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Pre-emptive planning to optimize safety and outcome is a defining principle of pediatric craniofacial surgery, in which "procedures that come before" should enhance and not compromise procedures that are planned to follow.A technical modification of fronto-orbital advancement/remodeling in 2-stage hypertelorism surgery for craniofrontonasal dysplasia is presented, where orbital hypertelorism is accompanied by coronal craniosynostosis. Fronto-orbital advancement/remodeling undertaken by this approach preserves bone in the supero-lateral bandeau and provides optimal quality bone stock for the subsequent orbital box shift osteotomy. In this way the second procedure is protected and enhanced by optimal planning of the primary procedure, with potential benefits to safety, quality, and outcome of the final result.

Ocular hypertelorism was introduced by Greig as an increased interpupillary distance. The paranasal sinus mucoceles are acquired lesions for various reasons; however, their behavior is progressive, capable of eroding the bone and extending to the orbital and intracranial regions. The objective is to present a clinical case of orbital hypertelorism secondary to mucocele in the paranasal sinuses. This is a 72-year-old male patient who came presenting an increase in volume in the right nasoorbitoethmoidal region. The isodense lesion occupying the maxillary and right ethmoidal sinuses was confirmed by an intimate relationship with the ipsilateral frontal and sphenoidal sinus, with osteolytic involvement of the orbit and nasal region. After incisional biopsy with mucocele results, a wide resection plus facial reconstruction was performed with autologous grafts and osteosynthesis material. Currently, the patient has 1 year of evolution, without significant functional commitment. It is important to consider giant mucoceles as part of the differential diagnoses in patients with deformities in the middle and upper third of the face.

Normal pre- and post-natal changes in the interorbital distance are described. Causes of illusory hypertelorism include flat nasal bridge, epicanthic folds, exotropia, widely-spaced eyebrows, narrow palpebral fissures, and dystopia canthorum. Measurements of hypertelorism may involve soft tissues or bone, and a number of indices have also been proposed. Various types of measurements are evaluated and recommendations suggested. Possible pathogenetic mechanisms for hypertelorism include: early ossification of the lesser wings of the sphenoid; failure in nasal capsule development allowing the primitive brain vesicle to protrude into the space normally occupied by the capsule resulting in morphokinetic arrest in the position of the eyes; and disturbances of the cranial base in Apert syndrome. Associations with increased interorbital distance are also discussed: orofacial clefting, nonprotruding lipomas of the corpus callosum, calcification of the falx cerebri, duplication of the crista galli, wrinkling of the nose, and tissue tags of the nose. Finally, experimental models of hypertelorism in animals are discussed.

A retrospective statistical analysis of orbital hypertelorism correction was performed by comparing the preoperative and postoperative intercanthal distances of these patients with published age-matched normal values. Forty-five patients who had undergone surgery over a 15-year period with an average follow-up of 5 years (6 months to 14 years) were evaluated. Comparison of age-normalized preoperative and postoperative intercanthal distances revealed a significant difference for orbital hypertelorism patients as a group (p < 0.0001), patients with clefts (p < 0.0001), patients with nasoencephalocele (p < 0.01), and patients with frontonasal dysplasia (p < 0.05), but not for those patients with craniofacial dysostosis (p < 0.20). Multiple analyses of variance revealed a significant interaction existing between the extent of preoperative deformity and the cause of hypertelorism for both the postoperative deformity and the total amount of correction achieved, but not for the type of surgery or for the age at which the surgery was performed.

This investigation was designed to test hypothesized pathogenetic mechanisms for orbital hypertelorism (OrH). Serial measurements of bony interorbital distance (BIOD), level of cribriform plate relative to orbital height (LOCP), and cranial width (CW) were made from postero-anterior cephalometric radiographs on two pathologic groups craniofacial clefts (FC) and premature craniofacial synostosis syndromes (PCS) compared with normal controls matched for age and sex. Both groups of malformations showed significantly larger mean values (P less than 0.01) for BIOD alone and when adjusted for CW. The LOCP relative to the orbital height was found to be positioned at a significantly lower level (P less than 0.01) than the norm in both groups. When the growth increments for BIOD were plotted to analyze rates of growth, individuals with FC showed increments similar to those seen for the normal. However, patients with Apert and Crouzon syndromes showed greater than normal increments for BIOD. In these cases, the LOCP remained at a relatively lower level in relation to orbital height. These findings support the hypothesis of a time-specific event during fetal development causing morphokinetic arrest in FC syndromes. In Apert and Crouzon, another mechanism continuing postnatally produces OrH.

In midfacial fractures the crucial area is the upper portion of the midfacial skeleton which lodges the orbits, the interorbital space with its anatomic relationship with the anterior cranial fossa, the lacrimal apparatus, the levator muscle, and the skeletal structures of the nose. Because of the severity of the injuries in a multisystem injured patient, these fractures may be neglected or receive inadequate primary treatment. In some cases the damage is so extensive that primary treatment can only accomplish part of the task. Late reconstruction is necessary, therefore, and is the subject of this paper.