Silent Sinus Syndrome

Etiology and Pathophysiology

• Silent sinus syndrome (SSS) is characterized by spontaneous, progressive enophthalmos and hypoglobus due to atelectasis of the maxillary sinus. This occurs in the absence of sinonasal symptoms.
• The initial insult is obstruction of the maxillary sinus ostium within the osteomeatal complex.¹ This is usually due to the lateral displacement of an inflamed medial infundibular wall.²  
• Although it was initially thought that preexisting hypoplasia of the maxillary sinus was the culprit, case reports have described patients with normal sinus anatomy on imaging prior to developing SSS, ruling out existing sinus abnormality as the cause of the disease.³
• As trapped air along with the aqueous component of the maxillary sinus secretions are resorbed, sinus pressure drops and becomes subatmospheric.^2,3
• This chronic negative pressure causes sinus walls to bow inward. The orbital floor, being the thinnest sinus wall, descends most prominently, expanding the orbital volume and leading the globe and orbital fat to redistribute posteriorly and inferiorly, manifesting as enophthalmos and hypoglobus.^4,5
• CT scans have shown the orbital floors of patients with silent sinus syndrome to be thinned and demineralized, possibly secondary to reduced osteoblastic activity in the chronically inflamed sinus, making it more likely for the bone to collapse downward.^6,7

Epidemiology

• The most comprehensive epidemiologic data derive from the systematic review by Michelle et al., including 153 articles and 558 patients.⁸
• The condition predominantly affects adults in the third to fifth decades of life (mean age 38.8 ± 14.1 years; range 7–76).⁸
• There is a slight male predominance (44.1% male vs. 39.6% female).⁸
• Among cases with documented laterality, right-sided disease is slightly more common (39.1% right, 31.0% left).⁸
• SSS is almost exclusively unilateral. Bilateral disease accounts for only 2.5% of cases.⁸
• Vahdani et al. described a case of sequential SSS, initially on the left side, followed by the right side years later.⁹
• The majority of cases are idiopathic.
• A post-traumatic SSS variant, namely due to orbital floor and medial wall fractures, may present months to years after the inciting injury.¹⁰
• Rose et. al reported six patients who suffered from SSS after undergoing orbital decompression for thyroid eye disease. They suggest that the orbital fat displaced from decompression occluded the maxillary sinus os.¹¹

Signs and Symptoms

Patients typically present to an ophthalmologist rather than an otolaryngologist,¹² as orbital findings dominate and sinonasal symptoms are by definition absent. A high index of suspicion for SSS should be maintained in any patient with spontaneous, unexplained enophthalmos.

• Time course
• Silent sinus syndrome is a gradual process, with signs and symptoms typically developing over weeks to months (average 4 to 8 months).^4,7,13
• Authors have reported symptoms occurring from “overnight” to as long as 2.5 years.⁷
• Ocular symptoms:
• The hallmark presentation is spontaneous, progressive, painless enophthalmos, present in 79.1% of cases (mean 2.67 ± 1.39 mm), with accompanying hypoglobus in 71.2% (mean 2.22 ± 1.43 mm).⁸
• Hollow superior sulcus, due to expansion of orbital volume and orbital fat redistribution.
• Upper eyelid pseudoretraction (in 90% of patients), due to descent of the globe.⁷
• Diplopia, in 36.3% to 65% of cases.^8,14
• Blepharoptosis, rarely.¹⁵
• Other symptoms:
• Facial pressure (in 29.3% of patients).⁸
• Headache (7.0% of patients).⁸ 
• However, significant symptomatic sinonasal disease, by definition, excludes the diagnosis of SSS in favor of chronic maxillary atelectasis, a similar but distinct entity.

Imaging

• CT of the orbits and paranasal sinuses is the diagnostic imaging modality of choice and is required to confirm SSS. Characteristic findings include:
• Ipsilateral maxillary sinus shrinkage (aka maxillary sinus atelectasis).¹⁴
• Collapse, or inward bowing of at least one of the maxillary walls was present in 92.2% of CT studies in a large review.⁸
• The orbital floor is typically inferiorly displaced, which produces enophthalmos and hypoglobus.
• Rarely, the ipsilateral ethmoid sinus can also collapse.⁴
• Expansion of the pterygopalatine fossa.⁴
• Due to collapse of the posterolateral wall of the maxillary sinus. 
• Ipsilateral maxillary sinus opacification.
• In a large review, complete opacification was noted in 18.4% and partial in 7.1% of CT studies.8 These sinus contents are sterile.^11,9
• Thinned and demineralized sinus walls.⁴
• From chronic negative-pressure bone remodeling.⁷
• Rose et al. also explains that later in the disease process, chronic inflammation may lead to local hyperostosis.⁷
• Nasal septal deviation to the affected side.^4,7,16
• Associated in 32% to 83% of cases; may contribute to ostial obstruction.

• Idiopathic cases, without identifiable structural or historical risk factors, constitute the majority of SSS cases.
• The primary risk factor for SSS is an abnormal nasal anatomy, causing predisposition to osteomeatal complex obstruction. This includes:
• Ipsilateral nasal septal deviation.^4,7,16
• Laterally deviated middle turbinate towards the osteomeatal complex of the affected side.^4,16
• Narrowed infundibular passage.²    
• Prior orbital fractures constitute a distinct risk factor for post-traumatic SSS.
• Patients suffered from orbital floor fractures, with few patients also sustaining a medial wall fracture.¹⁰ Brown et al. reported 6 cases from a single institution, who presented three to 16 months following orbital trauma.¹⁷ Wladis et al. further documented 20 cases of post-traumatic SSS, with presentation ranging from 3 months to 30 years after the initial trauma (mean 6.34 years).¹⁰
• In vein with “regular” SSS, orbital blowout or floor fractures are believed to cause obstruction of the maxillary ostium, negative sinus pressure, and subsequent collapse of the sinus walls.¹⁷
• Patients have been noted to develop SSS after bony orbital decompression for thyroid eye disease.¹¹
• Prolapsed orbital fat into the ethmoidal infundibulum during surgery may occlude the maxillary sinus os. Removal of the inferomedial strut during surgery may accentuate this risk.^7,11 In their series of six patients with post-decompression SSS, Rose et al. found that when antral implosion had occurred, the strut was absent and the infundibulum was occluded.¹¹ Some authors recommend performing a concurrent prophylactic middle meatal antrostomy with orbital decompression if the bone strut is to be removed, in order to prevent future obstruction.⁷

• Orbital floor fracture / post-traumatic enophthalmos
• However, late-onset post-traumatic SSS may complicate this distinction. In such cases, CT scans should demonstrates the characteristic sinus atelectasis with inward wall bowing.
• Congenital enophthalmos
• Due to congenital maxillary sinus hypoplasia, or craniofacial anomalies.
• Chronic maxillary atelectasis
• CMA and SSS share identical imaging features but differ in symptomatology. CMA patients report significant sinonasal symptoms (nasal congestion, rhinorrhea, facial pain, headaches), often with a history of chronic sinusitis or prior sinonasal trauma. SSS patients have no sinonasal symptoms by definition.
• Fibrosing Orbital Metastasis
• Most commonly metastatic breast carcinoma
• Parry-Romberg Syndrome
• Mucocele
• Post-Decompression Enophthalmos

• Observation is reasonable for minimal or subclinical deformity without functional complaint.¹⁸
• If there is clinical enophthalmos and/or hypoglobus, management of SSS is primarily surgical, aiming to restore maxillary sinus ventilation and correct of orbital volume and floor position. This is achieved through functional endoscopic sinus surgery (FESS) and orbital floor reconstruction (OFR), respectively. The central management decision is whether to combine these procedures or stage them, and whether OFR is required at all.
• Of note, the maxillary antrostomy was initially performed through a Caldwell-Luc approach,¹⁹ but preference has since shifted to an endoscopic technique.
• Functional Endoscopic Sinus Surgery (FESS)
• FESS should be performed in all patients as the initial step. The procedure typically comprises uncinectomy and maxillary antrostomy, creating a nasoantral window that equalizes sinus pressure, arrests further atelectasis, and restores sinus drainage. If a lateralized middle turbinate is present, it can be trimmed and medialized to prevent re-occlusion of the maxillary ostium.¹⁶ FESS was employed in 87% of patients in the largest systematic review.⁸
• Of note, penetration of the lamina papryacea might occur in cases with altered uncinate process anatomy, and care should be taken to avoid this.¹²
• By releasing the subatmospheric sinus pressure, FESS may permit some degree of spontaneous elevation of the orbital floor as the sinus expands. Thus, for mild enophthalmos without significant hypoglobus or diplopia, FESS alone may be sufficient.
• In a volumetric analysis of 13 patients who underwent endoscopic antrostomy alone, maxillary sinus volume increased by 9.8% and orbital height decreased by 5.7%, with clinical and/or radiographic resolution of enophthalmos and globe displacement in all patients.²⁰ 
• Thomas et al. reported that of 4 patients treated with FESS alone, 2 achieved complete resolution of enophthalmos, while 2 required second-stage orbital floor reconstruction (OFR).²¹ In another series of 14 patients with SS who underwent FESS, only two required further OFR.¹⁶ In their review, Brandt et al. noted that 34% of patients received FESS only.¹⁴ After endoscopic maxillary antrostomy, the range of reduction in enophthalmos is on average 1–2 mm.²¹
• However, FESS alone has limited efficacy for significant enophthalmos. In Wladis et al.’s post-traumatic SSS series, only 14.2% (1 of 7) of patients treated with FESS alone achieved complete resolution of enophthalmos, with a mean improvement of 1.0 mm (from 2.86 to 1.93 mm). In contrast, 76.9% (10 of 13) of patients undergoing combined FESS and OFR achieved complete globe position symmetry, with a mean improvement of 3.0 mm (from 3.42 to 0.39 mm; p = 0.00028).¹⁰
• Orbital Floor Reconstruction (OFR)
• OFR is recommended if there is clinically significant enophthalmos and/or hypoglobus, or is there is failure of adequate globe repositioning after FESS alone.
• The technique for orbital floor reconstruction is similar to that for orbital fracture repairs. The orbit is typically approached via a transconjunctival incision, with or without lateral canthotomy for wider exposure. Subperiosteal dissection exposes the inferior orbital wall, and an implant is placed to restore the floor to its pre-disease position, repositioning the globe.
• Some authors always repair the orbital floor,⁷ while others recommend waiting six months after FESS to evaluate whether ORF is necessary.¹⁶
• Rose et al. have surgically managed SSS with orbital surgery alone, placing a silicone block subperiosteally on the orbital floor.⁴ They warn that if the silicone is not carefully shaped to rest on healthy bone in addition to the bowed orbital floor, the implant may sink out of position.⁷
• A single-stage approach, combining endoscopic antrostomy and orbital floor reconstruction, has also been reported with good outcomes.^6,22,23 In one of the largest SSS reconstruction, Clarós et al. performed simultaneous FESS with OFR in 13 patients, and  reported significant correction of enophthalmos (mean 2.6 mm) and hypoglobus (2.7 mm).²⁴ In 2025, Shoji et al. reported 12 patients who underwent simultaneous FESS with OFR.¹⁸ Compared to patients who were treated with observation, or sinus surgery alone, these patients had significantly worse enophthalmos and hypoglobus, and had excellent outcomes after combined surgery.¹⁸ The authors argue that this combined technique can reduce the time and morbidity associated with a second surgery.
• No head-to-head comparison of implant materials for orbital reconstruction specifically within SSS exists. Here are materials used for this purpose reported in the literature:
• Porous polyethylene (Medpor).^{11,14,17,18,21,23}
• Titanium mesh.^14,25
• Titanium-Medpor composite.^13,17,24 
• Shaped silicone implant.^4,7,16 Some authors have seen late implant sinking between 3-7 years postoperatively with recurrent enophthalmos, and now anchor the implant against bone to prevent this.⁷
• Autologous bone (nasal septal cartilage, maxillary bone, iliac crest).^6,19
• To summarize, if there is no functional or cosmetic deficit, observation alone may suffice. If there is mild globe dystopia, enophthalmos, or hypoglobus, FESS alone can be performed, and globe position can be reassessed postoperatively. For patients with marked or symptomatic enophthalmos and/or hypoglobus, combined sinus surgery with orbital reconstruction should be considered.
• Hyaluronic acid gel (HAG) injection
• Mavrikakis et al. described one patient with 2mm of enophthalmos but no hypoglobus six months after endoscopic antrostomy for SSS. The patient received two milliliters of HAG in the intraconal space with resolution of enophthalmos. The patient had transient diplopia after the injection which resolved within 30 minutes.²⁶

Follow-Up

Follow-up in SSS should focus on confirming maxillary sinus re-aeration, monitoring globe position for adequacy of correction or late relapse, and if orbital reconstruction was performed, surveillance for implant-related complications. 

• If a FESS was performed, the patient should also be followed by an otolaryngologist to confirm patency of the maxillary antrostomy.
• Persistence of sinus opacification, or failure of the sinus to re-expand should prompt reconsideration.
• In terms of oculoplastic follow up, serial measurements of enophthalmos and hypoglobus should be obtained.
• If sinus surgery alone was performed, the postoperative assessments help decide whether orbital reconstruction is still needed. As discussed above, certain authors recommend waiting 6 months after FESS before considering OFR. 
• Recurrence of sinus obstruction should be excluded in any patient with postoperative progression of enophthalmos.
• Repeat CT can be obtained if clinically indicated, e.g., inadequate globe correction, suspected implant malposition, recurrent sinus opacification, or planning of staged reconstruction. 

The overall complication rate of SSS treatment is low. Michelle et al. reported adverse events in 11 of 146 patients (7.5%) across the systematic review.⁸ Wladis et al. reported no intra- or postoperative complications in either the FESS-alone or combined groups.¹⁰

• FESS-Related Complications
• Acute sinusitis (n=3 in systematic review).⁸
• Nasolacrimal duct obstruction.⁸
• OFR-Related Complications
• Lower eyelid retraction. Less common with the transconjunctival approach compared to the transciliary approach.⁸
• Transient diplopia. Typically resolves within weeks. Persistent diplopia warrants implant repositioning or resizing.⁸
• Overcorrection with exophthalmos.¹⁸ The staged approach theoretically mitigates this risk by allowing for sinus expansion and orbital improvement to plateau before OFR.
• Persistent enophthalmos. Residual enophthalmos after OFR may require revision.
• Implant extrusion or infection.

When SSS is undiagnosed, misdiagnosed, or untreated, progressive orbital and ocular complications may develop.

• Progressive Enophthalmos and Hypoglobus
• Delay in diagnosis, and more severe orbital floor descent, may amplify the reconstructive challenge.
• Lagophthalmos and Ocular Surface Disease
• Liss et al. reported the case of a 56-year-old man who was referred for tarsorrhaphy to treat recurrent bilateral corneal ulceration and central corneal thinning, and was found to have bilateral SSS as the underlying etiology.²⁷
• Diplopia
• Wladis et al. reported that all 6 patients with preoperative diplopia in their cohort achieved complete resolution of symptoms after combined FESS and ORF.¹⁰

Montgomery first described this phenomenon in 1964 in two cases of diplopia and enophthalmos associated with collapse and opacification of the ipsilateral maxillary sinus.²⁸ Later, Blackwell helped refine our understanding of this entity, suggesting that chronic maxillary hypoventilation and negative pressure resulted in the inward collapse of the maxillary sinus walls.²⁹ The term “silent sinus syndrome” and was formally coined by Soparkar et al. in 1994.¹ The alternate name “imploding antrum syndrome,” introduced by Rose et al. in 2003, captures the disease’s pathophysiology of negative sinus pressure leading to collapse of the sinus walls with descent of the orbital floor.⁴

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