Table of Contents  
CASE REPORT
Year : 2013  |  Volume : 6  |  Issue : 4  |  Page : 421-424  

Ophthalmologists saving life of a young patient presenting with sudden simultaneous bilateral retinal artery occlusions secondary to calcific emboli of cardiac origin


1 Department of Ophthalmology, Padmashree Dr. D. Y. Patil Medical College, Hospital and Research Centre, Dr. D. Y. Patil Vidyapeeth, Pimpri, Pune, India
2 SBKS Medical Institute & Research Center, Vadodara, Gujarat, India

Date of Web Publication17-Sep-2013

Correspondence Address:
Kavita R Bhatnagar
B 4/21, Brahma Aangan, Off Salunke Road, Kondhwa, Pune - 411 048, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.118268

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  Abstract 

We present a case report of a young 35-year-old previously healthy male with simultaneous central retinal artery occlusion in the right eye and branch retinal artery occlusion in the left eye with visible calcific emboli in both eyes from calcified mitral valve diagnosed on trans-esophageal echocardiography. Patient underwent an urgent life-saving mitral valve replacement surgery within 2 days as Ophthalmologists immediately referred him to Cardiologist moment they visualized calcific emboli in both eyes with bilateral retinal artery occlusions on fundoscopy. Bilateral retinal artery occlusions suggest a source of emboli at the level of the heart or aortic arch. All patients with retinal ischemia should have a complete cardiovascular evaluation supplemented by Transesophageal echocardiography. Many times an Ophthalmologist might be the physician of first contact for patients with cardiac diseases and awareness of the disease is therefore important for all Ophthalmologists. Timely referral and management by Cardiologist/cardiac surgeon may protect patient against serious life-threatening complications.

Keywords: Bilateral retinal artery occlusions, calcific emboli, mitral valve calcification


How to cite this article:
Bhatnagar KR, Gupta D. Ophthalmologists saving life of a young patient presenting with sudden simultaneous bilateral retinal artery occlusions secondary to calcific emboli of cardiac origin. Med J DY Patil Univ 2013;6:421-4

How to cite this URL:
Bhatnagar KR, Gupta D. Ophthalmologists saving life of a young patient presenting with sudden simultaneous bilateral retinal artery occlusions secondary to calcific emboli of cardiac origin. Med J DY Patil Univ [serial online] 2013 [cited 2024 Mar 29];6:421-4. Available from: https://journals.lww.com/mjdy/pages/default.aspx/text.asp?2013/6/4/421/118268


  Introduction Top


Several cardiovascular causes of retinal ischemia have been described. Retinal artery occlusion is rare, but potentially devastating complication of calcified mitral valve stenosis resulting as a consequence of the retrograde arteriolar micro embolus into the ophthalmic artery. [1] These cases can easily be missed as they have few cardiac symptoms or physical signs until late stage. Patients may first present with amaurosis fugax or rarely retinal artery occlusion as was the case with us and awareness of the disease are important for all Ophthalmologists as timely referral and management by Cardiologist/cardiac surgeon may protect patient against serious life-threatening complications.

We report a case of 35-year-old young male with simultaneous central retinal artery occlusion (CRAO) in the right eye and branch retinal artery occlusion (BRAO) in the left eye with visible calcific emboli in both eyes from calcified mitral valve diagnosed on trans-esophageal echocardiography.


  Case Report Top


A previously healthy young 35-year-old male patient reported to eye out-patient department of a tertiary care teaching hospital with complaints of sudden painless diminution of vision, right eye more than left eye of 10 days duration. He gave a history of breathlessness on exertion of recent onset for which he never visited a physician as he never realized the seriousness of his illness. He had been a chronic smoker since teenage.

On examination, visual acuity in the right eye (oculus dexter [OD]) was a perception of light with accurate projection of rays and 20/200 improving to 20/60 in the left eye (oculus sinister [OS]). Applanation tonometry revealed 7.0 mm of Hg pressure in both eyes. Pupil showed relative afferent pupillary defect in OD. Rest of anterior segment was normal in both eyes. Fundus examination showed a cherry red spot with pale white retinal background, presence of a normal patent cilioretinal artery, with an area of normal retina between the optic disc and central macular region and embolus in the central retinal artery just before its bifurcation into superior and inferior division over the optic nerve head OD [Figure 1]a and b and a large area of segmental infarction of the retina along the inferotemporal arcade with an embolus in the inferior-temporal branch just after bifurcation, better delineated in red free photograph OS [Figure 1]c and d. The extent of sparing of part of the macular retina between optic disc and fovea due to the presence of a patent cilioretinal artery is better delineated in red free photograph [Figure 1]b. Fundus Fluorescein angiography showed delayed arteriovenous transit time of 14 s, normal choroidal filling with normal filling pattern seen in the area supplied by patent cilioretinal artery and narrowed arterioles at perifoveal regions OD and delayed arteriovenous transit time in the inferotemporal branch OS. Based on these findings a clinical diagnosis of OD: CRAO and OS: Inferotemporal branch retinal artery occlusion (BRAO) was made. Emergency ophthalmic management is useful only if patient reports within few hours of catastrophe. [2] Our main aim was to find out the source of emboli and treat the associated systemic problems. A physician and Cardiologist reference was immediately made. Carotid ultrasound, magnetic resonance imaging and magnetic resonance angiography of the brain, trans-thoracic echocardiogram and laboratory work-up, including coagulation profile, were within the normal limits. Trans-esophageal echocardiography revealed severe calcific mitral stenosis, moderate mitral regurgitation, calcification in proximal interventricular septum, dilated left and right atrium, normal aortic valve and moderate tricuspid valve regurgitation. Doppler study showed moderate pulmonary arterial hypertension. Chest X-ray revealed bilateral pulmonary emphysema. Mitral valve replacement surgery was performed with R27# TTK China Valve at our hospital. On follow-up after 2 months, OD vision improved to Counting finger at 1 m due to the presence of patent cilioretinal artery and OS improved to 20/20. Fundus showed reabsorption of retinal edema and resolution of retinal pallor in both eyes. Patient did not cooperate for the right eye visual field charting, but in the left eye there was a superonasal scotoma corresponding to the area supplied by occluded inferotemporal retinal artery branch.
Figure 1

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  Discussion Top


Arterial obstructive disease of the eye is frequently encountered in clinical practice, but simultaneous bilateral retinal artery occlusions are a rare occurrence. Simultaneous bilateral retinal artery occlusions with visible emboli in both eyes are rarer. Retinal arteriolar emboli can be found in approximately 1% of adults more than 40 years of age. The frequency of retinal emboli increases with age and are more common in men than in women. Bilateral retinal emboli are rare; although, multiple emboli in a single eye may be seen in up to one-third of cases. [3]

The common etiologies found in the literature are arteriosclerotic thrombosis, vasculitis, embolic impaction, vasospasm or systemic hypotension. Over 75% of patients with CRAO suffer from generalized atheromatous disease, which is frequently associated with hypertension or diabetes mellitus or both. [1] Hypercoagulable state has been found to be a major cause responsible in young patients. [4]

CRAO was first described by Von Graefe [5] in 1859 as an embolic event in a patient of endocarditis. Three types of retinal emboli are described, that is calcific, cholesterol and platelet-fibrin. [6]

Patients with CRAO present with a sudden painless loss of vision. The appearance of a cherry-red spot in the fundus is characteristic. The cherry-red spot appears because soon after obstruction of the blood flow to the inner retina, the normally transparent retina becomes opaque and blocks the brownish-red color from the underlying retinal pigment epithelium. Because the retina overlying the foveola is relatively thin; however, the normal color of the underlying retinal pigment epithelium is still visible in this area. An afferent pupil defect is usually present. With obstruction, virtually all eyes have narrowing and irregularity in the arteries and there is frequently an irregularity in the caliber of the retinal veins. Segmentation (boxcarring) of the blood column frequently develops. In approximately 20% of patients, an embolus is evident somewhere in the arterial system. [7],[8] Branch retinal artery occlusion may have peripheral or central visual loss or normal vision depending upon the branch affected.

Our patient had all these features. The marked improvement in the left eye visual acuity on follow-up after 2 months may be a natural course of the disease. [9] The presence of patent cilioretinal artery in the right eye explains the visual improvement to "counting fingers" in this eye. This eye had an intact island of visual field corresponding to that normal area of the retina as seen in [Figure 1]a and b. It is well-known that in eyes with Central retinal artery occlusion and sparing of the cilioretinal artery, visual recovery is better than in ordinary CRAO. This was reported in a large study published in the American Journal of Ophthalmology. [9]

Obstruction of the retinal arterial circulation is an important clinical event not only in terms of the visual outcome and ophthalmic complications, but also because of the increased systemic morbidity and mortality among these patients. [1] Patients with visualized retinal artery emboli, whether or not obstruction is present, have a 56% mortality rate over 9 years, compared to 27% for an age-matched population without retinal artery emboli. Life expectancy of patients with CRAO is 5.5 years compared with 15.4 years for an age-matched population without CRAO. [10]

Bilateral retinal artery occlusions suggest a source of emboli at the level of the aortic arch or the heart. [11] Appropriate evaluation requires a trans-esophageal echocardiogram because trans-thoracic echocardiography may miss cardiac sources of emboli and is not adequate for the assessment of the aortic arch atheroma in most cases. [12]

Our patient was unusual in having CRAO in the right eye and branch retinal artery occlusion in the left eye simultaneously with visible calcific emboli in both retinae. Carotid ultrasound, magnetic resonance imaging and magnetic resonance angiography of the brain, trans-thoracic echocardiogram and laboratory work-up including coagulation profiles were within the normal limits. Trans-esophageal echocardiography confirmed severe calcific mitral stenosis, moderate mitral regurgitation and calcification in proximal interventricular septum. From mitral valve calcific emboli might have gone to the retinal artery, which is a branch of the ophthalmic artery.

Eyes with a CRAO normally have a poor visual prognosis and nothing much can be carried out if patients report to Ophthalmologist after few hours of catastrophe. An experimental study in elderly, hypertensive, atherosclerotic rhesus monkeys showed that CRAO of only 4 h results in irreversibly ischemic retinal damage and there is no logical possibility of visual recovery after that. [2] But with timely management of systemic problems including cardiac surgery can save a life and prevent future ischemic attacks, particularly stroke.

Take home message

All patients with retinal ischemia should have a complete cardiovascular evaluation supplemented by trans-esophageal echocardiography. Many times an Ophthalmologist might be the physician of first contact for patients with cardiac diseases and awareness of the disease is therefore important for all Ophthalmologists. Timely referral to Cardiologist/cardiac surgeon may protect patient against serious life-threatening complications.

 
  References Top

1.Beatty S, Au Eong KG. Acute occlusion of the retinal arteries: Current concepts and recent advances in diagnosis and management. J Accid Emerg Med 2000;17:324-9.  Back to cited text no. 1
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2.Hayreh SS, Zimmerman MB, Kimura A, Sanon A. Central retinal artery occlusion. Retinal survival time. Exp Eye Res 2004;78:723-36.  Back to cited text no. 2
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3.Wong TY, Klein R. Retinal arteriolar emboli: Epidemiology and risk of stroke. Curr Opin Ophthalmol 2002;13:142-6.  Back to cited text no. 3
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4.Hayreh SS, Podhajsky PA, Zimmerman MB. Retinal artery occlusion: Associated systemic and ophthalmic abnormalities. Ophthalmology 2009;116:1928-36.  Back to cited text no. 4
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5.Von Graefe A. Ueber embolie der arteria centralis retinae als urscahe plotzlicher erblingdung. Albrecht Von Graefes Arch Ophthalmol 1859;5:236-57.  Back to cited text no. 5
    
6.Arruga J, Sanders MD. Ophthalmologic findings in 70 patients with evidence of retinal embolism. Ophthalmology 1982;89:1336-47.  Back to cited text no. 6
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7.Duke-Elder S, Dobree JH. System of Ophthalmology: Diseases of the Retina. Vol. 10. St. Louis: CV Mosby; 1967.  Back to cited text no. 7
    
8.Hayreh SS. Prevalent misconceptions about acute retinal vascular occlusive disorders. Prog Retin Eye Res 2005;24:493-519.  Back to cited text no. 8
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9.Hayreh SS, Zimmerman MB. Central retinal artery occlusion: Visual outcome. Am J Ophthalmol 2005;140:376-91.  Back to cited text no. 9
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10.Kedar S, Biousse V, Newman NJ. Simultaneous bilateral retinal artery occlusions associated with a mitral valve mass. J Neuroophthalmol 2005;25:215-6.  Back to cited text no. 10
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11.Nischal KK, Aclimandos WA. Bilateral symmetrical branch retinal artery occlusions. J R Soc Med 1995;88:416P-7.  Back to cited text no. 11
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12.van Rhee F, Blecher TE, DeLepeleire KA, Galloway NR. Bilateral retinal artery occlusion due to mitral valve prolapse. Br J Ophthalmol 1991;75:436-7.  Back to cited text no. 12
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