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An 80-year-old Caucasian female with a remote history of nonarteritic ischemic optic neuropathy of the left eye presented with transient vision loss in the right eye, occurring once or twice per week, for the month before presentation. The onset of each episode was abrupt, rather than gradual, and described as “things fading in the right eye,” and “objects looking duller than usual” over the entire visual field. She had no positive visual phenomena with these episodes, which often lasted approximately 1–5 minutes. Each episode was neurologically isolated, without headache or focal neurologic symptoms. After each episode, the vision slowly returned to her previous baseline. She identified no precipitating factors related to her symptoms.
She had a negative review of systems, including fevers, chills, weight loss, fatigue, headache, jaw claudication, scalp tenderness, weakness, numbness, vertigo, diplopia, oscillopsia, slurred speech, facial droop, chest pain, palpitations, dyspnea, cough, or hemoptysis.
Examination at presentation was notable for a visual acuity of 20/40 OD and count fingers OS, as well as a left afferent pupillary defect, which was unchanged from baseline with her left ischemic optic neuropathy. Intraocular pressures were 14 mm Hg OU. Slit-lamp and fundus examination of the right eye showed no anterior segment disease, vessel occlusion, Hollenhorst plaques, or other retinal or vascular abnormalities. Her temporal artery pulses were strong bilaterally and she had no scalp tenderness. She had no other focal neurologic defects and the rest of her physical examination was unremarkable.
She was hospitalized for urgent evaluation of transient monocular vision loss. Laboratory work-up was notable for a troponin elevation, as well as mild anemia, thrombocytopenia, and hyponatremia. Erythrocyte sedimentation rate and C-reactive protein were unremarkable. Head computed tomography (CT) was negative for intracranial hemorrhage. Brain magnetic resonance imaging (MRI) was obtained and revealed multiple punctate cortical and juxtacortical areas of diffusion restriction, involving all vascular territories (Figure 1).
Carotid Dopplers showed smooth plaques in the internal carotid arteries causing less than 50% stenosis, but were otherwise unremarkable.
Given the involvement of multiple vascular distributions, a trans-thoracic echocardiogram was performed, which was negative for valvular abnormalities or right-to-left shunt. A trans-esophageal echocardiogram was then performed, which showed characteristic mobile echodensities on both leaflets of the mitral valves, including a 6 × 5 mm lesion on the posterior leaflet and 4 × 1 mm lesion on the anterior leaflet, without significant regurgitation or valve destruction (Figure 2). Blood cultures were obtained and negative for bacterial or fungal growth.
A CT of the chest, abdomen, and pelvis was performed that showed spiculated lesions in the lingula and right upper lobe of the lung, as well as mediastinal lymphadenopathy.
Positron emission tomography–CT showed increased uptake in the spine, pelvis, sternum, and thoracic wall, consistent with metastatic osseous disease. An ultrasound-guided biopsy of a paratracheal lymph node was performed. Pathology revealed malignant cells, strongly positive for thyroid transcription factor (TTF-1) and NapsinA, consistent with metastatic pulmonary adenocarcinoma.
“Transient monocular vision loss” (TMVL) is a broad term used to describe sudden, nonpermanent vision loss in one eye. The etiology of TMVL comprises a wide range of ophthalmic, neurologic, and systemic disease. Commonly, “amaurosis fugax” is the term used when TMVL is secondary to vascular insufficiency or ischemia.
Identifying the cause is of critical importance in the correct diagnosis and subsequent management of the underlying condition.
In this case, we believe that the patient's symptoms were attributable to an embolic source, from nonbacterial thrombotic endocarditis (NBTE) associated with metastatic lung adenocarcinoma. Anterior segment and dilated fundus examination findings were normal, not supporting retinal or other ocular pathologies, including intermittent angle closure glaucoma or ocular surface disease. Carotid Dopplers were negative for clinically significant stenosis or plaque rupture. There were no cardinal symptoms of giant cell arteritis, and inflammatory markers were within normal limits. She also had no history of migraine, and the characteristics of the episodes, including the frequency and duration, would be unusual for retinal migraine or migraine aura with headache. Indeed, many cases of the so-called retinal migraine are vascular in origin.
NBTE is a rare condition that refers to noninfectious vegetations of cardiac valves, most commonly associated with advanced malignancy or autoimmune disease. Rates in autopsy series range from 0.6% to 1.6%.
In particular, diffusion-weighted MRI can guide work-up, because ischemic strokes in multiple distributions suggest a cardioembolic source. Carotid sources of TMVL are more common than cardiac emboli, but consideration of a cardiac source is important when clinical suspicion is high. TEE is more sensitive in identifying small lesions and can be pursued when TTE is negative, as in this case. In our case, the discovery of NBTE led to the diagnosis of lung adenocarcinoma. In cases where there are no obvious traditional causes of amaurosis, NBTE should be considered, even in the absence of a history of malignancy or hypercoagulability.