Orbital floor fractures may result when a blunt object, which is of equal or greater diameter than the orbital aperture, strikes the eye. The globe usually does not rupture, and the resultant force is transmitted throughout the orbit causing a fracture of the orbital floor. Signs and symptoms can be quite varied, ranging from asymptomatic with minimal bruising and swelling to diplopia, enophthalmos, hypo-ophthalmia (ie, hypoglobus), and hypoesthesia of the cheek and upper gum on the affected side. Treatment is titrated to the degree of injury.[1] See the image below.
View Image | Coronal CT scan of orbits demonstrating loss of orbital floor on the left in contrast to the normal orbital floor on the right. |
The orbit and its contents are affected by orbital floor fractures. Direct fractures of the orbital floor can extend from orbital rim fractures, while indirect fractures of the orbital floor may not involve the orbital rim. The cause of the fracture is thought to be from increased intraorbital pressure, which causes the orbital bones to break at their weakest point. This is usually the medial orbital floor. Another theory is that compression of the inferior orbital rim causes direct buckling of the orbital floor. In either case, if the intraorbital pressure is great enough at the time of injury, orbital contents can be forced into the fracture site and possibly into the maxillary sinus.[2]
With simple blowout fractures, there may be no morbidity at all, or the patient may complain of diplopia, enophthalmos, or hypoesthesia of the cheek and gum. Edema and ecchymosis of the eyelids and periorbital region usually are seen but are temporary. With any injury that involves a sinus, air may escape into the orbit or subcutaneous tissues. This is called orbital emphysema.
Vertical diplopia may be caused by entrapment of the perimuscular tissue surrounding the inferior rectus muscle in the fracture site. This results in limited upgaze and may cause pain on attempted upgaze as well. Damage to the third nerve branch to the inferior rectus muscle also may cause limited vertical motility. Severe pain with limited horizontal and vertical movements can be indicative of more severe orbital hemorrhage or edema.[3]
Enophthalmos may result when large orbital floor fractures occur and orbital contents prolapse into the maxillary sinus. If a medial wall fracture also has occurred, the enophthalmos may be compounded due to prolapse of orbital contents into the ethmoid sinus. Orbital edema that occurs at the time of injury initially may mask the enophthalmos, but the sunken eye appearance will become more apparent over the following 1-2 weeks as the edema subsides.
Fractures along the floor usually affect the infraorbital groove and therefore the infraorbital nerve. The resultant neuropraxia causes hypoesthesia of the cheek and upper gum on the affected side. This is usually temporary but can last up to 6 months or longer. In severe injuries, the hypoesthesia may be permanent.
Because the usual mechanism of injury is assault with a blunt object, the vast majority of cases occur in males. In a study of facial fractures in an urban population, 81% of the patients were males.
Because of the nature of the injury and its etiology (eg, assault), most orbital floor fractures occur in teenagers or young adults.[4]
Most cases do well, and most patients obtain resolution of diplopia and correction of enophthalmos.
Warn patients to avoid strenuous activity and to use common sense when determining their postoperative activity level.
Warn patients to avoid nose blowing for several weeks after the injury and repair.
Educate patients about nerve damage recovery. An injured motor nerve (third nerve branch) or sensory nerve (infraorbital nerve) can take weeks or months to return to normal. In some cases, the damage may be permanent.
For excellent patient education resources, visit eMedicineHealth's Eye and Vision Center and Skin Conditions and Beauty Center. Also, see eMedicineHealth's patient education articles Black Eye and Bruises.
Patients may relay a history of the eye being struck by an object larger than the diameter of the orbital entrance. Fists, balls, or car dashboards are examples.
Patients may have no complaints. However, they may complain of vision loss or diplopia. The double vision is often vertical and worse with attempted up or downgaze.
Numbness (hypoesthesia) of the cheek and gum on the affected side may be present. Ecchymoses, ptosis (droopiness of the eyelid), and swelling around the eye may be noted.
The examiner should obtain a past ocular history to assess whether any loss of vision or diplopia is due to the present accident or was established prior to this incident.
A complete ocular evaluation is essential to ensure that no injury to the globe or optic nerve has occurred.
Visual acuity and pupils should be evaluated to ensure that no loss of vision or traumatic optic neuropathy has occurred.[5]
The examiner should evaluate extraocular movements and document any restriction or palsy.
A complete slit lamp evaluation and measurement of intraocular pressures should be performed.
Most posterior segment injuries can be ruled out with a dilated funduscopic examination.
The physical findings may involve only periorbital edema and ecchymosis; however, more severe cases may demonstrate limited vertical movement, enophthalmos, ptosis, and possibly proptosis.
Unusually severe orbital edema may be associated with more severe fractures and can cause proptosis. Once the edema has subsided (usually 1-2 wk), enophthalmos may be present.
Limited vertical movement may be due to entrapment of the perimuscular fascia of the inferior rectus in the fracture site. However, traumatic palsy of the third nerve branch to the inferior rectus also may cause decreased extraocular movements. If a question exists, forced duction testing may differentiate between the two conditions.
Hertel exophthalmometry may demonstrate either proptosis or enophthalmos and should be documented.
In a study of orbital fractures in an urban population, 70% of the fractures were due to assault with a blunt object (eg, fist, baseball bat), and 13% occurred due to a motor vehicle accident, usually involving striking the dashboard. Falls accounted for 10%, and gunshot wounds contributed to 6% of orbital floor fractures.
The only lab studies are those needed for clearance for surgery (eg, CBC count, sequential multiple analysis, chest x-ray, bleed times).
For most orbital fractures, the imaging study of choice is CT scan. A CT scan with axial and coronal views is optimal. Ask for thin cuts (2-3 mm) with specific attention to the orbital floor and optic canal.[6, 7] See the image below.
View Image | Coronal CT scan of orbits demonstrating loss of orbital floor on the left in contrast to the normal orbital floor on the right. |
When the patient has severe head and neck trauma, the radiologist may have difficulty positioning the patient to obtain coronal views. Because these views are generally the most helpful for evaluating the integrity of the orbital floor, the surgeon may ask the radiologist to obtain very thin axial cuts to allow reconstructed coronal views to be obtained.
Forced duction testing may be performed in the office to confirm that limited extraocular movements are due to restriction of the inferior rectus muscle instead of third nerve branch palsy. Testing should be performed after the orbital edema subsides, usually 10 days to 2 weeks after the trauma.
Testing should be performed at the beginning of a surgery to repair the floor fracture as well as at the end of the case. This will assure the surgeon that he has completely reduced the herniated tissue and that any residual motility deficit is neurologic and not mechanical.
When orbital edema is severe, steroids may be used to decrease orbital edema. However, most cases do not require any medical intervention. In addition, most cases are managed on an outpatient basis.[8, 5] Elderly patients may require antibiotics given preoperatively and continued for 2 weeks postoperatively. Patients should be advised to avoid nose blowing for several weeks after the injury to prevent orbital emphysema and possible visual compromise.
The criteria for surgical intervention in blowout fractures are controversial; however, 3 general guidelines exist for surgical intervention.[9]
When surgery is indicated, it is usually best performed as close to 2 weeks from the trauma date as possible. This allows the swelling to subside and a more accurate examination of the orbit to be performed. Additionally, the scarring usually has not advanced enough to prohibit adequate surgical correction.
Access to the orbital floor usually is made through an inferior fornix approach. This allows the surgeon to avoid a cutaneous incision and scar. Alternatively, a lower eyelid subciliary incision can be used but will result in a cutaneous scar. Both approaches allow easy elevation of the periorbita along the floor and release of entrapped orbital contents. An implant (eg, MEDPOR, calvarial bone, Supramid, silicone) is placed over the fracture site. The surgeon must ensure that adequate ledges of stable bone are present for the implant to sit on. Then, the periorbita is closed over the implant along the orbital rim. If the orbital rim is involved and unstable, microplates may be screwed directly into the floating bone segment to anchor it to stable bone.
Physical activity is limited for about 3-6 weeks after surgery to prevent re-injury. This may involve restricting gym class for students. Any contact sports should be avoided for this period.
Nose blowing should also be avoided for about 4-6 weeks to prevent orbital emphysema.
Surgical complications may include loss of vision, traumatic optic neuropathy, diplopia, overcorrection or undercorrection of enophthalmos, lower eyelid retraction, bleeding, infection, extrusion of the implant, infraorbital nerve damage with resultant hypoesthesia, orbital congestion, and epiphora.
Most complications are the result of either malpositioning the implant or using the wrong size implant.
Occasionally, trauma to the inferior rectus occurs during the attempt to release it from the fracture site. Palsy may result. This usually resolves spontaneously but may take as many as 3 months to resolve.
The use safety glasses in all contact sports may prevent many eye injuries. The lenses should be made of polycarbonate, and the frames should be larger than the orbital entrance.
The surgeon should evaluate the patient's vision in the recovery room postoperatively as soon as the patient is alert enough to cooperate.
The vision after surgery should be essentially the same as preoperative vision, and no afferent pupil should be present (assuming no afferent pupil was present preoperatively).
The surgeon should inspect for signs of excessive retrobulbar hemorrhage, such as proptosis or increased intraocular pressure.
Patients should be seen the next day in the office and evaluated for vision, pupils, motility, and intraocular pressure.
Start patients on a combination steroid/antibiotic ointment on the wound 4 times per day and have them follow up in 1 week.
A broad-spectrum antibiotic is used postoperatively in elderly or immune-compromised patients along with analgesics of choice.