You are in: eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > TRAUMA Orbital FracturesArticle Last Updated: Apr 30, 2007AUTHOR AND EDITOR INFORMATIONAuthor: Neeraj N Mathur, MBBS, Professor, Department of Ear, Nose and Throat, Lady Hardinge Medical College, SK Hospital, Kalawati Saran Children's Hospital Neeraj N Mathur is a member of the following medical societies: Royal Society of Medicine Coauthor(s): Simon Frank Taylor, MBBS, FRANZCO, FRACS, Consulting Staff, Department of Ophthalmology, Westmead Hospital, New South Wales; Bhupendra C K Patel, MD, FRCS, Associate Professor of Ophthalmic Plastic and Facial Cosmetic Surgery, Department of Ophthalmology and Visual Sciences, University of Utah School of Medicine, John A Moran Eye Center Editors: M Abraham Kuriakose, MD, DDS, FRCS, Chairman, Head and Neck Institute, Amrita Institute of Medical Sciences; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Erik Kass, MD, Chief, Department of Clinical Otolaryngology, Associates in Otolaryngology of Northern VA; Christopher L Slack, MD, Otolaryngology-Facial Plastic Surgery, Private Practice, Associated Coastal ENT; Medical Director, Treasure Coast Sleep Disorders; Arlen D Meyers, MD, MBA, Professor, Department of Otolaryngology-Head and Neck Surgery, University of Colorado School of Medicine Author and Editor Disclosure Synonyms and related keywords: orbital fractures, blowout fractures, blow-in fracture, orbital floor fractures, midfacial trauma, orbit fractures, blow-out fractures, trapdoor fracture, medial blow-out fractures, lateral blow-out fractures, superior rim fracture, orbital apex fractures, diplopia, facial trauma, sports-related facial trauma, maxillofacial trauma, blunt orbital trauma, orbital-rim fractures, orbital-roof fractures, traumatic optic neuropathy INTRODUCTIONOrbital fractures are commonly seen with midfacial trauma. Fracture severity ranges from small minimally displaced fractures of an isolated wall (see Image 1) that require no surgical intervention to major disruption of the orbit (see Image 2). Orbital fractures may be defined in terms of anatomic considerations, including the following:
Although these classifications of orbital fractures are useful in communication, the assessment and treatment of each patient must be individualized. Any or all of the orbital bones (eg, ethmoid, frontal, palatine, maxilla) may be involved in trauma, and fractures vary in their displacement and comminution. Assessing injury to the soft tissues and globe, as well as orbital and periorbital bone injury, is important. This article focuses on fractures of the internal orbital skeleton. ZMC, NOE, and frontal-sinus fractures and traumatic optic neuropathy are discussed in other articles in this journal. For excellent patient education resources, visit eMedicine's Breaks, Fractures, and Dislocations Center and Eye and Vision Center. Also, see eMedicine's patient education articles Facial Fracture and Black Eye. ProblemThe management of orbital trauma and fractures is aimed at minimizing and preventing early and late sequelae and complications. The goal of intervention is to prevent vision loss and to minimize late problems, such as persistent diplopia and disfiguring globe malpositioning. EtiologyFacial trauma is largely the result of motor vehicle accidents, industrial accidents, sports-related facial trauma, and assaults. Motor vehicle accidents, particularly those in which seatbelts are not worn, are usually the most common cause of maxillofacial trauma, as shown in large series in developed nations. In the adult female population, nonaccidental injury in the form of domestic violence should be specifically assessed during history-taking because this is a common cause of orbital fractures in this group. PathophysiologyMost patients present with a history of blunt orbital trauma. Penetrating trauma is less common. Currently, the pathogenesis of orbital blow-out fractures follows 2 lines of reasoning. The Hydraulic theory advocates that increased intraorbital pressure causes a decompressing fracture into an adjacent sinus. The Buckling theory contends that the posterior transmission of a direct orbital rim force causes a buckling and resultant fracture of the orbital wall. Both mechanisms may be involved to various degrees to produce orbital blow-out fractures. Orbital tissue (fat, fibrous septa, extraocular muscle) may be involved with the fracture site, resulting in ocular motility disturbance, while volume augmentation leads to globe malpositioning. In classic blow-out floor fractures, the lateral extent is generally limited by the infraorbital neurovascular structures, and the medial extent is limited by the maxilloethmoidal strut of stronger bone. Blow-out fractures of the medial wall are limited by the stronger bone of the frontoethmoidal suture in the superior direction and by the maxilloethmoidal strut in the inferior direction. The medial wall is also intermittently supported by the bony septa between the ethmoidal air cells. In a combined fracture of the floor and medial wall, the maxilloethmoidal bony strut is also fractured. Blow-out fractures that are limited medially to the infraorbital nerve are more common than those that extend laterally to it, resulting usually from high-velocity trauma. A ZMC fracture is frequently associated with a direct blow to the malar eminence. Classic tetrapod fractures involve injury to each of the following supporting structures of the ZMC:
Once these buttresses are disrupted, the force of the external injury and the pull of the masseter muscle may cause posterior and inferior rotation of the zygoma. This displacement is evident by the palpable step-off of the orbital rim and zygomatic arch. The zygoma may be comminuted, especially near the ZMC and the zygomaticotemporal sutures. The frontozygomatic suture is the strongest of the 4 zygomatic buttresses, and consequently, it is usually not comminuted. Displacement of the body of the zygoma is necessarily associated with a fracture of the lateral orbital floor and lateral orbital rim. Orbital-rim fractures are generally the result of a direct blow. Orbital-roof fractures are usually the result of high-energy injuries. They may be anteriorly continuous with an injury to the supraorbital rim or frontal sinus, or they may extend posteriorly to the superior orbital fissure. Linear undisplaced, blow-out, and blow-in fractures have been described. Always consider associated brain parenchymal and dural injuries. ClinicalMost patients present with a history of blunt orbital trauma. Initial treatment in patients with facial injuries should be aimed at airway security, hemodynamic stability, and cervical-spine integrity. Head injuries must be ruled out. The patient should be evaluated for additional soft-tissue and bony injuries of the head and neck. Injury to the globe has been reported in as many as 30% of orbital fractures, stressing the importance of an ocular examination. Assessment of ocular function is important on presentation, during surgery, and after surgery. Remember that the function of the orbit is to protect the globe and support a functioning binocular visual system. The importance of recording visual acuity cannot be overemphasized. Check the patient's best-corrected vision, considering the refractive error and degree of presbyopia (if a near-chart is used). Spectacles are frequently broken or lost during the traumatic event. Record the patient's unaided and pinhole vision. Pupil function is important to assess and is abnormal in traumatic optic neuropathy (with a relative afferent pupil defect), as well as in cases of third nerve/ciliary ganglion injury and traumatic mydriasis. Referral to an ophthalmologist is advised for a more thorough assessment of intrinsic and extrinsic ocular anatomy and function. This assessment includes a dilated fundal examination with the use of a slitlamp and ophthalmoscope. In most cases of orbital fracture, significant periocular ecchymosis and edema are evident. The position of the globe should be assessed. However, enophthalmos is rarely evident in the first days after injury because of edema of the orbital tissues. Frequently, a degree of proptosis is evident early. Significant hypoglobus may be seen with severe floor disruption and also with a subperiosteal hematoma of the roof. Diplopia with inferior rectus muscle dysfunction is common, with muscle restriction associated with perimuscular tissue entrapment at the fracture. This is commonly a nonconcomitant vertical diplopia. Extraocular muscle edema, hemorrhage, and nerve neurapraxia may also cause diplopia. Forced duction tests, force generation tests, and coronal CT scanning aid in the clinical assessment. Vertical ocular motility disturbance suggests a fracture of the orbital floor. Traumatic rupture of an extraocular muscle has been reported and should be evident on the CT scan. Muscle entrapment is reported to be more likely with small fractures, which have less enophthalmos. In large fractures, enophthalmos is more likely and entrapment is less likely. Infraorbital nerve (with its anterior superior alveolar branch) hypesthesia is reported in as many as 60% of orbital floor blow-out fractures and in 71% of inferior orbital rim fractures. Disruption of the mucosal integrity of the maxillary or ethmoidal sinus may result in subcutaneous or intraorbital emphysema. A history of sudden orbital pressure and crepitus with postinjury nose blowing is relatively frequent. Medial-wall fractures (see Image 3) may be the result of direct naso-orbital trauma or may be a blow-out type of fracture. The medial-wall fracture may be isolated, but frequently, it is part of a medial wall-floor fracture complex with disruption of the maxilloethmoidal strut. Loss of medial wall stability is associated with enophthalmos and horizontal muscle imbalance (with medial rectus herniation into the ethmoid sinus). Severe epistaxis, cerebrospinal fluid (CSF) leakage, and lacrimal drainage problems have been reported. A subgroup of orbital floor fractures with a longitudinal medially based hinged fracture results in a trapdoor effect (see Image 4) with firm soft-tissue entrapment. Radiologically, these fractures may not seem impressive, with minimal bone displacement and minimal soft-tissue herniation. This pattern of injury is particularly frequent in the pediatric age group. Because of the greater elasticity of the orbital bones in children, their potential for these trapdoor fractures is greater. Attempted ocular movements in these patients may generate significant pain and intense parasympathetic autonomic features of nausea, vomiting, and bradycardia. Such fractures warrant early intervention, not only to alleviate the patient's symptoms but also to prevent compromise of the vascular supply to the entrapped tissue and an ischemic contracture of the entrapped tissue. Orbital-roof fractures are particularly important because of their association with intracranial injury. Dural tears are associated with CSF leakage and pneumocephalus. Subperiosteal hematoma may cause significant hypoglobus. Ptosis and vertical ocular motility disturbance are seen with injury to the levator-superior rectus muscle complex. Fractures of the orbital apex are rarely isolated and occur in association with or as an extension of fractures of the facial and orbital skeleton or base of skull. The anatomy of the orbital apex is significant for the complex association between bony, neural, and vascular elements, and morbidity is due to injury to these structures. Injury to the optic nerve leads to visual loss, most commonly resulting from an indirect posterior traumatic optic neuropathy. Injuries to cranial nerves III, IV, and VI manifest as extraocular muscle nerve palsy with manifest diplopia. Injury to cranial nerve V appears as sensory disturbance to areas supplied by branches of the trigeminal nerve. However, significant injury to the neurovascular structures of the orbital apex may be present without a fracture. Optic canal fractures are seen in about 50% of patients with posterior optic neuropathy due to trauma. Sensation of the superior orbital rim is supplied by the branches of the ophthalmic division of the trigeminal nerve, which remains uninjured in fractures of the orbital floor. Hypesthesia of the ipsilateral upper central incisor suggests a fracture of the orbital floor. Lateral-wall fractures (see Image 5) are generally part of a ZMC fracture. Clinical features include visible malar flattening, lateral canthal dystopia, globe displacement with enophthalmos, diplopia with muscle imbalance, and a palpable step at the orbital rim in the regions of the ZMC or frontozygomatic suture. Problems with mastication arise, especially with displaced zygomatic arch fracture impingement on the coronoid process of the mandible. NOE fractures generally occur with a traumatic telecanthus (due to lateral displacement of the medial canthal tendon/bony central segment complex) and abnormal projection of the nasal bridge. The lamina papyracea is commonly comminuted in these fractures. Associated injuries to the frontal sinus, nasofrontal duct, and cribriform plate are common. The 3 most important associated orbital injuries include the following:
Differential diagnoses include orbital edema and hemorrhage without orbital fracture and cranial nerve palsies. INDICATIONSThe aim of orbital reconstruction is to achieve normal bony projection, to reposition the globe, to release any entrapped orbital soft tissue, and to reconstitute normal orbital volume. The management of orbital fractures involves clinical evaluation of the patient; appropriate imaging; and an evaluation of whether, when, and how to repair the fractures. Not all patients with isolated orbital blow-out fractures require surgical intervention. Two variables dictate whether repair should be undertaken: ocular motility and orbital volume. The decision for intervention should be made with an understanding of the anticipated natural history over time. Indications are as follows:
A decision against early intervention should be balanced against an appreciation of the difficulties encountered when late reconstructive surgery for diplopia or enophthalmos is required. The coexistence of a floor and medial-wall fracture, especially with disruption of the maxilloethmoidal strut, frequently requires repair in view of the orbital volume expansion. However, both isolated floor and isolated medial-wall fractures may fulfill the motility- and volume-based criteria for surgery. Several groups have attempted to correlate the volume of herniated orbital tissue and the degree of enophthalmos, with results of one study suggesting that a 1-mL increase in orbital volume leads to 0.8 mm of enophthalmos. Generally, the presence of significant displacement or comminution of the orbital rim requires open reduction and internal fixation. Principles involve preservation of bone fragments and miniplate fixation. The timing of surgery has also been debated over the years. Except in the circumstance of a trapdoor fracture with the potential for an ischemic contracture of the entrapped tissue, the authors generally allow several days for orbital and eyelid edema to resolve. This delay also allows more accurate assessment of extraocular muscle function. However, the authors try to undertake repair within 2 weeks of the injury and prior to any early fibrosis of entrapped tissue. RELEVANT ANATOMYThe anatomy of the orbit is well described. However, features of relevance are noted here. The orbits are pyramidal-shaped structures with 4 walls that meet at the orbital apex. The superior orbital fissure, the inferior orbital fissure, and the optic canal are located toward the apex. Each orbital volume is about 30 mL. The orbital floor is the shortest of all the walls and does not reach the apex. It measures 35 X 40 mm and terminates just before the orbital apex and annulus of Zinn. A 3-mm downward displacement of the entire floor results in an orbital volume that is increased by 1.5 cm3 (a 5% increase), producing 1-1.5 mm of enophthalmos. The orbital wall is thinnest medial to the infraorbital canal, where it may just be 0.5 mm in thickness and, thus, most vulnerable to fracture. The floor inclines superiorly at a 30° angle from anterior to posterior and at a 45° angle from lateral to medial. The floor is not uniplanar, but it has post–rim concavity and posterior convexity. This postequatorial convexity must be accurately reconstructed to help prevent postoperative enophthalmos. The inferior orbital fissure defines the posterior limit of the orbital floor. The infraorbital neurovascular bundle crosses the floor and may define the extent of a floor fracture. Perforating vessels are frequently encountered in periosteal elevation of the orbital floor. Cauterization of these vessels prior to cutting is prudent. The infraorbital nerve exits the foramen of rotundum, traverses the pterygopalatine fossa, and exits through the infraorbital foramen as the infraorbital nerve. The orbital floor is separated into the medial and lateral segments by the infraorbital nerve. The medial segment is larger and more fragile. It is bounded by the infraorbital fissure, the bony canal of the V2, the orbital rim, and the inferior aspect of lamina papyracea. The lateral segment of the orbital floor is generally thicker and stronger than the medial segment and is bounded by the infraorbital fissure, the bony canal of the V2, the orbital rim, and the lateral orbital wall. In medial-wall dissection, the anterior and posterior ethmoidal vessels are situated just below the level of the frontoethmoidal suture and serve as important landmarks. The anterior ethmoidal foramen is about 24 mm posterior to the anterior lacrimal crest. The posterior ethmoidal foramen is about 12 mm posterior to the anterior ethmoidal foramen. The optic canal opens some 6 mm posterior to the posterior ethmoidal foramen. Periosteal dissection of the lateral orbital wall usually requires division of the zygomaticotemporal and zygomaticofacial nerves, causing hypesthesia to the lateral orbital rim. The lateral extent of the inferior orbital fissure is 15 mm from the rim. The superior orbital rim presents the superior orbital notch or foramen, which allows passage of the supraorbital neurovascular bundle. This bundle may be damaged in rim fractures or in surgical approaches to the rim or roof. The orbital roof may be very thin and deficient in places in the aged skull. All surgical approaches to the floor require knowledge of eyelid anatomy, and the reader is referred tothe eMedicine article Eyelid Anatomy. CONTRAINDICATIONSThe section above describes the indications for surgical intervention in orbital fractures. Although contraindications are relative, delaying intervention may be reasonable in the following cases: (1) in patients who are critically ill or who have head injuries, (2) in patients with a coexistent globe rupture in which globe repair takes precedence over fracture repair, and (3) in a patient who is monocular. In this last case, the patient does not experience diplopia, and intervention for volume reconstruction must be weighed against the potential for blindness in the only eye with vision. WORKUPLab Studies
Imaging Studies
Other Tests
TREATMENTMedical therapy
Surgical therapySurgical repair of orbital and maxillofacial fractures typically involves several steps, as follows:
Surgical management of orbital floor and medial-wall fractures is described below. Preoperative detailsOrbital fracture repair generally requires general anesthesia, and the patient requires a general medical assessment with this in mind. Diagnostic imaging studies should be made available in the operating room for intraoperative guidance. Intraoperative detailsPrior to exposure of any fractures, perform forced duction testing to confirm extraocular muscle restriction and to obtain preoperative results for comparison with those obtained later in the procedure. The success of blow-out fracture repair depends on adequate exposure, visualization of posterior bony shelf, and anatomic repair of the entire defect. A fracture of the orbital floor may be repaired through transcutaneous, transconjunctival, or endoscopic (transmaxillary or transnasal) approaches. Transcutaneous techniques may involve an approach through the subciliary area, lower eyelid crease, or orbital rim. Transconjunctival approaches may be subtarsal, preseptal, or inferior fornical. The medial orbital wall may be approached via a Lynch incision or a transcaruncular approach. With all approaches, dissection is carried down to the periosteum of the orbital rim, which may be incised and reflected. Once the orbital rim is exposed, a subperiosteal dissection completely exposes the limits of the fracture. Herniated and entrapped orbital soft tissue is reduced. Once the orbital soft tissues are repositioned, an orbital implant is placed to completely cover the orbital bony defect, preventing malpositioning of the soft tissue and restoring the native bony orbital anatomic volume. A forced duction test is performed at this point to confirm adequate relief of entrapment. Excessive pressure or traction is avoided on the globe and optic nerve during retraction. Careful dissection is required in the posterior orbit to prevent orbital apex injury. Important anatomic landmarks include the posterior wall of the maxillary sinus and the posterior ethmoidal vessels. Closure of periosteum may help prevent implant migration. Conjunctiva or skin may be closed with a 6-0 absorbable suture. The transmaxillary endoscopic approach offers excellent visualization of the entire orbital floor and is safe and efficacious and eliminates any postoperative eyelid complications. Trapdoor and medial blow-out fractures are the best candidates for an endoscopic approach. Dissection necessary for larger defects that extend lateral to the infraorbital nerve may place the infraorbital nerve at a greater risk for postoperative paresthesias. Complex 2-wall fractures cannot be managed endoscopically. The surgeon must discuss with the patient the possibility of using a transconjunctival/subciliary incision if the endoscopic approach fails. In the transmaxillary endoscopic approach, a sublabial incision is made over the canine fossa to expose the maxillary face in the subperiosteal plane; a maxillary osteotomy is performed and enlarged to approximately 1 X 2 cm about 1-2 mm below the infraorbital foramen and 1-2 mm lateral to the nasomaxillary buttress, thus avoiding injury to nerve, nasal aperture, and dental roots. An endoscope notch is then created at the central portion of the antrostomy; this helps in giving tactile feedback while the eyes of the surgeon are on the monitor. In trapdoor fractures (the most common type of orbital blow-out fracture), a stable hinge that consists of greenstick fracture and the sinus mucoperiosteum is usually present. Implant placement is usually not required, and a 1- to 1.5-mm malleable retractor passed through the maxillary sinus antrostomy can reduce the orbital contents. In medial blow-out fractures, a circumferential dissection is first made and, after the margins are defined, a 3- to 5-mm dissection is made on the orbital side of the defect. This releases more periorbita into the sinus and increases the prolapse of the orbital contents into maxillary sinus but is essential for placement of the implant. Endoscopic endonasal reduction of a blow-out fracture is possible using endonasal sinus surgery. This depends on the endoscopic view of orbital floor via middle meatus; in a few patients, a supplemental septoplasty and submucous conchotomy of inferior turbinate may be required to obtain such a view. The following implants have been used to reconstruct the orbital wall:
All implants have advantages and disadvantages, and the choice of implant is usually determined by the preference of the institution, surgeon, and patient. Autogenous bone grafts are the criterion standard to provide framework for facial skeleton and orbital walls. Cancellous bone grafts are preferred over cortical because cancellous bone grafts revascularize rapidly and completely, have an initial appositional bone formation followed by resorption (the opposite of a cortical bone graft), and repair completely, whereas the cortical graft remains an admixture of necrotic and viable bone. Repair of a complex orbital fracture, such as orbital rim, zygomaticomaxillary (ZMC), and naso-orbito-ethmoid (NOE) fractures, requires additional incisions for adequate exposure (eg, coronal, brow, upper eyelid crease, lateral canthus, transoral). Periosteal elevation and adequate exposure of the fracture is required to ensure anatomic alignment. The skeleton is rigidly fixated with miniplate and microplate systems. Soft-tissue resuspension at the time of primary reconstructive surgery may prevent early and late soft-tissue deformity. Postoperative detailsApplying an eye patch after orbital surgery to protect the cornea and to reduce conjunctival edema in the postoperative period is common practice. However, signs that indicate orbital hemorrhage or optic nerve compression (eg, visual loss, proptosis, chemosis, ocular motility disturbance, pupil abnormalities) progress unnoticed under an eye patch. The authors' policy is never to apply an eye patch after orbital surgery. The orbital surgeon should be familiar with the short-term management of an evolving orbital compartment syndrome. Recording the patient's visual acuity when the patient has regained consciousness is prudent. Nursing the patient in a head-up position and applying cool compresses may be useful to reduce postoperative edema. Analgesia and antiemetics are frequently required after orbital surgery. Follow-upThe nursing staff, the patient, and the family must be informed of the symptoms and signs of vision-threatening elevated orbital pressure. Emergency management of increased intraorbital pressure may prevent the loss of vision. The patient should promptly report symptoms of decreasing vision, increasing pain, and increasing nausea and vomiting and signs of increasing proptosis, eyelid ecchymosis, and decreasing motility. Diplopia secondary to neurapraxia and extraocular muscle contusion should be monitored for at least 6 months. This diplopia should be stable prior to surgical intervention. COMPLICATIONSComplications may result from the initial trauma or from the surgical repair. Complications due to the latter may be intraoperative or postoperative, and postoperative complications may be early or late. Intraoperative complications include, but are not limited to, the following:
Postoperative complications include, but are not limited to, the following:
OUTCOME AND PROGNOSISThe management of orbital fractures has been a source of controversy over the last century, particularly regarding indications for surgery and the optimal timing of surgery. More recently, high-resolution CT scanning has enabled assessment of the relationships between the bony orbital and orbital soft tissues. This imaging technique has also been a significant factor in determining which patients may benefit from surgery. The combination of the clinical examination and CT scanning facilitates surgical evaluation. The decision for early surgery should be balanced against possible perioperative complications, including blindness. The decision against early intervention should be balanced against the difficulties encountered when late reconstructive surgery for diplopia or enophthalmos is required. The risk of loss of vision with orbital exploration has been reported as 1 event in 500 cases. Despite surgery, 5-30% of patients have residual diplopia and may require other forms of strabismus management. This percentage is higher with combined medial-wall and floor fractures. FUTURE AND CONTROVERSIESInternal fixation devices and techniques have evolved rapidly over the past decades and will continue to do so. Bioabsorbable polymers (eg, polyglycolic acid and polydioxanone) have been used in plates and screws, with the advantage of their absorption after the fracture has healed. Minimally invasive endoscopic techniques have found applications in the treatment of blow-out fractures. The management of orbital fractures and their complications have benefited from a multidisciplinary approach. The continued relationship between facial plastic surgeons, maxillofacial surgeons, plastic surgeons, craniofacial surgeons, ophthalmic surgeons, and others will contribute to the progression of orbital reconstruction techniques. MULTIMEDIA
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