Enophthalmos in silent sinus syndrome.

[FIGURE 1 OMITTED]

Spontaneous unilateral enophthalmos with asymptomatic sinus disease was first described by Montgomery in 1964. (1) Soparkar et al introduced the term silent sinus syndrome in 1994. (2) The primary predisposing factor is an obstruction of the osteomeatal complex that leads to a hypoventilated maxillary sinus. Consequently, there is resorption of gases into the sinus capillaries, which creates a negative pressure. This negative pressure within the maxillary sinus, which has been demonstrated in animals and humans, (3-6) leads to a pressure-induced osteopenia and bone thinning, which ultimately causes an inward retraction of the maxillary sinus walls. (5-7)

Silent sinus syndrome is most common in the third and fifth decades of life; there is no predilection for either sex. (2,4,8) Patients typically are asymptomatic; when symptoms do occur (i.e., enophthalmos and associated inflammatory disease), the condition is called chronic maxillary atelectasis. (7) In this condition, the enophthalmos, which is the predominant finding, occurs secondary to a collapse of the orbital floor. (9) Other physical findings include upper-eyelid retraction, deepening of the superior orbital sulcus, loss of fat in the lower eyelid, and malar depression. (2-4) Widening of the middle meatus and ipsilateral retraction of the middle turbinate toward the affected side are seen on endoscopy. (10)

The imaging findings in patients with silent sinus syndrome are characteristic and essential for its diagnosis. Most of these findings have been described on computed tomography (CT), although magnetic resonance imaging is also performed. One finding that is always present is a fully developed, partially or completely opacified maxillary sinus with associated bony changes. (8-10) In order for enophthalmos to occur, retraction of the orbital floor is necessary; the retraction leads to an increase in orbital volume. The orbital floor is usually thinned and can actually demonstrate complete resorption. The other orbital walls can be thinned, thickened, or normal, and the degree of internal retraction is variable. (4,8-10) Other findings include occlusion of the maxillary sinus infundibulum (secondary to retraction of the uncinate process against the inferomedial orbital wall), an enlarged middle meatus with lateral retraction of the middle turbinate, deviation of the nasal septum, and an increase of adipose tissue in the pterygomaxillary fossa. (2,3,8,10)

[FIGURE 2 OMITTED]

We evaluated a 59-year-old man whose chief complaint was progressive facial asymmetry of approximately 3 months' duration. He denied any symptomatology or history of inflammatory sinus disease. Physical examination revealed left enophthalmos, deepening of the superior orbital sulcus, loss of the lower-eyelid fat, and malar depression (figure 1). CT findings included complete opacification of the left maxillary sinus, inward retraction and thinning of all sinus walls, enophthalmos, increased orbital volume, occlusion of the maxillary sinus infundibulum, an enlarged middle meatus with lateral retraction of the middle turbinate, and an increase in pterygomaxillary fossa adipose tissue (figure 2).

Differential diagnoses that should be considered in patients with asymptomatic enophthalmos are Parry-Romberg syndrome (facial hemiatrophy), linear scleroderma, metastasis, osteomyelitis, atrophy of the orbital contents, orbital varix, chronic sinusitis, cysts, and pseudoenophthalmos, among others. (2,4,9) As previously mentioned, imaging is essential for the adequate diagnosis of the disease process.

The main treatment goals are to relieve the osteomeatal obstruction, decompress the maxillary sinus, and repair the cosmetic defect. A two-stage approach has been used that entails giving the enophthalmos an opportunity to spontaneously resolve. If a significant cosmetic defect persists after several months of osteomeatal decompression, reconstruction of the orbital floor is performed. (4,7) Our patient underwent endoscopic uncinectomy, opening of the maxillary sinusostium, and orbital floor repair with alloplastic material. A follow-up clinic visit 6 months postoperatively demonstrated a near-complete resolution of the physical findings.

References

(1.) Montgomery WW. Mucocele of the maxillary sinus causing enophthalmos. Eye Ear Nose Throat Mon 1964;43:41-4.

(2.) Soparkar CN, Patrinely JR, Cuaycong MJ, et al. The silent sinus syndrome. A cause of spontaneous enophthalmos. Ophthalmology 1994;101(4):772-8.

(3.) Hourany R, Aygun N, Della Santina CC, Zinreich SJ. Silent sinus syndrome: An acquired condition. AJNR Am J Neuroradiol 2005; 26(9):2390-2.

(4.) Annino DJ Jr., Goguen LA. Silent sinus syndrome. Curr Opin Otolaryngol Head Neck Surg 2008; 16(1):22-5.

(5.) Vander Meer JB, Harris G, Toohill RJ, Smith TL. The silent sinus syndrome: A case series and literature review. Laryngoscope 2001;111(6):975-8.

(6.) Soparkar CN, Patrinely JR, Davidson JK. Silent sinus syndrome-new perspectives? Ophthalmology 2004;111(2):414-15; author reply 415-16.

(7.) Eloy JA, Jacobson AS, Elahi E, Shohet MR. Enophthalmos as a complication of rhinoplasty. Laryngoscope 2006;116(6):1035-8.

(8.) Rose GE, Sandy C, Hallberg L, Moseley I. Clinical and radiologic characteristics of the imploding antrum, or "silent sinus" syndrome. Ophthalmology 2003;110(4):811-18.

(9.) Burroughs JR, Hernandez Cospin JR, Soparkar CN, Patrinely JR. Misdiagnosis of silent sinus syndrome. Ophthal Plast Reconstr Surg 2003;19(6):449-54.

(10.) Illner A, Davidson HC, Harnsberger HR, Hoffman J. The silent sinus syndrome: Clinical and radiographic findings. AIR Am J Roentgenol 2002;178(2):503-6.

Juan Gomez, MD; Fernando Gomez Villafane, MD; Enrique Palacios, MD, FACR 

From the Department of Radiology, Tulane University Hospital and Clinic, New Orleans (Dr. Gomez and Dr. Palacios), and the Department of Radiology, Diagnostico Medico DIME, Cali, Colombia (Dr. Gomez Villafane).