Secondary Orbital Reconstruction

Background

Persistent enophthalmos and diplopia following primary orbital reconstruction lead to unsatisfactory aesthetic and functional outcomes, respectively. Diplopia after surgical repair of orbital fractures has been reported in 8%–52% of patients, while clinically significant enophthalmos has been reported in 27%. Large combined medial wall and orbital floor fractures tend to carry a higher risk of enophthalmos, particularly if the fracture compromised the inferonasal bony strut support. Secondary orbital reconstruction has traditionally been seen as extremely challenging, and keys to success are careful preoperative planning, appropriate imaging and identifying which patients are most likely to benefit from surgical treatment.

Changes in orbital volume as small as 2.1–2.3 mL have been shown to result in clinically significant globe malposition. Suboptimal reduction of orbital fractures in the acute setting results in increased orbital volume and in both secondary enophthalmos and diplopia. Symptoms may present in a delayed fashion, as a poorly fixed implant becomes displaced or changes in orbital anatomy after trauma are not considered properly. For instance, if the posterior bony orbit remodels following trauma, the retrobulbar volume may increase; the orbital fat is frequently repositioned posteriorly, further compromising support of the globe. Such anatomic reasons for globe malposition tend not to improve, and frequently worsen, over time following inadequate primary reconstruction.

Persistent diplopia following orbital fracture repair may be broadly categorized into either restrictive or paralytic etiologies. Poor primary reduction may lead to increased orbital volume and muscle impingement. Developing adhesions surrounding the implant and implant displacement may also restrict muscle movement. Such anatomic causes of symptoms result in restrictive strabismus and most often improve with revision surgery. Conversely, paralytic diplopia secondary to neuromuscular injury will not benefit from reoperation, although symptoms tend to improve over time with conservative management which depends upon nerve regeneration.

Clinical Presentation

Patient history and physical examination should include all details relevant to any orbital trauma patient. Specific details pertinent in secondary reconstruction include a thorough understanding of prior reconstructive procedures, and a timeline of presentation of symptoms. Operative reports should be obtained if possible, detailing surgical approaches, incision choice, and implant type. An understanding of how symptoms have been changing over time may lend clues to the etiology. Diplopia that has been improving very slowly suggests neurogenic causes; new onset symptoms that have worsened since primary repair are more suggestive of a restrictive process.

Compared to patients with acute orbital trauma, those who have undergone prior repair warrant a more thorough eye examination. Patients should be referred for strabismus evaluation by an extraocular muscle specialist. A detailed extraocular motion exam may help differentiate between restrictive and paralytic symptoms, as the latter is unlikely to improve with repeat surgery. Additionally, accurate measurements of the relative position of orbital rims, lateral, and medial canthi, and pupils should be taken. An exophthalmometer may be used to measure globe position relative to the lateral orbital rim, or the ear canal if necessary ( Fig. 3.7.1 ).