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Silent sinus syndrome is a condition in which chronic asymptomatic maxillary sinus disease presents with spontaneous unilateral enophthalmos and hypoglobus.1 Patients have inferior displacement of the orbit due to a downward bowing of the orbital floor and atelectasis of the maxillary antrum. Although the underlying maxillary sinus pathology is “silent” it has been suggested recently that “imploding antrum” more closely describes the acute nature of maxillary sinus collapse that occurs in the majority of cases.2 We present a typical case that appears to have been related to previous nasotracheal intubation.
A 27 year old woman was referred to ophthalmology outpatients complaining that her left eye was lower than the right and that when she looked down, she could see more of her left cheek than on the other side. She had started to notice this following an admission to hospital 6 months previously with viral meningitis. Since then, she had also experienced a “heavy blocked” feeling in the left side of her face together with some left nasal congestion. There was no history of acute sinusitis or chronic rhinosinusitis and, in particular, no history of trauma or surgery to the face—although she had had a nasotracheal intubation for a routine general anaesthetic 1 year earlier.
On examination, she had normal visual acuity and extraocular movements, but was found to have 2 mm of enophthalmos and 2 mm of hypoglobus. On subsequent review in the ENT clinic, nasendoscopy revealed a left deviated nasal septum with obstruction of the middle meatus, while the middle turbinate could not be visualised.
Magnetic resonance imaging clearly showed depression of the left orbit with thinning of the orbital floor and a marked reduction in maxillary sinus volume (fig 1). The maxillary antrum was opacified and the middle turbinate severely lateralised. The ethmoid, frontal, and sphenoid sinuses were clear.
She underwent septoplasty and functional endoscopic sinus surgery (FESS) during which a left middle meatal antrostomy was performed. Biopsies from the antrum demonstrated polypoid fibrinous and mucoid material with no viable cellular tissue. Bacterial and fungal cultures were negative.
At follow up she had reduced hypoglobus of the left eye, an improvement in the left nasal airway and resolution of facial pressure. Orbital floor reconstruction was not required.
Silent sinus syndrome generally occurs in the third to fifth decade, shows equal sex distribution, and presents with anything from 2–12 months history of enophthalmos. Other symptoms can include transient vertical diploplia, upper lid retraction, lagophthalmos, malar depression, and facial pressure.3 By definition, there is no history of acute or chronic sinusitis and no previous facial surgery or trauma.1 The amount of enophthalmos varies from 2–5 mm1 and visual acuity and extraocular movements are usually normal.4
Much speculation exists about the cause of silent sinus syndrome. The most popular theory of pathogenesis is that ostiomeatal obstruction results in reduced aeration of the antrum, causing negative sinus pressure and atelectasis.1,4–6 In the most recent review, Rose et al found that, as well as the orbital floor being drawn downwards, there was abnormal concavities in the medial and posterolateral walls of all the maxilla that could be assessed on CT scanning.2 They also describe an iatrogenic version of the disease occurring after orbital decompression.7 These relatively acute changes have led them to use the term “imploding antrum syndrome.”2
It is possible in our case that the patient’s previous nasotracheal intubation caused sufficient local damage as to occlude the ostiomeatal complex and create the conditions necessary for development of the syndrome. This supports the hypoventilation theory and also highlights the importance of careful history taking in establishing risk factors for this increasingly recognised condition.