THE CLINICAL CHALLENGE
Diplopia—colloquially referred to as “double vision”—is a challenging chief complaint in the emergency and urgent care setting. It is also an infrequent chief complaint in the emergency and urgent care setting, representing 0.1% of all ED visits.1
Diplopia may occur from a wide spectrum of pathologies including many benign causes (e.g. decompensated phoria, convergence or divergence insufficiency, and microvascular disease) as well as vision- or lifethreatening causes (e.g. stroke, cerebral aneurysm, brain tumor, intracranial hemorrhage, thyroid eye disease, giant cell arteritis, myasthenia gravis, meningitis, cavernous sinus thrombosis, or increased intracranial pressure). Structural lesions causing diplopia may localize to the cortical, subcortex, brainstem, subarachnoid, cavernous sinus or orbital level. A comprehensive review of all causes of diplopia is beyond the scope of this chapter, but several important causes to consider in the emergency and urgent care settings are listed in Table 49-1
The clinician should first determine whether the diplopia is monocular or binocular. Monocular diplopia is confirmed when covering the unaffected eye does not resolve the diplopia. This strongly suggests a single eye problem such as dry eye, refractive error, corneal pathology, cataract, or retinal disease. These patients warrant a thorough eye exam, but monocular diplopia is generally not an emergency.
In contrast, binocular diplopia resolves with occlusion of either eye indicating misalignment of the visual axes. This chapter describes the evaluation of binocular diplopia (henceforth referred to as diplopia) with an emphasis on identifying emergent disease entities that clinicians must consider.
APPROACH/THE FOCUSED EXAM
The first step in evaluating a patient with binocular diplopia is to determine whether the patient has isolated diplopia or diplopia with additional neurologic deficits suggestive of a posterior circulation stroke. Patients presenting with acute onset diplopia in combination with altered mental status, bulbar weakness, vertigo, ataxia, or “crossed” brain stem signs (ipsilateral CN deficits with contralateral limb weakness or sensory loss) should be considered to have a brainstem stroke until proven otherwise.
The evaluation of patients with diplopia in the absence of acute onset brainstem symptoms begins with a focused history. The clinician should first determine the orientation of the diplopia (horizontal, vertical, or oblique) and whether the diplopia worsens in a particular direction of gaze. CN palsies and restrictive processes (such as thyroid eye disease or muscle entrapment by orbital fractures) cause incomitant diplopia, that is, diplopia that worsens in a particular direction of gaze corresponding with the affected extraocular muscle(s). By contrast, neuromuscular disorders such as myasthenia gravis may cause comitant (the same in all gaze directions) or incomitant diplopia.
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