Journal of Clinical Ophthalmology and Research

: 2018  |  Volume : 6  |  Issue : 2  |  Page : 77--82

Evaluation and management of orbital trauma

Kirti Nath Jha, AR Rajalakshmi 
 Department of Ophthalmology, Mahatma Gandhi Medical College and Research Institute (Sri Balaji Vidyapeeth), Puducherry, India

Correspondence Address:
Kirti Nath Jha
Medical College and Research Institute, Pondy-Cuddalore Main Road, Pillaiyarkuppam, Puducherry - 607 402


Orbital injuries occur in a variety of settings, road traffic accidents (RTA) being the commonest. Injuries vary in severity and have potential for visual impairment and disfigurement. Diligent history-taking and careful examination is desirable in all cases. Circumstances of injury and subtle external wounds indicate orbital foreign body. CT scan of the orbits axial and coronal views and thin cuts around the apex of the orbit reveal the nature of injury and help plan management. Traumatic optic neuropathy (TON) and injury to the globe threaten vision. Management of traumatic optic neuropathy is controversial. Systemic steroid is considered harmful. Decompression of the optic nerve offers no benefit. Blow-out fracture of the orbit associated with diplopia and soft tissue entrapment may require surgery and interdisciplinary approach. Orbital compartment syndrome needs immediate reduction of orbital pressure. Type of the intraorbital foreign body, its mechanical effect, and presence of infection guide their management. This article presents an overview of evaluation and management of orbital injuries from the point of view of comprehensive ophthalmologists.

How to cite this article:
Jha KN, Rajalakshmi A R. Evaluation and management of orbital trauma.J Clin Ophthalmol Res 2018;6:77-82

How to cite this URL:
Jha KN, Rajalakshmi A R. Evaluation and management of orbital trauma. J Clin Ophthalmol Res [serial online] 2018 [cited 2021 Nov 30 ];6:77-82
Available from:

Full Text

Orbital injuries are common. Most often, they result from road traffic accidents.[1],[2] With India witnessing an epidemic of road traffic accidents, ophthalmologists are even more likely to come across orbital trauma. Orbital trauma may involve the eyeball, the orbital soft tissues or bones, or both. It is estimated that about two-thirds of patients with maxillofacial injuries suffer intraocular injuries.[3] Many of these injuries have, therefore, sight-threatening potential due the injuries to the eyeball, traumatic optic neuropathy (TON), orbital hematoma and orbital compartment syndrome (OCS), and orbital foreign bodies. Some of these injuries may result in facial disfigurement.[4] Therefore, a thorough evaluation and appropriate management are essential to save sight and prevent disfigurement.

This article aims to discuss the evaluation and management of orbital trauma from the perspective of a comprehensive ophthalmologist. Discussion includes the management of TON, orbital fractures, OCS, and orbital foreign bodies. This article does not discuss injuries to the eyelid, lacrimal apparatus, and eyeball.

 History and Examination

History aims to find the nature of object impacting the orbit, the mechanism of injury (blunt or penetrating), and the direction of impact. Knowledge of mechanism of injury indicates the likely injury and helps plan management. Small- and high-velocity objects may result in penetrating injury and intraorbital foreign body. Larger and denser objects transfer kinetic energy to bones and may result in fractures.[5] Direction of impact is another factor affecting orbital injury. Direct impact on supraorbital margin may impact the optic canal and intracanalicular optic nerve.[6] History of decreased vision, double vision, watering from the eye, and watering from the nose should be specifically sought. Decreased vision indicates injury to the globe or the optic nerve. Diplopia results from fracture of orbital floor with muscle or soft-tissue entrapment, injury to the extraocular muscle, injury to the nerves supplying extraocular muscles, or orbital hematoma. Acute proptosis results from edema, hematoma, orbital emphysema, and fractures and displacement of the orbital bones. Trauma to infraorbital nerve results in infraorbital anesthesia. Acute epiphora in a setting of injury to the medial canthus, and in naso-orbital bony injuries, indicate injury to the lacrimal drainage system. Rhinorrhea may be due to cerebrospinal fluid (CSF) leak.

Every case of orbital trauma deserves careful examination. Those with facial fractures need comprehensive ophthalmologic evaluation.[7] Understanding of orbital anatomy and its relationship with the nose, cranial cavity and brain, and maxilla is essential.[5] Record of visual acuity, pupillary reactions, and color vision helps assess optic nerve function. Patients with significant eye injuries may present with grossly normal eyes and good visual acuity.[8] Examination of ocular motility reveals injury to the extraocular muscles and nerves and entrapment of extraocular muscles. The eye should be examined with minimal manipulation. Points of interest during inspection include point of impact, obvious bony deformity, flattening of malar prominence, and displacement of canthi, globe ptosis, proptosis, points of penetration, epiphora, and rhinorrhea. Minor external wounds may indicate site of penetration of foreign bodies. Fracture displacement of the zygoma may alter the lateral orbital rim, and lateral canthal anatomy; it renders exophthalmometry prone to error. Careful palpation of orbital rim shall reveal step-off deformity, and crepitus indicating emphysema. Rule out tight orbit and high intraocular pressure (IOP). Detailed examination of the anterior and posterior segments reveals injury to the lens, uvea, vitreous, and retina and may also reveal retained intraocular foreign body. Hyphema indicates injury to the globe. In a setting of tight orbit, look in the fundus, specifically for the presence of retinal arterial pulsation that indicates catastrophic rise of IOP.


Computed tomography (CT) of the orbit is the investigation of choice. Both axial and coronal scans should be asked. Thin-section CT scans of the orbital apex and anterior clinoid process demonstrate fractures through or adjacent to the optic canal in many cases.[9] Three-dimensional (3D) reconstruction of the digitized CT images may facilitate assessment of complex orbital fractures.[5] In the absence of ferromagnetic metallic foreign bodies, magnetic resonance imaging (MRI) may be ordered to demonstrate subtle intracanalicular hemorrhage and intracanalicular optic nerve.[5] MRI scan is the imaging of choice if wooden orbital foreign bodies are suspected.[9]

 Traumatic Optic Neuropathy

TON is an acute injury of the optic nerve with disruption of visual function.[10] TON is estimated to occur in 4% of midfacial, supraorbital, or frontal sinus injuries.[3] Injury to the optic nerve may be direct/indirect. Pressure on the optic nerve by a bony fragment and avulsion of the optic nerve are examples of direct injury. Optic nerve injury following orbital hemorrhage and OCS falls into a separate category; in OCS, elevated orbital pressure compromises the circulation to the optic nerve.[11] Rapid deceleration, the third mechanism of TON, results from shearing of blood vessels, edema, and contusion necrosis of the relatively fixed intracanalicular portion of the nerve.[12] Decreased vision in the absence of injury to the globe indicates TON. Onset of visual loss due to trauma may be slightly delayed due to progressive compressive etiology, if intracanalicular optic nerve develops hemorrhage and edema, commonly observed with injuries involving frontal region referred above. Relative afferent pupillary defect suggests optic neuropathy. Initial fundus picture depends on the site of injury to the nerve. Injury to the intraorbital optic nerve may present with fundus picture resulting from central retinal artery occlusion, central retinal venous occlusion, vitreous/subhyaloid, or retinal hemorrhage radiating from the optic nerve head.[5] Avulsions of the optic nerve from the globe produce a distinct picture with a partial ring of hemorrhage at the optic nerve head.[13] Optic nerve may appear normal in case of more posterior injury.

Orbital CT scan allows assessment of the integrity of the optic nerve, presence of an optic nerve sheath hematoma, orbital hemorrhage, and fracture. Blood in the ethmoidal sinus may indicate fracture with intracanalicular extension.[5]

The management of TON is controversial.[5],[9] Spontaneous resolutions are known to occur. Observation alone, high-dose corticosteroids, and surgical decompression of the optic canal are all considered reasonable options.[9] Given the evidence of harmful effects and lack of clinical efficacy, some authorities believe that corticosteroids should not be used for TON.[13] Therefore, therapy remains a matter of clinical judgment of the treating surgeon in the light of informed consent and clinical setting of the patient.

 Surgical Decompression of Optic Canal

There is no clear indication of surgical decompression of optic canal.[13] Anecdotal reports suggest the benefit of optic nerve sheath decompression in cases of progressive visual loss in intrasheath hemorrhage.[14],[15] However, decompression of the optic nerve provides no additional benefit over observation alone while subjecting patients to the risks associated with surgery.[9],[13]

 Orbital Blowout Fracture

Orbital blowout fractures refer to the fractures of orbital floor that do not involve the orbital rim. These fractures are believed to result from compressing force directly impacting the inferior orbital rim.[9] Diagnosis of orbital blowout fractures is suggested by history of blunt injury with a large object. Enophthalmos and diplopia are the major sequelae of blowout fractures. Signs include ecchymosis, eyelid edema, diplopia with limitation of the movement of the eyeball in vertical gaze, enophthalmos, globe ptosis, hypoesthesia in the distribution of infraorbital nerve, and subcutaneous emphysema [Figure 1]. Restriction of passive movement of the eye on forced duction test indicates muscle entrapment. Positive forced duction test may result from edema and hemorrhage also. White-eyed blowout fracture with muscle entrapment and diplopia may occur in young adults. Visual loss in orbital floor fractures may be due to injury to globe, injury to the optic nerve, or OCS. CT scan of the orbits, axial and coronal views, is the investigation of choice. CT scan shows the size and location of the fracture and its relationship with the soft tissues including muscle entrapment, usually the inferior rectus. Plain radiographs are no longer used for diagnosis.{Figure 1}

 Treatment of Blowout Fracture

The majority of blowout or other orbital floor fractures do not require surgical intervention.[9] Majority of them are observed for 5–10 days for edema and hemorrhage to subside. Oral steroids (1 mg/kg body weight for 7 days) reduce edema and may reduce diplopia from edema and from inferior rectus contracture. Indications of surgery are controversial. Interventions fall into immediate surgery, surgery within 2 weeks of injury, and observation. Followings are useful guidelines to determine if surgery is indicated:[16]

Diplopia with limitation of upgaze and/or downgaze within 30° of the primary position with a positive forced duction test 7–10 days after injury and with radiologic confirmation of a fracture of the orbital floorEnophthalmos that exceeds 2 mm and is cosmetically unacceptable to the patientLarge fractures involving at least half of the orbital floor, particularly when associated with large medial wall fractures determined by CT.

When surgery is indicated, most prefer it within 2 weeks of trauma. Trapdoor fracture in pediatric patients with nonresolving oculocardiac reflex on the movement of the eyes requires immediate surgical repair. Surgery aims to release the trapped muscle and soft tissue, repair the fracture, and restore cosmetic appearance. The approach to the fracture site depends on the type of injury, surgeon experience, and available equipment. Subciliary, subtarsal, and transconjunctival incisions are the most commonly utilized. Medial wall fractures require transcutaneous (Lynch incision), transconjunctival inferior fornix, transcaruncular, and endoscopic transethmoidal approach. Repair of the orbital floor may require miniplating or microplating systems or implants (allogenic or autogenous). Each of these has their merits and demerits.[17]

Complications of blowout fracture surgery include decreased visual acuity or blindness, diplopia, undercorrection or overcorrection of enophthalmos, lower eyelid retraction, infraorbital nerve hypoesthesia, infection, extrusion of the implant, lymphedema, and damage to the lacrimal drainage system.[9]

 Orbital Roof Fracture

Orbital roof fractures mostly result from blunt trauma. They may cause injury to the brain, sinuses, and globe. Injury to the orbital roof with or without fracture has potential to cause injury to the optic nerve due to direct transmission of force to its intracanalicular portion.[6] Majority of roof fractures do not require repair. Indications for surgery are often neurosurgical. Ophthalmic indications of surgery include vertical diplopia, impingement of bone fragment on orbital structures, lagophthalmos, and foreign body removal.[9]

 Naso-Orbital Fractures/medial Wall Orbital Fractures

Naso-orbital-ethmoidal fractures involve the nasal bones, ethmoidal sinuses, and medial orbital wall. They may present with collapse of the sinuses and flattening and widening of the nasal bridge, telecanthus, enophthalmos, and medial rectus entrapment [5] [Figure 2]. 3D reconstruction of the CT scan reveals the relationship of the bony fragments and helps repair that requires multidisciplinary approach.[18],[19] Significant enophthalmos, entrapment of muscle, and diplopia need repair. Methods of fixation vary widely and are beyond the scope of this article. Treatment involves reduction of nasal fracture and miniplate fixation. Surgery is done through a Lynch incision or transcaruncular approach.[9] Complications include injury to the brain and the eye, orbital hemorrhage, CSF rhinorrhea, displacement of medial canthus, injury to the lacrimal drainage system, and enophthalmos if the fractures are large.{Figure 2}

 Zygomatic Fractures

Zygomatic fractures are called tripod fractures. They cause fractures at three articulation sites: the frontozygomatic suture, the zygomaticotemporal suture, and the zygomaticomaxillary suture.[5] They may involve orbital floor in varying degrees. If the zygoma is not significantly displaced, surgery is not required. However, cosmetic deformity, displacement of the globe, diplopia, and trismus may result. Since zygomatic fractures with displacement of bony fragments result in alteration of lateral canthal anatomy, they also interfere in the assessment of globe ptosis, enophthalmos, and proptosis [Figure 3]. When treatment is indicated, tripod fracture is managed by maxillofacial surgeons by open reduction through temporal skin incision or through sublabial or buccal sulcus incisions.{Figure 3}

 Le Fort Fractures

Le Fort fractures involve the maxilla and must pass through the pterygoid process.[9] They are classified as:

 Le Fort I Fractures

Le Fort Type I fractures are low transverse maxillary fracture above the teeth with no orbital involvement.

 Le Fort II (Pyramidal) Fractures

Le Fort Type II fractures generally have a pyramidal configuration and involve the nasal, lacrimal, and maxillary bones as well as the medial orbital floor.

 Le Fort III (Craniofacial Disjunction)

Le Fort Type III fractures cause craniofacial disjunction in which the entire facial skeleton is completely detached from the base of the skull and suspended only by soft tissues. The orbital floor and medial and lateral orbital walls are involved. The treatment of Le Fort fractures requires the help of maxillofacial surgeons.

 Orbital Hemorrhage

Orbital hemorrhage may be subperiosteal, extraconal, intraconal, or within extraocular muscle. Pain, nausea, diplopia, and decreased vision reflect mass effect of accumulating blood due to severe and progressive hemorrhage within the confines of bony orbit and orbital septum. Small hemorrhages resolve spontaneously. Rarely hemorrhage and emphysema may result in OCS.

OCS refers to acute, uncontrolled pressure rise within the confined orbital space/s due to expanding hemorrhage, edema, or emphysema resulting from trauma or surgery. This is an ophthalmic emergency, which if not recognized and treated immediately, may result in rapid loss of vision. OCS is essentially a clinical diagnosis.[20] Affected eye shows decreased vision, increased IOP, and relative afferent papillary defect. Orbital signs include proptosis, limitation of ocular movements, and tight orbit. Fundus may reveal optic disc edema, retinal venous congestion, and central retinal artery pulsations or occlusion or retinal edema. Lateral canthotomy under local anesthesia immediately relieves tight orbit. Before the procedure, 2% lignocaine with 1:100,000 epinephrine is injected into the lateral canthus area. A straight clamp is positioned in the lateral canthal angle and clamped for 10 s which provides adequate hemostasis. Lateral canthotomy incision performed usually with a Stevens scissors extends horizontally from the lateral canthal angle, beyond the lateral fornix, to the level of the lateral orbital rim. If lateral canthotomy does not relieve tight orbit, a lateral cantholysis is performed by positioning the Stevens scissors perpendicular to the canthotomy incision and releasing the lateral canthal ligament fibers in the lateral aspect of the upper and lower eyelids along their attachments to the orbital rim.[5] In case of no relief within a few minutes, the orbital septum should be divided from its attachment to the orbital rims.[21] Division of orbital septum can be achieved by transconjunctival route or transcutaneous route (transcutaneous transseptal decompression).[20],[21] Transcutaneous transseptal decompression involves division of the orbital septum by a horizontal incision through the skin and preseptal orbicularis oculi [Figure 4]. Care is taken during the procedure to protect the globe by pushing it away from the orbital margin. Lateral canthotomy, cantholysis, and transcutaneous transseptal division of orbital septum can be done in the emergency room. Additional decompression, if needed, can be done under general anesthesia.[5]{Figure 4}

 Orbital Emphysema

Air from the paranasal sinus forced into orbit leads to orbital emphysema. Eyelid emphysema reveals crepitus on palpation. Emphysema of the orbit can lead to proptosis and reduction in ocular motility. The patient should be advised against blowing nose and Valsalva maneuver in such a situation. Treatment is similar to the cases of increased intraorbital pressure. Extreme cases of orbital emphysema should be released by the method described by Hunt et al.[22] A saline-filled syringe with a large bore needle is introduced into the orbit toward air seen on CT scan. Air bubble escapes into the saline-filled syringes as the needle enters the pocket. Escape of air into syringe indicates release of emphysema.

 Intraorbital Foreign Body

Orbital and intraocular foreign bodies are common in war injuries. However, orbital foreign may be encountered in non-war injuries as well. Depending upon the setting of injury, foreign bodies include gun pellets, and fragments of pencil, pen, wood, nail, and glass.[5] These injuries occur most often in young men, during recreation in school-going children, and at the workplace in working-age men.[23] Circumstances of injuries and examination of the periorbital area provide clue in the absence of visible site of entry. In the absence of obvious signs, pain, impairment of vision, limitation of movement, proptosis, fundus findings (retinitis sclopetaria and vitreous hemorrhage), and a discharging sinus indicate intraorbital foreign body [Figure 5]. Plain radiograph, CT scan, and MRI reveal radiopaque intraorbital foreign bodies well. Wooden foreign body may be missed on CT scan and may require MRI.[24] Composition of foreign bodies, their mechanical effect, and presence of infection guide the management decision.[5] As such intraorbital foreign bodies carry risk of infection. Therefore, prophylaxis with a broad-spectrum antibiotic and tetanus toxoid is recommended in all cases.[5] Inert foreign body with smooth edges, such as lead pellets, particularly in posterior orbit may be left in place. Wooden foreign body and foreign body containing vegetable matter should be removed, cultured, and treated with antibiotics to prevent discharging fistula and granulomas.[5]{Figure 5}


Orbital injuries are common. They vary in nature and severity. History, clinical examination, and CT scan of the orbits aid the diagnosis. High index of suspicion of vision-threatening ocular injury is desirable. TON, orbital hemorrhage, and injuries to the globe may result in visual impairment; thus, they need immediate intervention. Orbital fractures may require multidisciplinary approach. Ophthalmologists should be aware of OCS, a rare entity that needs immediate reduction of orbital pressure. Nature of foreign body, its mechanical effect, and presence of infection guide management of intraorbital foreign bodies.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Einy S, Abdel Rahman N, Siman-Tov M, Aizenbud D, Peleg K. Maxillofacial trauma following road accidents and falls. J Craniofac Surg 2016;27:857-61.
2Hogg NJ, Stewart TC, Armstrong JE, Girotti MJ. Epidemiology of maxillofacial injuries at trauma hospitals in Ontario, Canada, between 1992 and 1997. J Trauma 2000;49:425-32.
3Holt JE, Holt GR, Blodgett JM. Ocular injuries sustained during blunt facial trauma. Ophthalmology 1983;90:14-8.
4Pushker N, Bajaj MS, Sharma V, Balasubramanya R. Profile of trauma-related residual periorbital deformities in Indian children. Int Ophthalmol 2004;25:239-42.
5Iwamoto MA, Iliff NT. Management of orbital trauma. In: Tasman W, Jaegar EA, editors. Duane's Ophthalmology. Revised Edition. Philadelphia: Lippincott Williams & Wilkins; 2013. p. 9569-90.
6Anderson RL, Panje WR, Gross CE. Optic nerve blindness following blunt forehead trauma. Ophthalmology 1982;89:445-55.
7Andrews BT, Jackson AS, Nazir N, Hromas A, Sokol JA, Thurston TE, et al. Orbit fractures: Identifying patient factors indicating high risk for ocular and periocular injury. Laryngoscope 2016;126 Suppl 4:S5-11.
8Larian B, Wong B, Crumley RL, Moeinolmolki B, Muranaka E, Keates RH, et al. Facial trauma and ocular/orbital injury. J Craniomaxillofac Trauma 1999;5:15-24.
9Orbital trauma In Basic and Clinical Science Course, Section 7, Orbit, Eyelid and Lacrimal System. San Francisco: American Academy of Ophthalmology 2016-2017: pp 94-101.
10Steinsapir KD, Goldberg RA. Traumatic optic neuropathies. In: Miller NR, Newman NJ, editors. Walsh & Hoyt's Clinical Neuro-Ophthalmology. 6th ed. Philadelphia: Lippincott Williams & Wilkins; 2005. p. 432-48.
11Frenkel RE, Spoor TC. Diagnosis and management of traumatic optic neuropathies. Adv Ophthalmic Plast Reconstr Surg 1987;6:71-90.
12Park JH, Frenkel M, Dobbie JG, Choromokos E. Evulsion of the optic nerve. Am J Ophthalmol 1971;72:969-71.
13Steinsapir KD, Goldberg RA. Traumatic optic neuropathy: An evolving understanding. Am J Ophthalmol 2011;151:928-33.
14Steinsapir KD, Goldberg RA. Traumatic optic neuropathy. Surv Ophthalmol 1994;38:487-518.
15Miller NR. The management of traumatic optic neuropathy. Arch Ophthalmol 1990;108:1086-7.
16Burnstine MA. Clinical recommendations for repair of isolated orbital floor fractures: An evidence-based analysis. Ophthalmology 2002;109:1207-10.
17Boyette JR, Pemberton JD, Bonilla-Velez J. Management of orbital fractures: Challenges and solutions. Clin Ophthalmol 2015;9:2127-37.
18Watamull D, Rohrich RJ. Zygoma fracture fixation: A graduated anatomic approach to management based on recent clinical and biomechanical studies. Probl Plast Reconstr Surg 1991;1:350.
19Mayer MH, Manson PN. Plate and screw fixation in craniomaxillofacial skeletal fractures. Probl Plast Reconstr Surg 1991;1:290.
20Lima V, Burt B, Leibovitch I, Prabhakaran V, Goldberg RA, Selva D, et al. Orbital compartment syndrome: The ophthalmic surgical emergency. Surv Ophthalmol 2009;54:441-9.
21Zimmerer R, Schattmann K, Essig H, Jehn P, Metzger M, Kokemüller H, et al. Efficacy of transcutaneous transseptal orbital decompression in treating acute retrobulbar hemorrhage and a literature review. Craniomaxillofac Trauma Reconstr 2014;7:17-26.
22Hunts JH, Patrinely JR, Holds JB, Anderson RL. Orbital emphysema. Staging and acute management. Ophthalmology 1994;101:960-6.
23Miller CF, Brodkey JS, Colombi BJ. The danger of intracranial wood. Surg Neurol 1977;7:95-103.
24McGuckin JF Jr, Akhtar N, Ho VT, Smergel EM, Kubacki EJ, Villafana T, et al. CT and MR evaluation of a wooden foreign body in an in vitro model of the orbit. Am J Neuroradiol 1996;17:129-33.