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| ARTICLE |
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| Year : 1970 | Volume
: 18
| Issue : 2 | Page : 78-81 |
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Sympathetic keratitis presumably herpetic
IS Jain, Sah Dev
The Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
Correspondence Address:
I S Jain
The Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh
India
 Source of Support: None, Conflict of Interest: None  | Check |
How to cite this article:
Jain I S, Dev S. Sympathetic keratitis presumably herpetic. Indian J Ophthalmol 1970;18:78-81 |
Since clinical case reports of sympathetic uveitis following Herpetic Keratouveitis in the other eye are rare, though such a possibility was suggested by Haldiman; [4],[1],[2],[8] therefore the authors feel reporting of the following case is of interest.
| Case Report | |  |
Patient named K. L. 55 years old Hindu male, presented in the eye O.P.D. on 14th of August, 1968, with the complaints of pain, redness, and complete loss of vision in the left eye for the past four weeks. The history dates back to March, 1968 when some rubbish fell in his left eye and the eye became red and painful. It became alright with treatment after some time. Four weeks ago, he again developed sudden redness and pain in the same eye, and the sight deteriorated rapidly to complete blindness over a period of 10 days.
Past history
Treated for syphilis 35 years ago but denies any history of exposure.
Personal and family history
Married, has got eight children, the eldest 40 years old, and youngest 10 years old. No history of abortions in his wife.
Examination
General physical examination: well built; pulse 96/mt regular, of good volume; B.P. 155/95 mm Hg.
Systemic examination : Central nervous system, cardiovascular, res. piratory and abdominal systems did not reveal anything of significance.
Ocular Examination: Visual acuity in the right eye was 6/24 unaided and 6/9 with -1.0 Dcyl. axis 165; There was not even perception of light in the left eye. Right eye was white and quiet and the fundus was normal. There was slight photophobia in the left eye, the patient tended to keep the eye closed. There was slight injection of the conjunctiva and lacrimation. The cornea showed epithelial oedema and folds in the descemet's membrane. The endothelium also showed oedema. Flare in the anterior chamber could not be judged with certainty because of corneal haze. Corneal sensation was absent. There was no corneal epithelial staining. Pupil was dilated due to atropine. Tension digitally was normal.
A provisional diagnosis of viral kerato-uveitis was made and the patient was admitted in the hospital on 21st Aug., 1968 for treatment. He was treated locally with chloromycetin ointment and atropine ointment 1% thrice daily and orally with Tab. Vitamin C. 500 mgm, b.d. and hot fomentations t.d.s. After two days the patient was put on Betnesol-N eye drops, 4 hourly.
Investigations
No organism could be grown on culture from a scraping of the corneal lesion. However epithelial scrapings from the cornea showed many mononuclear cells. Urine examination, total and differential blood-counts showed no abnormality. Haemoglobin was 15 gm%, ESR 20 mm Ist hr. (Wintrobe). Stool examination revealed cysts of E. Coli and Iodo entamoeba. Fasting blood sugar was 113 mgm%. ENT and dental check ups were normal. VDRL Test negative.
Progress:
With the above line of treatment the patient showed gradual improvement with subjective relief in the pain, redness, and watering in the left eye. Objectively corneal oedema started regressing and after three days the patient could count fingers close to the face. The visual improvement continued and vision was 6/60 on 30th August 1968; Funds examination at this stage revealed a normal optic disc and a white ill defined spot, of the size of a paise just below and nasal to the disc which appeared to be an isolated patch of opaque nerve fibres.
On 1st Sept. 1968, the patient suddenly developed watering redness and marked diminution of vision in the right eye, only counting fingers close to his face.. The condition in the left eye had almost fully recovered to normal by this date. On examination, the right eye revealed an almost similar clinical picture as it was in the left eye on admission. There was gross corneal oedema, folds in descemet's membrane, but no flare or KP's could be sen due to corneal haze. Corneal sensation dull. Pupil was small in size, non reactive. Eye ball was tender. No staining of cornea was present. A similar line of therapy was instituted in the right eye i.e. atropine drops 1% and local cortico-sterioid drops frequently. The eye condition completely recovered by 10th September, 1968, and the patient was discharged on 14th Sept., 1968 with the final visual acquity of 6/12 right eye and 6/24 in his left eye with glasses.
The patient was last seen on 6-11-1968 and the visual acquity was maintained and had no ocular complaints.
| Discussion | | |
The present case, showed mainly endothelial and stromal involvement primarily and there was no preceding epithelial involvement in the form of dendritic keratitis.
Irvine and Kimura[5] have supported the theory of primary involvement of the endothelium, by their ability to culture the virus from the endothelium and this confirmed their belief in the long-known entity of "Herpes cornea posterior."
The concept that Herpes simplex virus was strictly epitheliotropic has changed recently by the demonstration of virus in corneal stromal cells by flourescent - antibody technique in rabbits and by electron microscopy in both rabbits and humans.
There is however no unanimity of opinion yet, as to whether the virus spreads to the endothelium by a hematogenous route or through the cornea or limbus. Viraemia in rabbits has been demonstrated after three days of inoculation of the virus in the epithelium (Irvine and Kimura[5]).
The loss of even perception of light in the present case, suggests that there was involvement of the optic nerve as well. Rarely one does come across cases with retrobulbar neuritis or papillitis having no PL and then recovering good vision following treatment.
There is, however, ample experimental support to the above premise.
Goodpasture and Teague[3], and Marinesco and Diaganesco[9] demonstrated spread of the Herpes virus along the optic nerve to the central nervous system after inoculation of the eyes of animals with Herpes virus.
Vel Hagen[11], and Rinaldi[10] even demonstrated that 15% of their animals developed violent uveitis in the uninoculated eye, sometimes even associated with papillitis. Recently Kimura [7],[6] and his colleagues have verified these findings by demonstrating the presence of the virus in the uveal tract, retina and the opitic nerve of the sympathising eye. In the experimental model, the uveitis in the first eye usually subsided in about 12 days, while the inflammation in the fellow eye developed after 7-14 days, and during this period signs of encephalitis were sometimes evident. Histopathological studies of the sympathising uveitis showed that the inflammation spread by way of the optic nerve to the chiasma and across to the other eye.
In the present case report the other eye was involved after nearly 7-8 weeks of involvement of the first eye eye and coincided with almost full recovery of its condition. Complete loss of vision in the originally involved eye must be due to involvement of the optic nerve during the process of spread to the other eye, and its subsequent functional recovery demonstrates that the damage done to the optic nerve is transitory and not permanent.
The history of treatment for syphilis thirtyfive years ago is not sufficient to consider syphilis as the etiological agent in the present case for various reasons. The clinical picture in the eye was far from syphilitic in nature, as there was no vascularisation, no severe anterior uveitis, neither any residual changes of scarring, ghost vessels or iris atrophic changes after the condition cleared. There were no other signs of acquired or congenital syphilis in the body.
Although in the present case we could not culture any virus because of inadequate facilities, but the only clue of its being viral in origin was increased number of mononuclears in the epithelial scraping, which was done in the later recovering stage of the disease.
| Summary | | |
A rare clinical case report of sympathetic "Keratitis" presumably viral in origin is described, where along with deep stromal keratitis there was involvement of the optic nerve leading to complete loss of vision. Subsequently after 7-8 weeks, the other eye was similarly involved, giving rise to a condition of so called "sympathe. tic" Herpetic Keratitis. There was eventually good visual recovery in both the eyes.
| References | | |
| 1. | Cavara and di Ferdinando : Boll. Oculist, 28: 1 (1949).  |
| 2. | Ferrante and Moro : Atti Soc. Med. Chir. Padora, 27: 447 (1949). |
| 3. | Goodpasture and Teaque: J. Med. Res. 44: 121, 139 (1923). |
| 4. | Haldimann: Ophthalmologica, 99: 187 (1940). |
| 5. | Irvine, R. A., and Kimura, S. J. Experimental Stromal Herpes simplex keratitis in Rabbits. Tr. Am. Ophth. Soc. 65: P. 189-210 (1967). |
| 6. | Katsnelson; Voinov and Kaplina: Vestn. Ophthal. 3: 61 (1962). |
| 7. | Kimura, S. J. Trans. Amer. Ophthal. Soc. 60: 440 (1962). |
| 8. | Legrand : Bull. Soc. Ophthal. Fr., 592 (1959). |
| 9. | Marinesco and Diaganesco : Amn. Inst. Pasteur, 37: 753, 1923. |
| 10. | Rinaldi: Riv. Pato1, Sper. 12: 416, 1934. |
| 11. | Velhagen, V. G.. Arch. Ophthal. (Berlin), 119: 325, 1927. |
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