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Growth Plate (Physeal) Fractures Treatment & Management

  • Author: Charles T Mehlman, DO, MPH; Chief Editor: Dennis P Grogan, MD  more...
 
Updated: Dec 12, 2014
 

Medical Therapy

Very commonly, growth plate (physeal) fractures can be treated nonoperatively. Factors that affect treatment decisions include the following:

  • Severity of the injury
  • Anatomic location of the injury
  • Classification of the fracture
  • Plane of the deformity
  • Patient age
  • Growth potential of the involved physis

Most Salter-Harris (SH) I and II injuries can be treated with closed reduction and casting or splinting and then reexamination in 7-10 days to evaluate maintenance of the reduction.

Closed reductions through manipulation and traction must be performed carefully, with the patient (and the involved musculature) as relaxed as possible in order to avoid unnecessary wrestling of the bony components that may lead to grating of the physis on sharp metaphyseal bone fragments and potential damage to the physis.

Less-than-satisfactory reductions are preferred to repeated attempts at reduction that may damage the germinal layer of cells within the physis. To avoid physeal damage, efforts at reduction should focus more on traction and less on forceful manipulation of the bone fragments.

Disruption of the physis may warrant restoration of its congruency in order to ensure proper joint mechanics. Angular deformities may also occur as a consequence of malreduction or partial growth arrest. The location and direction of the deformity must be considered in planning treatment. In general, greater angular deformity can be tolerated in the upper extremity than in the lower extremity, more valgus deformity can be tolerated than varus, and more flexion deformity can be tolerated than extension.

More proximal deformities of the lower extremity (in the hip) are better compensated for than distal deformities (in the knee and, least of all, the ankle). Spontaneous correction of angular deformities is greatest when the asymmetry is in the plane of flexion or extension (ie, the plane of joint motion), with function often returning to normal unless the fracture occurs near the end of growth.

The age of the patient at the time of injury is of paramount importance in helping predict clinical outcomes because more correction can be anticipated in younger patients. For instance, injuries to the physes of 14- to 15-year-old girls or 17- to 18-year-old boys are of little consequence, given the limited growth potential. As a result, any growth plate injury is unlikely to be clinically significant. However, injuries in younger children with full growth potential can cause significant problems and a wide range of clinical effects.

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Surgical Therapy

More severe injuries involving intra-articular fractures (SH III and IV) typically require anatomic reduction with open reduction and internal fixation that avoids crossing the physis. Smooth pins should parallel the physis in the epiphysis or metaphysis, avoiding the physis. Oblique application of pins across the physis should be considered only when satisfactory internal fixation is unattainable with transverse fixation. Any internal fixation devices should be easily removable yet adequate for internal fixation.

Type V fractures are rarely diagnosed acutely, and unfortunately, treatment is often delayed until the formation of a bony bar across the physis is evident. A high level of clinical suspicion is necessary to detect this complication early. In many cases, "early" may mean 6 months or more after the injury.

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Follow-up

Long-term follow-up is essential for determining whether complications will occur. Most growth plate (physeal) injuries should be reevaluated in the short term to ensure maintenance of reduction and proper anatomic relations. Some growth plate fractures are more problematic than others when it comes to the risk of growth arrest. Physeal fractures that are considered to be at increased risk for growth arrest include fractures to the following growth plates:

  • Distal femur [13]
  • Distal tibia [14]
  • Distal radius and ulna
  • Proximal tibia
  • Triradiate cartilage

After initial fracture healing has occurred, physeal fractures require additional follow-up radiographs 6 months and 12 months after injury to assess for growth disturbance. Management of such physeal fractures can thus be divided into two phases. The first phase involves ensuring bone healing, and the second phase involves monitoring growth.

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Complications

Growth acceleration

Growth acceleration is a possible complication of physeal injuries; however, it is uncommon. This complication usually occurs in the first 6-18 months after the initial injury. The rapid healing of the physis enables an increased vascular response that is usually of shorter duration than that for healing of bony fractures. Accelerated growth patterns also may be associated with the use of implants and fixation devices that may stimulate longitudinal growth.

The greater growth is rarely significant but may require future assessment by the clinician. Treatment for this acceleration in adolescents may involve an epiphysiodesis of the longer limb to avoid producing disproportionate limbs. If more than 6 cm of correction is desired, this is not a treatment option, and the clinician may consider lengthening procedures for bilateral limb-length equilibration.

Growth arrest

Complete growth retardation or partial growth arrest may result in progressive limb-length discrepancies. Complete growth arrest is uncommon and depends on when the injury to the physis occurs in relation to the remaining skeletal growth potential. The younger the patient, the greater the potential for problems associated with growth.

Premature partial growth arrest is far more common and can appear as peripheral or central closures. These can result in angular deformities and limb-length discrepancies. Premature partial arrests are produced when a bridge of bone (bone bar/bridge) forms, connecting metaphysis to epiphysis and traversing the physis.

This bone bar inhibits growth, and its size and location determine the clinical deformity. For example, if the bar is located medially in the physis of the distal femur, the normal physis continues to grow laterally, producing a varus deformity (genu varum), and vice versa for a genu valgum deformity.

Investigation into gait analysis for patients with genu valgum deformity has revealed improvements in cosmesis and corrected joint kinematics with hemiphyseal stapling. Anterior bone bars in the distal femoral physis allow normal physeal growth posteriorly but result in a genu recurvatum deformity.

Similarly, central growth arrests result in tented lesions of the physis and epiphysis because of a central osseous tether with the metaphysis, resulting in the characteristic physeal coning. As the physis tries to push the epiphysis away from the metaphysis, the bony bridge hypertrophies in an effort to overcome the increased tension placed on it. Bone tissue under constant tension usually atrophies, but in this instance, a dense reactive cortical bone develops.

Some longitudinal growth continues in patients with growth retardation, though at a much slower rate; thus, a progressive shortening of the limb occurs. Partial growth arrests may be visible on radiographs as early as 3-4 months after injury or may be delayed as long as 18-24 months. Follow-up checks may be necessary for 1-2 years after injury to monitor physeal healing and growth response.

Articular problems are also a possibility, particularly in physeal fractures that lead to discontinuities of the articular surface (ie, SH III and IV). These lesions can result in intra-articular stepoffs and early degenerative joint disease if they are not properly treated and anatomically reduced. Central growth arrest can promote the physeal tenting phenomena and, ultimately, result in a deformed articular surface.

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Outcome and Prognosis

Distal femur fractures

Distal femoral fractures account for approximately 5% of all growth plate (physeal) fractures. Displacement of the fracture in the sagittal plane may be associated with neurovascular injury in the popliteal fossa and instability on closed reduction. A common mechanism of injury is hyperextension causing an anterior displacement of the epiphysis. Physeal fracture displacement in the coronal plane is not associated with other injuries, and the joint may be stable after closed reduction.[15]

Clinically, the thigh may appear angulated and shortened as compared with the contralateral thigh; and pain, knee effusion, and soft-tissue swelling usually are severe. Hemarthrosis may be more severe in SH III and SH IV fractures, and vascular examinations may reveal diminished or absent distal pulses. Neurologic symptoms also may be evident distally due to disruption of the posterior tibial and common peroneal nerve distributions.

Injuries to the distal femoral physis may result in angular deformities. Certain levels of angulation are acceptable. Posterior angulation up to 20° remodels in children younger than 10 years; but injuries in adolescent patients do not remodel, and these patients do not tolerate this degree of angulation. Varus and valgus angulations are less acceptable; no angulation greater than 5° is acceptable for the distal femoral physis.

Treatment for distal femoral physeal fractures varies according to severity of injury. Displaced SH I or SH II fractures are treated with closed reduction and splinting with hip spica. SH III and SH IV injuries usually require anatomic reduction, which cannot be obtained with closed reduction, and are very often unstable. Operative treatment is required because even slight residual displacement can result in formation of a bone bar that causes limb-length discrepancy and angular deformity.

Complications of distal femoral fractures include growth arrest (partial or complete) with progressive angulation, shortening, or both in 30-80% of patients. Physeal fractures of the distal femur (particularly the common SH I and SH II fracture patterns) have been shown to be associated with an approximately 50% rate of growth disturbance.[16]

Because the incidence of growth arrest is high, even with satisfactory reduction, a lower-extremity limb-length discrepancy of more than 2 cm may develop in one third of patients. Shortening and angulation are related more to degree of initial displacement than to the accuracy of the reduction. An angulation deformity of more than 5° may develop in one third of patients. A persistent angular deformity in the coronal plane may not correct spontaneously with further growth.

Distal tibia fractures

Fractures of the distal end of the tibia in children often involve the physis. They are of particular importance because partial growth arrest can occur and result in angular deformity, lower extremity limb-length discrepancy, incongruity of the joint surface, or a combination of these. Triplane and Tillaux fractures are the two distinct types of distal tibial fractures.

In a triplane fracture classification, two types of fractures exist: two-part and three-part fractures. A two-part fracture is a type of SH IV fracture that primarily occurs when the medial portion of the distal tibial epiphysis is closed.

A three-part fracture is a combination of SH II and SH III fractures that occurs when only the middle portion of the distal tibial epiphysis is closed. It involves fracture of the anterolateral portion of the epiphysis of the distal tibia (similar to Tillaux fracture) and fracture of a large posterior fragment comprising the posterior and medial portions of the tibial epiphysis plus a large metaphyseal fragment of variable size; the fibula also may be fractured. These injuries most commonly occur just before epiphyseal closure and are due to external rotation forces.

Tillaux fractures are SH III fractures involving avulsion of the anterolateral tibial epiphysis. This portion of epiphysis is involved because the physis of the distal tibia closes first in the middle, then in the medial portion, and finally in the lateral portion. This injury occurs in older adolescents (eg, 12-15 years), after the middle and medial parts of the epiphyseal plate have closed but before the lateral part closes. Because it occurs in adolescents with relatively mature growth plates, there is minimal potential for deformity due to growth plate injury.

Treatment of displaced SH III and SH IV fractures of the distal tibia requires open reduction. This injury leads to premature physeal closure unless it is anatomically reduced. Development of an angular deformity is possible. Varus deformities, secondary to an osseous bridge formation on the medial aspect of the plate, are the most common complications found with distal tibia growth plate injuries. Limb shortening is the second most common problem associated with these injuries.

Kling et al, evaluating distal tibial physeal fractures that required open reduction, suggested that SH III, SH IV, and perhaps SH II fractures of the distal end of the tibia commonly cause disturbance of growth in the tibia and that closed or open anatomic reduction of the physis may decrease the incidence of these disturbances of growth, including shortening and varus angulation of the ankle.[17] SH IV fracture of the distal tibia has indeed been associated with premature physeal closure unless anatomically reduced, usually with internal fixation.

A high rate of premature physeal closure (PPC) has been reported to occur in SH type I or II fractures of the distal tibia. Rohmiller et al reported a PPC rate of 39.6% in SH type I or II fractures of the distal tibia physis and determined that fracture displacement following reduction was the most important determinant of PPC development.[2]

Barmada et al investigated the incidence and predictors of PPC after distal tibia SH type I and II fractures and found that when residual gapping of the physis was greater than 3 mm following reduction, the incidence of PPC was 60%; when the physeal gap was less than 3 mm, there was a 17% incidence of PPC. Upon open reduction of residual gapping, the periosteum was found to be entrapped within the physis, thereby preventing closure of the gap and preventing appropriate recreation of the anatomy.[18]

Russo et al performed a retrospective study of 96 patients presenting with displaced SH II fracture who were initially treated with closed reduction.[19] Patients with less than 2 mm of postreduction displacement were treated with a nonweightbearing long leg cast (LLC; group 1). Those with 2-4 mm of displacement were treated with either LLC (group 2) or open reduction and internal fixation (ORIF) with removal of any interposed tissue (group 3). Those with more than 4 mm of displacement were treated with ORIF (group 4).

Of the 14 patients in group 1, 29% had a PPC and 7% had to undergo a subsequent procedure (eg, epiphsyiodesis or osteotomy).[19] Of the 33 patients in group 2, 33% had a PPC and 15% had to undergo a subsequent procedure. Of the 11 patients in group 3, 46% had a PPC and 18% had a second procedure. Of the 38 patients in group 4, 55% had a PPC and 23% had a subsequent procedure. No statistically significant differences in the rates of PPC or subsequent surgery were observed between groups.

Distal radius and ulna fractures

Physeal injuries of the distal ulna occur much less frequently than those of the distal radius, but physeal injuries of the distal ulna are associated with a higher incidence of growth arrest, due to the ulna deriving 70-80% of its longitudinal growth from its distal physis. As a result, growth arrest can cause significant ulnar shortening.

The distal radial physis is the most frequently injured physis in children, usually in those aged 6-10 years. Children typically sustain the injury by falling on an outstretched hand. A great majority of these injuries are SH I and SH II fractures. The distal radial and ulnar physes provide 75-80% of total forearm growth; thus, potential for remodeling and correction of any deformity is excellent.[20]

Lee et al found that significant distal radial growth disturbance occurred in about 7% of physeal fractures[21] ; the rate of distal ulnar growth arrest following physeal fracture is probably at least as high.

The acceptable amount of residual displacement for distal radial and ulnar fractures is not specifically known; however, 30% physeal displacement heals readily, and 50% displacement may often completely remodel in 1.5 years.

Proximal tibia fractures

Whereas fractures involving the tibia and fibula are the most common lower-extremity pediatric fractures, those involving the proximal tibial epiphysis are among the most uncommon but have the highest rate of complications. When displacement occurs, the popliteal artery is vulnerable. At the tibial metaphysis, the artery is just posterior to the popliteus. Moore and Mackenzie found that in SH I injuries, half are nondisplaced and diagnosed by stress radiographs.[22]

SH I injuries occur at an earlier age (average, 10 years). SH II are the most common type, and one third are nondisplaced. SH III injuries are often associated with lateral condyle fractures or medial collateral ligament (MCL) injury. SH IV injuries are often associated with angular deformity. SH V injuries are usually diagnosed retrospectively. Anterior physis closure can cause significant genu recurvatum.

Complications of these injuries include vascular insufficiency and peroneal nerve palsy, however transient.

Triradiate cartilage fractures

Traumatic disruptions of the acetabular triradiate cartilage occur infrequently and may be associated with progressive acetabular dysplasia and subluxation of the hip. The volume of cartilage in a child's acetabulum allows a greater capacity for energy absorption than in adults. Thus, in children, fractures of the acetabulum are consistently the result of high-energy trauma. Unfortunately, a younger age at the time of injury is associated with a greater chance of developing acetabular dysplasia.

Disruption of the acetabular triradiate cartilage in patients older than 12 years results in minimal subsequent growth disturbance; however, in younger patients, acetabular growth abnormality is a frequent complication. Growth abnormalities include shallow acetabula and progressive subluxation of the hip.

Triradiate cartilage injuries occurring during adolescence result in fewer growth changes in acetabular morphology and hip joint congruencies. However, in younger children, especially those who are younger than 10 years, acetabular growth abnormality is a frequent complication of this injury and may result in a shallow acetabulum similar to that seen in patients with developmental dysplasia of the hip (DDH).

By the time patients reach skeletal maturity, disparate growth increases the incongruity of the hip joint and may lead to progressively more severe subluxation of the hip. Acetabular reconstruction may be necessary to correct the gradual subluxation of the femoral head.

Bucholz et al found 9 patients with triradiate physeal-cartilage injury who were classified according to the degree of displacement and the probable type of growth-plate disruption.[23] They determined that two main patterns of injury occurred. The first was a shearing (SH I or II) growth mechanism injury, with central displacement of the distal portion of the acetabulum. This injury pattern seemed to have a favorable prognosis for continued normal acetabular growth, although occasional premature closure of the triradiate physes occurred.

The second injury pattern appeared to be a crushing SH V growth mechanism injury; this type has a poor prognosis, with premature closure of the triradiate physes occurring secondary to the formation of a medial osseous bridge.[23] Prognosis is dependent on the age of the patient at the time of injury and on the extent of chondro-osseous disruption.

Stubbed great toe

The images below illustrate the respective radiographic and clinical appearance of an injury that has been termed the pediatric stubbed great toe. It is a somewhat occult open fracture due to the fact that the growth plate of the distal phalanx is remarkably close to the nail plate. When a subungual hematoma occurs in conjunction with a growth plate fracture, this does in fact represent an open fracture.

Growth plate (physeal) fractures. Radiographic evi Growth plate (physeal) fractures. Radiographic evidence of a pediatric stubbed great toe.
Growth plate (physeal) fractures. Clinical appeara Growth plate (physeal) fractures. Clinical appearance of a pediatric stubbed great toe. Note the subungual hematoma, representative of an open fracture.

In the great toe (or at times lesser toes), this injury has been termed a Pinckney fracture or Pinckney lesion.[24] In the hand, such fractures of the terminal phalanx may be called Seymour fractures.[25]

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Future and Controversies

Growth plate transplantation

Several experiments have been performed to evaluate the efficacy of interpositioning materials (eg, bone wax, fat, cartilage, silicon rubber, and polymethylmethacrylate) into defects resulting from physeal bar excision. No single material has been deemed superior in the prevention of physeal bar reformation. Cartilage may prove ideal, and several possible sources for graft material exist, but each has associated difficulties, such as the following:

  • Apophyseal cartilage may lack the growth potential of epiphyseal cartilage
  • Laboratory-procured chondrocyte allograft transplants may take a long time to develop and may not have any real possibility for interhuman transfer, because of the impending immune response
  • In physeal cartilage transfer, difficulties abound in procuring and transferring physes from one site to another

Tissue engineering

Most of the research into cartilage regeneration has focused on articular cartilage, but much of what is learned through such research may be applicable to growth plate cartilage. At present, no reliable means of regeneration exists. Cartilage cannot regenerate itself, partly because of its low cellularity and lack of vascular supply. In addition, chondrocytes in articular cartilage are well differentiated, and multipotent progenitor cells are relatively few. Thus, cartilage can heal the margins of damage but does not form a scar to join the defect edges together.

Many tissue-engineering strategies have been developed (eg, implantation of chondrogenic cells at various developmental stages into the defect site, implantation of cartilage itself [osteochondral autograft/mosaic arthroplasty], cartilage transplantation, and allogenic grafts). Periosteal and perichondrial tissue grafts have been considered for their stockpile of multipotent osteochondral progenitor cells. Scaffolding to provide a substrate for chondroprogenitor cell attachment and migration across cartilaginous defects has been studied as well.

These techniques have had variable success. Tissue scaffolding has proved effective at overcoming some deficiencies in tissue engineering. Collagen, a natural tissue, and poly-lactide-co-glycolide (PLGA), a polymer that elicits small acute immune responses, have shown promise as cartilage repair scaffolds. Chitin has recently been determined to be effective as a scaffolding for attaching and carrying stem cells for the repair of growth plate defects.

Some studies have combined gene therapy and tissue-engineering to regenerate articular cartilage in the hope of applying this approach to epiphyseal cartilage repair. One study used a retroviral vector to introduce human bone morphogenic protein (BMP)-7 complementary DNA into periosteal-derived rabbit mesenchymal stem cells. BMP-7 stimulates synthesis of type II collagen and aggrecan. Grafts containing modified cells consistently showed complete or near-complete articular cartilage regeneration at 8 and 12 weeks; control grafts showed poor regeneration.

The future also holds promise for specific intracellular signaling approaches to posttraumatic disturbances of the growth plate. At the University of Massachusetts, Leboy et al found that important regulators of physeal chondrocyte hypertrophy include special bone morphogenic proteins: activated cytoplasmic proteins (called Smads) and multifunctional transcription factors (called Runx proteins).[26]

Another potent stimulator of embryonic epiphyseal cartilage is growth differentiation factor (GDF)-5. Buxton et al found that GDF-5 promoted both cell adhesion and proliferation during limb development.[27]

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Contributor Information and Disclosures
Author

Charles T Mehlman, DO, MPH Professor of Pediatrics and Pediatric Orthopedic Surgery, Division of Pediatric Orthopedic Surgery, Director, Musculoskeletal Outcomes Research, Cincinnati Children's Hospital Medical Center

Charles T Mehlman, DO, MPH is a member of the following medical societies: American Academy of Pediatrics, American Fracture Association, Scoliosis Research Society, Pediatric Orthopaedic Society of North America, American Medical Association, American Orthopaedic Foot and Ankle Society, American Osteopathic Association, Arthroscopy Association of North America, North American Spine Society, Ohio State Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Matthew E Koepplinger, DO Assistant Professor, Department of Orthopedic Surgery, Baylor College of Medicine; Staff Physician, Department of Orthopedic Surgery, Ben Taub General Hospital

Matthew E Koepplinger, DO is a member of the following medical societies: American Osteopathic Association, American Osteopathic Academy of Orthopedics

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

George H Thompson, MD Director of Pediatric Orthopedic Surgery, Rainbow Babies and Children’s Hospital, University Hospitals Case Medical Center, and MetroHealth Medical Center; Professor of Orthopedic Surgery and Pediatrics, Case Western Reserve University School of Medicine

George H Thompson, MD is a member of the following medical societies: American Orthopaedic Association, Scoliosis Research Society, Pediatric Orthopaedic Society of North America, American Academy of Orthopaedic Surgeons

Disclosure: Received none from OrthoPediatrics for consulting; Received salary from Journal of Pediatric Orthopaedics for management position; Received none from SpineForm for consulting; Received none from SICOT for board membership.

Chief Editor

Dennis P Grogan, MD Clinical Professor (Retired), Department of Orthopedic Surgery, University of South Florida College of Medicine; Orthopedic Surgeon, Department of Orthopedic Surgery, Shriners Hospital for Children of Tampa

Dennis P Grogan, MD is a member of the following medical societies: American Medical Association, American Orthopaedic Association, Scoliosis Research Society, Irish American Orthopaedic Society, Pediatric Orthopaedic Society of North America, American Academy of Orthopaedic Surgeons, American Orthopaedic Foot and Ankle Society, Eastern Orthopaedic Association

Disclosure: Nothing to disclose.

Additional Contributors

Mininder S Kocher, MD, MPH Associate Professor of Orthopedic Surgery, Harvard Medical School/Harvard School of Public Health; Associate Director, Division of Sports Medicine, Department of Orthopedic Surgery, Children's Hospital Boston

Mininder S Kocher, MD, MPH is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Sports Medicine, Pediatric Orthopaedic Society of North America, American Association for the History of Medicine, American Orthopaedic Society for Sports Medicine, Massachusetts Medical Society

Disclosure: Received consulting fee from Smith & Nephew Endoscopy for consulting; Received consulting fee from EBI Biomet for consulting; Received consulting fee from OrthoPediatrics for consulting; Received stock from Pivot Medical for consulting; Received consulting fee from pediped for consulting; Received royalty from WB Saunders for none; Received stock from Fixes-4-Kids for consulting.

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Growth plate (physeal) fractures. Clinical appearance of the knee of a patient with a minimally displaced Salter-Harris I fracture of the distal femur. Impressive swelling was noted adjacent to the joint, but no evidence of intra-articular swelling was present. The patient was markedly tender to palpation about the distal femoral physis.
Growth plate (physeal) fractures. Anteroposterior radiograph of the knee of the patient in the previous image. Note subtle physeal widening confirming the diagnosis of a Salter-Harris I fracture of the distal femur.
Growth plate (physeal) fractures. Anteroposterior ankle radiograph demonstrating an impressively displaced Salter-Harris II fracture of the distal tibial epiphysis (along with comminuted fracture of distal fibular diaphysis).
Growth plate (physeal) fractures. Displaced Salter-Harris II fracture of the distal femur. The large Thurstan Holland (metaphyseal) fragment may serve an important fixation point for either a Steinmann pin or a lag screw.
Growth plate (physeal) fractures. Multiple computed tomography (CT) scan images depicting a displaced Salter-Harris III fracture of the distal anterolateral tibial epiphysis (ie, Tillaux fracture).
Growth plate (physeal) fractures. Displaced Salter-Harris IV fracture of the proximal tibia. The lateral portion of the epiphysis (with the Thurstan Holland fragment) and the medial portion of the epiphysis are independently displaced (ie, each are free-floating fragments).
Growth plate (physeal) fractures. The Salter-Harris V fracture pattern must be strongly suspected whenever the mechanism of injury includes significant compressive forces. This is the initial injury radiograph of a child's ankle that was subjected to significant compressive and inversion forces. It demonstrates minimally displaced fractures of the tibia and fibula with apparent maintenance of distal tibial physeal architecture.
Growth plate (physeal) fractures. Follow-up radiograph of the ankle of the child in the preceding image. This radiograph depicts growth arrest secondary to the Salter-Harris V nature of the injury. Note the markedly asymmetric Park-Harris growth recovery line, indicating that the lateral portion of the growth plate continues to function and the medial portion does not.
Growth plate (physeal) fractures. Mortise radiograph demonstrating somewhat subtle physeal injury to distal tibia. The Salter-Harris VI pattern may be suspected based upon history and physical examination findings. In this case, the radiograph indicates that it is quite likely that a small portion of the peripheral medial physis (as well as a small amount of adjacent epiphyseal and metaphyseal bone) has been avulsed.
Growth plate (physeal) fractures. Clinical photograph of the patient above with the displaced Salter-Harris II fracture of the distal femur. This mechanism of injury and physical examination findings are consistent with the Salter-Harris VI physeal injury pattern. Some may also refer to this injury type as a Kessel fracture.
Growth plate (physeal) fractures. Radiographic evidence of a pediatric stubbed great toe.
Growth plate (physeal) fractures. Clinical appearance of a pediatric stubbed great toe. Note the subungual hematoma, representative of an open fracture.
 
 
 
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