In evaluating a patient with a possible medial wall fracture of the orbit, certain key points need to be elicited on history, especially since early symptoms may be minimal.
First, take a detailed history about the trauma. This should include the specific mechanism of trauma and when it occurred. A history of trauma from several years prior also could be significant. Any events associated with the actual trauma, such as loss of vision or loss of consciousness, need to be elicited. Also inquire about events since the recent trauma, such as nose blowing.
Current symptoms, such as any change in vision or diplopia, should be elicited. Although quite rare, a history of epistaxis and cerebrospinal fluid (CSF) rhinorrhea also should be elicited.
Isolated fractures of the medial orbital wall are infrequent. Although the medial wall is thinner than the floor, fractures of the medial wall are less common than fractures of the orbital floor, possibly because of additional support given to the medial wall from the adjacent trabeculae of the ethmoid air cells.
The incidence of isolated fractures of the medial orbital wall in the literature varies considerably. However, the incidence has increased in recent years because of a rise in the incidence of high-energy impact orbital injuries, coupled with improved radiographic diagnostic procedure of the orbital structure. Although data indicate that isolated medial wall fractures are not frequent, concomitant medial wall and floor fractures are more frequent.
Although medial wall fractures are known to occur in multiple races, de Silva and Rose reported an increased incidence of isolated medial wall fractures in Afro-Caribbean patients compared with white patients or those of Asian descent. They postulate that this disparity results from a thicker orbital floor in Afro-Caribbean patients than in those of other races. In white and Asian patients, isolated orbital fractures were more common in the floor than in the medial wall.
Orbital fractures occur when the force generated by blunt trauma exceeds the tolerances of the bony surfaces. Medial wall fractures can result from either directly as injuries to the face or indirectly as blowout fractures, theorized to occur from a direct buckling of orbital bones or a hydraulic mechanism involving indirect transmission of forces.
This 55-year-old man sustained an injury to his right orbit as a result of blunt trauma from a fist; shown in primary position.
When the fracture occurs as a result of a direct injury, it is usually in conjunction with a naso-orbital fracture, which results from direct application of blunt force to the naso-orbital area. The most frequent cause of these naso-orbital fractures is a motor vehicle accident that results in the face impacting against the steering wheel or dashboard; additional causes include blunt trauma from the fist or the elbow. Medial wall blowout fractures are potential sequelae of blunt periorbital trauma. Common causes for this type of medial wall fracture include fists, elbows, shoe kicks, baseballs, and tennis balls, all of which have a diameter greater than the orbital rim.
A naso-orbital fracture tends to consist of a comminuted, depressed fracture involving the nasal bones, ethmoid sinuses, and medial orbital walls. It occurs when a blow of sufficient force is applied to the nasal bridge area. Such blunt trauma can cause the medial wall to develop a fracture in 1 of 2 ways. First, when the nasal bone fragments are projected backward, the thin lacrimal bone and lamina papyracea are comminuted easily. The nasal bone and frontal process of the maxilla may be displaced posteriorly into the ethmoid sinus; as a result, an in-fracturing of the medial orbital wall into the orbit occurs. Therefore, the compressive force causing nasal fractures is a very important causative factor of pure medial wall fractures.
With blowout fractures, the medial wall is fractured indirectly. When an external force is applied to the orbital cavity from an object whose diameter is larger than that of the orbit, the orbital contents are retropulsed and compressed. The consequent sudden rise in intraorbital pressure is transmitted to the walls of the orbit, which ultimately leads to fractures of the thin medial wall and/or orbital floor. Theoretically, this mechanism should lead to more fractures of the medial wall than the floor, since the medial wall is slightly thinner (0.25 mm vs 0.50 mm). However, pure blowout fractures most frequently involve the orbital floor. This may be attributed to the honeycomb structure of the numerous bony septa of the ethmoid sinuses, which support the lamina papyracea, thus allowing it to withstand the sudden rise in intraorbital hydraulic pressure better than the orbital floor.
Medial wall fractures frequently remain undetected, either because the clinical signs and symptoms of such a fracture may be masked by extensive periorbital trauma or because they give clinical symptoms in only a few instances. Therefore, a thorough clinical examination is critical to suspecting this type of fracture.
Fractures of the medial orbital wall can result in various clinical presentations. The different clinical syndromes depend in large part on whether the fracture is caused by a blowout injury or whether it is part of an ethmoid-orbital fracture.
Clinical findings suggestive of a medial wall fracture include periorbital edema and ecchymosis, (nasal) subconjunctival hemorrhage (all nonspecific), subcutaneous emphysema, epistaxis, CSF rhinorrhea, narrowing of the palpebral fissure with forced lateral duction, restriction of abduction, limitation of adduction, the acquired retraction syndrome or retraction of the globe on attempted abduction or adduction, horizontal diplopia, and progressive enophthalmos. Medial wall fractures also tend to be commonly associated with nasal fractures. The most striking features of an isolated medial wall fracture are diplopia on medial and lateral gaze and/or enophthalmos.
Patient with an injury to his right orbit as a result of blunt trauma from a fist in right gaze, showing full abduction of the right eye.
Patient with an injury to his right orbit as a result of blunt trauma from a fist in left gaze, showing poor adduction of the right eye.
Blowout fractures and naso-orbital fractures of the medial wall can be associated with limitation of ocular motility. Medial rectus muscle incarceration is described more frequently in medial wall blowout fractures than in naso-orbital fractures.[5, 6] Medial orbital fractures with true incarceration of the medial rectus muscle are rare. However, diagnosis of a medial wall fracture is often suggested by medial rectus entrapment. Patients with restriction of the medial rectus muscle and/or its surrounding connective tissue may present with horizontal diplopia, pain on abduction, restriction of abduction and adduction, and horizontal limitation with the forced duction test.
This specific presentation with severe tissue entrapment is more common in children who sustain blunt trauma to the orbit. This is because blowout fractures in the pediatric age group tend to be trapdoor-type fractures. The orbital bones in a child's orbit are hypothesized to be more flexible than an adult's bones. Therefore, rather than buckling and breaking in pieces like the brittle adult bones and leading to tissue prolapse, the child's bones tend to return to their original position and, in the process, entrap surrounding soft tissue.
Although the vast majority of trapdoor fractures described in the literature are floor fractures, this type of fracture has also been described in the medial wall.[9, 10, 11]
Other associated features of these pediatric fractures include nausea, vomiting, dizziness, and lightheadedness due to a vasovagal response; pain with eye movement; and minimal external evidence of trauma despite marked motility restriction; therefore, the lack of ecchymosis or edema, which are common soft-tissue signs in orbital trauma, should not deter the clinician from suspecting a serious injury. The symptoms associated with increased vagal tone that stem from the oculocardiac reflex complicate examination in children; therefore, clinicians need to maintain a high index of suspicion and proceed to appropriate orbital imaging in these situations, as these symptoms can sometimes be mistaken for an intracranial injury rather than an orbital injury.
Double vision may exist in extremes of gaze only, if orbital congestion is excessive. An important test to determine whether a muscle is entrapped is forced ductions. Restriction on forced ductions usually distinguishes entrapment of orbital contents from a contusion of the extraocular muscle, a lesion of the nerve, or simple congestion of the orbit. However, early on, if a muscle is swollen, it may be difficult to differentiate the swelling from true entrapment. A pseudo–Duane retraction syndrome or retraction of the globe and narrowing of the palpebral fissure upon attempted abduction may occur with medial wall fracture associated with medial rectus entrapment, and it is pathognomonic for this complication.
Other signs that should raise the suspicion of a medial wall fracture in orbital trauma are epistaxis, orbital emphysema, and CSF rhinorrhea. These signs occur less frequently than motility disturbances. Be alert for CSF rhinorrhea because it represents injury to the layers enveloping the brain and, thus, is an indication for prophylactic broad-spectrum antibiotics and neurosurgical consultation. Epistaxis may occur either in isolated medial wall fractures or in conjunction with naso-orbital fractures.
Orbital emphysema is the result of a communication between the ethmoid cells and the orbital cavity. To produce this emphysema, the air pressure in the ethmoid cells should be very high, which is not produced easily because of the drainage of air into the nasal cavity. Therefore, orbital emphysema may occur when there is simultaneous injury of the naso-ethmoid-frontal area, a precondition of nasal obstruction, blowing of the nose after the injury, or Valsalva maneuver after injury, such as sneezing.
Severe orbital emphysema can lead to severe, though reversible, visual loss from the extremely high intraorbital pressure. Careful palpation of the periorbital soft tissues should always be performed to look for crepitus, which is a helpful diagnostic sign of orbital emphysema; however, it may not be present when proptotic orbital tissue is very inflated and eyelids are tense. The clinical picture of severe orbital emphysema may simulate a large orbital hemorrhage, which may occur with medial wall fracture if there is trauma to the ethmoidal vessels. The hemorrhage also may cause severe visual loss due to compression on the optic nerve. It is critical that this acute compartment syndrome with rapidly progressive proptosis and elevated IOP due to orbital hemorrhage be distinguished from muscle entrapment as the cause of globe restriction in all age groups.
Medial wall fractures with ethmoid-orbital fractures can cause damage to the nasolacrimal drainage system and the medial canthal ligament. In some of these fractures, the medial canthal tendon is injured, resulting in traumatic telecanthus. A clinical finding associated with such detachment or severance of the medial canthal tendon is loss of the angular shape of the canthus, thus appearing rounded as a result of the lateral pull of the orbicularis oculi muscle. Also, the laterally displaced tissues of the upper and lower eyelids may cover the caruncle, the semilunar fold, and a portion of the sclera. Damage to the lacrimal drainage apparatus may present as epiphora or chronic infection secondary to nasolacrimal duct obstruction. Any portion of the lacrimal excretory apparatus, including the canaliculi, the lacrimal sac, or the nasolacrimal duct, may be obstructed by compression from displaced bone fragments or severed by similar fragments.
Another presentation of a medial wall fracture is enophthalmos, which results from the prolapse of tissue from the orbital cavity or enlargement of the cavity itself. In later stages, it may be caused by contracting necrotic muscles, orbital fat atrophy, or cicatricial contraction of the retrobulbar tissues.
Fractures of the medial orbital wall may cause little, if any, symptomatology. Operative treatment is not necessary if a displaced medial wall fracture shows no clinical diplopia, minimal enophthalmos, and no signs of herniation of orbital contents into the ethmoid sinus. A good functional and cosmetic result can be expected in this situation.
On the other hand, if the fracture causes symptomatic horizontal diplopia within 25-30° of primary gaze or painful ocular motility, a positive forced duction test, and evidence of muscle entrapment on CT scan, repair of the fracture with release of the incarcerated tissue is warranted within 2 weeks of the injury. Within this period, the surgery becomes technically easier and more successful, especially because fibrous or osseous union has not progressed sufficiently to immobilize the fragments.
In addition, incarceration of tissues may lead to necrosis and deformity if not relieved soon after the injury. This compartment-type occurrence with ischemia of entrapped soft tissue (intraorbital fat or muscle) is frequently encountered in the trapdoor fractures that occur in the pediatric population. Therefore, in these patients, even earlier surgery, within the first 48-72 hours after the injury, is warranted to prevent any fibrosis of the muscular and perimuscular tissue, thereby restoring optimal muscle function.
Early enophthalmos of 2 mm or more, which may be cosmetically unacceptable to the patient, is also an indication for repair of an isolated medial wall fracture. However, it should be noted that if an isolated medial wall fracture causes enophthalmos only, it may be advisable to wait until the fracture has healed and then put material on the floor to repair the enophthalmos.
Displacement of bone fragments toward the globe or optic nerve merits surgical intervention and reduction as soon as possible. Both severe orbital emphysema and large intraorbital hemorrhage that cause acute loss of vision are indications for immediate exploration and possible orbital decompression. Repair of a concomitant orbital floor fracture may be an indication for repair of the medial wall.
A basic knowledge of the anatomy of the medial orbital region is necessary, first, to understand the complications that arise from fractures of this area and, second, to perform surgical intervention when it is required.
The 4 bones that make up the medial wall (anteriorly to posteriorly) are the frontal process of the maxilla, the lacrimal bone, the orbital plate of the ethmoid, and finally the lesser wing of the sphenoid, through which the optic nerve traverses in the optic canal. The rectangular lamina papyracea of the ethmoid, which has a convex orientation with respect to the orbital cavity, is the largest component of the medial orbital wall. It is extremely thin, varying 0.2-0.4 mm in thickness. The thick frontal process of the maxilla forms the medial orbital rim.
When operating in the medial area of the orbit, surgical landmarks that must be kept in mind are the medial canthal tendon, lacrimal sac, the area of the trochlea, and the anterior ethmoidal vessels. The fragile lacrimal bone and the frontal process of the maxilla form the lacrimal groove (or fossa), which houses the lacrimal sac. The trochlea is attached to the periorbita in the anterior portion of the superior medial orbit. The ethmoidal foramina, which are about 24 mm and 36 mm behind the orbital rim, respectively, transmit the anterior and posterior ethmoidal arteries. All these vessels can be significant sources of bleeding when the region is involved in trauma, but only the anterior ethmoidal vessels need to be avoided during surgery.
The lacrimal sac is intimately related to the medial canthal tendon, which is a major supporting structure of the superficial tissues of the medial orbital region. The tendon splits into 2 heads. The anterior head lies anterior to the lacrimal sac and inserts into the anterior lacrimal crest, which is formed by the frontal process of the maxilla; the posterior head courses posterior to the sac and attaches to the posterior lacrimal crest.
Small medial wall fractures that cause no clinical symptoms or signs do not need surgical repair. Such fractures heal on their own in approximately 3 weeks without any sequelae. Another contraindication to repair of the fracture would be a concurrent ruptured globe, which would need to be repaired prior to any orbital surgery. Finally, in patients with other life-threatening medical problems or severe neurologic damage from head trauma, repair of the medial wall fracture would not be indicated.
Radiographic evaluation of suspected medial wall fractures has evolved over the past several years. Conventional radiography or routine orbital x-rays generally are not helpful because of the compact overlapping anatomy of this region and the thinness of the medial orbital wall. Nonetheless, x-ray signs to look for include a disruption in the medial orbital wall, opacification of the ethmoid sinus, and presence of air in the orbit.
CT scan has greatly improved the evaluation of orbital fractures, and it should be completed in all patients suspected of having such an injury. Optimal information can be gained from both axial and coronal cuts of bone and soft tissue images (see the images below). With these appropriate views, the size, morphology, and exact seat of the fracture, which has the possibility to extend to the optic canal, can be visualized.
Coronal CT scan of the orbits of a patient with an injury to his right orbit as a result of blunt trauma from a fist reveals a right medial orbital wa....
Axial CT section.
CT scan accurately localizes the bone fragments of the fractured lamina papyracea even if the orbital sinus adjacent to the fracture is opacified. A variable degree of medial displacement of the thin lamina papyracea may be present, and density is often increased in the ethmoidal sinuses from edema and blood accumulation. CT scan also detects entrapment of the medial rectus muscle, recognized by displacement of the muscle into the fracture site, with or without bone displacement. In the pediatric trapdoor fractures described earlier, clinical evidence of entrapment will not necessarily correlate with the CT scan findings. In these cases, in which a trapdoor-type defect has occurred, there will be minimal or no evidence of bone displacement. In addition, the medial rectus could appear in a normal position, but the surrounding connective tissue is seen entrapped in the location of the fracture. A more rounded appearance of the medial rectus adjacent to the bone should also raise the index of suspicion for a trapdoor-type fracture.
A CT scan reliably demonstrates whether acute proptosis in a patient is secondary to orbital hemorrhage or orbital emphysema. Echography also could aid in distinguishing these 2 distinct entities. B-scan ultrasound has proven to be reliable in diagnosing medial wall fractures because a good correlation between ultrasound and CT scan was found. However, edema, hemorrhage, emphysema, and swelling may influence the accuracy of the scan.
See the list below:
Most isolated medial wall orbital fractures require no treatment other than applying ice compresses, warning patients to avoid blowing their nose, and providing decongestants and systemic antibiotics. The antibiotics are recommended to reduce the risk of sinusitis and orbital cellulitis; cephalexin at a dosage of 250 mg every 6 hours is a prophylactic regimen.
Small medial wall fractures may not even be clinically detectable. They tend to be asymptomatic unless the patient has orbital or eyelid emphysema; overwhelmingly, the orbital emphysema is minimal, requires no treatment, and resolves within several days. In many cases, it is appropriate to allow time for spontaneous improvement of the clinical findings in a patient rather than rush into surgical intervention; symptoms associated with this type of fracture may disappear with time. For example, if muscle edema is the cause of a motility abnormality, spontaneous improvement may occur without treatment as the edema resolves. With the resolution of the diplopia, observation is indicated in case of the development of late enophthalmos.
Early significant enophthalmos and motility problems also may be masked by edema of periorbital tissues. Systemic corticosteroids have been advocated to speed up the resorption of the edema, as well as hemorrhage, thus allowing the surgeon to more accurately assess any muscle entrapment and orbital damage. Prednisone (60-80 mg/d) is initiated within 48 hours of the injury and is continued for 5 days. Steroids also are indicated if severe loss of vision occurs. In this case, the dosage is higher, 250 mg of methylprednisolone administered intravenously every 6 hours.
Although early definitive treatment of a fracture is desirable, it may be wise to allow acute inflammation to subside before proceeding with surgery. The goals of surgical treatment for medial wall fractures are restoration of good ocular motility, including single binocular vision in all fields of gaze, and improvement of significant enophthalmos. The primary goal is the complete reduction of the entrapped medial rectus muscle along with any other herniated orbital soft tissues. This may be followed by covering of the bony defect with an appropriately sized and accurately placed implant to prevent prolapse of tissue with possible reincarceration of tissue or late enophthalmos.
Bony defects of the medial orbital wall have been covered historically, by both alloplastic materials and bone grafts. Potential autogenous bone graft sources are the rib, iliac crest, and calvarium. However, with the increasing availability of viable alloplastic implants (either permanent or absorbable), such as porous polyethylene, gel film, bioglass, silicone sheeting, or those composed of titanium, along with donor-site complications associated with bone grafts, their use has declined in orbital wall reconstruction.
Medial orbital wall fractures are usually repaired under general anesthesia. The patient is brought into the operating room suite and sedated. The forced duction test is repeated with the patient under anesthesia to reconfirm previous findings.
Numerous surgical approaches have been used to explore the medial orbital wall and to repair its fractures. The appropriate approach depends on both the extent of the fracture and its association with other fractures.
In the past, the traditional approach used to repair medial wall fractures was the Lynch incision. It involves incising skin directly over the superomedial orbital rim (between the medial canthus and the bridge of the nose) and provides excellent exposure, but it can result in severe scarring or webbing. Since the 1990s, the transcaruncular approach[16, 17] has become a major approach to the medial orbit, as it avoids leaving a visible scar and any potential disruption of the medial canthus or adjacent lacrimal structures.[18, 19] In isolated medial wall fractures, this approach provides adequate direct exposure to the medial wall and to the area of tissue incarceration similar to that of the Lynch approach.
Once the incision is made between the plica and the caruncle, blunt dissection to the periosteum is performed, and the periosteum is incised just beneath the posterior lacrimal crest. Care is taken to avoid damage to the lacrimal sac and the medial rectus muscle. A periosteal elevator is then used to carry the dissection posteriorly in a subperiosteal plane until the entire fracture is clearly visible. The anterior and posterior ethmoidal vessels are identified and coagulated. The periosteal elevator, along with malleable retractors, is used to gently remove the incarcerated tissues from the fracture.
Of prime importance during the procedure, once any entrapped orbital contents are freed, forced ductions should be performed to confirm complete release of the entrapped orbital contents or muscles. This is also recommended when an implant is inserted into position.
Finally, the transcaruncular incision site is closed with dissolvable sutures.
The patient is prescribed broad-spectrum antibiotics by mouth for at least 10 days. Some patients may be started on 40-60 mg of prednisone daily for 5 days.
Eye exercises are also initiated. In these exercises, the patient follows an object, such as a pencil, from right to left, in sets of 20 movements, 5 times a day. If residual postoperative diplopia is present, patients specifically are asked to follow the object from the point where they see double, to a point where they have single binocular vision. These exercises are performed to keep the affected extraocular muscles active, thereby preventing any subsequent postoperative fibrosis or scarring. They are continued until the eye clinically is moving well or until resolution of the diplopia occurs.
Finally, patients are warned not to blow their nose for several weeks to avoid air passing into the orbit from the sinuses, possibly resulting in severe orbital emphysema with secondary visual compromise.
Generally, patients are seen for follow-up at about 1 week following repair of their fracture and then weekly thereafter. Physicians will exercise their own judgement to determine whether earlier visits are warranted, such as when optic nerve compromise is a concern. Some physicians may choose to admit patients to the hospital overnight for close observation, especially when the risk for postoperative bleeding in the orbit is high. Regardless of when the patient is to be discharged, the vision does need to be assessed postoperatively at some point on the day of surgery (by a physician or a nurse). Simply determining if the patient can at least count fingers is adequate.
In the initial days following surgery, all patients need to be instructed to assess their vision on their own on a daily basis; this can be done by simply asking them to hold their hands in front of them and determine if they can see well enough to count their fingers. If at any point they feel they cannot do this, or have a sudden increase in pain or swelling around their eye, they should be instructed to contact their surgeon immediately.
Follow-up visits are used to gauge improvement (eg, diplopia, enophthalmos) and to look for any potential complications, even in patients who do not undergo surgical treatment. In some patients with medial wall fractures, motility may not improve fully for several weeks, with or without surgery.
Patients are allowed to start light lifting and straining approximately 3 weeks after surgery, and they are allowed to return to most sports with protective eyewear at least 6 weeks after surgery.
For patient education resources, see the Eye and Vision Center, as well as Black Eye.
Any surgery deep within the orbital cavity is fraught with potential complications, and patients should be counseled about these risks. Failure to diagnose fractures that require early treatment may result in complications due to fibrosis, contracture, and unsatisfactory union. Postoperative complications include residual or worsening motility disturbance and residual enophthalmos. Sometimes, the enophthalmos may be severe and permanent in spite of the reduction of prolapsed orbital tissues and repair of the fracture; this may be caused by fat atrophy or contracting necrotic muscles. At this point, its treatment also becomes more problematic.
Transient weakness of the medial rectus may occur after release of the entrapped muscle, resulting in persistent diplopia, but normally it does improve, sometimes up to a few months later. It also may occur from orbital edema.
Visual loss and even blindness, although extremely rare, are possible complications following surgical repair of medial orbital fractures. This has been attributed to direct damage to the optic nerve or its vascular supply at the time of surgery or from orbital hemorrhage in the immediate postoperative period.
The insertion of an implant has its own set of potential complications. First, it should be carefully and appropriately placed subperiosteally to avoid injury to the optic nerve and extraocular muscles. An implant must be removed emergently if any early loss of vision occurs following repair of the orbital fracture. Extrusion of the implant has been reported and is related to an implant that is too large and not stable enough to prevent migration. It also may follow infection, hemorrhage, or poor wound closure. Appropriate fixation of the implant avoids its extrusion; one report advocates the use of fibrin glue (Tisseel) to prevent this complication.
Overall, patients with medial orbital wall fractures have a prognosis that is usually favorable. Minimal fractures usually do not require any treatment and lead to no complications. Of the patients in whom surgical repair is indicated, it is possible to obtain a complete recovery of function, including motility, even several years after the initial surgical repair. However, medial wall fractures that are not repaired within 2 weeks of the initial trauma have a poorer prognosis. Those patients with trapdoor-type fractures consisting of incarceration of tissues in the fracture site are at serious risk for permanent motility defects if they are not treated expeditiously.
If complete resolution of diplopia does not occur, prisms or muscle surgery may be necessary. Any significant residual diplopia should be given at least 4-6 months to recover before any muscle surgery is performed. Persistent enophthalmos can be repaired late with various materials placed on the floor.
The treatment of isolated medial orbital wall fractures continues to evolve. It has been postulated that fractures of the medial orbit may be more prone to enophthalmos than other orbital blowout fractures. Does this mean they should all be repaired? Likely not, although it is becoming apparent that there is no absolute time (eg, greater than or less than 2 weeks) or absolute indication for surgical intervention of all medial wall fractures; rather, each clinical scenario must be treated accordingly, such as in a “white-eyed” medial wall fracture. A 2016 classification system described by Chung et al that differentiates medial wall fractures into 3 types based on their CT appearance may eventually be used as a guide to determine which method would be the most suitable to treat a particular medial wall fracture.
The use of endoscopy in the repair of these fractures has been demonstrated with the advent of improved technology of fiberoptic illumination and sophisticated imaging. It is clear that most orbital fractures can be visualized satisfactorily and repaired with surgical approaches without the use of endoscopic techniques. However, endoscopic endonasal visualization may be useful for the repair of more complex fractures involving the superior and posterior medial orbit. Its major benefit is no external incision. On the other hand, prolonged operative time, a need for an additional set of operative instruments, poor visualization from bleeding, difficulty in placing an implant of adequate size through the nose for larger fractures (therefore requiring use of nasal packing for several weeks to maintain reduction of the herniated contents), leakage of cerebrospinal fluid, and injury to extraocular muscles or the optic nerve are among some of the disadvantages of this procedure.
Controversy exists on whether an implant should be placed over medial wall defects. Several case reports in the literature support the use of various rigid materials to close the bony defects associated with medial wall fractures. However, an informal survey of several other oculoplastic surgeons suggests that they would rarely place a rigid implant over an isolated medial wall fracture during repair. This is because of the small risk of impingement on the optic nerve with these implants, along with the associated risks of extrusion and infection.