29 Orbit

Any related systemic or progressive disease processes should be addressed. Approximate the normal orbital bone positions before soft tissue volume loss is addressed.

The repair of orbital fractures should be as follows:

●Maintain the convexity of the posterior, medial orbital floor;

●Be certain to stabilize floor implants posteriorly on intact floor ledge;

●Release any major adhesions or scar bands to allow mobilization of soft tissues. In late post-traumatic cases, sharp rather than blunt dissection often is required;

●If using bone grafts, allow for 15% to 30% reabsorption;

●Overcorrect to obtain 1 to 2 mm of exophthalmos intraoperatively;

Soparkar CNS, Patrinely JR, Cuaycong MJ, et al: The silent sinus syndrome: a cause of spontaneous enophthalmos. Ophthalmology 101:772– 778, 1994.

321 EXTERNAL ORBITAL FRACTURES

802.8

Richard D. Lisman, MD, FACS

New York, New York

Jennifer Scruggs, MD

New York, New York

An external fracture of the orbit results in direct disjunction of

The replacement of lost orbital soft tissue volume should be as follows:

●Perform ‘forward traction’ test on the globe to determine the amount of correction possible;

●Augment from the orbital walls inward with bone or synthetic materials;

●Position augmentation material beneath and behind the equator of the globe to achieve forward and upward displacement, as needed.

COMPLICATIONS

●Blindness from optic neuropathy-ischemic or compressive; either may be related to malposition of orbital implant or implants or to orbital hemorrhage.

●Orbital cellulites.

●Exacerbation of any intraocular injuries.

●Ocular motility disturbance from unreduced fractures, implant position, iatrogenic myopathy, or neuropathy.

●Damage to the infraorbital nerve.

●Implant infection, inflammatory reaction, migration, and hematic cyst formation.

●Grafted bone reabsorption.

●In cases of autologous bone or cartilage grafts, donor site complications.

●Lower eyelid retraction and immobilization.

●Facial scars (if transconjunctival approach is not used).

●Undercorrection.

●Hyperglobus due to augmentation directly beneath the globe rather than behind the equator

involvement. These injuries may occur in isolation or in conjunction with multisystem trauma.

ETIOLOGY/INCIDENCE

Facial bones break in predictable patterns. The superior and lateral orbital rims are the strongest rims of the orbit, and fractures are rare except at suture lines. In contrast, the medial and inferior orbital rims are weaker and more commonly sustain comminuted fractures.

Fractures of the lateral orbital wall usually occur through bony suture lines; the zygomaticofrontal suture superolaterally and the zygomatiomaxillary suture inferonasally are the weakest portions of the orbital rim. A fracture in these regions may result in a ‘tripod’ fracture of the zygoma (malar eminence), with the third foot of the tripod at the zygomaticotemporal suture of the zygomatic arch. Orbital floor fractures are invariably a part of this fracture complex.

Naso-orbital ethmoid fractures involve the medial wall of the orbit and often its associated lacrimal system through direct laceration or associated bony injury. These fractures may be associated with craniofacial separation (Le Fort II or III) fractures of the maxilla.

The superior orbital rim is thick and fractures are uncommon. They are usually seen in association with severe head trauma and cerebral injury.

DIAGNOSIS

Clinical signs and symptoms

glion or parasympathetic in the inferior division of cranial nerve III.

REFERENCES

Baujat B, Derbez R, Rossarie R, et al: Silent sinus syndrome: a mechanical theory. Orbit 25:145–148, 2006.

Cline RA, Rootman J: Enophthalmos: a clinical review. Ophthalmology 91:229–237, 1991.

Davidson JK, Soparkar CN, Williams JB, et al: Negative sinus pressure and normal predisease imaging in silent sinus syndrome. Arch Ophthalmol 117:1653–1654, 1999.

Manson PN, Clifford CM, Su OT, et al: Mechanisms of global support and posttraumatic enophthalmos: I. The anatomy of the ligament sling and

mity as well as palpation for rim discontinuity.

●Tripod fractures of the zygoma:

●Flattened malar eminence secondary to posterior displacement of the zygoma;

●Palpable and painful step-offs at the zygomaticofrontal suture (lateral orbital rim) and zygomaticomaxillary suture (inferior orbital rim);

●Lateral canthal tendon displacement and globe ptosis when the zygoma is displaced inferiorly and posteriorly;

●Trismus, or pain and difficulty opening the mouth from irritation and contusion of the adjacent temporalis muscle or impingement of the coronoid process by displaced bone spicules;

●Hypesthesia of the infraorbital nerve with orbital floor involvement.

●Naso-orbital ethmoid fractures:

●Flattening of the nasal bridge and possibly the forehead;

●Telecanthus and inferior displacement of the medial canthal tendon. The ethmoid sinuses are crushed and the nasal bones and frontal process of the maxilla splayed laterally;

incisions to expose the bone fragments, manipulation to place them in proper anatomic position, and fixation, often with titanium microplates, to stabilize the bone.

The surgical management of a tripod fracture of the zygoma varies according to the severity of bone displacement. A depressed fracture with smooth edges may be approached through a Gillies incision posterior to the hairline at the temple. A Bristow elevator is placed between the temporalis muscle and temporalis fascia and is used to lift the zygoma into position

medial component);

●Lacrimal damage (canaliculi, lacrimal sac, or nasolacrimal duct) with tearing and/or dacryocystitis.

●Superior orbital rim fractures:

●Neurologic manifestations with concurrent head trauma and cerebral injury;

●Traumatic optic neuropathy: shearing injury as the force of impact at the superior orbital rim is transmitted along the orbital roof to the optic canal.

Laboratory findings

●Computed tomography:

●Imaging with computed tomography (CT) is the gold standard to confirm the diagnosis, delineate the extent of injury, and devise a treatment plan for external orbital fractures. Plain films are inadequate. Axial and coronal CT projections should be obtained, using fine cuts (preferably 1 mm) through the orbits. Newer helical CT scanners quickly acquire these projections with no need to reposition the patient. Three-dimensional CT reconstruction, which shows dramatic presentation of the spatial relationships of the bone fragments, may offer additional benefit in complex external orbital fractures.

●Ultrasonography:

●It has been suggested that ultrasound may play a role in visualizing fractures of the zygomatic arch and anterior wall of the frontal sinus. While ultrasound is insufficient as a diagnostic study, it has potential value intraoperatively to evaluate closed reduction of fractures where direct visualization of alignment is not possible.

approach).

A displaced or comminuted fracture requires direct visualization with rigid internal fixation. Exposure of the inferior orbital rim is gained through a transcutaneous or transconjunctival lower eyelid incision with a lateral canthotomy; the transconjunctival approach is preferred and decreases the risk of lower eyelid retraction. The zygomaticomaxillary buttress is exposed through a gingivobuccal sulcus incision. A coronal approach may be necessary to visualize and plate a severely comminuted fracture of the zygomatic arch. Extremely comminuted or absent bone may be replaced with a synthetic structural device or bone graft.

Repair of naso-orbital ethmoid fractures is complex and often requires a combined coronal, transconjunctival, and oral approach in order to reconstruct the nose, lacrimal apparatus, medial canthal tendon, and frontal sinus. Proper medial canthal tendon attachment is to the posterior lacrimal crest; transnasal wiring or miniplate fixation may be used. Posttraumatic dacryostenosis is common, especially with delayed fracture repair or bone loss in the lacrimal region. Subsequent dacryocystorhinostomy is indicated for persistent tearing or dacryocystitis.

COMPLICATIONS

●Ocular: paralytic or restrictive strabismus, enophthalmos.

●Eyelids: ptosis, lid retraction, lateral canthal displacement, telecanthus, ectropion, entropion.

●Lacrimal system: obstruction, tearing, dacryocystitis.

●Surgical: hemorrhage, infection, implant extrusion.

TREATMENT

Systemic

A complete history and physical exam are essential to evaluate for other concurrent injures. Intracranial injuries take precedence over the management of orbital rim fractures. In addition, a full ophthalmologic examination must exclude penetrating ocular injury prior to evaluation or repair of orbital fractures.

Observation and conservative management are often preferred for up to 2 weeks before surgical intervention to allow associated hemorrhage and swelling to subside. Broad-spec- trum antibiotics are commonly prescribed as communication invariably exists between the orbit and nasal cavity or sinuses. Corticosteroids may be useful to decrease edema. Minimally displaced tripod fractures of the zygoma may result in minimal or no deformity or functional disability and do not require intervention.

Surgical

Surgery is indicated when bone displacement causes cosmetic or functional defects. The surgical approach typically involves

COMMENTS

External orbital fractures occur in predictable patterns with an associated constellation of signs and symptoms. CT scanning is essential for diagnosis and surgical planning. Treatment may initially involve observation; surgery is warranted for cosmetic or functional deformities. Surgical repair may combine multiple incisions to gain access to bony fragments from different directions, with subsequent reduction and fixation of the fractures.

REFERENCES

Becelli R, Renzi G, Mannino G, et al: Posttraumatic obstruction of lacrimal pathways: a retrospective analysis of 58 consecutive naso-orbitoeth- moid fractures. J Craniofac Surg 15:29–33, 2004.

Bedrossian EH, Della Rocca RC, Brazzo BG: Management of zygomaticomaxillary (tripod) fractures. In: Nesi F, Lisman R, Levine M, eds: Smith’s ophthalmic plastic reconstructive surgery. St Louis, V Mosby, 1998.

Nerad, JA: Eyelid and orbital trauma. In: Nerad JA, ed: Krachmer JH (series ed.): Oculoplastic surgery: the requisites in ophthalmology. St Louis, Mosby, 2001:312–347.

Weseley R: Current techniques for the repair of complex orbital fractures: miniplate fixation and cranial bone grafts. Ophthalmology 99:1766, 1992.

Zingg M: Classification and treatment of zygomatic fractures: a review of 1,025 cases. J Oral Maxillofac Surg 50:778, 1992.

322 INTERNAL ORBITAL FRACTURES

802.8

Richard D. Lisman, MD, FACS

New York, New York

Jennifer Scruggs, MD

New York, New York

ETIOLOGY/INCIDENCE

Internal orbital fractures, commonly known as blowout fractures, involve the walls of the orbit, leaving the bony rim intact. The orbital floor is most commonly affected, followed by the medial wall; the orbital roof is rarely fractured in isolation, and the lateral wall of the orbit is fractured with involvement of the orbital rim (see External orbital fractures, discussion of tripod fracture of the zygoma).

Theories on the mechanism of injury of pure blowout fractures are twofold: the buckling theory and the hydraulic theory. The buckling theory describes direct force on the relatively thick orbital rim with transmission of that force to the thinboned walls of the orbit. The hydraulic theory states that a blow by an object of greater diameter than the orbital entrance leads to an increase in intraorbital pressure, resulting in a fracture at the weakest portion of the orbit. Thin bones of the orbital floor (typically medial to the infraorbital canal) or medial wall are ‘blown out’ and orbital contents pushed into the maxillary or ethmoid sinuses.

entrapment is rare in isolated medial wall fractures, but transient horizontal diplopia may occur due to contusion of the medial rectus muscle.

A characteristic constellation of findings can be found in children with orbital floor fractures with entrapped tissue and minimally displaced bone fragments, the so-called ‘trapdoor’ fracture. These children may have nausea and vomiting or bradycardia (oculocardiac reflex), which are predictive of muscle entrapment. Aside from marked motility disturbance, these patients may show few additional signs of orbital trauma; thus the term ‘white-eyed’ blowout fracture has been used. These patients need urgent surgical repair.

Laboratory findings

Computed tomography (CT) scans of the orbit are used to confirm the diagnosis and delineate the area of the fracture. Coronal and axial views of the orbit should be obtained, using fine cuts (preferably 1 mm) through the orbits. Newer helical CT scanners quickly acquire these projections with no need to reposition the patient. Herniation of orbital tissue is thus visualized, and the position and appearance of the extraocular muscles can be noted. Occasionally, a trapdoor fracture of the orbital floor will clearly delineate an entrapped inferior rectus muscle below the floor. Orbital emphysema is frequently evident with fractures of the medial orbital wall.

TREATMENT

A complete history and physical exam are essential to evaluate for concurrent injuries. A full ophthalmologic exam must exclude penetrating ocular injury prior to repair of orbital fractures.

Medical

●Broad-spectrum antibiotics are commonly prescribed, as communication invariably exists between the orbit and nasal or sinus cavities.

DIAGNOSIS

Clinical signs and symptoms

Patients with orbital floor fractures may present acutely with proptosis from swelling and/or hemorrhage. Later, enophthalmos may ensue from orbital expansion associated with larger medial wall and floor fractures. Enophthalmos may also result from incarceration of orbital tissues into the maxillary antrum with resultant cicatrization. Extreme herniation of tissue may result in hypoglobus.

Diplopia is the most common complaint of patients with blowout fractures. Restrictive strabismus from entrapped orbital tissue is characteristic of smaller orbital floor fractures. Diplopia most commonly involves the vertical positions of gaze; decreased motility in upgaze is typical. The affected eye may be hypotropic (with anterior fractures) or hypertropic (with posterior fractures).

Hypesthesia in the distribution of the infraorbital nerve is very common and involves the lower eyelid, cheek, and anterior (incisor) teeth on the affected side. Subcutaneous emphysema occurs from the connection to the nasal cavity and/or sinuses.

Medial wall fractures may present acutely with epistaxis and rarely show proptosis if in isolation. Frank extraocular muscle

Ocular

●Serial Hertel exophthalmometry and extraocular muscle measurements (with or without orthoptic documentation) are performed. Enophthalmos may develop or worsen as edema resolves. Conversely, early diplopia may improve with decreasing orbital edema.

●Forced duction testing may be performed to determine if the motility dysfunction is restrictive in nature.

Surgical

Controversy exists in the timing of the management of orbital blowout fractures. Most surgeons agree that early (before 5 days post-injury) intervention is difficult when there is excessive traumatic edema and hemorrhage; conversely, late surgery (after 14 days post-injury) may be hampered by the formation of fibrovascular scar tissue. The exception is children with a blowout fracture and restriction; in these patients scarring progresses rapidly and surgery should be performed as soon as possible.

●A conservative approach is often favored for the first 5 to 14 days after trauma to allow associated hemorrhage and swelling to subside. The patient should avoid the Valsalva maneuver, including sneezing, nose blowing, and strenuous activity (to avoid further orbital tissue incarceration or exacerbation of orbital and subcutaneous emphysema).

Indications for surgical repair of a blowout fracture include:

●Diplopia which is restrictive in etiology and is persistent or progressive, occurring in near primary or reading position;

●Enophthalmos which is cosmetically unacceptable (typically 2 mm or more). Extensive disruption of the orbital floor and/or medial wall is considered a precursor to enophthalmos and therefore a relative indication for repair.

The goal of surgery is to release entrapped orbital tissue from the fracture and to restore normal orbital volume. Multiple surgical approaches are available; some surgeons are now advocating endoscopic methods for orbital fracture repair. However, the favored approach remains as follows:

●The transconjunctival approach with a lateral canthotomy and cantholysis is preferred to expose the orbital floor; the medial wall is also accessible or may be further exposed through a transcaruncular approach. Alternatively, a cutaneous approach via an infraorbital or subciliary incision may be used.

●The preseptal plane is entered down to the inferior orbital rim.

●The periosteum is incised along the orbital rim; periorbita is elevated off the orbital floor until the fracture is reached.

●The hand-over-hand technique is used to free the orbital contents from the maxillary antrum and reduce the fracture.

●The orbital floor is typically restored with an implant (such as porous polyethelene or silastic); the implant should cover the entire floor defect with no tissue prolapsing around the implant.

●Forced duction testing of the inferior rectus muscle is used to confirm release of any entrapment before closure.

Postoperative vision assessment is important in the first several hours after surgery; corticosteroids and antibiotics are usually administered for 1 week.

COMPLICATIONS

Lisman RD, Smith B, Rodgers R: Volkman’s ischemic contractures and blowout fractures. Adv Plastic Reconstr Surg 7:117–131, 1988.

323 ORBITAL INFLAMMATORY

SYNDROMES 377.398

Peter J. Dolman, MD, FRCSC

Vancouver, British Columbia, Canada

Jack Rootman, MD, FRCSC

Vancouver, British Columbia, Canada

This chapter reviews a heterogeneous group of orbital inflammatory syndromes (OIS) defined by clinical and histologic signs of orbital soft tissue inflammation that cannot be attributed to local injury or to infection or to Graves’ orbitopathy.

Traditionally, these syndromes were clumped together under the generic term ‘inflammatory pseudotumor,’ defined loosely as a non-neoplastic orbital inflammatory mass. Included in this broad group were lymphoid proliferations, which now are considered a separate disease spectrum ranging from benign lymphoid hyperplasia to lymphoma, (including Sjögren’s disease of the lacrimal gland).

More recently, the term ‘idiopathic non-specific orbital inflammatory syndromes’ has been used to describe the balance of diseases, but as subsets are identified with their own characteristic clinical and pathologic patterns, this term may become obsolete. As the molecular pathways of inflammatory cascades are progressively understood, further disease subcategories will probably be described.

For now, a simple classification for OIS can be based on the primary histopathology: acute polymorphous, sclerosing, granulomatous, and vasculitic.

ETIOLOGY/INCIDENCE

OIS account for 5–10% of cases of orbital disease. The cause is unknown, but they are likely immune disorders, perhaps initi-

lopia or enophthalmos.

●Surgical: hemorrhage, infection, implant extrusion, diplopia not improving after 6 months postoperatively, eyelid malpositions (ectropion, entropion, ptosis), pseudoptosis, lacrimal obstruction, sinus disease.

Chronic fibrosis of the inferior rectus muscle may be due to ischemic (Volkmann’s) contracture of the muscle resulting from hemorrhage and edema within the muscle sheath thereby leading to a compartment syndrome. In this subgroup of patients, systemic steroids are thought to be beneficial.

REFERENCES

Converse JM, Smith B: Enophthalmos and diplopia in fractures of the orbital floor. Br J Plast Surg 9:265–274, 1957.

Chang EL, Bernardino CR: Update on orbital trauma. Curr Opin Ophthalmol 15:411–415, 2004.

Cruz AAV, Eichenberger GCD: Epidemiology and management of orbital fractures. Curr Opin Ophthalmol 15:416–421, 2004.

Kersten RC: Blowout fracture of the orbital floor with entrapment caused by isolated trauma to the orbital rim. Am J Ophthalmol 103:215–220, 1987.

dilection for most of these diseases, although acute polymorphous myositis is more common in females.

COURSE/PROGNOSIS

Acute polymorphous OIS develop over several days to weeks with pain, redness, edema, and local dysfunction. Their clinical presentation relates to the principle area of orbital involvement: anterior (globe and surrounding orbital fat), myositis (extraocular muscle), dacryoadenitis (lacrimal gland), apical (orbital apex and cavernous sinus), and diffuse (entire orbital involvement).

Sclerosing OIS develop more insidiously and lead to orbital dysfunction as a result of progressive scarring and inflammation. This disease may be linked to multifocal fibrosclerosis, including retroperitoneal fibrosis and sclerosing cholangitis.

Granulomatous OIS develop subacutely to chronically with minimal inflammatory signs around a palpable mass. Sarcoidosis is a recognized systemic syndrome with granulomata developing in the conjunctiva, uvea, skin and lungs. Xanthogranulomatoses show fat-laden histiocytes and multi-nucleated giant cells on histopathology and may have significant systemic features involving the lungs, heart or retroperitoneum.