Medial Wall Orbital Fracture Treatment & Management
- Author: Aftab Zafar, MD; Chief Editor: Hampton Roy, Sr, MD more...
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 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 polyethylene, nylon foil, Gelfilm, 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[14, 15] 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.[16, 17] 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.
Any surgery deep within the orbital cavity is fraught with potential complications. 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.
Outcome and Prognosis
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.
Future and Controversies
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.
The use of endoscopy in the repair of these fractures has been demonstrated and is becoming more popular 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, 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.
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