Orbital Fractures 

Updated: May 11, 2020
Author: Neeraj N Mathur, MBBS, MS, DNB(ENT), MNAMS, FAMS; Chief Editor: Arlen D Meyers, MD, MBA 

Overview

Practice Essentials

Orbital fractures are commonly seen with midfacial trauma. Fracture severity ranges from small minimally displaced fractures of an isolated wall that require no surgical intervention to major disruption of the orbit as seen in the images below.

Minimally displaced orbital floor fracture. Minimally displaced orbital floor fracture.
Left orbital floor fracture. This patient presente Left orbital floor fracture. This patient presented with little motility disturbance; however, because of the large defect in the orbital floor, late enophthalmos was predicted. Surgical repair was undertaken. Note the pneumo-orbitum.

Orbital fractures may be defined in terms of anatomic considerations, including the following:

  • Fractures may be limited to the internal orbital skeleton. This type includes blow-out and blow-in patterns, as seen in isolated fractures of the orbital floor, medial wall, and roof. Orbital blow-out fractures can be divided into the following fractures:

    • Trapdoor fractures - Caused by low force

    • Medial blow-out fractures - Caused by intermediate force

    • Lateral blow-out fractures - Caused by high force

  • Fractures may involve the orbital rim. An inferior, lateral, or superior rim fracture may be an isolated injury, or it may be contiguous with an internal-wall fracture.

  • Fractures may be associated with other fractures of the facial skeleton. Orbit involvement is seen in various facial fracture patterns, including zygomaticomaxillary (ZMC), naso-orbito-ethmoid (NOE), frontal-sinus, Le Fort II, and Le Fort III fracture patterns.

  • Orbital apex fractures are important to identify because of their association with damage to the neurovascular structures of the superior orbital fissure and optic canal (including traumatic optic neuropathy).

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. Zygomatic maxillary complex (ZMC), nasoorbitoethmoid (NOE), and frontal sinus fractures and traumatic optic neuropathy are discussed in other articles in this journal.

Diagnosis and management of orbital fractures

Computed tomography (CT) scanning is considered the top choice in imaging studies for evaluating orbital trauma. The study should be performed with nonenhanced axial and coronal 3-mm cuts; multiplanar reformation sections are then performed. The use of contrast material is generally not required. Sections of 1-mm thickness may be useful to assess optic-canal fractures and traumatic optic neuropathy. Three-dimensional reconstructed images of the orbit are useful adjuncts in planning the surgical repair of complex fractures.

Medical therapy

Patients should avoid blowing their nose and performing Valsalva maneuvers to limit intraorbital emphysema. Oral antibiotic therapy may be considered. Fractures that involve the medial wall and floor may be considered open fractures, as laceration of the sinus mucosa is inevitable.

Analgesia and antiemetics may be required. The use of oral steroids (prednisone 1 mg/kg/d) has been advocated to decrease soft-tissue edema.

The management of traumatic hyphema responds well to outpatient care and topical aminocaproic acid.

Surgical therapy

A fracture of the orbital floor may be repaired through transcutaneous, transconjunctival, or endoscopic (transmaxillary or transnasal) approaches.[1, 2]

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 tissues are 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.

For patient education information, visit eMedicineHealth's First Aid and Injuries Center and Eye and Vision Center. Also, see eMedicineHealth's patient education articles Facial Fracture and Black Eye.

Problem

The 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.

Epidemiology

Frequency

Trauma to the eye represents approximately 3% of all emergency department visits in the United States.[3] Frequency of orbital fractures in them is however not reported.

Etiology

Facial 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.

A study by Wasicek et al, using the National Trauma Data Bank, found evidence that among pediatric patients aged 5 years or younger who sustain abuse-related/nonaccidental facial fractures, the rate of orbital fractures is lower than among children who suffer accidental facial fractures (31.1% vs 53.4%).[4]

Pathophysiology

Most 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. Both in adults and children, the medial and inferior orbital walls are the most vulnerable to fracture owing to their thin bony structure.

A retrospective study by Kim et al indicated that in pure orbital blow-out fractures, delayed orbital tissue atrophy resulting from soft tissue injury greatly contributes to the development of late enophthalmos. (Unlike other studies, however, this report did not find that bony defect size or the volume of displaced soft tissue were significantly related to late enophthalmos.)[5]

Because of progressive calcification, the bones of adults lack the elasticity found in those of children.[6] Hence, the greenstick fracture is a pediatric response to external deforming forces. The ophthalmic equivalent of the greenstick fracture is the trapdoor variant of the blow-out fracture. Here, intra-orbital soft tissue (fat and muscle) may become entrapped within the fracture as the elastic bones snap back into place, resulting in potentially severe restrictive external ophthalmoplegia; this clinical scenario is further complicated by the relative lack of external periocular signs of trauma in many pediatric cases, known as the white-eyed blow-out fracture (WEBOF).[7]

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:

  • Superiorly, in the regions of the frontozygomatic suture

  • Laterally, the zygomaticotemporal suture

  • Medially, the ZMC suture

  • Within the lateral orbital wall, the zygomaticosphenoidal suture

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.

Presentation

Most 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.

A 10-year, retrospective study by Büttner et al indicated that the presence of a black eye in patients with minor head injuries predicts the existence of orbital fracture. The investigators found that out of 1676 patients with minor head trauma who presented with one or two black eyes, computed tomography (CT) scanning showed a maxillofacial skeletal fracture in 1144 (68.3%) of them. The report therefore recommended that all minor head trauma patients presenting with a black eye undergo CT scanning.[8]

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.[9] 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.

A study by Boffano et al indicated that the characteristics of diplopia vary according to the type of orbital wall fracture. The report, in which just over 50% of 447 patients with pure blow-out fractures presented with evidence of diplopia, found statistically significant associations between orbital floor fractures and diplopia on eye elevation, and between medial wall fractures and horizontal diplopia. The investigators suggested, therefore, that the form of diplopia that a patient demonstrates may offer clues to the type of orbital fracture present.[10]

Forced duction tests, force generation tests, and coronal CT scanning aid in the clinical assessment of orbital fracture. 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 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. Medial-wall fracture is seen in the image below.

Medial-wall fracture with significant herniation o Medial-wall fracture with significant herniation of the orbital contents into the ethmoid sinus. Horizontal diplopia was evident.

A study by Ordon et al found that subjects with an orbital floor fracture who had a concomitant medial wall fracture presented with more severe enophthalmos than did those with an isolated floor fracture. Following orbital reconstruction, however, no enophthalmic difference was seen between the two groups, although the investigators did report that the medial wall fracture patients were more likely to have postoperative vertical diplopia.[11]

A subgroup of orbital floor fractures with a longitudinal medially based hinged fracture results in a trapdoor effect 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. Trapdoor fracture is seen in the image below.

Orbital floor fracture with significant soft-tissu Orbital floor fracture with significant soft-tissue entrapment, a so-called trapdoor fracture. Note the relatively small amount of herniated tissue and the air-fluid level in the maxillary sinus. This patient had a significant vertical ocular motility disturbance.

One must remember that because of the subtle external and radiologic signs, WEBOF, often seen in pediatric group (as described above), is easily overlooked in a busy emergency department.[12] The diagnosis may be delayed further by symptoms of nausea and vomiting, which often lead to radiologic investigation of the head, rather than the orbit, in search of intracranial injury.

To diagnose WEBOF in the emergency department, Lane et al (2007) recommend the following for all children who present with nausea and vomiting following orbital trauma:[13]

  • These patients must be specifically asked about the presence and pattern of diplopia (horizontal, vertical).

  • These patients must undergo an extraocular motility examination.

If extraocular motility dysfunction is noted (or cannot be documented to be normal), patients must undergo dedicated orbital CT scanning with axial and coronal views with bone and soft tissue windows, along with CNS imaging, as indicated clinically.

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 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. Lateral-wall fracture is seen in the image below.

This lateral-wall fracture is part of a zygomatico This lateral-wall fracture is part of a zygomaticomaxillary complex fracture that was classified as a tripod fracture.

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:

  • Traumatic retrobulbar hemorrhage and the development of an orbital compartment syndrome

  • Traumatic optic neuropathy

  • Coexistent ocular injury (including a globe rupture)

Differential diagnoses include orbital edema and hemorrhage without orbital fracture and cranial nerve palsies.

Indications

The 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:

  • Large orbital-floor fractures, ie, those with radiologic evidence of significant displacement or comminution of more than 50% of the orbital floor, with prolapse of orbital soft tissue, that are likely to lead to significant enophthalmos (usually reported as >2 mm) (However, a study by Vicinanzo et al suggested that in cases of orbital-floor fracture, clinical findings, rather than computed tomography [CT] scan assessments of fracture size, should be used to determine the need for surgery, since the investigation, which involved 23 patients, showed only moderate agreement between neuroradiologists in their evaluation of the extent of floor fractures.[14] )

  • Persistent diplopia accompanied by positive forced duction results and radiologic evidence of perimuscular tissue entrapment (Patients with diplopia within 30° of the primary position are likely to have persistent diplopia; therefore, surgical intervention is warranted.)

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 Anatomy

The 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 to the Medscape Reference article Eyelid Anatomy.

Contraindications

The 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.

 

Workup

Laboratory Studies

Laboratory studies are limited to those required for preoperative assessment in patients who require operative repair.

Imaging Studies

Computed tomography

CT scanning is considered the top choice in imaging studies for evaluating orbital trauma.

  • The study should be performed with nonenhanced axial and coronal 3-mm cuts; multiplanar reformation sections are then performed. The use of contrast material is generally not required.

  • Sections of 1-mm thickness may be useful to assess optic-canal fractures and traumatic optic neuropathy.

Three-dimensional reconstructed images of the orbit are useful adjuncts in planning the surgical repair of complex fractures.

When evaluating a patient with an orbital injury, the radiologist should do the following:[15]

  • Evaluate the bony orbit for fractures, note any herniations of orbital contents, and pay particular attention to the orbital apex.

  • Evaluate the anterior chamber.

  • Evaluate the position of the lens (the lens may be displaced, and may be either completely or partially dislocated).

  • Evaluate the posterior segment of the globe, look for bleeds or abnormal fluid collections, and evaluate for radiopaque or radiolucent foreign bodies.

  • Evaluate the ophthalmic veins and optic nerve complex, especially the orbital apex.

A study by Bruneau et al indicated that CT scan–based evaluation of pure orbital floor blowout fractures can be used to predict ophthalmologic outcomes, with, for example, the area ratio of the fractured orbital floor and the maximum height of periorbital tissue herniation being predictive for enophthalmos and diplopia, respectively.[16]

As previously mentioned, a study by Vicinanzo et al suggested that in cases of orbital floor fracture, clinical findings, rather than CT scan assessments, should be used to determine the need for surgery. The study, which involved 23 patients, showed only moderate agreement between neuroradiologists in their evaluation of the size of floor fractures, even though fracture size is considered to be an indication as to whether or not surgery should be performed. The magnitude of agreement between the neuroradiologists regarding anterior to posterior length of the fracture, as assessed using the intraclass correlation coefficient, was 0.66, while for transverse width, the magnitude of agreement was 0.44.[14]

Magnetic resonance imaging

See the list below:

  • The poor resolution of bone on magnetic resonance imaging (MRI) significantly limits its role in orbital trauma.

  • However, in cases of orbital-apex trauma and traumatic optic neuropathy, MRI may be useful for defining the anatomy of the apex and for depicting hemorrhage in the sheath of the optic nerve.

  • Before this is undertaken, one must make sure that no metallic foreign bodies are in the orbit.

Plain radiography

See the list below:

  • Prior to the use of CT scans, a facial radiographic series was used to assess facial fractures.

  • Waters, Caldwell, submental, anteroposterior (AP), and lateral views depict the facial skeleton.

  • Radiographic evidence of orbital fractures includes fragmentation and misalignment of bone contours, a fluid level in the maxillary sinus, air in the orbit, and prolapse of orbital soft tissue into the maxillary sinus.

  • Submental vertex images provide an excellent view of the zygomatic arch.

Angiography

This study may be considered in patients with orbital apex fractures and in those patients with clinical features consistent with a carotid-cavernous fistula or carotid artery injury.

Other Tests

See the list below:

  • Assessment of field of binocular single vision

  • Forced duction test

 

Treatment

Medical Therapy

Patients should avoid blowing their nose and performing Valsalva maneuvers to limit intraorbital emphysema.

Visual loss with acute orbital emphysema has been reported.

Oral antibiotic therapy may be considered. Fractures that involve the medial wall and floor may be considered open fractures, as laceration of the sinus mucosa is inevitable.

Analgesia and antiemetics may be required. The use of oral steroids (prednisone 1 mg/kg/d) has been advocated to decrease soft-tissue edema.

The management of traumatic hyphema responds well to outpatient care and topical aminocaproic acid.

In a study of 58 patients with orbital blow-out fractures, 46 of whom underwent nonsurgical treatment, Jansen et al found evidence that such injuries can often be handled through conservative management with repeated orthoptic evaluation.  In the report, 45 of the 58 patients had, by completion of 3-, 6-, and/or 12-month follow-up, recovered. This included a large percentage of patients with orbital floor and/or medial wall fracture who recovered spontaneously and had neither lasting diplopia nor cosmetically disfiguring enophthalmos.[17]

Surgical Therapy

Surgical repair of orbital and maxillofacial fractures typically involves several steps, as follows:

  1. Exposure with degloving the facial skeleton

  2. Anatomic reduction

  3. Rigid fixation with replacement of lost or comminuted bone

  4. Soft-tissue resuspension

  5. Closure

Surgical management of orbital floor and medial-wall fractures is described below.

Management of other associated injuries to globe are described in other Medscape Reference articles; however, management of traumatic cataracts has been enhanced with new iris-fixated lens implants.[18]

A retrospective study by Scawn et al indicated that surgery for orbital blow-out fractures can be successful even when performed more than 6 weeks after injury in late-presenting patients. The study involved 20 patients, including 10 with isolated floor fractures and 10 with combined floor and medial wall fractures, with surgery performed a mean 19 months after injury. Successful resolution or reduction of enophthalmos, hypoglobus, and diplopia was reported.[19]

However, a literature review by Damgaard et al indicated that in patients with isolated blow-out fractures, the chance of persistent postoperative diplopia is greater (odds ratio = 3.3) when surgery takes place more than 14 days after the trauma.[20]

Preoperative Details

Orbital 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 Details

Prior 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.[1, 2]

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 tissues are 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.

Suzuki et al described a modified transnasal endoscopic approach designed to address problems with repairing anterior and lateral orbital floor fractures that have been encountered with previous transnasal endoscopic techniques. The modified approach involves going through the anterior space to the nasolacrimal duct, with surgeons removing the medial maxillary bone, shifting the lateral wall of the nose medially to provide greater access to the maxillary sinus, carefully removing bone fragments entrapping the orbital content, and correcting the periorbita (orbital periosteum).[21]

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:

  • Autogenous materials (eg, bone [cortical and cancellous], cartilage, fascia)[22]

  • Alloplastic materials

    • Nonabsorbable titanium,[23] silicon, porous polyethylene, and Teflon

    • Absorbable - Polydioxanone, polylactide, and polyglactin

  • Allogenic dura

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.

A retrospective study by Seen et al reported that in the treatment of patients with isolated orbital floor blow-out fractures, the safety and efficacy of bioresorbable implants are comparable to those of permanent implants. The two types of implants demonstrated similar results for all fracture sizes with regard to diplopia, enophthalmos, and ocular motility restriction.[24]

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.

Posttraumatic enophthalmos is a relatively common problem following orbitozygomatic fractures. Bony-volume expansion and soft-tissue atrophy are considered the main etiological causes of this condition. Making fine adjustments to soft-tissue volume and orbital size during the same actual surgery is extremely difficult, if not impossible, which constitutes the biggest challenge in the treatment of enophthalmos. A novel protocol of one-stage treatment for correction of disfiguring enophthalmos has been described by Lee (2008), in which (in addition to the standard fracture-reduction methods) the author uses an autologous, 3.0-5.5 mL diced-cartilage graft to augment the orbital-tissue volume.

Postoperative Details

Applying 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-up

The 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.

Complications

Complications 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:

  • Globe and optic nerve injury caused by direct trauma, excessive retraction, or vascular compromise (eg, central retinal artery occlusion)

  • Injury to the infraorbital nerve

  • Inadequate reduction of prolapsed tissue

  • Orbital hemorrhage

Postoperative complications include, but are not limited to, the following:

  • Blindness

  • Persistent diplopia

  • Globe malpositioning, particularly enophthalmos or hypoglobus

  • Infection that presents as orbital cellulitis

  • Infraorbital nerve dysfunction in an orbital floor repair

  • Lid malpositioning, especially lower-lid retraction or entropion

  • Implant infection, migration, or extrusion

  • Epistaxis or cerebrospinal fluid (CSF) leakage in medial wall repairs

  • Sinus disease, especially sinusitis

A study by Jacobs et al indicated that in patients with multiple facial fractures undergoing orbital floor repair, a 6.45% chance exists that a blinding surgical complication will occur.[25]  

Outcome and Prognosis

The 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. Although 14 days after trauma is commonly cited as a timeline target for orbital blow-out repair, Dal Canto and Linberg (2008) believe that effective fracture repair can be performed up to 29 days after trauma.[26] Patients with improving diplopia who are at low risk for enophthalmos can be observed for 3-4 weeks prior to surgery. This may help prevent unnecessary surgery in some cases.

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.

Remember that endophthalmitis after ocular trauma carries a significantly worse prognosis, which may be reduced by early referral and intervention.

Future and Controversies

Internal 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.

 

Questions & Answers

Overview

What are orbital fractures?

What are the types of orbital fractures?

How are orbital fractures diagnosed?

Which medications are used in the treatment of orbital fractures?

What is the role of surgery in the treatment of orbital fractures?

What are the goals of treatment for orbital fractures?

What is the prevalence of orbital fractures?

What causes orbital fractures?

What is the pathophysiology of orbital fractures?

What is the role of zygomaticomaxillary complex fracture (ZMC) structures in the pathophysiology of orbital fractures?

What is the role of the zygomatic buttresses in the pathophysiology of orbital fractures?

Which clinical history findings are characteristic of orbital fractures?

Which physical findings are characteristic of medial-wall orbital fractures?

How is white-eyed blow-out fracture (WEBOF) diagnosed in the emergency department (ED)?

Which orbital fractures are associated with intracranial injury?

Which clinical history and physical findings are characteristic of orbital apex fractures?

What are the signs and symptoms of cranial nerve injury in orbital fractures?

Which physical findings are characteristic of lateral-wall orbital fractures?

Which physical findings are characteristic of NOE orbital fractures?

How are orbital fractures treated?

What are the indications for surgical intervention to treat orbital fractures?

What is the timing for surgical intervention to treat orbital fractures?

What is the anatomy of the orbit relevant to orbital fractures?

What is the anatomy of the infraorbital nerve relevant to orbital fractures?

What is the anatomy of the superior orbital rim relevant to orbital fracture?

What are contraindications to surgical intervention for orbital fractures?

Workup

What is the role of lab tests in the workup of orbital fractures?

What is the role of CT scanning in the diagnosis of orbital fractures?

What is the role of MRI in the diagnosis of orbital fractures?

What is the role of radiography in the diagnosis of orbital fractures?

What is the role of angiography in the diagnosis of orbital fractures?

Which ocular tests are performed in the diagnosis of orbital fractures?

Treatment

What is the role of medical therapy in the treatment of orbital fracture?

What steps in the surgical repair of orbital and maxillofacial fractures?

What is the role of surgery in the treatment of orbital fractures?

What is included in preoperative care for orbital fractures?

What is the role of forced duction testing in the preoperative evaluation of orbital fractures?

Which approaches are used for the surgical repair of orbital floor fractures?

What is a transcutaneous approach to surgical repair of orbital fractures?

How is dissection performed in the surgical repair of orbital fractures?

What is the transmaxillary endoscopic approach to the surgical repair of orbital fractures?

What is the modified transnasal endoscopic approach to the surgical repair of orbital fractures?

How it the surgical repair of trapdoor orbital fractures performed?

How is the surgical repair of blow-out orbital fractures performed?

What is the role of implants in the treatment of orbital fractures?

What is included in postoperative care following surgery for orbital fractures?

What is included in the long-term follow-up following treatment of orbital fractures?

What are the possible intraoperative complications of orbital fracture surgery?

What are the possible postoperative complications of orbital fracture surgery?

What is the prognosis of orbital fractures?

What treatments for orbital fractures are being investigated?