Mechanism: Many mechanisms may play a role in pediatric trauma. Falls, injuries at play, and motor vehicle accidents account for a majority of childhood fractures.⁵ Unfortunately, younger children may suffer fractures as a consequence of nonaccidental trauma (child abuse). These injuries are often characteristic and are covered in Chapter 144. Children of all ages are increasingly involved in and dedicated to athletics and competitive sports. Certain types of fractures, including stress fractures, are often associated with sporting injury. These fractures are addressed Chapter 145. Pathologic fractures may be seen with bone tumors, and insufficiency fractures may be seen with metabolic bone disease (see Chapter 140).

Fracture Description and Nomenclature: Understanding basic fracture nomenclature is important for effective communication with clinicians and other radiologists. Fractures are subdivided into two basic categories: (1) incomplete (plastic) and (2) complete. Incomplete fractures include greenstick and buckle fractures. Complete fractures should be described based on orientation: transverse, oblique, longitudinal, and spiral. Spiral fractures are defined by an approximately 180-degree or greater twist in the fracture plane. For any fracture, angulation, displacement, diastasis, comminution, and impaction must be described. On follow-up radiographs, any change, in addition to the presence or absence of fracture healing, should be described. The term dislocation should be reserved for joints only, not fracture sites. In addition, whenever describing fractures, involvement of an open physis and articular surface should be described. For physeal fractures, it is acceptable to describe the fracture using the Salter-Harris classification.

Fracture Healing: Fracture healing in children has been described in three phases: (1) inflammatory, (2) reparative, and (3) remodeling (e-Fig. 143-1).⁶ At the time of fracture, bone and periosteum are disrupted. A hematoma is formed at the site of fracture enveloping the ends of the fractured bone. The hematoma may also contain necrotic fragments of bone, bone marrow, and adjacent tissues. An inflammatory response is initiated (inflammatory phase), and the organization of a hematoma then begins. Osteoclasts and osteoblasts arise from precursor cells of the involved tissues. Bone resorption occurs at areas of necrosis.⁷ This peaks 2 to 3 weeks after injury and appears as a poorly defined fracture line.⁸ Initial callus (immature woven bone) is formed during the reparative phase.⁶ Osteoid and chondroid material (callus) forming within the hematoma envelops the fracture fragments, joining and stabilizing them. Endosteal callus also forms within the fracture fragments and is seen as increased density on radiographs. Devitalized portions of bone at the margin of the fracture fragments may undergo resorption and appear demineralized on radiographs. An injury that is less than 5 to 7 days old will not show any of these described radiographic features.⁷ With time, the woven bone of callus is replaced by organized lamellar bone during the remodeling phase. With remodeling, excess thickness from the callus is resorbed and the medullary canal is reestablished. Remodeling lasts months, and occasionally years.^6,7 The healing process is more rapid and complete in children than in adults. Most childhood fractures heal completely and without residual deformity.

Complications: Complications may occur at the time of fracture, during treatment, or as a failure of normal, complete fracture healing. Box 143-1 lists potential complications of pediatric fractures. The incidence of a particular complication varies, depending on many factors, including the site and severity of the fracture, complicating factors (i.e., open fracture), the age and overall health of the patient, associated injuries, and the adequacy of therapy.⁹

In nonunion, healing stops before osseous continuity of the fracture fragments occurs. The fracture fragments may form a pseudoarthrosis. Pseudoarthrosis is most common in the clavicle, humerus, and tibia. Nonunion and pseudoarthroses are uncommon in normal children but may be seen with underlying abnormalities such as neurofibromatosis or congenital insensitivity to pain.10,11 The incidence of nonunion is increased with greater injury, comminution, and distraction and with open fractures complicated by substantial soft tissue injury, infection, or both.¹¹ Delayed union is defined as failure of bone union to occur in the expected time. Malunion indicates fusion in a nonanatomic orientation. Mild degrees of malalignment are well tolerated and usually result in no permanent deformity and resolve overtime because of remodeling. Surgical interruption of the healing process to correct residual malalignment is occasionally necessary. Posttraumatic synostoses are most common in the paired bones of the forearm and leg. Infection may occur due to an open fracture or as a complication of surgery or percutaneous pinning.¹¹

Fracture at certain sites may result in neurovascular injury; however, such injuries are rare and usually only seen with substantial displacement and deformity, as may occur with supracondylar fractures of the distal humerus.⁹ Compartment syndrome is an uncommon complication of extremity fractures, most commonly in the leg or with supracondylar elbow fractures, and may lead to Volkmann contracture caused by ischemia.⁹

Reflex sympathetic dystrophy syndrome (RSDS; also called “Sudeck atrophy”) is a poorly understood dysfunction of the autonomic nervous system after injury. RSDS most commonly affects the lower extremities in children. Patients present with pain, swelling, joint stiffness, and exquisite sensitivity to touch.¹² Onset of symptoms is within 1 week to several months after injury.⁹ Radiographs show osteopenia that is difficult to distinguish from disuse osteoporosis. Magnetic resonance imaging (MRI) can show patchy bone marrow edema; however, at times it may be normal.¹³ Bone scintigraphy is usually abnormal. Early, increased activity is seen on perfusion, blood pool, and delayed phases. Later, decreased activity may be seen on both perfusion and blood pool phases, with increased activity remaining during the delayed phase for months.¹⁴ The characteristic imaging findings seen in adult patients may not be seen in children.¹⁵ RSDS has been more recently categorized under the more general term bone marrow edema syndrome, which includes other transient clinical conditions with an unknown underlying mechanism, such as transient osteoporosis of the hip.¹⁴

Premature fusion occurs in approximately 15% of physeal fractures.¹⁶ A bony “bridge” or “bar” forms across the physis.¹⁷ Prognosis depends on the involved bone, the extent and location of the physeal bar (central versus eccentric), and the amount of remaining growth.^11,16 Morbidity is greater when the remaining growth potential is higher. The phalanges and distal radius are the most common sites of physeal fracture; however, growth arrest is rare.¹⁶ The distal femur and proximal tibia have high incidence of posttraumatic physeal fusion but are less common sites for physeal fracture.¹⁶ Premature fusion in the distal femur and tibia is also of greater clinical importance because of possible resultant leg length discrepancy or angular deformity.¹⁶ Indirect physeal insult such as burns, frostbite, and electrical injury, which are discussed later in this chapter, and other processes such as infection and secondary ischemic insult related to meningococcemia can also cause premature physeal fusion (Box 143-2).

Central fusions cause loss of growth potential. Central fusions result in a cupped appearance of the physis, with the epiphysis and physis invaginating into the center of the metaphysis.11,16 Peripheral fusions result in angular deformity.^11,16 Premature physeal fusion usually occurs approximately 3 months after injury.¹⁶ Radiographs may show obliteration of the physeal clear space. Comparison views are often helpful, particularly when evaluating an older child in whom the time of normal physeal closure is near. A secondary sign of premature physeal fusion is tethering of growth lines.¹⁶ Growth lines normally form during the healing process. Normal growth lines parallel the physis, whereas with premature fusion, growth lines are angled toward a bony bar.¹⁶

Both computed tomography (CT) and MRI have been used to diagnose and map areas of premature fusion. With CT, a limited scan with narrow collimation is obtained through the physis. A standard protocol obtains 1.25-mm images overlapping at 0.625-mm intervals. Sagittal and coronal reformats will show the area of fusion. Small bars may be seen as a sclerotic band across the physis, whereas with larger areas of fusion, continuity of the marrow space across the fusion is seen.11,16,18 Cartilage-sensitive sequences (proton density with fat saturation, three-dimensional spoiled gradient recalled echo with fat saturation) can be employed on MRI to delineate the physis (Fig. 143-2). Areas of fusion will be seen as defects within the bright signal of the cartilaginous physis.^16,19 These sequences can also be helpful to detect the potential fracture complication of trapped periosteum within the physis.²⁰ With either CT or MRI, maps can be created showing the degree and site of fusion.

When a child is less than 2 years old or has 2 cm of growth remaining or when the bar involves less than 50% of the physis, resection of the bar can be considered.11,21 A plug of fatty tissue can be placed in the void.²¹ Premature fusion may recur. If greater than 50% of the physis is fused, resection of the bar may be impractical. Depending on the deformity and growth potential of the patient, other orthopedic techniques may be utilized to minimize morbidity from the premature fusion, including osteotomy and contralateral epiphysiodesis (surgical physeal fusion).¹¹

Imaging: Radiographs are the mainstay of imaging of traumatic injuries to the pediatric skeleton. As a general rule, two orthogonal views are obtained to assess for fracture at nonosteoarticular locations and an additional oblique view at osteoarticular locations. At some locations, normal anatomy limits the value of orthogonal projections (i.e., the pelvis). At other locations, unique projections are helpful for delineation of anatomy (i.e., an axillary view of the shoulder, and a sunrise view of the knee). When imaging a long bone, both the proximal and distal joints must be included.

Contralateral comparison views are not routinely obtained, but frequently aid in differentiating normal developmental variation from pathology.²² Comparison views are most helpful in areas of complex anatomy such as the elbow. Normal variants are common and may mimic fracture.

At certain sites and with complex patterns of injury, CT is very helpful in diagnosing fractures and delineating the anatomy of fracture planes and resultant deformity. Occasionally, MRI or ultrasonography can be used to diagnose fractures in children; however, these modalities excel in delineating associated soft tissue injury rather than osseous injury. Ultrasonography, however, may be particularly helpful in infants whose epiphyses are not yet ossified. It also can be used to detect lipohemarthrosis as an indirect sign of fracture or to aid in diagnosis of an occult fracture.²³ The cartilaginous epiphysis is well seen with ultrasonography, and its relationship and continuity with an adjacent metaphysis can be readily assessed. With the increasing capabilities of cross-sectional imaging, nuclear scintigraphy is less utilized than in the past. Nonetheless, scintigraphy can be a valuable tool to identify an occult fracture. Bone scans typically become positive 24 to 48 hours after a fracture.

Etiology, Pathophysiology, and Clinical Presentation: The composition of bones in a child is different from that of bones in an adult.²⁴ The most apparent anatomic difference in the pediatric skeleton is the presence of the physis and a thick periosteum.²⁵ The plasticity of a child’s bones allows for substantial deformity prior to fracture (e-Fig. 143-3).² Bone may give way and may become permanently deformed prior to a complete break. The result is an “incomplete fracture” or a “plastic fracture.”

A greenstick fracture occurs when a cortical fracture occurs on the tension side of bone with intact cortex on the loading side of bone. A torus or buckle fracture is a cortical fracture occurring on the loading side of bone with intact cortex on the tension side. A bowing deformity does not have a radiographically identifiable fracture line on either the tension or loading side of bone.

Greenstick fractures most commonly occur in long bones, particularly the radius and ulna.² These fractures are most common in the first decade of life, are uncommon in the second decade of life, and are not seen in normally developed and mineralized bones of adults.² Buckle fractures most commonly affect the distal radius and ulna, tibia, and proximal first metatarsal bone.

Imaging: Radiographs are the standard method of evaluation and advanced imaging is usually not indicated. Subtypes of incomplete fractures are buckle or torus fractures (Fig. 143-4), lead pipe fractures (part transverse fracture or part buckle fracture), greenstick fractures (Fig. 143-5), and bowing deformities (e-Fig. 143-6). With incomplete fractures, the periosteum is intact wherever the cortex is intact.²

Treatment: Cast and splinting is usually performed for pain control since most of these fractures are stable. Plastic fractures usually heal completely and have a good prognosis. Rarely, it may be necessary to operatively “complete” the fracture for reduction of severe angular deformity. Mild angular deformities (<15 degrees) usually do not need to be reduced and will remodel nicely without permanent sequelae.

Etiology, Pathophysiology, and Clinical Presentation: For the musculoskeletal unit of the child, the physis and physeal equivalent regions are points of relative weakness and are thus predisposed to mechanical failure leading to fractures.²⁶ The physis usually fails before ligamentous or tendinous soft tissue structures fail after biomechanical stress. This occurs more frequently during growth spurts, and affects the lower extremities more frequently than the upper extremities. Once the physis fuses, ligamentous and tendon soft tissue injuries become more frequent, as do metadiaphyseal fractures. Fracture patterns in older children are similar to fracture patterns seen in adults.

Approximately 18% of pediatric fractures involve the physes.²⁷ Physeal fractures are classified by the system of Salter and Harris (Fig. 143-7). The Salter-Harris classification is a well-accepted classification scheme for describing physeal fractures and therefore facilitates efficient communication between clinicians and radiologists.

Imaging: Most physeal fractures are adequately delineated by radiography. Since these fractures are at the ends of bones, potential epiphyseal and intraarticular extent of fracture may be present and therefore, three views are necessary (frontal, lateral, oblique). The Salter-Harris classification of fractures, the degree of diastasis and angulation, if present, loose bodies, and any intraarticular involvement should be considered.

Fractures through the physis may pass solely and directly through the physis (Salter-Harris I; e-Fig. 143-8), involve the physis and a portion of the metaphysis (Salter-Harris II; Fig. 143-9), involve the physis and a portion of the epiphysis (Salter-Harris III; e-Fig. 143-10), or cross the physis in single plane involving both epiphysis and metaphysis (Salter-Harris IV; e-Fig. 143-11). Crush injury of the physis (Salter-Harris V) is rare as an isolated injury to the bone and is rarely, if ever, diagnosed prospectively. Although not in common use, additional fracture types are included in an expanded Salter-Harris classification. A Salter-Harris VI fracture occurs at the perichondral ring at the edge of the physis. A Salter-Harris VII fracture is confined to the epiphyses.^2,26,28

Many lesser grades of Salter-Harris fractures that proceed to premature physeal fusion probably have a component of Salter-Harris V injury. The Salter-Harris classification serves to assign prognosis. Higher grade Salter-Harris fractures have a higher incidence of premature physeal fusion. Most physeal fractures, however, are either Salter-Harris I (approximately 10%) or Salter-Harris II (approximately 75%). Thus, although premature physeal fusion is more likely to occur with a higher grade Salter-Harris fracture, this complication is probably more commonly the result of a lower grade Salter-Harris fracture.

Fracture planes within the physis pass through the zone of calcified cartilage and adjacent newly formed bone, which represent the point of least resistance to fracture forces. Fracture lines that extend into the epiphysis (Salter-Harris III and IV) cross the zone of proliferating cartilage, which is more susceptible to damage leading to premature physeal fusion. The zone of proliferating cartilage is thought to be damaged by Salter-Harris V fractures. Malalignment of Salter-Harris IV fracture fragments may promote formation of a bridge across the healing fracture from metaphysis to epiphysis.²⁸

At certain locations, CT or MRI may be used to confirm or further delineate fractures, especially for defining exact measurements of fracture diastasis and whether involvement of an articular surface exists. Defining exact measurements of fracture diastasis is important especially when an articular cartilage is involved, especially at weightbearing zones (e.g., tibial plafond). On MRI, physeal fractures are diagnosed by widening and increased T2-weighted signal within the fractured portion of the physis, adjacent bone marrow edema, associated metaphyseal (Salter-Harris II) or epiphyseal (Salter-Harris III) fracture lines, and periosteal disruption.²⁹ The most significant complication of physeal injuries is growth arrest (see Fig. 143-2), which can lead to deformity and limb length discrepancies.³⁰ A rare complication of physeal fracture diagnosed by MRI is entrapment of periosteum within the fracture (e-Fig. 143-12). The entrapped periosteum will prevent complete reduction of the fracture. MRI can also be used to evaluate physeal fractures that have a significant risk of complications.³¹

Treatment: Salter-Harris I and II fractures are usually treated by closed manipulation followed by casting. Salter-Harris type III and IV fractures usually require open reduction and internal fixation, as often, these types of fractures are displaced and extend to the joint. To prevent posttraumatic osteoarthritis, it is important to create a smooth articular surface; therefore, Salter-Harris fractures with epiphyseal involvement and greater than 2 mm of diastasis or significant angulation usually need the epiphyseal component surgically reduced with orthopedic fixation.

Most (85%) of growth plate injuries heal without complication; however, in a subset of patients angulation and growth arrest may occur, and this depends on the location of the physeal insult.28,32 Angular deformities tend to occur when the physeal insult is eccentric, and limb shortening without angulation may occur when the physeal insult is central. Sometimes, paradoxic overgrowth may result after a Salter-Harris fracture. This is related to regional trophic effects associated with fracture healing.

Etiology, Pathophysiology, and Clinical Presentation: Injury to the proximal humerus varies with the age of the child. Infants and toddlers are likely to have a Salter-Harris I fracture of the proximal humeral physis. From 5 to 10 years of age, buckle fractures of the proximal humeral metaphysis are most prevalent (e-Fig. 143-13). These fractures may have considerable angulation. In older children, Salter-Harris II fractures predominate (e-Fig. 143-14). Fractures of the humeral diaphysis are also common.³³

Glenohumeral dislocation and instability is uncommon in younger children.³⁴ This is because the physis and metaphysis are less resilient to biomechanical stress compared with the glenohumeral capsule and ligaments. Glenohumeral dislocation is common in older teens and patterns of injury are similar to those in young adults.

The proximal humeral physis can be a site of birth trauma with the middle third of the humerus most commonly fractured.³⁵ Similar injuries can also be seen with child abuse.

Imaging: Anteroposterior and lateral radiographs of the humerus should be obtained to initially evaluate a fracture. If the fracture is near or involves the glenohumeral joint, an additional axillary view is recommended. If a Salter-Harris type I fracture is suspected in the neonate, evaluation with ultrasonography is preferable, as the proximal humeral epiphysis is cartilaginous and therefore better assessed with ultrasonography. For older patients or those with complex proximal humeral fractures, CT or MRI may be useful to evaluate for intraarticular extension and for involvement of the greater and lesser tuberosities.

Radiographically, since the humeral head is usually not ossified or only slightly ossified at birth, fracture through the physis mimics dislocation of the shoulder (e-Fig. 143-15). The humeral metaphysis may appear to align inferior to the glenoid. In the newborn, Salter-Harris I fracture of the proximal humerus is much more common than glenohumeral dislocation.³⁶ Ultrasound may be used to diagnose the fracture by showing malalignment of the cartilaginous humeral head with the proximal humeral metaphysis and showing motion at the physis (e-Fig. 143-16).^36,37

Salter-Harris fractures of the proximal humerus in older children are usually Salter-Harris II fractures, although the metaphyseal fragment is often very small. Occasionally, no metaphyseal fragment exists. Such Salter-Harris I fractures are sometimes called “slipped capital humeral epiphysis.” Typically, with a Salter-Harris I or II fracture of the proximal humerus, the epiphyseal fragment rotates medially because of unopposed pull by the rotator cuff.³⁵ Salter-Harris III and IV fractures of the proximal humerus are extraordinarily rare. Avulsion of the greater tuberosity is a Salter-Harris III fracture. Avulsions of the lesser tuberosity caused by hyperextension with avulsion of the subscapularis tendon are rare and often delayed in diagnosis and are best delineated by an axillary view.^38,39 Chronic avulsive injury of the deltoid insertion site has been reported.⁴⁰

In very young children, fractures of the humeral diaphysis may be incomplete fractures; however, beyond the toddler years, most fractures of the humeral diaphysis are complete fractures. The humerus is one of the more common sites for a pathologic fracture because of its propensity to develop bone cysts.⁴¹ The positioning and alignment of the fragments of a humeral fracture are dependent on the site of fracture and its relationship to the deltoid and pectoral muscular insertions.

Management: Treatment is variable. Proximal humeral fractures are usually treated nonsurgically, including those with significant angulation and displacement. Fractures will heal and remodel without long-term orthopedic sequelae. However, some advocate operative management in certain situations.42,43 Reduction may be necessary in patients near skeletal maturity if the fracture has more than 50 to 70 degrees of angulation in the coronal or sagittal plane.⁴⁴ Operative intervention also is indicated in those patients with associated neurovascular injury or who have intraarticular or open fractures.

Etiology, Pathophysiology, and Clinical Presentation: Supracondylar fractures of the distal humerus account for 60% of pediatric elbow fractures.⁶⁶ The usual mechanism of injury is hyperextension with impingement of the olecranon on the posterior distal humerus.⁶⁷ Fractures vary widely in severity from a faintly perceptible buckle fracture to a complete fracture with marked displacement and angulation. A significant percentage of patients with a supracondylar fracture will have an ipsilateral forearm fracture.⁶⁸

Imaging: Anteroposterior, oblique, and lateral radiographs are required not only for diagnosis but also to guide appropriate management.⁴⁷ Comparison with the contralateral elbow may be helpful in some instances but is not routinely necessary.⁶⁹ The distal fragment of a supracondylar fracture is often displaced or angulated posteriorly. As a result, the anterior humeral cortical line will not bisect the capitellum. In a normal elbow, anterior angulation of the distal humeral condyles causes the anterior humeral cortical line to pass through the center of the capitellar ossification center. If this line passes through the anterior third of the capitellar ossification center or anterior to it, then a supracondylar fracture is likely present.⁶⁵ It is important to assess for this finding on a properly positioned lateral view of the distal humerus. Obliquity of the distal humerus may cause the capitellar ossification center to appear falsely posterior relative to the anterior humeral cortical line.⁶⁵ Supracondylar fractures invariably involve the distal humeral metaphysis but physeal involvement is unusual.

The modified Gartland classification system of supracondylar fractures is the most commonly used to succinctly describe the fracture and for treatment planning.⁷⁰ Type I supracondylar fractures are nondisplaced or minimally displaced less than 2 mm and have an intact anterior humeral line (see Fig. 143-18). Type II fractures are displaced greater than 2 mm with angulation and disruption of the anterior humeral line, but with an intact posterior cortex. Type III fractures are displaced with no cortical continuity (e-Fig. 143-20). Type III fractures are subdivided into posteromedial and posterolateral fractures on the basis of displacement. Most type II and all type III fractures are treated surgically.⁶⁷ The risk of developing epiphyseal osteonecrosis of the trochlea should be considered if surgery is delayed.⁷¹ Neurovascular injury may occur with displaced supracondylar fractures.

Underreduced supracondylar fractures may cause clinically significant limitations in elbow flexion.⁷² After reduction, supracondylar fractures often demonstrate a mild degree of posterior displacement or angulation. This will not adversely affect functional outcome; however, fusion with loss of normal cubitus valgus will potentially inhibit the range of motion of the elbow. Normally, slight lateral angulation of the radius exists relative to the humerus (cubitus valgus) and is greater in females. The Baumann angle is created by the intersection of the humeral axis with a line tangent to the physis of the lateral condyle (e-Fig. 143-21). The normal angle is approximately 75 degrees. With posttraumatic cubitus varus, the Baumann angle is greater than 83 degrees.⁷³ Unfortunately, the Baumann angle is somewhat dependent on positioning. Cubitus varus deformity is thought to occur secondary to medial angulation of the distal fracture fragment.⁷⁴ Severe deformity of the distal humerus with cubitus varus has been called “gun stock deformity.”

Treatment: Conservative versus operative management generally depends on the degree of displacement, age of the patient, location of the fracture, stability of the fracture, and associated injuries. A nondisplaced or acceptably displaced fracture will be treated conservatively; an acceptable displacement is defined as one that will be corrected by expected growth and thickness of the injured bone.⁷⁵ For example, most type I or nondisplaced supracondylar fractures can be treated conservatively in a long arm cast for 3 to 4 weeks with the elbow held in 90 to 110 degrees of flexion. Most type II and III supracondylar fractures are treated operatively with closed reduction and percutaneous pinning.^76,77 Most supracondylar fractures can be electively treated (i.e., next morning for a fracture identified afterhours), including type III fractures. Patients exhibiting neurovascular compromise, however, require immediate treatment.

Etiology, Pathophysiology, and Clinical Presentation: Lateral condylar fractures are the second most common type of fracture of the pediatric elbow, accounting for 12% to 20% of pediatric elbow fractures.⁷⁸ The mechanism is hyperextension with varus stress.⁶⁶ Lateral condylar fractures are considered Salter-Harris IV fractures until proven otherwise.

Imaging: In addition to the standard anteroposterior and lateral radiographs, some advocate obtaining an internal oblique view to better delineate the lateral condylar fracture gap.⁷⁹ External oblique views tend to obscure the lateral condylar fracture but are better for delineating the radial head and neck. MDCT may be useful in certain cases to decide between surgical and nonsurgical management.⁸⁰ The severity of lateral condylar fractures varies considerably. The fracture may or may not extend through the unossified portion of the distal humeral epiphysis (e-Fig. 143-22). “Stable” lateral condylar fractures (type I) do not traverse the cartilaginous epiphysis and are incomplete and thus nondisplaced or minimally displaced (Fig. 143-23). Type II lateral condylar fractures are complete and thus “unstable” but with little or no displacement. The lateral condylar fracture line may be quite subtle, often paralleling the adjacent metaphyseal margin.

In the past, arthrography (with or without CT) was occasionally used to assess for the epiphyseal fracture line.⁸¹ Both MRI and ultrasonography have proven capable of demonstrating the fracture through epiphyseal cartilage indicating a Salter-Harris IV fracture.⁸² With complete or “unstable” fractures, the lateral condylar fragment is displaced and rotated (type III; e-Fig. 143-24).

Treatment: Lateral condylar fractures that are nondisplaced (stable) or are displaced 2 mm or less are managed with cast immobilization. Those that are displaced greater than 2 mm (unstable) are treated with surgical fixation with lateral entry pins.⁷⁸ A lower threshold exists for surgical intervention of lateral condylar fractures compared with supracondylar fractures because these fractures involve the physis and may have an intraarticular component. Physeal growth arrest and posttraumatic osteoarthritis are more common complications of lateral condylar fractures compared with supracondylar fractures. The most common long-term deformity is relative lateral overgrowth with subsequent cubitus varus.⁸³

Etiology, Pathophysiology, and Clinical Presentation: The medial epicondyle ossifies by age 7 years and fuses by age 16 years.⁸⁴ The medial epicondyle is the origin of the forearm flexor mechanism and ulnar collateral ligaments. Avulsions thus occur within this age range, although rare avulsions of the unossified medial epicondyle have been reported.⁸⁵ The two chief mechanisms of acute avulsion fracture of the medial epicondyle are (1) throwing injury and (2) elbow dislocation.^84,86 Acute avulsion of the medial epicondyle is but one of several injuries that can occur in the elbow of a skeletally immature throwing athlete.⁸⁷ The avulsion occurs because of hyperextension, with valgus stress producing traction on the apophysis by the flexor tendons and pronators. In the setting of an acute avulsion, the child will experience sudden-onset medial elbow pain while throwing and have point tenderness over the medial epicondyle.⁸⁷ Rarely, the medial epicondyle may displace into the joint mimicking a trochlear ossification center. This occurs because the valgus stress of throwing temporarily widens the joint.

Imaging: Initial assessment should include anteroposterior, oblique, and lateral radiographs of the elbow (Fig. 143-25). With elbow dislocation in the skeletally immature patient, the medial epicondyle is often avulsed from its normal location. When assessing the images of a dislocated elbow, the status of the medial epicondyle should be specifically addressed (e-Fig. 143-26). In addition, radiographs should address the type of avulsion fracture when present at the level of the medial epicondyle chondro-osseous junction, physeal equivalent, or at the juxtaphyseal metaphyseal equivalent region with displaced and fragmented bone.

Some cases of medial epicondyle avulsion fracture occur with a transient, unrecognized dislocation. When an elbow dislocation is reduced, the medial epicondyle may be trapped in the elbow joint (Fig. 143-27). A trapped medial epicondyle may superficially mimic a trochlear ossification center in the first decade of life. However, absence of the medial epicondyle at its normal location should prompt a search for it within the joint. If the trochlea is ossified, the medial epicondyle should be as well. Visualization of the trochlea without the medial epicondyle may be caused by displacement of the medial epicondyle or by a displaced medial epicondyle being mistaken for the trochlea.

Comparison views may be helpful in confirming mildly displaced medial epicondylar avulsion injuries at the level of the medial epicondyle physeal equivalent region; however, they are usually not necessary. MRI and CT will often demonstrate associated findings such as injury to the ulnar collateral ligament and the sublime tubercle of the ulna, as well as compression-type injuries in the lateral compartment, such as radiocapitellar osteochondral injuries and bone contusions. However, these additional findings often will not change clinical management.88,89 MRI and CT are useful when radiographs do not demonstrate a clear fracture and an alternative etiology for the child’s symptoms are sought. Avulsion of the medial epicondyle prior to its ossification is distinctly rare but has been reported. Ultrasonography as well as CT or MRI can be used for fracture delineation.⁹⁰

Treatment: Both surgical and nonsurgical management has been supported in the literature.⁶⁵ Indication for operative treatment include entrapment of the medial epicondyle in the joint and the uncommon occurrence of an open fracture.⁶⁵ Medial epicondyle avulsion fractures can be treated conservatively if the avulsed fragment is not intraarticular, if the child is less than 5 years of age or the degree of displacement is less than 4 mm. Generally, the need for intervention increases with the age of the child, degree of dislocation, and athletic activity.⁹¹

Etiology, Pathophysiology, and Clinical Presentation: Medial condylar fracture, not to be confused with medial epicondylar avulsion (see above), has an appearance similar to the more common lateral condylar fracture. Medial condylar fractures are uncommon and account for 1% to 2% of pediatric elbow fractures.⁶⁶ These are typically Salter-Harris type IV fractures.

Imaging: Initial assessment should include anteroposterior, external oblique, and lateral radiographs of the elbow. The fracture line extends through the medial metaphysis separating the metaphysis and medial epicondyle from the remainder of the humerus; the fracture line extends to the trochlear articular surface. MRI can also be useful to evaluate these fractures particularly in young children in whom the diagnosis can be difficult.⁹²

Treatment: Most minimally displaced fractures can be treated conservatively with immobilization. Surgical treatment is usually performed if displacement at the fracture site is greater than 2 mm.⁹²

Etiology, Pathophysiology, and Clinical Presentation: Distal humeral Salter-Harris I fracture is an uncommon fracture that occurs from birth to approximately age 7 years, peaking at age 2.5 years. It is typically an injury of infants and young toddlers and is caused by child abuse in half of the cases, or by a rare birth injury.66,93

Imaging: Radiographically, the fracture may be mistaken for a dislocation of the elbow, as the bones do not appear to align. The radial axis will be normally aligned with the capitellum, but the capitellum itself will be abnormally related to the distal humeral metaphysis (e-Figs. 143-28 through 143-30). The radius, ulna and humeral epiphysis will be medially displaced. Fractures may occur prior to capitellar ossification.⁹⁴

Treatment: Nondisplaced fractures will be treated with splinting or percutaneous pinning. Displaced fractures usually are treated with open reduction and internal fixation.

Etiology, Pathophysiology, and Clinical Presentation: Fractures of the radial head and neck account for 5% of pediatric elbow fractures.⁶⁶ Mechanism of injury is falling on an outstretched hand. Fractures in children often occur at or just distal to the physis; this is unlike the adult population where fractures typically involve the radial head.⁶⁶ Associated injuries include fracture of the olecranon, avulsion of the medial epicondyle, or medial collateral ligament injury.⁶⁶

Imaging: Radiographs are usually sufficient for diagnosis and follow-up. External oblique views best delineate the radial head and neck morphology, whereas internal oblique views are better for delineating the lateral condylar region. Radial neck fractures are usually buckle fractures followed by Salter-Harris fractures. Isolated radial neck fractures as well as fractures with extension to the radial head are unusual. The radiocapitellar joint is often preserved even when radial neck fractures are displaced and angulated (e-Fig. 143-31).