|Year : 1969 | Volume
| Issue : 6 | Page : 270-272
Embolism of central retinal artery originating from mitral valves (mitral stenosis)- case report
OP Kulshreshtha, MR Jain, MM Singh, S Bhargawa
Department of Ophthalmology, R.N.T. Medical College, Udaipur, India
|Date of Web Publication||11-Jan-2008|
O P Kulshreshtha
Department of Ophthalmology, R.N.T. Medical College, Udaipur
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Kulshreshtha O P, Jain M R, Singh M M, Bhargawa S. Embolism of central retinal artery originating from mitral valves (mitral stenosis)- case report. Indian J Ophthalmol 1969;17:270-2
|How to cite this URL:|
Kulshreshtha O P, Jain M R, Singh M M, Bhargawa S. Embolism of central retinal artery originating from mitral valves (mitral stenosis)- case report. Indian J Ophthalmol [serial online] 1969 [cited 2020 Aug 4];17:270-2. Available from: http://www.ijo.in/text.asp?1969/17/6/270/38554
It is currently presumed that the embolism of Central retinal artery is not so common though embolism of cerebral vessels is not uncommon. This is understandable as an embolus can readily pass from the ascending aorta into the innominate and the left common carotid artery which are continuous with it. The rarity of embolism in the central retinal artery is explained on the basis of the fact that these emboli must first pass the perpendicular ramifications of the artery from the internal carotid and then the perpendicular ramifications of the central retinal artery from the ophthalmic artery.
A typical case of occlusion of central retinal artery with embolus from mitral valves in a young female with mitral stenosis is described.
| Case Report|| |
Mrs. M., 26 years old Mohammedan widow attended the eye out-door on 3rd August, 1968, with a complaint of sudden loss of vision in the right eye since 8.00 A.M. While washing her clothes, she felt sudden clouding and loss of vision in her right eye leading to complete blindness.
On examination, the right pupil was found to be slightly dilated and sluggishly reacting to light directly, but reacting briskly consensually. Perception of light was absent. Fundus showed typical picture of central artery obstruction : Optic-disc was pale and showed slight oedema with indistinct margins. Retina was dull, oedematous, pale opaque white in colour showing a characteristic cherry-red spot at the fovea. Larger arteries were reduced to thread like dimensions and small arteries were invisible. Veins showed typical cattle-truck appearance with the blood thrown into columns or beads.
Following treatment was immediately instituted : Ocular massage accompanied with retrobulbar injection of Atropine 1/100 grain and tablet Nicotinic acid 50 mg each, 3 tablets stat. A hot bath was also given. At 12 o'clock, Inj. Duadilan 2 c.c. (isox suprine HCL 5 mg/ml) with 20 c.c. of 5%, glucose slowly was given intravenously followed by tablet Arlidine (nylidrine hydrochloride N.F. 6 mg.) stat and 4 hourly.
At 12.00 P.M. the patient developed perception of light, recognised a few objects dimly around her and even could count fingers in the temporal field at a distance of about 8 inches. At 1.00 P.M. her vision improved to finger counting at 2 meters. On fundus examination, the arteries over and near the disc became visible though markedly attenuated. Rest of the picture was the same. At 5.00 P.M. vision was finger counting at 5 meters in the temporal field. Pallor of the disc was as before. Retinal arteries were visible all over the fundus except in the temporal region. Rest of the picture was the same.
With continued administration of retrobulbar injection of Atropine 1/100 gr. twice a day and Nicotinic acid 100 mg. intravenously twice a day along with oral vasodilators (Tab. Arlidine 6 mg. thrice daily) and anticoagulant therapy (Dindivan 50 mg. tablet 8 hourly), the patient's vision improved to 6/12 in the temporal field and hand movement in the central and nasal field. Perimetry was not possible due to lack of fixation. After 6 days since the attack, fundus still showed pallor of the optic disc. The retina on the nasal side of the disc was normal in appearance, colour and reflex. Vessels in the nasal quadrant appeared perfectly normal but the lower temporal vessels (arteries) were still attenuated and showed a probable impaction of an embolus two disc diameters away from the disc. Smaller vessels around the macula were visible and instead of cherry-red spot, the macular area showed fine punctate pigmentary spots with an absent foveal reflex. Slight perimacular oedema still persisted.
Ten days later, the examination showed vision of 6/9 with glasses (-0.5 D. Sph) with slight eccenteric fixation. The disc was comparatively less pale and only the lower temporal vessel showed constriction with the lodged embolus. Macular area showed punctate pigment deposits.
General Examination and Investigations
Cardiac examination showed a late diastolic murmur of crescendo character with presystolic accentuation, suggestive of mitral stenosis. Blood pressure was 112/80 mm Hg. and electrocardiogram was normal.
Blood tests were as under :-
Total lececocytes 7,500 c mm.
Differential: count polymorphs 66%, lymphocytes 32%, monocytes 1%, basophils 1%.
Kahn's Test : Negative.
Coagulation time and clotting time were within normal limits.
No septic focus was present anywhere in the body and there was no history of any joint pains or of prolonged illness.
| Discussion|| |
The case is of clinical interest because the effected eye showed typical clinical picture of central retinal arterial obstruction due to embolism with clinical evidence of mitral stenosis and presence of impacted embolus in the lower temporal retinal vessel. Embolism as a cause of central arterial obstruction is presumed to be uncommon though various workers have demonstrated various embolic agents. von Graefe  and Manchot  have demonstrated endocarditis as a cause of retinal embolism. Fat (Fritz and Hogan  ), Mercury (Vallotton and Stokes  ) and Loiasis (Toussaint and Danis  ; Corrigan and Hill  ) have also been demonstrated as rare embolic agents. In the case cited above an embolus originating from the mitral valves was lodged in the central retinal artery probably at the cribriform plate (where there is physiological narrowing) leading to rapid loss of vision. Vasodilator drugs used dislodged the embolus from the central artery but it got finally lodged in the lower temporal branch. Early recovery of vision in the temporal field synchronises immediate reestablishment of blood circulation after the treatment.
Urgency of treatment is imperative. Once total occlusion has been present for some time, there is retinal ischtemia specially to the nerve fibre layers and irrepairable damage is done. Treatment consisting of intensive vasodilators systemically combined with retrohulbar injection of atropine, ocular massage and hot bath are essential. Anticoagulant therapy may also be of some value.
| Summary|| |
A case of central retinal arterial obstruction due to embolism arising from mitral valves (mitral stenosis) is reported. The diagnosis of embolism was supported by clinical evidence of mitral stenosis and ophthalmoscopic evidence of impacted embolus in lower temporal retinal artery. The embolus finally got lodged in the inferior temporal branch of retinal artery.
Intensive treatment resulted in reestablishment of retinal circulation and considerable improvement in visual acuity.
| References|| |
Corrigan, M. J.. and Hill, D. W.: Retinal Artery Occlusion in Loiasis. Brit. J. Ophth. 52: 477 (1968).
Fritz. M. H.. and Hogan, M. J.: Fat Embolization involving the human Eye. Amer. J. Ophth., 31: 527 (1948).
Graefe. A, von: On Embolism of the central retinal Artery as a cause of sudden Blindness (in German) Arch. f. Ophth. 5: 136 (1959).
Manchot. W. A.: Embolism of Central Retinal Artery Originating from a endocardial Myxoma. Amer. J. Ophth. 48: 381-385 (1959).
Toussaint. D.. and Danis. P.: Arch. Ophthal. (Chicago) 74: 470 (1965).
Vallotton, W. W., and Stokes, H. R.: Mercury_ Embolism of Central Retinal Artery. Amer. J. Ophth. 57: 476 (1964).