Silent sinus syndrome
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The silent sinus syndrome represents maxillary sinus atelectasis that results in painless enophthalmos, hypoglobus and facial asymmetry 1-3. Some authors restrict the term to patients with no history of sinusitis, trauma or surgery 2. Some authors suggest that is part of the spectrum of chronic maxillary atelectasis 6.
Silent sinus syndrome usually presents in the 3rd to 5th decade, without a gender predilection. In general, the condition is idiopathic. However, in a small number of patients, trauma to the lateral nasal wall and ostiomeatal complex may be the cause, e.g. endonasal intubation 1,2.
The presentation is typically with painless and usually relatively long-standing (months to years) facial asymmetry, enophthalmos of 2-5 mm, and hypoglobus 1-3. Symptoms of sinusitis are not always present 1. When there is significant deformity of the orbital floor, patients may develop diplopia. However, extraocular movements are usually normal 2.
Chronic occlusion of the maxillary sinus ostium/ostia results in gradual resorption of the air. Subsequently, negative pressure is generated within the sinus 3. This, in turn, results in gradual inward bowing of all four of the maxillary walls: roof (orbital floor), medial, posterolateral and anterior walls. Orbital volume increases with resultant enophthalmos and variable flattening of the malar eminence 1.
A number of other hypotheses have been advanced, including inflammatory erosion and softening of walls due to chronic sinusitis; or sinusitis in a hypoplastic sinus 4. However, manometric measurement in a number of cases have confirmed the presence of negative pressures, as well as proof of normal-sized sinuses on previous imaging 3 - these make the latter two hypotheses unlikely.
Although the diagnosis is usually made clinically, usually by otolaryngologists and ophthalmologists, imaging of the sinuses confirms the findings. Additionally, the diagnosis may be made incidentally on imaging of the region for other reasons.
Plain radiographs are no longer considered sufficiently sensitive or specific for the assessment of paranasal sinus disease. However, they are still not infrequently performed. The findings are the same as those seen on CT (see below).
CT, preferably performed as a volumetric acquisition with three-plane orthogonal reformats, is able to elegantly demonstrate changes in the sinus and the adjacent structures.
The sinus is fully formed but fully opacified and reduced in volume with inward bowing of all four walls. This manifests as 1:
- inferior bowing of the roof (orbital floor): increased orbital volume and enophthalmos
- lateral bowing of the medial wall: lateral displacement of the middle and inferior turbinate
- posterior bowing of the anterior wall: flattening of the malar eminence
- anteromedial bowing of the posterolateral wall
MRI is not required for the diagnosis. If it is performed, it will demonstrate (in addition to the anatomical changes above) a fully opacified sinus with thickening and enhancement of the mucosa. The secretions are of variable intensity.
Treatment and prognosis
The condition is benign but may result in diplopia. Treatment involves the creation of a drainage route for the sinus. This can be with a nasal antral window or maxillary antrostomy.
Once drainage is established, no further volume loss will develop. However, any deformity at the time of surgery will be permanent and may require surgical correction, especially if diplopia is present.
The differential is usually small. However, conditions to be considered include:
congenital maxillary sinus hypoplasia
- more common and does not present with a developing facial deformity
- post-traumatic maxillary sinus deformity
- inferior orbital decompression
- mucocele: similar process but the expansion of sinus due to build-up of secretions
- chronic sinusitis with mucoperiosteal thickening
- 1. Illner A, Davidson H, Harnsberger H, Hoffman J. The Silent Sinus Syndrome: Clinical and Radiographic Findings. AJR Am J Roentgenol. 2002;178(2):503-6. doi:10.2214/ajr.178.2.1780503 - Pubmed
- 2. Hobbs C, Saunders M, Potts M. "Imploding Antrum" or Silent Sinus Syndrome Following Naso-Tracheal Intubation. Br J Ophthalmol. 2004;88(7):974-5. doi:10.1136/bjo.2003.035386 - Pubmed
- 3. Davidson J, Soparkar C, Williams J, Patrinely J. Negative Sinus Pressure and Normal Predisease Imaging in Silent Sinus Syndrome. Arch Ophthalmol. 1999;117(12):1653-4. - Pubmed
- 4. Eto R & House J. Enophthalmos, a Sequela of Maxillary Sinusitis. AJNR Am J Neuroradiol. 1995;16(4 Suppl):939-41. PMC8332249 - Pubmed
- 5. Kilty S. Maxillary Sinus Atelectasis (Silent Sinus Syndrome): Treatment with Balloon Sinuplasty. J Laryngol Otol. 2014;128(2):189-91. doi:10.1017/S0022215113003538 - Pubmed
- 6. Mangussi-Gomes J, Nakanishi M, Chalita M, Damasco F, De Oliveira C. Stage II Chronic Maxillary Atelectasis Associated with Subclinical Visual Field Defect. Int Arch Otorhinolaryngol. 2013;17(4):409-12. doi:10.1055/s-0033-1351679 - Pubmed