Orbital Fractures

Updated: Jan 31, 2017
  • Author: Neeraj N Mathur, MBBS, MS, DNB(ENT), MNAMS, FAMS; Chief Editor: Arlen D Meyers, MD, MBA  more...
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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

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.



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.




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.



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.



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.) [4]

Because of progressive calcification, the bones of adults lack the elasticity found in those of children. [5] 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). [6]

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.



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. [7]

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. [8] 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. [9]

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 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. [10] 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: [11]

  • 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.



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. [12] )
  • 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.



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.