Disclaimer: The information contained within the Grand Rounds Archive is intended for use by doctors and other health care professionals. These documents were prepared by resident physicians for presentation and discussion at a conference held at Baylor College of Medicine in Houston, Texas. No guarantees are made with respect to accuracy or timeliness of this material. This material should not be used as a basis for treatment decisions, and is not a substitute for professional consultation and/or peer-reviewed medical literature.

Concepts of Orbital Reconstruction
Masayoshi Takashima, M.D.
February 11, 1999

If one critically assesses the long-term problems of facial fractures that cause the most difficulty in treatment, they virtually all relate to the orbit. A crooked nose, a depressed maxilla, a frontal deformity, or malocclusion can be treated by well established methods, which on most occasions will give a good correction of the deformity. Consider, however, enophthalmos, diplopia, telecanthus, and orbital dystopia. Often very different methods of treatment are available, depending on the surgeon and his or her experience, but it is relatively rare to achieve perfect symmetry even when using the newer techniques that have become available over the past few years. It is therefore important to look at the fractures that mainly account for these particular problems.

The axiom of orbital surgery is to restore the anatomic structure of the orbit to its natural and aesthetic form with preservation of function. Accurate realignment and replacement of the components are essential. To have an optimal result, the surgeon has to have a fundamental appreciation of the orbital anatomy. Even though orbital anatomy is complex, with some details still being actively researched, adherence to several anatomic principles will aid in the restoration of the traumatized orbit. Today I plan to provide a review and an update of the concepts involved in the treatment of orbital reconstructive problems. However, instead of focusing on rigid fixation, I would like to discuss the basic tenets that provide the guidelines for the reconstruction of the simple to the complex traumatized orbit.

Briefly, the eyelids represent specialized structures of the face designed to protect, moisten, and cleanse the ocular surfaces. The eyelids can be thought of as 2 leaves, an anterior consisting of skin and orbicularis muscle, and a posterior consisting of a tarsal plate, the conjunctival layer, and the eyelid retractors. A layer of fascia, the orbital septum, running from the peripheral ring of the orbital margin towards the lids where it fuses, separates these leaves.

Because of the abundant vascularity of the eyelids, wounds should seldom become acutely infected and are capable of healing under conditions of trauma and contamination that would cause wound breakdown, and even necrosis, in less vascular tissues. As a result of this, eyelid wounds should almost never be debrided, unless there is gross contusion of the tissues that are obviously thrombotic.

One complication which can occur with the eyelids after orbital trauma is ectropion or vertical lid shortening. This is thought to be secondary to overcorrection of the globe at the time of fracture reduction or can be due to scar adhesion between the orbital septum and orbicularis muscle upon reattachment.

Ectropion is more likely to arise in partial thickness lacerations, in which only skin and orbicularis are damaged, rather than in full thickness injuries where contraction of both the deep and the superficial layers more often tends to give rise to notching of the lid margin. Injuries of the lower lids are better tolerated than those affecting the upper lid. Even quite marked distortion, and even partial absence, of the lower lid may often be present without any serious consequences, while notching or ectropion, even of mild degree, affecting the upper lid can cause exposure of the cornea during sleep, and give rise to desiccation and ulceration with serious consequences to vision.

The canthal regions formed by union of the lid are firmly anchored in place by the connective tissue of the canthal tendon on the medial side and the canthal ligament on the lateral side, both of which attach to the bony margins of the orbit. The canthal attachments are extremely strong and are composite structures in which extensions of the fibrous tarsus, the orbital septum, the lateral horns of the aponeurosis of the levator palpebrae superioris and, in the medial canthus, the tendons of the various heads of the orbicularis muscle all share.

Both lateral and medial attachments are inserted into the bony orbit behind the plane of the cornea, the lateral canthal ligament into the orbital tubercle just within the bony margin and the medial canthal tendon into the anterior lacrimal crest. Disinsertion of either the lateral or medial attachment will produce at least temporary shortening of the length of the palpebral fissure, partly owing to contraction of the orbicularis muscle and partly due to retraction of the more elastic tissues of the eyelids.

The structure of the eyelids at the medial canthus is rendered even more complicated than at the lateral because of the presence of the lacrimal drainage apparatus. Lacerations or tissue loss at this site present a more difficult problem for repair than do similar injuries at the lateral canthus and elsewhere along the lids. Consequently, canthorraphy of the medial canthus is rarely performed.

Telecanthus may result from improper transnasal reduction of the canthus bearing central bone fragments. Common contributing factors include inadequate exposure, transnasal wiring performed anterior to the medial canthus, and detachment of the canthal insertion. Lateral displacement of the central fragments may occur when transnasal wires are placed anterior to the medial canthus; such reductions produce increased interorbital distance and telecanthus. Accidental stripping of the medial canthus requires reinsertion, adding another order of complexity to the fracture repair. It is technically difficult to restore preinjury aesthetics if the medial canthus must be reattached. Superior aesthetic results are usually only obtained when the canthus remains attached to its bony insertion. Secondary reconstruction of telecanthus may involve osteotomies of the central fragments to reduce the intercanthal distance. Complete subperiosteal dissection and mobilization of the orbital soft tissues allow an unstressed repositioning of the canthal ligament.

If suturing the medial canthal tendon to the periosteum does not produce a permanent correction of the canthal displacement, the canthal tendon must be held in place by a soft stainless steel wire passed across the nasal cavity through a hole drilled in the opposite nasal bone.

Repair and reconstruction involving the lateral canthus is considerably simplified when compared with similar surgical procedures at the medial canthus. This is chiefly because of the absence of the lacrimal drainage apparatus but, at least as far as reconstruction is concerned, is also partly due to the greater ease with which tissue may be introduced into this area.

Traumatic lateral canthal dislocation is repairable by suturing the divided ligament with non-absorbable suture to the inside of the orbital margin in the vicinity of the orbital tubercle to which the ligament is normally attached. If the displacement of the canthus is considerable, a more secured canthopexy may be achieved by drilling a small hole in the lateral wall at the site of the orbital tubercle and suturing the cut ligament through this hole.

Damage to the tear passages may occur as a result of direct or indirect trauma to the region of the inner canthus of the eye. Such injures are usually the result of traffic accidents, assaults, animal bites, or surgery in the region. Incorrect management may condemn the patient to a lifetime of artificial tears or the indefinite use of a bypass tube.

Whether an eye waters or not depends on the volume of tears produced. Anatomically, 30 % of tears drain via the upper canaliculus, and 70 % through the lower, while the tear sack drains though gravity. Most eyes with an obstructed lower canaliculus do not water under normal circumstances because the upper canaliculus will absorb the extra tears. Retrospective studies reveal that, unless both upper and lower canaliculi are injured, canalicular repair should not be undertaken secondary to the unlikelyhood of achieving permanent patency. In addition, this maneuver or the presence of a stent can compromise the integrity of the uninjured canaliculus.

The periorbita is a variable adherent and highly innervated fibrous layer that covers the bones of the orbit. The periorbita has several firm attachment points in the orbit including the suture lines, the foramina, the fissures, the orbital rim, and the lacrimal crest. At other locations, the periorbita can be lifted from the bone with relative ease, both by the surgeon getting exposure to the bone or by accumulations of blood or pus. Both the optic foramen and the superior orbital fissure periorbita are thick and continuous with the dura mater posteriorly. Therefore, surgery or trauma posteriorly may result in CSF leaks.

The vertical level of the globe is partially maintained by a sling of fascia that extends from the medial to the lateral wall of the orbit and effectively cradles the eyeball. This fascial web is known as Lockwood's suspensory ligament and is a direct component of the fascia of the inferior rectus and inferior oblique muscles. Mustarde demonstrated that Lockwood's ligament will support the eye even when the orbital floor is completely absent, so long as its anchoring points - to Whitnall's tubercle of the zygoma laterally and the lacrimal crest medially - are preserved. These anchoring points are only disrupted after a high velocity impact injury.

The spatial configuration and relationships of the orbits are best understood by examining a human skull. The bony orbit may be regarded as a quadrilateral pyramid that becomes three-sided near the apex. This base consists of a circumferential rim of thick, resilient bone that serves to resist and dissipate impact forces. Further support is provided by buttresses in the contiguous facial bones, oriented into vertical and horizontal pillars. The orbital rim, therefore, presents an anterior abutment that reinforces and protects the skeletal framework of the orbital cavity.

There are seven bones that make up the orbit: frontal, maxilla, zygomatic, ethmoid, lacrimal, greater and lesser wings of the sphenoid, and palatine. The first three constitute the strong outer buttress. They provide protection for the more delicate bones that make up the orbital walls. The bony orbit has been divided into four compartments: superior, lateral, inferior, and medial. Each has unique characteristics that influence its response to trauma.

The superior wall, or orbital roof, with its arched shape is moderately resistant to fracture. The orbital roof is 3 mm thick posteriorly and is thinnest just behind the superior rim anteriorly. Posteriorly, the roof remains flat and receives a contribution from the lesser wing of the sphenoid. The incidence of orbital roof fracture is uncommon, and is estimated at less than 5% of all facial fractures. They often present as orbital rim disruptions. It is postulated that the arched shape of the roof as well as the buttress effect of the brain dura and frontal sinuses contribute to the resilience of this structure. Limited orbital roof fractures need not be repaired unless the posterior table of the frontal sinus is injured. However, if there is fragment displacement and associated change in eye position, particularly with a CSF leak, then the area should be explored. Complications of incorrect fracture reduction include difficulties with upward and downward movement of the eye and defect in the orbital roof resulting in pulsating exophthalmamos.

The lateral wall is bounded by the superior and inferior orbital fissures. The greater wing of the sphenoid forms the posterior aspect of the lateral wall while anteriorly it is met by the zygoma and the zygomatic process of the frontal bone. Just inside the lateral orbital rim is the lateral orbital tubercle of Whitnall where the lateral canthal ligament, Lockwood's suspensory ligament of the eye, orbital septum and lacrimal fascia attach. The lateral wall has the lowest frequency of injury of all facial fractures. The rim is formed by the frontal and zygomatic bones, which are both moderately strong. Fracture of the lateral wall is found typically in association with the trimalar fracture. If the fracture is insufficiently reduced, then the bony orbital volume will be increased and there will be enophthalmos. In addition, there will be displacement of the eye since insufficient correction results in the whole lateral orbit being in the wrong position. As discussed previously, a lateral canthus detachment can also occur.

The medial wall is composed of mostly thin bones ranging from 0.2 to 0.4 mm in thickness. The length of the wall is approximately 5 cm. The ethmoid bone makes up most of the medial wall with contributions from the lacrimal bone. The medial wall thickens posteriorly near the body of the sphenoid and anteriorly near the lacrimal crests and fossa. The anterior and posterior ethmoidal foramina are located along the frontoethmoidal suture. These foramina mark the horizontal level of the cribriform plate, which is of critical importance during surgical decompression of the medial wall. The ethmoidal air cells, with the bony trabeculae, provide some strength to the medial wall, which it less susceptible to injury than the orbital floor. There are several major structures near the medial wall, including the lacrimal system and the medial canthal tendon, that make repair complex and hazardous. The significance of medial wall injury is four-fold. Firstly, the medial canthal tendon is usually displaced. Secondly, the medial wall may be blown out leading to an increase in orbital volume. Thirdly, there may be damage to the medial rectus muscle with medial displacement of eye. And lastly, damage to the lacrimal system may occur.

The inferior wall is the most vulnerable to injury. Most of the floor is composed of the orbital plate of the maxillary bone with a small contribution from the palatine bone posteriorly and the zygoma anterolaterally. Blowout fractures typically involve the medial orbital floor where the bone is thinnest. The inferior orbital fissure is approximately 2cm long and is a bony defect between the orbital floor and the lateral wall in the posterior orbit. This fissure is an important surgical landmark since it is the posterior limit of a subperiosteal dissection along the orbital floor and is about 20mm posterior to the anterior orbital rim. Anesthesia of the cheek secondary to trauma to the maxillary division of the cranial nerve V can be caused by a fracture that disrupts the infraorbital canal. Surgery is indicated if a large fracture with substantial orbital soft tissue herniation is seen on CT scan. Unfortunately, there is no accepted definition of "significant herniation," although one study found no significant enophthalmos in patients with orbital floor dehiscence of less than 2.5cm2, regardless of the soft tissue prolapse.

The position of the ocular globe and its relationship to the skeletal framework of the orbit requires further discussion. The precise location of the ocular globe in three dimensions is determined by several factors: the relative volume of the orbital cavity and that of its soft tissue contents, the configuration of the walls of the orbit, and the orientation and insertion of tendon attachments to the bony rim.

The coronal plane through the equator of the ocular globe divides the orbital cavity into anterior and posterior segments. It extends from the lateral orbital rim, through the center of the globe, to the medial orbital wall anterior to the lamina papyracea. The pathological features and reconstructive requirements of fractures in these two segments are entirely different, and will be discussed separately.

The anterior segment is defined as that part of the orbital cavity that is situated at or in front of the transverse axis of the globe. It comprises the bony rim of the orbit and the anterior portions of the orbital walls. In this region, both the medial wall and the floor of the orbit are concave in shape. Defects anterior to the axis generally do not cause significant changes in the volume of the orbital cavity and therefore do not alter the degree of ocular projection. These defects are usually seen in minor to moderate orbital trauma and can be repaired quite easily with autogenous or nonautogenous materials. Posttraumatic enophthalmos is not likely to occur. The one exception to this rule is the anterior floor fracture that entraps the inferior rectus and inferior oblique muscles. This is commonly a longitudinal fracture that runs posteriorly along the floor of the orbit toward the inferior orbital fissure. Although anterior to the axis of the globe, extraocular muscles entrapped within this narrow defect retract the globe, producing enophthalmos. It is important to note that whereas the dimensions and configuration of the anterior orbital segment do not significantly affect the forward and backward projection of the globe, they do determine ocular position in the coronal plane.

Poorly contoured grafts that do not duplicate the normal concavity of the anterior orbital floor are likely to cause superior globe displacement in the absence of enophthalmos or proptosis. A displaced segment of the orbital rim can also result in ocular transposition in a transverse or vertical dimension. Precise skeletal reconstruction at the level of the ocular axis is particularly important in ensuring accurate positioning of the globe.

The shape and volume of the orbital cavity posterior to the axis of the globe determine ocular projection in the a/p plane. Within the posterior segment of the orbit, the medial wall is parallel to the sagittal plane; the lateral wall diverges at 45-degree angle and is entirely posterior to the axis of the globe. Small changes in the orientation or position of the lateral wall profoundly affect orbital volume and globe projection. The lateral orbital wall is resilient and rarely comminutes. However, malrotation of the lateral wall due to poor reduction of a zygomatic fracture is frequently observed and is a leading cause of posttraumatic enophthalmos. Defects in the medial orbital wall are often overlooked. Isolated blowout fractures at this site cause an increased orbital volume posterior to the globe axis as well as enophthalmos. In rare instances, entrapment of the medial rectus muscle causes restricted ocular motility and retraction of the globe.

Appreciation of the anatomic configuration of the junctional area between the medial wall and floor in the posterior third of the orbit is particularly important. The upper portion of the maxillary antrum produces a characteristic bulge in this region, obliterating the angle between the orbital floor and the medial wall. This prominence is crucial in maintaining the forward projection of the globe. Failure precisely to recreate this contour invariable leads to posterior globe displacement, even in the presence of small fractures
.
Gross instability of orbital fractures predisposes to massive swelling of soft tissue. Within restricted anatomic spaces, such as the superior orbital fissure or optic canal, progressive edema can result in pressure neuropathy, causing disturbances in visual acuity and ocular motility. In the absence of adequate fixation, the skeletal framework of the orbital rim tends to collapse, and the overlying soft tissues become scarred and constricted. Failure to restore continuity to the walls of the orbital cavity inevitably leads to atrophy and contraction of herniated or incarcerated intraorbital contents. Major orbital trauma, therefore, results in a deformity that becomes progressively more severe with time. Shrinkage and contracture of associated soft tissues amplifies the deformity and jeopardizes the results of reconstruction.

Operative complications include visual loss, although this is rare. Nicholson and Guzak surveyed the literature and found 8 cases of blindness after facial fracture, six of them from their own series of 72 blow out fractures. The etiology was thought to be either increased intraorbital pressure - edema or hemorrhage, with vascular embarrassment or direct damage to the optic nerve. Ten years later, Lederman scanned the literature and noted only 5 cases of blindness after facial fracture. Other authors note a 2%-3% incidence of visual loss associated with fracture of the facial bones involving the orbit.

Measures that can be implemented to try to prevent visual loss include: using an implant or bone graft that is not too thick and not placed too far back in the orbit, avoiding external pressure on the globe, and immediate decompression if intraorbital hemorrhage is suspected. A high resolution CT is imperative in the early diagnosis and detection of the cause of visual impairment after facial fracture.

Orbital hemorrhage occurs in approximately 1% of all facial fractures. Bleeding tends to originate from the branches of the infraorbital artery or the penetrating venous branches transversing the floor, and usually resolves spontaneously. Steroids and orbital decompression may be necessary if visual acuity is threatened.

Infection and inflammation occurs postoperatively in 3%-4% of all facial fracture repairs. Due to the high vascularity of the tissues in this region, infection is quite rare even in those cases when a dirty wound exists. Goldfarb and colleagues discuss the contraction of orbital cellulitis after orbital fracture. Orbital cellulitis is commonly associated with sinusitis because of the close anatomic relationships between the two structures. Orbital cellulitis more commonly occurs when there is a break in the walls of the sinuses to permit direct extension of a sinus infection into the periorbital region. Thus the development of sinusitis must be closely monitored in patients who have sustained an orbital fracture.

Reports of host tissue reaction to Teflon, steel, aluminum and silastic implant materials over the last 13 to 20 years have recently come to light. In all cases, the presenting symptoms are proptosis and diplopia. CT and surgical exploration have found cyst-like inflammatory lesions at the floor of the orbit and histologic studies revealed hyperplastic, inflammatory tissue that should be excised.

Extrusion of foreign implants occurs in 3% of the cases. Data regarding long term extrusion rates are scarce, but Polley and Bingley had no rejection of implants in 230 reconstruction cases that were followed for an average of 30 months.

Infraorbital neuralgias is a rare complication of orbital fracture fixation. Infraorbital pain is often secondary to pressure on the nerve by an implant, and notching the posterior end of the prosthesis takes care of the problem. The pain can also be caused by fracture fragments impinging on the nerve at the infraorbital foramen, in which case decompression is needed.

Persistent diplopia occurs in 2%-50% of cases. Diplopia occurring immediately after an orbital fracture may be due to soft tissue entrapment by the bone fragments, orbital hemorrhage and edema with increased intraorbital pressure, or extraocular muscle or cranial nerve palsy. Diplopia due to neuromuscular contusions can take up to 6 months to resolve, but correct muscle surgery should be contemplated if it persists beyond this point. Residual diplopia may also be secondary to inadequate relapse of the original incarceration, reincarceration, or adhesions to either the bone graft or perforated alloplast.

Enophthalmos occurs in approximately 15%-22% of patients post surgery. The causes are escape of orbital fat, incorrect correction of deformity, enlargement of the bony orbital volume, muscle entrapment causing backward traction on the globe with secondary contractions, and orbital fat necrosis. In evaluating the late results of surgery vs. observation in 103 patients with confirmed "pure" blow out fractures, Dulley and Fells noted that patients repaired 6 months or longer after their injury showed a 72% incidence of enophthalmos, as opposed to 20% when surgery was performed within 14 days. In the late surgery group, 40% needed additional eye muscle or orbital surgery and binocular vision was achieved only to a moderate degree.

It can be seen that in orbital wall trauma, it is important to have a very accurate assessment as to where the trauma exists, the extent of the displacement, whether there is fragmentation or not, what has happened to the soft tissue and whether the orbital volume has changed. If these are not carefully assessed and appreciated, then unfortunate long-term sequelae will result. Although we are becoming more experienced and better equipped to deal with these problems, our ability to correct them completely still eludes us. This is probably due to the fact that, although we have a better understanding of what maintains the eyeball in position in the orbit, we do not yet know how to deal with the problems arising from disruption of these delicate structures. There is no doubt, however, that with a better understanding of orbital trauma, the results of primary treatment have improved considerably. As the anatomy of the traumatized orbit is better understood, further advances in treatment and even better results can be anticipated.

Case Presentation

J.S. is a 28-year-old Hispanic male who presented to the Ben Taub emergency center on 4/3/98 after shooting his girlfriend in the chest and then trying to commit suicide with a self-inflicted GSW to the head. On evaluation, the patient was alert and oriented times three. An obvious entrance wound was present at the right temple with an exit wound present just lateral to the left orbit in the left temporal bone. There existed a large tympanic membrane perforation with a laceration of the posterior bony external auditory canal on the right. The left tympanic membrane was intact, although there also existed a left external auditory canal laceration. Examination of the eyes revealed bilateral open globes. No other injuries were noted. Plain films revealed multiple facial fractures along with a metallic density seen overlying the anterior portion of the left inferior orbit.

Bibliography

Altobelli DE, Kikinis R, Mulliken JB, Cline H, Lorensen W, Jolesz F. Computer-assisted three-dimensional planning in craniofacial surgery. Plast Reconstr Surg 1993; 992:576-585.

Brody GS, Wheeler ES. Medial canthal tendon reconstruction. Plast Reconstr Surg 1981;68:789-791.

Friesenecker J, Dammer R, Moritz M, Niederdellmann H. Long-term results after primary restoration of the orbital floor. J Craniomaxillofac Surg 1995;23:31-33.

Goldfarb MS, Hoffman DS, Rosenberg S. Orbital cellulitis and orbital fractures. Ann Ophthalmol 1987;19:97.

Grant MP, Iliff NT, Manson PN. Strategies for the treatment of enophthalmos. Clin Plast Surg 1997;24:539-550.

Hammer B, Prein J. Correction of post-traumatic orbital deformities: operative techniques and review of 26 patients. J Craniomaxillofac Surg 1995;23:81-90.

Howard G, Osguthorpe JD. Concepts in orbital reconstruction. Otolaryngol Clin North Am 1997;30:541-562.

Janecka IP. Correction of ocular dystopia. Plast Reconstr Surg 1996;97:892-899.

Janecka IP. Orbital reconstruction. Plast Reconstr Surg 1983;71:20-26.

Klimek L, Wenzel M, Mosges R. Computer-assisted orbital surgery. Ophthalmic Surg 1993;24:411-417.

Lederman IR. Loss of vision associated with surgical treatment of zygomatic-orbital floor fracture. Plast Reconstr Surg 1981;68:94.

Leibsohn JM, Hahn F. Medial canthal tendon reconstruction with nasal periosteum. Ophthal Plast Reconstr Surg 1992;8:35-40.

Leone C R Jr. Lateral canthal reconstruction. Ophthalmology 1987;94:238-241.

Manson PN, Ruas EJ, Iliff NT. Deep orbital reconstruction for correction of post-traumatic enophthalmos. Clin Plast Surg 1987;14:113-121.

Manson PN, Clifford CM, Su CT, Iliff NT, Morgan R. Mechanisms of global support and posttraumatic enophthalmos: I. The anatomy of the ligament sling and its relation to intramuscular cone orbital fat. Plast Reconstr Surg 1986;77:193-202.

Mathog RH. Reconstruction of the orbit following trauma. Otolaryngol Clin North Am 1983;16: 585-607.

Marin PC, Love T, Carpenter R, Iliff NT, Manson PN. Complications of orbital reconstruction: misplacement of bone grafts within the intramuscular cone. Plast Reconstr Surg 1998;101:1323-1327.

Marschall MA, Cohen M, Garcia J, Schafer ME. Craniofacial approach for the reconstruction of severe facial injuries. J Oral Maxillofac Surg 1988;46:305-310.

Martinez-Lage JL. Bony reconstruction in the orbital region. Ann Plast Surg 1981;7:464-479.

Merkx MA, Freihofer HP, Borstlap WA, van't Hoff MA. Effectiveness of primary correction of traumatic telecanthus. Int J Oral Maxillofac Surg 1995;24:344-347.

Mustarde JC. Repair and Reconstruction in the Orbital Region. New York: Churchill Livingstone, 1991.

Nguyen PN, Sullivan P. Advances in the management of orbital fractures. Clin Plast Surg 1992;19:87-98.

Nicholson DH, Guzak SV. Visual loss complicating repair of orbital floor fractures. Arch Ophthalmol 1971;86:369.

Ortiz-Monasterio F, Molina F. Orbital hypertelorism. Clin Plast Surg 1994;21:599-612.

Penfold CN, Lang D, Evans BT. The management of orbital roof fractures. Br J Oral Maxillofac Surg 1992;30:97-103.

Perry M, Banks P, Richards R, Friedman EP, Shaw P. The use of computer-generated three-dimensional models in orbital reconstruction. Br J Oral Maxillofac Surg 1998;36:275-284.

Piotrowski WP, Beck-Mannagetta J. Surgical techniques in orbital roof fractures: early treatment and results. J Craniomaxillofac Surg 1995;23:6-11.

Polley JW, Ringler SL. The use of teflon in orbital floor reconstruction following blunt facial trauma: a 20 year excperience. Plast Reconstr Surg 1987;79:39.

Putterman AM, Scott R. Deep ocular socket reconstruction. Arch Ophthalmol 1977;95:1221-1228.

Raveh J, Laedrach K, Vuillemin T, Zingg M. Management of combined frontonaso-orbital/skull base fractures and telecanthus in 355 cases. Arch Otolaryngol Head Neck Surg 1992;118:605-614.

Rodriquez RL, Zide BM. Reconstruction of the medial canthus. Clin Plast Surg 1988;15:255-262.

Sewall SR, Pernoud FG, Pernoud MJ. Late reaction to silicone following reconstruction of an orbital floor fracture. J Oral Maxillofac Surg 1986;44:821-825.

Sires BS, Lemke BN, Kincaid MC. Orbital and Ocular Anatomy. Baltimore: Williams & Wilkins, 1997.

Smith B, Nesi FA. Orbital fractures and medial canthal reconstruction. Clin Plast Surg 1978;5: 505-511.

Spinelli HM, Jelks GW. Periocular reconstruction: a systematic approach. Plast Reconstr Surg 1993;91:1017-1024.

Waitzman AA, Posnick, JC, Armstrong DC, Pron GE. Craniofacial skeletal measurements based on computed tomography: Part II. Normal values and growth trends. Cleft Palate Craniofac J 1992;29:118-128.

Whitaker LA, Vander Kolk C. Orbital reconstruction in hypertelorism. Otolaryngol Clin North Am 1988;21:199-214.

Yab K, Tajima S, Imai K. Clinical application of a solid three-dimensional model for orbital wall fractures. J Craniomaxillofac Surg 1993;21:275-278.

Yaremchuk MJ, Gruss JS, Manson PN. Rigid Fixation of the Craniomaxillofacial Skeleton. Boston: Butterworth-Heinemann, 1992.

Ziccardi VB, Patterson GT, Ramasastry S, Sotereanos GC. Management of a severe zygomatico-orbital fracture with dislocation of the globe into the antrum. J Craniofac Surg 1993;4:95-101.

Zide BM, Jelks GW. Surgical Anatomy of the Orbit. New York: Raven, 1985.

Grand Rounds Archive | Department Home page

BCM Public | BCM Intranet | Privacy Notices | Contact BCM | BCM Site Map |

©2001-2006 Baylor College of Medicine
Bobby R. Alford Department of Otolaryngology-Head and Neck Surgery
Mail: One Baylor Plaza, NA102, Houston, TX 77030
Phone: 713-798-5906
E-mail: oto@bcm.edu

Last modified: Feb. 16, 2006