Silent Sinus Syndrome

Silent sinus syndrome (imploding antrum syndrome) is a rare condition in which chronic maxillary sinus hypoventilation causes spontaneous, progressive collapse of the maxillary sinus walls. The result is enophthalmos, hypoglobus (inferior displacement of the globe) and facial asymmetry, without symptoms of sinusitis (such as pain, congestion and discharge).

Typical patients are 30 to 50 years (range 20 to 70), with equal sex distribution. It is unilateral in over 95 percent (bilateral cases are rare).

The mechanism is chronic obstruction of the maxillary sinus ostium or ostiomeatal complex. Causes include a variation such as an uncinate process that is atelectatic and lateralised, a retained secretion, or mucosal thickening.

Resorption of the trapped gases and mucosal oxygen absorption produce negative pressure in the sinus. This draws the thin bony walls inwards: the sinus volume decreases, with inward bowing of the posterolateral wall and the orbital floor. The orbital floor is lowered, causing the globe to sink (enophthalmos and hypoglobus) and orbital volume to increase.

It can be a complication of trauma, and is associated with chronic sinus disease and the use of nasal decongestants. It was described first as a condition of the maxillary sinus and also in the frontal sinus and ethmoid sinuses (rare).

• Painless, progressive enophthalmos (a sunken eye, about 2 to 4 mm or more) and hypoglobus (the eye appears lower), over weeks to months. It is noticed by the patient or by family and friends.
• Associated lid changes: a deepened upper lid sulcus, ptosis like appearance (pseudoptosis), and a widening of the palpebral fissure with upper lid retraction or a higher upper lid crease.
• Facial asymmetry: flattening of the malar eminence and the cheek, with a depression of the infraorbital region.
• Diplopia (vertical, in about 10 to 20 percent), and sometimes visual symptoms of pseudoptosis.
• Absence of sinus symptoms: no facial pain, nasal obstruction, discharge or fever; occasionally mild facial pressure and a sense of cheek fullness or numbness.
• Nasal examination: lateralisation of the uncinate process, and a retracted lateral nasal wall, with a narrow middle meatus (endoscopy may show a lateralised uncinate process and a retracted posterior fontanelle); the nasal cavity appears widened.
• Normal visual acuity, and no proptosis or inflammation.

• Clinical diagnosis based on the triad: spontaneous enophthalmos, hypoglobus, and facial asymmetry, in the absence of sinusitis, trauma or previous surgery; measure using Hertel exophthalmometry (a difference of at least 2 mm).
• CT of the sinuses and orbits (axial and coronal, thin cuts; the diagnostic standard) shows:
  • opacified, small maxillary sinus with inward bowing of the walls (the antral walls retracted)
  • the orbital floor lowered and enlarged orbital volume
  • a lateralised uncinate process with obstruction of the infundibulum
  • an enlarged nasal cavity (an increased nasal-cavity-to-sinus ratio)
  • often a mucocele like content
  The sinus appears as a "pseudo atrophic" opacity without an air fluid level or bone erosion. Compare with the contralateral side.
• Ophthalmologic evaluation: visual acuity, ocular motility, diplopia assessment, and exophthalmometry.
• Nasal endoscopy for the middle meatus, uncinate process lateralisation and the maxillary ostium.
• Rule out other causes of enophthalmos: orbital blowout fracture, orbital tumour with scirrhous reaction (metastatic breast carcinoma), Parry-Romberg syndrome, atrophy of the orbital fat, chronic invasive fungal sinusitis, and vasculitis; MRI if there is a doubt (the normal sinus content in an imploding sinus is low signal).

• Surgical correction is the definitive therapy and aims to restore sinus ventilation, stop further collapse, and, if needed, reconstruct the orbital floor.
• Functional endoscopic sinus surgery (FESS) with uncinectomy and a wide middle meatal antrostomy re-establishes ventilation and drainage of the maxillary sinus. Uncinate removal exposes the infundibulum. The ostium is then enlarged with the retrograde removal of the posterior fontanelle, and the sinus contents are cleared. It is an under-the-microscope or endoscopic approach under general anaesthesia.
• The goals are re-aeration of the sinus and stabilisation, which usually halts progression. In some cases (about 20 to 30 percent over months) it permits spontaneous partial re-expansion of the orbital floor and resolution of the enophthalmos, with improved diplopia.
• Orbital floor reconstruction is indicated for persistent enophthalmos (above 2 mm) or hypoglobus and diplopia after sinus ventilation (usually at 3 to 6 months after endoscopic sinus surgery). It is done simultaneously in some.
• Techniques include placement of an implant (porous polyethylene, titanium mesh, or autologous bone or cartilage graft) through a subciliary or transconjunctival incision, or the endoscopic transantral approach, to restore the orbital volume and floor position. Caldwell-Luc is not recommended.
• Observation: for patients with minimal asymmetry and no functional disturbance, with endoscopic surgery to stop progression recommended in most.
• Perioperative care: saline nasal irrigation, topical nasal steroid (mometasone 50 micrograms per spray, 2 sprays in each nostril daily), and antibiotics for infection (amoxicillin clavulanate 625 mg three times daily for 7 to 10 days), and postoperative endoscopic debridement and follow up at 1 to 2 weeks and 6 weeks.
• Follow up: clinical and imaging, serial exophthalmometry and CT after 3 to 6 months to assess re-expansion of the sinus and orbital floor.
• Prognosis: surgery arrests the collapse, and the enophthalmos is corrected in most after floor reconstruction; recurrence of obstruction can occur if the antrostomy closes.