The unique anatomy and physiology of the growing craniofacial skeleton predispose children to different fracture patterns as compared to adults. Diagnosis and treatment of pediatric orbital fractures can be challenging. A thorough history and physical examination are essential for the diagnosis of pediatric orbital fractures. Physicians should be aware of symptoms and signs suggestive of trapdoor fractures with soft tissue entrapment including symptomatic diplopia with positive forced ductions, restricted ocular motility (regardless of conjunctival abnormalities), nausea/vomiting, bradycardia, vertical orbital dystopia, enophthalmos, and hypoglobus. Equivocal radiologic evidence of soft tissue entrapment should not withhold surgery. A multidisciplinary approach is recommended for the accurate diagnosis and proper management of pediatric orbital fractures.
Key points
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Different orbital wall fracture patterns exist in children, compared with adults, due to the unique anatomy and physiology of their developing craniofacial skeleton.
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A thorough history and physical examination are essential in the assessment of children with suspected orbital fractures.
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Physicians should be aware of symptoms and signs suggestive of trapdoor fractures with soft tissue entrapment that should prompt surgery within 48 hours of injury.
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Equivocal radiologic evidence of trapdoor fractures with soft tissue entrapment should not withhold surgery; imaging should only supplement the overall clinical picture.
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A multidisciplinary approach is recommended for the accurate diagnosis and proper management of pediatric orbital fractures.
Background
Although the orbit is a commonly fractured region of the face in both the pediatric and adult populations, there are significant differences in the clinical presentation, management, and outcomes between these two patient populations. This is attributed, in part, to anatomical and physiological differences between the developing pediatric skeleton versus adult skull. Despite the advancements in craniomaxillofacial surgery in children, the choice of operative management of pediatric orbital fractures (POF), as well as surgical timing, remain areas of controversy and active research. Only a minority of pediatric patients present with absolute indications for reduction and internal fixation of POF, whereas the majority of patients present with a more complicated clinical picture. Workup of POF can be further complicated by limitations in patient compliance to physical examination and imaging, leading to missed diagnoses. In POF, the decision to operate must balance surgical and anesthetic risk with potential benefits of intervention, such as the prevention of ocular motility disorders and globe malposition. In this article, we highlight the unique aspects of POF with regard to epidemiology, anatomy, clinical presentation, assessment, surgical indications, and complications.
Epidemiology
According to a review of the National Trauma Data Bank based on 12,739 pediatric patients with facial fractures, POF was the least common fracture type (9%) compared with mandibular (32.7%), nasal (30.2%), and maxillary/zygomatic (28.6%) pediatric facial fractures ( Fig. 1 ). In other studies, POF ranged from 5% to 56% of pediatric facial fractures. The incidence of POF varies according to age, sex, etiology, season of the year, and fracture site. Although several attempts have been made to quantify the characteristics and outcomes surrounding POF, the topic on a whole is significantly less well researched than adult orbital fractures; evidence on POF and its relation to the aforementioned factors is based on either small case series investigating POF or large trauma series investigating pediatric facial fractures in general.
In general, POF is often more likely to occur in boys , and during the summertime. The most common etiology of POF has been attributed to activities of daily living, assault, , , sports injuries, falls, or motor vehicle collision. , , This inconsistency regarding the most common etiology of POF might be due to the different age groups analyzed by the different studies, because the etiology of pediatric facial fracture has been shown to vary according to the child’s age.
Facial fractures, including orbital fractures, are significantly less common in children compared with adults. , , Only 1% of facial fractures have been reported to occur in children aged younger than 1 year. Although the overall incidence of POF does not seem to significantly vary across age groups in children (see Fig. 1 ), different age groups tend to have different POF patterns. For example, orbital roof fractures are predominant in children aged younger than 7 to 10 years compared with orbital floor fractures, which become more common afterwards and with increasing age. , , , , This is attributed to the changing anatomy and physiology of the developing craniofacial skeleton which will be discussed below.
Development and Anatomy
The Neurocranium and Face
The human skull is composed of the neurocranium and the facial skeleton. Neurocranial development is continuous, driven by the enlarging brain, and occurs in all directions. The majority of neurocranial development occurs before the age of 2 years, at which the neurocranium reaches around 75% of its adult size. Neurocranial growth then gradually decreases and is 95% complete by the age of 10. The facial skeleton, in contrast, has discontinuous growth and shows vectored expansion along various anatomic sites. It is driven by bone apposition, resorption, and affected by hormonal changes during puberty. The majority of facial skeletal development occurs before the age of 5 years, at which the facial skeleton reaches around 80% of its adult size. , Facial skeletal development decreases thereafter before accelerating again at puberty and abates around the age of 17 years. The asynchronous growth of the neurocranium and facial skeletons results in various neurocranium-to-face size ratios of 8-to-1 at birth, 4-to-1 at the age of 5 years, and 2.5-to-1 in adulthood ( Fig. 2 A, B, D , respectively). , , This difference in neurocranium-to-face size ratios is one reason behind the greater incidence of intracranial injury and craniofacial to maxillofacial fractures in children compared with adults. , , , ,
Another reason for the difference in susceptibility to facial fractures, including orbital fractures, is the differences in facial bone composition and resultant changes in mechanical properties in children compared with adults. The process of bone mineralization, which mainly occurs after 2 to 3 years of age, transforms the immature, elastic, and cancellous bone of the growing facial skeleton into the mature, mineralized, and cortical bone of the adult facial skeleton. , This provides the pediatric facial bones with a greater ability to bend, rather than break, and withstand traumatic forces compared with adult facial bones. As a result, children are more likely to develop incomplete fractures, also known as “greenstick” fractures, compared with adults. The bony composition of the pediatric facial skeleton also confers the advantage of greater bone healing and remodeling, which supports the nonoperative management of pediatric facial fractures. However, the elasticity of the pediatric facial skeleton, as well as the presence of rudimentary sinuses, permits an easier transmission of traumatic forces to the neurocranium increasing the risk of intracranial injury.
The Orbit and Adjacent Sinuses
The 2 orbits are a pair of quadrangular truncated pyramids whose contents are arranged according to the rule of 7; there are 7 bones, 7 intraorbital muscles, and 7 nerves in the orbit. The 7 bones of the orbit are the frontal, maxillary, zygomatic, ethmoid, lacrimal, palatine, and greater and lesser wings of the sphenoid. These bones make up the 4 orbital walls (roof, floor, lateral wall, and medial wall) and the first 3 make up the outer orbital rim.
As the facial skeleton develops, paranasal sinuses undergo pneumatization, and the orbital walls change configuration and thickness. Three of the 4 orbital walls (roof, floor, and medial wall) are adjacent to paranasal sinuses ( Fig. 3 ). Initially, the sinuses and the nasal cavity are merged in utero, until the frontal, maxillary, and ethmoid sinuses separate from the nasal cavity in the second trimester. The maxillary sinuses are the first to pneumatize and expand rapidly from birth to 3 years of age and from 7 to 12 years of age. The intermediary delay in maxillary sinus pneumatization coincides with a period of mixed dentition where the unerupted maxillary teeth are immediately below the orbital floor, shielding it and mitigating fracture risk. The subsequent resumption of maxillary sinus pneumatization beyond 7 years coincides with eruption of permanent dentition and ends at 16 to 18 years of age when it reaches adult size. In contrast to the biphasic growth pattern of the maxillary sinuses, the ethmoid sinuses continuously expand from birth to 12 years of age. As the ethmoid sinuses pneumatize, the medial orbital walls gradually become thinner and more susceptible to fracture (see Fig. 3 ). The maxillary and ethmoid sinuses growth patterns thus help explain the greater susceptibility of children aged older than 10 to 12 years to orbital floor and medial wall fractures. , , , , ,
The frontal sinuses start to pneumatize around 5 to 7 years of age (see Fig. 2 B). Before that, the lack of well-developed frontal sinuses allows facial traumatic forces to be directly transmitted to the orbital roof without force dissipation. This phenomenon, as well as the high cranium-to-face ratio discussed earlier, explains the greater susceptibility of children aged younger than 7 years to orbital roof fractures, as previously mentioned. , ,
The orbital cavity contains the globe, vessels, nerves, extraocular muscles, tendons, lacrimal gland, trochlea, periorbital fat, and other connective tissues. The orbital septum, check ligaments, and Lockwood’s suspensory ligament constitute the periorbital structures that provide ligamentous support to the globe. These periorbital soft tissues retain elasticity that helps provide stability, resist traumatic forces, protect the pediatric orbit against fractures, and even splint orbital contents in case of fractures ( Fig. 4 ). This characteristic of periorbital soft tissues may explain the relatively lower incidence of enophthalmos in children. Besides the bone composition of the pediatric facial skeleton discussed earlier, the resilience of the periorbital soft tissue also supports the nonoperative management of pediatric facial and orbital fractures.
Presentation and Assessment
The presentation of pediatric orbital and facial fractures is significantly different than that of adult orbital and facial fractures due to the previously discussed differences in the anatomy and physiology of the growing facial skeleton. The elasticity of the pediatric facial skeleton makes it less prone to fractures compared with the adult facial skeleton. Therefore, when pediatric facial fractures occur, strong traumatic forces are usually the cause and associated injuries should be suspected. It was reported that among children presenting with POF, 43.4% had concomitant intracranial injury and 20% had significant injury beyond the head and neck. POF with concomitant head and/or chest injuries are significantly associated with greater odds of mortality. Furthermore, a greater risk of concurrent intracranial injury is seen in patients presenting with fractures of multiple orbital walls. Sobol and colleagues reported an interesting case of a 3-year-old child with combined orbital roof and floor fractures with concomitant epidural hemorrhage ( Fig. 5 ). When one orbital wall is fractured, practitioners should carefully assess the other orbital walls for concomitant fractures. Coon and colleagues found that around 40% of children presenting with orbital roof fractures also have another orbital wall fracture. It is recognized that looking for associated fractures and injuries is challenging due to the generally uncooperative nature of pediatric patients. Nonetheless, a thorough traumatic survey and having a low threshold for obtaining radiographic imaging when facial fracture or intracranial injury is suspected are of paramount importance.
Orbital Floor Fractures
Orbital floor fractures can be classified as unentrapped/communited, also known as “open-door” fractures (see Fig. 4 ), or entrapped, known as “trapdoor” fractures ( Fig. 6 ). The elastic nature of the growing facial skeleton predisposes to minimally displaced greenstick fractures compared with blowout fractures in adults. Greenstick fractures can recoil back to their initial position, trapping the bulging periorbital soft tissues, hence the trapdoor nomenclature and the preponderance of these fractures in the pediatric population. , , , The inferior rectus muscle depresses and adducts the eye. Patients with entrapped inferior rectus muscle often present with vertical gaze diplopia and restriction of upgaze/supraduction (see Fig. 6 ). This entrapment inflicts high compartment pressure on the inferior rectus muscle and other periorbital soft tissues, potentially leading to ischemia and/or infarction and long-term motility problems. This is the reason extraocular muscle entrapment is considered a surgical emergency and should be addressed urgently. When blow-out fractures occur in pediatric patients (without extraocular muscle entrapment), enophthalmos and/or hypoglobus are rarely seen as presenting signs, due to the periorbital supporting structures described earlier that mitigate risk of globe malposition.
Patients with POF can present with classical symptoms and signs including pain, diplopia, limited extraocular motility, conjunctival erythema, subconjunctival hemorrhage, and periorbital soft tissue swelling. However, trapdoor fractures can cause entrapment and significant extraocular motility restriction without any periorbital ecchymosis, edema, conjunctival or subconjunctival abnormalities, or significant imaging findings. These trapdoor fractures are termed white-eyed fractures (see Fig. 6 ). When muscle gets entrapped in trapdoor fractures, it may be engulfed with fat in between the muscle and bone. This makes it hard for the muscle to be visualized on traditional computed tomography (CT) scans, which is often missed in 50% of the cases of muscle entrapment. One study revealed that patients with white-eyed fractures were less likely to undergo orbital imaging in the emergency department, less likely to be seen urgently by an ophthalmologist, and had a 4 to 5 days delay in follow-up with an ophthalmologist compared with other patients. Hence, practitioners should not solely rely on overt ocular abnormalities, like subconjunctival hemorrhage, or radiographic evidence alone for the diagnosis of entrapment. Instead, a thorough physical examination with a proper assessment of extraocular muscle motility should be performed and supplemented with radiographic evidence to arrive at an accurate diagnosis and management plan. Surgery within 24 to 48 hours of presentation for patients presenting with white-eyed fractures is favorable and leads to better long-term motility compared with surgery after 2 weeks of presentation.
Another potential manifestation of trapdoor fractures is the oculocardiac reflex, characterized by the triad of bradycardia, nausea/vomiting, and syncope. The extraocular muscle entrapment triggers an afferent signal via the ophthalmic division of the trigeminal nerve to the main sensory nucleus of the trigeminal nerve, which in turn sends back an efferent signal via the motor nucleus of the vagus nerve increasing parasympathetic tone and bradycardia. Of children with trapdoor fractures, it has been reported that 95% to 100% present with restricted extraocular motility , and that up to 63% present with nausea/vomiting. Nausea/vomiting has been reported to have a positive predictive value of 83.3% for entrapment in trapdoor fractures. Hence, the oculocardiac reflex has been considered as highly suggestive of inferior rectus entrapment and another indication for urgent surgical repair of POF. Surgical intervention allows for the prompt resolution of the symptoms of the oculocardiac reflex. This, again, signifies the importance of a thorough physical examination including assessment of vital signs, extraocular motility, visual acuity, forced ductions, and pupillary function for the diagnosis of possible extraocular muscle entrapment.
Orbital Medial Wall Fractures
Orbital medial wall fractures are prone to the entrapment of the medial rectus muscle ( Fig. 7 ). The function of the medial rectus muscle is to adduct the eye. Patients with entrapped medial rectus muscle often present with horizontal diplopia and lateral gaze restriction (see Fig. 7 A).
