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Year : 1975  |  Volume : 23  |  Issue : 1  |  Page : 36-38

Ocular manifestations of pulseless disease

Nehru Institute of Ophthalmology and Research, Eye Hospital, Sitapur, India

Correspondence Address:
A K Paul
Nehru Institute of Ophthalmology and Research, Eye Hospital, Sitapur
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Source of Support: None, Conflict of Interest: None

PMID: 1158422

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How to cite this article:
Paul A K. Ocular manifestations of pulseless disease. Indian J Ophthalmol 1975;23:36-8

How to cite this URL:
Paul A K. Ocular manifestations of pulseless disease. Indian J Ophthalmol [serial online] 1975 [cited 2021 Mar 5];23:36-8. Available from: https://www.ijo.in/text.asp?1975/23/1/36/31332

Pulseless disease is a form of chronic circulatory insufficiency characterised by pro­gressive obliteration of the great vessels arising from the arch of the aorta leading to arterial hypotension and a diminution or absence of pulsation of the vessels in the neck and arms and is associated with hypertension in the lower extremities. [1],[2],[15],[17]

In India few cases have been reported so far [5],[7],[9],[10],[11],[14]

Two types of the disease occur. The first, is common in females between the age 20 and 30 years, frequently seen in. Japanese and is mainly inflammatory in origin known as Takayasu's disease. The main characteristic changes are diffuse and non-specific arteritis, in vascular wall particularly of adventitia with inflammatory reaction containing giant cells leading to thrombosis [18] It is associated with raised sedimentation rate, leucocytosis and occasional fever. The second type, is found in patients with degenerative in nature and also known as Takayasu's syndrome or aortic arch syndrome. It occurs in older patients of either sex without racial predilection usually during 5th or 6th decades of life. The etiology of occlusion is principally the result of syphilitic aortitis and aneurysm [13] and atherosclerosis with thrombosis and atheroma to be common basis of the syndrome [19] .

The most common ocular findings described are [13] : 1. Atrophy of ciliary muscle and processes, 2. Cataractous change in the lens 3. diminis­hed central retinal arterial blood flow 4. Retinal arteriovenous anastomoses and new vessels formation in nerve fibre layers. 5. Clumping of rods and cones. 6. Decrease in the number of ganglion cells and 7. Demyelinization of optic nerve.

  Case Report Top

A Hindu female aged 30 years was admitted with history of progressively severe episodes of transient loss of vision, headache, fainting and weakness with tingling sensation in limbs since one year. The fainting was precipitated on standing from lying down position or on looking up. She had also noticed that if she put her hand under her head, or pillow while resting, the fingers would get numb.

A young moderately built woman, married 12 years back, has three children and all are healthy. The heart was slightly enlarged but sounds were normal. radial, brachial and temporal arteries were not palpa­ble and were without pulsation. Blood pressure could not be recorded in the upper limb but in the lower limb (Popliteal artery) it was 210/100 mm of Hg. Her speech was slow and face looked exhausted. Routine laboratory tests were within normal limits, except that the haemoglobin percentage was slightly low. The fasting blood sugar was 90 mg%.

Vision in right eye was finger counting one meter and in left eye it was only perception of light. The con­junctiva and cornea showed no abnormalities. Both the pupils were dilated and reacting sluggishly to light and convergence. There were patches of atrophy in the iris. Fine vessels could be seen on the surface e€ the iris mostly in the ciliary region. The lens showed posterior subcapsular opacity in both the eyes.

The intra ocular pressure in right eye was 17.3 mm. and in the left eye was 14.2 mm. (Schiotz). The ophthalmodynamometric pressure of the central retinal artery was found to be very low.

The most significant abnormalities were seen in the retina and pictures were almost same in both eyes. The discs were pale and covered with dilated and tortuous blood vessels. Arteries were almost untrace­able from the discs. The veins were tortuous, irregular with dilatations and showed segmentation of the mov­ing blood columns. There were peripapillary arterio­venous communications. There were superficial haemorrhages around the disc and few exudative spots were seen in the para macular area.

Fluorescein angiography showed delayed arm to retina circulation time (28 seconds) [Figure - 1] The arteries were seen occluded about 2 disc diameters from the disc. The veins were also similarly obliterated. There were dilated arteriovenous communications [Figure - 2]. The fine blood vessels on the disc were dilated tortuous and were showing aneurysmal dilatations. The dye [Figure - 3]was freely leaking from these vessels.

The essential ocular lesions described relate to persistent chronic ischaemia as a result of stenosis or occlusion of the great vessels originating from the arch of the aorta. This case presents a unique picture of vaso-occlusive disease. The extensive occlu­sion of the large branches of the central retinal blood vessels a small distance away from the disc seems to be a part of the primary disease process. The arterio­venous communications, and other micro-vascular anomalies could be due to general state of chronic anoxemia.

  Summary Top

A case of pulseless disease showing exten­sive retinal vascular occlusion with consequent vascular anomalies on and around the disc has been presented with fluorescein retinal photographs.

  References Top

Adams, R., 1928 Dubl. Hosp. Reg. 4, 443.  Back to cited text no. 1
Dowling L.J. and Taylor R.S., 1960 Arch­Ophthol. 64, 236.  Back to cited text no. 2
De Bes, Sanchez and Barcons, 1955, Brit. Heart. J. 17, 484.  Back to cited text no. 3
Due Elder, S., 1964 System of Ophthalmology, 10, 367, Henry Kimpton London.  Back to cited text no. 4
Damny, S.J. and Shah, R.M., 1960, of Indian Med. Association 35, 124.  Back to cited text no. 5
Gibbons, T.B. and King, R.L., 1957 Circulation (Quoted by Dowling and Taylor) 15, 845.  Back to cited text no. 6
Jain & Grover, 1963, Brit. J. Ophthal, 47,304.  Back to cited text no. 7
Kurachi, Hirose and Yonemura 1966, Jap. J. Ophthal. 10, Suppl. 106.  Back to cited text no. 8
Misra S. and Satya Prakash, 1959 Heart J. 57, 177.  Back to cited text no. 9
Pahwa, J.M., Pandey and Gupta, D.P., 1959, Brit. Med, J., 2, 1439.  Back to cited text no. 10
Pahwa J.M. and Gupta D.P., 1961, The Medicine & Surgery, 139,  Back to cited text no. 11
Ross R.S. and Me Kusick V.A., 1953, A.M.A. Arch. Intern. Med. 92, 701.  Back to cited text no. 12
Pinkam R.A., 1954, Acta-XVII Conciliurn Ophth. 1,348.  Back to cited text no. 13
Sen Gupta and Ghosh J.C., 1957, Brit. Med. J. 1, 137.  Back to cited text no. 14
Shimizu K., 194; , Rinsho Geka, 3, 377.  Back to cited text no. 15
Shimuzu K. and Sano, K., 1956, J. Neuropath, Clin. ,Veurol, 1, 37.  Back to cited text no. 16
Takayasu M., 1908, Acta Soc. Ophthal, Japan, 12, 554.  Back to cited text no. 17
Takeda, Ooneda, Suto, K & H, and Kubota, 1961, Gunma J. Med. Soc. 10, 27.  Back to cited text no. 18
Thurlbeck and Currens., 1959, Circulation, 19 499.  Back to cited text no. 19


  [Figure - 1], [Figure - 2], [Figure - 3]


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