Orbital Floor Fractures

Updated August 2024

Establishing the diagnosis

Anatomy

The orbital plate of the maxilla forms the largest part of the floor.
The orbital surface of the zygoma forms the anterolateral portion.
The orbital process of the palatine bone forms a small area of the floor behind the maxilla.
The orbital floor slopes upward medially at 45° and ascends posteriorly at about 30°.
The floor of the orbit is traversed by the infraorbital sulcus or groove, which runs almost straight forward from the inferior orbital fissure and becomes the infraorbital canal carrying the infraorbital nerve and vessels.
The floor of the orbit is separated from the medial wall by a thin suture line.
The floor is separated from the lateral wall posteriorly by the inferior orbital fissure. Anteriorly the floor is continuous with the lateral wall.
The medial floor is about 0.4–0.5-mm thick. It is most thin over the infraorbital canal.
The lateral orbital floor is much thicker than the medial floor and is approximately 1.25-mm in thickness.
Below the floor of the orbit, for nearly its whole extent, lies the maxillary sinus.

Etiology

Low-velocity blunt trauma to the lids and globe can raise hydrostatic pressure in the orbit and fracture the thin medial portion of the floor causing it to “blow out” into the maxillary sinus.
The weakest point on the orbital floor is usually along the infraorbital groove, therefore the greatest point of separation of the bone fragment in a blowout fracture is usually along the infraorbital groove.
“Hinged” bone fragment can be separated at the infraorbital groove and attached to the medial wall (Figure 1).
Alternatively, 2 points of separation can develop — along the infraorbital groove and at the junction with the medial wall — causing the medial orbital floor to be displaced downward into the maxillary sinus.
Rarely, the separation is primarily at the junction with the medial wall causing the bone to be “hinged” in the opposite direction, with remaining attachment along the infraorbital groove.
Rarely, a hinged fracture is lateral to the infraorbital groove — the thin bone fragment remaining attached to the thick lateral zygomatic bone (JAMA Ophthalmol 2013; 131:1492).
High-velocity blunt trauma absorbed directly by the bone along the orbital rim is more likely to displace the zygoma, possibly causing the orbital floor to buckle and fracture in an anterior-posterior direction.
Can be associated with other orbital and facial fractures as well as intracranial or soft tissue trauma
Rarely, fractures can be spontaneous, such as with Graves disease (OPRS 2010; 26:301).

Figure 1. CT exam of a medial hinged floor fracture. Note the concomitant medial-wall fracture and orbital contents herniating into the maxillary sinus. Inferior rectus muscle is rotated 90 degrees.

Epidemiology

Among 133 orbital floor fractures with CT scans treated at Moorfields Eye Hospital in London from 1991 to 2008, 72 (54%) had isolated involvement of the floor; the remainder had concomitant medial wall fractures.
Among 113 orbital floor fractures treated at Fukushima University in Tokyo from 1999 to 2002, 87 (77%) were males, reflecting a predominance of men in most series of orbital fractures (AJO 2006; 142:1019).
There were 19 females among 54 orbital fractures treated at Penn State University from 1989 to 1993, the majority due to domestic violence/sexual assault and motor vehicle accidents (6/19 or 31% each) (Ophthalmology 1996; 103:953).

Intimate partner violence is an important factor to recognize; surgical intervention has secondary implications in helping to emphasize the severity of the experience and injury (OPRS 2014; 30:508).

There can be variation in anatomic predisposition: Afro-Caribbean patients sustained medial wall fractures more commonly (only 2/19 or 10% had isolated floor fractures) than Caucasians and Asians in the Moorfields study (Ophthalmology 2011; 118:1677).
Adult patients are more likely than pediatric patients to develop floor fractures.
Orbital fractures in children are most commonly associated with sports injuries.

Pathophysiology

In classic (indirect) blowout fracture, also known as orbital hydrostatic theory, low-velocity blunt force to the soft tissue raises the intraorbital pressure fracturing the thin medial orbital floor (Figure 2).

Relative weakness in the orbital floor provides an energy outlet to protect the globe from mechanical displacement and rupture (OPRS 2000; 16:188).
Based on cadaver studies the estimated energy required to fracture the bone of the orbital floor according to the hydrostatic theory is about 71-78 mJ (OPRS 2000; 16:188).

Direct fractures are caused by strong forces applied directly to the malar eminence or inferior orbital rim causing buckling of adjacent floor in an anterior-posterior direction.

Because the rim is the thickest portion of the orbit, stronger forces (such as those in a motor vehicle accident) are required to fracture this bone.

“Trapdoor” fractures are more common in younger patients.

Sometimes referred to as white-eyed fractures because other signs of periocular trauma such as bruising or subconjunctival hemorrhage can be absent.
Pediatric bones have a higher proportion of osteocytes than osteoblasts with a smaller amount of calcified osseous tissue, so they are more pliant.
Entrapment of orbital soft tissue is more common in greenstick fractures than in blowout type fractures.
Perimuscular fascia is more commonly entrapped than the actual inferior rectus muscle.

If the muscle or its fascia is entrapped, vertical diplopia with an inability to fully elevate the eye is common.

The patient often refuses to look upward secondary to pain and nausea. The oculocardiac reflex with bradycardia on elevation might also be seen.
Muscle entrapment is a relative emergency as the blood supply to the inferior rectus can be compromised and muscle necrosis can occur.
After surgery, the patient might continue to have vertical diplopia for some time secondary to trauma to the inferior rectus muscle. Damage to the third nerve branch or hematoma of the muscle might prevent it from working normally.

Figure 2. Illustration of the mechanism for entrapment with a floor fracture.

History

Elicit a detailed and extensive history of the mechanism of injury.
Most commonly the mechanism is a traumatic event, but can be seemingly incidental in children.
Of particular importance is the patient’s visual acuity immediately after the event.

Roughly 70% of all orbital trauma patients will have a globe injury.

Elicit a list of comorbidities that can influence your surgical decisions.

Clinical features

Life-threatening injuries and vision-threatening injuries always take precedent.

If the globe has ruptured, diplopia and enophthalmos, potential sequelae of the floor fracture, become less relevant.

Visual acuity and pupil evaluation

Check pupil size and shape.
Is there a possibility of traumatic optic neuropathy?

Slit lamp or pen light evaluation

Is there a hyphema?
Other intraocular injuries such as traumatic iritis, lens subluxation, angle recession, commotio retinae etc?

Intraocular pressure evaluation — unless the globe is obviously open
Extraocular motility evaluation

Check ductions and versions; pain on upgaze might suggest orbital tissue and/or inferior rectus muscle entrapment.
Diplopia — check forced ductions.

Globe position evaluation

Hertel measurements.
Is there hyper or hypo globus?
Large fractures can induce luxation of the globe through the bony defect (OPRS 1991; 7:303) (Figure 3).
Severe injury resulting in globe luxation into the maxillary sinus can cause irreversible complete visual loss (OPRS 2007; 23:156).
Late visual recovery to 20/20 six weeks after repositioning a subluxed globe has been reported in a patient also treated with intravenous methylprednisolone (250 mg every 6 hours), but the patient was left with a severely constricted visual field (OPRS 2011; 28: e17).

Canthal evaluation

Check for telecanthus.
Is the canthus stable to bimanual palpation?

Cranial nerve V evaluation

Hypesthesia, dysesthesia, or hyperalgesia in V1 and V2.

Palpation

Is there a step-off deformity of the orbital rim?
Is trismus present?
Is there crepitus?
Is there decreased retropulsion or a tense orbit?
Is there palatal movement?
Is there mandibular stability?

Check for periorbital edema, ecchymosis, subcutaneous emphysema
In children and young adults with a “trap-door” fracture

Minimal signs of external trauma.
Double vision on upgaze and less commonly on downgaze
Supraduction can illicit nausea, vomiting, and bradycardia because of the oculocardiac reflex

Figure 3A. Coronal CT exam demonstrating hypoglobus with subluxation of the globe into the maxillary sinus.

Figure 3B. Same CT in the sagittal plane.

Testing

Facial computed tomography (CT) scan

Thin cuts (2–3 mm) without contrast
Axial, coronal and sagittal views
Bone and soft tissue windows
Extensive (panfacial) fractures can be evaluated with a 3D CT (Figure 4).
Floor fractures are best evaluated in the coronal and sagittal views.
Look for a trapdoor type fracture with entrapped orbital tissue especially in children and teens.
Look for opacification or air/fluid level in maxillary sinus
X-rays are of very limited use.

Can be of use when evaluating for metallic foreign bodies.

Bone windows

Look for location, size and morphology of the fracture.
Coronal views allow the surgeon the best medial/lateral evaluation to judge the extent of medial wall and lateral floor involvement.

If severe head or neck trauma does not allow for direct coronals then reconstructed views can be obtained.

Sagittal views allow the surgeon to evaluate the anterior/posterior aspect of the fracture and judge the size of the posterior ledge.
Axial views allow the surgeon to judge the involvement of the medial and lateral walls of the orbit and optic canal.
Look for other facial fractures

Medial wall, lateral wall, orbital roof
Maxillary, ethmoid, frontal sinuses
Lateral maxillary buttress
Medial maxillary buttress
Zygomatic arch
Nasal fractures
Nasoethmoidal (NOE) fractures
Mandible fractures
Pterygoid plates

Soft-tissue windows

Rule out ruptured globe by evaluating the shape of the globe, location of the lens and intraocular hemorrhage.
Look for orbital hemorrhage/hematoma.
Look for orbital emphysema.
Look for intraocular or intraorbital foreign bodies.
Evaluate for proptosis or enophthalmos.
Evaluate for hyper or hypoglobus.
Look for signs for extraocular muscle trauma such as hematoma
Look for signs of venous congestion such as a dilated superior orbital vein.

Figure 4. 3D CT exam showing a panfacial fracture.

Differential diagnosis

Direct damage to the inferior rectus muscle and/or its innervation

Intrinsic injury to the inferior rectus muscle is marked by hypertropia with limitation of downgaze and a negative forced duction test.
Inferior rectus muscle injury can be corrected by ipsilateral superior rectus muscle recession and partial transposition of the lateral and medial rectus muscles (J Craniofacial Surg 2013; 24:e590).
Transection of the inferior rectus muscle also induces a large exotropia (Internat Ophthalmol 2014; 34;341).
Hematoma in the inferior rectus can present as weakness several days after the injury (JAMA Ophthalmol 2013; 131:1492).
Isolated inferior rectus muscle paresis can be from trauma, congenital or vascular anomaly (Strabismus 2014; 22:58).
Third nerve branch palsy.

Direct damage to the superior rectus muscle and/or its innervation

Muscle hematoma
Third nerve branch palsy

Patient management: treatment and follow-up

Medical therapy

Can observe for 7–10 days for resolution of motility disturbance resulting from edema, hemorrhage, rectus muscle contusion.
If the fracture is large and associated with early enophthalmos then a period of observation is not indicated.
Medications

Nasal decongestants
Oral steroids
Oral antibiotics — infection occurred in 0.8% of orbital fractures in 1 study; 3 of the 4 patients with infection received antibiotics (Ben Simon, Ophthalmology 2005).

Botulinum toxin injection is less effective in correcting vertical deviation from orbital fractures, compared to similar ocular deviation from other orbital pathology (Strabismus 2013; 21:165).
Avoid nose blowing
Ice packs for 2–3 days.

Surgery

Surgical criteria should be treated more as guidelines than strict rules. Indications for repair:

“Trap-door” or “white-eyed” floor fractures can have severe restriction, which can cause pain and vagal symptoms of nausea, vomiting and bradycardia

Urgent surgical intervention might be required to prevent inferior rectus ischemia.
Surgical repair more than 48 hours after injury with white eyed blowout fracture has resulted in residual limitation in upgaze, despite adequate surgical repair (Arch Dis Child 2013; 98:445).
Typically do not have significant enophthalmos, and the degree of fracture might appear limited on orbital imaging (OPRS 1998; 14:379).

Unresolved diplopia in useful fields of gaze suspected to be restrictive in nature or secondary to globe malposition

Check forced ductions

Early enophthalmos > 2 mm
Large fracture (> 50% of orbital floor on CT scan) indicates that enophthalmos is likely to occur.

Concomitant medial orbital wall fracture can increase risk of progressive enophthalmos. Orbital floor fracture repair might be indicated in this setting for small or medium sized defects.
Appropriate timing is based on the clinical exam and imaging.

Oculocardiac reflex — bradycardia and nausea from traction on orbital contents with significant herniation of orbital contents; can be without clinical evidence of extraocular muscle entrapment (OPRS 2009; 25:496).

Has been observed with clinical evidence of entrapment, bradycardia with vomiting was exacerbated by upgaze (BMJ Case Reports 2014, 2014).
Oculocardiac reflex can also resolve spontaneously without surgery (Orbit 2014; 33:286).

Infraorbital nerve hypesthesia — rarely an indication for surgical intervention

Mostly resolves spontaneously
Severe, progressive nerve pain and paresthesia can be an indication for surgery (OPRS 1994; 10:271).

Timing of surgery:

Early intervention

Trapdoor fractures with signs of severe restriction and nausea/pain
Intervention should occur within first few days to prevent permanent motility deficits (Jordan DR, Ophthal Plast Reconstr Surg, 1998)
Early intervention improves likelihood of complete recovery in motility deficits in pediatric population (Mehta et al. Effect of Time to Operative Intervention on Motility Outcomes Following Orbital Floor Fracture Repair in Children. Ophthalmic Plastic and Reconstructive Surgery)

Delayed intervention

Typically 7–14 days after trauma to allow for edema to subside making the surgery easier and safer by decreasing the chances for a compartment syndrome.
In a comparison of 36 orbital floor fractures with diplopia repaired early (average 9 days after injury), versus 22 late repairs (average 19 days after trauma), there was no significant difference in postoperative diplopia (OPRS 2008; 24:437).

Late intervention

Might be weeks to months after injury; repair more than 6 weeks after injury can still have good outcomes, but prognosis is more varied. (OPRS 2015).
Some surgeons will wait until visually significant enophthalmos develops or diplopia remains.
Additional reports have indicated that outcomes of fractures in which repair was delayed might be similar to those of more acutely repaired fractures among oculoplastic surgeons (Dal Canto, Ophthal Plast Reconstr Surg 2008)

Preoperative evaluation:

Enophthalmos

In addition to Hertel measurements, volumetric analysis of CT images can have predictive value, estimating bone displacement (BJO 1993; 77:100).
CT images can be more helpful early after the injury, with clinical exam altered by edema and hemorrhage.
As an approximation, volumetric expansion of 1 cm³ correlates with 0.8 mm of induced enophthalmos (BJO 1994; 78:618).
A 1.5-cm-wide fracture, involving half the typical orbital floor, with 2 cm in depth, typical of the maxillary sinus, and 1 cm displacement, potentially creates volumetric expansion of 1.5 x 2 x 1 = 3 cm,³ presenting concern about postoperative enophthalmos.
Because a hinged fracture creates a bisecting triangle, it might induce only half the volumetric expansion.
When floor fractures are combined with medial wall and zygoma fractures the likelihood of enophthalmos is greater.

Diplopia

Hess screen can confirm restriction of muscle movement and isolate involved muscle (AJO 2006; 142:1019).
Hess area ratio (HAR) is defined as percentage of total measured ocular motility on the affected side compared to movement on the unaffected side.
In a study of 30 patients with orbital fractures and diplopia undergoing repair within 7 days after injury, 13 (43%) with HAR > 85% had no postoperative diplopia while 5/8 (52%) with HAR <65% had postoperative diplopia at four months (OPRS 2009; 25:123).

Stop anticoagulants if possible.

Surgical approach:

Transconjunctival approach (Figure 5).

Probably the most common approach used by oculofacial surgeons.
Without or with lateral canthotomy (“swinging eyelid”) for better exposure.
Conjunctival incision

Subtarsal
Midfornix

Can be extended for access to medial and lateral orbital walls.
Advantages

No visible scar
Wide access to the inferior orbit
Less chance for postoperative lid retraction
No damage to the orbicularis or its innervation

Disadvantages

Less direct approach
Higher learning curve

Transcutaneous (Figure 6).

Less commonly used by oculofacial surgeons
Skin incision

Subciliary
Subtarsal
Orbital rim

Advantages

More direct approach
Less of a learning curve

Disadvantages

Visible scar
Higher chance of cicatricial lower lid retraction

Transantral endoscopic

Rarely used
Requires endoscopic equipment

Figure 5. Illustration of the transconjunctival approach to the orbit.

Figure 6. Illustration of the transcutaneous approach to the orbit.

Transconjunctival procedure:

General anesthesia, lidocaine with epinephrine into the lower lid.
Perform forced ductions. (Figure 7).
Evert the lower lid.
Open conjunctiva (e.g., with monopolar knife) with or without release of the lateral canthus.
Sharply and bluntly dissect posterior to the orbicularis and anterior to the orbital septum.
Blunt retractor in lower lid and conjunctiva/lower lid retractors on bridle suture over cornea.
Open the periosteum of the rim and dissect in the plane inferior to the periosteum posteriorly in the orbit.
Careful release of entrapped tissue from the fracture.
Placement of implant to reproduce the anatomic position of the orbital floor.

Posterior aspect of the implant must rest on the posterior ledge.

Perform forced ductions and ensure release of any entrapped tissue.
Close periosteum over the rim.
Close conjunctiva and repair lateral canthus if it was released.
No patch.

Figure 7. Illustration of forced duction testing.

Orbital floor implants:

Autologous material

Bone

Calvarial
Anterior maxillary wall

Cartilage

Nasal septal
Conchal/auricular

Fascia lata
Periosteum

Allogenic material

Irradiated bone
Lyophilized dura
Lyophilized cartilage
Fascia lata
Bovine bone

Alloplastic material

Metallic

Titanium mesh (Figure 8 and Figure 9)
Vitallium mesh

Nonmetallic

Silastic (silicone) sheet
Marlex mesh (crystalline polypropylene)
Bioactive glass (glass/ceramic)
Teflon
Porous polyethylene — with titanium reinforcement (Figure 8) and without

Resorbable

Polylactic/polyglycolic (PLA/PGA) acid copolymer
Polydioxanone (PDS)
Seprafilm — carboxymethylcellulose and hyaluronate hybrid (OPRS 2009; 25:2011).
Polyglactin 910 polydioxanone (OPRS 1993; 9:191).

Figure 8. Illustration of various titanium implants used for orbital fracture repair. A. Titanium fan-shaped plate. B. Porous polyethylene covered titanium fan-shaped plates. C. Titanium floor and medial wall plate. D. Preformed right and left anatomic titanium floor plates.

Figure 9. Illustration of titanium implant placed on the floor of the left orbit.

Postoperative care:

Typically the surgery is outpatient and the patient is allowed to go home after the surgery.
Medications

Pain control medication
Lubricating ointment

Antibiotic ointment with or without steroid (e.g., Tobradex)

Possibly antinausea medication
Possibly oral steroids

No nose blowing
No contact sports
No patch

The patient might develop a hematoma with optic nerve compromise, and the patch can mask this.

Ice packs for the first 2–3 days, then heat packs
Instructions to call the surgeon ASAP at any hour if uncontrolled bleeding or vision loss is experienced
Note: Some surgeons will place a drain in the orbit and admit the patient overnight.
Follow-up in the surgeon’s office in a few days to 1–2 weeks

Preventing and managing treatment complications

Postoperative orbital hemorrhage

Stop all anticoagulants if possible prior to surgery.

Might require discussion with the primary care provider or other provider such as the cardiologist or cardiothoracic surgeon.

Meticulous hemostasis during surgery.

Consider thrombin and gel foam if excessive oozing is encountered.

Control blood pressure during and after surgery.
Apply cold compresses after surgery.
Consider placing a drain if bleeding is an issue during the surgery.
Consider removing the implant and surgically draining the hematoma if the vision is compromised.

Postoperative vision loss or blindness

Monitor the pupil during surgery
Take care to monitor the retractors held by the assistants.
Size the implant appropriately and place it very carefully.
Treatment of the vision loss depends on the etiology

Optic nerve trauma

Consider removing the implant.
Consider high dose corticosteroids.

Orbital hemorrhage

Infection

Consider pre and intraoperative intravenous antibiotics
Use sterile technique
Routine postop antibiotics are controversial (Wladis, Orbit 2013)
If postoperative infection is confirmed, treatment varies

Confirm infection; patients often think the wound is infected when it is actually not infected
Consider location of infection: orbital versus skin/subcutaneous tissue
Consider source of infection: sinuses versus superficial source.
Consider obtaining cultures tissue for microbiology.
If no cultures, can treat empirically with IV or oral antibiotics.
Consider draining and packing of an abscess
Consider removal of implant.
Reconsider the type of implant and potential need for replacement if implant is removed.

Implant related morbidity

Extrusion

Can be caused by infection, hemorrhage, oversized implant or poor fixation
Treatment depends on cause and degree of migration
Infection would be treated with antibiotics and implant removal
Can require repositioning or replacement

Cyst

Fibrotic capsule or respiratory epithelium surrounds implant (OPRS 2008; 24:498).
Cyst exacerbated by hemorrhage can become large (OPRS 2011; 27:e117).
Can present as a mass several years after the injury (OPRS 2009; 25:238).

Inflammation

Some implant materials such as silicone can produce inflammation that can simulate myositis in addition to a hematic cyst (OPRS 1991; 7:267).

Hypesthesia

Can take up to 12 months to resolve following injury or surgery
Postop CT scan to evaluate implant and/or screw placement if hypesthesia not resolving as anticipated

Eyelid retraction or ectropion

The transconjunctival approach has lower risk for lid retraction
Avoid excessive traction and cautery of the lower eyelid.
Careful wound closure to avoid shortening the orbital septum.
Take great care to cover any titanium on the orbital rim with periosteum or other soft tissue to keep the orbicularis from sticking to and scarring the implant.
Treatment depends on the severity of the scarring.

Injection of steroid into the scar with vigorous massage might release the cicatrix.
Surgery typically requires removal of the rim titanium implant
Spacer material is typically required to prevent rescarring

Hard palate mucosa works very well
Upper lid free tarsal graft
Auricular cartilage (can be bulky)
Alloderm (human cadaveric dermis)
Tarsys (decellularized porcine derived membrane)
Tutoplast (human preserved sclera)
Porous polyethylene (high complication rate)
Others

Keeping the eyelid on stretch over the cornea for several days can be very helpful.

Persistent restriction of motility

Treatment depends on etiology.
Ensure release of all entrapped tissue after the implant has been placed into position.
Perform forced ductions prior to closing of the wound.
Consider follow-up imaging studies to evaluate implant position and possibility of residual tissue incarceration.
Restricted motility secondary to rectus muscle damage will typically resolve over weeks to months.

Muscle hematoma
CN III branch trauma

Enophthalmos undercorrection

Ensure that the orbital implant is placed adequately on the posterior ledge and is nonmobile.
Ensure that all fractures are adequately addressed (e.g., floor and medial wall)
Evaluate for incorrect implant placement with follow-up CT scan.
Consider implant replacement or augmentation of orbital volume.

This can be difficult because of orbital scarring, rectus muscle retraction, and fat atrophy.
Augmentation material must be placed behind the globe and not underneath or hyperglobus will result.

Enophthalmos overcorrection

Ensure that the proper size and thickness of implant is used
Ensure proper placement of the implant
The overcorrection typically improves with time as edema resolves.

Persistent lymphedema

Most commonly seen with cutaneous approach
Ensure the incision placement does encroach on the lymphatic vessels of the lateral canthus.
Warm compresses to increase blood flow and decrease healing time.
Typically improves over time.

Disease-related complications

Soft-tissue emphysema

Commonly seen after facial trauma can be introduced by nose blowing or sneezing.
Orbital emphysema with proptosis typically resolves without intervention.
In severe cases, release of the intraorbital air pocket with a large gauge needle might be indicated.
Severe subcutaneous emphysema can extend beyond the orbit and sinus onto the neck and chest, causing airway obstruction and necessitating intubation (OPRS 2005; 21:465).

Orbital hemorrhage

Commonly seen after orbital trauma, typically resolves without intervention.
In severe cases, the increased orbital pressure can cause compromise of blood flow to the optic nerve.
Emergent release of the lateral canthus via lateral canthotomy and cantholysis might be required.
Out-fracturing of orbital walls and/or drainage of the hematoma with drain placement might be required.

Persistent diplopia

There are multiple potential causes for persistent diplopia including injury to the muscle and/or innervation of the extraocular muscle.
Can be caused by persistent muscle entrapment
In a study of 19 patients younger than 20 years old and treated 2000–2008 for entrapment, delaying surgery more than a week after the injury increased the likelihood of postoperative upgaze diplopia, but this resolved within 2 months without additional surgery (BJO 2010; 94:736).
Can require prism glasses or strabismus surgery
When scarring limits strabismus repair to ipsilateral inferior rectus muscle, moderate vertical deviation can also be corrected by contralateral superior oblique posterior tenotomy (Strabismus 2013; 21:29).

Enophthalmos

Relatively common, especially if multiple orbital walls are involved.
Early enophthalmos can continue to worsen over time.
Late enophthalmos might be seen as edema resolves.
Typically easier to repair in the first 2–3 weeks after injury but can be repaired weeks to months later.

Aberrant maxillary sinus drainage

Prolapsed orbital contents can potentially interfere with drainage of maxillary sinus.
Can produce congestion and silent sinus syndrome with secondary enophthalmos; can be corrected with maxillary antrostomy (OPRS 2004; 20:241).
Fistulous tract between orbit and maxillary sinus can predispose to orbital emphysema; can be repaired with a patch graft (OPRS 1995; 11:66).

Orbital cellulitis

Uncommon after orbital fractures
Can be secondary to sinus infection or from direct communication between the nose and orbit.
Can be secondary to foreign matter (e.g., plant material) introduced at time of the trauma.
Treat with topical and systemic antibiotics.
Might require surgical drainage with cultures.

Sinusitis

Uncommon after orbital fractures.
Oxymetazoline (alpha adrenergic agonist) induces vasoconstriction and improves airflow and drainage.
Treat with systemic antibiotics.
Might require ENT referral

Patient instructions

Typically the surgery is outpatient.
Medications

Pain control medication
Lubricating ointment
Antibiotic ointment with or without steroid (e.g., Tobradex)
Possibly antinausea medication
Possibly oral steroids

Avoid nose blowing
No contact sports until cleared by physician
No patch — can develop a hematoma with optic nerve compromise and the patch can mask this.

Ice packs can be helpful for the first 2–3 days
Instructions to call the surgeon ASAP if uncontrolled bleeding or vision loss is experienced.

Some surgeons will place a drain in the orbit and admit the patient overnight.

Follow up in the surgeon’s office in a few days to 1–2 weeks.
Avoid swimming or scuba diving or other activities associated with substantial changes in pressure.

References and additional resources

AAO, Basic and Clinical Sciences Course. Section 2: Fundamentals and Principles of Ophthalmology; Section 6: Pediatric Ophthalmology and Strabismus; Section 7: Orbit, Eyelids, and Lacrimal System, 2013-2014.
AAO, Surgical Anatomy of the Ocular Adnexa, 1996, p.52, 80.
AAO Focal Points. Vol. XXXI, Number 1.
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Ben Simon GJ, et al. Orbital cellulitis: a rare complication after orbital blowout fracture. Ophthalmology. 2005; 112: 2030.
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