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A 63 year-old woman with enophthalmos
Digital Journal of Ophthalmology 2005
Volume 11, Number 12
July 10, 2005
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Michelle Yao | University of Wisconsin
Mark Lucarelli, M.D. | University of Wisconsin
Diagnosis and Discussion
Soparkar and colleagues (1) described a clinical phenomenon that consisted of the asymptomatic, unilateral, and spontaneous enophthalmos and hypoglobus, unrelated to local tumor or systemic diseases, in 14 patients at mean age of 37. The characteristic radiological manifestations of the silent sinus syndrome include dramatic thinning or complete resorption of the orbital floor with downward migration of the orbital contents. There were also various degrees of smooth inward bowing or implosion of the antral walls, of which attenuation of the medial wall occurred in 71%, of the posterior wall in 43%, of the anterior wall in 29%, and of the lateral wall in only one patient of the total of 14 patients. They hypothesized that a unilateral mild to moderate maxillary sinus hypoplasia in sinus development in such patients along with some event or combination of events could cause temporary obstruction of the maxillary sinus ostium. Continuous mucoid secretion with hormonal and local influences may result in maxillary bone remodeling. They thus coined the term “silent sinus syndrome.” In a subsequent report, Soparker and Patrinely’s (4) group documented negative maxillary sinus pressure.
Rose et al (2) applied the term “imploding antrum syndrome” to describe 14 patients with mean age of 41 years who presented with the very characteristic clinical features similar to those reported by Soparkar et al (1). They reported average enophthalmos being 2.8 mm compared with 3.0 mm in the Soparkar series, and a mean hypoglobus of 2.2 mm compared with 3.4 mm. The concavity of maxilla walls including medial, posterolateral, and/or anterior was universally present, with anterior walls absent in 2 of 14 patients. However, this series showed various changes in the maxillary walls—with thickening, generalized thinning, or focal loss of bone. This study also demonstrated that, in 10 of 14 patients, nasal septal deviation occurred toward the involved side. This contrasted to Soparker and Patrinely’s (5) updated series in which only 32% of patients had deviations towards the affected side. There were abnormalities of the ipsilateral middle turbinate and osteomeatal complex. Interestingly, where the posterolateral maxillary wall was affected, there was a concomitant increase in the fat content in the pterygopalatine fossa. They preferred the term “imploding antrum syndrome” to “silent sinus syndrome”.
Rose et al (3) recently proposed a hypothesis to explain the underlying pathophysiology for iatrogenic and idiopathic “imploding antrum” (silent sinus) syndrome. They described features and treatment of late enophthalmos in six patients who underwent three-wall orbital decompression for thyroid eye disease. All six patients had a satisfactory degree of decompression in the early postoperative period. However, over a few months after surgery, they experienced enophthalmos and hypoglobus. Two patients had a clear history of ipsilateral sinusitis shortly before the onset of enophthalmos. Radiologically, 5 of 6 patients displayed inward bowing of the posterolateral antral wall. There was occlusion of the ethmoidal infundibulum by prolapsed orbital fat, with secondary opacification of the maxillary antrum in all six patients. In the unaffected maxillary antrum of all 6 patients, aeration was present, and the unoperated walls were normal. When the maxillary-ethmoidal interface was intact, the ethmoidal infundibulum was found to be patent with normal maxillary antral aeration. When there was prolapse of orbital fat into the ethmoidal infundibulum obstructing aeration of the maxillary antrum, drainage of sinus secretions into the middle meatus was blocked, and the opacification of the sinus ensued. With ongoing resorption of antral fluid, pressure in the sinus might become sub-atmospheric, resulting in downward movement of the orbital floor producing secondary enophthalmos and hypoglobus. Inferior soft tissue prolapse further blocks antral drainage and worsens aeration. The impact of the long-standing subatmospheric pressure within the maxillary sinus may lead to implosion of the other walls of the sinus. This process may eventually stabilize when the antral walls have undergone maximal remodeling.
During orbital decompression, it is critical to retain the maxillo-ethmoidal interface (inferomedial bone strut). Retaining the maxillo-ethmoidal strut also helps prevent large inferomedial displacement of the globe following orbital decompression. In the event that the bone strut is removed, medial antrostomy should be considered.






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