Summary
Strabismus and other ophthalmic complications due to acute severe sinusitis have long been known, but less well appreciated is the association of strabismus with subacute, subclinical, or asymptomatic sinusitis. Sinus-related strabismus presents with fibrosis of the extraocular muscles that are adjacent to the involved sinuses. The medial rectus muscles and superior obliques are adjacent to the ethmoid sinuses, and the inferior rectus muscles and inferior obliques sit above the maxillary sinuses. Strabismus patterns seen include esotropia, hypotropia with extorsion of the lower eye, V-pattern esotropia, Brown’s syndrome, and high AC/A ratio. Acute esotropia is frequently mistaken for sixth cranial nerve (CN) palsy, but true sixth CN palsy can be seen with mastoiditis or cavernous sinus involvement. Fourth CN palsy may precede the Brown syndrome. Diagnosis is made by otolaryngologic examination and sinus imaging. Treatment of sinusitis medically (and sometimes surgically) may reverse strabismus if caught early, but strabismus surgery is frequently required. If sinusitis is ignored, strabismus will usually recur despite initial surgical success.
13 Presumed Sinus-Related Strabismus
13.1 Introduction
During routine strabismus surgery, this author noticed that the extraocular muscles most frequently showing signs of perimuscular inflammation and fibrosis were the inferior rectus (IR) and medial rectus (MR) muscles. The oblique muscles were sometimes involved, the superior rectus muscles were rarely involved, and the lateral rectus muscles never showed these changes. It was hypothesized that the proximity of these muscles to the maxillary and ethmoid sinuses was a possible explanation for this pattern. Patients referred by this author for sinus evaluation by an otolaryngologist had a much higher incidence of positive findings of sinusitis on computed tomography (CT) scan than is found in the general population (Box 13.1). 1 , 2
Box 13.1
Twenty-six patients with suspected sinus-related strabismus were referred for otolaryngologic evaluation. 1 Of these, 92% had positive findings on CT scan, whereas the normal population has positive findings in 15 to 17%. Our population had a rate of 58% showing active sinusitis, with a 2% rate of active sinusitis incidentally found in normals.
Of the 59 patients in our series, 10 experienced improvement of strabismus with treatment of sinus disease alone. Forty required strabismus surgery, and all had positive forced duction testing suggesting extraocular muscle fibrosis, usually of the IR and MR muscles. Sixteen had tight superior oblique (SO) muscles, and 13 had tight inferior oblique (IO) muscles.
In seven patients the diagnosis of sinusitis was not picked up until after strabismus recurred following initial good alignment after surgery. Since the study, this author has followed numerous patients who have ignored the strabismus surgeon’s recommendation of sinus evaluation by an otolaryngologist. Almost invariably there has been recurrence of strabismus within one to several years. Progression of strabismus stopped only after successful control of sinusitis was achieved.
One child required intensive care hospitalization to treat bacterial meningitis originating from bilateral maxillary sinusitis 2 months after presenting with new onset high accommodative convergence to accommodation (AC/A) ratio. Her mother, a pediatrician herself, ignored advice to image or prophylactically treat the sinuses, as the child was otherwise asymptomatic. The motility evaluation returned to normal after her sinusitis was cleared.
An ophthalmologist underwent bilateral orbital decompression followed by successful strabismus surgery for thyroid ophthalmopathy. He developed recurrence of strabismus coincident with an upper respiratory infection with sinusitis and required repeat strabismus surgery. He has been controlled since with meticulous control of his sinus disease, as well as range of motion eye rolling to stretch his eye muscles whenever diplopia recurs.
Sinusitis was known in the past to cause strabismus, usually with severe consequences such as cranial nerve (CN) palsies or blindness due to cavernous sinus involvement, orbital floor collapse, and orbital abscess. 3 , 4 , 5 , 6 , 7 , 8 , 9 These patients were usually seriously ill, suffering acute, fulminant sinusitis. These cases became rare with the advent of the antibiotic era. A gradual, subacute development of strabismus due to adjacent chronic sinusitis is now the typical clinical presentation of “presumed sinus-related strabismus.” Proving the causation is difficult due to the common occurrence of sinusitis in the general population, but the association is frequent and worthy of consideration. It has been this author’s experience that whenever adjacent sinusitis in a suspected case of presumed sinus-related strabismus is ignored, there is a high strabismus recurrence rate after initially successful eye muscle surgery (Box 13.1). Sinus treatment usually stabilizes strabismus and reduces the rate of reoperation. In some cases, if diagnosis and sinus treatment are prompt, strabismus can resolve without surgery.
13.2 Anatomy and Mechanism
The IR and IO muscles are adjacent to the maxillary sinuses, and the MR and SO muscles are adjacent to the ethmoid sinuses. The bones of the orbital floor and medial orbital wall are thin, and they contain fissures and foramina, through which pass vessels and nerves. Congenital dehiscences in the medial orbital wall and orbital floor are also known to exist. 3 Additionally, subclinical trauma can lead to small bony defects, which may not be easily detected on routine imaging. 10 It is therefore plausible that inflammatory cells and infectious organisms may pass into adjacent orbital tissue. The extreme result of this process would be orbital cellulitis and abcess, which are well-known complications of upper respiratory disease and sinusitis. 3 , 4 , 5 , 11 Subclinical smoldering inflammation without overt symptoms is very common with sinusitis, and there is probably a parallel situation for adjacent orbital inflammation. A rare but known complication of chronic asymptomatic sinusitis is orbital floor erosion and collapse and resultant vertical diplopia and hypoglobus. 8
The subset of patients with prior orbital decompression for thyroid ophthalmopathy are at increased risk of strabismic complications of sinusitis (Chapter 12). Also at increased risk are those with repaired orbital fractures with implants.
The orbital connective tissue structures (“pulleys”) and orbital fat are also impacted by inflammation and fibrosis. These changes to the pulleys are likely to contribute to sinus-related strabismus and motility restriction.
13.3 Clinical Features and Diagnosis
13.3.1 History
Cases of strabismus due to sinusitis may be categorized as acute, subacute, chronic–intermittently relapsing, and chronic–slowly progressing. 1
Acute cases usually present with esotropia or hypertopia, which may be mistaken for sixth or fourth CN palsy, respectively. Coincident upper respiratory infection is frequently present. Imaging is often obtained due to fear of a neurologic disorder, but the physician may ignore the finding of incidental sinusitis. Acute onset cases seem to be more prevalent in children. Gradenigo’s syndrome, which is a true sixth CN palsy due to mastoid sinusitis, should also be considered, especially in association with otitis media.
Subacute cases have a more vague history of onset, over several weeks to months. These patients have gradually increasing strabismus and may be unaware of sinusitis, which is of a more chronic nature. Specific questioning about sinus symptoms may prove positive, but otolaryngologic examination and imaging are usually required for diagnosis.
Chronic–intermittently relapsing cases have a seasonal pattern to their worsening strabismus, coincident with flare-ups of allergies and sinusitis. Some observant patients have noticed that the prisms in their glasses need increasing yearly during allergy season.
Chronic–slowly progressing cases are unaware of a relapsing pattern to strabismus, and feel there is a very slow increase in the deviation over time. They may have chronic unremitting sinus inflammation, gradually leading to perimuscular and intramuscular inflammation and fibrosis.
13.3.2 Motility Examination and Strabismus Patterns
Hypertropia may develop due to fibrosis of one IR, with asymmetrical maxillary sinusitis. The pattern of deviation may simulate an SO palsy, but the extorsion is mild and is seen in the lower eye. This finding is pathognomonic of a fibrotic IR. Limitation of upgaze in the affected eye may also be seen. Bilateral maxillary sinusitis with bilateral IR fibrosis may be associated with vertical deviation if the IR involvement is asymmetrical. 1 , 6
SO palsy followed by Brown’s syndrome has been observed with adjacent ethmoid sinusitis. The sinusitis initially causes muscle weakness, but subsequent peritrochlear fibrosis then leads to contracture and a clinical picture of Brown’s syndrome. 11 , 12
Acquired high AC/A ratio due to contracture of the MR muscles is sometimes the first sign of sinus-related strabismus. With progression, this can increase to manifest esotropia, for distance and near vision. 1
Esotropia may be comitant or incomitant, depending upon the symmetry or asymmetry of sinus disease. Many sinus-related esotropia cases are initially misdiagnosed as sixth CN palsy, especially in children, who quickly begin to suppress one eye and are loath to switch fixation. This can cause them to resist full abduction of the suppressed eye, simulating a partial sixth CN palsy 1 (Fig. 13‑1). Persistence of the examiner will usually succeed in pushing the child to full abduction.
Pseudo–sixth CN palsy due to asymmetrical sinusitis can cause unilateral limitation of abduction due to MR fibrosis, but the limitation is usually mild. Mild incomitance of alignment measurements may also be seen. If the patient is old enough to perform, force generation testing of the lateral rectus reveals normal strength. 1
V-pattern esotropia with extorsion is seen with bilateral pansinusitis, which primarily impacts the IR and MR muscles. The IOs may also be affected, contributing to the pattern.
Fig. 13.1 The 3-year-old on right developed acute esotropia along with otitis media. He was diagnosed with viral sixth cranial nerve palsy and had normal head computed tomography (CT) scan. He did not respond to injection of botulinum toxin, hyperopic spectacle correction (+2.00 with +2.50 bifocals), or recession of the left medial rectus. His identical twin (left side of photo) had no strabismus, and there was no family history of strabismus. By age 5, he had V-pattern esotropia and high accommodative convergence to accommodation (AC/A) ratio, and was fully glasses dependent. CT scan showed severe pansinusitis, including the sphenoid sinuses. The radiologist felt this was an emergency, and sinusitis treatment was immediate, first medical, then surgical. Repeat strabismus surgery was required, and marked fibrosis of both medial and inferior rectus muscles was observed. (Used with permission from Ludwig and Smith. 1 )
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
