CHAPTER
49

The frontal sinus is absent at birth. Frontal bone pneumatization begins at age 3 years and reaches the nasion by age 4 years. The frontal sinus is only pea-sized by age 7 years. Full adult size and conformation is not reached until age 15 to 19 years.1 The maxillary sinus also starts as a bud at birth. By age 7 years the maxillary sinus has extended laterally to the midpupillary line. Growth continues as permanent dentition erupts.

Nasal Bones and Septum

The pediatric nose possesses several unique traits compared with an adult. The growing nose is less projected. The nasal framework is more cartilaginous and the nasal bone suture is open. Nasal growth is biphasic. The first growth phase occurs between ages 2 and 5 years, and the second occurs during puberty.² Most nasal growth is completed by age 16 years for young women. Growth may continue beyond age 18 years for young men.³

Mandible and Dentition

Most of the development of the mandible derives from growth at the condyle and ramus.⁴ Tooth eruption and development of the alveolar process also contributes to mandible maturation. The body and symphysis remain relatively unchanged.

Deciduous tooth eruption begins at approximately 6 months. It is complete at 2 years. Exfoliation begins around 6 years through root resorption. Concurrently, eruption of permanent dentition begins and continues through age 12 years. Incisors erupt around age 6 years, and canines around age 9 years. Wisdom teeth usually erupt in early adulthood.⁵ During the transition through mixed dentition, there is relatively low bone stock. Permanent tooth follicles occupy a large portion of mandibular volume.

Epidemiology of Pediatric Facial Fractures

Demographics

Between 6 and 15% of all facial fractures occur in pediatric patients.^6,7 The incidence is lowest for patients age 0 to 5 years (0–1% of all facial fractures) and increases thereafter.^6,8–15 Sex distribution, male to female, is 1.7:3.1.^8,9,16

The causes of pediatric fractures are diverse. Between 10 and 38% of fractures are caused by falls, and 27 to 34% by play accidents. Between 17 and 54% are by motor vehicle accidents, 1 to 21% are by sporting injuries, and 3 to 48% are caused by assault.7–10,17–19 Though rare, there have been a few documented cases of facial fracture from traumatic birth.^9,16,18,20

Fracture Types

Fracture distribution is unique compared with adult facial fractures^{7–10,16–19,21–27} (Box 49.1).

Associated Injuries and Complications

Associated injuries are more common in pediatric maxillofacial trauma than in adult cases. Depending on the case series, 36 to 89% of patients experience other injuries concurrent with facial fractures^6,7,9,16,19:

• Soft tissue lacerations: 14 to 88%

• Extremity injuries: 2 to 70%

• Head trauma: 4 to 80%

• Facial nerve palsy: 1%

• Abdominal trauma: 1 to 18%

• Cervical spine trauma: 1 to 2%

• Globe trauma: 1 to 8%^7,9,19,20,22

Overall complication rates range from 12 to 26%.^9,18,22 Details regarding specific complications are reviewed later in this chapter.

Principles of Evaluation and Management

As in any trauma case, surgeons must follow proper protocol in the management of the airway, breathing, and circulation A primary survey will prompt the surgeon to secure the airway. Pediatric patients, especially younger ones, require greater attention because of the size and position of the larynx. The secondary survey includes examination of the head and neck for cranial nerve and ocular function, skeletal stability, and any sources of hemorrhage.

Appropriate imaging of the facial skeleton and cervical spine, as prompted by physical examination, will assist in determining the presence and extent of fractures. Once the patient’s age, severity of injury, and presence of concurrent injuries have been accounted for, specific treatment planning for facial fractures can be initiated.

Associated Acute Sequelae

Skull Fracture and Intracranial Injury

Intracranial injury associated with facial bone fractures occurs at a relatively high frequency in the pediatric age group. Lack of paranasal sinus development in children may contribute to forces being transmitted to the cranium and its contents.²⁸ As such, computed tomography (CT) is indicated to evaluate the status of the cranium and underlying intracranial contents. Injuries requiring neurosurgical intervention may require craniotomy, craniectomy, or repair of dural tears. If the frontal sinus is present and involved, it must be managed accordingly.

Patients with facial fractures and associated cranial or skull base injury are at risk for further complications.²⁹ Structural deformity, olfactory nerve dysfunction, and surgical-site infection may occur. Ophthalmic complications, such as ptosis, visual field disturbances including blindness, diplopia, telecanthus, or enophthalmos are potential sequelae. Persistent cerebrospinal fluid (CSF) leakage may result as well. Prolonged neurological deficits and posttraumatic hypopituitarism are further sequelae that warrant extended follow-up and observation.

Cerebrospinal Fluid Rhinorrhea

Fourteen percent of naso-orbital-ethmoidal (NOE) fractures are associated with CSF rhinorrhea.^14,25 Between 70 and 85% of traumatic CSF leaks resolve within 1 week.^30,31 If CSF leak persists beyond 1 week, placement of a lumbar drain usually satisfactorily decompresses the site of leakage. This allows for dural tear closure. If the lumbar drain fails to resolve the CSF leak, neurosurgical repair of the skull base defect should be performed. Unrecognized CSF leak or fistula may progress to meningitis, encephalitis, or even brain abscess.

Superior Orbital Fissure and Orbital Apex Syndrome

Injury to the contents of the superior orbital fissure and the optic canal is usually secondary to a skull base or orbital roof fracture. Prompt diagnosis by cranial nerve and ophthalmologic evaluation is vital to prevent a permanent visual disturbance and blindness.

The overall incidence of soft tissue injury with pediatric facial trauma is 14 to 42%.9,32 Severe injuries may result in a soft tissue defect from avulsion. Between 1 and 56% of cases have a significant soft tissue defect.^9,33,34 Suboptimal long-term outcomes in the appearance of these scars has been reported at 6.5%.³⁵ As in other laceration repairs, the surgeon should monitor wounds for hypertrophic scars. Revision techniques include steroid injection, laser therapy, scar revision, and reorientation of scar via z-plasty or geometric broken lines.

Unfavorable Results and Complications in Postoperative Facial Fracture Repair

Infection, Malunion, Nonunion, and Osteomyelitis

Complications of bony healing are relatively rare in pediatric facial fractures. They are usually associated with comminuted fractures.³⁶ A growing facial skeleton heals faster than that of an adult.³⁷ Furthermore, few fractures are comminuted or significantly displaced, facilitating appropriate reduction. Infection may occur and osteomyelitis can occur at any fracture site. Overall incidence ranges from 8 to 9%.⁹ Four percent of cases are complicated by malunion.⁹ Early definitive treatment and appropriate surgical technique will minimize cases of infection. If hardware is present and infection persists, eventual removal may be necessary.

Sequelae of Rigid Reduction

Research in cleft lip and palate repair has demonstrated an association with wide subperiosteal undermining and potential future adverse alterations in bony growth.³⁸ Al though this study has not been extended to the repair of maxillofacial fractures in the growing skeleton, minimizing periosteal elevation in fracture repair is prudent for preserving normal craniofacial growth patterns.

The role of rigid fixation in the development of a cranio-facial growth disturbance remains controversial. In animal studies, both wire and compression plate fixation of the craniofacial skeleton have resulted in growth alterations.^39–41 These studies involved disruption of the coronal suture line as well. No animal models have investigated removal of hardware or wiring and the subsequent growth patterns. Furthermore, no studies exist that examine changes in the growing mandible, the most common site undergoing open reduction for trauma. Regardless, there are several case reports detailing migration of retained fixation hardware during growth.^42–45 Some case series have reported intracranial migration of hardware and association with injury to the globe, seizure activity, meningitis, and damage to underlying cortex.^46,47

Because of the risk of growth disturbance and hardware migration, some have advocated resorbable hardware. Resorbable plates are typically manufactured as a blend of materials. Poly-L-lactic acid (PLLA) maintains its strength for up to 6 months. It is less malleable than other resorbable materials. Polyglycolic acid, poly-DL-lactic acid, and polydioxanone are weaker but more malleable. Current resorbable plates are typically composed of a blend of PLLA and one of the other materials to achieve desirable physical characteristics. All resorbable plates are mechanically weaker than titanium fixation plates. To circumvent this, resorbable plates are usually larger in profile. Manufacturers effectively exchange strength and low profile for resorbability. Some cases of device extrusion and sterile abscesses have been reported.⁴⁸

In their series of 1,884 pediatric craniofacial patients, Eppley et al⁴⁹ reported outcomes in patients treated with resorbable poly-L-lactic-polyglycolic acid (PLLA-PGA) plates. There were five cases of resorbable device failure requiring reoperation. Failure was the result of plate fracture rather than screw pullout. Twelve patients suffered from foreign body reaction presenting at 4 to 10 months after surgery.

Imola et al48 published a case series of 57 patients treated with resorbable plates, 11 of whom underwent facial fracture repair. Two of three mandibular fracture cases experienced delayed union. One of those two patients required revision surgery via metal plate fixation because of plate extrusion and surgical site infection. With continued improvement in biomaterial technology, more recent case series have reported few complications with resorbable plates for mandible fractures.^50–52 These included infection requiring removal of hardware (1 of 22 patients).

Unfavorable Results Involving the Upper Third of the Face

Posttraumatic Growing Skull Fracture

Although uncommon in adults, superior orbital fractures are more common than floor fractures in children younger than age 7 years.²⁵ This is most likely related to the timing of the development of the frontal and maxillary sinuses. As such, supero-orbital fractures are more likely to be associated with a dural tear. They are at risk for progressive diastasis of the fracture line. Although only 0.03 to 2.2% of all pediatric skull fractures result in growing skull fractures, 90% occur in patients younger than 3 years. Fifty percent occur in those younger than 1 year.^53–57 Younger children are susceptible because of their malleable cranial vault and rapidly growing brain.^53,58,59 The presence of a dural tear at the time of injury seems to be necessary for the development of a growing skull fracture.^58,60–63 Typically, the scalp is intact. A collection of CSF at the fracture site (cephalhydrocele) indicates the dural tear. Other presenting symptoms may include diplopia, proptosis with or without pulsatility, eyelid edema, or orbital asymmetry. Patients may present 2 to 18 months after injury.⁶⁴

Without proper recognition and treatment, the skull fracture will continue to expand with destruction of the bony vault, porencephalic cyst, epilepsy, paresis, cerebral scarring, brain atrophy, and cerebral herniation.^63,65,66 A significant mass effect on the orbit may result in optic nerve compression.⁶⁷

Prompt diagnosis and treatment of a dural tear associated with a fracture is vital to avoid a growing fracture. If the injury has already progressed to a growing skull fracture, surgical treatment with wide exposure using a coronal incision is advocated. Dural edges are usually retracted at the time of repair.^66,68 Havlik et al⁶⁶ recommend for mal craniotomy with removal of meningovascular cicatrix; drainage of cystic structures; dural repair, which may require grafting; and reconstruction of the cranial vault. Rongeuring bone rather than performing a craniotomy will result in loss of bone stock. This makes healing difficult. Bone grafting of the anterior skull base or orbital roof may be indicated. Patients may require secondary procedures for persistent orbital asymmetry.⁵⁷

Mucocele

Mucoceles are the result of fractures involving the frontal sinus associated with mucosal tear.⁶⁹ Mucosa entrapped in a fracture line may result in cyst formation. Growing mucoceles produce several inflammatory cytokines, such as prostaglandin and collagenase. These can erode surrounding bone.^70,71 Mucocele development occurs over a span of years. They are only likely to present in adulthood.⁷² Furthermore, mucoceles originating from trauma in childhood are rare, given that the frontal sinus is not present before age 4 years and is not fully developed until adulthood.¹

Treatment of a mucocele remains controversial. Integrity of the posterior table, dura, frontal recess, and any other bony defects must be assessed. All diseased mucosa must be removed. If the frontal recess is patent and functional, then the frontal sinus may be left intact. Otherwise, obliteration or cranialization with occlusion of the frontal recess is indicated. Orbital roof or frontal bone defects should be reconstructed as needed.

Unfavorable Results Involving the Middle Third of the Face

Telecanthus

NOE fractures are the major cause of telecanthus in pediatric facial trauma. Comminuted NOE fractures usually require transnasal fixation to properly reposition the medial canthal tendon. A drill hole is placed posterior to the lacrimal fossa and linked to the fragment containing the medial canthal tendon with a small-gauge wire.⁷³ This technique usually provides an anatomical reduction of the fracture. Alternatively, permanent sutures anchored to a miniplate can achieve the same result. Regardless of the technique used, anatomical repositioning requires satisfactory superior and posterior positioning of the canthal remnant. Residual telecanthus may nevertheless result even after satisfactory initial treatment. In Singh and Bartlett’s series⁷⁴ of 20 pediatric patients with NOE fractures, 6 required further canthal repositioning.

Any fracture involving the orbital floor may cause entrapment of orbital contents. Trimalar, Le Fort, and simple floor fractures are all susceptible. Pure orbital wall fractures are more common in children than adults because of their incomplete pneumatization of the paranasal sinuses. As stated previously, children older than 7 years are more likely to experience floor fractures, whereas those younger than 7 years are more susceptible to pure orbital roof fractures. Furthermore, because most pediatric facial fractures occur after the age of 5 years, most simple orbital fractures in children involve the floor.75,76 Orbital floor fractures are typically classified as “direct,” involving a direct impact to the orbital rim with subsequent fracture of both the inferior orbital rim and the orbital floor, or “indirect,” consisting of a force impacting the orbital contents and causing them to break through the weakest point of the orbital walls. In the pneumatized maxilla, this is the orbital floor.

Because of the propensity of pediatric bone to greenstick fracture, entrapment is significantly more common in children.⁷⁷ Patients with entrapment may present with symptoms of oculocardiac reflex: bradycardia, nausea, and syncope.⁷⁸ Surgeons should nevertheless perform forced duction testing at the time of injury to rule out entrapment even if symptoms are absent. Children may present without any associated findings. This has been termed “white-eyed” blowout.⁷⁹ Patients without entrapment can be observed for enophthalmos and diplopia during the days after injury. Entrapment can also occur during surgical repair of an orbital floor fracture. Before closure during orbital floor reconstruction, the surgeon should repeat forced duction testing to rule out entrapment of orbital contents.

Although inferior rectus entrapment with symptoms of oculocardiac reflex is considered a surgical emergency, the timing of orbital floor repair with asymptomatic entrapment remains unsettled. Some authors advocate treatment within 1 or 2 days.^77,79,80 Prolonged entrapment may predispose the inferior rectus to ischemic contracture and necrosis.⁸¹ Fibrosis and adhesions of intraorbital contents may also be a causative factor of ocular restriction.⁸² Furthermore, some studies have shown that most cases have no muscle within the entrapped contents.^83,84 Regardless of the cause, no definitive treatment protocol currently exists. Cases of restricted movement with onset as early as 72 hours after injury have been documented.⁷⁸ Conversely, some evidence suggests that immediate repair is not necessary. Egbert et al⁸⁵ reported a case series of 34 patients. They reported no difference in mobility or diplopia for children treated within 1 month of fracture. However, patients receiving therapy within 7 days had a more rapid improvement in symptoms than those treated later. They recommended early treatment for patients with severe symptoms of entrapment.

Data regarding long-term outcomes and complications of surgical intervention in pediatric floor fractures are lacking. Nevertheless, surgeons typically advocate surgical approaches that allow for adequate exposure and proper implant placement. A transconjunctival approach allows for a “scarless” surgery but has limited exposure compared with external approaches. Lateral canthotomy can improve exposure, but the surgeon must repair the canthal ligament before case completion. “Middle lamella” syndrome, violation and subsequent scarring of the orbital septum with resultant lower lid malpositioning, has not been investigated in detail in the pediatric literature. Measures should be taken to avoid its occurrence. In the external approach or the preseptal subconjunctival approach, surgeons should incise the orbital septum below the orbital rim to allow for appropriate graft coverage and suture reapproximation. Nonresorbable alloplastic implants are at risk for migration in the growing orbit and should be avoided. They may impinge on orbital structures and adversely affect movement. Infection is also an increased risk. It is treated with implant removal. In the case of supramid, the foreign body capsule should be marsupialized into the maxillary sinus, because spontaneous hemorrhage has been reported.⁸⁶

Persistent diplopia after orbital trauma may also result from transient muscle ischemia with subsequent strength imbalance. Injury to cranial nerves III, IV, or VI may also negatively affect ocular motility. Any suspected impingement should be evaluated and imaged as necessary. In cases of muscular imbalance, prism glasses can be used for conservative management. More aggressive therapies include botulinum toxin injections into restricted extraocular muscles or strabismus surgery to address muscle length.⁸⁷

Either a pure orbital floor fracture or a zygomaticomaxillary complex fracture involving the orbital floor will result in enophthalmos if the floor defect is not properly assessed and corrected (Fig. 49.1). Most surgeons recommend a period of observation to allow for resolution of periorbital edema to ascertain true extent of enophthalmos. Losee et al⁷⁶ examined their series of patients with orbital fractures and the outcomes with conservative management. Three of ten pure orbital fractures managed conservatively had detectable enophthalmos. These patients had higher energy impact trauma, larger fracture widths, greater fracture area, displacement, and soft tissue herniation. None of the patients with enophthalmos demonstrated any functional deficit. Degree of enophthalmos for all three patients measured no more than 1 mm. These findings suggest that conservative management of pediatric enophthalmos without further complication of dystopia or entrapment may be considered. This may be related to the elasticity of the orbital connective tissue in a child and the ability of their periosteum to resist tearing.^26,76 However, some cases do require secondary surgery. In their review of complex orbital fractures, Nowinski et al88 documented 3 of 14 patients with persistent enophthalmos or ocular dystopia requiring surgical revision.

Fig. 49.1 A pediatric patient after an orbital blowout fracture. (a) Radiological findings of the floor blowout, with herniation of the orbital contents into the maxillary sinus and a “greenstick” fracture of the floor. (b) The intraoperative view of the placement of an orbital floor implant via a transconjunctival approach.

Accurate incidence of nasal fractures has been difficult to ascertain. Many are managed in an outpatient setting. Inpatient statistical analysis may therefore omit many cases. Regardless, most authors regard the nose as the most common site of pediatric facial fractures.8,9,16–19,21–23,89

Several nasal fracture classification schema exist. Moran⁹⁰ specifically described patterns seen in children. Lateral fractures are the most common. These involve ipsilateral infracture and contralateral outfracture of the junction of the ascending process of the maxilla and the nasal bone. Linear fractures are nondisplaced and without comminution. Frontal fractures, like those in adults, are more likely to cause greater trauma. Vector of force may transmit injury posteriorly to the lacrimal and ethmoid bones, or posterior telescoping of the nasal tip or pyriform aperture may occur. “Open book” fracture is a type of frontal fracture particular to the pediatric population related to incomplete nasal bone fusion. Nasal bones separate at the midline, causing central depression and lateral flaring and displacement over the frontal process of the maxilla.

Verwoerd and Verwoerd-Verhoef² described common patterns of pediatric nasal septal fractures. Vertical fractures involve fractures caudal to the insertion of the upper lateral cartilages and extend to the anterior nasal spine. Left untreated, they will result in deviation of the caudal septum and nasal tip. A “C-formed fracture” extends posteriorly and superiorly from the central cartilaginous septum to the perpendicular plate. These fractures result in both bony and cartilaginous septal deviation. Recognition of these fracture patterns during physical examination will assist the surgeon in performing the appropriate treatment and reduction maneuvers in these patients. This requires both external and internal nasal examination. External examination should focus on inspection of the deformity and palpation of crepitus, mobility, and step-offs. Proper instrumentation is paramount to complete intranasal examination and will allow the surgeon to evaluate the presence of a septal hematoma, septal fracture or deviation, epistaxis, intranasal lacerations, and patency of the internal nasal valve. Headlight illumination, suction, topical decongestants, and a nasal speculum are all necessary for adequate exposure and examination.

Researchers have postulated two models of nasal growth and development. According to Verwoerd and Verwoerd-Verhoef’s model,2 two growth centers exist in the nose. The sphenodorsal zone extends from the sphenoid to the nasal dorsum and results in increased length and height of the nasal dorsum. The keystone area, the junction of the upper lateral cartilages and the nasal septum at the bony–cartilaginous interface, is part of this growth zone. The sphenospinal zone extends from the sphenoid to the anterior nasal spine and results in increased projection of the nose and maxilla. Injury to either growth center may result in progressive deformity in the dimensions each growth center controls. Another model describes a two-phase growth of the premaxilla.⁹¹ In this model, the septo-premaxillary ligament transmits an inferior and anterior force from the growing nasal septum to the premaxilla until the maxillae reach their definitive boundaries. A second phase of growth then occurs, intrinsic to the orbital and posterior surfaces of the maxillae. Saddle nose deformity of the nasal dorsum (Fig. 49.2), widening of the nasal bridge, widening of the nasal base, decreased nasal length, and decreased projection are all possible sequelae in patients even after satisfactory surgical treatment of a nasal fracture.^92,93

Because the nose continues to grow into late adolescence or even adulthood for men, most surgeons recommend a conservative approach to the management of nasal fractures. Furthermore, the younger the patient at the time of injury, the more likely long-term deformities will occur. Although cases of nasal trauma at birth may resolve with no intervention, some authors advocate immediate treatment regardless of nasal airway patency.^94,95 They propose that the ease and safety of the maneuver weighed against the risk of functional and developmental abnormality justifies intervention. Otherwise, pediatric nasal fractures should be treated within 3 to 5 days after injury. Bony healing is more rapid than that of adults.⁹⁶ Closed reduction under anesthesia permits proper examination, reduction, and splinting of the fracture. Older children may tolerate treatment with regional nerve blocks. In cases of severe nasal obstruction, some surgeons recommend open septorhinoplasty.^97–101 Care must be taken to avoid the aforementioned growth centers whenever possible. Resection of septal cartilage should always be minimal, unless septal deflection is the major contributor to airway obstruction. Bony and cartilaginous septal continuity should be maintained. Resected cartilage should be recontoured and replaced. Surgeons may opt to use polydiaxone scaffolding to support the regrafted cartilage. Animal studies have demonstrated normal cartilage growth after a cartilage defect has been bridged with polydiaxone.¹⁰² Spreader grafts should be avoided. They disrupt the dorsoseptal growth center. Crushed cartilage can fill areas at risk for perforation. However, it lacks the mechanical strength to support the growing nose.¹⁰³

Unfortunately, replacement of cartilage does not guarantee normal nasal growth after repair. Several case series have reported deformities and growth disturbances that have arisen years after surgical treatment.^104–106 This is most likely related to injury and repair occurring before the adolescent growth spurt. Reestablishing the end-to-end relationships of cartilage fragments should be the surgeon’s goal to minimize future growth disturbance. If saddle nose deformity does develop, secondary surgery is required to establish satisfactory dorsal height and length (see Fig. 49.2).

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