Three presentations of monocular vision loss

Transcription

1 Optometry (2006) 77, Three presentations of monocular vision loss Melissa E. Trego, O.D., a,b and Jean Marie Pagani, O.D. a,c a The Eye Institute, Pennsylvania College of Optometry, Philadelphia, Pennsylvania; b Cardiff University, School of Optometry and Vision Sciences, Cardiff, Wales, United Kingdom; and c Nemours Health Clinic, Wilmington, Delaware. KEYWORDS: Retinal emboli; Carotid artery disease; Transient ischemic attack Abstract BACKGROUND: Carotid artery disease is estimated to affect 30% of persons older than 50. Risk factors include hypertension, cigarette smoking, hyperlipidemia and diabetes mellitus. Symptoms ascribed to carotid artery lesions with stenosis of the artery or plaque formation include monocular vision loss and transient ischemic attacks. Patients can present with transient monocular vision loss as their initial symptom. CASE REPORTS: Three patients from a geriatric clinic in Wilmington, Delaware presented with different complaints of vision loss with similar overall outcomes. Patient A was an 87-year-old woman who presented with dimming of vision on extreme left head turn. Dilated fundus examination found a retinal arterial emboli in the left eye (O.S.). Carotid duplex examination found 50% to 79% left internal carotid stenosis with no hemodynamic stenosis of the right internal carotid. Patient B was a 78-year-old woman who presented with a right superior altitudinal defect and transient vision loss in the right eye. Dilated fundus examination found retinal arterial emboli in the right eye (O.D.). Carotid duplex examination found 50% to 79% carotid stenosis in both the left and right internal carotids. Patient C was an 84-year-old man who complained of a superior altitudinal visual field defect O.D. Dilated fundus examination found a retinal arterial emboli O.D. Carotid duplex results showed calcified atherosclerotic plaques present at the level of the common carotid artery bifurcations bilaterally, with 50% to 70% narrowing of the right internal carotid artery with no significant narrowing of the left internal carotid artery. CONCLUSIONS: These 3 presentations show that in patients older than 50 who present with chief complaints of monocular vision loss, a differential diagnosis of carotid artery disease must be considered. Patients who exhibit retinal arterial emboli are at increased risk for stroke and vascular death. Appropriate measures for confirming a diagnosis include duplex ultrasound imaging, magnetic resonance angiography (MRA), and carotid angiography. Surgical techniques such as carotid angioplasty and carotid endarterectomy may be recommended. Optometry 2006;77:82-87 Carotid artery disease is estimated to affect 30% of individuals older than 50. A number of vascular risk factors have been associated with carotid disease including hypertension, cigarette smoking, diabetes mellitus, and hyperlipidemia. 1-7 The retinal vasculature of the eye can provide an Corresponding author: Jean Marie Pagani, The Eye Institute, 1200 W. Godfrey Avenue, Philadelphia, Pennsylvania jpagani@pco.edu excellent window for the analysis of the cerebral microvasculature. Any type of emboli (calcific, cholesterol, fibrinoplatelet) lodged within the retinal arterial system may represent the potential for the presence of emboli elsewhere within the cerebral or cardiovascular circulation. 2-4 Patients with carotid artery disease may present with monocular, ipsilateral vision loss; transient vision loss; asymptomatic retinal emboli; or central retinal artery occlusion. The detection of emboli as an initial presentation of an underlying /06/$ -see front matter 2006 American Optometric Association. All rights reserved. doi: /j.optm

2 Trego and Pagani Clinical Care 83 systemic disease may afford the opportunity for early intervention. 1-3,6-7 In the following case presentations, all 3 patients presented with monocular vision loss with concurrent detection of retinal emboli warranting further carotid evaluation, ultimately leading to the diagnosis of carotid artery disease. Case presentation 1 (Patient A) Patient A was an 87-year-old woman who presented with a chief complaint of blurry vision on extreme left head turn 3 months before her examination. Ocular history was remarkable for bilateral pseudophakia. Her systemic history was remarkable for hypertension and hyperthyroidism. Patient A had no known drug allergies and was taking hydrochlorothiazide and propylthiouracil for her systemic conditions. Best-corrected visual acuities at distance were 20/40 in the right eye (O.D.) and in the left eye (O.S.). Pupils, confrontation visual fields, and ocular motilities were within normal limits. Slit lamp examination found scleromalacia and epithelial basement membrane dystrophy of the cornea in both eyes (OU). Intraocular pressures were 18 mmhg O.D. and 14 mmhg O.S. Dilated fundus examination found cellophane maculopathy OU and a plaque at the bifurcation of the inferior retinal arteriolar tree O.S. No carotid bruit was heard on the left or right side. The patient was referred for an immediate carotid workup, which included a carotid duplex examination. Results of carotid studies showed 50% to 79% stenosis of the left internal carotid artery with no stenosis of the right internal carotid. The patient declined surgery and is being monitored for ocular sequelae of carotid artery disease. Case presentation 2 (Patient B) Patient B was a 78-year-old woman who presented with a chief complaint of a black spot over her right eye and transient visual loss O.D. Ocular history was remarkable for pseudophakia OU, nonproliferative diabetic retinopathy OU, and maculopathy OU. Her systemic history was remarkable for hypercholesterolemia, acne rosacea, hypertension, type II diabetes mellitus (for 10 years), and kidney problems. Patient B was taking nifedipine, metoprolol, aprazolam, atorvastatin, furosemide, glipizide, doxazosin, and lisinopril for systemic conditions. Best-corrected visual acuities at distance were 20/30 O.D. and O.S. Pupils and ocular motilities were within normal limits. Confrontation visual fields showed a superior altitudinal defect O.D. and were full O.S. Slit lamp examination was unremarkable, and intraocular pressures were 11 mmhg OU. Dilated fundus examination found moderate nonproliferative diabetic retinopathy OU and a retinal plaque in the inferior arteriolar tree O.D. (see Figure 1). The patient was referred for an immediate carotid workup, which included a carotid duplex Figure 1 Fundus exhibiting a Hollenhorst plaque in the inferior arteriolar tree. (Photo compliments of Jodi Pukl, O.D.) examination. Results of carotid studies showed 50% to 79% stenosis of both the left and right internal carotids. The patient is being followed up by a vascular specialist and is being monitored closely for ocular sequelae of carotid artery disease. Case presentation 3 (Patient C) Patient C was an 84-year-old man who presented with a chief complaint of not being able to see in his superior field of vision O.D. for 2 weeks before his examination. Ocular history was remarkable for pseudophakia and nonproliferative diabetic retinopathy OU. Systemic history was remarkable for type II diabetes mellitus (for 7 years), hypertension, and a previous cerebral vascular accident, for which the patient showed a left homonymous superior quadrantanopia (see Figures 2A and B). Patient C was taking lisinopril, amlodipine besylate, clopidogrel, propranolol, metformin, and aspirin for his systemic conditions. Best-corrected visual acuities at distance were 20/40 O.D. and 20/30 O.S. Pupils and ocular motilities were within normal limits. Slit lamp examination was unremarkable, and intraocular pressures were 18 mmhg OU. Dilated fundus examination found an inferior ischemic retina O.D. with a plaque at the bifurcation of the retinal arteriolar tree O.D. No carotid bruit was heard on the left or right side. The patient was referred for an immediate carotid workup, which included a carotid duplex examination, magnetic resonance angiography (MRA) of the neck (see Figure 3), and a magnetic resonance image (MRI) of the head. Automated threshold visual fields were also completed. Results of carotid studies showed calcified atherosclerotic plaques present at the level of the common carotid artery with 50% to 79% stenosis of the right internal carotid artery

3 84 Optometry, Vol 77, No 2, February 2006 Figure 2 Automated threshold visual fields for Patient C.

4 Trego and Pagani Clinical Care 85 Figure 3 with no stenosis of the left internal carotid. MRI studies showed a right cerebral peduncle (brainstem) infarct. Visual fields showed a superior altitudinal field loss O.D. ( see Figures 2C and D) compared with the previous visual fields, which showed a left homonymous superior quadranopsia (see Figures 2A and B). The patient is being followed up by a vascular specialist and is being monitored closely for ocular complications of carotid artery disease. Discussion MRA shows stenosis of the internal carotid artery. A variety of transient visual signs or symptoms may develop in patients with disease of the carotid arteries. Ultimately, the hallmark of these disturbances is their monocular nature, ipsilateral to the carotid disease. Such ocular signs and symptoms include transient monocular visual loss (amaurosis fugax), venous stasis retinopathy or ocular ischemic syndrome, central retinal artery occlusion, ischemic optic neuropathy, Horner s syndrome, and oculomotor nerve palsy. 2-4 A recent study performed by McCullough et al., 8 found that the predictive value of ocular fundoscopic findings for identifying carotid artery occlusive disease is variable but generally poor. Ocular findings of moderate predictive values that warranted further diagnostic testing included retinal emboli, venous stasis retinopathy, and amaurosis fugax. Other ocular findings with poor prediction of carotid occlusive disease included ischemic optic neuropathy, retinal artery or vein occlusion, asymmetric diabetic retinopathy, optic atrophy, and ocular ischemic syndrome. 8 Yet, of all presenting symptoms, transient monocular vision loss (TMVL) is the most universal and perhaps the most important ophthalmic symptom of carotid occlusive disease. 1 Patients with TMVL typically complain of acute, monocular loss of vision that may be partial or incomplete. In the North American Symptomatic Carotid Endarterectomy Trial (NASCET), 53.4% of 554 patients reported sudden, painless, and diffuse loss of vision and altitudinal visual loss with a descending or ascending shade reported in 28.8% of patients. 1,4 Most episodes of TMVL last 2 to 30 minutes and then resolve spontaneously, usually over seconds and minutes. Lesions of the common or internal carotids often cause this TMVL, secondary to emboli within the retinal circulation. With emboli, most commonly a black or dark shade spreads across the visual field of the affected eye, disappearing after a few seconds or minutes at most. Less commonly, severe stenosis of the carotid artery causes TMVL secondary to retinal or choroidal hypoperfusion. 1 All 3 patients presented with some form of monocular vision loss. Patient A presented with blurring of vision upon extreme left head turn, Patient B presented with a black spot over her right eye, and Patient C noted the inability to see the upper half of his visual field in the right eye. Although all 3 were different in presenting symptoms, all reported the visual loss ipsilateral to the stenosed carotid artery. In addition to the presenting symptom of monocular vision loss ipsilateral to the stenosed carotid, which is significant clinical evidence for carotid occlusive disease, all 3 patients exhibited retinal emboli in their arteriolar trees. Common locations for emboli include the origins of the major arteries such as the internal carotid artery, middle cerebral artery, basilar artery, vertebral arteries, and aortic arch (see Figure 4). Emboli, often asymptomatic, may consist of calcium from a diseased heart valve, organisms, or foreign materials such as talc, fat, or tumor cells and cholesterol. 5 The presence of retinal emboli carries implications for the patient s future health status and is often associated with systemic vascular disease (see Table). Results of the Beaver Dam Eye Study showed that the overall prevalence of retinal emboli in a population of 4,926 patients was 1.3%, increasing to 3.1% in patients 75 years or older. 5,6 Researchers of this study also found an increase in stroke and cardiac-related deaths among those patients with retinal emboli. This study supports the notion that patients with retinal emboli are more systemically ill than patients without emboli. 6 In addition to plaques at the bifurcation of their arteriolar trees, all 3 patients also exhibited systemic vascular diseases often associated with retinal emboli, in- Table Concomitant medical conditions associated with retinal arterial emboli 29 Systemic vascular disease Incidence of concurrence with retinal arterial emboli (%) Hypertension 70.0 Diabetes mellitus 45.0 Cardiac disease 41.0 Elevated cholesterol levels 59.0 Carotid stenosis ipsilateral 55.2

5 86 Optometry, Vol 77, No 2, February 2006 Figure 4 Diagram of blood flow from the carotid system. (Reprinted from ica.htm with permission from Loyola University Medical Education (LUMEN) and Christopher Ladner, M.D., Ph.D. cluding hypertension, diabetes mellitus, and high cholesterol. As primary eye care providers, we play a pivotal role in the recommended followup and referral of these at risk patients. Patients suspected of having carotid artery disease require prompt, noninvasive vascular evaluation to confirm the carotid lesion, establish its cause (atheroma, dissection, vasculitis, compression), and assess the severity of the lesion (percentage of occlusion/stenosis) and its ocular and cerebral tolerance (hypoperfusion of the ipsilateral eye and hemisphere). 1,3 Oculoplethysmography (OPG) is a wellknown noninvasive test used to detect the presence of blockage in the carotid arteries by changes in flow and pressure from the hemodynamically significant lesions. 9 OPG can be used as an initial semiquantitative measurement in the estimation of blockage in the carotid arteries and their tributaries in symptomatic or asymptomatic patients with bruits. 9,10 However, clinical evidence has shown that OPG is not a reliable screening test for carotid artery disease, particularly in nonocclusive unilateral disease or bilateral disease. 11 A recent study examined the use of pulsatile ocular blood flow (POBF) as a noninvasive technique to examine severe stenosis of the internal carotid artery. 12 POBF repeatedly measures intraocular pressure with a pneumatic applanation tonometer during the cardiac pulse cycle and, based on intraocular pressure variation with time, calculates the pulsatile ocular blood flow. 13 Although not a direct reflection of blood flow of the internal carotid artery, low or unrecordable POBF may signify severe stenosis and alert the primary eye care provider that further investigation is needed. 12 Carotid duplex ultrasonography is the singular noninvasive diagnostic tool for the evaluation of extracranial carotid disease. Carotid duplex scanning can accurately measure the degree of extracranial carotid artery stenosis and can provide important information about the vessel wall configuration and plaque morphology. 1,14-18 In addition to carotid duplex ultrasonography, MRA can also be a diagnostic tool in screening for carotid arteriosclerosis and evaluating intracranial hemodynamics. MRA is not as efficient as a carotid duplex in the analysis of plaque morphology, in the estimation of stenosis, and in carotid interpretation. 16,17,19 Although an MRA is diagnostic, it carries a higher morbidity and mortality rate than ultrasonography. 2 However, by combining the carotid Doppler with the MRA, the information obtained on carotid artery disease morphology is revealing. All 3 patients underwent carotid duplex testing, which revealed the stenosis of their respective internal carotid arteries. In addition, Patient C also underwent an MRA, to further support the diagnosis. Two major prospective studies, North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST) provide strong evidence for the benefit of carotid endarterectomy in symptomatic patients when performed by experienced surgeons. 1,5,15,20-21 Both studies showed that in patients with retinal or hemispheric symptoms attributed to severe (70% to 99%) carotid stenosis, endarterectomy was superior to medical care alone. There was no benefit of carotid endarterectomy in symptomatic patients with mild stenosis ( 50%). 5,20-21 Patients with carotid artery disease, who are asymptomatic, are prevalent in the general population. However severe ( 70%) carotid stenosis of the asymptomatic patient is rare in comparison with symptomatic patients. Four randomized clinical trials were conducted (Carotid Artery Surgery Asymptomatic Narrowing Operation Versus Aspirin [CASANOVA], Mayo Asymptomatic Carotid Endarterectomy [MACE] Trial, Veterans Affairs Asymptomatic Carotid Endarterectomy Trial, and the Asymptomatic Carotid Atherosclerosis Study [ACAS]) to determine the risks and benefits of carotid endarterectomy in asymptomatic patients. CASANOVA, MACE, and the Veteran Affairs Asymptomatic Trial found no benefit from surgery in asymptomatic patients. 5,15,22-27 Based on a 5-year projection, the ACAS found that carotid endarterectomy reduced the risk of absolute stroke by 5.9% and the relative risk of stroke and death by 53%. Patients enrolled in ACAS were younger than 80 years and had asymptomatic carotid stenosis of 60% or more. 15,26 The overall benefit of endarterectomy strongly depends on surgical risk. Mortality and morbidity rates associated with carotid endarterectomy are significantly lower in asymptomatic patients than in symptomatic patients. 15,25-27 Because all 3 patients chose not to undergo carotid endartectomy, optometric management should include a dilated fundus examination every 6 months, monitoring closely for ocular complications of carotid artery disease and ocular ischemic syndrome. In addition to careful ocular examination, comanagement with their primary provider and a vascular specialist is recommended.

6 Trego and Pagani Clinical Care 87 Conclusion These 3 presentations show that through proper management of patients over 50 who present with chief complaints of monocular vision loss, a differential diagnosis of carotid artery disease should be considered. Patients who exhibit retinal arterial emboli are at an increased risk for both stroke and vascular death. Appropriate measures for confirming a diagnosis include carotid duplex ultrasound imaging, MRA, and carotid angioplasty. Proper management of these patients includes a dilated fundus examination every 6 months and monitoring closely for ocular complications of carotid artery disease. Further medical management with antiplatelet therapy, risk factor modification, as well as surgical techniques such as carotid angioplasty and carotid endarterectomy may be recommended. 28 References 1. Biousse V. Carotid disease and the eye. Curr Opin Ophthalmol 1997;8: Alexander LJ. Variations in physicians response to consultation requests for Hollenhorst plaques: a pilot study. J Am Optom Assoc 1992;63(5): American Heart Association Medical/Scientific Statement. Guidelines for the management of patients with transient ischemic attacks. Stroke 1994;25: Streifler JY, Eliaziw M, Benavente OR, et al, for the North American Symptomatic Carotid Endarterectomy Trial. The risk of stroke with first-ever retinal vs hemispheric transient ischemic attacks and high grade stenosis. Arch Neurol 1995;52: Egan RA, Biousse V. Update on ischemic stroke. Curr Opin Ophthalmol 2000; 11: Klein R, Klein BEK, Jensen SC, et al. Retinal emboli and stroke: The Beaver Eye Dam Study. Arch Ophthalmol 1999;117: Recchia FM, Brown GC. Systemic disorders associated with retinal vascular occlusion. Curr Opin Ophthalmol 2000;11: McCullough HK, Reinert CG, Hynan LS, et al. Ocular findings as predictors or carotid occlusive disease: is carotid imaging justified? J Vasc Surg 2004;40: Wasserman DH, Hobson RW, Lynch TG, et al. Ultrasonic imaging and oculoplethysmography in diagnosis of carotid occlusive disease. Arch Surg 1983;118: Graham AA. Plethysmography: safety, effectiveness, and clinical utility in diagnosing vascular disease. Health Technol Assess (Rockv) 1996;7: Blakeley DD, Oddone EZ, Hasselblad V, et al. Noninvasive carotid artery testing: a meta-analytic review. Ann Intern Med 1995;122: Barkana Y, Harris A, Hefez L, et al. Unrecordable pulsatile ocular blood flow may signify severe stenosis of the ipsilateral internal carotid artery. Br J Ophthalmol 2005;87: Silver DM, Farrell RA. Validity of pulsatile ocular blood flow measurements. Surv Ophthalmol 1994;38:S Sharma S, Brown GC, Pater JL, et al. Does a visible retinal embolus increase the likelihood of hemodynamically significant carotid artery stenosis in patients with acute retinal arterial occlusion? Arch Ophthalmol 1998;116: Biller J, Thies W. When to operate in carotid artery disease. Am Fam Physician 2000; 61: Garcia JH, Khang-Loon H. Carotid atherosclerosis: definition, pathogenesis, and clinical significance. Neuroimaging Clin North Am 1996; 6: El-Barghouty N, Nicolaides A, Bahal V, et al. The identification of the high risk carotid plaque. Eur J Vasc Endovasc Surg 1996;11: Hatsukami TS, Ferguson MS, Beach KW, et al. Carotid plaque morphology and clinical events. Stroke 1997; 28: Golinik KC, Hund PW, Stroman GA, et al. Magnetic resonance imaging in patients with unexplained optic neuropathy. Ophthalmology 1996;103: North American Symptomatic Carotid Endarterectomy Trial (NASCET) Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med 1991;325: European Carotid Surgery Trialists Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70-99%) or with mild (0-29%) carotid stenosis. Lancet 1991;337: Norris JW, Zhu CA, Bornstein NM, et al. Vascular risks of asymptomatic carotid stenosis. Stroke 1991;22: CASANOVA Study Group. Carotid surgery versus medical therapy in asymptomatic carotid stenosis. Stroke 1991;22: Mayo Asymptomatic Carotid Endarterectomy Study Group. Results of a randomized controlled trial of carotid Endarterectomy for asymptomatic carotid stenosis. Mayo Clin Proc 1992;67: Hobson RW 2nd, Weiss DG, Fields WS, et al. Efficacy of carotid endarterectomy for asymptomatic carotid stenosis. N Engl J Med 1993;328: Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid stenosis. JAMA 1995;273: European Carotid Surgery Trialists Collaborative Group. Risk of stroke in the distribution of an asymptomatic carotid artery. Lancet 1995;345: Wijman C, Gomes JA, Winter MR, et al. Symptomatic and asymptomatic retinal embolism have different mechanisms. Stroke 2004;35: e Schwarcz TH, Eton D, Ellenby MI, et al. Hollenhorst plaques: Retinal manifestations and the role of carotid endarterectomy. J Vasc Surg 1990;11: