Postoperative Decompensated Strabismus Following Otherwise Uncomplicated Ocular Surgeries
Disease Entity and Epidemiology
Strabismus is a common ocular disease defined as a misalignment of the eyes. It affects approximately 4% of the United States population. Fortunately, many patients with long-standing strabismus may retain fusion which mitigates the diplopia . Loss of this fusional ability however can lead to decompensation of previously well-controlled and asymptomatic or intermittently symptomatic diplopia. Many otherwise uncomplicated ocular surgeries can lead to visual blur which can break the patient’s fusion and lead to post-operative diplopia. Binocular single vision is achieved through the coordinated use of both eyes so that separate and dissimilar images arising in each fovea are unified as a single image. This occurs as optical stimuli excite neurons in two cortical fields simultaneously. The two receptive fields detect the object and assign it to a single locus in space, thus creating the basis of binocular vison. The normal fusional process requires clear visual input from both eyes, appropriate communication of the retinal and cortical elements, and precise coordination of gaze in all directions. Disruption of the sensory or motor aspects of fusion can induce diplopia .
Sensory fusion describes the process of combining an image from each eye to create a single image. For sensory fusion to occur, the images must be located on corresponding areas of the retina as well as be similar in size, shape, and clarity. Asymmetric and distorted visual input poses a significant obstacle to fusion .
Motor fusion describes the ability to align the eyes in positions that allow the preservation of sensory fusion. To prevent diplopia, images must be kept within the region of visual space in which single vison is perceived, known as Panum's fusional area. Objects in front or behind this area induce physiological diplopia .
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Decompensation of longstanding fusion in strabismus can occur following prolonged sensory deprivation or from any ophthalmologic surgery that causes visual blur . Loss of fusion in patients with preexisting strabismus has been documented following many otherwise uncomplicated ocular procedures such as laser in situ keratomileusis (LASIK) and cataract extraction and intra ocular lens (CEIOL) .
A review of cataract surgeries noted up to 3% of patients experience diplopia following cataract extraction. The causes of diplopia following the procedure vary, however of the 150 patients that experienced diplopia, the leading cause was decompensation of pre-existing strabismus (34%). Similarly, refractive diplopia (8.5%) and disruption of central fusion (5%) were prominent causes of diplopia following CEIOL. Similarly, the most common cause of binocular diplopia in patients that underwent LASIK surgery was also decompensation of pre-existing strabismus .
In normal binocular single vision, optical stimuli excite cortical neurons and is presented to the respective cortical fields simultaneously. This process requires images similar in size, shape, and clarity. However, as discussed above, patients with long standing strabismus may develop adequate fusion despite eye misalignment and preclude development of diplopia . In these patients, development of temporary uniocular blurriness due to media opacities, changes in refractive error, or optic nerve lesions can alter this process and force reliance on input from the not affected eye. As the visual impairment resolves, sometimes the previously well controlled fusion fails to recover and the patient experiences significant diplopia .
A thorough history should be taken prior to any ocular surgery. Asking if the patient has noticed drifting of their eye, if they underwent childhood patching or strabismus surgery, and examination of old photographs can help establish the presence of a preexisting strabismus. Similarly, asking if the patient’s family has noted anomalous head positioning can help determine if the lesion is long standing. The use of any prior prism therapy in spectacle correction should also be noted. Thyroid eye disease (TED) and Myasthenia gravis (MG) can also present as a new onset ocular motility defect after ocular surgeries. Review of systems and obtaining history about weight loss/gain, cold or heat intolerance, hair loss, dry skin, systemic signs of shortness of breath, difficulty swallowing, and fatigable weaknesses should be performed .
A complete ocular examination, including thorough motility testing, is recommended prior to any ophthalmologic procedure. Incomitant strabismus may indicate restrictive disease, cranial neuropathy, supranuclear disorders, ocular myopathies, and neuromuscular junction disorders. Comitant strabismus, however, more likely indicates a long-standing strabismus. Similarly, presence of large fusional amplitudes, facial asymmetry, spread of comitance, and full ductions increase the likelihood of postoperative decompensation in a formerly well-controlled fusion.
Family members, friends, or a “FAT” (family album tomography) scan of old photographs may demonstrate a pre-existing anomalous head or face tilting or turning that might reflect underlying well controlled strabismus.
Symptoms may include headaches, difficulty reading, eyestrain, and diplopia,
Diagnosis of decompensated cranial nerve palsy or fusional decompensation are made by cover uncover and other strabismic physical examinations.
There are no laboratory abnormalities specific to detect decompensation of strabismus. However, as thyroid eye disease and myasthenia gravis may present as a new onset motility defect following ocular surgeries, laboratory tests to rule out these pathologies should be performed .
• Decompensated childhood strabismus
• Thyroid Eye Disease
• Myasthenia Gravis
• Diabetic microvascular damage
Management of decompensated strabismus depends on the underlying etiology, however, most cases can be symptomatically managed with prism glasses .
If the misalignment cannot be corrected using prism glasses, surgical intervention specific to the deviation may be recommended .
Most patients with postoperative decompensated strabismus can be corrected with prism glasses or strabismus surgery. However, a minority of patients will have persistent diplopia and require long term occlusion therapy .
The best treatment of post operative decompensated strabismus is prevention with a thorough history and ocular motility exam. In all patients presenting for ophthalmologic procedures, specific inquiries regarding personal or family history of strabismus can prevent unexpected and devastating results.
Clinicians performing ocular surgery should be aware that any post-operative visual blur can decompensate previously well controlled and asymptomatic strabismus. Visual blur induced breakdown of fusional mechanisms is believed to be the cause of most strabismus following ocular surgeries. Prior restrictive or paretic ocular misalignment should be documented as well as any prior strabismus history, strabismus surgery, or strabismus treatment (e.g. patching or prism). The informed consent process likely should include the possibility of decompensation of fusion and post-operative diplopia both for medical and potentially medicolegal reasons.
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