Clin Plastic Surg 31 (2004) 499 – 518
Pediatric craniofacial fractures: long-term consequences Davinder J. Singh, MDa,b, Scott P. Bartlett, MDa,b,* a
Division of Plastic Surgery, University of Pennsylvania School of Medicine, 3400 Spruce Street, 10 Penn Tower, Philadelphia, PA 19104, USA b The Children’s Hospital of Philadelphia, Wood Building, 1st Floor, 34th Street and Civic Center Blvd., Philadelphia, PA 19104, USA
Compared with adult facial fractures, fractures of the pediatric craniofacial skeleton are uncommon. However, they are frequently more difficult to manage because of the anatomical differences and the evolving potential for growth and development [1 – 6]. The overall treatment goal of structural restoration is similar in adults and children, but the longevity of this restoration in children remains largely unknown owing to a paucity of literature documenting long-term follow-up, particularly in upper and midfacial fractures [7 – 9]. The potential growth disturbances and need for secondary surgery associated with early condylar injury have been well documented, but the growth and developmental problems resulting from upper and midfacial fractures are elusive [10 – 16]. This article discusses the growth and development of the pediatric craniofacial skeleton. It also reviews the literature on pediatric craniofacial fractures with particular emphasis on the effects of craniofacial trauma on the evolving pediatric craniofacial skeleton. The authors present their long-term data from a retrospective review of pediatric craniofacial fractures treated operatively at the Children’s Hospital of Philadelphia.
Epidemiology The overall incidence of craniofacial trauma is higher in children than in adults; however, the inci* Corresponding author. Division of Plastic Surgery, University of Pennsylvania Health System, 3400 Spruce Street, 10 Penn Tower, Philadelphia, PA 19104. E-mail address:
[email protected] (S.P. Bartlett).
dence of pediatric maxillofacial fractures is lower, accounting for only 8% of all pediatric facial injuries [17]. The lower incidence of pediatric maxillofacial fractures is due to several factors, including a protected environment, a low ratio of facial mass to cranium, and the greater elasticity of immature bone. The incidence and distribution of facial fractures vary with age. Retrospective reviews of maxillofacial trauma involving both adults and children report that approximately 1% of the fractures occur in patients younger than 5 years of age, and that 1.5% to 23% occur in those who are younger than 16 years of age [1,2,4 – 6,18 – 20]. The wide range in incidence is due to changes in diagnostic radiographic studies with the advent of CT and to underreporting of two of the more common pediatric facial fractures, nasal and dentoalveolar, which are frequently treated nonsurgically and excluded from studies [2,4]. Pediatric facial fractures are almost twice as common in boys as in girls [6]. The incidence and distribution of fractures vary considerably with age as the facial skeleton becomes more prominent and increasingly mineralized. After the age of 2 to 3, the facial bones lose much of their elasticity [21]. With age, fractures shift from the upper to the lower aspect of the face, with frontal and orbital fractures having a higher incidence in the 0 to 5-year-old age group and midface and mandibular fractures having a higher incidence in the 6 to 16-year-old age group [17,22,23]. Looking at all age groups, we see that nasal and mandibular fractures are the most common, followed by orbital, midface, and cranial vault in that order [5,17 – 19,22,23]. Kaban [18], in his initial review, reported a 45% incidence of nasal fractures and a 32% incidence of mandibular fractures, whereas McCoy reported a higher inci-
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dence of mandibular fractures at 41% and a lower of nasal at 23%. In a subsequent review, Kaban reported five midface fractures (LeFort [LF] III level) in a review of 184 fractures over 10 years [19,20]. McCoy et al [5] reported a 16.3% incidence for orbital or malar complex fractures, a 5.8% incidence for maxillary fractures, and a 4.7% incidence for zygomatic fractures. Causes of pediatric fractures include motor vehicle accidents (MVA), falls, and sports [6,24 – 27]. MVAs account for the more severe midface fractures, with all-terrain vehicles (ATVs) and motorized bikes becoming a more frequent source of injury in the adolescent age group. Of all facial injuries resulting from ATV accidents, 37% included facial fractures [28]. Concomitant injury is high in pediatric patients with craniofacial fractures and ranges between 10.4% to 88% [5,6,18,22,23,28,29]. These associated injuries include facial wounds, concussions, cerebrospinal fluid rhinorrhea, extremity fractures, ocular injury, closed chest injury, and abdominal injury.
sutures, and apposition-resorption. The face is affected by growth spurts differing in direction, location, and time. Facial dimensions at the age of 3 months are equivalent to 40% of those of the adult, those at the age of 2 years to 70%, and those at the age of 5 years to 80%. The speed of growth decreases from 5 years of age until the arrival of puberty. This period is associated with an acceleration of growth of a hormonal origin and is followed by rapid retardation to stop at the age of 17 years [31]. The two more vulnerable periods during which injury or disturbance may result in facial asymmetry are the transition between deciduous and adult dentition, and puberty with its spurt of mandibular growth [30]. While brain growth is the primary initiator of cranial growth, the growth of the central face is dependent on the ‘‘median-sagittal sector,’’ which is comprised of the chondrocranial spheno-ethmoidonasal portion and the vomeropremaxillary and pterygo-palatomaxillary portions (Fig. 1). The sphenoethmoidonasal portion terminates in the nasal septum and the lateral cartilaginous expansions and plays no role in the shape or position of the premaxilla. The vomeropremaxillary portion propels the premaxilla
Growth and development To understand pediatric fracture patterns, means of management, and potential long-term sequelae of craniofacial fractures, one must study the growth and development of the craniofacial skeleton. The craniofacial skeleton grows differentially according to location, with different regions reaching adult dimensions at different times. A discrepancy between the growth of the cranium and the face creates a ratio of 8:1 at birth, which becomes 4:1 at around 5 years and 2:1 in the adult. At birth, the neurocranium has achieved only 25% of its growth potential, and it continues to expand rapidly to complete 75% by 2 years. By 10 years, the neurocranial growth is 95% complete, whereas the facial growth is only 65% complete [22,30,31]. Cranial growth is an example of continuous development in short periods of time and is activated in large part by the brain and partially by means of the sutures. The brain doubles its volume in the first 6 months and triples it at the end of the first year, thus acting as a ‘‘functional matrix’’ in determining the extent of cranial bone growth. Postnatal bone growth results in narrowing of the sutures and closure of the fontanelles. Growth continues rapidly until the age of 3, waning thereafter into adulthood [30]. The face demonstrates discontinuous growth until the completion of adolescence. It is multifactorial, with successive mechanisms such as synchondroses,
Pt
mes P
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Fig. 1. Median sagittal sector. (Modified from Stricker M, Raphael B, Van der Meulen J, Mazzola R. Craniofacial development and growth. In: Sticker M, Van der Meulen R, Raphael B, Mazzola R, editors. Craniofacial malformations. New York: Churchill Livingstone; 1990. p. 82; with permission.)
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forward. The pterygo-palatomaxillary portion controls the position of the middle face by supporting the palatine bone, which serves as a transition with the maxillary bone [30]. Upper facial growth is secondary to cerebral and ocular growth, which primarily expands the orbit. Orbital growth is complete by age 6 to 8 years. Frontal sinus aeration becomes evident at age 4 to 5 years and finishes after puberty. Midfacial growth varies according to stages of dental development. Transverse maxillary growth is near completion by age 2 years. The palatal and midline maxillary sutural growth are usually finished between ages 8 and 12 years. The pneumatization of the maxillary antra correlates with dental eruption. The maxillary sinuses approach the nasal floor by approximately 12 years of age, when most of the permanent teeth have erupted, but do not reach full size until after puberty [30,31]. The lower facial growth occurs in different stages as well. The mandibular symphysis undergoes complete fusion by age 2 years, at which point the deciduous teeth are erupting. The condyle contributes primarily to vertical growth, which is activated by muscular activity. Most of the mandible’s surfaces undergo bone remodeling, which typically occurs with puberty and takes place via apposition and resorption [7,12,22]. Mechanisms of growth involve both the cartilage and the periosteum. The cartilage constitutes a primary active area of growth because it is stimulated by intrinsic dynamic forces. The condylar cartilage is
Table 1 Distribution of operatively treated pediatric craniofacial fractures at the Children’s Hospital of Philadelphia from 1986 to 2002 Nasal Dentoalveolar Condyle Condyle and mandible Mandible Maxilla Orbitozygomatic Isolated orbital Frontal bone/Sinus Frontal/SOR/Roof Frontal/SOR/Roof/NOE Frontal/SOR/Roof/NOE/Sinus NOE NOE and maxillary Panfacial
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Fig. 2. Age distribution of facial fractures treated at the Children’s Hospital of Philadelphia.
an exception to this in that it is a site of secondary passive growth dependent on forces acting on it, specifically the pterygoid muscles. The periosteal system is also an area of passive secondary growth and is composed of three structures: the sutures, intermediary periosteum, and expanding joints. The periosteum is influenced by muscular insertions, which are responsible for apposition and resorption according to Enlow’s theory [30,31] of 1968. Synchondroses are areas of growth cartilage that separate the zones of ossification in the cartilage of the base and are vulnerable to insults and trauma [32,33]. Controversy exists as to how much the cartilaginous septum contributes to growth [8,9,12, 33,34]. Moss et al [33] believed that this cartilaginous component has no intrinsic growth and only acts passively by transmission of pressure. Powell et al
33 4 4 2 25 0 19 8 3 8 2 7 7 1 5
Abbreviations: NOE, naso-orbito-ethmoidal; SOR, superior orbital rim.
Fig. 3. Six-year-old girl with bilateral condylar fractures.
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Fig. 4. (A,B) Postoperative occlusion in Class I relations.
[35] reviewed their pediatric patients (average age 13.8 years) who underwent maxillary removal and reinsertion for anterior cranial base tumors and found no major complications with regard to growth during a mean 14-month follow-up. However, other authors [36] have demonstrated intrinsic growth disturbances by division of the upper portion of the cartilaginous septum. In animal studies, surgical manipulation of the septal cartilage and vomer resulted in significant growth disturbances [37 – 39]. In addition to its intrinsic growth capacity, the facial skeleton is responsive to growth activators. Cellular proliferation, cerebral expansion, and function are the key activators of craniofacial growth [30]. The facial skeleton has cavities that expand and contribute to growth. The growth of the pneumatic cavities as well as the orbits and buccal cavity all
result in facial expansion in three dimensions. The deposition of bone on one site and resorption on the opposite site—as demonstrated by Enlow, particularly in the maxilla and mandible—is the primary growth mechanism [12,22,31,40]. An understanding of the growth centers and development of the craniofacial skeleton enables one to comprehend the pediatric facial fracture patterns and the challenges of their management, as well as their long-term sequelae.
Pediatric facial fracture patterns Fractures shift from the upper to the lower aspect of the face with increasing age, primarily because of the later growth and development of the
Fig. 5. (A,B) At 4 months post-injury, mild Class II occlusion and good jaw opening.
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maxilla and mandible and the decreasing elasticity of the bone. The decreasing elasticity results from increasing mineralization, which occurs exponentially after the age of 2 to 3 years. Children often sustain incomplete ‘‘greenstick’’ fractures, or less comminuted fractures than adults when receiving equivalent traumatic force [21,41,42]. In contrast to adults, the LeFort facial fracture patterns are rare in the pediatric population before significant development of maxillary sinuses. If they do occur, they are typically in combination with other fractures and are often unilateral [21,42]. In 1990, Moore and David [42] described the typical oblique fracture patterns seen in high velocity accidents in children. The fracture runs obliquely across the frontal bone with radiation into the cranial base and extension across the orbit and maxilla.
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There is infrequent extension to the mandible. The reason for the fracture’s oblique nature in the pediatric population is the lack of the structural pillars or buttresses that determine adult fracture patterns. These facial buttresses are not fully developed because of mixed dentition with unerupted teeth, less paranasal sinus pneumatization, and a higher ratio of cancellous bone.
Management Concerning management, there is still controversy on the issue of the closed versus the open approach and the long-term sequelae of potential disturbance of growth with the latter [3,29]. Contradictory evidence exists regarding subperiosteal undermining and
Fig. 6. (A – C) At 1.5 years post-injury, minimal mandibular hypoplasia and development of Class II malocclusion.
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growth restriction, with some authors having demonstrated growth retardation following wide dissection and devascularization in the growing skeleton [43]. Conversely, broad undermining of the fronto-orbital region, as in the treatment of unicoronal synostosis, is not observed to place any significant restriction on growth [44]. Because the growing child has the capacity for remodeling of the bone post-injury, particularly of the condyle and mandible, a more conservative approach is frequently taken, in contrast to the concept of accurate anatomic reduction in adults [11,16]. In general, if a reasonable anatomic position can be
obtained by means of the closed approach or a limited exposure, it is preferred. Any consequent minor occlusal disturbances are acceptable and can be treated with orthodontics at a later age. When deciding upon an open versus closed approach and a method of fixation in pediatric craniofacial fractures, one must consider the severity of the fracture and the age at the time of injury [21]. Pediatric craniofacial fractures pose many challenges, ranging from timing to technique to the potential growth sequelae. Because of the rapid bone healing in pediatric patients, fractures should ideally be treated within 3 to 4 days, in contrast to the
Fig. 7. At 3 years post-injury, progression of mandibular hypoplasia (A,B), with CT scan demonstrating flattening of both condylar heads and glenoid fossae (C,D).
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Fig. 8. A 6-year-old girl who sustained frontal bone, cranial base, and naso-orbitoethmoidal fractures (A,B), as demonstrated on her CT scans (C,D). (E) Intraoperative photograph showing degree of centrofacial injury. (From Bentz ML. Pediatric plastic surgery. Stamford (CT): McGraw Hill; 1997. p. 483; with permission.)
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2-week window in adults. The high incidence of concomitant injury occasionally delays treatment and results in significant difficulty in reducing fractures [21]. The various stages of mixed dentition pose limitations on methods of fixation and raise concern about damage to permanent teeth. Greenstick or minimally displaced fractures can be treated conservatively with closed reduction and no fixation. If fixation is needed, wires and microplates should be used [15,22]. Microplates provide stable but not rigid fixation and avoid the potential growth restric-
tion. Studies involving this potential remain controversial, with some demonstrating growth disturbances secondary to the rigid fixation [38,45 – 47]. Another concern is the migration or translocation of these plates as the pediatric skeleton expands via apposition and resorption [48]. Rigid fixation serves a clear purpose in the severe, complex pediatric craniofacial fractures, but consideration should be given to interval removal, depending on the age of the child and the location and size of the plates [3]. In recent years, the use of the resorbable plating systems in the growing craniofacial skeleton has become
Fig. 9. (A – C) Postoperative CT and photos showing good restoration of frontal bone and upper facial contour. (B,C From Bentz ML. Pediatric plastic surgery. Stamford (CT): McGraw Hill; 1997. p. 483; with permission.)
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Autogenous bone grafts are more predictable, but should be used judiciously in the growing craniofacial skeleton. Onlay grafts with rigid fixation for contour may result in a secondary growth disturbance; however, if they are placed in a precise soft tissue pocket, such as the nasal dorsum, and with minimal fixation, they serve to restore contour in the severely fractured midface [3]. In deciding upon surgical technique and in advising the patient and family, thought must be given to the long-term effects of the trauma and treatment on the growth and development of the pediatric craniofacial skeleton.
Long-term consequences Fig. 10. Nine-month follow-up illustrating good upper and midfacial projection on lateral profile.
more popular, with the goal of preventing growth restriction and obviating the need for removal of titanium hardware secondary to palpability or infection [49 – 51]. Another question in management concerns the use of bone grafts and alloplastic materials, both of which are used frequently in the adult population. In the pediatric patient, the long-term results of alloplastic materials for reconstruction are unpredictable.
Despite timely and appropriate treatment of pediatric fractures, growth and developmental disturbances may result because of damage to active growth centers. There have been case reports of late craniofacial deformities secondary to trauma during the growth years and numerous studies documenting the sequelae of mandibular trauma [10 – 16]. However, there has been no longitudinal study of patients treated in infancy and childhood and followed into adolescence by the same surgeon. Growth disturbances have been associated with nasal trauma by means of premature ossification of the septovomerine suture [52]. The role of the septum in facial growth has been documented by several
Fig. 11. (A,B) Two years post-injury, the patient has developed a mild saddle nose deformity and frontal bone irregularity.
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Fig. 12. (A,B) Three years post-injury, photographs demonstrate the progression of her growth disturbance.
authors [8,53 – 55]. Zygomatic fractures are said to pose little concern for growth disturbance [18,19, 23,29]. Fronto-orbital injury occurs with a frequency of 3% to 35% in the pediatric population. It is more common in the younger age group, where the cranium and upper face are more prominent in comparison with the mid- and lower face. Before age 7 years, because of the presence of only rudimentary sinuses, internal orbital injury occurs almost
exclusively at the orbital roof with linear extension to the frontal bone. After age 7, internal orbital injury of the roof, floor, and medial and lateral walls occurs along with frontal sinus fractures. At this point, the growth is complete and concern for growth disturbance is minimal [6,29,41,42]. Naso-orbital-ethmoidal injuries are relatively infrequent, but are the most technically challenging to treat in children [56,57]. Anatomic reduction and
Fig. 13. (A,B) Five years post-injury, photographs illustrate the severity of the saddle nose deformity and the marked irregularity of the central frontal bone. The patient underwent secondary frontal bone contouring and augmentation rhinoplasty with cranial bone graft.
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Fig. 14. Seven-year-old boy who sustained a LeFort II and mandibular fractures (A), as seen on his CT scans (B,C).
fixation are mandatory in an attempt to prevent growth disturbances. Growth in this area is dictated by development, and sutural growth at the frontoethmoidal, frontolacrimal, frontomaxillary, ethmoidomaxillary, nasomaxillary, and septovomerine sutures is dictated by expansion of the cranium to compensate for the brain. Premature ossification or obliteration of these sutures may result in midfacial hypoplasia in the vertical and anterior – posterior direction [6,22]. The maxilla is the least frequently injured pediatric facial bone [58 – 62]. Anatomic reduction is necessary to ensure proper growth and development, with attention directed to the nasofrontal and fronto-
maxillary sutures and the septum. The septovomerine suture has been associated with midfacial growth disturbances after trauma [9,63]. Osterhout et al [63] published case reports of three adolescent patients who needed LeFort III midface advancement. They had a history of midface trauma in childhood but had not been treated at that time by the authors. Osterhout hypothesized that the growth disturbance was secondary to ossification of sutures and damage to cartilaginous growth sites. In 1995, Iizuka et al [23] reviewed 54 pediatric patients with 70 midface fractures and a mean age of 10.3 years. They reported 5% secondary surgery for
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Fig. 15. (A,B) Three months postoperatively, after reduction of fractures into Class I occlusion, the patient exhibits good midface projection.
Fig. 16. (A – D) At 1.5 years post-injury, the patient has developed midface hypoplasia and a Class III malocclusion.
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Fig. 17. At 2.5 years post-injury, the patient has progression of the growth disturbance (A), as shown in flattening of his midface on profile (B), and in his occlusal relations (C,D).
insufficient reduction and no issues with growth disturbance, but conducted only a 14.2-month average follow-up. Because of this lack of long-term follow-up of patients by the primary surgeon, little is known about the outcomes of pediatric facial trauma and intervention. The authors performed a retrospective review of all patients who underwent surgical treatment for craniofacial fractures at the Children’s Hospital of Philadelphia between 1986 and 2003. Charts were reviewed for causes, distribution of fractures, age at time of injury, operative management, and outcome. The investigation revealed 125 patients treated operatively. The mean age at time of injury was 10.9 years, with a range from 8 months to 17 years. The mean follow-up was 5 years, with a range from 5 months to 12 years. The most common fractures were nasal and mandibular, followed by upper facial fractures and then the combined oblique craniofacial fractures. The
distribution of fractures can be seen in Table 1, and the distribution of patients into different age groups can be seen in Fig. 2. The incidence of fractures rose sharply from ages 3 to 6 years and reached a peak in adolescence. In assessing long-term effects, the nasal and dentoalveolar fractures were excluded because of lack of adequate follow-up. Of the remaining 88 craniofacial fractures, most were mandibular fractures, which were underreported because many were treated conservatively with soft diet and observation. In reviewing these patients for growth and developmental anomalies, the authors found that 10 patients (11.4%) were identified as having undergone or requiring secondary surgery. Two of the ten patients had condylar injury in childhood, one unilateral and the other bilateral. Eight patients required secondary surgery following significant midface trauma with resultant growth and developmental disturbances.
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Fig. 18. At 4 years post-injury, the patient has gone from a convexity of his mid- and lower face to a concavity secondary to disruption of normal midfacial growth (A,B). Flattening of the midface can be appreciated on submental view (C). Worsening of his Class III malocclusion is seen (D).
Fig. 19. An 8-year-old girl presented with rhinorrhea secondary to the frontal bone, cranial base, and naso-orbitoethmoidal region fractures (A) as seen in her CT (B). (From Bentz ML. Pediatric plastic surgery. Stamford (CT): McGraw Hill; 1997. p. 477 – 8; with permission.)
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Fig. 20. (A,B) One year post-ORIF and bilateral cranialization of frontal sinuses, she had no symptoms and had good facial symmetry.
A total of 20 patients were identified as having been treated for midface fractures, either in isolation or in combination with upper and lower face fractures. A fracture common to all these patients was the naso-orbitoethmoid fracture. Eight of twenty patients (40%) required or will require secondary surgery. Mean age at time of injury for these eight patients was 9.3 years, compared with 10.8 years for the 12 patients who sustained midface trauma but no growth disturbance. One patient had a developmental anomaly, a frontal mucocele, after repair of a nasoorbitoethmoidal and frontal sinus fracture with open reduction and internal fixation (ORIF) and bilateral frontal sinus cranialization at age 8 years. Six patients required cranial bone graft to the nasal dorsum and canthal repositioning, despite immediate cranial bone graft to the nasal dorsum and anatomic reduction of the naso-orbito-ethmoidal (NOE) fractures and canthi at the time of primary surgery. One of these six also required frontal bone contouring. One patient is being followed until growth is complete and has demonstrated a progressive midface hypoplasia with Class III malocclusion, despite having undergone ORIF with Class I occlusion postoperatively.
Case reports Below are case reports illustrating the severity of the primary injury, the treatment, and the long-term
follow-up, as well as documenting growth and developmental disturbances. Case 1 (Figs. 3 – 7) T.G., aged 6 years, presented with bilateral condylar fractures, a neck fracture on the right, and an intracapsular fracture on the left after a fall. She underwent closed reduction and a brief period of maxillo-mandibular fixation (MMF). Her 1- and 4-month follow-up occlusal photos illustrate Class I occlusion and good jaw opening. Her 1.5-year follow-up shows very minimal mandibular hypoplasia, which is more evident on her 3-year follow-up at age 9. Her CT scan at this time demonstrated flattening of both glenoid fossae and greater flattening of the right condylar head. She is currently being followed on a yearly basis for mandibular growth. Case 2 (Figs. 8 – 13) A.R. sustained severe centrofacial trauma at the age of 6 years when she was riding an ATV and was struck in the face by a piece of farm machinery. She suffered fractures of the frontal bone, cranial base, and naso-orbitoethmoidal region. Axial CT scans demonstrate the degree of bony displacement. Intraoperative photographs illustrate the injury. She underwent acute cranial bone graft to the orbital roof, right orbital floor, and nasal dorsum, in addition to bilateral medial canthopexies and a galeal frontalis
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Fig. 21. Six years post-injury, she presented with complaint of headaches and orbital asymmetry (A,B). CT scans demonstrated a frontal sinus mucocele on the right (C,D).
flap to the cranial base. Her 1- and 9-month follow-up photos show good facial proportions and projection on lateral profile. In her 2- and 3-year follow-up photos, the development and progression of a saddle deformity of the nasal dorsum are seen, along with a contour irregularity of frontal bone. On her 5-year follow-up, there is lack of growth and projection of the nose and more grooving of the frontal bone. She underwent secondary contouring with bone substitute and rhinoplasty with cranial bone grafting to the nasal dorsum. Case 3 (Figs. 14 – 18) K.M. was involved in an MVA at the age of 7 years and sustained an LFII fracture and mandibular body and parasymphaseal fractures. He underwent ORIF of the LFII fracture with cranial bone graft to
the orbital floors and IMF via suspension wires for treatment of his mandibular fractures and was restored to a Class I occlusion. His 3-month postoperative photographs show stability of the reduction with good mid- and lower facial projection. His 1.5-year follow-up revealed lack of maxillary growth and a Class III malocclusion. His 2.5- and 4-year follow-ups showed a progressive maxillary hypoplasia with flattening of the malar region and a Class III malocclusion, with an approximately 10-mm negative overjet. He awaits completion of facial growth and will need either a LeFort I or III to correct his midface deficiency. Case 4 (Figs. 19 – 23) D.D., aged 8 years, sustained a frontal sinus and naso-orbitoethmoidal fracture and presented with
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Fig. 22. (A – C) She underwent direct excision, obliteration, and reconstruction of the orbital roof with cranial bone grafts.
significant rhinorrhea. She underwent a transcranial open reduction and internal fixation with bilateral frontal sinus cranialization. She also had bone graft reconstruction of her cranial base and nasal dorsum. Her 1-year postoperative photographs show good
facial symmetry and nasal projection. Six years postinjury, she presented with orbital asymmetry and complaint of headaches. Her photographs illustrate the decreased height of her right palpebral fissure and prominence of her right supraorbital bar. CT
Fig. 23. (A,B) One year post-secondary surgery, she had no complaints and good orbital symmetry.
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scans revealed a right frontal sinus mucocele, and she underwent obliteration of the right frontal sinus and reconstruction of the orbital roof with cranial bone grafts. Her 3-month and 1-year follow-up photographs show restoration and maintenance of orbital symmetry and no further problems with mucocele formation.
Discussion Based on the information at hand, it seems that operatively treated facial fractures in children have a favorable outcome for growth and development in most patients. In particular, isolated injuries to the orbit, zygoma, forehead, and mandibular corpus, exclusive of the condyle, are associated with normal subsequent growth and development. Two contrasting groups remain in which growth outcomes may be less than optimal: those with a direct injury, often limited to the condyle, and those with complex centrofacial injury. Despite the differences in the complexity and severity of the injury causing the subsequent growth disturbance in these two regions, this altered growth pattern is most likely related to disruption of a growth center in both cases. The condylar cartilage is the only clinical example of secondary cartilage that contains very young prechondroblasts. These cells have not undergone differentiation and are extremely sensitive to mechanical pressures; hence the growth at this site is dependent primarily on the cartilages’ activators or muscles [30]. The condyle, a relatively small part of the facial mass, is intricately attached to adjacent muscle, most notably the medial and lateral pterygoids. The thin, localized functional matrix of the condyle, if not righted by closed or open reduction, may disallow normal growth and redirect it according to displaced forces, potentially altering mandibular growth. Similarly situated but in a much larger functional matrix is the central face. Contributors to the matrix include the brain above, the orbits adjacent, and the aerated sinuses of the maxilla. Tessier dubbed the intersection of these multiple functional structures the ‘‘crossroads of the face.’’ The septum may have a specific growth focus that is disrupted by severe trauma, but in order for more significant growth disturbance to occur, as in the patient in Case Report 3, more members of this functional matrix need to be injured or altered. Anatomic repair may go only so far in rectifying this disjunction, explaining the enigma of why some injuries heal and allow growth without incident, while in others an altered state persists. To a degree, secondary growth disruptions are related to the force of injury, but, as we have seen
in the examples above, the disruption of the functional matrix may occur irrespective of the force. Also relevant may be the timing of the injury. It is likely that each growth center or functional matrix complex goes through a more vulnerable period in its growth wherein an injury will cause more secondary sequelae than it would if it occurred at a different point in time. Investigation focused on the effects of treatment, such as subperiosteal undermining, rigid fixation, and bone grafting, is needed to clarify the role of each of these on growth and development. Although we have focused primarily on facial bone growth following injury and repair, mention should also be made of other structures—for instance, in Case Report 4, a frontal sinus mucocele that developed 6 years after complete cranialization of the sinus. Despite appropriate primary management of frontal sinus fractures, a late frontal sinus mucocele may develop [64,65]. This example implies, though it does not prove, the notion that ‘‘development of the sinus must go on’’ despite the anatomic limitation imposed by cranialization. Biological determinism, the programming of specific growth processes adapted to survival, seems to have a role here. Another example is that of injured tooth buds that despite damage from injury and treatment continue to erupt, often in disadvantaged positions. Yet another is the injured nasal septal cartilage and its supporting upper and lower lateral cartilages, which may develop curvature over time after injury in childhood, a process most of us have heard about from our patients and witnessed as well. It is difficult to predict with precision which pediatric patients will have secondary growth and developmental disturbances after craniofacial fractures. Many factors play a role in determining this, and more research in the field of developmental biology is needed to answer questions about the effects of trauma, both incidental and surgical, on the functional matrix of the craniofacial skeleton.
Summary The majority of pediatric facial fractures are associated with favorable long-term outcome, with only 11.4% requiring secondary surgery. The vast majority of the patients requiring secondary surgery sustained severe centrofacial bony and cartilaginous injury, which may be associated with secondary growth and developmental disturbances. It is crucial that pediatric patients be informed of the potential for growth and developmental disturbances at the time of
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the primary injury and that they be followed on a yearly basis until growth is complete.
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