Determination of disease type is the first step in creating a customized plan for orbital decompression. Clinical examination and orbital imaging both aid to categorize a patient’s disease as fat or muscle predominant. As stated before, many patients may demonstrate expansion of both tissues. Patients with fat predominant disease typically have more proptosis, and reduced rates of diplopia and compressive optic neuropathy as compared to patients with muscle predominant disease [14]. Furthermore, patients with fat predominant disease generally have reduced resistance to retropulsion. On CT scan, proptosis is observed without substantial enlargement of extraocular muscles. In such patients, isolated fat decompression can significantly reduce axial proptosis with minimal risk of consecutive diplopia. Heterogenous fibrosis of orbital fat may influence the decompressive effect; however, this has not yet been fully elucidated. Figure 11.2 demonstrates the computed tomography (CT) scan of a patient with fat predominant disease. Notably, the extraocular muscles appear to be of normal caliber on imaging. This patient underwent bilateral orbital fat decompression, with significant improvement in proptosis and symptoms of exposure keratopathy. An improvement in inferior scleral show was also noted, thus obviating the need for lower lid retraction repair (Fig. 11.2c, d). In cases where fat decompression alone is not sufficient to achieve the desired degree of proptosis reduction (for example in cases with significant fibrosis of fat or severe proptosis), it can be combined with bony decompression of the lateral orbital wall for additional proptosis reduction with minimal postoperative risk of diplopia.

In cases of muscle predominant disease, fat decompression is rarely used as an isolated procedure to decompress the orbit. This is due to the fact that fat decompression may be more technically challenging due to minimal fat expansion, variable fibrosis of fat, potentially increased risk for muscle injury due to enlargement, and propensity for bleeding related to increased orbital congestion and dilation of vasculature. Therefore in these cases, removal of bone is generally always performed in the stepwise approach as listed in Table 11.1, while also taking into consideration the individualized factors in Fig. 11.1. If the patient has no preoperative diplopia and mild to moderate exophthalmos (less than 6 mm), fat and lateral wall (including deep, lateral orbit) decompression is a preferred surgical approach as it provides excellent proptosis reduction while minimizing postoperative diplopia. In cases of severe exophthalmos (greater than 6 mm) where “maximal” axial proptosis reduction is required, one may consider additional decompression of the medial wall despite the increased risk for diplopia. Although this modified “3 wall” (balanced bone and fat) decompression poses an increased risk for diplopia compared to lateral and fat decompression, the risk appears to be less than traditional 3 wall bony decompression of the orbital floor, medial and lateral walls [13]. Furthermore, sparing of the anterior orbital strut provides a “ledge” for the globe, preventing inferomedial globe dystopia [15].

If additional axial proptosis reduction is required, removal of the deep portion of the frontal bone in the superolateral orbit can be performed to maximize the decompressive effect, as shown in the CT scan in Fig. 11.3. This can also be performed through an eyelid crease incision during standard lateral decompression, obviating the need for craniotomy. In this manner the bone surrounding the superior orbital fissure (greater wing of sphenoid and frontal bones) can be removed in entirety baring dura and substantially expanding orbital volume.