| Article Access Statistics|
| Viewed||1168 |
| Printed||26 |
| Emailed||0 |
| PDF Downloaded||0 |
| Comments ||[Add] |
Click on image for details.
|Year : 1957 | Volume
| Issue : 4 | Page : 102-106
Clinical study of non-traumatic intra-ocular haemorrhage with particular reference to Eales' disease
Satya Pal Gupta
King George's Medical College, Lucknow, India
Satya Pal Gupta
King George's Medical College, Lucknow
|How to cite this article:|
Gupta SP. Clinical study of non-traumatic intra-ocular haemorrhage with particular reference to Eales' disease. Indian J Ophthalmol 1957;5:102-6
|How to cite this URL:|
Gupta SP. Clinical study of non-traumatic intra-ocular haemorrhage with particular reference to Eales' disease. Indian J Ophthalmol [serial online] 1957 [cited 2013 Jun 18];5:102-6. Available from: http://www.ijo.in/text.asp?1957/5/4/102/40736
The following conclusions have been derived from 100 cases of intraocular haemorrhage (non-traumatic) studied at the eye department, King George's Medical College, Lucknow. It includes 33 cases of Eales' desease, 10 cases of retinitis proliferans, 10 cases of macular haemorrhage, 6 cases of bilateral papilloedema, 15 cases of diabetes, 5 cases of leukaemia, 15 cases of arterio-sclerosis and 5 cases of severe anaemia.
Intraocular haemorrhage is quite a common condition. Of this a large number of cases belong to the younger age group, usually males, who apparently look healthy. The usual complaint is of sudden painless diminution of vision. Though such a case was first described by McKenzie in 1854, it was not until 1880 when Henry Eales gave it the clinical entity. The condition is characterised by recurrent retinal and preretinal haemorrhages associated with perivasculitis occurring mostly in young adult males.
The distribution is world wide and is more common in the tropics. It is usually prevalent amongst people with a low income group and leads to marked diminution of vision to such an extent that the victim becomes a liability to his family and the community at large.
The overall incidence of Eales' disease in our hospital is 33 per cent amongst all non-traumatic intraocular haemorrhage cases, which is possibly due to high incidence of tuberculosis in this part of the world.
Although it is usually stated that Henry Eales of Burmingham in 1880 first defined this group of cases, McKenzie has described a clinical case in a: young man in 1854. Von Graefe recognised this condition as a separate disease in 1855. In Eales' study of five cases the patients were young men, having the history of constipation, headache, dyspepsia, epistaxis, bradycardia, high blood pressure, and low spirits. Eales attributed it to neurosis inhibiting the musculature of alimentry tract and thereby causing engorgement of cranial venous system leading to rupture of venules in the retina and nasal mucous membrane due to compensatory capillary dilatation. On account of the resemblance to the spontaneous nose bleeding in young people, Panas in 1887 suggested the name ocular epistaxis '. Simon 1896 observed tuberculous disease of retinal vessels leading to recurrent intraocular haemorrhage and Harms described it as tubercular periphlehitis. Stoch 1911 suggested that the eye lesions are due to focal reaction of tuberculous toxin on the retinal vessels. Evidence of active tuberculosis has also been presented. Young 1930 reported 3 cases of recurrent vitreous and retinal haemorrhage in adolescent, and one of his cases showed deficiency in blood calcium. During the last 25 years various workers have investigated and reviewed this disease. But no uniform conclusion has yet been arrived at.
Many workers have ascribed it variously to endocrinal dysfunction in females, vitamin C deficiency in diet, blood dyscresias, thromboangeitis obliterans and allergy whereas in Madras it has been attributed to filariasis. Very little light has been thrown in recent years on its etiology except that the retinal perivaculitis at the periphery may cause neovascularisation which may be inter-retinal, vitreal, or uveal, these new vessels in the event of any trauma or even otherwise may rupture intermittently leading to recurrent intraocular haemorrhage. The various causes so far attributed are tuberculosis, septic foci, high blood pressure, and capillary fragility.
In our study of 100 cases, we have carried out all possible investigations including W. R. and Kahn test, capillary fragility test, blood calcium, total and differential W. B. C. count, platelet count, sinus examination and Mantaux test were done, and were found to be within normal limits except the Mantaux which was positive in all cases of Eales' disease with 1:10,000 dilution.
In our series of 33 cases of Eales' disease 32 were males and one female.
Half the cases were intelligent enough to narrate their history. No case gave a history of having suffered from ocular tuberculosis.
They all belonged to the poor or low middle class, majority of them having no balanced diet.
A history of constipation and headache did not form an important feature of our cases. Only three cases complained of occasional constipation.
Eales said that in a patient with recurrent intraocular haemorrhage, his spirits are moderate. It seems quite natural that a man should be in low spirits whose visual acuity in both the eyes is repeatedly interfered with and each time it is going down due to irreversible changes. The mental fit up appears to be due to the anxiety caused to the patient in the face of impending blindness, and has no clinical significance.
Though vales observed raised blood pressure, in my series all had normal blood pressure. Bradycardia has not been observed in any case. Majority of them were thin built and three developed active tuberculosis later on.
Occupation and habits
All patients except four were active subjects.
Two patients suffered from tuberculous infection, one of tuberculosis of knee from six months and the other of urinary tract from two months.
The average age of occurrence of the haemorrhage in the first eye was 23.9 years. Eales in support of his theory said that left eye is mainly affected, there being direct vascular channels on the left side supplying and draining the head area.
Any eye may be affected. In my series of cases the right eye was affected in 18 and left eye in 15 cases. In majority, the other eye was affected sooner or later, usual interval being 2 to 6 months. If proper early treatment is taken it is possible that the other eye may remain normal.
It varies very much from one to five times, sometimes the eye that was affected late showed more recurrence than the eye affected first.
The treatment is not very satisfactory, all sorts of treatments have been tried including endocrines, X-ray therapy. In my series of cases I have divided the treatment in three groups. Each group consisting of II cases.
This group was given antitubercutar treatment :-
Streptomycin I Gm. intra-muscularly, once daily for one month.
P. A. S. 4 Gm. T.D.S. orally for one month.
This group was given coagulant therapy including :-
Calcium gluconate 10% 10 c.c. intra-venously on alternate days, such 10 injections.
Vitamin C. 500 mgm. intra-venously on alternate days, such 10 injections.
Vitamin K. 10mgm.subcutaneously alternate days, such 10 injections.
This group was given Endocrinal Threapy
Testosteron propionate starting with 5 mgm. increased up to 10mgm. was given alternate days intramuscular for one month.
In this present series of hundred cases 33 eases were found to be of Eales' disease. The commonest cause is said to be a tuberculosis, though I have no histopathological evidence due to lack of material. To consider a lesion as tubercular on the basis of tuberculin test and or a healed lung lesion will be inconclusive. Although the tuberculin positive percentage in Eales' patients is definitely more whereas the same in unaffected group comes to about 5o per cent. Similarly one can argue that the same percentage of similar - headed lung tuberculous lesions may be obtained by doing mass screening of the chest.
Septic foci may undoubtedly be responsible for considerable number of cases in whom the most exhaustive search for tuberculosis locally or systemically has been negative. But to blame septic foci in the absence of a contributable cause of the condition is not scientific.
Clinically none of the patients showed any picture of endocrinal disturbances, but it may be suggested that some sex hormone may be responsible for the condition as it is seen in male and female in ratio of 9 :I and in this series 32 were males and only one female.
Though different lines of treatment including antitubercular, endocrinal and coagulant therapy have been tried, no satisfectory response as yet has been obtained as regards the cure of the disease. The antitubercular therapy seems to be effective in checking the frequency of recurrence. The coagulant and endocrinal therepy did not, prove to be of much avail.
1. In this series the commonest cause of intraocular haemorrahage (Non-traumatic) was found to be Eales' disease which account for 33 per cent of cases.
2. The disease is mostly seen in males only one female patient has been observed.
3. The average age group is 23.9 years.
4. No predilection to any particular eye was noticed.
5. The tuberculin test has been found to be positive in all cases, two cases showed tuberculous focus elsewhere in the body.
The present study consist of hundred cases of (non traumatic) intraocular haemorrhage out of which 33 cases were of Eales' disease, lo cases of Retinitis proliferans, ro cases of Macular haemorrhage, 6 cases of bilateral papilloedema, 15 cases of Arteriosclerosis and 5 cases of severe aueamia. Eales' disesase was found to be the most common cause. Various types of therapy were tried but none satisfactory. The other group of cases such as diabetes, leukaemias and anemias though responded to proper treatment, a lasting cure has not been obtained.
| References|| |
|1.||Tassman I. S. M. D. Philadelphia, Ocular changes in blood dyscresia (Arch. Ophth. Jan. 1947). |
|2.||Townley Paton, M. D., Eales' disease with historic review (arch. Opth. Aug. 1938). |
|3.||Wendling M., Retinal periphlebitis and tuberculous etiology (arch. Opth 1938 141 : 198). |
|4.||Rordon Flint, M. D., New vessel formation in vitreous (B. J. 01934). |
|5.||Ballentyne and Nichaelson, Case of perivasculities retinal associated with retinal disease (B. J. 0. 1932). |
|6.||Hutchinson M. D., Recurrent intraocular haemorrhage in young adults (B. J. 0.). |
|7.||Sir Stenwart Duke Elder, 'Vol, III-1940. |
|8.||Elliot, A. J., Recurrent intraocular haemorrhage (Tr. Ophth Soc. Am. 1954/ 811). |