Indian Journal of Ophthalmology

ARTICLES
Year
: 1979  |  Volume : 27  |  Issue : 4  |  Page : 200--202

Short posterior ciliary artery block (a case report)


SRK Malik, S Malik 
 Sir Ganga Ram Hospital, New Delhi, India

Correspondence Address:
SRK Malik
Sir Ganga Ram Hospital, New Delhi
India




How to cite this article:
Malik S, Malik S. Short posterior ciliary artery block (a case report).Indian J Ophthalmol 1979;27:200-202


How to cite this URL:
Malik S, Malik S. Short posterior ciliary artery block (a case report). Indian J Ophthalmol [serial online] 1979 [cited 2024 Mar 29 ];27:200-202
Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?1979/27/4/200/32628


Full Text

Case History

A young lady aged 20 years came to the eye department in April, 1977 with the complaints of a persistent black net in front of the left eye and a gradual diminution of vision of the same eye. Her complaints started in late 1975 (around October) when one day she suddenly had bleeding from her nose and gums followed 3-4 days later by profuse bleeding per vagina. The last symptom was not menstrual because she had just finished her last cycle 15 days prior to the beginning of these complaints. She became very weak and was finally prostrated- Some local doctor was consulted and with his medication bleeding from nose and gums stopped. The weakness continued and finally after about 20 days she was admitted to the Holy Family Hospital. Her haemoglobin at the time of admission was 5 gm% and by this time bleeding from vagina bad also stopped. All other investigations were normal except for a slightly raised ESR, lowered platelet count and a peripheral smear which showed hyperchromatic, microcytic anaemia.

She was then given 21 units of fresh blood in siliconised bottles over a period of about 1 month. In the midst of these transfusions, one day, she developed the present eye complaint in the form of sudden blurring of vision and then the persistence of black net in front of her left eye. Her complaint was disregarded at that time as a part of the generalised weakness. She was given supportive therapy in the form of Prednisilone tablets (Total of approx. 400 tabs). and ampiciilin capsules with iron and vitamin. Gradually her haemo�globin came up to 8 gm%. In between transfusions there was no other complaint, and she was finally discharged after 1 month. However, within 15 days she was readmitted with high-grade fever which was diag�nosed as Malaria and blood smear was positive for the parasite. Peripheral blood picture at this stage showed toxic granules on polymorphs, and blood culture was positive for mimapolymorpha. She was treated with chloroquin. She responded to it and was again dis. charged with a Haemoglobin of 8 gm%.

Her eye complaint in the meantime had remained stationery and she, herself did not take much notice of it. In 1976, she went to an eye hospital for a check up, where she was told that she had a retinal haemorrhages which was incurable and prescribed zincosulpha eye drops. This year in April, she came to Mool Chand Hospital and has been under our care since.

On examination we found that her right eye is normal. Her left eye to all external appearances is normal but the vision is 6/60 with the head tilted slightly upwards.

On direct ophthalmoscopy, the media were clear, vessels were normal but the disc showed a marked temporal pallor. Along the lower retinal vessels, there is a fairly large area of yellowish-brown depigmentation in the midst of which are seen several round, circums�cribed, well defined yellowish-grey spots. The macula showed stippling [Figure 1].

The visual field of the left eye showed a sectorial scotoma in the upper field corresponding to the defect seen in the fundus [Figure 2].

Flourescence angiography was done. Yellowish grey round areas appeared as dark, round areas devoid of flourescence amidst a greyish haze of choroidal flourescence. [Figure 3].

 Discussion



There have been very few cases described previously with a similar clinical appearance, and at times, it is often difficult to determine the exact mode and site of lesion. Condon, Sergeant and Ideda (1973) described 2 cases in which an unusual chorioretinopathy was seen. These patients had reduced visual acuity and visual field loss associated with an unusual chorioretinal atrophic condition which they attributed to a vascular occlusive process charac�teristic of sickle cell disease affecting posterior ciliary vessels. In each case, the fluorecein angio�graphic picture showed a mottled appearance with pale yellow tracks interspersed with areas of brownish red apparently normal retina. In case there was typical multiple small round white area in the active phase. This case was not followed up by authors as we feel that in late stage it would have resembled our case.

Before discussion it would be essential to give a brief description of the pattern of post�erior ciliary arteries in man, and the blood supply of the optic disc and optic nerve, so as to make the discussion more explicit.

Hayreh's studies (1970) have demonstrated that the posterior ciliary can be designated as medial, lateral and superior depending on their relationship with the optic nerve.

(a) The medial posterior ciliary artery may be one (in 70% of cases) or two (in 30% of cases).

(b) The lateral posterior ciliary artery may be one (75% cases), two (20% of cases), three (less than 2% of cases), and more (3% of cases).

(c) The superior posterior ciliary artery may be seen in only 9% of cases and may be one in 7% of cases and two in 2% of cases.

The mode of origin of the posterior ciliary arteries from the ophthalmic artery varies. The medial posterior ciliary artery arises in common with the central retinal artery in 44� % of cases. In the remainder, it is usually single and occasioally arises with other branches of the ophthalmic artery. The lateral artery arises with the central retinal artery in 12% cases, but is usually an independent branch, and more rarely with any other branch.

At the point of crossing of the ophthalmic artery over the optic nerve, the medial branch arises first in 53% of cases and the lateral branch in 22% of cases. According to Wolff (1948) and Duke-Elder (1961), the posterior ciliary arteries divide into 10-20 small branches as they run forwards, and pierce the sclera near the optic nerve. Of these larger numbers of branches, one on the medial side and another on the lateral side form the long posterior ciliary arteries, while the rest have been named short posterior ciliary arteries. The two long posterior ciliary arteries pierce the sclera on the medial and lateral sides slightly further away from the optic nerve than the short ones. Notwithstanding the number of posterior ciliary arteries, the lateral distribution is usually greater than the medial, and there is consistently a discrete submacular artery. The posterior ciliary arteries are often markedly tortuous.

Waybar (1954) basing his opinion on his injection studies of the short posterior ciliary arteries concluded that these arteries were segmental in arrangement and that each branch supplied a localised zone of the choroid with a network of arterioles and capillaries. He had, however, denied any anatomical concept that these arteries were true end-arteries. In Hayrch's studies (1970) in vivo, a well demarcated segmental distribution by the posterior ciliary arteries in the choroid and optic disc was seen. In 80% of these cases, the temporal and nasal half of the choroid and optic disc filled with the dye completely, while the other half remained devoid of it, and the two areas were sharply outlined. In the remaining 20%, a similar phenomenon was seen in the upper and lower half of the choroid and optic disc.

On repeated fiourescence antiography in some, only a quadrantic filling of the choroid and optic disc was observed, the rest remaining empty. These studies suggest a well-demarcated segmental distribution, by the posterior ciliary arteries in the choroid and the optic disc. This is further suggested by the selective localisation of pathological lesions in the choroid and the disc in relation to its vascular anatomy.

The vascular lesions responsible for nerve fibre bundle defects lie either in the optic disc or in the optic nerve. In the prelaminar region, it seems that each branch of the posterior ciliary artery supplies a well-defined sector. The involvement of one of the arteries thus produces a sectoral nerve fibre bundle defect. Occlusion of one of the posterior ciliary arteries or its smaller divisions, therefore would involve a sector of the lamina cribrosa, the prelaminar part of the optic disc and the retro laminar part of the optic nerve. When a sector of the peripapillary choroid only is involved, the region of the lamina may be spared. A poste�rior ciliary artery occlusion may result from any form of arterities or embolism, thrombosis, or arterioschlesesis. The area of infarction involved would depend on the size of artery occluded, i.e., occlusion of the main posterior ciliary artery would involve a larger area, while occlusion of one of its subdivisions would affect a much smaller area, in fact a sectoral lesion would be produced. In these cases retinal vessels are normal.

Hence, any lesion destroying the peripapillary choroid in a sector will interfere with the blood supply to the corresponding sector of the disc and a complete occlusion of the posterior ciliary artery, produces ischaemic optic neuropathy. Considering this study of the segmental choro�idal supply and applying this basic anatomy to the clinical appearances of our cases, we would postulate that the unusual choroidal atrophy

and the sectorial field defect seen in our cases is due to a vascular occlusive process affecting one of the short posterior ciliary artery, pro�bably an embolism or thrombosis following blood transfusion.

 Summary



This case is being presented because of the unusual clinical appearance and associated clinical history. It is being discussed as a case of possible short posterior ciliary vessel occlu�sion leading to an unusual type of choroidal atrophy and associated with a sectoral nerve fibre bundle defect. The case is probably an embolism or thrombosis following the adminis�tration of several bottles of blood.