Visual-field loss caused by sinusitis: a case report. (Original Article).

Abstract

The author reports a case of visual-field loss that was not characterized by any direct compression or external signs of sinus disease. The patient's hemianopia was found to be associated with severe sinusitis, which had not been clinically apparent and which had not extended beyond the bony walls of the sinuses. Following surgical drainage of the affected sinuses, the hemianopia resolved immediately and completely.

Introduction

Descriptions of visual-field loss associated with lesions that affect the sinuses have been published since before the onset of imaging. (1) Such cases were most likely associated with either destruction of the bony wall of the affected sinus or compression of the optic nerve in patients with sinusitis/sphenoethmoiditis, (2,3) mucoceles, (4) Wegener's granulomatosis, or tumors of sinusoidal origin. Optic neuropathy is thought to be caused by infective, inflammatory, compressive, neoplastic, or vascular processes. (5)

Digre et al (6) and more recently Moorman et al (7) suggested that sphenoid sinus opacification on computed tomography (CT) or magnetic resonance imaging (MRI) is a significant finding. Cadaveric studies have shown a highly variable anatomy in the relationship of the optic nerve to the posterior sphenoethmoid sinus. In some cases, the optic nerve was found to traverse the posterior air cells, which would render it particularly vulnerable to damage by infection, compression, or trauma in this part of the sinus. (8)

In this article, the author describes a case of visual-field loss in a patient who had no outward signs of sinusitis.

Case report

A 29-year-old man, an electronics engineer, experienced a sudden onset of right temporal visual-field loss. His condition was pain-free and did not involve his central vision. His visual acuity was 6/6 right and 6/5 left, he had no relative afferent pupillary defect, and his ocular movements were normal. Findings on examination of the anterior chambers and fundus were normal, as was his ocular pressure. The right temporal visual-field defect was observed on confrontation visual-field testing and confirmed by Humphrey 24-2 automated visual-field analysis (figure 1). MRI (figure 2) and CT (figure 3) detected gross bilateral sinusitis, but no evidence of a mucocele; the optic nerve was unaffected on all slides. Measurements of the complete blood count, erythrocyte sedimentation rate, antineutrophil cytoplasmic antibody (ANCA) level, and antinuclear antibody (ANA) level were all within normal ranges.

Following a course of intravenous antibiotics, endoscopic ethmoidectomy was performed 1 month following the onset of symptoms. The patient reported a complete resolution of his visual-field loss immediately after surgery. A repeat Humphrey's 24-2 visual-field analysis shortly after surgery confirmed the complete recovery (figure 4).

Discussion

This patient's extremely rapid recovery suggests that the mechanism of injury involved either vascular or direct compression that led to relative ischemia of the optic nerve immediately adjacent to the sphenoethmoid sinus (the retinotopic arrangement of axons in the optic nerve corresponds to the affected area). He had exhibited no radiologic evidence that the optic nerve had traversed the posterior air cells. The relationship between surgical intervention and the rapid recovery is highly suggestive that the patient's sinusitis was the cause of his visual-field loss.

Endoscopic nasal procedures are an effective treatment in cases where optic neuropathy is believed to have occurred secondary to sinus pathology. (9, 10) CT is mandatory because a significant percentage of MRIs in a normal population will incorrectly demonstrate sinus abnormalities. (11)

References

(1.) Loeb HW. A study of the anatomic relations of the optic nerve to the accessory cavities of the nose. Ann Otol Rhinol Laryngol 1909;18:243-73.

(2.) Awerbuch G, Labadie EL, Van Dalen JT. Reversible optic neuritis secondary to paranasal sinusitis. Eur Neurol 1989;29:189-93.

(3.) Slavin ML, Glaser JS. Acute severe irreversible visual loss with sphenoethmoiditis-'posterior' orbital cellulitis. Arch Ophthalmol l987;105:345-8.

(4.) Newton N, Jr., Baratham G, Sinniah R, Lim A. Bilateral compressive optic neuropathy secondary to bilateral sphenoethmoidal mucoceles. Ophthalmologica 1989;198:13-9.

(5.) Albert DM, Jakobiec FA. Principles and Practice of Ophthalmology. 2nd ed. Vol. 5. Philadelphia: W.B. Saunders, 1994:4176-9.

(6.) Digre KB, Maxner CE, Crawford S, Yuh WT. Significance of CT and MR findings in sphenoid sinus disease. AJNR Am J Neuroradiol 1989;103:603-6.

(7.) Moorman CM, Anslow P, Elston JS. Is sphenoid sinus opacity significant in patients with optic neuritis? Eye 1999;13(Pt 1): 76-82.

(8.) Yeoh KH, Tan KK. The optic nerve in the posterior ethmoid in Asians. Acta Otolaryngol 1994;114:329-36.

(9.) Kountakis SE, Maillard AA, Stiernberg CM. Optic neuritis secondary to sphenoethmoiditis: Surgical treatment. Am J Otolaryngol 1995;16:422-7.

(10.) Rice DH, Schaefer SD. Endoscopic paranasal sinus surgery. New York: Raven Press, 1988.

(11.) Gordts F, Clement PA, Buisseret T. Prevalence of paranasal sinus abnormalities on MRI in a non-ENT population. Acta Otorhinolaryngol Belg 1996;50:167-70.

From the West of England Eye Unit, Royal Devon and Exeter Hospital, Exeter, U.K.

Reprint request: Mr. Pieter Gouws, West of England Eye Unit, Royal Devon and Exeter Hospital, Barrack Rd., Exeter EX2 5DW, U.K. Phone: [phone]; fax: [phone]; e-mail: [e-mail]