Classification

Fractures can be classified as complete or incomplete and open or closed (Figure 44-1). In a complete fracture the bone is broken all the way through, whereas in an incomplete fracture the bone is damaged but still in one piece. Complete or incomplete fractures also can be classified as open (formerly referred to as compound) if the skin is broken or as closed (formerly called simple) if it is not. A fracture in which a bone breaks into more than two fragments is termed a comminuted fracture. Fractures are classified also according to the direction of the fracture line. A linear fracture runs parallel to the long axis of the bone. An oblique fracture is a slanted fracture of the shaft of the bone. A spiral fracture encircles the bone, and a transverse fracture occurs straight across the bone.

Incomplete fractures tend to occur in the more flexible, growing bones of children. The three main types of incomplete fractures are greenstick, buckle or torus, and bowing. A greenstick fracture perforates one cortex and splinters the spongy bone and is relatively unstable.³ The name is derived from the damage sustained by a young tree branch (a green stick) when it is bent sharply. The outer surface is disrupted, but the inner surface remains intact. Greenstick fractures typically occur in the metaphysis or diaphysis of the tibia, radius, and ulna. In a buckle or torus fracture, the cortex buckles but does not break; this is a relatively stable fracture. Bowing fractures usually occur when longitudinal force is applied to bone. This type of fracture is common in children and usually involves the paired radius-ulna or fibula-tibia. A complete diaphyseal fracture occurs in one of the bones of the pair, which disperses the stress sufficiently to prevent a complete fracture of the second bone, which bows. A bowing fracture resists correction (reduction) because the force necessary to reduce it must be equal to the force that bowed it. Treatment of bowing fractures is difficult also because the bowed bone interferes with reduction of the fractured bone. A fracture that results from a low-level trauma (one that would not normally cause a fracture) is called a fragility fracture, which is often seen in osteoporosis. Types of fractures are summarized in Table 44-1.

Fractures may be further classified by cause as pathologic, stress, or transchondral. A pathologic fracture is a break at the site of a preexisting abnormality (such as a tumor), usually by force that would not fracture a normal bone. Any disease process that weakens a bone (especially the cortex) predisposes the bone to pathologic fracture, commonly associated with tumors, osteoporosis, infections, and metabolic bone disorders.

Stress fractures occur in normal or abnormal bone that is subjected to repeated forces, such as occurs during athletics. Fatigue fractures are caused by abnormal stress or torque applied to a bone with normal ability to deform and recover (e.g., joggers, dancers, military recruits) and are a type of stress fracture. Insufficiency fractures include fragility fractures of osteoporosis and osteomalacia, and occur in bones lacking normal ability to deform and recover (i.e., normal weightbearing or activity fractures the bone).

A transchondral fracture consists of fragmentation and separation of a portion of the articular cartilage that covers the end of a bone at a joint. (Joint structures are defined in Chapter 43.) The fragments may consist of cartilage alone or cartilage and bone. Typical sites of transchondral fracture are the distal femur, the ankle, the kneecap, the elbow, and the wrist. Transchondral fractures are most prevalent in adolescents.

Pathophysiology

When a bone is broken the periosteum and blood vessels in the cortex, marrow, and surrounding soft tissues are disrupted. Bleeding occurs from the damaged ends of the bone and from the neighboring soft tissue. A clot (hematoma) forms within the medullary canal, between the fractured ends of the bone, and beneath the periosteum. Bone tissue immediately adjacent to the fracture dies. This necrotic tissue (along with any debris in the fracture area) stimulates an intense inflammatory response characterized by vasodilation, exudation of plasma and leukocytes, and infiltration by inflammatory leukocytes and mast cells. Cytokines, including transforming growth factor-beta (TGF-β), platelet-derived growth factor (PDGF), prostaglandins, and other factors that promote healing are released. Within 48 hours after the injury, vascular tissue invades the fracture area from surrounding soft tissue and the marrow cavity, and blood flow to the entire bone is increased. Bone-forming cells in the periosteum, endosteum, and marrow are activated to produce subperiosteal procallus along the outer surface of the shaft and over the broken ends of the bone (Figure 44-2). Healing generally occurs in three overlapping phases. The initial inflammatory phase of healing lasts 3 to 4 days. During the next few days, the repair phase begins and capillary ingrowth, together with mononuclear cells and fibroblasts, begins the transformation of a hematoma into granulation tissue. Osteoblasts within the procallus synthesize collagen and matrix, which becomes mineralized to form callus. As the repair process continues, remodeling occurs, during which unnecessary callus is resorbed and trabeculae are formed along lines of stress; at the end of this stage, bone can withstand normal stresses. The last phase, remodeling, lasts for months to years. Except for the liver, bone is unique among all body tissues in that after a fracture it will heal with normal, not scar, tissue.

Clinical Manifestations

The clinical manifestations of a fracture vary according to the type of fracture, site of the fracture, and associated soft tissue injury. In general, the signs and symptoms of a fracture include impaired function, unnatural alignment (deformity), swelling, muscle spasm, tenderness, pain, and impaired sensation. The position of the bone segments is determined by the pull of attached muscles, gravity, and the direction and magnitude of the force that caused the fracture. One or both segments may be rotated inward or outward on the bone’s long axis (rotation), be misaligned at an angle (angulation), slide over the other segment (overriding), or be out of normal position (displaced).

The immediate pain of a fracture is severe and usually caused by trauma. Subsequent pain may be produced by muscle spasm, overriding of the fracture segments, or damage to adjacent soft tissues. Numbness is common and is caused by swelling, pinching or severing of a nerve, trauma, or by bone fragments. Pathologic fractures can cause angular deformity, painless swelling, or generalized bone pain. Stress fractures are painful, not because of trauma, but because of accelerated remodeling. The pain occurs during activity and is usually relieved by rest. Stress fractures also cause local tenderness and soft tissue swelling. Transchondral fractures may be entirely asymptomatic or painful during movement. Range of motion in the joint is limited, and movement may evoke audible clicking sounds (crepitus).

Evaluation and Treatment

Treatment of a displaced fracture involves realigning the bone fragments (reduction) to their normal or anatomic position and holding the fragments in place (immobilization) so that bone union can occur. Several methods are available to reduce a fracture: closed manipulation, traction, and open reduction. Many fractures heal without manipulation—they require only adequate immobilization. A fracture that is malaligned, however, requires more aggressive treatment.

Many fractures can be reduced by closed manipulation: the skin is not opened, and the bone is moved or manipulated into place. Closed manipulation is used when the contour of the bone is in fair alignment and can be maintained well with immobilization.

Traction is used to accomplish or maintain reduction. When bone fragments are displaced (not in their anatomic position), weights are used to apply firm, steady traction (pull) and countertraction to the long axis of the bone. Traction stretches and fatigues muscles that pull the bone fragments out of place, allowing the distal fragment to align with the proximal fragment. Traction can be applied to the skin (skin traction), directly to the involved bone, or distal to the involved bone (skeletal traction). Skin traction is used when only a few pounds of pulling force are needed to realign the fragments or when the traction will be used for brief times only, such as before surgery or, for children with femoral fractures, for 3 to 7 days before applying a cast. In skeletal traction, a pin or wire is drilled through the bone below the fracture site, and a traction bow, rope, and weights are attached to the pin or wire to apply tension and to provide the pulling force needed to overcome the muscle spasm and help realign the fracture fragments.

External fixation can be used to reduce and immobilize significantly displaced open fractures. Pins are placed in the bone proximal and distal to the break and then stabilized by an external frame of clamps and rods (Figure 44-3).

Open reduction is a surgical procedure that exposes the fracture site; the fragments are brought into alignment under direct visualization. Some form of prosthesis, screw, plate, nail, or wire usually is used to maintain the reduction (internal fixation).

Splints and casts are used to immobilize and hold a reduction in place. Improper reduction or immobilization of a fractured bone may result in nonunion, delayed union, or malunion. Nonunion is failure of the bone ends to grow together (Figure 44-4). The gap between the broken ends of the bone fills with dense fibrous and fibrocartilaginous tissue instead of new bone. Occasionally the fibrous tissue contains a fluid-filled space that resembles a joint and is termed a false joint, or pseudarthrosis. Delayed union is union that does not occur until approximately 8 to 9 months after a fracture. Malunion is the healing of a bone in a nonanatomic position. Treatment of delayed union and nonunion includes use of various modalities designed to stimulate new bone formation. Physical modalities, such as implantable or external electric current devices, electromagnetic field generations, and low-density ultrasound, have been effective in stimulating bone formation.⁴ Stem cells and gene therapy also show promise in promoting formation of new bone.^5,6 Large defects in bone can be filled with bone graft or synthetic materials, such as calcium phosphate cement.

Dislocation and Subluxation

Dislocation and subluxation are usually caused by trauma but can also be due to ligamentous laxity, nerve injury, rheumatoid disease, or genetic problems. Dislocation is the temporary displacement of a bone from its normal position in a joint. If a dislocation does not involve a fracture, it is considered a simple dislocation; if there is an associated fracture, it becomes a complex dislocation. If the contact between the two joint surfaces is only partially lost, the injury is called a subluxation.

Dislocation and subluxation are most common in persons younger than 20 years and are generally associated with fractures. Dislocation and subluxation, however, may result from congenital or acquired disorders that cause (1) muscular imbalance, as occurs with congenital hip dislocation or neurologic disorders; (2) incongruities in the articulating surfaces of the bones, such as with rheumatoid arthritis (see p. 1568); or (3) joint instability.

Most often dislocated or subluxated are the joints of the shoulder, elbow, wrist, finger, hip, and knee (Figure 44-5). The shoulder’s glenohumeral joint is a relatively unstable joint because the articular surface of the glenoid cavity is only one third as large as the surface of the humeral head. As a result, the glenohumeral joint is often injured. Physical trauma to the shoulder can cause anterior, posterior, superior, or inferior dislocation. Anterior dislocation is the most common and is usually the result of an indirect force that places the shoulder in extreme external rotation. Posterior dislocations usually occur as a result of trauma. A superior dislocation is rare and usually the result of an extreme forward and upward force on an adducted arm. Inferior displacement is often seen in persons with neurologic injuries of the brachial plexus and is believed to be caused by stretching of the supporting muscles or by joint effusion.

Traumatic dislocation of the elbow joint is common in the immature skeleton. In adults an elbow dislocation is usually associated with a fracture of the ulna or head of the radius. Posterior dislocations occur when the individual falls on an outstretched hand with the elbow extended. Anterior dislocations are usually the result of a direct blow to the flexed elbow.

Traumatic dislocation of the wrist usually involves the distal ulna and carpal bones. Any one of the eight carpal bones can be dislocated after an injury. The most common cause is a fall on the hyperextended hand.

Dislocation in the hand usually involves the metacarpophalangeal and interphalangeal joints. Dislocation of the metacarpophalangeal joint is often the result of a fall on the outstretched hand that forces the joint into hyperextension. Dislocation of the interphalangeal joint occurs as a result of injury to the fingers in a hyperextended position.

Considerable trauma is needed to dislocate the hip. Anterior hip dislocation is rather rare and is caused by forced abduction, for example, when an individual lands on the feet from a high fall. Posterior dislocation of the hip can occur in an automobile accident in which the flexed knee strikes the dashboard.

The knee is a relatively unstable joint that depends heavily on the soft tissue structures around it for support. Because the knee is an unstable weightbearing joint exposed to many different types of motion (flexion, extension, rotation), it is one of the most commonly injured joints. A knee dislocation can be anterior, posterior, lateral, medial, or rotary. It is often the result of a hyperextension injury that occurs during sports activities.

Pathophysiology

When a tendon or ligament is torn, an extensive cascade of inflammatory processes begins. An inflammatory exudate develops between the torn ends. Later, granulation tissue containing macrophages, fibroblasts, and capillary buds grows inward from the surrounding soft tissue and cartilage to begin the repair process. Within 3 to 4 days after the injury, collagen formation begins. At first, collagen formation is random and disorganized. As the collagen fibers interweave and connect with pre-existing tendon fibers, they become organized parallel to the lines of stress. Eventually vascular fibrous tissue fuses the new and surrounding tissues into a single mass. As reorganization takes place, the healing tendon or ligament separates from the surrounding soft tissue. Usually a healing tendon or ligament lacks sufficient strength to withstand strong pull for 4 to 5 weeks after the injury. If strong muscle pull does occur during this time, the tendon or ligament ends may separate again, which causes the tendon or ligament to heal in a lengthened shape with an excessive amount of scar tissue that renders the tendon or ligament functionless. Scar remodeling may take months to years before it is complete.⁷

Clinical Manifestations

Tendon and ligament injuries are painful and are usually accompanied by soft tissue swelling, changes in tendon or ligament contour, and dislocation or subluxation of bones. The pain is generally sharp and localized, and tenderness persists over the distribution of the tendon or ligament. Painful joint swelling usually can be seen in finger and elbow sprains. Flexion deformities of the fingers and thumb occur in injuries to the extensor tendons. Crepitus may accompany tendon injury in the wrist. Pain in the elbow may be accentuated by flexion, supination, and extension of the elbow or by extension of the wrist. Lifting small objects requires extension of the wrist and therefore aggravates the pain. Tendon injuries in the upper arm cause weakness when the individual tries to flex the forearm. Pain is often the key symptom of shoulder injuries. It may be referred to the deltoid muscle or extend down the arm and is aggravated by attempts to actively raise the arms. Depending on the ligament or tendon involved, tendon and ligament injuries in the knee may produce pronounced immobility, absence of lateral movement, instability when walking down stairs, flexion deformity, crepitus, or an upward or downward shift of the patella.

Evaluation and Treatment

Evaluation is based on clinical manifestations, stress radiography, arthroscopy, or arthrography. When possible, treatment consists of protection of the involved structures (splinting), promotion of early motion, and rehabilitation. Suturing the tendon or ligament ends in close approximation may be necessary to treat complete rupture. If this is not possible because of the extent of damage, tendon or ligament grafting may be necessary. Prolonged rehabilitation exercises help ensure that the individual regains nearly normal functions.

Tendinopathy and Bursitis

Trauma and repetitive stress can cause painful degradation of collagen fibers (tendinosis), inflammation of tendons (tendinitis), or inflammation in bursal sacs (bursitis). The term tendinopathy includes tendinitis, tendinosis, and paratendinitis. Studies have shown that vascular ingrowth in tendinopathy (neovascularization) is accompanied with nerve ingrowth, facilitating pain transmission in Achilles and patellar tendinopathies.⁸ Other causes of tendinopathy include crystal deposits, postural misalignment, and hypermobility in a joint. Table 44-2 summarizes classes of tendinopathies.

Epicondylitis is inflammation of a tendon where it attaches to a bone (at its origin). Most tendon pathology, however, is caused by tissue degeneration rather than inflammation.⁹ Epicondylar areas of the humerus, radius, or ulna and the area around the knee are most often involved. Lateral epicondylopathy, commonly called tennis elbow, is the result of tissue degeneration or irritation of the extensor carpi radialis brevis tendon at its origin. Medial epicondylopathy, referred to as golfer’s elbow, is a degenerative process of the pronator teres, flexor carpi radialis, and palmaris longus tendons at the medial humeral condyle (Figure 44-6). Epicondylopathy is also related to smoking, obesity, and work activities that involve forceful or repetitive cyclic flexion and extension of the elbow, or cyclic pronation, supination, extension, and flexion of the wrist that generates loads to the elbow and forearm region.

Bursae are small sacs lined with synovial membrane and filled with synovial fluid; they are located between tendons, muscles, and bony prominences. Their primary function is to separate, lubricate, and cushion these structures. When irritated or injured, these sacs become inflamed and swell. Because most bursae lie outside joints, joint movement is rarely compromised with bursitis. Acute bursitis occurs primarily in the middle years and is often caused by trauma; repetitive irritation can cause chronic bursitis. Septic bursitis is caused by wound infection or bacterial infection of the skin overlying the bursae. Bursitis commonly occurs in the shoulder, hip, knee, and elbow.

Pathophysiology

In tendinitis, inflammatory fluid accumulates causing swelling of the tendon and its enclosing sheath. Inflammatory changes cause thickening of the sheath, which limits movements and causes pain. Microtears cause bleeding, edema, and pain in the involved tendons or surrounding structures. At times, after repeated inflammations, calcium may be deposited in the tendon origin area, causing a calcific tendinitis.

The typical bursitis is an inflammation that is reactive to overuse or excessive pressure. The inflamed bursal sac becomes engorged, and the inflammation can spread to adjacent tissues (Figure 44-7). The inflammation may decrease with rest, heat, and aspiration of the fluid. (Inflammation is discussed in Chapter 7.)

Muscle Strains

Mild injury such as muscle strain is usually seen after traumatic or sports injuries. Muscle strain is a general term for local muscle damage. It is often the result of sudden, forced motion causing the muscle to become stretched beyond normal capacity. Strains often involve the tendon as well. Muscles are ruptured more often than tendons in young people; the opposite is true in older adults. Muscle strain may be chronic when the muscle is repeatedly stretched beyond its usual capacity. There is evidence of tissue disruption with subsequent signs of muscle regeneration and connective tissue repair when a biopsy is performed. Hemorrhage into the surrounding tissue and signs of inflammation also may be present. Knife and gunshot wounds also cause traumatic rupture. Regardless of the cause of trauma, muscle cells usually can regenerate. Regeneration may take up to 6 weeks, and the affected muscle should be protected during this time. Types of muscle strain, together with their manifestations and treatment, are summarized in Table 44-4.

A late complication of localized muscle injury is abnormal bone formation in soft tissue, often called myositis ossificans or heterotopic ossification (HO). Its exact pathophysiology remains unknown, but the basic problem seems to be the inability of mesenchymal cells to differentiate into osteoblastic stem cells and the improper development of fibroblasts into bone-forming cells. Though uncommon, HO is associated with burns, joint surgery, and trauma to the musculoskeletal system or central nervous system. HO may involve muscle or tendons, ligaments, or bones near a muscle.¹⁰ Examples include “rider’s bone,” in which the adductor muscle of the thigh of equestrians becomes calcified, as well as in football players after muscle injury to thigh muscles; and “drill bone,” in which the same complication is seen in the deltoid and pectoral muscles of fencers and infantry soldiers.

Rhabdomyolysis

Once used interchangeably with the term myoglobinuria, rhabdomyolysis is the rapid breakdown of muscle that causes the release of intracellular contents, including protein pigment myoglobin, into the extracellular space and bloodstream. Physical interruptions in the sarcolemmal membrane, called delta lesions, suggest that the sarcolemmal membrane is the route through which muscle constituents are released. Myoglobinuria, first described in victims of crush injuries in London during World War II, refers to the presence of the muscle protein myoglobin in the urine. More recently, myoglobinuria has been reported in individuals found unresponsive and immobile for long periods, such as drug and alcohol overdoses.

Pathophysiology

Rhabdomyolysis is sometimes incorrectly used interchangeably with crush injury (a description of injuries resulting from crushing of a body part), compartment syndrome (the consequences of increased intracompartmental pressures of a muscle), or crush syndrome (the pathophysiologic events caused by rhabdomyolysis, primarily involving the kidneys and coagulation syndrome).¹¹ Although relatively rare, rhabdomyolysis has many causes (Box 44-1) and can result in serious complications, including hyperkalemia (because of the release of intracellular potassium into the circulation), metabolic acidosis (from liberation of intracellular phosphorus and sulfate), acute renal failure (myoglobin precipitates in the tubules, obstructing flow through the nephron and producing injury), and even disseminated intravascular coagulation (DIC) (likely caused by activation of the clotting cascade by sarcolemma damage and release of intracellular components from the damaged muscles). Even the weight of a limp extremity can generate enough pressure to produce muscle ischemia (Figure 44-8).

BOX 44-1   SELECTED CAUSES OF RHABDOMYOLYSIS

Medications and Toxic Substances That Increase the Risk of Rhabdomyolysis

Direct Myotoxicity

HMG-CoA reductase inhibitors (statins), especially in combination with fibrate-derived lipid-lowering agents such as niacin (nicotinic acid; Nicolar)

Cyclosporine (Sandimmune)

Itraconazole (Sporanox)

Erythromycin

Colchicine

Zidovudine (Retrovir)

Corticosteroids

Other Medications and Toxins

Amphetamines

Anesthetic and paralytic agents (halothane, propofol, succinylcholine—malignant hyperthermia syndrome)

Antihistamines (diphenhydramine, doxylamine)

Anti-hyperlipidemic agents (statins, clofibrate, bezafibrate)

Antipsychotics and antidepressants (amitriptyline, doxepine, fluoxetine, haloperidol, lithium, protriptyline, perphenazine, promethazine, chlorpromazine, trifluoperazine)

Caffeine

Cocaine

HIV integrase inhibitor (raltegravir)

Hypnotics and sedatives (benzodiazepines, barbiturates)

Heroin

LSD

Methamphetamine

Methadone

Methylenedioxymethamphetamine (MDMA; “ecstasy”)

Miscellaneous medications (amphotericin B, azathioprine, epsilon-aminocaproic acid, quinidine, penicillamine, salicylates, theophylline, terbutaline, thiazides, vasopressin)

Phencyclidine

Protease inhibitors

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