final pathway to achieving nerve regeneration requires the plasticity or re-education of the central nervous system. The brain must undergo some re-education to interpret the stimulus correctly.
Some basic principles are discussed in Box 1.4.17. Motor recovery is unlikely if there is lack of reinnervation by 18 months, and results are worse if repair is performed 6 months after the injury.
The following key concepts underpin successful nerve repair:
1) Microsurgical techniques with adequate magnification, instrumentation, and microsuture
2) Adequate exposure of both ends followed by debridement and resection of the damaged nerve section to minimize scar tissue formation
3) Reapposition of nerve ends tension-free with avoidance of extreme positioning of the extremity
4) Primary nerve repair should be performed whenever possible
5) Align fascicles accurately.
Accurate nerve alignment is critical for optimal outcome. The simplest method is using anatomical landmarks such as epineural blood vessels and fascicle arrangement. Electrical stimulation in the awake patient can help delineate motor and sensory fascicles in the proximal stump. Staining of the nerve ends using acetylcholinesterase (motor) and carbonic anhydrase (sensory) may be performed on sections of proximal nerve ends to identify sensory and motor fascicles of the proximal stump only.
Three types of direct repair are available to the surgeon: epineural, group fascicular, and fascicular. Factors influencing results of nerve repair are summarized in Box 1.4.18.
♦ Epineural repair is used when internal topography of the nerve is unclear. Fascicles are aligned using fine monofilament suture under high-power magnification. Sutures are placed only through the epineurium to avoid bunching. Tension must be assessed after the repair and the extremity taken through a gentle range of motion
♦ Group fascicular repair is most useful in nerves with few groups and in partial lacerations where complete fascicular groups are lacerated. The fascicle groups are exposed by splitting the epineurium longitudinally. The largest identifiable fascicle group should be repaired first. The epineurium is finally repaired to minimize tension
♦ Fascicular repair is useful in partial lacerations and in nerves with few fascicles. The technique requires dissection of external and internal epineurium to expose the fascicles. Repair is effected using one or two sutures of 10-0 or 11-0 nylon placed in the perineurium.
Complex crush and blast injuries are best treated with nerve grafts. When there is no recovery after approximately 3 months, exploration and repair may be indicated. The success of grafting and sources of nerve graft are documented in Box 1.4.19.
The site of the nerve repair, or the proximal and distal ends of a nerve grafts, are carefully documented. The extremity is immobilized in a position that relaxes all suture lines which may be maintained for 4 weeks. Regeneration is monitored by physical examination and electrical studies. As sensory axons may regenerate to sensory end-organs, the signal the brain receives may not correspond to the actual stimulation. The patient must be re-educated to interpret the new signal. Children accomplish this much more readily than older patients. Placing the cut nerve endings into a tube (silicone, biodegradable material, or vein) has demonstrated excellent results in pure sensory nerve injuries.
Proprioception gives us a sense of position and movement in relation to space, and initiates and coordinates the muscle functions that first stabilize a joint and then make it the fulcrum of a precise, coordinated motion. Deficits occur when afferent sensory nerve fibres are interrupted (injury or disease) and can affect entire limb function. Vision can be a substitute but is less effective in the lower than in the upper extremity. Proprioception relies on information from sensory, visual, and vestibular inputs. Based on afferent information, efferent stimuli are generated centrally. These stimuli activate agonistic and antagonistic muscle groups to reposition joints and extremity segments.
Sensory input derives from muscle spindles, Golgi tendon organs, Pacinian corpuscles, Meissner’s corpuscles, and other receptors in muscles, tendons, ligaments, joints, and skin. The cell bodies of these nerve fibres are located in the dorsal root ganglia. From here, fibres connect to neurons relaying information centrally to the cerebellum, medulla, thalamus, and the cerebral cortex (Figure 1.4.11). Isolated injuries to ligaments, joints, muscles, or other end-organs results in a focal loss of feedback.
Head injuries: presentations and outcomes
Head injury is often associated with major musculoskeletal disruptions and cerebral lesions are commonly diagnosed late or managed inadequately. Head injuries are two to three times more common in males and have a higher incidence in summer months. The commonest mechanism of injury is motor vehicle accidents. Although many head injuries present similarly, they can be differentiated by the type of pathological lesion as follows.
♦ Shearing/diffuse axonal injuries Shearing is a consequence of acceleration, deceleration, and rotational forces which damages the brain by stretching and compressing fibre tracts; and moving the brain over bony prominences. Shearing and diffuse axonal injuries are rarely picked up on initial computed tomography (CT) scans. Magnetic resonance imaging (MRI) is the gold standard in detecting these injuries.
♦ Contusions These are bruises or haematomas on or close to the brain’s surface. They commonly affect the frontal and temporal lobes. They may be asymptomatic or associated with severe neurological deficits and seizures.
♦ Epidural haematoma This refers to a collection of blood between the dura mater and the skull and occurs secondary to a tear of the middle meningeal artery. They can cause sudden compression of the brain and be fatal. Clinically, a short lucid interval is typical, followed by loss of consciousness.
♦ Subdural haematoma The bleeding occurs within the subdural space. Onset may be acute or, especially in the elderly, chronic. Chronic lesions are commonly caused by linear and rotational forces which tear the veins between the brain and the dura mater. Most subdural haematomas result in significant focal damage of the cortex and co-exist with brain contusions.
♦ Subarachnoid haemorrhage Bleeding into the subarachnoid space is often caused by trauma but may occur spontaneously after rupture of a berry aneurysm. The bleeding is usually diffuse and does not cause a space-occupying lesion.
♦ Intracerebral haematomas and brain displacement These space-occupying lesions are often accompanied by swelling of surrounding brain tissues. They may cause life-threatening brain herniation following expansion.
Classification and assessment of head injuries
The Glasgow Coma Scale provides a score (in the range 3–15) to initially assess the likelihood of a brain injury. A score of 3 indicates that the patient is unresponsive. A score less than 9 must prompt an urgent evaluation of the airway. With a score of 15, the patient is alert, oriented, and able to follow commands. While the Glasgow Coma Scale is an excellent predictor of gross outcome, it is less reliable in predicting neurobehavioral outcomes. The most reliable predictor of neurobehavioral outcome is the duration of post-traumatic amnesia. When the patient has sustained post-traumatic amnesia of 24h or less, the head injury is classified as mild. If the post-traumatic amnesia lasts from 24h to 7 days, the head injury is considered moderate. Post-traumatic amnesia beyond 7 days indicates a severe head injury.
CT scans and MRI scans provide additional parameters to assess head injury. However, a patient with a very severe head injury may have negative initial findings on both CT and MRI scans.
In summary, the key factors that predict the severity of a head injury are as follows:
♦ The Glasgow Coma Scale score
♦ Duration of loss of consciousness or coma
♦ Duration of post-traumatic amnesia
♦ The nature and extent of the cerebral lesion as seen on CT or MRI.
Positive prognostic factors include high premorbid intelligence quotients and socioeconomic status, as well as a supportive family structure.
Clinical presentation: postconcussive syndrome
Neurobehavioral symptoms following head injuries are often missed because of inexperience or masking secondary to pain medication. Typical symptoms of postconcussive syndrome include inhibition, euphoria, emotional lability, confusion, memory disturbance, disturbance of social or occupational functions, concentration, and higher-order thought deficits.
Many head injuries have psychological sequelae such as irritability and agitation as well as exaggerated reactions to painful stimuli. Protracted malaise and depression may be the sequelae of a concomitant head injury. Diagnosis and management of many head injuries can be improved by consulting an experienced clinical neuropsychologist skilled in cognitivebehavioural techniques such as desensitization or hypnotherapy.
Acute and chronic higher cortical deficits due to head injuries
Patients with significant head injuries are usually comatose or obtunded on presentation. With recovery, the level of cortical arousal becomes heightened and the mental status improves. Postcomatose patients, display moderate to severe global and diffuse deficits of cognitive function.
Influence of age
Adult patients may remain in a coma for long periods and only gradually recover their mental capabilities. Children tend to improve quickly or perish. Typical symptoms resulting from traumatic brain injury in adults are either absent or short-lived in the paediatric population.
Most adult patients sustaining injury to the temporal lobe will experience severe aphasia, difficulties in comprehension, naming, repetition, reading, and writing. If children present with aphasic symptoms, recovery is often rapid. Complete mutism, which resolves in 1 or 2 weeks, may be pronounced. Similar differences have been observed with respect to visual and visuospatial dysfunction.
Adults may suffer a range of psychiatric conditions, from mild anxiety disorders to psychosis. Children under 10 years of age frequently suffer attention-deficit disorders without the hyperactive component. Adolescents tend to experience depression, anxiety, and explosive behaviour.
Most neurobehavioral recovery occurs 12 months after injury. Improvement up to 3 years is not uncommon. Residual deficits usually involve attention and concentration, verbal and visual memory, and higher-thought processes including planning, problem solving, and strategy formation. Resolution of these symptoms is usually much more complete in the paediatric population.
Allgower, M. and Spiegel, P. (1979). Internal fixation of fractures: Evolution of concepts. Clinical Orthopaedics and Related Research, 138, 26–9.Find this resource:
Anderson, H. (1990). The role of cells versus matrix in bone induction. Connective Tissue Research, 24, 3–12.Find this resource:
Blenman, P., Carter, D., and Beaupre, G. (1989). Role of mechanical loading in the progressive ossification of a fracture callus. Journal of Orthopaedic Research, 7, 398–407.Find this resource:
Buckwalter, J. and Cooper, R. (1987). Bone structure and function. Instructional Course Lectures, 36, 27–48.Find this resource:
Cruess, R. and Dumont, J. (1975). Fracture healing. Canadian Journal of Surgery, 18, 403–13.Find this resource:
Ilizarov, G. (1989). The tension-stress effect on the genesis and growth of tissues: Part I. The influence of stability of fixation and soft tissue preservation. Clinical Orthopaedics, 283, 249–81.Find this resource:
Ilizarov, G. (1989). The tension-stress effect on the genesis and growth of tissues: Part II. The influence of the rate and frequency of distraction. Clinical Orthopaedics, 283, 249–81.Find this resource:
Katz, J.L. (1981). Composite material models for cortical bone. In: Cowin, S.C. (ed) Mechanical Properties of Bone, pp. 171–84. New York: American Society of Mechanical Engineers.Find this resource:
Kenwright, J., Richardson, J., Cunningham, J., et al. (1991). Axial movement and tibial fractures: a controlled randomised trial of treatment. Journal of Bone and Joint Surgery, 73-B, 654–9.Find this resource:
Müller, M., Allgöwer, M., Schneider, R., et al. (1991). Basic aspects of internal fixation. In: Allgöwer, M. (ed), Manual of Internal Fixation. Techniques Recommended by the AO-ASIF group, 3rd edition, pp. 1–158. Berlin: Springer-Verlag.Find this resource:
Perren, S. (1979). Physical and biological aspects of fracture healing with special reference to internal fixation. Clinical Orthopaedics and Related Research, 138, 175–96.Find this resource:
Seddon, H. (1943). Three types of nerve injury. Brain, 66, 237–88.Find this resource:
Sunderland, S. (1951). A classification of peripheral nerve injuries producing loss of function. Brain, 74, 491–516.Find this resource:
Wolff, J. (1892). Das Gesetz der Transformation der Knochen. Hirschwalk, Berlin.Find this resource: