In deep lateral orbital decompression for thyroid eye disease (TED), the diploic space of the greater wing of the sphenoid is typically removed and the posterior table of the skull base thinned to eggshell bone over the middle cranial fossa.1 , 2 The posterior table is typically preserved as it was thought that dural exposure did not increase decompressive effect, and may, in fact, reduce decompression if the cranial contents expanded in the orbit.3
The authors hypothesize that removal of the posterior table with wide exposure of the dura of the middle cranial fossa will allow orbital expansion in the cranial fossa and allow profound decompressive effect. While the concept of wide orbitocranial exposure in the treatment of TED was originally conceived by Naffziger,4 only recently the transorbital craniotomy through the greater sphenoid wing has been shown to be technically feasible.5–7 In this study, the authors aim to understand the dynamic relationship between the orbital and cranial spaces after deep lateral and medial decompression with wide exposure of the middle cranial fossa through a minimally invasive transorbital approach.
In this cross-sectional cohort study, consecutive patients with TED who underwent extradural transorbital decompression (as depicted in Fig. 1, Video, Supplemental Digital Content 1, available at http://links.lww.com/IOP/A176) by a single surgeon (Y.W.) in Beijing, China, between January 2009 and January 2011 were screened for entry. Indication for surgery was the patient’s desire for cosmetic or rehabilitative proptosis reduction. Inclusion criteria were euthyroid state, quiescent TED for at least 6 months prior to surgery, and sufficient quality preoperative and postoperative CT scans. Exclusion criteria included prior orbital radiotherapy and inadequate data for analysis. This study protocol was approved by the Institutional Review Board of the institute for each author and is in compliance with the Health Insurance Portability and Accountability Act and all tenets of the Declaration of Helsinki.
The primary outcome measure was change in percentage of orbital and brain tissue within a predefined triangular window. Secondary outcome measures were posterior displacement of the anteriormost aspect of the temporal lobe, reduction in clinical proptosis, reduction in clinical activity score (CAS), and postoperative incidence of diplopia. Patients were assessed on clinical parameters at the preoperative and 6-month postoperative time points.
CT scanning was obtained routinely preoperatively and postoperatively at 6 months as per the operating surgeon’s (Y.W.) standard of care. Representative imaging is shown in Figure 2. Preoperative and postoperative axial CT slices in a standard soft tissue window were selected for review at the level of the superior orbital fissure immediately below the anterior clinoid process. Preoperative and postoperative slices were aligned and superimposed by aligning the sphenoid sinus, the remaining edges of the lateral orbital wall and temporal bone, and the posterior clinoid processes, and a new composite image was created.
To measure percentage area change, a triangular window was then defined and placed over the composite image with the following borders: anteriorly, the orbital surface of the lateral orbital wall in the preoperative CT, posteriorly, a horizontal line that crosses the tip of the sphenoid at the superior orbital fissure, and laterally, a vertical line that crosses the medial edge of the remaining greater sphenoid wing postoperatively (Fig. 3). The percentage area of this window occupied by orbital and brain tissue preoperatively and postoperatively was measured by 2 examiners (S.R., A.N.). The preoperative window necessarily excludes any orbital tissue from being present.
Anterior–posterior displacement of the anteriormost aspect of the temporal lobe was measured by placing a horizontal reference line at the anteriormost extent of the brain preoperatively and set at 0 mm, and a similar horizontal line in the postoperative slice; the distance between the 2 lines was measured (Fig. 4). Clinical proptosis was measured with a Hertel exophthalmometer by a single examiner (Y.W.). Clinical activity score was measured on a scale of 7 points,8 and groups were segregated into 2 categorical groups: CAS <3 and CAS ≥3, based on literature support for a threshold CAS of 3. Diplopia was evaluated according to a previously described method,9 , 10 quantified as: no diplopia (0), diplopia in extreme gaze (+), intermittent diplopia in primary and/or reading positions (++), or continuous diplopia in primary and/or reading positions (+++).
Continuous variables were tested for significance with a paired t test, and categorical variables were tested for significant with a chi-square test. Data were analyzed using Statistical Package for the Social Sciences version 22.0 (SPSS Inc., Chicago, IL) software.
Surgery was initiated through a lateral upper eyelid crease incision, with exposure of the lateral orbital rim, subsequent subperiosteal dissection, and exposure of the bony orbit from the superior to inferior orbital fissures. This was followed by removal of the sphenoid diploe to the level of the temporalis fossa periosteum and middle cranial fossa dura between the superior and inferior orbital fissures with a high-speed neurosurgical drill and rongeurs (Fig. 1). Medial decompression was subsequently performed via a transcaruncular approach, with titrated removal of the medial orbital wall and ethmoid sinus from the posterior lacrimal crest to the orbital apex, tailored to reduce any residual proptosis after the deep lateral decompression was completed. The infraorbital strut and orbital floor were left intact. The orbital periosteum was opened laterally and medially, and limited intraconal fat that prolapsed freely was removed. Care was taken to maintain intact temporalis fossa periosteum. Surgical technique for wide dural exposure is shown in the Video Supplemental Digital Content 1, available at http://links.lww.com/IOP/A176.
Data from 36 patients (60 orbits) were included in this study; 12 patients (15 orbits) were excluded for incomplete clinical data. Demographic data are summarized in Table 1. All patients underwent deep lateral and medial orbital decompression. Intraoperative dural tear with cerebrospinal fluid leak was reported in 2 orbits (3%), which was successfully repaired with fibrin glue; these patients experienced no sequelae. No other complications were noted, including infection, spontaneous orbital pulsations, postoperative hemorrhage (intracranial or intraorbital), or reactivation of disease.
For the primary outcome measure, the mean composition of the window preoperatively was 0% orbital and 44% ± 15% brain tissue, compared with 70% ± 16% orbital and 28% ± 14% brain tissue postoperatively (p < 0.001). Posterior movement of the brain was demonstrated in all but 1 orbit, with a mean displacement of 2.0 mm ± 1.3 mm (p < 0.001). Mean clinical proptosis reduction was 11.2 mm ± 3.6 mm (p < 0.001). The proportion of patients with CAS <3 compared with CAS ≥3 was not significantly different after surgery (p = 0.163). Improved diplopia was noted in 5 patients (14%), and worsening diplopia noted in 3 patients (8%), although these changes were not significant (p = 0.772). Outcomes are summarized in Table 2. Incidence of diplopia is summarized in Table 3.
In this study, the authors observed significant orbital expansion in the cranial vault after wide transorbital dural exposure through the greater sphenoid wing. This expansion is further detailed by the observed posterior displacement of the anteriormost aspect of the temporal lobe after decompression in all but 1 orbit studied. Overall, these findings suggest that wide dural exposure of the middle cranial fossa through the greater sphenoid wing may enhance decompressive effect by allowing greater volume for orbital expansion posterior to the globe.
The average reduction in proptosis in their study was 11.2 mm. Such significant proptosis reduction has only been reported previously through neurosurgical approaches,11–15 with transorbital 3-wall decompression reported to provide only 6 mm to 8 mm of proptosis reduction16–20 prior to their study. Their data suggest that the extra 2 mm to 3 mm proptosis reduction provided is directly due to the wide dural exposure performed in their study, as this is the only new variable in surgical technique. A transorbital 4-wall decompression including the orbital roof, in combination with neurosurgery, was reported to provide a mean of 13 mm of decompression,21 although this approach has been rarely used. Their study is the first study to describe such profound proptosis reduction, by orbital surgeons, through a minimally invasive eyelid crease approach, and to quantify the subsequent orbital expansion in the cranial vault postoperatively.
Tissue compliance and resting tension in the brain and orbit are affected by both surgical and disease-specific factors, and these biomechanical forces may account for the observed phenomenon. Physiologic intracranial and intraparenchymal pressures range between 5 and 10 mm Hg22 , 23 in healthy subjects, and has been shown to decrease to 3 and 4 mm Hg after limited craniectomy.23 Comparatively, orbital pressure ranges from 4 to 6 mm Hg in healthy subjects and is increased to 8 to 12 mm Hg in patients with TED.24 , 25 Brain tissue compliance increases after limited craniectomy,23 whereas orbital tissue is already significantly less compliant in TED than in control orbits.25 This altered orbitocranial balance of pressure and compliance may explain the observed posterior expansion of the orbit after wide dural exposure.
The clinical implication of these findings is compelling, in that additional decompressive effect may be gained through wide dural exposure of the middle cranial fossa as the orbit in TED appears to overcome cranial gravitational and hydrostatic forces and occupy a portion of the middle cranial fossa. Of course, the point of equilibrium between the orbit and intracranial contents may vary among patients, dependent on disease severity, fat-predominant versus muscle-predominant disease, or other factors. Further studies will be required to understand the contribution of these factors. However, the ability of the orbit to access and expand into a new anatomic space is striking and may allow for such significant proptosis reduction.
This intracranial expansion does not seem to come at the price of worsening diplopia. Postoperative imaging did not reveal any radiologically significant fibrosis, and clinical examination of ocular movements at 6 months postoperatively did not suggest an adduction or other deficit indicative of lateral rectus or orbital fat fibrosis and tethering to the dura. This may be somewhat expected as the dura is analogous to the orbital periosteum, and if left intact, does not seem to provoke an exuberant fibrotic response. Moreover, traditional neurosurgical approaches12 , 13 , 15 for decompression or removal of orbital lesions routinely leave orbital tissue in contact with the dura, to no detriment.
This study has important limitations. Reduction in proptosis with this technique compared with preservation of the posterior table is not directly compared, and the primary outcome measure is a surrogate for orbital expansion in the cranial cavity. Patients were not segregated into fat- or muscle-predominant categories, and the technique appeared to be equally applicable to both, although this should be further elucidated.
The study was also not powered to assess safety, although the risk of cerebrospinal fluid leak or other complications is quite low and may be related to surgical technique. Both orbits with cerebrospinal fluid leak were managed successfully without subsequent complications, and the 8% rate of worsening diplopia is well under the reported rate for balanced decompression, possibly due to the need for less medial decompression. However, only highly skilled surgeons comfortable with the anatomy of the deep orbit should attempt this procedure.
The data are limited by radiologic follow-up at 6 months, and long-term changes in globe position or strabismus were not studied. However, prior studies11–15 utilizing the pterional approach suggest that wide exposure of the orbit to the dura is not associated with additional complications such as progressive enophthalmos or strabismus. Finally, a single surgeon study with a homogenous population may not be generalizable to the entire cohort of thyroid patients. Future studies may directly compare proptosis reduction, assess safety and longevity, and measure orbital biomechanics including tension and compliance after wide dural exposure to better understand these forces in a more heterogeneous population.
Overall, the authors find that the orbit tends to expand posteriorly in the cranial vault after wide dural exposure of the middle cranial fossa in extradural transorbital decompression. The surgeon may be able to exploit this phenomenon in surgical rehabilitation of TED.
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